RR - Cardiology 1, RR - Cardiology 2

Ischemic Heart Disease

#1 cause of death in USA • RFs: family hx, smoking, HTN, DM, cholesterol, male, age >55 • Stable angina: activity → chest pain (CP), relieved by rest, NTG • Unstable angina: CP at rest • CP, dyspnea, diaphoresis, nausea, hiccups, radiation to shoulder/jaw/back • Elderly, diabetics, females, hx of stroke or HF: ↑ risk for atypical presentation • Earliest ECG sign of MI: hyperacute T waves • Up to 50% of ECGs are negative or nonspecific • Highest S/S: troponin I

Lower Limits of Pediatric Systolic Blood Pressure

0-28 days: 60 mm Hg • 1-12 months: 70 mm Hg • 1-10 years: 70 mm Hg + (2 x age in years) • >10 years: 90 mm Hg

Why do H2 blockers help with cutaneous symptoms in allergic reactions?

10% of histamine receptors in the skin are of the H2 variety.

What is the normal range for the PR interval?

120-200 milliseconds.

What is the recommended blood pressure goal in patients with hypertension?

139/89 mm Hg or less.

What is the volume of physiologic fluid in the pericardial space?

15 to 30 mL.

Paroxysmal junctional tachycardia is usually in what range of heart rates?

150-250 beats per minute.

Which of the following patients should receive prophylactic antibiotics to prevent endocarditis? 18-year-old pregnant woman with a history of a repaired congenital heart defect, with an impending vaginal delivery 19-year-old woman with a history of endocarditis who is undergoing a dental extraction 20-year-old man with a prosthetic heart valve who requires a Foley catheter due to urinary obstruction 21-year-old man with a history of a heart transplant and valvulopathy who is undergoing suture repair of a facial laceration

19-year-old woman with a history of endocarditis who is undergoing a dental extraction This patient meets high-risk criteria (history of endocarditis) and requires antibiotic prophylaxis. The American Heart Association has published guidelines regarding prophylaxis for infective endocarditis in high-risk patients undergoing dental or invasive respiratory procedures. High-risk patients who are undergoing vaginal delivery (A), Foley catheterization (C), and suture repair (D) do not require antibiotic prophylaxis. In fact, prophylactic antibiotics are generally not needed with any genitourinary or gastrointestinal instrumentation and nearly all procedures that are performed in the ED.

A patient with an intermediate risk of coronary artery disease is undergoing an exercise stress test. Which of the following is the most specific finding for myocardial ischemia? 2 mm downsloping ST-segment depression 2 mm upsloping ST-segment depression Increase of systolic blood pressure Sporadic premature ventricular complexes

2 mm downsloping ST-segment depression 2 mm downsloping ST-segment depression is the most specific finding for myocardial ischemia during an exercise stress test. Subendocardial ischemia during exercise produces ST-segment depression or elevation or both. ST-segment depression that occurs during exercise testing is one of the most identifiable ECG signs of myocardial ischemia. The ECG portion of the exercise test is generally considered abnormal, or positive for ischemia, when there is ≥ 1 mm horizontal or downsloping ST-segment depression in one or more leads. Horizontal or downsloping ST-segment depression is generally more specific for ischemia than upsloping ST-segment depression. An increase in systolic blood pressure (C) is an expected physiologic response during an exercise stress test and is not a sign of myocardial ischemia. Sporadic premature ventricular complexes (D) are not uncommon during peak exercise and do not indicate myocardial ischemia. Although 2 mm upsloping ST-segment depression (B) could be suggestive of myocardial ischemia, it is less specific than downsloping or horizontal ST-segment depression.

How long should an individual undergo treatment for an isolated pulmonary embolism with no other risk factors?

3 months.

What is the biological half-life of warfarin?

36 to 42 hours

What is the desired heart rate in the treatment of chronic stable angina with beta-blocker therapy?

55-60/min.

What percent of aortic aneurysms >5 cm can be palpated?

75%, but only 5-10% of patients with an AAA have an abdominal bruit.

What ankle-brachial index measurement is frequently seen with resting pain?

< 0.4

What duration of CPR constitutes a relative contraindication to fibrinolytic use for STEMI?

> 10 minutes.

Ventricular Tachycardia

>3 consecutive ectopic ventricular beats • Monomorphic, polymorphic • Bidirectional: digoxin toxicity • Wide complexes • Pulseless: immediate defibrillation • Unstable: synchronized cardioversion • Stable: procainamide, amiodarone, synchronized cardioversion (refractory) • If unsure, manage all wide complex tachycardias as ventricular tachycardia

Which of the following patients is considered hypotensive? A 1-year-old boy with a systolic blood pressure of 75 mm Hg A 2-year-old girl with a systolic blood pressure of 80 mm Hg A 3-year-old girl with a systolic blood pressure of 70 mm Hg A 6-year-old boy with a systolic blood pressure of 85 mm Hg

A 3-year-old girl with a systolic blood pressure of 70 mm Hg A 3-year-old girl with a systolic blood pressure of 70 mm Hg is considered to be hypotensive. The minimum systolic blood pressure in a child (1-10 years) is calculated by the formula: Minimum SBP = 70 + (2 x age in years). Therefore, the minimum systolic blood pressure for a 3-year-old is 76 mm Hg. The minimum systolic blood pressure for a neonate (0-28 days) is 60 mm Hg and an infant (1-12 months) is 70 mm Hg. Based on the formula, a systolic blood pressure of 75 mm Hg is considered normal for a 1-year-old (A). A systolic blood pressure of 80 mm Hg is normal for 2-year-old (B) and a systolic blood pressure of 85 mm Hg for a 6-year-old (D).

Which of the following patients requires endocarditis prophylaxis for a dental procedure that requires manipulation of the gingival tissue? A 14-year-old boy with a Still's murmur A 25-year-old man with a grade 3/6 systolic ejection murmur A 35-year-old man with a prosthetic mitral valve A 45-year-old man with aortic stenosis

A 35-year-old man with a prosthetic mitral valve To prevent adverse complications from infective endocarditis, recent guidelines indicate that only high-risk cardiac patients should receive bacterial endocarditis prophylaxis when undergoing dental procedures that involve manipulation of gingival tissue or periapical teeth or perforation of oral mucosa. The routine use of infective endocarditis prophylaxis before gastrointestinal or genitourinary tract manipulation is not recommended, except in patients with active GI or GU infections.The high-risk cardiac patients include those with prosthetic cardiac valves or prosthetic material used for cardiac valve repair, prior history of infective endocarditis, unrepaired congenital heart disease, or repaired congenital heart defect with a prosthesis during the first 6 months after the procedure. Heart murmurs do not require prophylaxis for dental procedures unless they fall in high-risk category described above. Therefore a 3/6 systolic ejection murmur (B), Still's murmur (A) and aortic stenosis (D), do not require antibiotic prophylaxis.

Which of the following clinical scenarios can be defined as a hypertensive emergency? A 25-year-old pregnant woman in her second trimester with a blood pressure of 155/100 mm Hg with a normal urinalysis A 55-year-old man with a blood pressure of 185/90 mm Hg whose creatinine has increased from 1.0 to 2.5 mg/dL within 36 hours A 59-year-old asymptomatic man requesting a medication refill and is found to have a blood pressure of 210/110 mm Hg and an ECG consistent with left ventricular hypertrophy (LVH) A 63-year-old woman with a history of poorly controlled hypertension who presents with a finger laceration and is noted to have a blood pressure of 200/105 mm Hg

A 55-year-old man with a blood pressure of 185/90 mm Hg whose creatinine has increased from 1.0 to 2.5 mg/dL within 36 hours Hypertensive emergency is generally defined as a markedly elevated blood pressure in the setting of acute end-organ damage of the cardiovascular, neurologic, or renal organ system. This condition is a true medical emergency and warrants early reduction of blood pressure (preferably within one hour of identification of the condition) with titratable intravenous medications. It is important to understand, however, that an elevated blood pressure in response to an acute condition is often physiologic; aggressive lowering of the pressure in these conditions (e.g., ischemic stroke) may actually increase morbidity and mortality. Renal failure can be seen as both a consequence and cause of hypertension. Uncontrolled hypertension may cause acute kidney injury and can accelerate the progression of injury in patients with chronic renal failure. Acute worsening of kidney function as seen in this patient whose creatinine increased acutely from 1 to 2.5 mg/dL—in the setting of elevated blood pressure—should be considered a hypertensive emergency and warrants immediate treatment. Hypertension is one of the most common complications in pregnancy. Hypertension in pregnancy is defined as a systolic pressure > 140 mm Hg or a diastolic pressure > 90 mm Hg. Severe hypertension is classified as a systolic pressure > 160 mm Hg or diastolic > 105 mm Hg. Pre-eclampsia is defined as hypertension occurring after 20 weeks gestation with proteinuria or any signs or symptoms of end-organ damage (e.g., elevated LFTs) and should be considered a hypertensive emergency. Hypertension occurring after 20 weeks gestation without these signs or symptoms (A) is termed gestational hypertension. Patients who are hypertensive, but asymptomatic, and show no evidence of acute end-organ damage (C and D) in most cases, do not need acute lowering of their blood pressure. Patients with chronic hypertension may have an altered autoregulatory range; rapid normalization of their elevated blood pressure may in fact lead to hypoperfusion and ischemia. In response to chronic hypertension, the heart is remodeled in a cycle starting with increased wall stress that leads to hypertrophy and impaired diastolic function. When LVH is present in the setting of hypertension, early follow-up should be arranged because such patients are at increased risk for MI, heart failure, stroke, and sudden death.

Which of the following patients with atrial fibrillation has the greatest risk for complications from anticoagulation therapy? A 64-year-old woman with hypertension and history of colon cancer A 66-year-old man with a history of hypertension, diabetes, and ethanol abuse A 79-year-old man with a history of congestive heart failure A 90-year-old otherwise healthy woman

A 66-year-old man with a history of hypertension, diabetes, and ethanol abuse Atrial fibrillation is associated with arterial thromboembolism and ischemic stroke; therefore, anticoagulation is recommended in most cases. The HAS-BLED risk score is based upon seven risk factors for bleeding, including age > 65 years, and has been recommended within the European Society of Cardiology and Canadian guidelines for assessing the risk of bleeding in atrial fibrillation management. The 66-year-old man with a history of hypertension, diabetes, and ethanol abuse has a HAS-BLED score of 3 which corresponds to a high risk for bleeding. The 64-year-old woman with hypertension and history of colon cancer (A) has a score of 1. The 79-year-old man with a history of congestive heart failure (C) has a score of 1. The 90-year-old otherwise healthy woman (D) has a score of 1.

A diagnosis of orthostatic hypotension can be made in which of the following scenarios? A drop in diastolic blood pressure of 5 mm Hg upon standing A drop in systolic blood pressure of 20 mm Hg upon standing An increase in heart rate of 35 beats per minute upon standing An increase in heart rate of 5 beats per minute upon standing

A drop in systolic blood pressure of 20 mm Hg upon standing Orthostatic hypotension is defined as a decrease in systolic BP of 20 mm Hg or diastolic BP of 10 mm Hg within 3 minutes of standing from a seated or supine position. Symptoms may include positional syncope, dizziness, generalized weakness or fatigue. Once underlying cardiac, endocrine, neurologic and medication side effect etiologies are ruled out, treatment options include increasing water intake, sodium supplementation, abdominal or lower extremity binders, a physical therapy conditioning program and medications. A diagnosis of orthostatic hypotension requires a drop of 10 or more mm Hg (A) in diastolic BP upon standing. Although commonly checked along with blood pressure measurements during supine and standing position, baseline heart rate, or changes in heart rate (C), are not included in the latest definition of orthostatic hypotension. Postural orthostatic tachycardia syndrome, not orthostatic hypotension, should be considered if the heart rate increases ≥ 30 beats per minute (D) upon standing.

What is the classic physical sign associated with tricuspid regurgitation?

A large, bounding v wave is seen during jugular vein inspection. Also, a pulsatile liver may be palpable.

In which of the following clinical scenarios is an implantable cardioverter-defibrillator indicated for the prevention of ventricular dysrhythmias and sudden cardiac death? A patient with a left ventricular ejection fraction < 35% and heart failure NYHA Functional Class II or III A patient with a normal left ventricular ejection fraction and asymptomatic structural heart disease A patient with sustained ventricular tachycardia in the setting of an acute myocardial infarction A patient with sustained ventricular tachycardia in the setting of hyperkalemia

A patient with a left ventricular ejection fraction ≤ 35% and heart failure NYHA Functional Class II or III A patient with a left ventricular ejection fraction ≤ 35% and heart failure NYHA Functional Class II or III is a clinical scenario in which an implantable cardioverter-defibrillator is indicated. An implantable cardioverter-defibrillator is a small device combining a cardioverter and defibrillator into one implantable unit that is surgically placed in the chest or abdomen. It is battery powered and programmed to detect dysrhythmias, mainly sustained ventricular tachycardia and ventricular fibrillation, which can lead to sudden cardiac death. It has a very high success rate in rapidly terminating ventricular dysrhythmias and evidence shows that it improves survival. Implantable cardioverter-defibrillator implantation is generally considered the first-line treatment for the secondary prevention of sudden cardiac death in patients who have survived an event and for primary prevention in certain high risk populations. Published guidelines exclude cases that are considered "reversible causes." Some of the major indications are as follows. A patient with asymptomatic structural heart disease (B) is not an indication for implantable cardioverter-defibrillator. Only when a patient with structural heart disease, such as hypertrophic cardiomyopathy, has symptoms or unexplained syncope with inducible dysrhythmia on electrophysiological studies is it indicated for an implantable cardioverter-defibrillator. Patients with sustained ventricular tachycardia in the setting of hyperkalemia (D) or acute myocardial infarction (C) are not indicated for an implantable cardioverter-defibrillator. Hyperkalemia and acute ischemia are considered "reversible causes" and correction of the metabolic derangement and revascularization are often adequate measures to reduce the risk of sudden cardiac death.

What are Osler's nodes?

A sign of subacute bacterial endocarditis, these are the result of immune complex deposition, leading to tender nodules in the digit pads.

Chronic congestive heart failure is managed with which outpatient medications?

ACE-inhibitors, beta-blockers and diuretics, with consideration of aldactone, nitrates and inotropes.

What agents should be avoided in patients with atrial fibrillation and Wolf-Parkinson-White (WPW) syndrome?

AV-nodal blocking agents such as adenosine, calcium channel blockers, beta-adrenergic blockers, and digoxin. This can lead to cardiovascular collapse due to preferential accessory pathway conduction.

A woman with chest pain presents to the ED. Her electrocardiogram shows ST elevation in leads V3 and V4. She is started on oxygen, intravenous nitroglycerin, and aspirin. You are preparing her for transfer to the interventional cardiac unit for primary percutaneous cardiac reperfusion. Her heart rate has been consistently < 60, averaging 54 over the past 30 minutes. Which of the following medications is also appropriate treatment at this time? Abciximab Infliximab Metaproterenol Metoprolol

Abciximab ST-elevation myocardial infarction in the anterior heart is evidenced by chest pain and ECG changes as above. The most likely site of complete arterial thrombus in this scenario is the left anterior descending artery. In a percutaneous coronary intervention (PCI) capable hospital, the goal is to get the patient to PCI within 90 minutes. Once this is possible, it is recommended to administer a GP IIb/IIIa inihibitor, such as abciximab, eptifibatide or tirofiban. Some research has shown a 60% decrease in death and further MI with this class of medications. Abciximab is a platelet aggregation inhibitor mainly used during and after coronary artery procedures like angioplasty to prevent platelets from sticking together and causing thrombus formation within the coronary artery. The use of abciximab in this setting is associated with a decreased incidence of ischemic complications due to the procedure and a decreased need for repeated coronary artery revascularization in the first month following the procedure. Infliximab (B) is an anti-tumor necrosis factor alpha antibody used in the treatment of autoimmune disease, not STEMI. Beta-2 agonists, such as metaproterenol (C), are used in the acute management of asthmatic bronchospasm, not STEMI. Beta-blockers, such as metoprolol (D), do have an anti-arrhythmic benefit in STEMI, however, their use is contraindicated if pulse is < 60 bpm or systolic blood pressure is < 120 mm Hg.

Which of the following conditions is most suggestive of an asymptomatic abdominal aortic aneurysm? Abdominal bruit Abdominal mass Hypertension Hypotension

Abdominal mass An abdominal mass is most suggestive of an asymptomatic abdominal aortic aneurysm. An abdominal aortic aneurysm is defined as a focal, full-thickness dilation of the aorta that is greater than 50% larger than its normal diameter. Most patients with abdominal aortic aneurysms do not have any symptoms. Asymptomatic abdominal aortic aneurysms may be discovered as a result of screening in patients with risk factors for abdominal aortic aneurysm, on routine physical examination, or on imaging studies to evaluate an unrelated complaint. An abdominal aortic aneurysm does not typically cause symptoms unless the aneurysm is expanding rapidly, has become large enough to compress surrounding structures, is an inflammatory or infectious aneurysm, or has ruptured. Patients with symptomatic abdominal aortic aneurysms most commonly present with abdominal, back, or flank pain, which may or may not be associated with abdominal aortic aneurysm rupture. The classic triad of severe acute pain, a pulsatile abdominal mass, and hypotension occurs in about 50% of patients with ruptured abdominal aortic aneurysm. An abdominal bruit (A) is not most suggestive of an asymptomatic abdominal aortic aneurysm, but is more suggestive of renal artery stenosis. Hypertension (C) is not most suggestive of an asymptomatic abdominal aortic aneurysm. Hypertension is a risk factor for development of an aortic aneurysm. Hypotension (D) is not most suggestive of an asymptomatic abdominal aortic aneurysm but could result from a ruptured abdominal aortic aneurysm with hypovolemic shock.

What is the classic triad of AAA?

Abdominal/back pain, hypotension and a pulsatile abdominal mass.

What is the preferred therapy for the prevention of recurrent preexcited atrial fibrillation?

Ablation of the accessory pathway.

Aortic Regurgitation

Acute MCC: endocarditis • Chronic MCC: rheumatic heart disease • Blowing diastolic murmur at left sternal border • Pulse pressure: normal (acute), widened (chronic) • de Musset sign: head bobbing with systole • Quincke's pulse: prominent nail pulsations • Duroziez murmur: "singsong" murmur over femoral artery • Austin-Flint murmur: mid-diastolic murmur in severe AR • Rx objective: ↓ afterload

A 54-year-old man presents to the hospital in acute respiratory distress. He was released from the hospital three days ago after undergoing a cardiac stent placement secondary to an acute myocardial infarction. His hospital course was uncomplicated. On exam, his BP is 110/60 mm Hg, HR is 115, RR is 28, and pulse oximetry is 91% on room air. Cardiopulmonary exam reveals a midsystolic murmur with bibasilar crackles. An ECG shows sinus tachycardia. Which of the following is the most likely diagnosis? Acute aortic insufficiency Acute mitral regurgitation Postmyocardial infarction syndrome Ventricular aneurysm rupture

Acute mitral regurgitation Acute mitral regurgitation is the result of rupture of the chordae tendineae, papillary muscle, or valve leaflet. Its etiology can be idiopathic due to acute ischemia, a complication of infective endocarditis, or trauma. As with this patient, it may also occur as a delayed consequence of acute myocardial infarction (usually two to seven days post-event). Patients typically present in fulminant pulmonary edema rapid in onset. It is associated with a midsystolic murmur. Patients generally have no history of heart failure, and the ECG may be normal or display signs of ischemia or infarction. Acute aortic insufficiency (A) is most commonly due to infective endocarditis, aortic dissection, or trauma. As in acute mitral regurgitation, patients present with severe dyspnea due to a rapid rise in left ventricular end-diastolic pressure leading to pulmonary edema and cardiogenic shock. Notable findings on physical exam include signs of decreased cardiac output (cool, pale extremities, cyanosis), a loud S3, and a short diastolic murmur best heard at the left sternal border with the diaphragm of the stethoscope. Postmyocardial infarction syndrome (C) is also known as Dressler's syndrome and is associated with pericarditis that occurs in the setting of injury to the heart or pericardium. Patients typically present with fever, pleuritic chest pain, and a pericardial effusion. While left ventricular aneurysm (D) may result from an acute myocardial infarction, rupture is rare because the aneurysm wall is lined by scar tissue. However, when present, it may block the aortic outflow tract leading to reduced cardiac output.

A 42-year-old man presents to the Emergency Department with acute onset of severe shortness of breath. He was recently discharged from the hospital with endocarditis. Vital signs include temperature 37.6oC, HR 110, BP 110/50, RR 24, Pox 93%. On examination, he is ill appearing with a new harsh apical systolic murmur and bibasilar rales. Which of the following is the most likely diagnosis? Acute mitral regurgitation Aortic regurgitation Health care associated pneumonia Pulmonary embolism

Acute mitral regurgitation Acute mitral regurgitation presents with acute onset of severe dyspnea and signs of pulmonary edema. Patients can rapidly decompensate into cardiogenic shock or cardiac arrest. A harsh systolic apical murmur and S4 gallop are present. It is most commonly due to rupture of the papillary muscle or chordae tendinae secondary to myocardial infarction. Other causes include rupture due to infective endocarditis, blunt chest trauma or spontaneous rupture. Chest x-ray will show signs of pulmonary edema with a normal heart size (unless the patient has chronic ischemic or valvular heart disease). Echocardiography will confirm the diagnosis and assess the degree of regurgitation. Emergency Department management includes oxygen and positive pressure ventilation as needed for respiratory failure. Nitrates and diuretics are indicated for treatment of pulmonary edema. An intra-aortic balloon pump may be needed for stabilization of the hypotensive patient until definitive treatment with surgery. Emergent cardiology and surgical consultation is imperative. Aortic regurgitation (B) can also present with severe dyspnea but is associated with a high pitched blowing diastolic murmur. Health care associated pneumonia (C) typically presents with fever, cough and findings of consolidation on lung exam. Although dyspnea may be severe and acute in onset in patients with pulmonary embolism (D), they do not typically present with a new heart murmur.

A 34-year-old woman presents to the ED with chest pain that is worse with inspiration and better upon leaning forward. She has had a runny nose and cough for the last week. In the ED, her vital signs are BP 134/78, HR 86, RR 14, oxygen saturation 99% on room air, and T101°F. On exam, a friction rub is heard. An ECG displays global ST segment elevation with PR segment depression. What is the most likely diagnosis and what would be the next step in management? Acute myocardial infarction; give aspirin, nitroglycerin, consult cardiology, and activate the cath lab Acute pericarditis; give nonsteroidal anti-inflammatory drugs Cardiac tamponade; perform immediate pericardiocentesis Pulmonary embolism; order CT angiography of the chest

Acute pericarditis; give nonsteroidal anti-inflammatory drugs This patient most likely has acute pericarditis, which is inflammation of the pericardial sac. Patients present with pleuritic chest pain that is typically worse when lying supine, deep inspiration, or swallowing. The pain is usually relieved by leaning forward. On auscultation, a pericardial friction rub may be heard. Pulsus paradoxus may also be observed, which is a fall in systolic blood pressure of greater than 10 mmHg with inspiration. Pericarditis can have many etiologies including infection, systemic connective tissue diseases, uremia, post-radiation, or post-myocardial infarction (Dressler's syndrome). Although there is no definitive diagnostic test, an ECG can demonstrate diffuse ST segment elevation, diffuse PR segment depression, and PR elevation in aVR (thumbprint sign). Treatment of pericarditis is mainly supportive. NSAIDs will reduce inflammation and pain. Steroids or colchicine may be given for refractory cases. An acute myocardial infarction (A) is less likely in this patient given her age and clinical presentation (fever, runny nose, and cough). A pericardial effusion may accompany acute pericarditis but rarely leads to cardiac tamponade (C). The clinical triad of pericardial tamponade is hypotension, jugular venous distension, and muffled heart sounds. A pulmonary embolism (D) is less likely in this patient given her ECG findings, vital signs, and clinical presentation.

A 70-year-old woman with a long history of coronary artery disease is seen in cardiology clinic for routine follow up. She complains of continued angina despite medical therapy. She reports chest pain every time she walks to her mailbox. It does not occur at rest and is relieved by sublingual nitroglycerin. Her medications include carvedilol, amlodipine, daytime transdermal nitroglycerine, sublingual nitroglycerin, aspirin, and simvastatin. On physical exam her BP is 105/72, HR is 51 and RR 16. What is the next step in management? Add ranolazine Increase the dose of carvedilol Increase the dose of simvastatin Schedule 24 hour usage of transdermal nitroglycerin

Add ranolazine The addition of ranolazine should be considered in patients with chronic stable angina who remain symptomatic despite optimal doses of beta blockers, calcium channel blockers and nitrates. Stable angina refers to chest discomfort that occurs predictably and reproducibly at certain levels of exertion and is relieved by rest or nitroglycerine. This patient remains symptomatic on carvedilol, amlodipine and two different preparations of nitroglycerine. Ranolazine is a novel anti-anginal agent that causes selective inhibition of the late sodium channel. It is approved for the treatment for chronic stable angina for those who have failed standard medical therapy. It has been shown to be effective in reducing anginal symptoms and improving exercise capacity when added to conventional medical therapy. Ranolazine can prolong the QT interval and it should be used with caution in patients with kidney or liver disease. It is not safe to increase the dose of carvedilol (B) as this patient's blood pressure and pulse are too low for up-titration of her beta-blocker. Statin therapy is important for the treatment of this patient's coronary artery disease; however it is not appropriate to increase the dose of simvastatin (C) in this situation as statin therapy does not have anti-anginal properties. Long acting nitroglycerin preparations are very useful in the treatment of chronic stable angina; however, they require a nitrate free period of 8-12 hours, typically at night, to obviate nitrate tolerance. Therefore, 24 hour use of transdermal nitroglycerin (D) would not be beneficial.

Why should beta-blockers be avoided in the treatment of patients with cocaine related chest pain or hypertension?

Administration of a beta-blocker can cause unopposed alpha effects leading to worsening symptoms and blood pressure.

A 22-year-old man presents to the Emergency Department after a syncopal episode. His ECG is shown above. He is currently asymptomatic with normal vital signs. Which of the following is the most appropriate next step in management? Admit to a telemetry unit for cardiology consult and AICD placement Discharge with cardiology follow up as an outpatient Order emergent echocardiogram Start amiodarone for treatment of presumed ventricular tachycardia

Admit to a telemetry unit for cardiology consult and AICD placement Brugada syndrome was initially described in 1992 and is an inherited disorder that is the result of a mutation in the cardiac sodium channel gene. Patients are predisposed to malignant dysrhythmias and sudden death. The mean age of sudden death is 41 years and males are significantly more likely than females to be affected. Most patients are asymptomatic and found only by incidental ECG. The type 1 ECG pattern characteristic of Brugada syndrome is coved ST segment elevation of greater than 2 mm in V1-V3. It can be transient and may be augmented by fever or pharmacologic stimulation (particularly sodium channel blockers). The type 1 pattern is considered diagnostic when combined with clinical criteria such as syncope, family history of early sudden death, characteristic ECG changes in family members, or history of ventricular fibrillation or ventricular tachycardia. The type 2 ECG pattern of saddleback ST segment elevation in V1-V3 is suggestive of Brugada syndrome but not diagnostic. Management involves admission to a telemetry unit for cardiology consultation. Definitive treatment is implantable cardioverter defibrillator placement. Patients with characteristic ECG changes and clinical criteria such as syncope are at a high risk for malignant dysrhythmias and sudden death and should not be discharged (B). There is no structural defect associated with Brugada syndrome so an echocardiogram (C) is not indicated in the the workup. Medications such as amiodarone (C) do not play a role in the management of Brugada syndrome. The only proven therapy to prevent sudden death in these patients is AICD placement.

Abdominal Aortic Aneurysm (AAA)

Advanced age, male, smoking hx, HTN • Acute abdominal pain + hypotension + pulsatile abdominal mass • US: 100% sensitive • CT: 100% sensitive, detects rupture/leak • AAA > 5 cm: ↑ risk of rupture • Renal colic in elderly: r/o AAA

What is the most common reason sick sinus syndrome occurs?

Age and replacement of SA node with fibrous tissue.

Atrial Fibrillation

Alcohol • Irregularly irregular • No P waves • Narrow QRS unless conduction block or accessory pathway • Unstable: cardioversion • Stable: . Rate control with CCBs, ßBs . <48 hours duration: cardiovert to sinus rhythm . >48 hours duration: anticoagulate, echo to r/o thrombus, then cardioversion

What are Roth spots and Osler nodes?

All are manifestations of left-sided endocarditis. Roth spots are retinal hemorrhages and Osler nodes are painful nodes on the digits both caused by immunologic vasculitis.

Supraventricular Tachycardia

All tachydysrhythmias that arise above the bifurcation of the bundle of His • Characteristics: . Atrial rate 120-200 . Rhythm: regular . Narrow QRS • Causes . Pre-excitation syndromes (WPW) . Mitral disease . Digitalis toxicity . Drugs and toxins . Hyperthyroidism • Treatment: . Vagal maneuvers (Valsalva) . Adenosine (first-line medication), ßBs, CCBs . Unstable: synchronized cardioversion

Supraventricular Tachycardia amended 6/20/16

All tachydysrhythmias that arise above the bifurcation of the bundle of His • Characteristics: ◦ Atrial rate 120-200 ◦ Rhythm: regular ◦ Narrow QRS • Causes ◦ Pre-excitation syndromes (WPW) ◦ Mitral disease ◦ Digitalis toxicity ◦ Drugs and toxins ◦ Hyperthyroidism • Treatment: ◦ Vagal maneuvers (Valsalva) ◦ Adenosine (first-line medication), ßBs, CCBs ◦ Unstable: synchronized cardioversion

An inotropic drug works by which of the following mechanisms? Alter cardiac conduction velocity Alter the force of myocardial contraction Alter the heart rate Dilate blood vessels

Alter the force of myocardial contraction Inotropic drugs alter the force of myocardial contraction. Inotropic, chronotropic and dromotropic are different classifications of cardiac drugs. Chronotropic drugs effect the heart rate and dromotropic drugs affect the conduction velocity though the myocardium. These cardiovascular drugs differ from each other primarily on the basis of the aspects related to cardiac performance which they influence or affect. There are two types of inotropic agents- positive and negative. Positive inotropic agents increase the force of myocardial contraction by increasing intracellular calcium concentrations. Increased contraction results in increased stroke volume and cardiac output for each ventricular filling. These agents are used to support impaired systolic function in conditions such as decompensated systolic heart failure, cardiogenic shock, septic shock and myocardial infarction. Examples include dopamine, dobutamine, norepinephrine, epinephrine and milrinone. Negative inotropic agents decrease the force of myocardial contraction and are used to decrease cardiac workload. This can be useful in different clinical situations such as angina or hypertrophic cardiomyopathy. Negative inotropic agents include beta blockers, calcium channel blockers, quinidine, and flecainide. Chronotropic drugs alter the heart rate (C). They are further classified into positive and negative chronotropic agents. Positive chronotropic drugs increase the heart rate by acceleration the rate of impulse formation in the SA node. Negative chronotropic drugs slow down the heart rate by decreasing impulse formation. Dromotropic drugs alter the conduction velocity (A). Positive dromotropic drugs increase the rate of conduction, whereas negative dromotropic drugs decreases the rate of electrical conduction. Vasodilators dilate blood vessels (D) and include drugs such as nitrates, calcium channel blockers and angiotensin converting enzyme inhibitors

Heart Failure Staging/Classification

American Heart Association/American College of Cardiology staging: . Stage A: high risk without symptoms/disease . Stage B: structural disease without sx . Stage C: structural disease + sx . Stage D: refractory heart failure • New York Heart Association classification: . I: asymptomatic . II: sx with ordinary activity . III: asymptomatic only at rest . IV: sx at rest

A 67-year-old African-American man established care with you two months ago after being told at a community health fair that his blood pressure was elevated. The blood pressure readings done in your office include 168/94, 158/98 and 162/96. You determine that the patient has primary essential hypertension. Lifestyle measures have already been instituted but you decide that medication is also warranted at this time. Which of the following is the best initial agent for blood pressure control in this patient? Amlodipine Clonidine Metoprolol Prazosin

Amlodipine Current studies suggest that the best initial choice for treating hypertension in African-American patients without diabetes or chronic kidney disease is either a calcium-channel blocker or a thiazide-type diuretic. When used as monotherapy, either of these agents is more effective at lowering blood pressure than drugs in other classes, though many patients require the addition of a second anti-hypertensive agent for adequate control. Clonidine (B) is a central alpha sympathetic agonist used for the treatment of hypertension. It is associated with several drug-drug interactions and orthostatic hypotension. Although it is used as an anti-hypertensive in some patients, it is not recommended as first-line therapy. Metoprolol (C) is a cardioselective beta-blocker used in the management of hypertension. Beta-blockers have been found to be comparatively less effective agents for the treatment of hypertension in African Americans, and in recent years have fallen out of favor as the best initial option for managing hypertension in other patients groups, as well. Prazosin (D) is one of several alpha-adrenergic receptor blockers which work to lower blood pressure by decreasing peripheral vascular resistance. It is not recommended as a first-line agent.

What antibiotic is recommended as prophylaxis for high-risk patients undergoing a dental extraction?

Amoxicillin (2 grams by mouth).

What is the most common cause of restrictive cardiomyopathy?

Amyloidosis.

What is rheumatic heart disease (also known as rheumatic fever)?

An antibody-cross reactivity inflammatory disease which follows Streptococcus pyogenes infection and causes heart (myocarditis), joint, skin and brain inflammation, most commonly occurring in 6-15 year olds.

What is a DeBakey type 2 dissection?

An aortic dissection that only involves the ascending aorta.

What is malignant hypertension?

An outdated term which has been replaced by hypertensive emergency.

A 62-year old man presents complaining of crushing substernal chest pain for the last two hours associated with diaphoresis, nausea, and lightheadedness. His pain improved with sublingual nitroglycerin. Electrocardiogram obtained in triage shows deep Q waves and ST segment elevation in leads V1-V4, with ST depression in leads III and aVF. This pattern on electrocardiogram represents infarction of which area of myocardium? Anterior Inferior Lateral Posterior

Anterior Anterior wall myocardial infarction is characterized by ST elevation in leads V1-V4, with reciprocal changes in the inferior leads (III and aVF). Septal involvement is reflected by changes in V1 and V2. The left anterior descending artery serves the anterior wall.

In patients with aortic dissection, what is the recommended blood pressure goal?

Antihypertensives should be titrated to a systolic blood pressure of 110 mm Hg.

List some medications whose side effects can cause symptoms of orthostasis?

Antiparkinsonian drugs, antiadrenergics, anticholinergics, antidepressants, antiarrhythmics, antipsychotics, diuretics, narcotics and sedatives.

A 58-year-old man is undergoing a pre-operative evaluation before an elective surgery. An ECG shows atrial fibrillation with rapid ventricular response. The patient has no symptoms and is completely unaware of his dysrhythmia. He has a past medical history significant for obesity and hypertension that is treated with lisinopril. His vital signs are BP 120/80, HR 150, RR 16 and oxygen saturation is 100% on room air. What is the appropriate management with regards to anticoagulation? Antiplatelet or anticoagulation Diltiazem No therapy Warfarin and aspirin

Antiplatelet or anticoagulation An antiplatelet or anticoagulant can be used to treat this patient with atrial fibrillation. Atrial fibrillation is caused by rapid and uncoordinated electrical activation within the atria. The most serious complication is arterial thromboembolism. Antithrombotic therapy with oral anticoagulation has been shown to lower the risk of thromboembolism in virtually all patients with atrial fibrillation. However, in the lowest-risk patients, the risk of anticoagulant-related major bleeding may equal or exceed the risk of thromboembolism without therapy. Thus, clinicians need guidance regarding when to recommend such therapy. Risk prediction models have been developed for this purpose. The CHA2DS2-VASc score is used for estimating the risk of stroke in patients with non-valvular atrial fibrillation. The score is used to determine whether or not treatment is required with anticoagulation therapy or antiplatelet therapy. The patient in the above scenario has a CHA2DS2-VASc score of 1 is considered low-moderate risk. This risk score is associated with the recommendation for antiplatelet or anticoagulant therapy. In regards to the upcoming surgery, the patient should initially be anticoagulated and then the anticoagulation be re-addressed at the time of surgery. Diltiazem (B) is appropriate for this patient as a rate control agent. However, diltiazem does not provide anticoagulation. No therapy (C) is not appropriate as this patient has risk factors that require further therapy. Warfarin + Aspirin (D) is not appropriate as combination anticoagulation and antiplatelet therapy is not recommended for atrial fibrillation therapy and increases the risk of bleeding in this patient.

Antithrombotics include which medications?

Antiplatelets (aspirin, glycoprotein IIb/IIIa, adenosine diphosphate, cyclooxygenase, phosphodiesterase, and thromboxane inhibitors), anticoagulants (vitamin K, factor Xa and thrombin inhibitors) and thrombo-fibrinolytics (plasminogen activators).

Who should be screened for an abdominal aortic aneurysm?

Any man between the ages of 65 and 75 years who has ever smoked.

A careful cardiac examination requires close attention to the heart sounds. The second heart sound, S2, is produced by which of the following structures? Aortic and pulmonic valves Mitral and tricuspid valves Pericardium and chest wall Posterior and anterior cusps of the mitral valve

Aortic and pulmonic valves The cardiac cycle begins with ventricular contraction, or systole. The pressure generated closes the mitral and tricuspid valves, producing S1, and opens the aortic and pulmonic valves. As the ventricles relax, the previously "pumped-out" blood pushes back on the heart, closing the aortic and pulmonic valves and producing the second heart sound, S2. The ECG's P wave comes before S1, the QRS complex occurs during S1 and the T wave occurs between S1 and S2. S1 is produced by the closure of the mitral and tricuspid valves (B). A friction rub may be appreciated when there is fluid or irritation between the pericardium and the chest wall (C). Functional abnormalities of the mitral valve's posterior and anterior cusp (D) may lead to a stenotic or regurgitant murmur.

A careful cardiac examination requires close attention to the heart sounds. The second heart sound, S2, is produced by which of the following structures? Aortic and pulmonic valves Mitral and tricuspid valves Pericardium and chest wall Posterior and anterior cusps of the mitral valve

Aortic and pulmonic valves The cardiac cycle begins with ventricular contraction, or systole. The pressure generated closes the mitral and tricuspid valves, producing S1, and opens the aortic and pulmonic valves. As the ventricles relax, the previously "pumped-out" blood pushes back on the heart, closing the aortic and pulmonic valves and producing the second heart sound, S2. The ECG's P wave comes before S1, the QRS complex occurs during S1 and the T wave occurs between S1 and S2. S1 is produced by the closure of the mitral and tricuspid valves (B). A friction rub may be appreciated when there is fluid or irritation between the pericardium and the chest wall (C). Functional abnormalities of the mitral valve's posterior and anterior cusp (D) may lead to a stenotic or regurgitant murmur.

A 65-year-old man presents to your office with sudden severe chest pain, asymmetric blood pressures in his arms with a new evolving aortic regurgitation murmur. The patient describes the chest pain as 10 out of 10 in severity. You decide to call 911 as you suspect what acute emergency? Acute pericarditis Aortic dissection Myocardial infarction Pulmonary embolism

Aortic dissection Aortic dissection has a typical clinical presentation of sudden onset of severe chest pain often described as sharp, tearing, or ripping. Pain can be anterior with ascending aortic dissection or back pain with descending aortic dissection. Pulse and blood pressure differentials commonly can be caused by partial compression of subclavian arteries. Most patients present with markedly elevated blood pressure. Hypotension can indicate hemorrhage, cardiac tamponade, or severe aortic regurgitation. Risk factors include chronic hypertension, atherosclerosis, family history of aortic aneurysms, trauma, collagen disorders, bicuspid aortic valve, aortic coarctation, vasculitis, Turner's syndrome and cocaine abuse. Aortic dissection has a typical clinical presentation of sudden onset of severe chest pain often described as sharp, tearing, or ripping. Pain can be anterior with ascending aortic dissection or back pain with descending aortic dissection. Pulse and blood pressure differentials commonly can be caused by partial compression of subclavian arteries. Most patients present with markedly elevated blood pressure. Hypotension can indicate hemorrhage, cardiac tamponade, or severe aortic regurgitation. Risk factors include chronic hypertension, atherosclerosis, family history of aortic aneurysms, trauma, collagen disorders, bicuspid aortic valve, aortic coarctation, vasculitis, Turner's syndrome and cocaine abuse.

Other than cardiac ischemia or infarct, what are some other cardiac causes of chest pain?

Aortic dissection, pericarditis and myopericarditis.

Which of the following statements is true regarding giant cell arteritis? Aortic involvement can lead to valvular disease and dissection Corticosteroid therapy should be initiated only when biopsy confirms the disease Histologic findings of inflammation are irreversible It is associated with sudden, painful binocular vision loss

Aortic involvement can lead to valvular disease and dissection Temporal arteritis is a chronic segmental vasculitis of medium and large vessels. Although it most commonly affects one or more branches of the carotid artery (temporal artery, ophthalmic artery, and posterior ciliary artery), the aorta can also be involved. Aortic involvement can lead to valvular insufficiency, aortic arch syndrome, and dissection. The carotid and vertebrobasilar arteries can also be affected, which can lead to neurologic complications. The condition is associated with a markedly elevated erythrocyte sedimentation rate (50-100 mm/hr). Histologic findings (C) are rapidly reversed with steroid therapy. Temporal arteritis is a sight-threatening disease, but timely administration of high-dose corticosteroids can prevent blindness. For this reason, if the diagnosis is suspected, corticosteroids should be administered immediately (B) while awaiting the results of temporal artery biopsy. Symptoms suggestive of temporal arteritis include headache, jaw claudication, and visual disturbances. Temporal arteritis is associated with a sudden painless monocular loss of vision (D) due to vascular occlusion of the ophthalmic or posterior ciliary artery with infarction of the optic nerve or retina.

Which of the following valvular disorders is characterized by any of the following: a low-pitched diastolic murmur heard best over the apex, an early high-pitched, blowing diastolic murmur heard best over the left sternal border, and a wide pulse pressure? Aortic regurgitation Aortic stenosis Mitral stenosis Tricuspid stenosis

Aortic regurgitation Physical signs of aortic regurgitation (AR) include a rapid, quick arterial pulse (Corrigan's pulse), a wide pulse pressure, an early high-pitched, blowing diastolic murmur heard best over the left sternal border, an S3 gallop, and a low-pitched diastolic murmur at the apex (Austin-Flint murmur). Aortic valve regurgitation is defined as blood flow from the aorta to the left ventricle in diastole because of an incompetent aortic valve. Aortic valve insufficiency is generally acquired through valve infection, dilation and dissection of the aortic root, trauma, or long-term degenerative change of the valve, particularly in the setting of hypertension. Patients with a history of prosthetic valves can also have aortic valve insufficiency. Aortic insufficiency can also be caused by a congenital bicuspid aortic valve. The surgical treatment of AR is indicated in symptomatic patients with dyspnea, angina, or CHF. Asymptomatic patients should undergo surgery if left ventricular ejection fraction is 55% or less, or left ventricular end-systolic dimension approaches 5.5 cm. Patients with moderate to severe AR should avoid competitive sports, heavy workloads, and weightlifting. The typical physical signs of severe aortic valve stenosis (B) are diminished carotid pulses (delayed and weak), a sustained apical impulse, a single second heart sound, an S4 gallop, and mid-systolic crescendo-decrescendo murmur late peaking best heard at the base of the heart. Most auscultatory signs of mitral stenosis (C) are missed if not performed in the left lateral decubitus position. Typically, the first heart sound (S1) is accentuated. A low-pitched diastolic rumble heard with the bell of the stethoscope over the apex is also present. The high-pitched opening snap, caused by the abrupt stopping of the domed mitral valve into the left ventricle is also appreciated in most patients midway between the left sternal border and apex. Tricuspid valve stenosis (D) is mostly caused by rheumatic heart disease and is typically associated with other valvular involvement. Patients can be dyspneic with activity. Typically, there is an increase in the jugular vein with a large a wave, indicating atrial contraction against a stiff tricuspid valve.

A 75-year-old otherwise healthy woman states that she has passed out three times in the last month during her daily brisk walk. Which one of the following is the most likely cause of her syncope? Aortic stenosis Atrial myxoma Orthostatic hypotension Vasovagal syncope

Aortic stenosis Syncope with exercise is a manifestation of organic heart disease in which cardiac output is fixed and does not rise with exertion. Syncope, commonly occurring with exertion, is reported in up to 42% of patients with severe aortic stenosis. The pathology of aortic stenosis includes processes similar to those in atherosclerosis, including lipid accumulation, inflammation, and calcification. The development of significant aortic stenosis tends to occur earlier in those with congenital bicuspid aortic valves. During the asymptomatic latent period, left ventricular hypertrophy and atrial enlargement of preload compensate for the increase in afterload caused by aortic stenosis. As the disease worsens, these compensatory mechanisms fail, leading to symptoms of heart failure, angina, or syncope. Doppler echocardiography is the recommended initial test for patients with classic symptoms of aortic stenosis. It is helpful for estimating aortic valve area, peak and mean transvalvular gradients, and maximum aortic velocity. Aortic valve replacement should be recommended in most patients with any of these symptoms accompanied by evidence of significant aortic stenosis on echocardiography. Vasovagal syncope (D) is associated with unpleasant stimuli or physiologic conditions, including sights, sounds, smells, sudden pain, sustained upright posture, heat, hunger, and acute blood loss. Orthostatic hypotension (C) is associated with changing from a sitting or lying position to an upright position. Atrial myxoma (B) is associated with syncope related to changes in position, such as bending, lying down from a seated position, or turning over in bed.

What is Heyde's syndrome?

Aortic stenosis and gastrointestinal bleeding from gastrointestinal angiodysplasia.

A 62-year-old man with a history of ongoing tobacco abuse, hypertension, dyslipidemia and erectile dysfunction complains of progressive aching pain in his right buttock and hip. The pain is worse with walking and is relieved with rest. Physical exam of the lower extremities reveals slightly diminished femoral, popliteal, and dorsalis pedis pulses. Which of the following is the most likely site of this patient's peripheral arterial disease? Aortoiliac artery Common femoral artery Popliteal artery Superficial femoral artery

Aortoiliac artery This patient most likely has peripheral arterial disease in the right aortoiliac artery. Peripheral arterial disease is physiologically significant atherosclerosis of the aortic bifurcations or arteries of the lower limbs. It is strongly associated with smoking, diabetes mellitus, and aging and shares all the risk factors common to atherosclerosis. This patient presents with right hip and buttock claudication, diminished femoral pulses and erectile dysfunction. This presentation commonly represents atherosclerotic disease within the aortoiliac system and is sometimes referred to as Leriche syndrome. Classic claudication is characterized by leg pain that is consistently reproduced with exercise and relieved with rest. The degree of symptoms of claudication depends upon the severity of stenosis, the collateral circulation, and the vigor of exercise. Patients with claudication can present with buttock, hip, thigh, calf, or foot pain, alone or in combination. The usual relationships are between pain location and corresponding anatomic site of arterial occlusive disease. Peripheral arterial disease in the common femoral artery (B) may cause thigh pain with effort but would not result in erectile dysfunction. Peripheral arterial disease in the popliteal artery (C) would produce pain in the lower one-third of the calf. Peripheral arterial disease within the superficial femoral artery (D) usually produces an effort-related discomfort in the upper two-thirds of the calf.

A 45-year-old man with a history of paroxysmal atrial fibrillation presents to the ED with acute onset of severe pain and paresthesias in his right calf. On exam, you note lower extremity pallor and an absent dorsalis pedis pulse. Which of the following is the most likely diagnosis? Arterial atheroembolism Arterial thromboembolism Arterial thrombosis Arterial vasospasm

Arterial thromboembolism Arterial embolism can be divided into thromboembolic and atheroembolic causes. Most arterial thromboemboli originate in the left side of the heart and are frequently associated with a recent myocardial infarction, atrial fibrillation, or valvular abnormalities. Acute arterial thromboembolism results in the sudden loss of a previously present pulse. In general, patients with arterial thromboembolism have few physical findings suggestive of long-standing peripheral vascular disease and will have normal proximal and contralateral limb pulses. These patients typically do not have well-developed collateral circulation and are at high risk for limb ischemia. Arterial atheroemboli (A) refers to microemboli consisting of cholesterol, calcium, and platelet aggregates dislodged from proximal complicated atherosclerotic plaques. In the peripheral vascular system, atheroemboli characteristically present with cool, painful, and cyanotic toes ("blue-toe" syndrome). Arterial thrombosis (C) is a chronic condition associated with progressive development of complicated atherosclerotic plaques. Peripheral arterial thrombi are usually firmly attached to the damaged arterial wall and rarely embolize. Patients will exhibit signs of longstanding atherosclerosis in their lower extremities (atrophy, loss of hair growth, thickened toe nails) and often have a history of claudication. These patients have well-developed collateral circulation, which helps protect them from limb-threatening ischemia. Arterial vasospasm (D), such as Raynaud's disease, causes a sharp border between ischemic and normal tissue. This condition is characterized by intermittent attacks of triphasic color changes (pallor, cyanosis, rubor).

Which of the following medications has the greatest impact on reducing mortality in patients presenting with acute coronary syndrome? Aspirin Beta blocker Morphine Nitroglycerin

Aspirin Of the medications listed above, aspirin has been shown to have the greatest effect on reducing mortality in patients with acute coronary syndrome (ACS). Aspirin is an irreversible antiplatelet agent. It inactivates platelets for the life span of the platelet (8-10 days). ISIS-2 demonstrated a 23% reduction in mortality for patients with acute myocardial infarction (AMI) that received aspirin but not thrombolytic therapy. It also demonstrated that aspirin was synergistic with thrombolytics (42% reduction in mortality). Overall, aspirin has a number needed to treat (to prevent death) of 42. Administration of aspirin (chewed and swallowed) is recommended in any patient with suspected ACS. Beta-blockers (B) are used in STEMI to prevent ventricular dysrhythmias but have shown only a small (0.5 - 1%) improvement in this outcome. Morphine (C) is an opiate that has been used as an adjunct for relief of ischemic pain but has never been shown to improve mortality (and some studies have shown harm). Nitroglycerin (D) is a vasodilator that reduces anginal pain but has also never been shown to improve outcomes.

In patients with a myocardial infarction, which three drugs have been shown to decrease mortality?

Aspirin, beta-blockers, and ACE-inhibitors.

Which other antiplatelet medications are recommended for treating STEMI?

Aspirin, clopidogrel, ticagrelor and prasugrel.

Acute Coronary Syndrome: Management

Aspirin: ↓ mortality, ↓ infarct size, ↓ reinfarction rate • Clopridogrel: patients with aspirin allergy • Heparin: ↓ DVT, ↓ reinfarction, ↓ stroke, ↓ LV thrombus, ↓ reocclusion • Nitroglycerin: . Coronary artery dilation/vascular smooth muscle relaxation → ↓preload/afterload → ↓ myocardial O2 demand . Contraindications: sildenafil use within 24 hrs, RV infarction • ß-blockers: . ↓ Myocardial O2 demand, ↓ ventricular fibrillation . IV indications: tachydysrhythmias, intractable HTN • Morphine: . ↓ Preload/afterload, ↓ sympathetic activity . No mortality benefit • Glycoprotein IIb/IIIa inhibitors: benefit in patients undergoing PCI • PCI: . Preferred over thrombolytics in all STEMI patients . PCI center: <90 minutes contact to device time . Non-PCI center: transfer to PCI center if contact to device time can be <120 minutes . Non-PCI center: thrombolytics if contact to device time to be >120 minutes • Thrombolytics: begin within 30 minutes of ED arrival if selected

Hypertrophic Cardiomyopathy

Asymmetric LV septal wall hypertrophy → outflow obstruction • Autosomal dominant (familial form) • Young patient • Exertional syncope • Sudden cardiac death • S4 gallop • Midsystolic murmur (↑ as preload ↓) • Rx: ßBs or CCBs

Ethanol Intoxication

Ataxia, gait instability, slurred speech • Severe intoxication: 4 Hs (Hypotension, Hypoventilation, Hypothermia, Hypoglycemia) • Usually supportive care • Severe case rx: glucose, thiamine

Which of the following is an important predisposing factor for the development of the condition seen in this radiograph? Atherosclerosis Hernia Hyperparathyroidism Ulcer disease

Atherosclerosis The calcified wall of an abdominal aortic aneurysm (AAA) is visualized in this radiograph. The most common plain-film findings of an AAA is a curvilinear calcification of the aortic wall or a paravertebral soft tissue mass. Rarely with longstanding aneurysms, is the erosion of one or more vertebral bodies seen. Atherosclerosis, age >60 years, smoking, and family history are all important predisposing factors for the development of AAA. An AAA is a disease of aging and is rare before age 50 years. It is found in 5%-10% of elderly men screened with ultrasound. AAAs progressively enlarge, weakening the vessel wall, and ultimately rupture resulting in fatal hemorrhage. The most important factor in determining the risk of rupture is the size of the aneurysm. The rupture risk increases dramatically with increased aneurysmal size, and most ruptured AAAs have diameters >5 cm. Rupture usually occurs in the retroperitoneum; even those who make it to the OR still have a mortality close to 50%. The classic triad of a ruptured AAA is pain, hypotension, and a pulsatile abdominal mass, although many patients have only 1 or 2 of these components. Pain usually localizes to the abdomen, back, or flank, and is sometimes tragically misdiagnosed as renal colic. Treatment involves hemodynamic support and definitive repair by a vascular surgeon. Hernias (B) are the second most common cause of bowel obstruction, preceded by adhesions. Air fluid levels and dilated loops of bowel are radiographic findings associated with bowel obstruction. Primary hyperparathyroidism (C) is associated with some patients with recurring renal calculi. Secondary hyperparathyroidism can lead to abnormal bone resorption and manifests as bone syndromes such as rickets, osteomalacia, and renal osteodystrophy. Duodenal and gastric ulcers (D) are complicated by perforations that can lead to the detection of free air in the abdominal cavity. Free air is generally seen under the diaphragm in an erect patient.

A 74-year-old man is having a preoperative ECG performed. What is your interpretation of his ECG? Atrial fibrillation Atrial flutter Normal sinus rhythm Sinus tachycardia

Atrial fibrillation Atrial fibrillation is an irregularly irregular rhythm due to uncoordinated atrial activation and random occurrence of ventricular depolarization. The atria are not contracting, but they do discharge electrical impulses to the ventricles. However, no single impulse depolarizes the atria completely, so only an occasional impulse gets through the AV node. It is the most common sustained dysrhythmia in clinical practice. Atrial flutter (B) is a rapid atrial rhythm, but due to nodal delay, ventricular response rate is slower. Therefore, atrial flutter always occurs with some sort of AV block so that not all impulses are conducted. The resulting block is often variable (2:1, 3:1, 4:1). P waves have a characteristic sawtooth pattern. In normal sinus rhythm (C) and sinus tachycardia (D), the SA node is the pacemaker that causes the atria to depolarize regularly and, thus, the ventricles to depolarize regularly. Therefore, the ECGs for both of these rhythms have P waves and QRS complexes that occur regularly. The difference between these two rhythms is with the rate. The rate of sinus rhythm is 60-99. The rate of sinus tachycardia is >100.

A 65-year-old man presents to the Emergency Department complaining of palpitations for the last week. The palpitations are intermittent, but more severe in the last 3 hours. His heart rate is 140 and blood pressure is 130/80 mm Hg. His ECG is shown above. What is the cardiac rhythm shown on the ECG? Atrial fibrillation Atrial flutter Paroxysmal atrial tachycardia Sinus tachycardia

Atrial fibrillation To analyze the heart rhythm on this ECG, a systematic approach is recommended.. First, look at the rate. This rate is fast (tachycardia), greater than 100 beats per minute. Then, look at the width of the QRS complex for a clue to where the impulse originates. The QRS complexes here are narrow so this is a supraventricular tachycardia. Next, evaluate the regularity of the rhythm. Is it regular or irregular? If the rhythm is irregular, is there still a pattern to the beats? If there is no pattern to the beats, it is irregularly irregular. If a rhythm is irregularly irregular, ask, "Is this atrial fibrillation?". This rhythm is irregularly irregular. Last, look for P waves and their relationship to the QRS. In this case there are no consistent P waves, confirming the diagnosis of atrial fibrillation. Atrial flutter (B), paroxysmal atrial tachycardia (C) and sinus tachycardia (D) are all supraventricular tachycardias (i.e.fast rhythms with narrow QRS complexes). Atrial flutter is usually regular, but may be irregular due to varying degrees of atrioventricular block. Large, fast F waves, called flutter waves, should be seen in at least one lead in atrial flutter. Paroxysmal atrial tachycardia is regular with rates of 180-240. Sinus tachycardia is regular and will have P waves prior to each QRS. These P waves should be upright in leads I and AVF.

What dysrhythmia is most commonly associated with tricuspid regurgitation?

Atrial fibrillation (80% of patients with tricuspid regurgitation).

Which dysrhythmia is commonly associated with mitral regurgitation?

Atrial fibrillation.

A 69-year-old man with atherosclerosis presents with calf pain during ambulation. He notices a blanching of the leg skin when the pain is at its worst. If he stops walking, the pain ceases within 5 minutes. He has a 120 pack-year history of tobacco use. Examination of the toes reveals prolonged capillary refill but normal sensation. A recent work-up revealed normal cardiac function. Which of the following abnormalities would most likely be found during examination of this patient's lower extremities? Atrophic, shiny skin Intrinsic foot muscle weakness Pitting edema Varicose veins

Atrophic, shiny skin Occlusive peripheral arterial disease results from atherosclerotic changes of vessels outside of the heart. It is heralded by intermittent claudication, a physical activity induced extremity pain that ceases with a few minutes of rest. Other classic symptoms include the 5 P's: pulselessness, pallor, pain, paresthesias and paralysis. Limb-threatening ischemia, suggested by paresthesias and paralysis, necessitate immediate evaluation and treatment. Prolonged capillary refill is also a common finding. Chronic poor blood supply causes the typical atrophic, shiny, dry skin changes seen with peripheral arterial disease. Evaluation includes pulse examination, abdominopelvic auscultation, Doppler assessment and ankle-brachial index testing. Diagnosis can be confirmed with Duplex ultrasonography, CT-angiography or MRI-angiography. Treatment begins with lifestyle modifications, namely tobacco cessation and regular exercise. Medications include lipid lowering statins, aspirin and other antiplatelet drugs like clopidogrel and cilostazol. Distal muscle weakness (B) and atrophy occurs more with peripheral neuropathy and myopathy than with peripheral arterial disease. If distal sensation is intact, peripheral neuropathy is less likely. Peripheral edema (C) occurs more commonly with cardiac failure, venous disturbance, lymphatic disturbance or infection than with peripheral arterial disease. It would not be the most expected finding in someone with a recent normal cardiac function test. Venous varicosities (D) suggest venous, not arterial, insufficiency, and rarely presents with intermittent claudication symptoms.

A 50-year-old woman presents to the Emergency Department following a syncopal episode. On physical exam she is diaphoretic, but alert and orientated. Her blood pressure is 100/50 mm Hg, heart rate 46 beats per minute, and respirations 12 per minute. Her rhythm strip is shown above. What is the most appropriate treatment for this patient's condition? Adenosine Amiodarone Amlodipine Atropine

Atropine Sinus bradycardia is a rhythm that originates from the sinoatrial (SA) node with a rate of less than 60 per minute. The SA node is the heart's normal pacemaker, and sinus bradycardia may be normal in some patients such as conditioned athletes. In these cases, patients will have a resting heart rate of less than 60 per minute, but will not exhibit any other symptoms. Other times, sinus bradycardia may be due to organic heart disease such as coronary artery disease, cardiomyopathy, or myocarditis, resulting in symptomatic sinus bradycardia. Therefore, treatment largely depends on whether the patient is symptomatic (unstable) or not. An unstable patient is anyone who shows signs of poor perfusion such as altered mental status, diaphoresis, dizziness or syncope. A stable patient may be monitored closely, with ECG and vital signs, but initial treatment for an unstable patient is atropine. Since this patient presents with both a syncopal episode and diaphoresis, she is unstable and atropine is the appropriate therapy. After an initial dose of atropine, infusions of epinephrine or dopamine may also be considered, and for more emergent cases transcutaneous pacing may be necessary. Adenosine (A) is the treatment for supraventricular tachycardia , not bradycardia, and so is not appropriate for this patient. Amiodarone (B) is used to treat dysrhythmias such as ventricular tachycardia, not a sinus rhythm, while amlodipine (C) is a calcium channel blocker that helps to control blood pressure and chest pain.

A 55-year-old man presents after a syncopal event. He states he just started a new blood pressure medication. His heart rate is 41 beats/minute and his blood pressure is 95/60 mm Hg. Electrocardiogram shows sinus bradycardia. Which of the following medications should be administered? Adenosine Atropine Diltiazem Procainamide

Atropine Sinus bradycardia refers to a discharge rate from the sinoatrial node of < 60 beats/minute. Sinus bradycardia can be a result of pathologic factors like hypoxia, hypothermia, cardiac ischemia or infarction, hypothyroidism, or increased intracranial pressure. Many medications also cause sinus bradycardia, including beta-blockers, calcium-channel blockers, digoxin, and opioids. Sinus bradycardia may also be a normal finding in well-conditioned young people, athletes, during sleep, or as a result of vagal stimulation. On electrocardiogram, sinus bradycardia is indistinguishable from sinus rhythm other than having a slower rate. Patients with sinus bradycardia may be asymptomatic or may complain of dizziness or lightheadedness. An especially slow rate may result in signs of hypoperfusion (e.g. hypotension, altered mental status, or ischemic chest pain). The treatment of sinus bradycardia depends on the underlying cause and the clinical effects. Underlying causes should be corrected. Unstable patients should be treated with atropine while transcutaneous pacing is initiated and arrangements for transvenous pacing are made. Infusions of dopamine or epinephrine are also indicated to increase the heart rate if atropine is ineffective. Glucagon is used to treat cardiotoxicity from beta-blocker or calcium channel blocker overdose. Adenosine (A) is an atrioventricular (AV) nodal blocker used in the treatment of supraventricular tachycardias. Diltiazem (C) is a calcium channel blocker used in the treatment of tachydysrhythmias. Procainamide (D) is an antiarrhythmic used in the treatment of tachydysrhythmias.

Hypertrophic cardiomyopathy is passed on through what genetic inheritance pattern?

Autosomal dominant pattern. This means one copy of the altered gene in each cell is sufficient to cause the disorder.

JNC 8 Treatment for HTN

BP goals: . Age < 60 or Diabetic: 140/90 . Age > 60: 150/90 • Treatment: . #1 is always lifestyle modifications . Nonblack: Thiazide, ACE inhibitor, or ARB or calcium channel blocker alone or in combination . Black: Thiazide or calcium channel blocker alone or in combination . CKD (with or without diabetes): all races ACE inhibitor or ARB alone or in combination with other drug classes

A 27-year-old woman presents to the emergency department with complaints of fever, rash, and myalgias. She also admits to night sweats and nausea. On exam, there are multiple scars in her left antecubital fossa, scattered petechiae, and tender nodules on the tips of her digits. Cardiac auscultation reveals a murmur. Which of the following is the most likely diagnosis? Acute pericarditis Bacterial endocarditis Community-acquired pneumonia Hypertrophic cardiomyopathy

Bacterial endocarditis This woman most likely has bacterial endocarditis caused by intravenous drug use. Infective endocarditis is an infection of the endocardial or valvular surfaces of the heart. Underlying valvular disease is present in about half of cases. Colonization of the valve by bacteria or fungi can occur during dental, upper respiratory, urologic, or surgical procedures. Intravenous drug use (IVDU) is also a source of bacteremia. Most cases of native valve endocarditis are caused by Streptococcus species, including S viridans. Staphylococcus aureus accounts for over 60% of endocarditis associated with IVDU. The tricuspid valve is most commonly affected in IVDU associated endocarditis. Almost all patients have fever. Other nonspecific symptoms include chills, anorexia, weight loss, myalgias, and malaise. Dyspnea and cough are common complaints when the tricuspid valve is affected due to embolic showering of the pulmonary vasculature. Roth spots (retinal hemorrhages), Osler nodes (distal digital subcutaneous nodules), and Janeway lesions (nontender maculae on palms and soles) are caused by peripheral emboli. Petechiae are the most common skin finding. Blood cultures are key in the diagnosis of infective endocarditis. Three sets of blood cultures should be obtained prior to initiating antibiotics. Transthoracic echocardiography can be used initially, but cannot be used to rule out endocarditis due low sensitivity. Transesophageal echocardiography has a sensitivity of 90-100% for valvular lesions. Electrocardiography is usually nonspecific. The Modified Duke criteria can aid in the diagnosis. Treatment depends on underlying history and suspected etiology, but empiric IV antibiotic regimens should be initiated prior to obtaining culture results. Acute pericarditis (A) commonly presents with acute onset of pleuritic, positional chest pain. Auscultation may reveal a scratchy, grating rub. Acute pericarditis does not cause petechiae or Osler nodes. Nonsteroidal anti-inflammatory drugs are the mainstay of treatment. Community-acquired pneumonia (C) is typically characterized by fever, dyspnea, and cough. Physical exam may reveal dullness to percussion, rhonchi or crackles. A chest radiograph may show a lobar infiltrate. Treatment of community-acquired pneumonia is typically with a fluoroquinolone or macrolide. Hypertrophic cardiomyopathy (D) is a genetic disorder that can cause sudden cardiac death. Dyspnea and syncope are the most common presenting symptoms of hypertrophic cardiomyopathy. Echocardiography is diagnostic for hypertrophic cardiomyopathy.

A woman presents for her annual examination. She is treated for stable angina with aspirin and a statin. She continues to have angina 3-4 times a week, but its character, intensity, frequency and duration is unchanged. She has no history of myocardial infarction, diabetes or pulmonary disease. Which of the following interventions is most appropriate at this time? Begin atenolol Begin lisinopril Begin nitroglycerin Continue current medications and follow-up in 1 month

Begin atenolol Chronic stable angina is properly managed with lifestyle modifications and statin, antihypertensive and antiplatelet therapies. Concerning antihypertensive therapy in patients with documented coronary artery disease and chronic stable angina, first-line therapy is accomplished with beta-blockers. Even if patients do not have hypertension, beta-blockade is recommended. Their β1 and β2 antagonism decreases myocardial demand by decreasing heart rate and myocardial contractility, as well as increasing diastolic filling time. Other antihypertensive agents include ACE-inhibitors, ARBS and calcium-channel blockers. ACE-inhibitors (B) are considered first-line if the patient has had an MI or currently has diabetes. They are considered second-line therapy in all other hypertensive patients once beta-blockade therapy has been established. Nitrates (C) may be considered in patients with continued stable angina if they have failed beta or calcium-channel antagonists. This patient has not been trialed on either. Proper management of stable angina includes three classes of medications. This patient is missing an antihypertensive agent, and should be started on one at today's visit (D).

A 65-year-old man presents to the emergency department with chest pain and ST-segment elevation in leads II, III, and aVF. The patient is hypotensive and physical exam reveals jugular venous distention, clear lung fields and tachycardia. No murmur or S3 is appreciated. What is the next step in management? Administer a beta blocker Administer morphine sulfate Administer sublingual nitroglycerin Begin intravenous hydration

Begin intravenous hydration This patient has an ECG concerning for a right ventricular infarct. In this situation, the patient becomes preload dependent (essentially the right ventricle is impaired so there is "passive" flow into the left ventricle). When these patients become hypotensive, the immediate treatment is intravenous hydration to increase preload. Right ventricular infarction is represented on an ECG by noting ST elevation in right-sided leads (V3R and V4R). Because the right coronary artery often supplies the right side of the heart and the inferior wall of the heart, any ECG with ST elevations in leads II, III, and aVF (inferior leads) should have another ECG performed with right-sided lead placement. Aggressive volume loading with normal saline boluses is used to restore blood flow to the right ventricle and inotropic support is indicated if hypotension persists. Early percutaneous coronary intervention or thrombolytic therapy should be initiated as soon as possible. In general, patients' with right ventricular myocardial infarction are treated in a manner similar to those with acute ST-elevation myocardial infarction. This includes the early use of dual antiplatelet therapy, statin therapy, and an anticoagulant. Medications that lower preload such as nitroglycerin (C) and morphine (B) or drugs that slow heart rate such as beta blockers (A) should be avoided or used with extreme caution.

What is an example of a drug that reduces cardiac contractility?

Beta blockers

What medication is contraindicated in the treatment of Prinzmetal's angina?

Beta-blockers

A 58-year-old woman presents with progressive orthopnea and peripheral edema. She also gets "winded" when she climbs a full flight of stairs. Which of the following laboratory tests helps define a cardiac versus a pulmonary cause of dyspnea? Beta-2 microglobulin Beta-type natriuretic peptide Erythrocyte sedimentation rate Homovanillic acid

Beta-type natriuretic peptide Cardiomyopathy is defined as a group of diseases which involve the muscle or electrical system of the heart. There are several causes, most of which are genetic in nature. Other etiologies are related to infectious, autoimmune, inflammatory, infiltrative, toxic, electrolytic, endocrine, nutritional and radiation etiologies. There are four main types: dilated, hypertrophic, restrictive and arrhythmogenic-right-ventricular (fibro fatty infiltration of the right ventricle). Dilated cardiomyopathy (DCM) is the most common subtype. It is the third most common cause of cardiac failure, behind coronary artery disease and hypertension. Adult DCM is most commonly caused by hypertension and coronary artery disease, but also is caused by genetic and infectious etiologies. Patients usually present with symptoms of heart failure, such as peripheral and pulmonary edema, cough, orthopnea and dyspnea at rest, with exertion or of the paroxysmal-nocturnal type. Initial evaluation of a patient with these symptoms includes electrocardiography, echocardiography, chest radiography and baseline chemistries, namely Beta-type (Brain) natriuretic peptide (BNP). BNP is secreted by the cardiac myocytes in response to increased volume and filling pressures. Beta-2 microglobulin (A) is used to evaluate hematologic disorders like multiple myeloma, lymphoma and leukemia. It is also associated with multiple sclerosis and other CNS disorders, as well as renal tubular disorders. Erythrocyte sedimentation rate (C) is a marker of inflammation. It is not a reliable test in differentiating cardiac from pulmonary dysfunction. Homovanillic acid (D) is a biomarker of metabolic stress in the central nervous system, not the cardiac or pulmonary systems.

Which of the following is a risk factor for the condition shown above? Bicuspid aortic valve Chronic heroin use Fibromuscular dysplasia Tobacco use

Bicuspid aortic valve Aortic dissection is an uncommon but life-threatening phenomenon that occurs when damage of the intima allows the entry of blood between the intima and media, creating a false lumen. The most important risk factor for aortic dissection is hypertension. Other risk factors include chronic cocaine use, bicuspid aortic valve, collagen disorders, pre-existing aortic aneurysm, aortic surgery or instrumentation, vasculitis involving the aorta, pregnancy and delivery, and aortic coarctation. Aortic dissection has a bimodal age distribution, with a peak under 40 years of age associated with connective tissue disorders and another peak at greater that 50 years of age associated with chronic hypertension. The presentation of aortic dissection depends on the anatomic location of the dissection, with the most common presentation being sharp or tearing chest pain. More distal aortic dissections may present with abdominal or flank pain. A history of diabetes, prior aortic surgery, or pre-existing aortic aneurysm may cause a painless presentation. Other presentations include syncope, stroke from carotid involvement, and spinal cord syndromes. CT angiogram is the gold standard for diagnosis of dissection. Chronic cocaine and amphetamine use, rather than chronic heroin use (B), are associated with aortic dissection as they accelerate atherosclerosis, weakening the aortic wall. Fibromuscular dysplasia (C) is an non-inflammatory, non-atherosclerotic disorder than can lead to arterial stenosis, aneurysm and dissection. Fibromuscular dysplasia typically affects the renal and internal carotid arteries rather than the aorta. Tobacco use (D) does not significantly increase the risk of aortic dissection.

Which of the following is a marker of high ventricular filling pressures? Brain natriuretic peptide Creatine kinase-MB Creatinine Troponin

Brain natriuretic peptide Brain natriuretic peptide is a marker of high ventricular filling pressures. It is a natriuretic hormone that was initially identified in the brain but is also released from the heart, particularly the ventricles. It is released in response to volume expansion and increased wall stress in the ventricles. Increased plasma concentrations are found in heart failure in response to increased ventricular filling pressures from volume overload. Troponin (D) and creatine kinase-MB (B) are markers for cardiac muscle damage as in an acute myocardial infarction or ischemia. Troponin is the preferred marker for the diagnosis of myocardial injury for all diagnostic categories because of its increased specificity and better sensitivity compared to creatine kinase-MB. Creatinine (C) is a marker of renal function, not increased ventricular filling pressures.

What is the most likely underlying chronic medical problem in the patient with the following ECG? Cardiomyopathy COPD Hyperthyroidism Mitral stenosis

COPD This electrocardiogram demonstrates multifocal atrial tachycardia, a form of atrial tachycardia diagnosed on the electrocardiogram by three distinct p-wave morphologies. In approximately 60% of cases, patients have underlying pulmonary disease, most commonly COPD. Patients may have a primary cardiac pathology although this is much less common. Cardiomyopathy (A) is not commonly associated with atrial dysrhythmias, but may be the causative agent of ventricular dysrhythmias, particularly ventricular tachycardia. Hyperthyroidism (C) is on the differential diagnosis of atrial fibrillation and should be excluded in cases of new onset atrial fibrillation. Valvular disease, particularly mitral stenosis (D) may also lead to atrial fibrillation as the atrium dilates over time as a result of the stenosis.

What are the three primary causes of aortic stenosis?

Calcification of a congenitally abnormal valve, calcification of a normal valve, and rheumatic heart disease.

What are the main actions of diltiazem?

Calcium channel blockade into myocardial cells resulting in decreased contraction, AV nodal conduction, and, to a lesser degree, vasodilation.

What is the medical treatment of symptomatic premature atrial contractions?

Calcium-channel blockers or beta-blockers.

What is the formula for cardiac output?

Cardiac output (Q) = stroke volume (SV) x heart rate (HR).

Which of the following conditions is a result of a rapid increase in pericardial pressure and a clinical picture of acute restrictive cardiomyopathy? Cardiac tamponade Constrictive pericarditis Pericardial effusion Pneumopericardium

Cardiac tamponade Cardiac tamponade results from acute compression of the myocardium by rapid fluid (or gas) accumulation in the pericardial sac. Tamponade develops when fluid filling the pericardial sac accumulates faster than the rate of stretch in the parietal pericardium. The resulting extrinsic pressure on the myocardium exceeds right atrial pressure leading to a reduction in right ventricular filling. With a continued rise in pericardial pressure, cardiac compliance decreases. Flow of blood into the right side of the heart ceases, leading to a precipitous decline in cardiac output. Key to remember: the rate of fluid accumulation, not the absolute volume, is the important factor in the development of tamponade. Constrictive pericarditis (B) usually results from fibrous reaction of the pericardium and is characterized by impaired diastolic filling from external cardiac compression caused by a thickened pericardium. It is usually due to a late consequence of viral pericarditis, or even tuberculosis, and presents with a more indolent course than tamponade. A characteristic auscultatory finding is a pericardial knock in early diastole. A friction rub may also be heard. Pericardial effusions (C) are often asymptomatic and are due to a variety of diseases such as malignancy, renal failure, uremia, trauma, and radiation therapy. If the pericardial effusion accumulates rapidly, it can result in pericardial tamponade. Pneumopericardium (D) is a rare disorder that results in air around or within the pericardial space. It is classically associated with Hamman's sign, which is a loud crunching sound—best heard with the patient in a left lateral recumbent position—and is pathognomonic for mediastinal air.

What does hypotension in the setting of aortic dissection usually indicate?

Cardiac tamponade or aortic rupture.

A patient with dyspnea and angina fails medication management of his symptoms with beta-blockers, ACE-inhibitors and calcium channel blockers. He undergoes complete cardiac evaluation which uncovers the presence of nonobstructive, end-stage hypertrophic cardiomyopathy. Which of the following is the most appropriate treatment at this point in time? Aggressive diuresis Cardiac transplantation Implantable intracardiac pacing Surgical myectomy

Cardiac transplantation The management of hypertrophic cardiomyopathy should follow heart failure treatment guidelines. This includes a careful use of diuretics, as many patients with HCM require higher filling pressures to maintain cardiac function. This is especially true if edema is not a main finding. Negative inotropes and negative chronotropes are also recommended, and include beta-blockers and calcium channel blockers. If pharmacotherapy is unsuccessful, further treatment is dictated by whether the hypertrophic cardiomyopathy is obstructive or nonobstructive. If obstructive physiology is detected, surgical options may be required, and include cardiac pacing, surgical myectomy or septal ablation. If nonobstructive physiology is found, cardiac transplant is usually the only viable solution. Diuresis (A) is cautioned in those with hypertrophic cardiomyopathy. Acute, aggressive diuresis may likely push the patient into further decompensation. Pacing (C) and myectomy (D) may be viable treatment options for obstructive HCM but not for nonobstructive HCM.

A patient with dyspnea and angina fails medication management of his symptoms with beta-blockers, ACE-inhibitors and calcium channel blockers. He undergoes complete cardiac evaluation which uncovers the presence of nonobstructive, end-stage hypertrophic cardiomyopathy. Which of the following is the most appropriate treatment at this point in time? Aggressive diuresis Cardiac transplantation Implantable intracardiac pacing Surgical myectomy

Cardiac transplantation The management of hypertrophic cardiomyopathy should follow heart failure treatment guidelines. This includes a careful use of diuretics, as many patients with HCM require higher filling pressures to maintain cardiac function. This is especially true if edema is not a main finding. Negative inotropes and negative chronotropes are also recommended, and include beta-blockers and calcium channel blockers. If pharmacotherapy is unsuccessful, further treatment is dictated by whether the hypertrophic cardiomyopathy is obstructive or nonobstructive. If obstructive physiology is detected, surgical options may be required, and include cardiac pacing, surgical myectomy or septal ablation. If nonobstructive physiology is found, cardiac transplant is usually the only viable solution. Diuresis (A) is cautioned in those with hypertrophic cardiomyopathy. Acute, aggressive diuresis may likely push the patient into further decompensation. Pacing (C) and myectomy (D) may be viable treatment options for obstructive HCM but not for nonobstructive HCM.

Which cardiac biomarker has the highest sensitivity and specificity?

Cardiac troponin.

How does carotid massage affect second degree type I and type II heart block?

Carotid massage will typically worsen second degree type I block and improve second degree type II block.

Which vagal maneuver is relatively contraindicated in the elderly population?

Carotid massage, as the risk of embolic stroke from underlying carotid atherosclerosis is present.

Dilated Cardiomyopathy

Causes: idiopathic > viral myocarditis, Chagas disease • Echo: 4 dilated chambers (ventricles > atria) • Systolic pump failure → heart failure • S3, S4 • Peripheral embolization of mural thrombi • MC dysrhythmia: atrial fibrillation • ßBs, ACEIs, diuretics, digoxin, anticoagulation, AICD

Mitral Regurgitation (MR)

Causes: ischemic heart disease, endocarditis, MI, trauma Acute sx: dyspnea, pulmonary edema, cardiogenic edema Chronic sx: asymptomatic until CHF onset, S3 Acute rx: nitroprusside, dobutamine, intra-aortic balloon pump, emergency surgery Chronic rx: anticoagulation, CHF rx, valve replacement

Tricuspid Regurgitation

Causes: tricuspid ring stretching > pulmonary HTN, endocarditis, rheumatic heart disease • Pansystolic murmur at left sternal border • JVP: giant c-v wave • Atrial fibrillation

What is the most common presenting symptom in patients with acute ischemic heart disease?

Central-chest discomfort.

A 35-year-old man is evaluated in the emergency department after being the restrained driver in a motor vehicle collision. At presentation, the patient is alert, anxious, and able to verbalize a complaint of chest pain associated with some anterior chest wall bruising. There are no gross deformities on exam. Suddenly, the patient becomes unresponsive. Telemetry shows the rhythm above. No pulse can be palpated. Which of the following is the most appropriate next step in the management of this patient? Amiodarone drip Chest compressions Epinephrine Synchronized cardioversion

Chest compressions Pulseless Electrical Activity (PEA) is defined as an organized electrical rhythm without sufficient mechanical ventricular contraction to result in a palpable pulse or measurable blood pressure. PEA is thought to be the presenting rhythm in almost half of cardiac arrests. PEA is a non-perfusing rhythm and requires the immediate initiation of cardiopulmonary resuscitation with chest compressions. Cardiopulmonary resuscitation, vasopressor administration and recognition and reversal of the underlying cause are the cornerstones of the management of PEA. Causes of PEA can be summarized by "The H's and T's," and include hypovolemia, hypoxia, hydrogen ion excess (acidosis), hyper- and hypokalemia, hypothermia, toxins, tamponade (cardiac), tension pneumothorax and thrombosis (coronary and pulmonary). Hypovolemia and hypoxia are the most common causes of noncardiac PEA. Synchronized cardioversion (D) is the intervention of choice in narrow complex tachydysrhythmias with hemodynamic instability or hemodynamically unstable ventricular tachycardia with a pulse. Synchronized cardioversion is not effective in PEA arrest. Epinephrine (C) should be administered in PEA arrest after the initiation of chest compressions, not before. Amiodarone (A) is an important anti-arrhythmic in wide- and narrow-complex tachycardias but does not have a role in PEA arrest.

What is the most commonly seen symptom or sign in patients with acute aortic dissection? Aortic insufficiency murmur Chest pain Pulse deficit Syncope

Chest pain Chest pain is the most common symptom seen in patients with acute aortic dissection. Aortic dissection is an uncommon presentation but it represents a difficult and life-threatening diagnosis. Difficulty in diagnosing the disease stems from the myriad of presentations and manifestations the disease can assume. Approximately 73% of patients with acute aortic dissection will present complaining of chest pain. This symptom is more common in those patients with ascending dissections whereas back pain is more common in those with descending thoracic dissections. Some complaint of pain is seen in up to 96% of patients. The pain is classically described as ripping or tearing but only about 50% of patients will describe it in this way. Aortic insufficiency murmur (A) results from an ascending dissection that compromises the aortic valve but is only seen in about 32% of patients. Pulse deficit (C) is even less common (15%). Syncope (D) is seen in approximately 9% of aortic dissections.

You are seeing an African-American 42-year-old man for an initial primary care visit. His medical history is significant for diabetes, seasonal allergies, obesity, and rotator cuff repair. His medications include insulin and desloratadine. Proper blood pressure readings are taken: 154/98 and 148/94. Which of the following medications is most appropriate when initiating antihypertensive management in this patient? Candesartan Captopril Carvedilol Chlorthalidone

Chlorthalidone JNC-8 has published recommendations for hypertensive management in early 2014. The goal for all patients < 60 years of age is < 140/90 mm Hg. JNC-8's Initial antihypertensive choice for African-Americans is a thiazide-type diuretic or a calcium channel blocker. In comparison, the initial antihypertensive choice in the non-African-American population is a thiazide-type diuretic, calcium channel blocker, angiotensin-converting enzyme inhibitor (ACEI), or angiotensin receptor blocker (ARB). In both sub-populations, these recommendations hold true even if the patient also has diabetes mellitus. calcium channel blocker choices include amlodipine, nitrendipine and diltiazem ER. thiazide-type diuretic choices include indapamide, hydrochlorothiazide, chlorthalidone and bendroflumethazide. Angiotensin receptor blockers, like candesartan (A), are not recommended as first-line antihypertensive therapy in the African-American population. Angiotensin-converting enzyme inhibitors, like captopril (B), are not recommended as first-line antihypertensive therapy in the African-American population. Beta-blockers (C) are not recommended for treating hypertension. JNC-8 determined that current data showed beta-blockers resulted in a higher rate of cardiovascular death, myocardial infarction or stroke as compared to ARBs. Also, other data showed beta-blockers to perform similarly to the above four medications or there wasn't enough evidence to make such a determination.

What is proBNP?

Cleavage of the prohormone proBNP produces biologically active 32 amino acid BNP (brain natriuretic peptide) as well as the biologically inert 76 amino acid N-terminal proBNP (NT-proBNP).

An elderly man presents with 4 episodes of angina in the past 24 hours. His medical history includes diabetes and advanced COPD. Based on initial testing, you diagnose non-ST-elevation myocardial infarction. You are waiting for the cardiac team to admit him to the critical care unit. In the interim, which of the following is the most appropriate medication to begin? Atelplase Clopidogrel Digoxin Metoprolol

Clopidogrel Non-ST-elevation myocardial infarction (NSTEMI) treatment begins with a basic anti-ischemic regimen consisting of oxygen, morphine, nitrates, and possibly beta-blockers and ACE-inhibitors. Antiplatelet medications are then considered. Choices include aspirin, clopidogrel, and prasugrel. NSTEMI treatment is rounded out with anticoagulants such as enoxaparin, bivalirudin, and fondaparinux. Based on risk stratification, definitive treatment may include medications-alone, angiography, percutaneous cardiac intervention or coronary artery bypass surgery. Clopidogrel acts by irreversibly inhibiting a platelet receptor that is needed for activation, thereby inhibiting platelet function. Thrombolytics (fibrinolytics), such as alteplase (A), reteplase and tenecteplase, are contraindicated in the treatment of NSTEMI, as they have shown worse outcomes with their use. Digoxin (C), a cardiac glycoside, is used in treating certain dysrhythmias and heart failure, not myocardial infarction. Beta-blockers such as metoprolol (D) carry a relative contraindication in patients with severe COPD, asthma, atrioventricular block, hypotension or bradycardia.

What antipsychotic drug has a black-box warning for the development of pericarditis and myocarditis?

Clozapine.

What medication may prevent recurrent episodes and is also used in the treatment of refractory pericarditis?

Colchicine.

What therapy, when used in the acute phase, may be effective in preventing recurrent symptoms of pericarditis?

Colchicine.

What medical condition is associated with Streptococcus bovis endocarditis?

Colorectal cancer.

Which of the following best describes the rhythm seen in the ECG above? Complete heart block First degree heart block Mobitz I (Wenckebach) Mobitz II

Complete heart block Third degree, or complete, heart block is characterized by absent conduction of all atrial impulses and complete electrical AV dissociation. The hallmark findings of third-degree AV heart block are regular PP intervals unrelated to regular R-R intervals with P waves that appear to march through the QRS-T complexes. There are two independent pacemakers: one in the S-A node and one either in the AV junction (narrow QRS complexes) or within the Purkinje fibers in the ventricles (wide QRS complexes). First degree heart block (B) is defined by normal AV conduction with a prolonged PR interval (>200 ms). There is a 1:1 relationship between P waves and QRS complexes. In Mobitz I (C), the PR interval progressively lengthens and the R-R interval progressively shortens until a beat is dropped. This cycle repeats itself, producing a pattern of "grouped beating." In Mobitz II (D), the PR interval is constant, but there are nonconducted P waves that lead to dropped beats. This block can deteriorate into third-degree heart block.

A previously healthy 38-year-old woman presents to your office with complaints of dilated veins and itching in both lower legs that has been worsening since the birth of her last child. The symptoms are improved with elevation of her legs. Which of the following is the most effective management? Compression stockings Laser therapy Sclerotherapy Venous reconstruction

Compression stockings Varicose veins are a type of chronic venous disease or venous insufficiency. The spectrum of disease in venous insufficiency ranges from mild to severe, with milder forms being uncomfortable and cosmetically unappealing and more severe forms causing serious systemic manifestations. Venous insufficiency may or may not be symptomatic. When symptoms are present, they can range from venous dilation to skin changes to ulceration. The dilation of the veins occurs due to increased venous pressure, resulting in varicose veins or telangiectasias, which are smaller, spider veins seen on the surface of the skin. Varicose veins are more frequently seen in women and are a very common finding, occurring in approximately a quarter of all adults in the United States. Risk factors for the development of venous insufficiency include advanced age, pregnancy, prolonged standing, obesity, smoking, prior venous thrombosis, sedentary lifestyle and lower extremity trauma. Patients generally present with complaints of heaviness or pain in the legs, pruritus, burning sensations, restless legs or night cramps, edema and skin changes. Diagnosis is initially clinical and then confirmed with duplex ultrasound. Conservative management with leg elevation, compression stockings and exercise is the initial treatment in the majority of cases of varicose veins. Laser therapy (B) is used to treat small surface vessels on the face, but is not recommended for use in primary treatment of varicose or spider veins on the extremities. Laser therapy is painful and the deeper vessels that feed the surface vessels need treatment before the surface area can be effectively treated. Sclerotherapy (C) is the chemical ablation of a vein. An irritant agent is injected into the vein, causing damage to the epithelial tissue. Sclerotherapy is used in the treatment of varicose veins, but is generally used after conservative measures have been tried and failed. Venous reconstruction (D) involves the surgical repair of deep vein valves that are damaged. Patients with primary valvular incompetence may consider this option. Those with secondary valvular incompetence following a thromboembolism may also benefit. In both cases, conservative measures should be tried initially before pursuing a more invasive option.

Aortic stenosis can lead to which of the following general patterns of left ventricular remodeling? Asymmetric left ventricular hypertrophy Concentric left ventricular hypertrophy Eccentric left ventricular hypertrophy Mixed concentric/eccentric left ventricular hypertrophy

Concentric left ventricular hypertrophy Aortic stenosis increases afterload to the left ventricle resulting in concentric left ventricular hypertrophy. Pressure overload leads to concentric left ventricular remodeling with or without an overall increase in myocardial mass. Concentric remodeling is characterized by increased relative wall thickness or ventricular wall thickness as compared to cavity size. With concentric hypertrophy, cardiac sarcomeres are added in parallel and individual cardiomyocytes grow thicker. This pattern of hypertrophy is adaptive to the increased wall stress of the left ventricle and helps maintain normal systolic function of the left ventricle. However, as severity of stenosis and left ventricular remodeling progresses, abnormal diastolic function typically occurs. This usually precedes systolic dysfunction and results in increased left ventricular filling pressures and symptoms of angina and dyspnea. In contrast, pure regurgitant lesions, such as mitral valve regurgitation cause volume overload to the left ventricle. The remodeling pattern involves eccentric left ventricular hypertrophy; a compensatory mechanism that maintains ventricular compliance. This allows increased left ventricular volume without increased left ventricular filling pressure. With progression of regurgitation and left ventricular dilation, left ventricular contractility or systolic function is impaired. Patients with mixed stenotic and regurgitant lesions such as combined aortic stenosis and regurgitation, may develop concentric and eccentric hypertrophy. In this scenario the dominant lesion determines left ventricular remodeling, clinical presentation, and management. Eccentric left ventricular hypertrophy (C) is characterized by increased cardiac mass and chamber volume and is caused by volume overload or isotonic exercise. Relative wall thickness may be normal, increased, or decreased. With eccentric hypertrophy, sarcomeres are added in series and individual cardiomyocytes grow longer. This pattern of left ventricular remodeling is not seen in aortic stenosis. Mixed concentric/eccentric left ventricular hypertrophy (D) can occur in mixed stenotic and regurgitant lesions or following myocardial infarction. Myocardial infarction causes stretched, infarcted tissue which increases left ventricular volume, leading to combined volume and pressure load on noninfarcted zones. Asymmetric left ventricular hypertrophy (A) is typical of hypertrophic cardiomyopathy and is not associated with aortic stenosis.

Which of the following conditions is associated with a pericardial knock on auscultation? Acute pericarditis Constrictive pericarditis Pericardial tamponade Restrictive cardiomyopathy

Constrictive pericarditis Constrictive pericarditis is associated with a pericardial knock. On cardiac auscultation, an early diastolic sound, the pericardial knock, may be heard at the apex 60 to 120 msec after the second heart sound (S2). The pericardial knock sounds like a ventricular gallop but occurs earlier than the S3 of heart failure, which it may mimic. The knock is due to accelerated right ventricular inflow in early diastole and early myocardial distention, followed by an abrupt slowing of further ventricular expansion. There is usually no pericardial friction rub. Constrictive pericarditis is pathologically distinct from acute pericarditis. Constrictive pericarditis is caused by the resultant inflammatory and reparative process from a pericardial injury. This leads to a fibrous thickening of the pericardium. Clinical presentation mimics heart failure and restrictive cardiomyopathy. Physical exam is associated with Kussmaul's sign (inspiratory neck vein distention) and pulsus paradoxus. Severe cases require surgical treatment with a pericardiectomy. Acute pericarditis (A) is associated with a pericardial friction rub. It is best heard with the diaphragm of the stethoscope at the lower left sternal border or apex when the patient is sitting and leaning forward or in the hands-and-knees position. The classic cardiac auscultation findings of pericardial tamponade (C) include distant heart or soft heart sounds. Restrictive cardiomyopathies (D) result from systemic disorders such as amyloidosis, sarcoidosis, hemochromotosis, scleroderma, carcinoid heart disease, and endomyocardial fibrosis. Findings on physical exam depend on the stage or severity of myocardial involvement. An S3 is almost always present, and an S4 is often heard.

Which of the following conditions is associated with a pericardial knock on auscultation? Acute pericarditis Constrictive pericarditis Pericardial tamponade Restrictive cardiomyopathy

Constrictive pericarditis Constrictive pericarditis is associated with a pericardial knock. On cardiac auscultation, an early diastolic sound, the pericardial knock, may be heard at the apex 60 to 120 msec after the second heart sound (S2). The pericardial knock sounds like a ventricular gallop but occurs earlier than the S3 of heart failure, which it may mimic. The knock is due to accelerated right ventricular inflow in early diastole and early myocardial distention, followed by an abrupt slowing of further ventricular expansion. There is usually no pericardial friction rub. Constrictive pericarditis is pathologically distinct from acute pericarditis. Constrictive pericarditis is caused by the resultant inflammatory and reparative process from a pericardial injury. This leads to a fibrous thickening of the pericardium. Clinical presentation mimics heart failure and restrictive cardiomyopathy. Physical exam is associated with Kussmaul's sign (inspiratory neck vein distention) and pulsus paradoxus. Severe cases require surgical treatment with a pericardiectomy. Acute pericarditis (A) is associated with a pericardial friction rub. It is best heard with the diaphragm of the stethoscope at the lower left sternal border or apex when the patient is sitting and leaning forward or in the hands-and-knees position. The classic cardiac auscultation findings of pericardial tamponade (C) include distant heart or soft heart sounds. Restrictive cardiomyopathies (D) result from systemic disorders such as amyloidosis, sarcoidosis, hemochromotosis, scleroderma, carcinoid heart disease, and endomyocardial fibrosis. Findings on physical exam depend on the stage or severity of myocardial involvement. An S3 is almost always present, and an S4 is often heard.

Which cardiac disorder is similar to restrictive cardiomyopathy?

Constrictive pericarditis, which is caused by viral or TB infection, uremia, radiation and post-cardiac-surgery fibrosis.

While performing a routine physical examination, a provider notices a distinct decrease in the strength of the patient's radial pulse during inspiration. Which of the following conditions does this patient likely have? Constrictive pericarditis Diabetes mellitus Subclavian steal syndrome Tietze syndrome

Constructive pericarditis Pulsus paradoxus is an abnormally large decrease in systolic blood pressure and pulse wave amplitude during inspiration. The normal fall in pressure is less than 10 mm Hg. When the drop is more than 10 mm Hg, it is referred to as pulsus paradoxus. Pulsus paradoxus has nothing to do with pulse rate or heart rate. As a breath is taken in, the negative intrathoracic pressure within the chest increases venous return to the right side of the heart (increases right ventricular volume). Under normal circumstances, the right ventricle is able to expand into the pericardial space and has very little impact on the left ventricle. Pulsus paradoxus is a sign that is indicative of several conditions, including cardiac tamponade, constrictive pericarditis, chronic sleep apnea, croup, and obstructive lung disease. The paradox in pulsus paradoxus is that, on clinical examination, one can detect beats on cardiac auscultation during inspiration that cannot be palpated at the radial pulse. It results from an accentuated decrease of the blood pressure (due to reduced stroke volume), which leads to the radial pulse not being palpable and may be accompanied by an increase in the jugular venous pressure height (Kussmaul's sign). As is usual with inspiration, the heart rate is slightly increased, due to decreased left ventricular output. Diabetes mellitus (B), subclavian steal syndrome (C), and Tietze syndrome (D) are not associated with pulsus paradoxus.

You are managing the blood pressure of a 49-year-old Caucasian woman with enalapril 20 mg twice a day. She does not have diabetes or chronic kidney disease. She has been taking the enalapril for over 1 month. Repeated blood pressure readings in both arms average out to 138/96. Which of the following is the most appropriate treatment at this time? Continue enalapril and add amlodipine Continue enalapril and add losartan Continue enalapril and add nothing, as she is at goal with just one medication Double the dose of enalapril

Continue enalapril and add amlodipine According to JNC-8, first-line antihypertensives in the African-American population include thiazide-type diuretics (TTD) or calcium channel blockers (CCB), while first-line medications in the non-African-American population include thiazide-type diuretics (TTD) or calcium channel blockers (CCB), in addition to angiotensin-converting enzyme inhibitors (ACEI) or angiotensin receptor blockers (ARB). If the blood pressure goal is not achieved during one month of treatment, clinicians should increase the dose of the first drug, or continue the first drug and add a second drug. The patient above is already taking max dose enalapril. Therefore, a second agent (e.g. amlodipine) should be added to her regimen. If two drugs fail, a third drug should be added. If three drugs fail, or contraindications limit the use of any combination of the above four drugs, other antihypertensives can be used. These include alpha1-blockers, alpha2-agonists, beta-blockers, loop diuretics, aldosterone-receptor-blockers, adrenergic neuronal depleting agents and vasodilators. Furthermore, the clinician should consider referral to a hypertension specialist if 4 drugs are necessary to achieve a goal pressure. ACEIs and ARBs, like losartan (B), should never be used together. She is < 60 years old, and does not have DM or chronic kidney disease. Proper blood pressure goal is < 90 mm Hg diastolic. There is insufficient evidence to recommend a systolic goal in this age group, however, the consensus is to use < 140/90 mm Hg as a final goal (C) in those < 60 years of age. She is already at the maximum target dose of enalapril (40 mg per day). Doubling this dose (D) is not recommended, but adding a second class is.

You are managing the blood pressure of a 49-year-old Caucasian woman with enalapril 20 mg twice a day. She does not have diabetes or chronic kidney disease. She has been taking the enalapril for over 1 month. Repeated blood pressure readings in both arms average out to 138/96. Which of the following is the most appropriate treatment at this time? Continue enalapril and add amlodipine Continue enalapril and add losartan Continue enalapril and add nothing, as she is at goal with just one medication Double the dose of enalapril

Continue enalapril and add amlodipine According to JNC-8, first-line antihypertensives in the African-American population include thiazide-type diuretics (TTD) or calcium channel blockers (CCB), while first-line medications in the non-African-American population include thiazide-type diuretics (TTD) or calcium channel blockers (CCB), in addition to angiotensin-converting enzyme inhibitors (ACEI) or angiotensin receptor blockers (ARB). If the blood pressure goal is not achieved during one month of treatment, clinicians should increase the dose of the first drug, or continue the first drug and add a second drug. The patient above is already taking max dose enalapril. Therefore, a second agent (e.g. amlodipine) should be added to her regimen. If two drugs fail, a third drug should be added. If three drugs fail, or contraindications limit the use of any combination of the above four drugs, other antihypertensives can be used. These include alpha1-blockers, alpha2-agonists, beta-blockers, loop diuretics, aldosterone-receptor-blockers, adrenergic neuronal depleting agents and vasodilators. Furthermore, the clinician should consider referral to a hypertension specialist if 4 drugs are necessary to achieve a goal pressure. ACEIs and ARBs, like losartan (B), should never be used together. She is < 60 years old, and does not have DM or chronic kidney disease. Proper blood pressure goal is < 90 mm Hg diastolic. There is insufficient evidence to recommend a systolic goal in this age group, however, the consensus is to use < 140/90 mm Hg as a final goal (C) in those < 60 years of age. She is already at the maximum target dose of enalapril (40 mg per day). Doubling this dose (D) is not recommended, but adding a second class is.

The emergency department staff began treatment for a woman who presented with chest pain. The pain is described as retrosternal, worse with minimal activity, better with rest, sharp in character and 9/10 in intensity. You are paged to admit her to the intensive care unit under the working diagnosis of unstable angina. Her vitals have remained stable after beginning antiplatelet, antihypertensive and antithrombotic medications. Two hours after admission, a repeat history and physical and review of available test results offers the following information: Serial electrocardiograms reveal increasing R wave amplitude; An echocardiogram calculates an ejection fraction of 50%; Angina is reported as 9/10 in intensity; Atrial natriuretic peptide levels are elevated. Which of the following historical facts would prompt you to immediately consult interventional cardiology for invasive coronary revascularization? 50% ejection fraction Continued chest pain Elevated atrial natriuretic peptide R wave progression

Continued chest pain Patients with unstable angina are mostly admitted to a critical care unit after initial presentation. There, an anti-ischemic regimen, if not already begun, is initiated. This typically includes oxygen, nitrates, analgesics and beta-blockers. Serial monitoring for new dysrhythmias, recurrent ischemia, dynamic electrocardiography, changing laboratory results and worsening angina is necessary to maximize patient outcomes. Further management includes risk stratification to determine if early invasive treatment is appropriate. High-risk indicators that favor early invasive treatment strategies include hemodynamic instability, elevated troponin I or T levels, a history of CABG, a history of percutaneous coronary intervention (PCI) within the past 6 months, recurrent angina despite anti-ischemic therapy, symptoms of congestive heart failure (S3, pulmonary edema, crackles, mitral regurgitation) or an ejection fraction < 40%. An ejection fraction < 40%, not 50% (A), favors early invasive treatment of unstable angina. Whereas elevated B-type natriuretic peptide is associated with poor outcomes in patients with unstable angina, atrial natriuretic peptide (C) is not. It is however responsible for water, sodium and potassium homeostasis. Its action is opposite of aldosterone. R wave progression (D) is not indicative of invasive management of unstable angina. New or presumably new ST depression is, however.

What is the name of the rapid quick arterial pulse seen in aortic regurgitation?

Corrigan's pulse.

Which virus is the most common cause of acute viral pericarditis?

Coxsackie virus.

What is the diagnostic murmur auscultated in aortic stenosis?

Crescendo-decrescendo systolic murmur.

Which of the following describes the correct management of aortic dissection? All aortic dissections eventually need surgical or endovascular repair Crystalloids are the preferred treatment of hypotension in the setting of aortic dissection Stanford type A dissections should be managed chronically with negative inotropes Vasodilators are the preferred treatment of hypertension in the setting of aortic dissection

Crystalloids are the preferred treatment of hypotension in the setting of aortic dissection Aortic dissection is an uncommon but life-threatening phenomenon that occurs when damage of the intima allows the entry of blood between the intima and media, creating a false lumen. The most important risk factor for aortic dissection is hypertension. Aortic dissection has a bimodal age distribution, with a peak under 40 years of age associated with connective tissue disorders and another peak at greater that 50 years of age associated with chronic hypertension. CT angiogram is the gold standard for diagnosis of dissection. Aortic dissections are defined by their anatomic locations, with Stanford Type A dissections involving the ascending aorta and Stanford Type B dissections involving only the descending aorta. Control of hypertension and heart rate are the cornerstones of acute management of aortic dissection. Negative inotropes are the preferred agents for the control of hypertension in aortic dissection. This is due to their ability to lower blood pressure without increasing heart rate, which would increase shearing force against the intimal flap and lead to propagation of the dissection. Short-acting beta-blockers such as labetalol, esmolol, and propranolol are the first line agents. Calcium channel blockers can be used in the event of contraindication to beta-blockers, though there is more limited literature on their use in this setting. For persistent hypertension, vasodilators such as nitroprusside or nicardipine can be used. Aortic dissection typically presents with hypertension and hypotension, when present, is a poor prognostic indicator and should be managed with crystalloids. Definitive management depends on the anatomic location of the dissection. Type A and complicated type B dissections typically require surgical repair while uncomplicated type B dissections are typically medically managed. Uncomplicated Stanford Type B dissections can be managed chronically with negative inotropes and do not need surgical or endovascular repair (A). Stanford Type A dissections, which involve the ascending aorta, need emergent surgical or endovascular repair and cannot be managed chronically with negative inotropes (C). Negative inotropes are first line agents for hypertension in the setting of aortic dissection as vasodilators (D) can cause a rebound tachycardia that increases shear force on the aorta.

What are some examples of newer oral anticoagulation agents?

Dabigatran, apixaban, rivaroxaban, edoxaban.

Orthostatic Hypotension

Decrease in systolic blood pressure ≥ 20 • Decrease in diastolic blood pressure ≥ 10 • Inadequate physiologic response to postural changes

You prescribe ramipril to a 65-year-old man with uncontrolled hypertension and severe renovascular disease. At a follow-up visit four weeks later his creatinine is noted to be 2.3. His creatinine before starting the ramipril was 1.0. By what mechanism did the ACE inhibitor cause this change? Activating the arachidonic acid pathway Decreasing glomerular blood flow Increasing angiotensin II activity Increasing serum kinin levels

Decreasing glomerular blood flow One of the actions of angiotensin II is to vasoconstrict efferent arterioles as they leave the glomerulus. This vasoconstriction stabilizes renal perfusion pressure and helps maintain normal creatinine levels. ACE Inhibitors block the conversion of angiotensin I to angiotensin II which causes a modest reduction in renal blood flow. This reduction may be severe in patients with bilateral renal artery stenosis, hypertensive nephrosclerosis, congestive heart failure, polycystic kidney disease or chronic kidney disease. In all of these cases renal perfusion is already compromised. By blocking angiotensin II with an ACE inhibitor, glomerular blood flow is decreased even further thus worsening the patient's creatinine. Activation of the arachidonic acid pathway (A) and increased serum kinin levels (D) are thought to be involved in the classic ACE inhibitor cough. Increased angiotensin II (C) activity would increase renal perfusion pressure and stabilize the creatinine, not worsen it.

A woman with known coronary artery disease presents to the ED with chest pain and ventricular tachycardia. Five minutes after admission she becomes unresponsive. Her rhythm strip is seen above. Which of the following is the most appropriate intervention? Beta-blockade Cardioversion Defibrillation Vasopressin

Defibrillation Ventricular fibrillation is the most common dysrhythmia in cardiac arrest patients. Instead of coordinated ventricular depolarization and contraction, ventricular fibrillation (VF) is characterized by rapid disorganized excitation potentials that amount to ineffective contraction. VF occurs with acute infarct or ischemia as well as old infarct or ischemia. Common triggers include electrocution, myocardial ischemia, and hypoxia. Electrocardiographically, VF appears as a chaotic, disorganized waveform that has no discernible typical morphology. Ventricular fibrillation is incompatible with life. Treatment is with immediate defibrillation. Vasopressin (D) was previously part of the ACLS protocol for pulseless ventricular tachycardia (pVT) and ventricular fibrillation (VF). However, the new 2015 AHA guidelines, have removed vasopressin all together. Beta-blockers (A) are not indicated for VF. Cardioversion (B) is only used in patients with organized electrical activity and who have a pulse.

What is beriberi?

Deficiency of thiamine (vitamin B1).

What are some triggers that can precipitate cardiac arrest in long QT syndrome?

Depending on the specific channel affected, various triggers can precipitate cardiac arrest including exercise, sudden loud noises or sleep.

According to JNC-8, special attention is given to which two diseases in hypertensive patients ≥ 18 years old?

Diabetes and chronic kidney disease (goal is < 140/90 mm Hg, no matter what age over 18 years).

A 68-year-old woman presents to the ED with chest pain. It occurs at rest, and has been getting worse over the past 2 hours. Her past medical history includes COPD, GERD, diabetes, urinary incontinence and Factor V Leiden. Her past surgical history is significant for carpal tunnel release four years ago and total hip arthroplasty 18 months ago. Blood pressure is 168/118 mm Hg, heart rate is 100 BPM and oxygen saturation is 95% on room air. An electrocardiogram reveals ST-elevation. An initial cardiac panel shows a positive troponin level. In this scenario, which of the following in this patient is a relative contraindication to fibrinolytic therapy? Diastolic blood pressure Factor V Leiden Gastroesophageal reflux disease Total hip arthroplasty

Diastolic blood pressure These symptoms are concordant with acute coronary syndrome, notably, acute ST-elevation myocardial infarction. While percutaneous coronary intervention is recommended, it is not always possible, due to facility abilities and services. In addition, fibrinolytic therapy is recommended, as ST elevation is indicative of complete coronary thrombotic obstruction. There are however absolute and relative contraindications to this type of therapy as the risk of internal hemorrhage could produce catastrophic events. Absolute contraindications include a history of any intracranial hemorrhage, cerebral vascular structural lesions or intracranial neoplasm. Others include ischemic stroke or head or facial trauma within the past 3 months and active bleeding or bleeding diathesis. Relative contraindications include systolic BP ≥ 180 or diastolic BP ≥ 110 mm Hg, as well as uncontrolled chronic hypertension, pregnancy and anticoagulant use. This patient's DBP is 118 mm Hg, above the recommended 100 mm Hg. Bleeding diatheses (tendency or predisposition), such as von Willebrand's disease and Factor V deficiency, are absolute contraindications to fibrinolytics. Factor V Leiden (B) is a pro-thrombotic coagulopathy, not a bleeding diathesis. As such, this is not a contraindication. Active peptic ulcer disease, not GERD (C), is a relative contraindication to fibrinolytic therapy. Major surgery, such as total hip arthroplasty (D), is a relative contraindication if it occurred within 3 weeks of acute coronary symptom onset.

Which value has greater influence on the mean arterial pressure, the diastolic or systolic blood pressure?

Diastolic blood pressure.

Syncope

Differentiate between syncope and seizure • ECG for all • San Francisco Syncope Rule (high-risk criteria): CHESS . ​CHF . Hematocrit <30% . ECG abnormal . SOB . Systolic BP <90 mm Hg • Adolescent athlete + syncope: HOCM • Young woman + abdominal pain + syncope: ectopic pregnancy • Older male + abdominal/flank pain + syncope: AAA • Sudden onset severe HA + syncope: SAH • Woman + prodrome of nausea, sweating, warmth + syncope: vasovagal • Malignancy + sudden onset SOB + syncope: PE

Which drug used for the treatment of heart failure has been shown to reduce hospitalizations, but has no effect on mortality?

Digoxin

An elderly man with congestive heart failure presents to the ED with a complaint of "not feeling normal." He is on several different medications. His ECG is shown above. Which of the following medications is the most likely cause of this ECG abnormality? Digoxin Furosemide Metoprolol Warfarin

Digoxin Digoxin is a cardiac glycoside derived from the foxglove plant. It is used to increase the force of myocardial contraction in systolic heart failure and to decrease AV nodal conduction in atrial fibrillation. It works by inactivating the Na+ K+ ATPase pump on the cardiac cell membrane which leads to increased intracellular calcium and extracellular potassium. In individuals taking digoxin, there is a characteristic ECG pattern commonly referred to as the "digoxin effect." The presence of the "digoxin effect" on the ECG is not a marker of toxicity, rather it indicates that the patient is taking digoxin. The "digoxin effect" is characterized by (1) downsloping ST depression with a characteristic "slurred" appearance; (2) flattened, inverted, or biphasic T waves; (3) shortened QT interval. The overall morphology is commonly compared to the shape of a mustache. Furosemide (B) is a diuretic that is not directly related to changes in ECG morphology. However, in extreme cases it can lead to electrolyte abnormalities that are represented by ECG changes. Metoprolol (C) and other beta-blockers may cause a first-degree heart block (PR interval > 200 msec). Warfarin (D) does not affect the cardiac electrical pathway to produce ECG changes.

What is Digoxin classified as?

Digoxin is a positive ionotrope and negative chronotrope. It augments pumping while decreasing heart rate.

Which of the following conditions is associated with low output heart failure? Anemia Dilated cardiomyopathy Pregnancy Thyrotoxicosis

Dilated cardiomyopathy Low output cardiac failure is more common than high output cardiac failure. Low output failure is typically associated with a dilated cardiomyopathy, which may occur as a result of poorly controlled chronic hypertension, ischemic heart disease, or valvular heart disease. Low output failure is characterized by a decreased cardiac output (systolic dysfunction), an increase in left ventricular end-diastolic pressure, and an increased systemic oxygen extraction ratio. Anemia (A), pregnancy (C), and thyrotoxicosis (D) are associated with high output cardiac failure, which is caused by excessive demand for tissue perfusion resulting in hyperdynamic cardiac dysfunction with a supranormal cardiac output and decreased oxygen extraction ratio. Pulmonary congestion and peripheral edema occur as a result of elevated diastolic pressures. Over time, systolic myocardial dysfunction occurs, and patients develop classic heart failure indistinguishable from other end-stage cardiomyopathies.

You are examining an afebrile 78-year-old woman in the emergency department. During cardiac examination, you auscultate a low intensity, low pitch extra heart sound which occurs in early diastole. You do not appreciate any murmurs. Her ECG appears normal. Which of the following is the most likely diagnosis? Bacterial endocarditis Dilated cardiomyopathy Right bundle branch block Tricuspid stenosis

Dilated cardiomyopathy The third heart sound (S3) is a low-frequency, brief vibration occurring in early diastole, at the end of the rapid diastolic filling period of the right or left ventricle. It is best appreciated at the apex in the left lateral position. It may be a normal variant in patients younger than age 40. After age 40, the presence of an S3 is usually abnormal, and correlates well with ventricular dysfunction, namely volume overload. However, any cause of ventricular dysfunction may be causative: dilated or ischemic cardiomyopathy, conduction abnormalities, left-to-right intracardiac shunts, ischemic heart disease, myocarditis or valvular regurgitation. High output states, such as anemia, thyrotoxicosis or pregnancy, also are causative. Although conduction abnormalities can cause ventricular dysfunction, bundle branch block (C) is unlikely in a patient with a normal ECG. Patients with bacterial endocarditis (A) are typically febrile. These patients usually have tricuspid or mitral valve vegitations. Tricuspid stenosis (D) is a rare complication of rheumatic fever. It is associated with a diastolic murmur.

What type of cardiomyopathy is most common in patients who consume alcohol?

Dilated cardiomyopathy.

An 85-year-old woman presents with generalized weakness for five days. Her vital signs are unremarkable except for a HR of 130 bpm. Her ECG is shown above. Which of the following represents the first-line treatment for this patient? Adenosine Amiodarone Diltiazem Synchronized cardioversion

Diltiazem The patient has atrial fibrillation with rapid ventricular response. Treatment of atrial fibrillation starts by distinguishing it from other chaotic rhythms (e.g., multifocal atrial tachycardia) and recognition of any underlying causes. Asymptomatic atrial fibrillation at a rate of <100 bpm requires no specific emergent therapy. Stable patients who have a rapid ventricular response (>100 bpm) should receive rate or rhythm control. Because the onset of atrial fibrillation in this patient is unknown, rhythm control in the ED is contraindicated. Intravenous calcium channel blockers (diltiazem, verapamil) or beta-adrenergic blockers (metoprolol) are first-line rate-controlling agents for stable atrial fibrillation. Adenosine (A) is a short-acting AV-nodal blocking agent used in the treatment of AV-nodal re-entry tachycardia (AVNRT), not atrial fibrillation. Amiodarone (B) is a class III antidysrhythmic that is used for the treatment of both ventricular and supraventricular dysrhythmias. It has the ability to cardiovert an irregular rhythm (atrial fibrillation) and should be avoided in this patient. In addition, amiodarone has an unfavorable side effect profile compared to calcium channel blockers. Synchronized cardioversion (D) should not be performed for atrial fibrillation when the exact onset is unknown. Patients should undergo an echocardiogram to evaluate for an atrial thrombus prior to cardioversion. However, in the unstable patient, the benefit of cardioversion outweighs the risk of thromboembolism, and cardioversion is indicated.

Which two calcium channel blockers should be used most cautiously in conjunction with beta-blockers due to the increased risk of AV conduction depression?

Diltiazem and verapamil, the two nondihydropyridine calcium channel blockers, pose the greatest risk of depressing AV node conduction and sinus node automaticity when combined with beta-blockers.

A 67-year-old man with diabetes mellitus, chronic lower back pain and previously stable systolic heart failure now has increasing orthopnea and shortness of breath. Physical exam reveals pulmonary crackles, jugular venous distention and lower extremity edema. He is on carvedilol, lisinopril, furosemide, insulin and ibuprofen. Which of the following is appropriate for management of this patient? Add a calcium channel blocker Decrease the dosage of furosemide Discontinue the carvedilol Discontinue the ibuprofen

Discontinue the ibuprofen Non-steroidal anti-inflammatory drugs (e.g. ibuprofen) can worsen symptoms of heart failure. In fact, a number of medications that are in common clinical use are relatively or absolutely contraindicated in patients with heart failure. This is either because they can cause exacerbations of heart failure or because there is a higher risk of adverse events in such patients. Mechanisms by which some of these drugs can exacerbate heart failure relate to sodium retention, negative inotropic effects or direct cardiotoxicity. Non-steroidal anti-inflammatory drugs are associated with an increased risk of heart failure exacerbation, increased renal dysfunction and impairment of the response of angiotensin converting enzyme inhibitors and diuretics. Observational data has reported an association with non-steroidal anti-inflammatory drugs and increased mortality in patients with heart failure. It would not be correct to add a calcium channel blocker (A) as this class of medication has no direct role in the management of heart failure. Some studies have shown that their negative inotropic activity cause a greater clinical deterioration when compared to placebo, particularly with the first generation, non-dihydropyridines calcium channel blockers. It would also not be appropriate to decrease the dose of furosemide (B) as this patient is volume overloaded and needs diuresis to help alleviate his symptoms. It would not be appropriate to discontinue carvedilol (C) at this time. Although, generally, starting beta blocker therapy is not recommended in patients with decompensated heart failure, it is okay to continue beta blocker therapy if the patient has been previously stable on this medication.

A 58-year-old African-American man with a history of hypertension presents to your office for his annual exam. His BP is 145/95 and HR is 75. He is taking lisinopril as previously prescribed. Based on the most recent hypertension guideline, which of the following is the most appropriate next step in his management? Continue the lisinopril and start the patient on an angiotensin receptor blocker Continue the lisinopril and start the patient on hydrochlorothiazide Discontinue the lisinopril and start the patient on an angiotensin receptor blocker Discontinue the lisinopril and start the patient on hydrochlorothiazide

Discontinue the lisinopril and start the patient on hydrochlorothiazide The Report From the Panel Members Appointed to the Eighth Joint National Committee (JNC 8) provides the most updated guideline for treatment of hypertension. One change from the previous guideline, JNC 7, is the differentiation of drug therapy recommendations based on race. For the general African-American population, initial therapy includes a thiazide-type diuretic or calcium channel blocker. For the general non-black population, initial therapy includes a thiazide-type diuretic, calcium channel blocker, angiotensin receptor blocker, or ACE-inhibitor. ACE-inhibitors (A and B) are not recommended as first line treatment for the general African-American. Angiotensin receptor blockers (C) are also not first line treatment for this patient because of his race.

A 21-year-old woman with a history of intravenous drug abuse presents with fever, dyspnea, cough and chest pain. Examination reveals an ill-appearing woman with track marks on both upper extremities. A chest X-ray reveals no infiltrate and urinalysis is unremarkable. What management is indicated? Discharge with a prescription for azithromycin for a respiratory infection Draw blood cultures and admit for intravenous antibiotics and transthoracic echo Draw blood cultures and admit for intravenous antibiotics and valvuloplasty Start antibiotics for community acquired pneumonia and admit

Draw blood cultures and admit for intravenous antibiotics and transthoracic echo This patient's presentation is concerning for infective endocarditis and should have a minimum of three blood cultures drawn, started on intravenous antibiotics and ordered for a transthoracic echocardiogram (TTE). If the TTE is negative, the patient, since she is high risk (IVDA), should undergo a transesophageal echocardiogram (TEE). Infective endocarditis is a life-threatening disorder that most frequently occurs in patients with specific risk factors including a history of rheumatic heart disease, prosthetic cardiac valves and intravenous drug abuse (IVDA). There are a number of causative organisms for bacterial endocarditis but staphylococcus (42%) and streptococcus species (40%) are the most predominant. Staphylococcus species are most common in patients with IVDA. Additionally, the valve involved differs based on population factors as well. Patients with IVDA are more likely to develop right-sided (tricuspid and pulmonic valve) bacterial endocarditis. Patients with right-sided endocarditis typically have an acute presentation with fever, and respiratory symptoms as well as chest pain. Septic emboli can travel to the lung causing multifocal pneumonia but peripheral septic embolic events are rarely seen (as opposed to left-sided endocarditis). Right-sided endocarditis is often misdiagnosed as pneumonia due to the presence of respiratory symptoms. Additionally, less than 35% of patients with IVDA and endocarditis will present with a murmur. In this population, an unexplained fever should raise concern for bacterial endocarditis. TEE is the diagnostic modality of choice as it is highly sensitive and specific for diagnosing infective endocarditis. In patients without prosthetic valves, the negative predictive value of TEE approaches 100%. In patients with native valves and a history of IVDA, vancomycin can be started as single treatment. Although the patient has a predominance of respiratory features, the presence of fever and IVDA makes endocarditis a distinct possibility and the patient should not be discharged with the diagnosis of a respiratory infection (A). Valvuloplasty (C) uses a balloon catheter to open a stenotic valve. This is most often performed for aortic stenosis. Although this patient may one day require a valvuloplasty, it is not performed in the early stages of endocarditis. Fever, cough and chest pain may be consistent with pneumonia and early in the clinical course, the chest X-ray may not reveal an infiltrate. However, this patient is at high-risk for infective endocarditis and treatment for pneumonia (D) would not be appropriate.

A patient presents 2 weeks following a myocardial infarction. He complains of chest pain that improves with leaning forward, fever, and malaise. Vital signs are BP 125/70, HR 105, RR 14, and pulse oxygenation 98% on room air. Lab results reveal a leukocytosis and negative troponin. ECG shows sinus tachycardia. Which of the following is the most likely diagnosis? Acute myocardial infarction Bacterial pneumonia Dressler's syndrome Spontaneous pneumothorax

Dressler's syndrome Dressler's syndrome or postcardiotomy pericarditis is due to an inflammatory reaction to transmural myocardial necrosis. It usually presents as a recurrence of pain with pleural-pericardial features. On physical exam, a friction rub may be heard. The troponin may be residually elevated from the initial myocardial infarction. It can occur from 2-10 weeks post-myocardial infarction. Treatment is with NSAIDs, colchicine and steroids. The patient's ECG and troponin do not reveal any evidence of acute ischemia. Therefore it is unlikely the patient is experiencing an acute myocardial infarction (A). It is possible for the troponin to be residually elevated from the initial myocardial infarction. Bacterial pneumonia (B) is associated with fever and cough with yellow or rusty colored-sputum. Patients may experience pleuritic chest pain, but typically it is not affected by position. Spontaneous pneumothorax (D) is associated with decreased breath sounds on the side of the pneumothorax. It is not associated with fever or leukocytosis.

An elderly woman presents with intermittent leg pain. She states it is a burning heaviness that is not necessarily associated with activity. Inspection reveals several dilated and tortuous veins about the lower legs. The skin is edematous and speckled with dark brown areas of capillary dilation but no specific pallor. Distal motor and sensory examinations are intact. Which of the following is the most appropriate initial tests in the evaluation of these symptoms? Angiography Coagulation panel Duplex ultrasonography Electrodiagnostics

Duplex ultrasonography Venous insufficiency, mainly due to incompetent or absent venous valves, can lead to retrograde blood flow in the superficial or deep venous systems. Ultimately, this leads to the syndrome of chronic venous insufficiency, which is marked by poor cosmesis, pain, lipodermatosclerosis, ulceration and life-threatening infections. The pain is usually described as burning, cramping or heaviness that occurs constantly in almost 20%, and episodically in almost 50% of sufferers. Chronic venous stasis or hypertension causes the characteristic skin changes of capillary proliferation, red or brown coloring, fat necrosis and fibrosis. These may be associated with edema, cellulitis, ulceration and cutaneous infarction. Although typical, these physical findings are only suggestive of the condition. Any suspicion is best evaluated initially with duplex ultrasonography. Angiography (A) is the test of choice for patients with suspected arterial insufficiency and peripheral arterial occlusion disorder. These conditions are more commonly associated with pain with activity and skin pallor, atrophy and shiny appearance. A coagulation panel (B) is usually performed as a baseline test before initiating anticoagulation in a patient with documented deep venous thrombosis. The above symptoms do not confirm, but merely suggest, venous insufficiency, which may be due to superficial or deep venous thrombosis. A diagnosis needs to be made before preparing for treatment. Electromyography and nerve conduction studies (D) are recommended for those with complaints and findings of distal neuropathy or myopathy, not venous insufficiency.

A 32-year-old woman presents to the ED complaining of right calf swelling for one week. She is one week postpartum following an uneventful full-term vaginal delivery. She denies any chest pain, dyspnea, or cough. On examination, her right calf is 16 cm in circumference; her left calf is 10 cm. Which of the following is the most accurate test to confirm the diagnosis? Computed tomography D-dimer assay Duplex ultrasound Impedance plethysmography

Duplex ultrasound Duplex ultrasonography is currently the first-line imaging study to diagnose deep vein thrombosis (DVT) because of its relative ease of use, the absence of irradiation or contrast material, and a high degree of accuracy. In patients with clinically suspected disease, compression ultrasonography is 95%-99% sensitive for proximal venous thrombus. D-dimer (B) levels remain elevated in DVT for about seven days. Patients presenting late in the course, after clot organization and adherence have occurred, may have low levels of D-dimer. Similarly, patients with isolated calf vein DVT may have a small clot burden and low levels of D-dimer below the analytic cut-off value of the assay. This accounts for the reduced sensitivity of the D-dimer assay in the setting of confirmed DVT. In some countries, impedance plethysmography (IPG) (D) has been the initial noninvasive diagnostic test of choice and has been shown to be sensitive and specific for proximal vein thrombosis. However, IPG has several limitations, including insensitivity for calf vein thrombosis, non-occluding proximal vein thrombus, and iliofemoral vein thrombosis above the inguinal ligament. Computed tomography (A) can identify intravascular thrombi through demonstration of a filling defect with contrast-enhancement. There are few studies evaluating the true sensitivity of this test, but the current studies show that it can be as sensitive as 95% in diagnosis of DVT.

An elderly man presents with 6 months of progressive positional dyspnea. Nine months ago, he had a mild heart attack and was properly treated. Today, you appreciate a new loud, blowing holosystolic murmur heard at the apex. Which of the following color Doppler echocardiography findings would you most expect to find based on these signs and symptoms? During diastole, blood flows from the right ventricle into the right atrium During diastole, blood is seen flowing from the aorta into the coronary arteries During systole, blood flows from the left ventricle into the aorta During systole, blood is seen flowing from the left ventricle into the left atrium

During systole, blood is seen flowing from the left ventricle into the left atrium One of the most common cardiac valve abnormalities is mitral regurgitation (MR). Also known as mitral insufficiency, it can be caused by rheumatic fever, myocardial infarction, ruptured chordae or papillary muscles and cardiac myxomatous degeneration. In fact, the most common cause of mitral regurgitation is the myxomatous breakdown of this valve's connective tissue, a condition called mitral valve prolapse. Mitral prolapse can be heard at the apex and the left sternal border best when the patient is seated, and is typically described as a late systolic murmur preceded by an earlier systolic click. However, mitral regurgitation, also heard best at the apex is described as a holosystolic, plateau-shaped, loud blowing murmur, which may be associated with an apical thrill. An echocardiogram is used to confirm the diagnosis, the key finding of which is a stream of blood flowing out of the left ventricle into the left atrium during systole. Symptoms depend on presentation, acute or chronic. Acute MR includes dyspnea, orthopnea, pulmonary edema, poor exercise tolerance, palpitations and cardiogenic shock. Acute cases are mainly infectious in nature. Chronic compensated cases may be asymptomatic, whereas volume-overloaded decompensated cases will shows signs of congestive heart failure. Chronic cases are usually treated with ACE-inhibitors and hydralazine, the combination of which can effectively delay valve replacement surgery. Indications for surgery in chronic cases depends on the ejection fraction, the presence of new onset atrial fibrillation or severe pulmonary hypertension. Normally during diastole, the blood that was just pumped out of the left ventricle pushes back, closes the aortic valve and enters the ostia of the coronary arteries (B). Most of coronary blood flow occurs during diastole. During diastole, blood normally flows from the right atrium into the right ventricle (A), not vice-versa. During systole, blood normally flows out of the left ventricle into the aorta (C).

Which of the following is commonly the first reported symptom of aortic stenosis? Chest pain Dyspnea Syncope Vomiting

Dyspnea In aortic stenosis, structural damage to the aortic valve obstructs ventricular outflow. The most common cause of aortic stenosis in the United States is degenerative calcification, also known as calcific aortic stenosis. Incidence is associated with traditional cardiovascular risks factors of age, hypertension, hyperlipidemia, diabetes, and tobacco use. Bicuspid aortic valves, in which the normal trileaflet aortic valve has only two leaflets, is another cause of aortic stenosis, particularly in younger individuals. Worldwide, rheumatic heart disease is a major cause of aortic stenosis. When aortic stenosis develops, there is typically a long asymptomatic period, during which the left ventricular hypertrophies to compensate for the outflow obstruction, and cardiac output is preserved. However, when ventricular wall is so thickened as to impede diastolic filling, cardiac output is decreased and symptoms appear. The classic triad of aortic stenosis is known by the acronym SAD: syncope, angina, and dyspnea. Dyspnea is often the first symptom to appear, followed by chest pain, and then syncope (classically with exertion) and clinical signs and symptoms of heart failure. The characteristic murmur of aortic stenosis is a harsh systolic ejection murmur heard best at the right second intercostal space radiating to the carotids. A narrowed pulse pressure may also be present. Chest pain (A) usually develops after dyspnea. Syncope (C) is a late finding of aortic stenosis. Vomiting (D) is not a typical symptoms of aortic stenosis.

A patient is found to have a low pitched rumbling diastolic apical murmur. Which of the following is the most frequent presenting complaint associated with this murmur? Chest pain Dyspnea with exertion Hemoptysis Palpitations

Dyspnea with exertion Mitral stenosis is characterized by left ventricular inflow obstruction resulting in a low pitched rumbling diastolic apical murmur. Rheumatic heart disease is the most common cause worldwide. Valvular obstruction develops slowly over time, taking decades to become symptomatic. Less common causes of mitral stenosis include congenital mitral stenosis and mitral annular calcification. Mitral valve obstruction causes elevated left atrial pressures resulting in left atrial enlargement and pulmonary hypertension. Dyspnea with exertion is the most common presenting complaint, found in up to 70% of patients. It is exacerbated by factors that increase cardiac demand (eg. fever, anemia, pregnancy). As the degree of stenosis increases, less exertion is necessary to produce symptoms and orthopnea can occur. Chest pain (A) is an uncommon complaint in mitral stenosis. Hemoptysis (C) due to bronchial vein rupture can occur in mitral stenosis but is less common. Palpitations (D) can occur secondary to atrial fibrillation which is a common complication of mitral stenosis. The prevalence of atrial fibrillation increases with higher degrees of stenosis, advanced age and the presence of other valvular abnormalities. Patients with atrial fibrillation require rate control and anticoagulation.

Heart Block: Third Degree

ECG will show P waves "march through" QRS complexes. • Treatment is pacemaker • Comments: P-P and R-R rate intervals will be regular without dropped beats

Heart Block: First Degree

ECG will show PR interval > 200 msecs with regular rhythm • Treatment is not necessary • Comments: most common conduction disturbance and usually represents an incidental finding on an ECG

Torsades de Pointes (TdP)

ECG will show rhythm > 100 beats per minute and frequent variation in the QRS axis and morphology • Most commonly caused by acquired or congenital long QT interval syndrome • Treatment is . Unstable: defibrillation . Stable: intravenous magnesium sulfate and stopping the offending drug

Wolff-Parkinson-White (WPW) Syndrome

ECG will show short PR interval, delta wave, wide QRS • Most commonly caused by an accessory pathway (bundle of Kent) connects atria to ventricles, bypassing AV node • Definitive treatment is radiofrequency ablation

Left Bundle Branch Block

ECG will show: • Wide QRS >.12 sec • Broad, slurred R in V4 and V6 • Deep S in V1 and V2 • ST elevations in V1 - V3 • Comments: New LBBB + Chest Pain = MI until proven otherwise

Which of the following features can differentiate myocardial infarction from pericarditis? Chest pain ECG with reciprocal changes ECG with ST-segment elevations T wave flattening

ECG with reciprocal changes Reciprocal ST-segment depressions should never be seen in patients with pericarditis and an ECG with this finding should always be assumed to be from myocardial ischemia or infarction. There is no single best test for pericarditis but clinicians rely on the ECG as the best tool. Early in the disease, the ECG findings of acute pericarditis can mimic those of acute myocardial infarction (MI). The differentiation is critical as timely treatment of MI improves outcomes. Additionally, thrombolytic therapy should not be given to patients with pericarditis as it may precipitate hemorrhage into the pericardial space. Chest pain (A), ST-segment elevation (C) and T wave flattening (D) can be seen in both pericarditis and MI.

A 5-year-old girl with Turner syndrome is found to have systolic hypertension. Further examination reveals diminished femoral pulses. Which of the following is the best initial test for establishing the most likely diagnosis? Cardiac catheterization Chest X-ray Echocardiogram Electrocardiogram

Echocardiogram Patients with Turner syndrome are at increased risk for coarctation of the aorta and should have an echocardiogram to establish the diagnosis and determine the severity of the stenosis. Coarctation of the aorta is defined as a narrowing of the aorta. Most cases of coarctation of the aorta are congenital and associated with other congenital cardiac defects. Acquired cases are usually due to an inflammatory disease, such as Takayasu arteritis. Approximately 30% of patients with Turner syndrome have a coarctation. In order to maintain normal systolic function, several compensatory mechanisms arise to overcome the left ventricular outflow tract obstruction. These mechanisms include left ventricular hypertrophy and the development of collateral blood flow to circumvent the lesion. Systolic hypertension and diminished or delayed femoral pulses are classic physical exam findings. Older children and adults may complain of chest pain, cold extremities, and claudication. If collateral flow has had time to develop, a continuous murmur may be heard over the left anterior chest or left midline back. Initial diagnostic studies include electrocardiography, chest radiography, and echocardiography. Chest radiography may reveal notching of the ribs. In most patients, echocardiography with Doppler can establish the diagnosis, determine the severity, and evaluate for additional defects without the need for further imaging studies. Computed tomography and magnetic resonance imaging may be required in adults for complete evaluation of the thoracic aorta. Patients with coarctation of the aorta should be referred to a cardiovascular surgeon for evaluation. Accelerated coronary artery disease, aortic dissection, stroke, and heart failure are common complications in patients who do not undergo surgical repair for the lesion. Because of the invasive nature, cardiac catheterization (A) is typically performed in conjunction with therapeutic intervention. Cardiac catheterization involves inserting a catheter into an artery and then maneuvering the catheter into the aorta and left side of the heart. Relative contraindications for cardiac catheterization include severe, uncontrolled hypertension, dysrhythmias, allergy to contrast dye, and severe coagulopathy. A chest X-ray (B) and electrocardiogram (D) can both be used in the initial evaluation for coarctation of the aorta; however, both tests may be normal or have nonspecific findings. In adolescents and adults, the electrocardiogram may show left ventricular hypertrophy. Depending upon the degree of stenosis and resulting heart failure, chest radiography may show cardiomegaly, increased pulmonary vascular marking, or pulmonary edema. Notching of the ribs, as seen on chest radiography, is pathognomonic for coarctation of the aorta.

Which of the following will help to classify heart failure as being systolic or diastolic? Afterload Ejection fraction Heart rate Preload

Ejection fraction Ejection fraction is the percentage of blood that is ejected from the ventricle during systole. A normal ejection fraction is 55% or greater. Systolic dysfunction typically results from ischemic heart disease and myocardial cell death. It results in impaired contractility with an ejection fraction < 40%. Cardiac output is dependent on resistance (afterload) to emptying the ventricle. Diastolic dysfunction typically results from chronic hypertension and left ventricular hypertrophy. It results in impaired relaxation and ventricular filling with a normal ejection fraction. Output is dependent on ventricular filling (preload). Afterload (A) is the force needed to overcome both the volume of blood in the ventricle and the peripheral vascular resistance during ventricular contraction. The afterload is not specific for different types of heart failure. Heart rate (C) can also be variable in different types of heart failure. Preload (D) is the force or volume stretching the myocytes before contraction. It also can be thought of as the volume in the ventricle at the end of diastole just before the ventricle contracts. Output is dependent on preload in diastolic dysfunction, but it poorly differentiates diastolic from systolic heart failure.

What is the name of the ECG finding classically associated with large pericardial effusions?

Electrical alternans.

What is the treatment of hemodynamically unstable ventricular tachycardia?

Electrical cardioversion.

Which of the following is the most common cause of tricuspid regurgitation? Bacterial endocarditis Elevated right heart pressure Myxomatous degeneration Rheumatic heart disease

Elevated right heart pressure Tricuspid regurgitation refers to incompetence of the tricuspid valve leaflets such that some blood flows backwards from the right ventricle into the right atrium during systole, producing a blowing holosystolic murmur best heard at the left sternal border. Like all right heart murmurs, the murmur of tricuspid regurgitation is enhanced by inspiration. Tricuspid regurgitation is most commonly functional, caused by dilation of the right atrium or ventricle and subsequent stretching of the annulus of the valve. Pathologic tricuspid regurgitation occurs most often due to elevated right heart pressure, typically due to pulmonary problems such as COPD or pulmonary fibrosis, or volume overload. Tricuspid regurgitation can also result from seeding of the tricuspid valve with bacteria as seen in endocarditis, creating vegetations that render the valve leaflets incompetent. This is usually due to intravenous drug use, which introduces aggressive bacterial pathogens like S. aureus into circulation and the right heart. Bacterial endocarditis (A), especially from intravenous drug use, can cause tricuspid valve vegetations and incompetence. Still, primary tricuspid valve disease is less common than functional tricuspid valve disease. Myxomatous degeneration (C) is most commonly the cause of mitral valve prolapse with or without associated mitral valve regurgitation but may also be associated with the much more rare tricuspid valve prolapse. Rheumatic heart disease (D) is the most common cause of primary valvular heart disease in the non-industrialized world and usually causes mitral stenosis in the chronic setting. Tricuspid valve involvement is uncommon.

A 52-year-old man presents to discuss his elevated blood pressure. He brings in his home blood pressure readings which have been between 150-160/90-100 for the past two weeks. The patient's past medical history includes type 2 diabetes and hyperlipidemia. Which of the following is the most appropriate treatment for this patient's hypertension? Doxazosin Enalapril Furosemide Metoprolol

Enalapril The most appropriate antihypertensive agent for this patient is enalapril. Enalapril is an angiotensin-converting enzyme (ACE) inhibitor. ACE inhibitors are recommended as initial therapy for patients with hypertension and diabetes as they slow the progression of diabetic nephropathy. ACE inhibitors are also recommended as first-line agents in patients with heart failure, chronic kidney disease or history of a myocardial infarction. Doxazosin (A) is an alpha blocker which is not recommended for initial monotherapy. There may be some use for doxazosin in patients with hypertension and benign prostatic hyperplasia. Furosemide (C) is a loop diuretic which is commonly used to treat edema caused from heart failure or renal failure. Metoprolol (D) is a beta-blocker and is not typically used as a first-line agent for treating hypertension in a patient without a history of heart failure or myocardial infarction.

How do you definitively diagnose myocarditis?

Endomyocardial biopsy.

A 21-year-old woman presents with shortness of breath, rash and nausea after an insect bite. Her vitals are T 97.7°F, HR 128, BP 85/56, RR 28, oxygen saturation 93%. Exam reveals diffuse hives and posterior pharyngeal swelling. Which of the following should be immediately administered? Epinephrine 1:10,000, 0.3 mL IM Epinephrine 1:10,000, 10 mL IV Epinephrine 1:1000, 0.3 mL IM Epinephrine 1:1000, 0.3 mL IV

Epinephrine 1:1000, 0.3 mL IM This patient presents with anaphylactic shock from an insect bite and requires immediate administration of epinephrine. Epinephrine is potentially life-saving in severe anaphylactic reactions. During an anaphylactic reaction, mast cells degranulate leading to release of histamines and other immune mediators. These mediators lead to the hallmark symptoms of allergic reactions including hives, nausea and vomiting, airway edema, bronchoconstriction and hypotension. Epinephrine acts immediately on adrenergic receptors to reverse these symptoms. Inhaled beta agonists can also be given to rapidly reverse bronchoconstriction. Many of the other treatments in anaphylaxis have a delayed onset of action. Diphenhydramine (H1 receptor blocker) acts by blocking the effect of histamine on H1 receptors mainly in the skin. Ranitidine, famotidine and other H2 blockers can mitigate some of the gastrointestinal symptoms caused by histamine as well as some of the cutaneous manifestations. Steroids mainly act by stabilizing mast cells from further degranulation but this effect is usually delayed 4-6 hours after administration. Steroids also increase the expression of beta-receptors in the lung increasing the efficacy of inhaled beta-agonists. Epinephrine should be given as 300 - 500 mcg IM in the anterolateral thigh. This dose equates to 0.3 - 0.5 mL of the 1:1000 preparation. Giving epinephrine 1:1000, 0.3 mL IV (D) is a massive overdose and can cause dysrhythmias and cardiac ischemia. Cardiac epinephrine (A & B) (1:10,000 concentration) comes in vials of 10 mL for a total of 1000 mcg of epinephrine. This preparation of epinephrine is reserved for use in patients with cardiac arrest (ventricular fibrillation, pulseless electrical activity or asystole) and should not be given to patients with a blood pressure. 0.3 mL of cardiac epinephrine IM is a 10-fold underdose as this amount only contains 30 mcg of epinephrine.

Which drugs have been implicated as a possible cause of mitral regurgitation?

Ergotamine, bromocriptine, cabergoline, and anorectic drugs.

An 18-year-old woman presents after having a syncopal episode. She is complaining of a 2-day history of lower abdominal pain and vaginal spotting. Her BP is 86/42, HR is 128, RR is 18 breaths, and oxygen saturation is 99% on room air. She is drowsy, but answers questions appropriately. What is the most appropriate next step in management? Establish large-bore IV access and administer an IV fluid bolus Initiate rapid sequence induction and orotracheal intubation Perform a bedside urine pregnancy testing Perform an ultrasound of the abdomen to assess for free fluid

Establish large-bore IV access and administer an IV fluid bolus The patient is hypotensive and tachycardic. She is suffering from hypovolemic shock secondary to a ruptured ectopic pregnancy. Therefore she requires immediate intravenous access and volume resuscitation with Lactated Ringer's or normal saline. Emergency Department management of unstable patients includes rapid assessment of the ABC's (Airway, Breathing, Circulation). This patient is phonating, has a respiratory rate of 18 breaths per minute and an oxygen saturation of 99% on room air. There is no concern that her airway or breathing is in immediate jeopardy, therefore she would not require immediate rapid sequence induction and orotracheal intubation (B). Although a bedside pregnancy test (C) and abdominal ultrasound (D) would help make a diagnosis of ruptured ectopic pregnancy, the next step would be to resuscitate the patient.

Which of the following drugs is most likely to be associated with the development of atrial tachydysrhythmias? Ethanol Gamma hydroxybutyrate (GHB) Lorazepam Phenobarbital

Ethanol Ethanol abuse is associated with the development of atrial dysrhythmias, specifically, atrial fibrillation. Alcohol ingestion (acute or chronic) has multiple effects on the cardiovascular system. It can exacerbate coronary artery disease, lead to cardiomyopathy and produce dysrhythmias. Left ventricular dysfunction is common in patients with moderate alcohol consumption. Additionally, these patients may have diastolic dysfunction. Supraventricular and ventricular dysrhythmias are common. The so called "holiday heart" that occurs with heavy drinking can present as atrial fibrillation or, in unusual cases, ventricular tachycardia. Additionally, electrolyte deficiencies (hypokalemia and hypomagnesemia) predispose to dysrhythmias. GHB (B) has been associated with bradycardia and hypotension. Lorazepam (C) and phenobarbital (D) are generally not associated with cardiac dysrhythmias.

How often should patients be screened who are below the threshold for lipid-lowering therapy?

Every five years.

Acute Decompensated Heart Failure

Exertional dyspnea, orthopnea, paroxysmal nocturnal dyspnea, pitting edema S3 ↑ BNP CXR: cardiomegaly, cephalization, Kerley B lines, effusions Most useful study: echo Treatment: BiPAP: ↑ oxygenation, ↓ work of breathing, ↓ preload/afterload Nitroglycerin: ↓ preload/afterload Morphine: ↓ myocardial O2 consumption, ↓ preload Furosemide: diuresis Hypotension without signs of shock: dobutamine (may worsen hypotension) Severe hypotension with signs of shock: norepinephrine (↑ systemic vascular resistance, ↑ HR, ↑ BP, ↑ myocardial O2 demand)

Acute Decompensated Heart Failure

Exertional dyspnea, orthopnea, paroxysmal nocturnal dyspnea, pitting edema • S3 • ↑ BNP • CXR: cardiomegaly, cephalization, Kerley B lines, effusions • Most useful study: echo • Treatment: • . BiPAP: ↑ oxygenation, ↓ work of breathing, ↓ preload/afterload . Nitroglycerin: ↓ preload/afterload . Furosemide: diuresis . Hypotension without signs of shock: dobutamine (may worsen hypotension) . Severe hypotension with signs of shock: norepinephrine (↑ systemic vascular resistance, ↑ HR, ↑ BP, ↑ myocardial O2 demand)

Premature Atrial Contractions

Extra beats that originate outside sinus node • Originate from ectopic atrial pacemaker • Different morphology from sinus P waves • Appears interspersed throughout an underlying rhythm

You receive the laboratory report of a pericardial effusion sample sent yesterday from an inpatient with metastatic lung cancer. Which of the following results would you most expect? Exudate with Gram-positive bacilli Exudate with low-protein and high glucose levels Exudate with positive cytology Transudate with elevated carcinoembryonic antigen levels

Exudate with positive cytology There are several different reasons why the pericardial sac fills with fluid. Pericardial effusion often poses several diagnostic questions. In order to work through a differential, a sample of pericardial fluid can be sent to the lab for analysis testing. As is common with other fluid analyses, the first step in evaluating pericardial fluid is to differentiate transudate from exudate. Transudate represents an imbalance between vessel hydrostatic and oncotic pressure. Transudates are usually associated with some cardiac disease, such as congestive heart failure, or hepatic disease, such as cirrhosis. Other causes of transudative effusion include nephrotic syndrome, hypothyroidism and amyloidosis. On the other hand, exudates herald the presence of some traumatic injury or inflammation. Exudate can be infectious in nature, as in viral, bacterial or fungal pericarditis, or even myocarditis and endocarditis. Exudates are also commonly associated with autoimmune rheumatic conditions, such as rheumatoid arthritis or systemic lupus erythematosus. Cancer, either primary or metastatic, can also produce a pericardial exudate. In addition, exudates can be bloody, as in bleeding disorders or direct trauma. Once the pericardial effusion is deemed exudative, other tests are employed. Total cell counts, WBC differentials, fluid glucose, total protein and lactate dehydrogenase levels, microscopic examination, Gram stain, culture and susceptibility testing, AFB smear and culture, cytology and parasitic testing round out the typical battery of tests used to determine the source of a pericardial exudative effusion. Light's criteria are used to help differentiate transudative from exudative effusions - most commonly in pleural effusions but the table below can also be applied to pericardial effusions. Gram-positivity and the presence of bacteria (A) suggests infectious, not neoplastic, etiology. Exudates typically have a high total protein, low glucose (B) and high lactate dehydrogenase levels. Although malignancy is associated with pericardial effusion with elevated carcinoembryonic levels, they are mostly exudative, not transudative (D).

Anatomically speaking, what is the most common type of ectopic pregnancy?

Fallopian tube (97%) of which 80% are in the ampulla.

Which of the following is a minor Jones criteria for the diagnosis of acute rheumatic fever? Carditis Fever Polyarthritis Sydenham chorea

Fever Fever is one of four minor Jones criteria for the diagnosis of acute rheumatic fever (ARF). ARF results from molecular cross-reactivity between streptococcus and host cell proteins resulting in antibody formation. This is a type II hypersensitivity inflammatory reaction. Diagnosis is based on the Jones criteria, which contains major and minor criteria. A patient is determined to have ARF if they have evidence of a prior group A streptococcus infection along with either two major criteria or one major and two minor criteria. Aside from fever, the other minor criteria are arthralgia, elevated ESR/CRP, and prolonged PR interval. Patients should be investigated for rheumatic heart disease. Treatment usually starts with treating residual group A streptococcal infection and treatment of pain and inflammation with non-steroidal anti-inflammatory agents, salicylates and steroids. Carditis (A), polyarthritis (C), Sydenham chorea (D), erythema marginatum, and subcutaneous nodules are all major Jones criteria.

Which reperfusion medication is considered in ST-elevation myocardial infarction (STEMI) of < 12 hours duration?

Fibrinolytics

Constrictive Pericarditis

Fibrotic changes leading to reduced diastolic filling No wall enlargement Pericardial knock on cardiac auscultation Kussmaul's sign and pulsus paradoxus Pericardiectomy

Constrictive Pericarditis

Fibrotic changes leading to reduced diastolic filling • No wall enlargement • Pericardial knock on cardiac auscultation • Kussmaul's sign and pulsus paradoxus • Pericardiectomy

Which of the following antiarrhythmic medications is contraindicated in the setting of coronary artery or structural heart disease? Amiodarone Dofetilide Dronedarone Flecainide

Flecainide Flecainide is contraindicated in the setting of coronary artery or structural heart disease because of the increased risk of polymorphic ventricular tachycardia. Flecainide is a class IC antiarrhythmic and is an effective agent against both ventricular and supraventricular dysrhythmias. It is often used for atrial fibrillation and its use is sometimes referred to as the "pill-in-the-pocket" approach. In this approach, the patient takes the medication with episodes of paroxysmal atrial fibrillation, rather than taking medication on a daily basis. Flecainide is an attractive agent because of the relatively good side effect profile, efficacy, and ease of use. However, its use is limited, particularly its proarrhythmic effects. Flecainide should also not be used in the setting of sinus or AV node dysfunction, bundle branch block, or long QT syndrome. Patients should take a short acting beta blocker or calcium channel blocker 30 minutes before taking the antiarrhythmic agent or use background rate control therapy. Because of concern of a post conversion pause, patients should be monitored the first time flecainide is used. Dofetilide (B) and amiodarone (A) are class III antiarrhythmics. Class III agents are used for atrial and ventricular arrhythmias but can lengthen the QT interval; for this reason, they are often initiated in an inpatient setting over 3 days to monitor for torsades de pointes. Amiodarone can prolong the QT interval but has not been shown to cause torsades de pointes and does not have to be initiated as an inpatient. Dronedarone (C), the newest agent, can reduce the incidence of hospitalization for cardiovascular events or death in patients with atrial fibrillation or flutter. Dronedarone should not be used in patients with NYHA functional class II or III heart failure with recent decompensation or with class IV heart failure.

Name two medications used to treat orthostatic hypotension?

Fludrocortisone and pyridostigmine.

Light's Criteria

Fluid is exudate if one of the following Light's criteria is present: • Fluid protein/serum protein ≥ 0.5 • Fluid lactate dehydrogenase (LDH)/serum LDH ≥ 0.6 • Fluid LDH level > 2/3 the upper limit of normal of serum LDH

A 58-year-old man ran out of his congestive heart failure medications. He presents with significant dyspnea and altered mental status. Examination reveals bibasilar crackles and jugular venous distension. An electrocardiogram shows sinus rhythm with low voltage complexes. Which of the following is most appropriate at this time? Amiodarone Disopyramide Furosemide Ventricular assist device

Furosemide Acute or decompensated congestive heart failure may be the result of myocardial infarction, dysrhythmias, dietary noncompliance, medical noncompliance, kidney failure, pulmonary embolism, anemia or toxins. Acute failure typically requires hospitalization and critical care. In-house care is comprised of oxygen, nitrates, and furosemide. Furosemide is a loop diuretic that inhibits the transporter at the loop of Henle in the kidneys leading to free water clearance. Inotropic medications, such as dobutamine and dopamine, may also be necessary if there is evidence of impaired perfusion. Severe cases may require an intraaortic balloon pump or a ventricular assist device. Amiodarone (A) is an antiarrhythmic used in treating acute and chronic dysrhythmias. It is not routinely used in the acute decompensation of heart failure, especially when a patient is in normal sinus rhythm. Disopyramide (B) is used in treating hypertrophic cardiomyopathy and arrhythmias but not heart failure. A ventricular assist device (D) is reserved for cardiac failure that fails medication management, or as a bridge to cardiac transplant.

A 72-year-old man presents for evaluation of palpitations. He has a regular, wide complex tachycardia at a rate of 140 bpm. Which of the following supports a diagnosis of ventricular tachycardia? Discordance of the QRS axis in the precordial leads Fusion beats Leftward axis ST elevation greater than 5 mm

Fusion beats Ventricular tachycardia (VT) originates from a location within the ventricle typically outside of the normal conduction system. Increased automaticity or a reentry circuit may cause it. The majority of patients with VT have underlying cardiac disease. The most common form of VT is monomorphic where the QRS complexes appear the same morphologically. Since the electrical impulse originates outside of the conduction system, the QRS complex is wide. It is sometimes challenging to differentiate between VT and other wide complex tachycardias (eg, supraventricular tachycardia with aberrancy). VT is typically regular although there may be a small amount of irregularity helping to distinguish between it and supraventricular tachycardia. Fusion beats occur when impulses from two different locations (one within the ventricle and one in a supraventricular location) activate the ventricle. The result is a QRS complex with morphology resembling a hybrid of a sinus beat and intraventricular beat. These are diagnostic of VT because they represent AV dissociation. Capture beats occur when a sinus beat is normally conducted and a single beat with the sinus QRS morphology occurs within a wide complex tachycardia. Discordance of the QRS axis in the precordial leads (A) is NOT suggestive of VT. Typically across the precordium in VT the QRS complex demonstrates concordance or its polarity. A leftward axis (C) is not suggestive of VT and a more characteristic axis deviation is right superior. ST elevation greater than 5 mm (D) is not part any diagnostic criteria for the identification of VT.

A 64-year-old man with a history of hypertension presents to the Emergency Department requesting medication refills. He states that he has not taken his medications for the last 2 weeks. His blood pressure is 190/100. He has no complaints at this time. He has prescription bottles for atenolol and hydrochlorothiazide. What management is indicated? Change his medications to a calcium-channel blocker Give the patient a prescription for his medications and refer to his primary doctor in 48 hours Start intravenous labetalol and admit to the floor Start intravenous labetalol and admit to the intensive care unit

Give the patient a prescription for his medications and refer to his primary doctor in 48 hours This patient presents with asymptomatic hypertension in the setting of medical non-compliance and should be restarted on his medications and scheduled for follow up with a primary care provider. Accelerated hypertension is defined as markedly elevated blood pressure in the absence of symptoms. This is in contrast with hypertensive emergency where the patient has symptoms or evidence of end organ system dysfunction or both as a result of elevated blood pressure. Accelerated hypertension has a poor long-term prognosis if not controlled but does not pose an immediate threat. As such, it should not be aggressively treated with parenteral medications. Rapid lowering of blood pressure in patients with chronic elevated blood pressure can cause organ hypoperfusion, particularly brain hypoperfusion, and lead to serious sequelae. These patients should be restarted on their medications (if appropriate) and sent for follow up with a primary care physician to monitor and treat the elevated blood pressure. There is no reason to change the patient's medications (A) since he has not been taking them. Starting an intravenous medication (C and D) is required in the treatment of hypertensive emergency but may be dangerous in patients with asymptomatic elevated blood pressure.

What is the goal heart rate during an treadmill exercise stress test?

Goal= 85% of maximum predicted heart rate [220 - patient age].

Which gram-negative organisms which are difficult to culture can cause endocarditis?

HACEK group (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, and Kingella).

Which of the following is the most common physical finding in patients with infective endocarditis? Heart murmur Janeway lesion Osler nodes Splinter hemorrhages

Heart murmur Infective endocarditis occurs when pathogens introduced to the systemic circulation invade the endocardial surface of the heart, including the heart valves. Staphylococcal and Streptococcal bacteria are the most common culprits. The clinical signs and symptoms of endocarditis are varied. Symptoms include fever, chills, dyspnea, weakness, nausea, vomiting, cough, and chest pain. Regarding physical findings, fever is the most common abnormality, seen in 90%. The majority of patients with endocarditis will have a heart murmur (85%). Approximately half of patients with endocarditis develop embolic phenomena, where septic microemboli break off and lodge in downstream tissues. Characteristic skin findings are somewhat less common. Osler nodes, tender lesions on the pads of the fingers, are seen in 10-23% of patients with endocarditis. Janeway lesions, nontender erythematous lesions on the extremities, are seen in 10%, and splinter hemorrhages, linear lines in under the nails, are seen in 15% of patients. The treatment of infective endocarditis involves antibiotic therapy targeted to the suspected pathogen, and stabilization of any hemodynamic instability. Janeway lesions (B), Osler nodes (C), and splinter hemorrhages (D) are relatively uncommon physical findings of infective endocarditis.

Which of the following vital signs is considered abnormal in a 1-year-old patient? Heart rate of 160 beats per minute Oxygen saturation of 98% on room air Respiratory rate of 26 breaths per minute Systolic blood pressure of 85 mm Hg

Heart rate of 160 beats per minute A heart rate of 160 beats per minute would be considered tachycardia in a 1-year-old patient. The average heart rate for a 1-year-old is 120 beats per minute. An oxygen saturation of 98% on room air (B) is within normal limits for all aged patients, including a 1-year-old. The average respiratory rate for a 1-year-old is 26 breaths per minute (C) and is therefore considered normal. The average systolic blood pressure for a 1-year-old is 90 mm Hg (D) with a minimum systolic blood pressure of 72 mm Hg.

A 28-year-old woman with no past medical history presents to the emergency department with acute dyspnea. Physical exam reveals tachycardia, warm extremities, wide-pulse pressure, bounding pulses, a systolic flow murmur, exophthalmos and a neck mass. Which of the following is the most likely diagnosis? Aortic regurgitation High output heart failure Low output heart failure Methamphetamine intoxication

High output heart failure This patient most likely has high-output heart failure secondary to thyrotoxicosis. High output heart failure occurs when cardiac output is elevated in patients with reduced systemic vascular resistance. Examples include thyrotoxicosis, anemia, pregnancy, beriberi and Paget's disease. Patients with high output heart failure usually have normal pump function, but it is not adequate to meet the high metabolic demands. In high output heart failure the heart rate is typically elevated, the pulse is usually bounding and the pulse pressure wide. Pistol-shot sounds may be auscultated over the femoral arteries, which is referred to as Traube's sign. Subungual capillary pulsations, often referred to as Quincke's pulse, may also be present. Although these findings may be seen in other cardiac conditions, such as aortic regurgitation or patent ductus arteriosus, in the absence of those conditions, these signs are highly suggestive of elevated left ventricular stroke volume due to a hyperdynamic state. Patients with chronic high output also may develop signs and symptoms classically associated with the more common low-output heart failure; specifically, they may develop pulmonary or systemic venous congestion or both, while maintaining the above normal cardiac output. Low output heart failure (C) is often secondary to ischemic heart disease, hypertension, dilated cardiomyopathy, valvular and pericardial disease or arrhythmia. It can cause dyspnea but is not associated with symptoms of a hyperdynamic state. Aortic regurgitation (A) is classically associated with bounding pulses, a wide pulse pressure and subungual capillary pulsations; however, aortic regurgitation is less likely in a young woman with no past cardiac history. Additionally, this woman has exophthalmos and a goiter on exam, which support the diagnosis of thyrotoxicosis. Methamphetamine intoxication (D) usually presents with agitation, tachycardia, and psychosis; however, it is not associated with a hyperdynamic state, exophthalmos or a goiter.

A 35-year-old woman with alcohol abuse presents to clinic complaining of "skipped heart beats." Her examination is normal. An in-office ECG is also normal. Laboratory testing is nonspecific. Which of the following is the next most appropriate test? Echocardiogram Electromyography Holter monitor Sestamibi scan

Holter monitor Premature atrial contractions (PACs) are extra beats that originate outside the sinus node from ectopic atrial pacemakers. They appear interspersed throughout an underlying rhythm, usually sinus. Common symptoms include palpitations, described by many as a skipped beat or a missing beat. Others describe it as a stopping or flipping of the heartbeat. These symptoms mimic those of premature ventricular contractions. Causes include psychological stress, hypertension, valvulopathy, ischemic cardiac disease, stimulants (caffeine, tobacco, alcohol), digitalis toxicity, electrolyte abnormalities, and idiopathic. Most cases are asymptomatic and occur in otherwise healthy hearts. Many times one can only find them with continuous 24 hour monitoring via a Holter monitor. PACs are benign, however, a small amount may deteriorate into atrial flutter or fibrillation as well as supraventricular tachycardia. Although echocardiography (A) is usually part of the evaluation of PACs, one must first diagnose them by finding them on electrocardiography. Electromyography (B) is used in the evaluation of nerve and skeletal muscle disorders, not cardiac disorders. Sestamibi scanning (D) is a nuclear medicine test used in the evaluation of myocardial ischemia and infarction. It is not the next most appropriate test when the clinician does not have a working diagnosis of "skipped beats."

What is the earliest change seen on electrocardiogram in an acute ST elevation myocardial infarction? Hyperacute T waves J point elevation PR depression ST segment elevation

Hyperacute T waves Electrocardiogram abnormalities during an acute myocardial infarction follow a typical progression. The earliest ECG finding is the hyperacute T wave. They are usually broad based and slightly asymmetrical. Depending on the timing of presentation, this finding may not be seen. As infarction progresses, ST segment elevation becomes apparent in leads specific to the coronary artery involved. Reciprocal ST depression will be seen in electrically opposite leads (e.g. an inferior myocardial infarction will present with ST elevations in leads II, III and aVF with reciprocal ST depression in lead aVL and possibly lead I). Q waves are commonly seen after the development of ST segment elevation and may persist as a marker of previous infarction. The J point (B) is found at the end of the QRS complex and the beginning of the ST segment. A positive deflection of the J point is termed an Osborn wave and can be seen in hypothermia. Notching of the J point can be seen in benign early repolarization. PR depression (C) is not a typical component of a STEMI but can be seen in pericarditis. ST segment elevation (D) is the hallmark of acute myocardial infarction but is not the first change seen on an ECG.

Myocardial Infarction: ECG findings

Hyperacute T waves: earliest finding • ST elevation • Reciproacal ST depression • T wave inversions • New LBBB • Sgarbossa Criteria for STEMI with LBBB . Concordant ST elevation > 1 mm in leads with a positive QRS (5) . Concordant ST depression > 1 mm in V1-V3 (3) . Discordant ST elevation ≥5 mm in leads with a negative QRS (2) . ≥3 = STEMI

Which electrolyte abnormality can cause increased blood pressure?

Hypercalcemia

Hypertensive Emergency

Hypertension with acute end-organ system injury Encephalopathy, cardiac ischemia, renal ischemia Objectives: reduce MAP 25% in first hour, normalize BP over the next 8 to 24 hours Reduction of MAP > 25% may cause end-organ ischemia IV antihypertensives (labetalol or nicardipine)

Hypertensive Emergency

Hypertension with acute end-organ system injury • Encephalopathy, cardiac ischemia, renal ischemia • Objectives: reduce MAP 25% in first hour, normalize BP over the next 8 to 24 hours • Reduction of MAP > 25% may cause end-organ ischemia • IV antihypertensives (labetalol or nicardipine)

A 74-year-old man presents to the ED with chest pain radiating to the jaw and dyspnea. His past medical history is significant for hypercholesterolemia, hypertension and diabetes. He denies illicit drug use. His blood pressure is 210/122 mm Hg. Physical exam and chest X-ray are normal. His ECG is consistent with left ventricular hypertrophy. Which of the following is the most likely diagnosis? Autonomic dysreflexia Hypertensive emergency Hypertensive urgency Sympathetic crisis

Hypertensive emergency A hypertensive emergency is a severe elevation in blood pressure with evidence of end-organ damage. This requires immediate lowering of blood pressure. There is no specific blood pressure at which hypertensive emergency occurs, however, end-organ damage is less likely if the diastolic BP is < 130 mm Hg. With that being said, the well-accepted criteria for hypertensive crisis are systolic pressure ≥180 mm Hg or diastolic pressure ≥ 110 mm Hg. One must further consider the patient's baseline blood pressure, as a patient with chronic hypertension may not have end-organ damage with pressures around 200/150 mm Hg. Precipitants of hypertensive emergencies include progression of essential hypertension (especially if there is medical noncompliance), progression of renovascular disease, acute cardiac or cerebral ischemic injury and undiagnosed or progressive endocrinopathies. Symptoms of hypertensive emergency include chest pain, dyspnea and neurologic deficits. Associated clinical scenarios include encephalopathy, hemorrhagic or ischemic stroke, aortic dissection, acute myocardial infarction, acute coronary syndrome, acute renal failure, pulmonary edema with respiratory failure, microangiopathic hemolytic anemia and pre-eclampsia/eclampsia/HELLP syndrome. Autonomic dysreflexia (A) occurs in patients with spinal cord injury at T6 or above. A sensory stimuli, such as a urinary tract infection, caudal to the level of injury precipitates reflex vasoconstriction with resultant hypertension and bradycardia. This patient does not have spinal cord injury. Hypertensive urgency (C) was defined as a severely elevated blood pressure without evidence of end-organ damage. Hypertensive urgency is also known as severe asymptomatic hypertension. Sympathetic crisis (D) is associated with illicit drug use (cocaine, amphetamines and PCP). It is a rare condition which may also present, although infrequently, with pheochromocytoma, abrupt cessation of antihypertensives or high tyramine diet in patients on monoamine oxidase inhibitors.

A 32-year-old man presents after a syncopal episode. He was running on the track when he developed shortness of breath followed by witnessed syncope. He was not post-ictal and had no seizure activity. He reports that his father's brother died while playing basketball. Physical examination is notable for a midsystolic crescendo-decrescendo murmur. Which of the following is the most likely diagnosis? Aortic stenosis Arrhythmogenic right ventricular dysplasia Hypertrophic cardiomyopathy Wolff-Parkinson-White syndrome

Hypertrophic cardiomyopathy Hypertrophic cardiomyopathy is an autosomal dominant disease causing mutations in the cardiac sarcomere protein. This leads to abnormal muscle protein development and compensatory hypertrophy of the left ventricle. Most commonly, there is asymmetric hypertrophy with significant enlargement of the anterior interventricular septum. During exertion, patients may experience syncope associated with shortness of breath, chest pain or palpitations. In a large percentage of patients, the presenting symptom is sudden death. The ECG is abnormal in 90% of cases and abnormalities include left ventricular hypertrophy, "dagger-like" Q waves in the inferior and lateral leads, and nonspecific ST segment changes. The diagnosis is made by echocardiogram. Treatment and prevention of symptoms is aimed at maintaining adequate left ventricular filling and increasing diastolic time for filling. Aortic stenosis (A) can also be associated with exertional syncope and causes a crescendo-decrescendo murmur. However, these patients are typically older and often have other symptoms such as progressive dyspnea with exertion and angina. Arrhythmogenic right ventricular dysplasia (B) is another leading cause of sudden death in young athletes. Cardiomyopathy develops as the right ventricle is replaced by fat tissue. The ECG may demonstrate epsilon waves in 50% of people. This is a small positive deflection at the end of the QRS complex. The S wave upstroke may also be prolonged in leads V1-V3. The physical examination will not reveal a cardiac murmur. Wolff-Parkinson-White syndrome (D) is one of several pre-excitation syndromes that predispose patients to dysrhythmia. In Wolff-Parkinson-White an abnormal accessory pathway exists between the atria and ventricles. Sudden cardiac death is rare in patients with this syndrome. Classic ECG findings include a short PR interval with associated delta wave (upsloping of the QRS complex).

A man with dyspnea-on-exertion presents for cardiac evaluation. Physical exam is significant for a left sternal border systolic murmur which is louder during a Valsalva maneuver. An S4 is also appreciated. The ECG shows large QRS complexes. An echocardiogram reveals a decrease in left ventricular chamber volume and normal left atrial measurements. Which of the following is the most likely diagnosis? Aortic stenosis Dilated cardiomyopathy Hypertrophic cardiomyopathy Mitral stenosis

Hypertrophic cardiomyopathy Hypertrophic cardiomyopathy (HCM) results from left or right ventricular hypertrophy or both. This condition can be primarily caused by autosomal dominant genetic mutations of the cardiac sarcomere genes and myocardial fiber hypertrophy. Secondary causes include aortic stenosis, mitral valve abnormalities, coronary heart disease and chronic systemic hypertension. Most patients are asymptomatic upon presentation, however, the common clinical manifestations are dyspnea, angina and dysrhythmia. Decreased chamber volume and increased ventricular wall thickness are the key echocardiographic findings in HCM. Furthermore, the ECG typically shows left ventricular hypertrophy, T-wave inversion and large QRS complexes. A harsh, left sternal border, systolic, crescendo-decrescendo murmur which is worse with Valsalva maneuver is quite typical of HCM. Aortic stenosis (A) is associated with a right, not left, sternal border pansystolic murmur that is decreased, not increased, during a Valsalva maneuver. S3, normal or thin ventricular wall and enlarged ventricular chamber volume are more common with dilated cardiomyopathy (B). S4, thick ventricular wall and decreased ventricular chamber volume are more common with hypertrophic cardiomyopathy. Mitral stenosis (D) produces a diastolic, not systolic, murmur, and is associated with increased left atrial size and pressure.

What is the mechanism behind bradycardia in athletes?

Hypervagotonia is the primary mechanism of resting sinus bradycardia in well-trained athletes.

Which electrolyte abnormalities can cause a long QT syndrome?

Hypokalemia and hypomagnesemia.

What are some common electrolyte abnormalities found with hydrochlorothiazide?

Hypokalemia, hyponatremia, hypomagnesemia, and hypercalcemia.

What are the two major side effects of procainamide?

Hypotension and prolonged QT interval.

A 47-year-old man presents to the emergency department due to acute, sharp chest pain that is relieved by leaning forward. A pericardial friction rub is auscultated on cardiac examination and an ECG shows diffuse ST elevations. Echocardiography reveals a small pericardial effusion. Which of the following is the most appropriate initial treatment? Atenolol Ibuprofen Nitroglycerin Prednisone

Ibuprofen Pericarditis is defined as an inflammation of the pericardium and can be caused from an acute myocardial infarction, viral etiologies, medications, systemic disease and trauma to the chest cavity. A pericardial friction rub is often heard on auscultation and the patient presents with retrosternal chest pain that is relieved by leaning forward. Classic electrocardiographic changes include widespread concave upward ST-segment elevation without reciprocal T-wave inversions or Q waves. First-line treatment includes nonsteroidal anti-inflammatory drugs and colchicine. Beta-blockers such as atenolol (A) are used for cardiac arrhythmias such as atrial fibrillation. They are also used in the post myocardial infarction regimen as they help in the remodeling of the cardiac muscle. Nitroglycerin (C) is used for acute chest pain in the setting of a myocardial infarction as it reduces the afterload. Corticosteroids such as prednisone (D) are considered a second-line treatment for pericarditis when NSAID's and colchicine fail to relieve symptoms in severe or refractory cases that are often marked by systemic disease.

A 17-year-old man with no past medical history presents complaining of constant chest pain for 5 days. He states that he had a cold 2 weeks ago and feels like he never got better. His vitals are T 36.8°C, HR 91, BP 122/75, RR 18, and oxygen saturation 99%. A 12-lead ECG is performed as seen above. What is the appropriate immediate management for this patient? Aspirin 325 mg and activation of the cardiac catheterization lab Azithromycin 500 mg by mouth, followed by 250 mg once a day for 4 days Ibuprofen and prompt follow-up with his primary care doctor Serum d-Dimer test

Ibuprofen and prompt follow-up with his primary care doctor This patient presents with acute pericarditis. His ECG shows sinus tachycardia at 102 beats per minute with diffuse small ST elevations (II, aVF, V2-V6); PR depression (II, III, aVF, V2-V6); and no reciprocal ST depressions. The treatment of pericarditis consists of high-dose nonsteroidal anti-inflammatory medications (e.g., ibuprofen 400-800 mg 3 times per day for 7-14 days). Other treatment options include aspirin 2-4 grams per day and indomethacin 75-150 mg per day. This ECG does not demonstrate an acute myocardial infarction necessitating aspirin and possible cardiac catheterization (A). The ECG shows diffuse ST elevations in the limb and precordial leads, which would indicate involvement of more than 1 coronary vascular territory (a rare occurrence in acute myocardial infarction). Additionally, there are no reciprocal ST depressions. d-Dimer testing (D) is helpful in the diagnosis of pulmonary embolism but does not play a role in diagnosis or prognosis of pericarditis. Antibiotics, including azithromycin (B), do not aid in the treatment of pericarditis.

Which of the following medications can be used in the treatment of hemodynamically stable atrial fibrillation with concomitant Wolff-Parkinson-White syndrome? Adenosine Diltiazem Ibutilide Metoprolol

Ibutilide Ibutilide can be used for rhythm control in hemodynamically stable atrial fibrillation with concomitant Wolff-Parkinson-White syndrome, which is also referred to as preexcited atrial fibrillation. Atrial fibrillation can occur in up to one third of patients with Wolff-Parkinson-White syndrome. Tachydysrhythmias can be facilitated by direct conduction from the atria to the ventricles via the accessory pathway, bypassing the AV node, as seen with atrial fibrillation or atrial flutter in conjunction with Wolff-Parkinson-White. Treatment with AV nodal blocking drugs such as adenosine, calcium-channel blockers, beta-blockers and digoxin may increase conduction via the accessory pathway with a resultant increase in ventricular rate and possible degeneration into ventricular tachycardia or ventricular fibrillation. The goals of acute drug therapy for preexcited atrial fibrillation are prompt control of the ventricular response and, ideally, termination of atrial fibrillation. If the patient is unstable because of a rapid ventricular response, electrical cardioversion should be performed. For more stable patients, trials of intravenous medications can be performed cautiously. Treatment of preexcited atrial fibrillation requires a parenteral drug that lengthens antegrade refractoriness and slows conduction in both the AV node and the His-Purkinje system as well as the accessory pathway. Ibutilide is a class III antiarrhythmic drug that prolongs the refractoriness of the AV node, His-Purkinje system, and accessory pathway, and is useful for termination of atrial fibrillation and atrial flutter. If ibutilide is not available, or if the concern for drug-induced QT prolongation and polymorphic ventricular tachycardia is high, procainamide in another option. Adenosine (A), Diltiazem (B), and Metoprolol (D) are all AV nodal blocking agents and should be avoided in patients with preexcited atrial fibrillation. Blocking the AV node can promote and enhance conduction down the accessory pathway, which can deteriorate into an unstable rhythm such as ventricular tachycardia or ventricular fibrillation.

Acute Pericarditis

Idiopathic > viral (Coxsackie) • Pleuritic chest pain radiating to the back • Pain ↓ with leaning forward • Pericardial friction rub • ECG: diffuse STE, PR depression • NSAIDs

What is the treatment of atrial fibrillation with rapid ventricular response?

If stable, rate control via calcium channel blocker (e.g.) diltiazem or beta-blocker (e.g. metoprolol).

Anaphylactic Reaction

IgE-mast cell mediated • Airway management • Antihistamines, dexamethasone, IM epinephrine, IVF • Glucagon for refractory hypotension in patient with known HTN

What is the next step in management for secondary prevention of sudden cardiac arrest?

Implantable cardioverter-defibrillator (ICD).

Other than magnesium sulfate and cardioversion/defibrillation, what is another treatment for torsades de pointes?

Increase the heart rate to shorten ventricular repolarization, also known as overdrive pacing.

A 42-year-old man presents to the Emergency Department with fever, chills, cough, and hemoptysis. He has a history of intravenous opioid use. Vital signs include BP 110/65 mm Hg, HR 120 beats per minute, RR 20 breaths per minute, and T 103.4°F. Chest X-ray is shown above. Which of the following is the most likely diagnosis? Diffuse alveolar hemorrhage Infectious endocarditis Miliary tuberculosis Wegener's granulomatosis

Infectious endocarditis This patient is presenting with signs and symptoms of infectious endocarditis. Risk factors for infectious endocarditis include rheumatic heart disease, congenital or acquired valvular disease, and intravenous drug use. Infectious endocarditis is classified as acute or subacute depending upon the time course and presentation. Acute endocarditis more often affects normal valves in younger patients. Septic emboli (as shown in the above chest X-ray) and significant illness are common on presentation. Subacute endocarditis has a predilection for abnormal valves and more frequently occurs in older patients. These patients are typically less ill on presentation with intermittent fevers and constitutional symptoms. Left-sided endocarditis involves either the aortic or mitral valve. It is more common than right-sided endocarditis. Organisms often implicated in left-sided endocarditis include Streptococcus viridans, Staphylococcus aureus, and those in the Enterococcus family. Complications include systemic infarcts from septic emboli. Right-sided endocarditis involves either the pulmonic or tricuspid valve. It is classically seen in intravenous drug users. Organisms implicated in right-sided endocarditis include Staphylococcus aureus, Streptococcus pneumoniae, and gram negative bacteria. Presenting symptoms often include fever, cough, hemoptysis, chest pain, and dyspnea. Right-sided endocarditis is frequently misdiagnosed initially as pneumonia. Dermatologic and ocular manifestations of endocarditis are important indicators of the diagnosis. Roth spots are retinal hemorrhages with central clearing seen on funduscopic examination. Osler nodes are painful nodules on fingers and toes. Janeway lesions are painless erythematous plaques on the palms and soles. Splinter hemorrhages occur beneath the nails due to septic emboli. Diagnosis is made by having either both major criteria, 1 major and 3 minor criteria, or 5 minor criteria. Major criteria include 2 positive blood cultures with at least 3 sets sent one hour apart of organisms common to infectious endocarditis or abnormal echocardiography with either visible vegetation, new valvular regurgitation, prosthetic valve dehiscence, or myocardial abscess. Echocardiography is the hallmark of imaging for endocarditis and is preferably done via the transesophageal route. Minor criteria include predisposing risk factors or IV drug use, fever, vascular events such as septic emboli and Janeway lesions, immunologic events such as Osler nodes or Roth spots, echocardiographic findings consistent with endocarditis not meeting major criteria, and positive blood cultures not meeting major criteria. Management includes antibiotics for the suspected organism based on the clinical situation. In an IV drug user, coverage should include methicillin-resistant Staphylococcus aureus and Pseudomonas aeruginosa in addition to the typically implicated organisms. The most appropriate antibiotics for this patient would include cefepime and vancomycin. Diffuse alveolar hemorrhage (A) will often present with cough and hemoptysis; however, fever is uncommon. Chest X-ray will typically show bilateral infiltrates, primarily central. The classic finding in diffuse alveolar hemorrhage is return of increasing amounts of blood on bronchoalveolar lavage. Miliary tuberculosis (C) will often present with a diffuse reticulonodular pattern on chest X-ray as well as generalized malaise and fever, but rarely with hemoptysis. Also, intravenous drug use is a much more significant risk factor for infectious endocarditis. Wegener's granulomatosis (D) will often present with chronic low-grade fevers, night sweats, fatigue, and weight loss. Patients will often have chronic sinusitis, but not present until they have severe hemoptysis, vasculitis, or oral lesions. Chest X-ray will often show bilateral central infiltrates; however, the patient will not present with high fever and intravenous drug use is not a risk factor for this disease.

A previously healthy 27-year-old woman presents to your clinic with concerns about screening for cholesterol. She has never smoked, is physically active, and is in the normal range for body mass index and blood pressure. She says that her father started taking medication for hyperlipidemia at age 66 and she wants to know when she should start being screened. Which of the following is the most appropriate next step in management? Initiate lipid screening at age 35 Initiate lipid screening at age 45 Initiate preventative therapy with aspirin Initiate preventative therapy with lovastatin

Initiate lipid screening at age 45 Screening for lipid abnormalities is a part of determining overall cardiovascular risk. Lipid-lowering therapy is one way to improve cardiovascular outcomes and patients at risk should be screened to evaluate the need for treatment with aspirin or statins. The need for and timing of screening is determined by assessing patient risk factors including age, sex, and other risk factors for cardiovascular disease such as smoking, hypertension and family history of premature coronary heart disease. Patients are at higher risk if they have more than one risk factor or a single risk factor that is severe. Examples of severe single risk factors include a heavy smoking history or multiple first-degree family members with coronary heart disease at a young age. Women determined to be at low risk should start screening for lipid abnormalities at age 45. Men at low risk should start screening at age 35. Women determined to be at a higher cardiovascular risk by the presence of more than one risk factor or a severe single risk factor should start lipid screening at age 35 (A). Men at high risk should start screening at age 25. Therapy with aspirin (C) and statins (D) is recommended with a diagnosis of hyperlipidemia and not as a preventive measure.

A 28-year-old man presents to the emergency department with a one cm laceration to the left forearm. The patient is in good health and has no other complaints. At triage the patient's blood pressure was noted to be 155/94 mmHg; the remainder of his vital signs are normal. Following repair of the laceration, the patient's blood pressure is rechecked and is unchanged. What is the best approach to this patient's elevated blood pressure? Administer labetalol or nifedipine with observation until BP is <140 systolic Evaluate for end organ damage with chest X-ray, ECG, electrolytes, BUN/creatinine and urinalysis Instruct the patient to follow-up with his private physician within two months for recheck No further management required

Instruct the patient to follow-up with his private physician within two months for recheck All patients seen for emergency care, regardless of the complaint should have their blood pressure recorded. A vast majority of the hypertension encountered in the ED is either transient or mild. The most common cause of transient hypertension is pain and anxiety. In these patients, end-organ ischemia does not occur, and attention is focused on treatment of the primary process. If the pressure is elevated, it should be repeated prior to discharge. The patient is advised of this potential problem and appropriate follow up arranged. In adults, systolic blood pressure less than 120 mm Hg and diastolic pressure of less than 80 mm Hg are considered normal. If the diastolic pressure is between 80 to 104 mm Hg, the patient should have follow-up within two months. For diastolic blood pressure greater than or equal to 115 mm Hg, the patient should be evaluated immediately. The patient does not require diagnostic workup (B) or therapeutic intervention (A). The patient should be informed of his or her blood pressure and arrangements should be made for outpatient follow up (D).

A 77-year-old man presents with syncope. He states he was walking to the bus when he felt chest pain, shortness of breath and passed out. The patient has a history of hypertension. Examination reveals dry mucous membranes and a systolic murmur that radiates to the carotids bilaterally. The patient continues to complain of chest pain. Vitals are unremarkable and the ECG reveals left ventricular hypertrophy. What management is indicated? Intravenous fluids and cardiology consultation Morphine sulfate and admit to telemetry Sublingual nitroglycerin and activation of the cardiac catheterization lab Sublingual nitroglycerin and admit to telemetry

Intravenous fluids and cardiology consultation The patient presents with syncope and a systolic murmur radiating to the neck, which suggests the presence of critical aortic stenosis. Management should focus on restoring preload and cardiology consultation. Aortic stenosis is the most common cardiac-valve lesion in the U.S. A normal aortic valve has an area of 3 cm squared. Reduction by 50% causes significant obstruction and critical aortic stenosis occurs with a valve area <0.8 cm squared. As the disease progresses, left ventricular hypertrophy develops to maintain cardiac output. Patients often are asymptomatic until aortic stenosis has progressed to severe or critical levels. At this point, they often develop angina (due to increased demand and decreased supply), exertional syncope (fixed cardiac output), and congestive heart failure (diastolic and systolic dysfunction). The classic physical examination finding is a crescendo-decrescendo, systolic ejection murmur that radiates to the bilateral carotid arteries. Additionally, carotid pulses may be both diminished and delayed. Once patients develop symptoms, survival is markedly reduced unless the valve is replaced. 50% of patients with angina die within 5 years, 50% with syncope die within 3 years and 50% with dyspnea die within 2 years. Immediate medical management should focus on restoring preload with fluids or blood transfusion if significant anemia is present. The only definitive treatment is valve replacement. Patients with symptomatic aortic stenosis exhibit an extreme sensitivity to vasodilators. Sublingual nitroglycerin (C & D) treats typical anginal symptoms by vasodilation leading to decreased preload and decreased cardiac work load. In aortic stenosis patients, this vasodilation can precipitate worsening symptoms. Morphine (B) causes vasodilation through histamine and is also contraindicated.

Which of the following ECG findings is most characteristic of a premature junctional contraction? Inverted P' wave following the QRS Peaked T wave Premature P' wave Widened QRS > 120 msec

Inverted P' wave following the QRS An inverted P' (P-prime) wave following the QRS is most characteristic of a premature junctional contraction. A premature junctional contraction is the result of an irritable automaticity focus in the AV junction which fires a premature stimulus that is conducted to, and depolarizes, the ventricles and often the atria as well. The premature junctional contraction captures the atria in a retrograde fashion and the ventricles in an antegrade fashion. Since atrial and ventricular depolarizations are moving in opposite directions from the junctional focus, the premature P' wave is inverted or opposite the QRS. Bottom up depolarizations record as an inverted P' wave in ECG leads with an upright QRS. The retrograde P' wave may appear before, during, or after the QRS complex. A premature P' wave (C) is seen with premature atrial contractions which record as a P' on ECG. An atrial focus is the origin of this premature atrial contraction, not the SA node, so the stimulus produces a premature and unusually shaped P' wave that looks different than the normal sinus generated P wave. A widened QRS > 120 msecs (D) can be induced by intrinsic or extrinsic factors, including but not limited to, a premature ventricular beat, or pre-excitation of the ventricles via a bypass tract as in Wolff-Parkinson-White and intraventricular conduction delays. Intraventricular conduction delays refer to abnormalities in the intraventricular propagation of supraventricular impulses. These abnormalities of propagation give rise to changes in the shape and duration of the QRS complex. Examples include left and right bundle branch block patterns and their variants. Peaked T waves (B) can be seen with hyperkalemia and are not associated with premature junctional contractions.

Atrial Fibrillation

Irregularly irregular No P waves Narrow QRS unless conduction block or accessory pathway Variable ventricular response rate

Multifocal Atrial Tachycardia

Irregularly irregular • ≥ 3 different P waves • Rate: 100-180 • Nonconducted P waves are present • Pulmonary disease/COPD • Treat underlying condition • Symptomatic: CCBs for rate control

Which of the following best describes the underlying pathophysiology of ventricular tachycardia? Calcified mitral valve leaflets Electrical blockade in the atrioventricular node Irritable ventricular foci Reentrant pathway exists between atria and ventricles

Irritable ventricular foci Ventricular tachycardia (VT) is usually initiated by irritable ventricular automaticity foci. These foci may become irritable by several factors, three of which are hypokalemia, hypoxia and ischemia. Hypoxia may result from airway obstruction, lack of air (as in suffocation or drowning) and pulmonary compromise (as in pulmonary embolus or pneumothorax). Myocardial ischemia or infarction occurs in disease states such as chronic ischemic heart and coronary disease, or in emergent states, as in hypovolemic shock or cardiogenic shock. The more common causes of irritation are coronary insufficiency (vasospasm as with cocaine, atherosclerosis or thrombosis and embolus) and myocardial infarction. Once a ventricular foci is irritated enough, it will take over as the dominant pacemaker, suppressing the sinoatrial node, and resulting in a tachycardia usually between 150-250 bpm. Electrical blockade thru the atrioventricular node (B) is the basis of AV block, not ventricular tachycardia. Mitral stenosis is caused by rheumatic fever and leaflet calcification (A). A diseased mitral valve is associated with atrial fibrillation. A reentrant pathway between atria and ventricles (D) explains the basis of supraventricular tachycardia (SVT).

What is the most common cause of heart failure with reduced ejection fraction?

Ischemic cardiomyopathy.

What is the most common cause of heart failure in the United States?

Ischemic heart disease

Which of the following is the most common cause of sudden cardiac arrest and sudden cardiac death? Anomalous coronary artery Cardiomyopathy Ischemic heart disease Left ventricular hypertrophy

Ischemic heart disease Sudden cardiac arrest and sudden cardiac death usually occurs in people with some form of underlying structural heart disease, most notably ischemic heart disease. Sudden cardiac arrest and sudden cardiac death refer to the sudden cessation of cardiac activity with hemodynamic collapse. Events that are successfully treated leading to patient survival are referred to as sudden cardiac arrest, while those that lead to death are referred to as sudden cardiac death. As much as 70% of sudden cardiac arrest have been attributed to coronary or ischemic heart disease. Among patients with coronary heart disease, sudden cardiac arrest or death can occur both during an acute coronary syndrome and in the setting of chronic, otherwise stable coronary heart disease. Often such patients have had prior myocardial damage and scar that serves as a substrate for sudden cardiac arrest. Other forms of structural heart disease, both acquired and hereditary, account for approximately 10% of cases of sudden cardiac arrest or death. Examples of such disorders include heart failure, anomalous coronary artery (A), cardiomyopathy (B), left ventricular hypertrophy (C) due to hypertension or other causes, myocarditis, hypertrophic cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy, and mitral valve prolapse.

What effect will the administration of atropine have on third degree heart block?

It alters conduction ratios without changing the appearance of the ventricular escape rhythm.

Does the volume of a pericardial friction rub increase or decrease with inspiration?

It increases during inspiration.

What is a Still's murmur?

It is a short, vibrating, physiologic murmur which can be heard over the mid precordium in children in the absence of any other abnormality. This is a common and benign condition.

What is digoxin used for?

Its positive-inotropic and antidysrhythmic effects, at therapeutic doses, are used in treating atrial fibrillation and congestive heart failure.

18 months ago, an elderly patient received a mitral valve replacement. Unfortunately, for the past year, he has been fighting subacute bacterial endocarditis. He has been admitted to the hospital 3 times in the past 6 months. Of all things, he is most concerned with unsightly changes of his palms. During inspection, you appreciate that both palms have several nontender macules of red to brown to black coloration. His daughter is getting married in 3 weeks, and he doesn't want people to see these "weird rashes" on his hands. Which of the following correctly names these findings? Janeway lesions Raynaud's phenomenon Roth spots Splinter hemorrhages

Janeway lesions Bacterial endocarditis usually presents with persistent fever, bacteremia and constitutional symptoms. There are also several physical examination findings which clue the clinician into considering this diagnosis. A new onset murmur, a change in a previous murmur or a new thrill are common presenting signs. Conjunctival and palate petechiae are also common. Tender splenomegaly or tender joints may be present. Neurologic symptoms may be the result of septic emboli emanating from an acutely infected cardiac valve. Septic emboli can also present with cutaneous findings, namely Janeway lesions, however, these are usually present in subacute rather than acute endocarditis. They are described as multicolored hemorrhagic macules which appear on the palms and soles. Treatment of prosthetic valve endocarditis of >1 year's duration is vancomycin plus gentamicin plus ceftriaxone, adjusted, of course, to culture results. Raynaud's phenomenon (B) commonly occurs in rheumatologic disease, like systemic sclerosis. It represents a cold-induced distal digital vasoconstriction, which causes finger, not palmar, pallor, cyanosis or hyperemia and pain. Roth spots (C), also a common finding in bacterial endocarditis, represent retinal hemorrhages surrounding pale centers. They do not occur on the palms. Other cutaneous findings of bacterial endocarditis include proximal nail bed, not palmar, splinter hemorrhages (D).

When does the vessel-expansion, typically seen in the jugular vein as a double-pulsation, occur in the cardiac cycle?

Just after S1 and during S2.

A 58-year-old man with chronic hypertension presents to the ED with acute, 10/10 tearing substernal pain that radiates to the back. All you can gather from him is that he also has some type of "collagen disorder" and diabetes. A chest radiograph reveals a widened mediastinum. As you prepare for a transesophageal echocardiogram, you would most likely start which of the following medications as a first-line agent? Clonidine Labetalol Lisinopril Nitroprusside

Labetalol A classic aortic dissection involves an intimal tear and hemorrhagic extravasation into the intima-media space. Aortic dissections can be defined as proximal, affecting the ascending aorta, or distal, involving the descending aorta distal to the subclavian take-off. Several risk factors of this potentially fatal condition exist, and include hypertension, congenital aortic valve disorder (coarctation, root-dilatation or bicuspid valve), trauma, cardiac surgery, aortitis and connective tissue disorder. Both types are characterized by severe, "ripping or tearing" pain that is maximal at onset (as compared to the crescendo pain of an acute coronary syndrome) and located in the chest, back or abdomen. A new aortic insufficiency murmur is more common in proximal dissection, while a history of hypertension is more common in the distal type. Evaluation includes chest radiograph, chest CT and transesophageal echocardiogram. First-line therapy is intravenous beta-blockers, such as labetalol or esmolol, followed by vasodilators like nitroprusside. Emergency surgery is very likely, especially for proximal dissections. Alpha-2-agonists, like clonidine (A), and angiotensin-converting enzyme inhibitors, like lisinopril (C), are not the recommended treatment of aortic dissection. The goal in treating aortic dissection is to first use beta-blockers, and then use vasodilators, like nitroprusside (D). Administering beta-blockers first helps to protect against reflex tachycardia and positive inotropy that sometimes occurs with agents that cause profound vasodilation.

A 14-day old boy is brought to clinic for a well-child check. The boy was born full-term via normal spontaneous vaginal delivery to a G2, P2 mother who had limited prenatal care. There were no complications at delivery. The boy has not yet regained birth weight and has been breastfeeding poorly. On physical examination, you note bluish discoloration of the lips and oral mucosa, clear breath sounds and a harsh left upper sternal border murmur. Which of the following chest X-ray findings is consistent with Tetralogy of Fallot? Egg-shaped heart Heart shaped like a snowman Increased pulmonary blood flow Lack of vascular congestion

Lack of vascular congestion The boy has central cyanosis with a harsh murmur characteristic of pulmonary stenosis. These findings are suspicious for tetralogy of Fallot (TOF). TOF is composed of four anatomic defects consisting of an overriding aorta, right ventricular hypertrophy, pulmonary stenosis, and ventricular septal defect (VSD). The clinical presentation depends upon the degree of pulmonary stenosis. The more severe the stenosis, the greater is the reduction of pulmonary blood flow and increased cyanosis. On examination, the patients are usually comfortable and in no distress. During hypercyanotic (tet) spells, patients usually become hyperpneic or agitated. The murmur of TOF is usually due to pulmonary stenosis and not the VSD. The murmur is due to the degree of obstruction and to the amount of flow across the obstruction. The diagnosis of TOF is generally made by echocardiography. Other tests that are often performed during the evaluation of TOF include chest radiography and electrocardiogram. The classic chest X-ray in TOF demonstrates a "boot-shaped" heart with an upturned apex and a concave main pulmonary artery segment. The heart size is often normal, and pulmonary flow will appear normal or decreased. Treatment of TOF involves surgical closure of the VSD as well as repair of the pulmonary stenosis. The timing of this procedure depends upon the degree of obstruction to pulmonary blood flow. The following are possible chest radiography findings in cyanotic heart diseases: egg-shaped heart (A) is found in transposition of the great arteries, heart shaped like a snowman (B) is described in total anomalous pulmonary venous return, and increased pulmonary blood flow (C) can be found in truncus arteriosus, transposition of the great arteries, and total anomalous pulmonary venous return.

A 14-day old boy is brought to clinic for a well-child check. The boy was born full-term via normal spontaneous vaginal delivery to a G2, P2 mother who had limited prenatal care. There were no complications at delivery. The boy has not yet regained birth weight and has been breastfeeding poorly. On physical examination, you note bluish discoloration of the lips and oral mucosa, clear breath sounds and a harsh left upper sternal border murmur. Which of the following chest X-ray findings is consistent with Tetralogy of Fallot? Egg-shaped heart Heart shaped like a snowman Increased pulmonary blood flow Lack of vascular congestion

Lack of vascular congestion The boy has central cyanosis with a harsh murmur characteristic of pulmonary stenosis. These findings are suspicious for tetralogy of Fallot (TOF). TOF is composed of four anatomic defects consisting of an overriding aorta, right ventricular hypertrophy, pulmonary stenosis, and ventricular septal defect (VSD). The clinical presentation depends upon the degree of pulmonary stenosis. The more severe the stenosis, the greater is the reduction of pulmonary blood flow and increased cyanosis. On examination, the patients are usually comfortable and in no distress. During hypercyanotic (tet) spells, patients usually become hyperpneic or agitated. The murmur of TOF is usually due to pulmonary stenosis and not the VSD. The murmur is due to the degree of obstruction and to the amount of flow across the obstruction. The diagnosis of TOF is generally made by echocardiography. Other tests that are often performed during the evaluation of TOF include chest radiography and electrocardiogram. The classic chest X-ray in TOF demonstrates a "boot-shaped" heart with an upturned apex and a concave main pulmonary artery segment. The heart size is often normal, and pulmonary flow will appear normal or decreased. Treatment of TOF involves surgical closure of the VSD as well as repair of the pulmonary stenosis. The timing of this procedure depends upon the degree of obstruction to pulmonary blood flow. The following are possible chest radiography findings in cyanotic heart diseases: egg-shaped heart (A) is found in transposition of the great arteries, heart shaped like a snowman (B) is described in total anomalous pulmonary venous return, and increased pulmonary blood flow (C) can be found in truncus arteriosus, transposition of the great arteries, and total anomalous pulmonary venous return.

Large pericardial effusions (>250 ml) have what classic appearance on chest radiograph?

Large "water-bottle" cardiac silhouette with epicardial halo.

0.2 seconds on an ECG is one small or one large block?

Large. Each small block is 0.04 seconds. Therefore, 5 small blocks to every 1 large block (5 x 0.04 = 0.2).

What lead is most common used for a rhythm strip?

Lead II.

Ischemic Heart Disease

Leading cause of death in the USA in both men and women • RFs: family hx, smoking, HTN, DM, cholesterol, male, age >55 • Atypical presentations occur in up to one third of patients • Chest pain, diaphoresis, nausea, hiccups, radiation to shoulder/jaw/back • Elderly, diabetics, females, history of stroke or heart failure: increased risk for atypical presentation • ECG: hyperacute T waves earliest sign of MI • Up to 50% of ECGs are normal or nonspecific • Troponin I most specific for cardiac injury • Nitroglycerin contraindicated in right ventricular MI and recent sildenafil use • Aspirin, nitrates, clopidogrel, heparin, and beta-blockers (within 24 hours) • Preferred treatment for AMI: angioplasty or stenting

Restrictive Cardiomyopathy

Least common cardiomyopathy • Most common cause: amyloidosis • Impaired diastolic filling + preserved systolic function • Right-sided heart failure symptoms • ECG: low voltage, nonspecific changes

How does mitral stenosis result in hoarseness?

Left atrial enlargement can cause compression of the recurrent laryngeal nerve resulting in hoarseness.

What kind of axis deviation is described by an ECG with a positively deflected QRS complex in Lead I and a negatively deflected QRS complex in Lead II and aVF?

Left axis deviation.

Which of the following best describes the finding seen in the ECG above? Atrioventricular block Left bundle branch block Right bundle branch block Sinoatrial block

Left bundle branch block Bundle branch blocks are abnormal conduction abnormalities (not rhythm disturbances) in which the ventricles depolarize in sequence, rather than simultaneously, thus producing a wide QRS complex (> 120 msec) and a ST segment with a slope opposite that of the terminal half of the QRS complex. A left bundle branch block is a bifascicular block in which ventricular activation is by way of the right bundle branch. The impulse travels down the right bundle, activating the septum and the free wall of the right ventricle, and then continues on in the same direction to activate the free wall of the left ventricle. Because the dominant forces are traveling in the same direction, there is a tendency toward monophasic QRS complexes. The ECG in a LBBB will show a large wide R wave in lead I and a negative wave (QS or rS) in lead V1. AV block (A) produces PR interval lengthening, not R-R' complexes. The ECG in a RBBB (C) will show a wide S wave in lead I and a RSR' pattern in lead V1. Sinoatrial block (D) is represented electrocardiographically by a missed cycle or beat within otherwise normal appearing P waves and QRS complexes.

What is the most common cause of right heart failure?

Left heart failure.

What is the most likely culprit lesion in patients with acute ST elevation in lead aVR?

Left main coronary artery.

An 84-year-old woman is recovering in the hospital from an acute anterior ST elevation myocardial infarction four days ago without complication. The patient suddenly develops chest pain, tachypnea and dyspnea. Her pulse is 115 beats per minute, respiratory rate is 26 breaths per minute, blood pressure is 85/50 mm Hg in both arms. She has elevated jugular venous pulsations and distant heart sounds. Her lungs are clear to auscultation bilaterally and no new murmur is appreciated. What is the most likely etiology of her acute decompensation? Acute aortic dissection Acute mitral regurgitation Left ventricular free wall rupture Post infarction ventricular septal defect

Left ventricular free wall rupture Left ventricular free wall rupture usually leads to hemopericardium with cardiac tamponade, characterized by the classic triad of jugular venous distention, hypotension and muffled heart sounds. The presence of rupture is first suggested by the development of sudden profound right heart failure and shock, often progressing rapidly to pulseless electrical activity and death. Survival depends primarily upon the rapid recognition and immediate therapy. Patients displaying suggestive symptoms, signs, and ECG changes require a bedside echocardiogram for diagnosis. Treatment is emergent pericardiocentesis and hemodynamic support. Risk factors include first myocardial infarction, anterior location of the infarction, elderly age and female sex. The incidence of myocardial rupture after an MI is about 1% in patients. In about one-half of cases, myocardial rupture occurs within the first five days after a myocardial infarction and in over 90% of cases within two weeks. Acute aortic dissection (A), acute mitral regurgitation (B) and post infarction ventricular septal defect (D) are all major mechanical complications of acute myocardial infarction that can cause hemodynamic collapse. Acute aortic dissection is associated with inferior wall ST elevation myocardial infarction. Common clinical findings are asymmetric blood pressures and an early diastolic murmur of aortic regurgitation. Acute mitral regurgitation is another complication of myocardial infarction and presents with a new holosystolic murmur heard best at the left sternal border and apex that may radiate to the axilla. Post infarction ventricular septal defect is characterized by a new holosystolic murmur at the left sternal border associated with a thrill. Both acute ischemic mitral regurgitation and post infarction ventricular septal defect can result in acute pulmonary edema with respiratory distress. The diagnosis must be confirmed by echocardiography.

Chronic Heart Failure Treatment

Lifestyle modifications • Diuretics: used for acute pulmonary edema, no mortality benefit • ACEIs: ↓ mortality in all classes • BBs: ↓ mortality in classes II, III, IV • Hydralazine with nitrates: ↓ mortality in African-Americans • Digoxin: used in refractory systolic dysfunction, no mortality benefit • Spironolactone: ↓ mortality in class III/IV • Isolated diastolic dysfunction: HR and BP control • Advanced treatments: mechanical assist device, ICD, heart transplantation

Name a serious complication of mitral stenosis?

Long-standing mitral stenosis can lead to left atrial dilation, a prominent risk factor for atrial fibrillation and thromboembolism.

What is the mainstay of treatment for hypertrophic cardiomyopathy?

Long-term beta-blocker therapy.

What is a common side effect of amlodipine?

Lower extremity edema.

What infectious etiology is associated with complete heart block?

Lyme disease

Mean Arterial Pressure

MAP = (CO x SVR) + CVP • MAP = DBP + 1/3 (SBP-DBP) • Another way: MAP = [(2 x diastolic)+systolic] / 3

How do you calculate mean arterial pressure (MAP)? [DBP = diastolic blood pressure, SBP = systolic blood pressure] MAP = [DBP + (2 x SBP)]/3 MAP = DBP + 1/3(SBP-DBP) MAP = DBP + 2/3(SBP-DBP) MAP = SBP + 1/3(SBP-DBP)

MAP = DBP + 1/3(SBP-DBP) Calculation of the mean arterial pressure (MAP) provides a weighted average of the systolic blood pressure (SBP) and the diastolic blood pressure (DBP). It is a determination of tissue perfusion and is normally 70-100 mm Hg in adults. A MAP of approximately 60 is necessary to perfuse the coronary arteries, brain, and kidneys. MAP = [DBP + (2 x SBP)]/3 (A); MAP = DBP + 2/3(SBP-DBP) (C); and MAP = SBP + 1/3(SBP-DBP) (D) are incorrect formulas.

Asymptomatic Hypertension

MC causes of BP elevation: pain, anxiety • No workup indicated • Outpatient follow-up

A 54-year-old man with a history of schizophrenia presents to the ED after a syncopal episode. During your evaluation, he becomes diaphoretic and complains of dizziness. You are able to feel a radial pulse, and he is alert and talking with you. His rhythm strip is seen above. Which of the following represents the first-line treatment of this disorder? Amiodarone Labetalol Magnesium sulfate Synchronized cardioversion

Magnesium sulfate This ECG shows a rapid, irregular, wide-complex rhythm with multiple QRS morphologies or polymorphic ventricular tachycardia. This most commonly appears as a cyclical progressive change in cardiac axis—otherwise known as torsades de pointes. Torsades often occurs in the setting of a prolonged QT interval during sinus rhythm and is due to abnormal ventricular repolarization. The patient above has a history of schizophrenia. This condition is managed with antipsychotics (risperidone, olanzapine), which are associated with prolonging the QT interval. A QT interval of 500 msec (congenital or acquired) is a risk factor for development of torsades. In adults, however, most causes of QT prolongation are acquired and multifactorial involving drug interactions, myocardial ischemia, and electrolyte disturbances. The immediate management for a patient with torsades is IV magnesium sulfate given as a bolus. If this patient decompensates and loses his pulse, then he'll require defibrillation. Amiodarone (A) is an antidysrhythmic often used in patients with ventricular tachycardia and ventricular fibrillation. However, amiodarone itself causes QT prolongation and can be deleterious in patients with torsades. Labetalol (B) is a combination beta- and alpha-blocking agent that is contraindicated in ventricular dysrhythmias due to its AV-nodal effects. Administration during torsades will likely worsen the dysrhythmia. Although electrical cardioversion (D) is the standard treatment for many wide-complex tachycardias, torsades is less responsive to electricity. It is also difficult to synchronize due to the undulating axis of torsades. If the patient decompensates and loses his pulse, then defibrillation should be performed.

A patient with palpitations presents to the ED. Her rhythm strip is seen above. Which of the following is the most appropriate initial management? Amiodarone Cardioversion Magnesium sulfate Transvenous pacing at 60-80 bpm

Magnesium sulfate Torsades de pointes is a form of polymorphic ventricular tachycardia. It is characterized by a fluctuating amplitude of the QRS complexes which appear to twist around the isoelectric line. Torsades is associated with prolonged QT syndrome, hypokalemia and hypomagnesemia. It can deteriorate into ventricular fibrillation. Symptoms include palpitations, dizziness, syncope and sudden death. Acute management begins with intravenous magnesium. Amiodarone (A) prolongs the QT interval. As such, it is contraindicated in torsades de pointes. Cardioversion (B) is a last resort treatment of torsades due to the fact that many cases of torsades are self-limiting and improve with administration of magnesium. A transvenous pacer (D) is typically used to treat bradydysrhythmias. It also can be used to overdrive pace the ventricles which may lead to cessation of torsades. However, inserting a transvenous pacer is time consuming and the initial treatment of torsades is intravenous magnesium.

The presence of an implantable cardioverter-defibrillator is considered a strong relative contraindication for what diagnostic study?

Magnetic resonance imaging.

A 60-year-old woman with a history of hypertension, dyslipidemia and coronary artery disease was sent to the emergency department from her primary care physician's office for a heart rate of 40/min. She has no complaints except for mild fatigue. Her medications include metoprolol, atorvastatin, lisinopril and baby aspirin. Her ECG reveals sinus bradycardia and her physical exam is normal. Which of the following is the most appropriate next step in management? Administer atropine Make a medication adjustment Schedule her for a temporary pacemaker Watchful waiting

Make a medication adjustment Medication adjustment is the most appropriate in this clinical situation. This patient has sinus bradycardia associated with mild fatigue and is hemodynamically stable. She is currently taking a beta blocker, metoprolol, which can cause or exacerbate sinus bradycardia. Sinus bradycardia is usually asymptomatic. However, symptoms related to the slow heart rate can occur, including lightheadedness, pre-syncope or syncope, as well as worsening of angina pectoris or heart failure. Symptoms may be subtle, with many patients noting only fatigue. This is frequently overlooked and ascribed to aging rather than bradycardia. The underlying cause of pathologic sinus bradycardia in most patients is fibrotic replacement of the sinus node associated with aging. Other causes include node damage secondary to infarction or cardiac surgery, infiltrative causes such as amyloid or sarcoidosis, increased vagal tone secondary to a Valsalva maneuver or vomiting, medications such as beta blockers or calcium channel blockers, and rarely genetic diseases. Sinus bradycardia is not necessarily pathologic; athletes and other highly conditioned persons may have heart rates of 40/min and sleeping heart rates of 30/min. Treatment is not indicated in asymptomatic patients with sinus bradycardia. When symptoms occur it is appropriate to search for a medication that may be depressing sinus node function. This patient is taking a beta blocker. This should be either be dose adjusted or discontinued before any other medications or more invasive approaches are initiated. Atropine (A) and temporary pacemakers (C) are used in ACLS protocol for bradycardia in patients who are hemodynamically unstable. This patient is hemodynamically stable with no lightheadedness, pre-syncope or syncope. Temporary or permanent electrical pacing may be required in acute or chronic symptomatic sinus bradycardia. Watchful waiting (D) is inappropriate as this patient has symptoms of fatigue.

Pulmonary Hypertension

Mean PA pressure: >25/>30 mm Hg at rest/exercise • Exertional dyspnea • RVH • CXR: tapering PAs, RVH

What is the most common X-ray finding in acute aortic dissection?

Mediastinal widening is seen in the majority of aortic dissection cases.

What should be considered first when patients are not at therapeutic blood pressure goals?

Medication compliance and lifestyle intervention adherence.

A 33-year-old woman is seen in clinic for pregnancy induced hypertension. Which of the following antihypertensives is considered safe during pregnancy? Lisinopril Losartan Methyldopa Nitroprusside

Methyldopa Methyldopa is a drug of first choice for control of mild to moderate hypertension in pregnancy and is the most widely prescribed antihypertensive for this indication. Gestational hypertension refers to elevated blood pressure first detected after 20 weeks of gestation in the absence of proteinuria or other diagnostic features of preeclampsia. When hypertension is diagnosed in a pregnant woman, the major issues are establishing a diagnosis, deciding the blood pressure at which treatment should be initiated and avoiding drugs that may adversely affect the fetus. Methyldopa has been widely used in pregnant women and its long-term safety for the fetus has been demonstrated. During long term use in pregnancy, methyldopa does not alter maternal cardiac output or blood flow to the uterus or kidneys and for all these reasons is generally considered the agent of choice for blood pressure control in pregnancy. Labetalol, hydralazine and long-acting nifedipine are also acceptable oral antihypertensive options. Angiotensin converting enzyme inhibitors such as lisinopril (A), angiotensin II receptor blockers such as losartan (B), and nitroprusside (D) are contraindicated in all stages of pregnancy because of the risk of teratogenicity and toxic side effects.

What formula is used to calculate the minimum systolic blood pressure for a child age 1-10 years?

Minimum SBP = 70 + (2 x age in years).

In normal hearts, which of the following heart valves is composed of two cusps? Aortic Mitral Pulmonic Tricuspid

Mitral The mitral valve is the only heart valve with two cusps. Each cusp is a double layer of endocardium attached at its base to the fibrous skeleton of the heart. The margins of the cusps are attached to muscular projections from the ventricles (papillary muscles) via tendinous cords (chordae tendineae).

A 54-year-old woman presents with dyspnea on exertion. She states that it has been progressively worsening over the last few months and she is losing her ability to complete activities that she was able to do before without sitting down to "catch her breath." Cardiac auscultation over the apex reveals a low-pitched, diastolic murmur and an opening snap. Which of the following is the most likely diagnosis? Aortic regurgitation Aortic stenosis Mitral regurgitation Mitral stenosis

Mitral stenosis Mitral stenosis is best auscultated at the apex of the heart. The murmur is described as low-pitched and diastolic. An opening snap of the valve leaflets is heard at the beginning of S2 and can sometimes be confused with a splitting of the second heart sound. The sounds are diminished with inspiration and exaggerated with expiration. Mitral stenosis is most commonly caused by rheumatic fever in childhood but can also be congenital. Symptoms typically begin between ages 20 and 50 years and can include dyspnea on exertion, shortness of breath, and fatigue. Mitral stenosis is associated with atrial fibrillation which may be picked up on an electrocardiogram. Transthoracic echocardiography is used for diagnosis. This will demonstrate information regarding valve anatomy and blood flow dynamics. Doppler used during the echocardiogram can demonstrate concurrent atrial valve abnormalities as well as valve regurgitation. This information is used to stage the severity of stenosis. Stages are listed in severity from stage A to stage D with stage D being the most severe. Mitral regurgitation (C) and aortic stenosis (B) both present with systolic murmurs. Mitral regurgitation causes a mid-frequency holosystolic murmur and aortic stenosis presents with a crescendo-decrescendo systolic murmur. Aortic regurgitation (A) would best be heard near the base of the heart at the second right intercostal space. The murmur associated with chronic aortic regurgitation is an early diastolic murmur that is high-pitched and blowing in quality.

A 55-year-old woman presents to the office with progressive dyspnea, paroxysmal dyspnea, orthopnea, and fatigue over the last several months. On auscultation of her heart you hear a low-pitched diastolic rumble best heard in the left lateral decubitus position along with a high-pitched opening snap. Which type of valvular abnormality is associated with these findings? Aortic regurgitaion Aortic stenosis Mitral regurgitation Mitral stenosis

Mitral stenosis The main symptoms of mitral stenosis (MS) are slowly progressive dyspnea and fatigue. Most auscultatory signs of MS are missed if not performed in the left lateral decubitus position. Typically, the first heart sound (S1) is accentuated. A low-pitched diastolic rumble, heard with the bell of the stethoscope over the apex is also present. The high-pitched opening snap (OS) is caused by the abrupt stopping of the domed mitral valve into the left ventricle (also appreciated in most patients midway between the left sternal border and apex). A shorter A2-OS distance indicates a more severe MS. Signs of pulmonary hypertension such as a loud P2 and right ventricular hypertrophy can also be present as MS becomes more severe. Mitral stenosis is defined as the reduced ability of the blood to move from the left atrium to the left ventricle in diastole. It is mostly caused by dysfunction in the mitral valve, which lacks the ability to open its leaflets in diastole. Mitral valve stenosis (MS) is predominantly caused by rheumatic carditis and is more prevalent in female patients. Physical signs of severe aortic regurgitation (A) include a rapid, quick arterial pulse, a wide pulse pressure, an early high-pitched, blowing diastolic murmur heard best over the left sternal border, an S3 gallop, and a low-pitched diastolic murmur at the apex (Austin-Flint murmur).The typical physical signs of severe aortic valve stenosis (B) are diminished carotid pulses (delayed and weak), a sustained apical impulse, a single second heart sound, an S4 gallop, and midsystolic crescendo-decrescendo murmur with late peaking best heard at the base of the heart. In mitral regurgitation (C) patients will display a systolic murmur, most often holosystolic, high-pitched and present at the apex with radiation to the axilla, left scapula, middle back, or left sternal border, depending on the direction of the regurgitant jet.

Which valvulopathy is commonly associated with premature ventricular contractions (PVCs)?

Mitral valve prolapse.

Ventricular Fibrillation

Most common cause: ischemic heart disease • ECG: irregular chaotic pattern without P waves or QRS complexes • Immediate defibrillation

Tricuspid Stenosis

Most common cause: rheumatic heart disease • almost always occurs with mitral stenosis (MS) • Murmur: . Diastolic murmur along left sternal border . Louder than MS during inspiration • JVP: giant "a" waves

What is the treatment for multifocal atrial tachycardia?

Most commonly, treat the underlying cause which will often improve the dysrhythmia. Nodal agents are not as effective as in other dysrhythmias.

What trio of physical exam findings might be present in a patient with Pericardial Tamponade?

Muffled Heart Sounds, JVD, Narrowing Pulse Pressure/Hypotension (Beck's Triad).

What is Beck's triad for cardiac tamponade?

Muffled heart sounds, hypotension, and jugular venous distention.

What is the gold standard for diagnosing myocarditis?

Myocardial biopsy.

What is the most common cause of ventricular tachycardia?

Myocardial ischemia or infarct.

What is the most common etiology of ventricular fibrillation?

Myocardial ischemia.

A four-year-old girl is brought to the ED by her parents due to lethargy. A week prior, the girl had a cough and cold. Later, symptoms progressed to include fever and malaise. She has been less active with decreased appetite. A few hours prior to arrival in the ER, she was having difficulty breathing. On exam, temperature is 38.3°C, respiratory rate is 35, heart rate is 126, blood pressure is 90/60, with clear breath sounds, hepatomegaly, and poor pulses. Which of the following is the most likely diagnosis? Bronchiolitis Dysrhythmia Myocarditis Pneumonia

Myocarditis The girl demonstrates signs and symptoms that are suspicious for myocarditis, which is a condition that results from inflammation of the heart muscle. The majority of children present with acute or fulminant disease. Myocarditis can be caused by infectious, toxic, or autoimmune conditions. Common causes of viral myocarditis include enterovirus (coxsackie group B), adenovirus, parvovirus B19, Epstein-Barr virus, cytomegalovirus, and human herpes 6 (HHV-6). The presentation of the disease is variable, and patients can present with broad symptoms that range from subclinical disease to cardiogenic shock, arrhythmias, and sudden death. There is usually a history of a recent respiratory or gastrointestinal illness within the previous weeks. There is a prodrome of fever, myalgia, and malaise several days prior to the onset of symptoms of heart dysfunction. Then, patients present with heart failure symptoms that include dyspnea at rest, exercise intolerance, syncope, tachypnea, tachycardia, and hepatomegaly. Testing is focused on determining the severity of cardiac dysfunction and these include electrocardiography (ECG), cardiac biomarkers, chest radiography, and echocardiography. Confirmation of myocarditis is generally made by cardiac magnetic resonance imaging or endomyocardial biopsy. Dysrhythmia (B) usually presents with palpitations, syncope, and chest pain. In the vignette, the girl's symptoms are more consistent with myocarditis. A primary dysrhythmia resulting in myocardial injury is differentiated from myocarditis by an endomyocardial biopsy. Bronchiolitis (A) is typically a disease in children younger than two years of age. It is diagnosed clinically with the characteristic findings of a viral upper respiratory prodrome followed by increased respiratory effort. Pneumonia (D) usually presents with respiratory complaints, particularly cough, tachypnea, retractions, and abnormal lung examination, which were not present in the vignette.

A 62-year-old man with a history of hypertension and tobacco abuse presents with acute onset of sharp epigastric abdominal pain with radiation to his back. On arrival, his vitals signs are T 37.3°C, HR 100, BP 180/90 in the right arm and 80/40 in the left arm, RR 27. Which of the following agents is the first line management of this patient's condition? Diuretics Negative inotropes Vasodilators Vasopressors

Negative inotropes Aortic dissection occurs when damage of the intima allows the entry of blood between the intima and media, creating a false lumen. The presentation of aortic dissection depends on the anatomic location of the dissection, with the most common presentation being sharp or tearing chest pain. Hypertension is typically present and hypotension is a poor prognostic indicator. A difference in blood pressures between opposite arms and a pulse deficit may also occur. Aortic dissection has a bimodal age distribution, with a peak under 40 years of age associated with connective tissue disorders and another peak at greater that 50 years of age associated with chronic hypertension. Control of hypertension and heart rate are the cornerstones of acute management of aortic dissection. Negative inotropes are the preferred agents for the control of hypertension in aortic dissection. This is due to their ability to lower blood pressure without increasing heart rate, which would increase shearing force against the intimal flap and lead to propagation of the dissection. Short-acting beta-blockers, such as labetalol or esmolol, are the first line agents. For persistent hypertension despite maximal therapy with negative inotropes, vasodilators can be used. Diuretics (A) are used in the management of chronic hypertension but have no role in hypertension in the setting of aortic dissection. Vasodilators (C) should not be used as initial management of hypertension in aortic dissection. This is due to the possibility of reflex tachycardia associated with these agents, which would increase shearing force against the intimal flap. Negative inotropes should be used first to block the possibility of this reflex tachycardia. Vasopressors (D) should be avoided, if possible, in aortic dissection as they increase heart rate and shearing force against the dissecting aorta. Crystalloids are the treatment of choice in this setting.

Infantile dilated cardiomyopathy is most commonly caused by which etiology other than idiopathic causes?

Neuromuscular disorders such as Duchenne and Becker muscular dystrophy.

Which of the following drugs is classified as a calcium channel blocker? Alendronate Calcitonin Nicardipine Olanzapine

Nicardipine Nicardipine is a dihydropyridine calcium-channel blocking agent used for the treatment of vascular disorders such as chronic stable angina, hypertension, and Raynaud's phenomenon. It is available in oral and intravenous formulations. Its mechanism of action and clinical effects closely resemble those of nifedipine and the other dihydropyridines (amlodipine, felodipine), except that nicardipine is more selective for cerebral and coronary blood vessels. Furthermore, nicardipine does not intrinsically decrease myocardial contractility and may be useful in the management of congestive heart failure. Nicardipine also has a longer half-life than nifedipine. Alendronate (A) is a bisphosphonate that acts as an osteoclast inhibitor to inhibit bone resorption. Calcitonin (B) works to lower serum calcium concentration by inhibiting calcium absorption by the intestines, inhibiting osteoclast activity in the bones, and inhibits renal tubular cell reabsorption of calcium allowing it to be excreted in the urine. Olanzapine (D) is an atypical antipsychotic that is used for the treatment of schizophrenia and bipolar disorder. Olanzapine is structurally similar to clozapine and quetiapine, but is classified as a thienobenzodiazepine.

Patients with severe aortic regurgitation may benefit from which long-acting vasodilators?

Nifedipine XL or other long acting calcium channel blockers.

A patient presents with chest pain and the ECG seen above. Which of the following medications is contraindicated in this patient's management? Aspirin Clopidogrel Heparin Nitroglycerin

Nitroglycerin This patient presents with an inferior ST elevation myocardial infarction (STEMI) and the use of nitroglycerin is relatively contraindicated in management. In patients with myocardial ischemia or infarction, nitrates are used to decreased myocardial oxygen demand. They increase venous capacitance leading to decreased preload and are direct coronary artery vasodilators. Coronary artery vasodilation leads to increased blood flow to ischemic myocardium. The beneficial effects of nitrates are profound leading to their recommendation for most patients with a systolic blood pressure > 90 mm Hg. An inferior STEMI is one of these contraindications. Patients with an inferior STEMI may also have right ventricular infarct and be preload dependent. In a patient with an inferior STEMI, right ventricular infarct is suggested by the presence of ST elevation in lead III larger than that in lead II. A right ventricular infarct can be discovered by performing a right-sided ECG and looking for ST elevation in lead "RV4." In these patients, a preload reducing medication like nitroglycerin can lead to a precipitous drop in blood pressure. Aspirin (A) is the most beneficial treatment in patients with ACS and should be given to all patients unless they have a severe allergy. Clopidogrel (B) is an antiplatelet agent that is beneficial in patients that will be going to cardiac catheterization. Heparin (C) has also been found to be beneficial in STEMI and should only be withheld in patients with concomitant bleeding or a history of hypersensitivity reaction.

A 35-year-old woman is being evaluated at her annual well woman exam. She has no complaints and generally feels healthy. She has no past medical history and takes no medications. She walks 30 minutes five days per week with no dyspnea or discomfort. On physical exam her blood pressure is 118/68, pulse 64/min and respiration rate is 13/min. Her body mass index is 22. Cardiac auscultation reveals a 2/6 mid-systolic crescendo-decrescendo murmur heard best at the left lower sternal border without radiation. She has a normal S1 and S2 and normal cardiac impulse. Lungs are clear and peripheral pulses are normal. Electrocardiogram is normal. What is the next appropriate step in management? Cardiac magnetic resonance imaging No additional testing Transesophageal echocardiography Transthoracic echocardiography

No additional testing No additional testing is indicated in this patient. She most likely has a benign systolic ejection murmur. This is a common clinical situation and reassurance is appropriate. A systolic murmur is present in up to 60 % of patients, with 90 % being associated with a normal echocardiogram. A murmur is characterized by its intensity or grade, timing, configuration, frequency or pitch, and location. The most common causes of a mid-systolic murmur are innocent flow murmurs, an increase in flow rate across a normal semilunar valve, and aortic valve sclerosis. Innocent murmurs are typically systolic ejection murmurs located at the base of the heart, short and soft, grade 1/6 to 2/6, without radiation, with a normal S1 and S2, normal cardiac impulse, and no evidence of any hemodynamic abnormality. The benign characteristics of the murmur in this patient include a grade < 3/6, mid-systolic timing, lack of radiation, and the absence of additional abnormal heart sounds. The remainder of the physical examination and the electrocardiogram are normal, without any evidence of cardiac enlargement or dysfunction. Signs of more serious cardiac disease include an S4, grade >3/6 intensity, any diastolic murmur and fixed splitting of S2. Transthoracic echocardiography (D) is the primary test for diagnosis and assessment of valvular heart disease. The appropriateness of this test is guided by history and physical examination. It is indicated in symptomatic patients, in those with a systolic murmur grade 3/6 or greater, diastolic murmurs, continuous murmurs (begins after s1 and beyond s2), holosystolic murmurs, late systolic murmurs, murmurs associated with ejection clicks, or murmurs that radiate to the neck or back. This patient's murmur does not have any of these characteristics. Transesophageal echocardiography (C) may be useful in patients with poor imaging by transthoracic study or to evaluate the feasibility of surgical repair when surgery is planned. Cardiac magnetic resonance imaging (A) is indicated if both transthoracic and transesophageal echocardiograms are equivocal in a more suspicious murmur. It is good for the assessment of the aorta and cardiac chamber size and function.

A 60-year-old man with a history of hypertension and paroxysmal atrial fibrillation is scheduled to undergo an elective dental extraction. His paroxysmal atrial fibrillation is rate controlled with a beta blocker and he is on chronic anticoagulation with warfarin. Anticoagulation must be discontinued for the procedure. His medications include metoprolol tartrate, lisinopril and warfarin. In addition to discontinuing warfarin, which of the following is the most appropriate next step in management? Bridge with aspirin Bridge with intravenous unfractionated heparin Bridge with low molecular weight heparin No bridging agent is necessary

No bridging agent is necessary No bridging agent is necessary. Interruption of oral anticoagulation in patients with atrial fibrillation is sometimes necessary for invasive procedures, and it must be determined whether bridging is indicated. If the patient has a low short-term risk as determined by a CHA2DS2-VASc score of 0-1 and the duration of interruption is less than 1 week, then bridging is not needed. This patient has a CHA2DS2-VASc score of 1 due to his history of hypertension; therefore, no periprocedural bridging is necessary. In this scenario it would be recommended to simply discontinue warfarin approximately 5 days before the procedure with no bridging agent. Warfarin can often be resumed 12-24 hours after the procedure if there is no active bleeding. If the patient has a high short-term risk with a CHA2DS2-VASc score of > 2, recent stroke, mechanical or rheumatic mitral valve or if the interruption is more than 1 week, then use of a bridging agent should be considered more strongly. In this setting, it would be appropriate to bridge with intravenous unfractionated heparin (B) or low molecular weight heparin (C). For atrial fibrillation patients with moderate risk features with a CHADS2 score of 3-4, a history of remote transient ischemic attack or stroke, or a mechanical aortic valve, management is individualized according to risks and benefits and is patient and provider dependent. It would not be appropriate to bridge with aspirin (A) as aspirin has no role in bridging.

A 52-year-old man presents from his primary care physician's office for evaluation of an abnormal electrocardiogram. His ECG is seen above. He has no symptoms. What is the appropriate intervention? Measurement of cardiac enzymes No intervention Telemetry observation Transcutaneous pacer pad placement

No intervention This ECG demonstrates an example of Type 1 second-degree atrioventricular (AV) block. AV block results from impaired conduction through some portion of the electrical circuit impairing communication between the atria and ventricles. In first and second degree AV block there is a partial disruption of the electrical circuitry as opposed to third degree heart block when there is no electrical communication between the atria and ventricles (AV dissociation). In second-degree heart block, some sinus impulses do not reach the ventricles at all. In type 1 second-degree AV block, there is lengthening of the PR interval until ultimately a beat is dropped. This is also known as Wenckebach or Mobitz I. In many cases, type 1 second-degree heart block is a normal variant. Other times, the etiology is likely related to increased vagal tone and in most cases requires no treatment. It can also occur in a myocardial infarction and usually resolves after the infarct period. Type 2 second-degree heart block is characterized by a dropped beat without any prolongation of the PR interval. Type 2 is never considered a normal variant. In the absence of any cardiac symptoms, the measurement of cardiac enzymes (A) in type 1 second-degree heart block is not necessary. Telemetry observation (C) is not required in type 1 second-degree heart block because it does not typically progress into other forms of heart block. In patients with type 2 heart block, this interruption of the electrical pathway occurs below the level of the AV node and can progress. Transcutaneous pacer pads (D) are often placed on the chest of a patient with complete heart block (type 3) because of the high chance for impaired cardiac output. These patients will require pacemaker placement if the heart block is not due to a reversible cause (e.g. hyperkalemia).

Name some medications which are prescribed for venous insufficiency?

No oral medications have been shown to be beneficial in the treatment of this condition.

Are QRS complexes dropped in first degree heart block?

No, P wave conduction is delayed but not actually blocked, so no QRS complexes are dropped.

Can a S4 be heard in normal individuals?

No.

Is antibiotic prophylaxis indicated in patients with isolated aortic stenosis?

No.

Do all pericardial effusions cause tamponade?

No. Chronic effusions are less likely to cause tamponade than acute effusions.

A 49-year-old man presents with chest pain. His medical history does not list any cardiac murmur, however, during examination, you hear a mitral regurgitant murmur. Blood pressure is equal in both the left and right arms. Although you have none to compare to, you order an electrocardiogram and notice ST segment depression in three different leads and T-wave inversion in two different leads. No other abnormalities are appreciated. A chest radiograph is read as normal. Initial lab testing shows an elevated troponin level. Which of the following is the most correct diagnosis? Aortic dissection Non ST-segment elevation myocardial infarction ST-segment elevation myocardial infarction Unstable angina

Non ST-segment elevation myocardial infarction Myocardial infarction encompasses both non-ST-segment elevation myocardial infarction (NSTEMI) and ST-segment elevation myocardial infarction (STEMI). It is defined as myocardial cell death and necrosis as diagnosed by a rise and fall in cardiac enzymes (in association with appropriate clinical presentation) or by pathologic findings of prior myocardial infarction (e.g. new Q waves on ECG). NSTEMI represents subtotal coronary thrombosis and myocardial ischemia infarct. Common symptoms include angina less than 30 minutes duration, dyspnea, diaphoresis and palpitations. Myocardial insult is also associated with a new-onset mitral regurgitation murmur, newly-auscultated S4 and a paradoxical S2. New infarcts can be identified with a positive troponin on laboratory testing. Aortic dissection (A) is associated with severe, tearing, knifelike pain that may radiate to the midscapular region. It is associated with asymmetric blood pressures in the arms, aortic regurgitation murmur, widened mediastinum on radiography and neurologic deficits. It is less likely than NSTEM in this scenario. STEMI (C) is associated with positive troponins and ST-segment elevation, not depression. Unstable angina (D) is not associated with positive troponin levels, but it can be associated with T wave inversion and ST depression.

What is the role of antibiotics in the prevention of post-streptococcal glomerulonephritis (PSGN)?

None. Antibiotics do not prevent PSGN.

What is a typical chest radiograph finding in acute mitral regurgitation?

Normal cardiac silhouette with severe pulmonary edema.

A young woman with Raynaud's phenomenon presents with a 3 month history of cyclical short episodes of chest pain. Her social history is positive for intermittent cocaine use. The pain occurs most commonly after she wakes in the morning, lasts for 20 minutes, then resolves. This pain occurs at rest and is not worse with exercise or increased activity. Which of the following would you most expect to find during an evaluation of these symptoms? Coronary artery stenosis Normal exercise stress test Pain relief during ergonivine administration ST-segment depression

Normal exercise stress test Prinzmetal's angina, also known as variant angina, is due to endothelium dysfunction and coronary vasospasm. It can occur in normal or diseased arteries. It commonly occurs in younger women who do not have the typical cardiac risk factors, except for tobacco use, however, it can be associated with atherosclerosis as well. It is associated with other vasospastic conditions such as migraine headache and Raynaud's phenomenon. Predisposing factors in developing coronary vasospasm include cocaine and tobacco use, cold weather and psychological stress. Symptoms include cyclical angina that occurs at rest, most commonly in the early morning and late evening hours, and is not made worse with exercise or other cardiac loading. Dysrhythmias are common and can be fatal. It is diagnosed by observing angina with transient ST-segment elevation, especially with increasing doses of intravenous ergonovine or acetylcholine. Exercise treadmill testing is normal in patients with Prinzmetal's angina as this condition is not due to increasing cardiac demand. Successful treatment can be accomplished with medications. Prognosis is favorable when there is no concordant coronary atherosclerosis or stenosis. Patients with Prinzmetal's angina typically have minimal to absent coronary stenosis (A). More pain, not less (C), occurs during administration of ergonovine in a patient with coronary vasospasm. ST elevation, not depression (D), is seen during Prinzmetal anginal attacks.

A 46-year-old woman is in your office for her yearly physical. What is your interpretation of her ECG? Atrial fibrillation Atrial flutter Normal sinus rhythm Sinus tachycardia

Normal sinus rhythm The ECG is representative of normal sinus rhythm with a rate of 80. Normal sinus rhythm has a rate between 60-100. The rhythm is regular with a 1:1 relationship of the P to QRS. The PR interval is 120-200 msec, the QRS complex is 60-100 msec. P waves are upright in leads I, II, and aVF. Atrial fibrillation (A) is an irregularly irregular rhythm due to uncoordinated atrial activation and random occurrence of ventricular depolarization. The atria are not contracting but they do discharge electrical impulses to the ventricles. However, no single impulse depolarizes the atria completely, so only an occasional impulse gets through the AV node. It is the most common sustained dysrhythmia in clinical practice. Atrial flutter (B) is a rapid atrial rhythm but due to nodal delay, ventricular response rate is slower. Therefore, atrial flutter always occurs with some sort of AV block so that not all impulses are conducted. The resulting block is often variable (2:1, 3:1, 4:1). P waves have characteristic sawtooth pattern. In sinus tachycardia (D) the SA node is the pacemaker that causes the atria to depolarize regularly and, thus, the ventricles to depolarize regularly. P waves and QRS complexes occur regularly and the rate is >100.

Digoxin Effect

Not a marker of toxicity--only indicates patient is taking digoxin • Downsloping ST depression with a characteristic slurred appearance ("Salvador Dali mustache") • Flattened, inverted, or biphasic t waves • Shortened QT interval

Which of the following can decrease levels of brain natriuretic peptide? Elderly age Female sex Kidney failure Obesity

Obesity Obesity can decrease levels of brain natriuretic peptide. Brain natriuretic peptide is a natriuretic hormone that was initially identified in the brain but is also released from the heart, particularly the ventricles. It is released in response to volume expansion and increased wall stress in the cardiac ventricles. Increased plasma concentrations are found in heart failure in response to increased ventricular filling pressures from volume overload. An elevated serum brain natriuretic peptide is a nonspecific finding that does not establish the diagnosis of heart failure. However, levels > 500 pg/mL is consistent with heart failure, and a level < 100 pg/mL effectively eliminates heart failure as an acute cause of dyspnea. It is most useful in differentiating dyspnea due to heart failure verses that due to pulmonary disease. Brain natriuretic peptide is less helpful in the setting of increased body mass index as obese patients tend to have lower plasma levels of brain natriuretic peptide concentrations than nonobese patients. The etiology of this phenomena is not entirely understood. Elderly age (A), female sex (B) and kidney failure (C) can falsely elevate levels of brain natriuretic peptide, not decrease them. Plasma concentrations can vary with age, sex and renal function. Levels increase with renal failure secondary to reduced excretion and concentrations are inversely related to glomerular filtration rate.

A 32-year-old previously healthy man presents to the ED with a 4-hour history of palpitations. He denies chest pain, shortness of breath, or history of similar palpitations. He does admit to heavy alcohol use in the past week, drinking 1 pint of vodka and a 24-pack of beer each day. In the ED, his vital signs are BP 135/75, HR 115, RR 14, and oxygen saturation 98% on room air. An irregularly irregular rhythm is heard on auscultation and an ECG shows atrial fibrillation. What is the next step in management? Chemical cardioversion Observation Rate control Synchronized cardioversion

Observation This patient has holiday heart syndrome, which can produce atrial fibrillation, atrial flutter, or atrial tachycardia after excessive alcohol use. Patients generally present with palpitations. The rhythm tends to spontaneously convert back to a sinus rhythm within 24-48 hours; thus, the best step in management at this time is to observe the patient with cardiac monitoring. If the patient stays tachycardic beyond 24-48 hours, rate control (C) can be employed, using medications such as calcium channel blockers or beta-blockers. Chemical cardioversion (A) and synchronized cardioversion (D) are both unnecessary now, as the patient is likely to revert to a sinus rhythm on his own. However, if symptoms persist, cardioversion may be used to reduce the risk of thrombus formation in addition to the need for either anticoagulation or a transesophageal echocardiogram. In addition, if the patient becomes unstable at any time, synchronized cardioversion would be used.

A 32-year-old man with a history of intravenous drug use presents to the emergency department with complaints of chest pain, shortness of breath, cough and fever. Physical exam reveals a temperature of 102°F, new heart murmur, diffuse petechial rash and subungual hemorrhages. Which of the following is the most appropriate next step in management? Begin anticoagulation therapy Begin empiric antibiotic therapy Obtain three sets of blood cultures Order cardiovascular surgical consult

Obtain three sets of blood cultures Infective endocarditis (IE) affects the endocardial surface of the heart including the valves and mural endocardium. Different types of endocarditis have different pathogens and etiologies. Intravenous drug use is a risk factor for bacterial endocarditis. Diagnosis may be challenging and requires a high level of suspicion, as patients generally have no previous cardiac disease or heart murmurs. Patients often present with nonspecific complaints of fever, chills, night sweats, myalgias, joint pain, anorexia, and weight loss. Clinical manifestations include fever and heart murmurs. Classic signs of IE include petechiae, subungual hemorrhages, tender nodules on the fingertips, and nontender macules on the palms and soles. In the emergent setting, initial goals include stabilizing the patient and making the correct diagnosis. Three sets of blood cultures should be obtained over the first 60-90 minutes and then empiric antibiotic therapy may be administered based on the patient's history and risk factors. The use of anticoagulation therapy (A) is controversial in the treatment of IE and it does not play a role in initial management. One of the primary goals in the diagnosis of IE is to determine the correct diagnosis by identifying the pathogen involved. Administration of empiric antibiotic therapy (B) before obtaining blood cultures could interfere with determining the most appropriate anti-infective agent. Some patients with IE will eventually need surgery and a cardiovascular surgical consult (D) may be appropriate later in the treatment process, but is not part of the initial management of a patient with IE.

Premature Ventricular Contractions (PVCs)

Occur earlier than the next expected normal QRS • Wider than a normal QRS • QRS morphology is generally bizarre • No preceding P wave • Deflection of the ST segment and T wave is opposite that of the QRS • Followed by a compensatory pause

Which of the following should be assessed in the physical exam of a patient with essential hypertension? Costovertebral angle tenderness Deep tendon reflexes Ocular fundus Pupillary response

Ocular fundus Hypertension is defined as a systolic blood pressure of 140 to 159 mm Hg or a diastolic blood pressure of 90 to 99 mm Hg on two or more occasions. Hypertension is commonly seen in the primary care setting and risk factors include family history of hypertension, obesity, advancing age, African-American race, physical inactivity, high sodium diet, and diabetes. When taking the history of a patient with hypertension, questions should include duration of the diagnosis, previous treatment, and aggravating factors such as alcohol consumption, smoking, use of nonsteroidal anti-inflammatory agents and other prescription medications. The purpose of the physical exam is to assess for end-organ damage and cardiovascular disease as well as potential causes of secondary hypertension. Physical exam should include an accurate reading of blood pressure along with an assessment of general appearance, heart, lungs, neck, abdomen, and extremities. A fundoscopic exam of the eyes should be used to evaluate for hypertensive retinopathy including hemorrhage, papilledema and cotton wool spots. Costal vertebral angle tenderness (A) is assessed to rule out pyelonephritis or renal stones. Deep tendon reflexes (B) are evaluated in patients as part of a complete neurological exam. Neurological abnormalities seen in patients with hypertension include visual disturbance, focal weakness or confusion. Pupillary response (D) is assessed as part of cranial nerve testing in patients with neurological defects.

Which of the following should be assessed in the physical exam of a patient with essential hypertension? Costovertebral angle tenderness Deep tendon reflexes Ocular fundus Pupillary response

Ocular fundus Hypertension is defined as a systolic blood pressure of 140 to 159 mm Hg or a diastolic blood pressure of 90 to 99 mm Hg on two or more occasions. Hypertension is commonly seen in the primary care setting and risk factors include family history of hypertension, obesity, advancing age, African-American race, physical inactivity, high sodium diet, and diabetes. When taking the history of a patient with hypertension, questions should include duration of the diagnosis, previous treatment, and aggravating factors such as alcohol consumption, smoking, use of nonsteroidal anti-inflammatory agents and other prescription medications. The purpose of the physical exam is to assess for end-organ damage and cardiovascular disease as well as potential causes of secondary hypertension. Physical exam should include an accurate reading of blood pressure along with an assessment of general appearance, heart, lungs, neck, abdomen, and extremities. A fundoscopic exam of the eyes should be used to evaluate for hypertensive retinopathy including hemorrhage, papilledema and cotton wool spots. Costal vertebral angle tenderness (A) is assessed to rule out pyelonephritis or renal stones. Deep tendon reflexes (B) are evaluated in patients as part of a complete neurological exam. Neurological abnormalities seen in patients with hypertension include visual disturbance, focal weakness or confusion. Pupillary response (D) is assessed as part of cranial nerve testing in patients with neurological defects.

According to the new JNC8 guideline, how much time needs to pass before any adjustments to medication are made for hypertension management?

One month.

An elderly man complains of dizziness upon standing. He denies being dizzy once he has stood for 5 minutes, and also denies being dizzy when supine or seated. He denies associated chest pain, palpitations, or dyspnea. Which of the following tests should first be performed during the evaluation of this positional dizziness? Chest radiograph Head-up tilt-table testing Orthostatic vital signs Transesophageal echocardiography

Orthostatic vital signs Orthostatic hypotension is due to an inadequate physiologic response to postural changes. This condition mostly exists in the elderly population. It is estimated that nearly 25% of syncopal admissions to the ED are due to orthostatic hypotension. Symptoms of orthostatic hypotension include dizziness, weakness, fatigue, light-headedness, headache or syncope which occur after standing. Primary causes include frailty, dehydration, poor cardiac output or autonomic instability. However, there are a multitude of underlying conditions that can cause secondary orthostasis. These include anemia, hemorrhage, cardiac dysfunction, venous insufficiency, endocrine dysfunction (hypothyroidism, hypoaldosteronism, adrenal insufficiency, diabetes insipidus, hypokalemia) and neurologic dysfunction (autonomic neuropathy, vitamin B12 deficiency). If suspected, orthostatic vital signs must be obtained as follows: BP and heart rate must be measured in the supine position, then repeated after 3 minutes of standing. If normal, but orthostasis is still suspected, then the patient should be sent for head-up tilt-table testing. Head-up tilt-table testing (B) can help confirm a diagnosis of suspected orthostatic hypotension when orthostatic vital signs are nondiagnostic. It should be done after orthostatic vital signs are checked. A chest X-ray (A) and echocardiogram (D) may be used during the evaluation of orthostasis, but they would not be ordered initially. It is important first to consider orthostatic hypotension as the diagnosis, then once confirmed, begin evaluation of other causes with more specific testing.

What is the name of the tender nodules found on the fingertips of patients with infective endocarditis?

Osler nodes

A previously healthy 35-year-old woman presents to the emergency department with pleuritic chest pain and malaise. She has been feeling unwell for the past few days with intermittent fever. Her pulse is 87 beats/minute, respiratory rate is 19 breaths/minute, blood pressure is 122/82 mm Hg, and temperature is 37.0°C. On exam, a pericardial friction rub is appreciated. Echocardiography is negative for pericardial effusion. Which of the following is the most appropriate management? Admission and intravenous acyclovir Admission and intravenous gentamicin Outpatient follow-up and oral naproxen Outpatient follow-up and oral prednisone

Outpatient follow-up and oral naproxen The most appropriate treatment for this patient with acute pericarditis is on an outpatient follow-up and oral naproxen. Acute pericarditis is an inflammation of the pericardium. Acute pericarditis is most commonly seen in men under the age of 50 years. Viral infections are the most common cause of acute pericarditis in the United States. Worldwide, tuberculosis is the most common cause. Other causes of pericarditis include bacteria, uremia, neoplasms, myocardial infarctions (Dressler syndrome), radiation, and rheumatoid conditions. In most cases of acute pericarditis, the pericardium becomes inflamed and infiltrated with leukocytes. Pericardial effusions can develop during pericarditis. Effusions that accumulate rapidly may cause cardiac tamponade. Regardless of etiology, most cases of pericarditis present with pleuritic, postural chest pain. The pain may radiate to the neck, shoulders, back, or epigastric region. A pericardial friction rub is pathognomonic and is very specific, but lacks sensitivity. The friction rub is often transient and serial exams may be necessary for detection. Other physical findings may depend on the etiology. Viral pericarditis is usually accompanied by flu-like symptoms, low-grade fever, malaise, dyspnea, and tachypnea. Fever may be absent in uremic pericarditis. Patients with bacterial pericarditis often appear systemically toxic. Lab findings and diagnostics should be used to rule out other serious causes of chest pain, such as myocardial infarction, pulmonary embolism, or aortic dissection. Echocardiography should be used to evaluate for effusion. Electrocardiography may show generalized ST segment elevation and PR segment depression. Chest radiographs are usually normal unless a significant pericardial effusion is present. Nonsteroidal anti-inflammatory drugs (NSAIDs) are the first line treatment unless contraindicated. Colchicine and corticosteroids can be used in severe or refractory cases. Corticosteroids increase the risk of recurrence. Uremic pericarditis should be treated with urgent dialysis. Indications for admission include presence of effusion, fever, immunosuppression, trauma, oral anticoagulation therapy, myopericarditis, or failure of oral NSAIDs therapy. This patient does not have any signs of systemic toxicity or pericardial effusion, therefore, admission and intravenous acyclovir (A) or admission and intravenous gentamicin (B) is not warranted. If bacterial pericarditis were suspected, admission for IV antibiotics would be indicated. Intravenous acyclovir is used to severe manifestations of herpes viral infections. Outpatient follow-up and oral prednisone (D) may be used if this patient fails to respond to treatment with NSAIDs or has a contraindication to NSAIDs. Prednisone increases the risk for recurrence of pericarditis.

Coarctation of the Aorta

PE will show higher blood pressure in the arms than in the legs • EKG will show LVH • CXR will show notching of ribs • Diagnosis is made by echo • Treatment is balloon angioplasty with stent placement, or surgical correction • Comments: Associated with Turner's syndrome

A 44-year-old woman presents with a three day history of pleuritic chest pain radiating to the back. It is worsened by lying supine. On examination, a friction rub is appreciated when she leans forward. Which of the following would you expect to see on her ECG? Peaked T waves in V1-V6 PR depression in aVR PR depression in II, aVF, and V4-V6 ST segment elevation in the anterior leads with reciprocal changes inferiorly

PR depression in II, aVF, and V4-V6 Pericarditis is a syndrome characterized by inflammation of the pericardium. There are many possible causes including infectious, infiltrative, uremic, and post-MI, but most cases are idiopathic. Patients present with chest pain that is typically described as sharp and pleuritic and may radiate to the shoulder. It is worse with lying supine and improved with sitting forward. On exam, the friction between the inflamed visceral and parietal pericardium results in a rub which is best heard over the left sternal border and may be intermittent. It can be accentuated by having the patient lean forward in full expiration. The ECG is the most reliable diagnostic tool. Diffuse ST elevations and PR depressions in V2-V6, I, II, III, aVL and aVF are seen in the first hours to days of illness with reciprocal ST depression and PR elevation in aVR. In contrast to changes seen in acute myocardial infarction, the ST segments are concave, diffuse and not associated with T wave inversions initially. Over the course of one to three weeks, the ST segments will normalize and the T waves flattened. The flattened T waves can later become inverted followed by a return to a normal appearing ECG after many weeks. Peaked T waves (A) can be seen in hyperkalemia and early MI but are not seen in pericarditis. While PR depression is seen in most leads, the PR segment is elevated in aVR (B). The ST elevations in pericarditis are diffuse (D) and do not follow the typical patterns of acute myocardial infarction.

A 67-year-old woman with sick sinus syndrome complains of significant lightheadedness. If she is driving and a "dizzy spell" begins, she has to pull off the road and wait for it to pass. You capture an ECG during one of her spells in the office and note a bradycardia in the 50s. Which of the following is the best treatment recommendation? Atenolol Defibrillator Digitalis Pacemaker

Pacemaker Sick sinus syndrome occurs as a result of disease of the sinoatrial (SA) node. It is associated with tachycardia-bradycardia syndrome in which the sinus rate varies from fast to slow and back again. ECG shows an irregular rhythm with pauses in sinus activity. Many patients with sick sinus syndrome respond favorably to permanent pacemaker placement. In fact, the treatment of choice for any symptomatic bradycardia that accompanies sick sinus syndrome is pacemaker placement. Atenolol (A) and other beta-blockers may cause sinoatrial arrest or block in patients with sick sinus syndrome. Digitalis (C) may cause bradydysrhythmias in patients with sick sinus syndrome. Defibrillators (B) are not recommended in the treatment of sick sinus syndrome.

What is the treatment of choice for the bradycardic component of sick sinus syndrome? Ablation of accessory pathways Chronotropic medications No treatment is necessary Pacemaker

Pacemaker Treatment generally requires a permanent pacemaker to prevent sinus arrest. The term sick sinus syndrome was coined to describe patients with SA node dysfunction that causes marked sinus bradycardia or sinus arrest. Often, junctional escape rhythms occur, which may lead to symptoms of lightheadedness and syncope. In some patients with sick sinus syndrome, bradycardic episodes are interspersed with paroxysms of supraventricular tachycardia (atrial fibrillation, atrial flutter, PSVT). Sometimes the bradycardia occurs immediately after spontaneous termination of the tachycardia. An important subset of patients are those with paroxysmal atrial fibrillation that have marked sinus bradycardia and even sinus arrest after spontaneous conversion of atrial fibrillation. The term brady-tachy syndrome has been used to describe patients with sick sinus syndrome who have both tachydysrhythmias and bradydysrhythmias. The diagnosis of sick sinus syndrome and, in particular, the brady-tachy variant often requires monitoring the patient's heart rhythm over several hours, days, or even weeks. A single ECG strip may be normal or may reveal only the bradycardic or tachycardic episode. Ablation of accessory pathways (A) and medications (B) are often used after pacemaker placement to control the tachcycardias. Without pacemaker placement (C), these patients can have sinus arrest.

Varicose Veins

Patient will be a woman • Complaining of a dull ache in her legs after prolonged standing • PE will show dilated, elongated subcutaneous veins • Diagnosis is made by duplex ultrasound • Treatment is leg elevation and compression stockings

Pericardial Tamponade

Patient will be complaining of dyspnea and chest pain PE will show muffled heart sounds, JVD, hypotension (Beck's triad), pulsus paradoxus ECG will show low voltage QRS, electrical alterans Echocardiography will show diastolic collapse of RV Treatment is pericardiocentesis

Pericardial Tamponade

Patient will be complaining of dyspnea and chest pain • PE will show muffled heart sounds, JVD, hypotension (Beck's triad), pulsus paradoxus • ECG will show low voltage QRS, electrical alterans • Echocardiography will show diastolic collapse of RV • Treatment is pericardiocentesis

Endocarditis

Patient will be complaining of fever, rash, cough and myalgias • PE will show Fever, Roth spots, Osler nodes, Murmur, Janeway lesions, Anemia, Nailbed hemorrhages, Emboli (FROM JANE) • Diagnosis is made by echocardiography and Duke's criteria • Most commonly caused by: . IVDA: S. aureus, tricuspid . Native valve: Streptococci, mitral • Treatment is antibiotics • Comments: GI malignancy: S. bovis

Hyperthyroidism

Patient will be complaining of heat intolerance, palpitations, weight loss, tachycardia, and anxiety PE will show hyperreflexia Labs will show low TSH and high free T4 Most commonly caused by Graves disease (autoimmune against TSH receptor) Treatment is methimazole or PTU Comments: Propylthiouracil (PTU) P for pregnant

Pericarditis

Patient will be complaining of pleuritic chest pain radiating to the back that is worse when laying back and improved when leaning forward • PE will show tachycardia and pericardial friction rub • ECG will show PR depression, PR elevation (aVR), diffuse ST segment elevation (concave) • Most commonly caused by Idiopathic then viral (Coxsackie) • Treatment is NSAIDs

Aortic Dissection

Patient will be older • With a history of HTN, smoking, Marfan syndrome • Complaining of sudden "ripping" or "tearing" CP radiating to back • PE will show asymmetric pulses/BP • CXR will show widened mediastinum • Diagnosis is made by CT or transesophageal echocardiogram (TEE) • Treatment is reduce BP, surgery

Aortic Stenosis

Patient will be older • With a history of diabetes, hypertension • Complaining of dyspnea, chest pain, syncope • PE will show crescendo-decrescendo systolic murmur that radiates to the carotids, paradoxically split S2, S4 gallop • Most commonly caused by degenerative calcification • Treatment is aortic valve replacement • Comments: murmur decreases with Valsalva

Aortic Stenosis

Patient will be older • With a history of diabetes, hypertension • Complaining of dyspnea, chest pain, syncope • PE will show crescendo-decrescendo systolic murmur that radiates to the carotids, paradoxically split S2, S4 gallop • Most commonly caused by degenerative calcification • Treatment is aortic valve replacement • Comments: murmur decreases with valsalva

Rheumatic Fever

Patient with a history of GAS infection • Complaining of fever, red skin lesions on the trunk and proximal extremities, and small, non-tender lumps located over the joints • PE will show JONES criteria: Joints, Oh, no carditis!, Nodules, Erythema marginatum, Sydenham's chorea • Labs will show anti-streptolysin O, anti-DNase B, positive throat culture, or positive rapid antigen test • Treatment is antibiotics, NSAIDs • Comments: Modified Jones Criteria for a first episode of acute rheumatic fever: need 2 major or 1 major and 2 minor

Prinzmetal Angina (Variant Angina)

Patient with a history of HTN, smoking, DM, obesity, or cocaine use • Complaining of squeezing, pressure-like chest discomfort at rest • ECG will show transient ST-segment elevations and cardiac enzymes will be normal • Diagnosis is made by cardiac stress test • Most commonly caused by coronary artery spasm • Treatment is calcium channel blockers and nitrates

Dressler's Syndrome

Patient with a history of MI • Complaining of pleuritic chest pain radiating to the back, worse when laying back, improved when leaning forward • PE will show tachycardia and pericardial friction rub • ECG will show PR depression, PR elevation (aVR), diffuse ST segment elevation (concave) • Treatment is colchicine, steroids, NSAIDs

Tetralogy of Fallot

Patient with a history of episodes of cyanosis (tet spells) and squatting for relief • PE will show pulmonic stenosis, right ventricular hypertrophy, overriding aorta, VSD • CXR will show "boot-shaped" heart • Comments: Most common cyanotic congenital heart disease • Mnemonic: PROVe:: Pulmonic stenosis, Right ventricular hypertrophy, Overriding aorta, VSD

Tetrology of Fallot

Patient with a history of episodes of cyanosis (tet spells) and squatting for relief • PE will show pulmonic stenosis, right ventricular hypertrophy, overriding aorta, VSD • CXR will show "boot-shaped" heart • Comments: Most common cyanotic congenital heart disease • Mnemonic: PROVe:: Pulmonic stenosis, Right ventricular hypertrophy, Overriding aorta, VSD

Mitral Regurgitation

Patient with a history of ischemic heart disease, endocarditis, MI, trauma • Complaining of dyspnea • PE will show blowing holosystolic mumur, best heard at apex with radiation to axilla, pulmonary edema, cardiogenic edema • Diagnosis is made by echo • Treatment is nitroprusside, dobutamine, intraaortic balloon pump, emergency surgery

Hyperkalemia

Patient with a history of renal failure, DKA, rhabdomyolysis, tumor lysis Complaining of lethargy, weakness, paralysis PE will show bradycardia, hypotension, cardiac dysrhythmia ECG will show peaked T waves, prolonged PR, wide QRS Treatment is calcium gluconate, insulin, albuterol, kayexalate, bicarbonate

Mitral Stenosis

Patient with a history of rheumatic heart disease Complaining of exertional dyspnea, hemoptysis PE will show loud S1, opening snap, low-pitched, rumbling diastolic apical murmur Most commonly caused by rheumatic heart disease Comment: Antibiotic prophylaxis for procedures prone to bacteremia

Mitral Stenosis

Patient with a history of rheumatic heart disease • Complaining of exertional dyspnea, hemoptysis • PE will show loud S1, opening snap, low-pitched, rumbling diastolic apical murmur • Most commonly caused by rheumatic heart disease

A patient is being evaluated for dyspnea and lower extremity swelling. On physical exam the patient has jugular venous distention with inspiration and 2 + pedal edema. Hepatojugular reflex is present. The patient has clear lung fields and no murmur is appreciated. Which of the following findings would support the diagnosis of constrictive pericarditis over restrictive cardiomyopathy? Cardiomegaly Left bundle branch block Pericardial knock S3 heart sound

Pericardial knock A Pericardial knock is associated with constrictive pericarditis, which is the most likely diagnosis in this patient. Approximately 50% of patients with constrictive pericarditis present with a pericardial knock, which is an accentuated heart sound occurring slightly earlier than a third heart sound. This would not be expected in restrictive cardiomyopathy. Conversely, an audible S3 is frequently present in persons with restrictive cardiomyopathy because of the abrupt cessation of the rapid ventricular filling. Constrictive pericarditis is a rare but disabling condition characterized by impaired filling resulting from restraint of ventricular diastolic expansion by a stiff pericardium. Any cause of pericarditis can lead to the condition. Some common causes include viruses, cardiac surgery, mediastinal irradiation and connective tissue disease. Patients present with dyspnea, fatigue and peripheral edema. Examination may show evidence of right sided heart failure including ascites, pedal edema, hepatojugular reflex and jugular vein engorgement with inspiration, also known as a Kussmaul sign. Pulmonary congestion is absent. Both constrictive pericarditis and restrictive cardiomyopathy can present with signs and symptoms of right sided heart failure making it difficult to distinguish one from the other. Further diagnostic testing and specific physical exam findings can aid in making the correct diagnosis. A S3 heart sound (D) is frequently present in persons with restrictive cardiomyopathy while an accentuated S2 or pericardial knock is associated with constrictive pericarditis. Cardiomegaly (A) on chest x-ray is more suggestive of restrictive cardiomyopathy whereas radiographic evidence of a calcified pericardium strongly suggests constrictive pericarditis. Depolarization abnormalities, such as a left bundle branch block (B) on electrocardiogram strongly favor restrictive cardiomyopathy.

A 76-year-old man with colorectal cancer presents to the ED with dyspnea and fatigue. He is hypotensive, tachycardic, tachypneic and afebrile. The jugular venous pulse rides high on lateral neck inspection. Cardiac sounds, but not breath sounds, are distant. There is no discernable friction rub or murmur, however, his blood pressure decreases during inspiration. An ECG reveals normal rhythm, increased rate and decreased voltages. Which of the following treatments is most appropriate in this patient's plan of care? Cardioversion Endarterectomy Hemodialysis Pericardiocentesis

Pericardiocentesis This scenario most likely represents cardiac tamponade. Pericardial tamponade refers to the dampening effect of rapidly accumulating pericardial effusion. An increase in intrapericaridal pressure compresses the heart chambers, decreases venous return and ultimately decreases cardiac output. As this occurs, it becomes ever more difficult for blood to flow from chamber to chamber. Causes include pericarditis, traumatic aortic dissection and myocardial rupture. Patients usually present with severe dyspnea, fatigue and hypotension. Typical exam findings include Beck's triad of hypotension, distant heart sounds and increased jugular venous pressure. Tachycardia and clear-sounding tachypnea are common. Pulsus paradoxus, a decrease in systolic blood pressure more than 10 mm Hg during inspiration, is also commonly present. However, pulsus paradoxus also accompanies constrictive pericarditis, congestive heart failure, pulmonary embolism, and end-stage obstructive pulmonary disease. Distant heart sounds and friction rubs may be present. Chest radiographs show large cardiac silhouettes, and ECGs may reveal a widespread decrease in voltage with an effusion and electrical alternans in tamponade. Classic echocardiographic findings are effusion, interventricular septal shift during inspiration, diastolic collapse of the right atrium and respiration-timed alterations in transvalvular flow. This medical emergency is treated with cardiopulmonary stabilization, pericardiocentesis (percutaneous drainage of pericardial fluid), cautious volume replacement and inotropic medications such as dobutamine. Cardioversion (A) is an electrophysiological treatment used to reverse arrhythmias, such as atrial fibrillation. This patient has a normal rhythm. Endarterectomy (B) is a surgical procedure used to remove atheromatous plaque from within a vessel. It is commonly used in the carotid arteries and aorta of patients with chronic atherosclerosis and distal ischemia, such as stroke symptoms or painful distal vasculopathy. This patient does not present with neurologic or peripheral arterial disease complaints. Hemodialysis (C) is used for patients with end-stage renal failure.

A 55-year-old man is being evaluated for sudden onset of chest pain. He describes the pain as sharp that is improved by sitting up and leaning forward. The chest pain is made worse by inspiration or coughing. An ECG shows new widespread ST segment elevation. Auscultation over the left sternal border is heard in the above audio clip. Which of the following is the most likely diagnosis? Aortic stenosis Mitral stenosis Patent ductus arteriosus Pericarditis

Pericarditis A pericardial friction rub is most commonly associated with pericarditis. It resembles the sound of squeaky leather and is often described as grating, scratching, or rasping. The pericardium is a double-walled sac around the heart. The inner (visceral) and outer (parietal) layers are normally lubricated by a small amount of pericardial fluid, but when inflammation of pericardium is present, the 2 walls move against each other with audible friction (the rub). In children, rheumatic fever is often the cause of pericardial friction rub. The friction rub is usually best heard between the apex and sternum but may be audible across the precordium. The murmur associated with aortic stenosis (A) is associated with an easily heard systolic, crescendo murmur loudest along the upper right sternal border at the 2nd right intercostal space radiating to the carotid arteries bilaterally. The murmur associated with mitral stenosis (B) is mid-diastolic and has a rumbling character. It is best heard with the bell of the stethoscope in the left ventricular impulse area with the patient in the lateral decubitus position. It usually starts with an opening snap. A patent ductus arteriosus (C) is classically associated with a machinery, crescendo/decrescendo murmur continuous from systole to diastole.

A 15-year-old male presents with sharp substernal chest pain that is relieved by sitting up and leaning forward. Cardiac auscultation is normal. What is his chest pain most likely due to? Coronary ischemia Costochondritis Esophageal spasm Pericarditis

Pericarditis Pericarditis is caused by isolated inflammation of the pericardium. Its etiology is primarily idiopathic. Other causes include infection (Coxsackie most common), malignancy, drug-induced, connective tissue disorders, and postinfarction (Dressler syndrome). Patients often complain of pleuritic chest pain that radiates into the back. Pain is classically worse when lying back and relieved by sitting up and leaning forward. On exam, patients may be tachycardic and have a pericardial friction rub, which is often difficult to hear and may vary in intensity over time. Characteristic ECG findings include PR depression, PR elevation (aVR), and diffuse concave ST segment elevation most prominent in the precordium. Management usually includes supportive care and NSAIDs. The patient is unlike to have coronary ischemia (A) given his age. Costrochondritis (B) is also an inflammatory condition that is often seen in young patients. This condition will cause pain in the costrochondral joints that worsens with all movements. It is generally not relieved by sitting forward. Esophageal spasm (C) can cause intense, sharp chest pain, but is not positional.

The ankle-brachial index is used to evaluate which disease?

Peripheral arterial disease (normal is 0.9-1.4; < 0.9 = PAD; >1.4 = calcified PAD).

What is the definitive treatment for sinus bradycardia?

Permanent pacemaker.

What vascular emergency of the leg results from a large DVT?

Phlegmasia cerulea dolens.

A 62-year-old man reports to the ED with new-onset, crushing, left-sided chest pain, radiating to the left arm that began suddenly 35 minutes prior to arrival. The patient has a history of hypertension, hypercholesterolemia, diabetes mellitus, and a 60-pack-year smoking history. His EMS ECG demonstrates ST-segment elevation in leads II, III, and aVF. In the ED, his vital signs are BP 135/75, HR 98, and RR 18. What is the most appropriate next step? Arrange for the patient to have an emergent stress test Call the cath lab emergently and prepare the patient for transport Give the patient nitroglycerin and draw labs, including troponins Place the patient on a cardiac monitor, give the patient oxygen if hypoxic and administer aspirin

Place the patient on a cardiac monitor, give the patient oxygen if hypoxic and administer aspirin This patient has an acute myocardial infarction (MI). An acute MI is clinically characterized by left-sided, substernal, chest pain (often described as an "elephant on my chest," tightness, or pressure rather than pain itself) that radiates down the left arm or left jaw, diaphoresis, nausea/vomiting, and shortness of breath. These symptoms are a result of myocardial death due to coronary vessel occlusion or vasospasm, often as a result of rupture of an atherosclerotic plaque. The definition of an acute MI, as described by the European Society for Cardiology and American College of Cardiology (ACC) is a rise and fall of a cardiac biomarker (troponin) in addition to clinical symptoms, ECG changes, or coronary artery changes as noted on an interventional level. Risk factors for an acute MI include hypertension, hypercholesterolemia, diabetes, tobacco, male, increased age, and family history. This patient has ST-segment changes in leads II, III, and aVF, correlating to an inferior wall MI. In a patient with an acute MI, the first step in management is to place the patient on a cardiac monitor to recognize any dysrhythmias, establish a peripheral IV, give oxygen if hypoxic, and administer aspirin. An ischemic right ventricle becomes preload dependent because it can no longer pump blood to the left side of the heart. Administering nitroglycerin (C) (a preload reducer) to a patient having ischemia of the right ventricle can lead to severe hypotension. Because the right coronary artery often supplies the inferior aspect of the heart and the right ventricle, whenever there is evidence of ST-segment elevation in the inferior leads (II, III, aVF), it is important to exclude a right ventricular infarct by obtaining "right-sided leads." This is performed by placing the precordial leads on the right side of the patient's chest instead of the left. Lead rV4 is thought to be the most sensitive in identifying a right ventricular infarct. Similarly, labs, including serial cardiac biomarkers (troponin) should be drawn; however, this is not the most appropriate next step. It is important to notify the cath lab (B) of the patient's need for percutaneous intervention, but the first priority are the ABCs and administering an aspirin. The cath lab should be notified immediately after this is performed. Although a stress test (A) would be useful in a patient with cardiac risk factors, this patient has active cardiac symptoms and the ACC/AHA guidelines recommend such testing be performed when patients are free of ischemic or heart failure symptoms for at least 8-12 hours. In addition, this patient has evidence for a STEMI and should undergo percutaneous intervention in the cath lab.

Name three genetic disorders, and their respective protein abnormalities, that are associated with aortic dissection?

Polycystic kidney disease (polycystin), Marfan's syndrome (fibrillin) and Ehlers-Danlos IV (type 3 procollagen).

A previously healthy 16-year old boy presents to your office after having a syncopal episode at the start of track practice. An ECG reveals a QTc of 520 ms. This is confirmed on a subsequent ECG. This finding is associated with which one of the following rhythm abnormalities? Paroxysmal supraventricular tachycardia Polymorphic ventricular tachycardia Sinus arrest Third degree atrioventricular block

Polymorphic ventricular tachycardia Patients with repeated ECGs showing a QTc interval > 480 ms with a syncopal episode, or > 500 ms in the absence of symptoms, are diagnosed with long QT syndrome if no secondary cause such as medication use is present. Prolong QT interval is associated with polymorphic ventricular tachycardia, including torsades de pointes, and sudden cardiac death. Most cardiac events are precipitated by vigorous exercise or emotional stress, but they also can occur during sleep. Long QT syndrome is usually diagnosed after a person has a cardiac event such as syncope or cardiac arrest. In some situations, this condition is diagnosed after a family member suddenly dies. It may be treated with beta-blockers and implanted cardioverter defibrillators. Patients with long QT syndrome should avoid participation in competitive sports, strenuous exercise, and stress-related emotions. Epinephrine adrenaline for local anesthesia and asthma medication should be avoided in patients with long QT syndrome. Other medications that should be avoided include certain antibiotics, antifungals, antihistamines, antiarrythmics and psychotropic medications which prolong the QT interval. Third-degree atrioventricular block (D) results from various pathologic states causing infiltration, fibrosis, or loss of connection in portions of the healthy conduction system. Third-degree atrioventricular block can be either congenital or acquired. Paroxysmal supraventricular tachycardia (A) is a narrow-complex tachycardia that has a regular, rapid rhythm and is triggered by a reentry mechanism. This may be induced by premature atrial or ventricular ectopic beats. Other triggers include hyperthyroidism and stimulants, including caffeine, drugs, and alcohol. Paroxysmal supraventricular tachycardia is observed not only in healthy individuals; it is also common in patients with previous myocardial infarction, mitral valve prolapse, rheumatic heart disease, pericarditis, pneumonia, chronic lung disease, and current alcohol intoxication. Sinoatrial arrest (C) is when the sinoatrial node of the heart transiently ceases to generate the electrical impulses that normally stimulate the myocardial tissues to contract. It is defined as lasting from 2.0 seconds to several minutes. None of the above are associated with long QT syndrome.

What other disease do up to 50% of patients with temporal arteritis also have?

Polymyalgia rheumatica, which manifests as proximal muscle pain and stiffness, often involving the upper > lower extremities.

What is Dressler's syndrome?

Post-myocardial infarction pericarditis.

Hypertension: Eighth Joint National Committee (JNC 8) Recommendations

PreHTN: systolic blood pressure (SBP) 120-139 mmHg or diastolic blood pressure (DBP) 80-89 mmHg • Stage I HTN: SBP 140-159 mmHg or DBP 90-99 mmHg • Stage II HTN: SBP >160 mmHg or DBP >100 mmHg • Treatment goals: . >60 years: SBP <150, DBP <90 . All others: SBP <140, DBP <90 • 1st line rx for general population: thiazide, CCB, ACEI, or ARB • 1st line rx for African Americans: CCB or thiazide • Chronic kidney disease: Rx should include ACEI or ARB

A patient with sarcoidosis presents with progressive peripheral edema. Echocardiography reveals restrictive cardiomyopathy. In addition to diuresis and heart rate control, which of the following is also appropriate? Buspirone Melphalan Phlebotomy Prednisone

Prednisone Infiltrative myocardial deposition usually results in restrictive cardiomyopathy (RCM). Evaluation begins with the typical heart failure work-up of chest radiograph, ECG, echocardiogram, cardiac MRI and possibly cardiac catheterization. A chest radiograph may show enlarged atria and normal ventricles. ECG may reveal low voltages and tachyarrhythmias. Echocardiographic findings typical of RCM include bilateral atrial enlargement, normal or thickened ventricular walls, decreased right > left ventricular walls, mural thrombi and diastolic dysfunction. A cardiac MRI may show myocardial inflammation or infiltrates. Endocardial biopsy may be necessary to confirm a diagnosis. Treatment of RCM is difficult due to the relative refractoriness of many of the underlying pathologies. Specific augmentative treatments are aimed at the underlying disorder. One example is corticosteroids, like prednisone or prednisolone, used to control sarcoidosis and Loeffler's endocarditis. Gentle diuresis may be helpful. Anticoagulation is usually considered. Serotonin agonists are contraindicated in patients with restrictive cardiomyopathy, as these drugs, like buspirone (A), cisapride and sumatriptan, can cause decreased compliance of the endomyocardium, and actually lead to restrictive cardiomyopathy. Chemotherapy, like melphalan (B) and cyclophosphamide, is used to decrease the amount of abnormal cells in amyloid restrictive cardiomyopathy. Phlebotomy (C) and chelation therapy are used to control the complications of hemochromatosis.

What is the diagnostic criteria for pre-eclampsia?

Preeclampsia refers to the syndrome of new onset of hypertension and either proteinuria or end-organ dysfunction during pregnancy.

What are contraindications to lower extremity ablation therapy?

Pregnancy, thromboembolism, moderate to severe peripheral artery disease, joint disease that affects mobility, and congenital venous abnormality.

A 78-year-old man complains of his "heart -stopping". After reviewing his ECG, you appreciate intermittent, large, wide QRS complexes which are not preceded by a P wave. Otherwise, the rhythm strip appears normal without PR interval, ST segment, P wave or T wave abnormalities. Which of the following is the most likely diagnosis? Atrial fibrillation Multifocal atrial tachycardia Non-ST-elevation myocardial infarction Premature ventricular contraction

Premature ventricular contraction Premature ventricular contractions (PVCs) appear as abnormal QRS complexes and T waves that occur in another underlying rhythm. PVCs have 6 characteristics: (1) Occur earlier than the next expected normal QRS; (2) Wider than a normal QRS; (3) QRS morphology is generally bizarre; (4) Preceding P wave is absent; (5) Deflection of the ST segment and T wave is opposite that of the QRS; (6) Followed by a compensatory pause. In general, PVCs are benign. However, when more than 3 occur simultaneously at a rate greater than 100, it is considered ventricular tachycardia. Atrial fibrillation (A) is diagnosed when disorganized electrical activity is seen in place of normal P waves. Apart from the intermittent oddly shaped QRS complex, the remainder of this patient's ECG shows normal P waves. Multifocal atrial tachycardia (B) is characterized by an irregular rhythm with rate > 100 and 3 or more P waves of variable morphology and PR interval variability. NSTEMI (C) is associated with T wave inversion and ST segment depression.

What is the carotid sinus reflex?

Pressure applied to the carotid sinus enhances the baroreceptor firing rate and activates vagal efferents, thereby slowing the heart rate and reducing blood pressure.

Which of the following is an independent cause of secondary hypertension? Addison's disease Atrial fibrillation Hypercholesterolemia Primary aldosteronism

Primary aldosteronism Primary aldosteronism is a potential cause of secondary hypertension. Hypertension can be divided into essential or secondary hypertension. Approximately 95% of patients with elevated blood pressure have essential hypertension. Secondary cause of elevated blood pressure should be suspected in patients with severe or resistant hypertension, in patients younger than 30 years without risk factors for hypertension, in patients with malignant hypertension, or hypertension onset before the age of puberty. Potential causes of secondary hypertension include renovascular disease, primary kidney disease, primary aldosteronism, obstructive sleep apnea, long-term corticosteroid use, coarctation of the aorta, thyroid disease, drugs, or pheochromocytoma. Renovascular disease is the most common potentially correctable cause of secondary hypertension. Signs, symptoms, and laboratory findings are dependent upon the etiology. Patients with secondary hypertension due to renovascular disease may present with an abdominal bruit or decreased kidney function after initiating antihypertensive therapy. Primary aldosteronism typically causes hypokalemia, mild hypernatremia, or drug-resistant hypertension. Patients with sleep apnea are usually obese and may complain of daytime somnolence, fatigue, headache, or depression. Drug-induced hypertension can be caused by oral contraceptives, decongestants, nonsteroidal anti-inflammatory drugs (NSAIDs), or cocaine. The treatment of secondary hypertension is based upon the underlying etiology. Complications of untreated hypertension include heart failure, cerebrovascular disease, renal insufficiency, and aortic dissection. Addison's disease (A), or chronic adrenocortical deficiency, is a result of dysfunction or absence of the adrenal cortices. This results in a loss of cortisol production and subsequent elevation of serum adrenocorticotropic hormone (ACTH). Autoimmune destruction is the most common cause of Addison's disease in the United States. Patients with Addison's disease typically present with hyperpigmentation of the skin, weakness, weight loss, anorexia, irritability, and hypotension. The majority of patients with Addison's disease have a systolic blood pressure of less than 110 mm Hg. Atrial fibrillation (B) is not a cause of secondary hypertension. Atrial fibrillation has the potential to cause severe hypotension and shock due to insufficient cardiac output. Hypercholesterolemia (C) is not an independent cause of secondary hypertension. However, hypercholesterolemia is a risk factor for the development of atherosclerosis. Atherosclerosis can cause renal vascular stenosis, which is potential cause of secondary hypertension.

A 65-year-old man is brought to the ED complaining of nausea for the last two hours. On arrival to the emergency department, he has the cardiac rhythm seen above. His blood pressure is 110/70 mm Hg. He denies any headache, chest pain, or difficulty breathing. Which of the following is the most appropriate next step in management? Defibrillation Magnesium sulfate Procainamide Synchronized cardioversion

Procainamide The rhythm seen in the image is a monomorphic ventricular tachycardia. This occurs in most cases due to the presence of scar tissue in the myocardium. The first objective for treating any patient with a wide-complex tachycardia (WCT) is to evaluate for hemodynamic instability (hypotension, chest pain, dyspnea, altered mental status) because any patient with a WCT can deteriorate quickly as the rhythm degenerates into ventricular fibrillation. In stable patients, procainamide is the drug of choice and will terminate the rhythm in the vast majority of cases. It is superior to amiodarone and lidocaine. Not only is it useful in the termination of stable ventricular tachycardia, but it also blocks accessory pathway conduction, which terminates preexcited tachycardias. Sotalol, a class III antidysrhythmic with beta-blocker properties, can also be used in such patients though it is considered a second-line alternative. Defibrillation (A) is reserved for pulseless ventricular tachycardia and ventricular fibrillation. Magnesium sulfate (B) is the treatment of choice for polymorphic ventricular tachycardia (torsades de pointes). If medical management fails or the patient begins to decompensate, the patient should immediately receive synchronized cardioversion (D).

What drug is safe to administer to a patient with wide complex irregular tachycardia?

Procainamide.

Second Degree Heart Block, type I (Wenkebach/Mobitz I)

Progressive prolongation of PR interval until one QRS complex is dropped

What is the other class IC antiarrhythmic medication?

Propafenone

Which of the following is a medical treatment for congenital long QT syndrome? Flecainide Propafenone Propranolol Quinidine

Propranolol Propranolol is the appropriate treatment for congenital long QT syndrome as beta blockers are the mainstay of treatment for this condition. Long QT syndrome is the most common channelopathy and is thought to affect 1 in 5000 persons. It is a disorder of myocardial repolarization characterized by a prolonged QT interval on ECG and an increased risk of sudden cardiac death: QTc is usually > 460 ms. This syndrome is associated with an increased risk of a characteristic life threatening polymorphic ventricular tachycardia known as torsades de pointes or "twisting of the points." The primary symptoms in patients with long QT syndrome include palpitations, syncope, seizures, and cardiac arrest, and patients usually have syncope related to polymorphic ventricular tachycardia. Factors conferring the highest risk for sudden cardiac death include a history of sudden cardiac arrest, recent syncope, and QTc interval greater than 500ms. Beta blockers, such as propranolol, have shown to reduce both syncope and sudden cardiac death. The goal of beta blocker therapy is to blunt the maximal heart rate achieved during exertion and are thought to interrupt the "trigger" for torsades de pointe and shorten the QT interval. Flecainide (A) and propafenone (B) are both class IC III antiarrhythmics which are commonly used for atrial and ventricular dysrhythmias; however, they can lengthen the QT interval. Quinidine (D) is a class IA antiarrhythmic that can also lengthen the QT interval.

Cor Pulmonale

Pulmonary HTN + RVH → right heart failure • Most common chronic cause: COPD • Most common acute cause: PE • Right heart catheterization

Which of the following is most closely associated with the development of acute cor pulmonale? Acute bronchitis Health care associated pneumonia Heart failure Pulmonary embolism

Pulmonary embolism Cor pulmonale is defined as an alteration in the structure and function of the right ventricle caused by a primary disorder of the respiratory system. Pulmonary hypertension is the common link between lung dysfunction and the heart in cor pulmonale. Cor pulmonale is usually a chronic condition, but acute pulmonary embolism (more common) and acute respiratory distress syndrome are associated with acute cor pulmonale. The underlying pathophysiology in massive pulmonary embolism causing cor pulmonale is the sudden increase in pulmonary resistance. In chronic cor pulmonale, RV hypertrophy (RVH) generally predominates. In acute cor pulmonale, right ventricular dilation mainly occurs. Acute bronchitis (A) is not associated with cor pulmonale. Heart failure (C) results from an abnormality in systolic or diastolic cardiac function. Chronically increased left heart pressures in poorly controlled heart failure can lead to cor pulmonale, but in most patients, this does not occur. Pneumonia (B) can increase cardiac demands but generally does not lead to pulmonary hypertension or right ventricular dilation.

Which of the following conditions would most likely result in right axis deviation on an ECG? Aortic valve stenosis Chronic hypertension Excess abdominal fat Pulmonary hypertension

Pulmonary hypertension Axis is the direction of depolarization in the heart, from the atria and spreading to the ventricles. Because the left ventricle makes up the bulk of ventricular depolarization, the resultant normal axis for the heart is toward the left ventricle. In pulmonary hypertension, the right side of the heart must work harder to overcome the increased resistance, or afterload, of the higher pressures in the pulmonary vasculature. This results in right ventricular hypertrophy; the direction of depolarization is now in the right axis. Aortic valve stenosis (A) is a condition where the aortic valve does not completely open, resulting in the left ventricle having to work harder to overcome this resistance. This often leads to left ventricular hypertrophy. This is associated with a left axis deviation because there is even more left ventricular muscle depolarizing. Excessive abdominal fat (C) can also cause left axis deviation because the heart may sit more horizontally because it is being pushed up by the excessive adipose tissue in the abdomen. Chronic hypertension (B) is associated with increased afterload, which leads to left ventricular hypertrophy and left axis deviation.

Which of the following is the most common physical exam finding in an abdominal aortic aneurysm? Abdominal bruit Diminished femoral pulses Duodenal obstruction Pulsatile abdominal mass

Pulsatile abdominal mass A pulsatile abdominal mass is the most common physical examination finding in a patient with an abdominal aortic aneurysm (AAA). Patients with unruptured AAA rarely have any symptoms. If pain is present, it is usually gradual in onset and dull. Patients occasionally describe colicky pain that can be in the back or stomach making it easy to confuse this diagnosis with renal colic. The presence of acute severe pain typically heralds rupture. The most prominent physical examination feature is a pulsatile abdominal mass. Typically, the mass is palpated at the level of the umbilicus. The ability to palpate an AAA depends on the size of the AAA and the patients body habitus. An abdominal bruit (A) is an uncommon finding. Generally, patients have good distal perfusion and so femoral pulses will not be diminished (B). Duodenal obstruction (C) may occur but is very rare.

Right Bundle Branch Block (RBBB)

QRS > 120 ms • RSR' pattern in V1-V3 • Wide, slurred S wave in lateral leads

Inferior ST-Elevation Myocardial Infarction

RCA occlusion • ST elevations: II,III, aVF • RV infarction . ST elevations: V4R and V5R . JVD, hypotension . Rx: IVF • NTG contraindicated

Normal sinus rhythm

Rate 60-100 • Regular rhythm with P for every QRS • PR interval 120-200 • QRS 60-100

A 30-year-old woman with no past medical history presents to the emergency department complaining of substernal chest pain for two hours. It is not worse with exertion and was not relieved by sublingual nitroglycerin. She admits to some mild nausea. She does not smoke cigarettes or use any illicit drugs. Her family history includes a grandmother who died of a myocardial infarction at 84-years-old. Labs in the emergency department are unremarkable. Point of care troponin is negative and ECG reveals sinus rhythm. What is your next step in management? Dobutamine stress test Exercise stress test Reassurance Stress echocardiography

Reassurance Reassurance is most appropriate for this patient as her pretest probability for coronary heart disease it is very low. An initial estimate of the likelihood of coronary heart disease is referred to as the pretest probability and is based upon the clinical history. The pretest probability determines the need for noninvasive diagnostic tests or even coronary arteriography. The pretest probability is calculated using patient's age, sex and classification of their angina. Angina is classified as "typical," "atypical" or "nonanginal." Typical angina has three components: (1) sub-sternal pain or discomfort; (2) provoked by exertion or emotional stress; (3) relieved by rest or nitroglycerin or both. Atypical chest pain has two of the three components and nonanginal chest pain has one or none of the three components. In this clinical scenario, the patient is 30 years old, a woman, and has chest pain classified as nonanginal. This gives her a 2% likelihood of having coronary heart disease and stress testing is not indicated. Stress testing is typically needed for initial diagnosis and subsequent clinical management in patient with potential cardiac disease. The utility of cardiac stress testing is determined in part by pretest probability. In patients with low pretest probability, false positive results may lead to potential downstream testing and treatment that may cause more harm than good. Conversely, in patients with high coronary heart disease pretest probability, falsely negative studies lead to false security and missed diagnoses. Therefore, the greatest benefit is in patients with an intermediate pretest probability, in whom a positive test significantly increases the disease likelihood and a negative test significantly decreases the likelihood. Dobutamine stress test (A), exercise stress test (B) and stress echocardiography (D) are different forms of stress testing that have distinct indications including, but not limited to, the patient's ability to exercise, resting electrocardiogram, prior cardiac history, and structural heart status.

A 23-year-old man is admitted for a femur fracture. An admission ECG is shown above. What management is indicated? Atropine Beta blocker Reassurance Transvenous pacing

Reassurance The patient's ECG shows a first degree AV block; a normal variant finding in 2% of the population that requires no specific management. First degree AV block is defined as prolonged conduction of atrial impulses. The PR interval > 0.20 seconds (200 msec) and there is no loss of any atrial impulse. All impulses result in a ventricular response. Although it can be a normal variant, it can be seen in pathologic conditions like Lyme disease and should be followed up. However, no specific management is needed. Nodal depressing agents should be avoided or used with caution. Atropine (A) is required for patients with symptomatic bradycardia. Beta blockers (B) are AV nodal blockers and should be used with caution in patients with first degree AV blocks. Transvenous pacing (D) is required for higher degree AV blocks (second degree type II and third degree heart block).

Nitrate therapy works by which of the following mechanisms? Reducing afterload Reducing both preload and afterload Reducing cardiac contractility Reducing preload

Reducing both preload and afterload Nitrates work by reducing both preload and afterload. Nitroglycerine was the first treatment for angina pectoris and dates back to the 1800s. It still remains first-line drug therapy for many patients. Nitrates dilate veins and coronary arteries and to a lesser extent systemic arteries by relaxing vascular smooth muscle. Thus, nitrates reduce preload by increasing venous capacitance and improve coronary blood flow by coronary vasodilatation. Decreased preload lowers left ventricular end-diastolic pressure, thereby decreasing wall stress, resulting in a decrease in myocardial oxygen demand. At higher doses the afterload effects cause a drop in systemic blood pressure further decreasing wall stress and oxygen demand. Nitrates do not have a direct effect on cardiac chronotropy or inotropy. The primary adverse effects induced by nitrate therapy include hypotension, headache, and tachycardia. Nitrates should be avoided in patients with one or more of the following: systolic blood pressure less than 90 mm Hg, heart rate less than 50/min, or heart rate greater than 100/min. It should also be avoided in known or suspected right ventricular infarction, in patients who have taken a phosphodiesterase inhibitor for erectile dysfunction within the last 24 hours, in patients with hypertrophic cardiomyopathy or severe aortic stenosis. Nitrates do not work by only reducing afterload (A) or preload (D). Nitrates do not directly reduce cardiac contractility (C).

By what mechanism do ACE inhibitors cause hyperkalemia?

Reduction of aldosterone secretion.

A 35-year-old woman on oral contraceptives presents for evaluation of thigh pain and swelling. She was seen six days ago for the same complaint and had a negative ultrasound. Which of the following is the most appropriate plan? CT venogram Diuretic therapy Reassurance Repeat Doppler ultrasound

Repeat Doppler ultrasound Venous doppler ultrasound performed by a qualified sonographer has a sensitivity and specificity of approximately 95% in the detection of deep vein thrombosis (DVT) of the proximal leg. The evaluation typically includes three different points: common femoral vein, superficial femoral vein and the popliteal vein. In patients with a high pre-test probability (as in this case of a woman on oral contraceptive medication), a repeat doppler ultrasound is indicated in patients with persistent symptoms. An alternative approach on the initial visit is to also perform a D-dimer which if negative in combination with the three-point ultrasound excludes the diagnosis of DVT. CT venogram (A) is not routinely performed in the evaluation of a patient for DVT. Some centers combine CT venogram of the legs with CT angiogram of the chest performed for the evaluation of pulmonary embolism. Using this in combination does increase the overall sensitivity of CT imaging for these diagnoses. Diuretic therapy (B) would not be initiated by the physician for unilateral leg swelling. A patient needs follow-up with a provider in order to monitor the effects of diuretic and also a complete evaluation to look for other causes of the leg swelling. While reassurance (C) should always be provided to patients, in this case, a diagnosis has not yet been made and further testing is indicated.

A 59-year-old woman has furosemide-resistant peripheral edema and ascites. Her medical history is significant for sarcoidosis. You order an echocardiogram which reveals right ventricle with increased wall thickness and decreased cavity size, enlarged atria and a normal appearing left ventricle. Cardiac MRI shows no fatty deposition in the ventricular walls. Which of the following is the most likely diagnosis? Arrhythmogenic right ventricular cardiomyopathy Dilated cardiomyopathy Hypertrophic cardiomyopathy Restrictive cardiomyopathy

Restrictive cardiomyopathy Restrictive cardiomyopathy (RCM) is caused by decreased myometrial compliance in the absence of pericardial disease. Several etiologies exist including infiltrative disorders (e.g. amyloidosis, sarcoidosis and hemochromatosis), autoimmune disorders (e.g. scleroderma and polymyositis), storage disorders (e.g. Gaucher's and Fabry's), toxin exposure (e.g. anthracyclines and radiation), esosinophilic disorders (e.g. Loffler's disease), metastatic cancer and diabetes mellitus. In RCM, myocardial compliance is decreased, ventricular cavity size is decreased and wall thickness is normal or increased in a symmetric fashion. Right-sided heart failure is more common than left sided disease, and as such, patients present more with peripheral edema than pulmonary edema. Common associated findings include tachyarrhythmias, thromboembolism (mural thrombi may be seen on echocardiogram), hepatomegaly and ascites, increased jugular venous pulsation, regurgitant murmurs and S3 or S4. It is also common for patients with RCM to fail diuretic management of peripheral edema. Arrhythmogenic right ventricular cardiomyopathy (A) is an autosomal dominant genetic condition which is characterized by fatty or fibrous myocardial deposition. Manifestations include syncope, arrhythmias and sudden death, and less commonly heart failure symptoms. Dilated cardiomyopathy (B) is characterized by thin walled, large cavity sized ventricles. As compared to hypertrophic cardiomyopathy (C), restrictive cardiomyopathy affects the right ventricle more than the left ventricle. RCM is also more likely to produce biatrial enlargement and a normal left ventricle.

A 62-year-old man with a history of sarcoidosis presents to his cardiologist with dyspnea, fatigue, and signs of right-sided heart failure. Physical exam shows elevated jugular venous pressure and hepatomegaly. Echocardiogram shows reduced diastolic filling. Magnetic resonance imaging shows gadolinium hyperenhancement. Which of the following is the most likely diagnosis? Dilated cardiomyopathy Hypertrophic cardiomyopathy Restrictive cardiomyopathy Takotsubo cardiomyopathy

Restrictive cardiomyopathy Restrictive cardiomyopathy occurs due to fibrosis or infiltration of the ventricular wall because of collagen-defect diseases. It can occur due to amyloidosis, endomyocardial fibrosis, hemochromatosis or sarcoidosis. Patients often present with decreased tolerance of exercise. Pulmonary hypertension is common. In advanced cases, patients develop right-sided congestive heart failure. Physical exam shows elevated jugular venous pressure (JVP) and Kussmaul's sign (a paradoxical rise in JVP on inspiration). Chest radiography shows mild to moderate cardiomegaly. Echocardiography is key to diagnosis, showing rapid, early diastolic filling and a small-normal sized, thickened left ventricle. MRI shows gadolinium hyperenhancement. Diuretics may be useful symptomatic treatment. Prognosis is poor if due to amyloidosis. Cardiac transplantation can be used if there is no systemic involvement Dilated cardiomyopathy (A) is often idiopathic or associated with longstanding alcohol abuse. Left ventricular dilation and cardiomegaly occur. Physical examination shows S3 and elevated jugular venous pressure. Hypertrophic cardiomyopathy (B) leads to an increased risk of sudden death in young athletes. Most patients are asymptomatic; others present with dyspnea on exertion, angina, or syncope. Takotsubo myopathy (D) occurs after a large discharge of catecholamines due to a major stressor. It is more common in postmenopausal women. Symptoms include angina and dyspnea.

What is the most common cause of mitral stenosis?

Rheumatic heart disease.

Which common systemic diseases are associated with pericarditis?

Rheumatoid arthritis and connective tissue diseases.

Which of the following states a correct order of electrical current through the heart during one cycle of normal cardiac depolarization? Atrioventricular node -> sinoatrial node Bundle of His -> atrioventricular node Left bundle branch -> right bundle branch Right bundle branch -> purkinje fibers

Right bundle branch -> purkinje fibers A normal cycle of cardiac depolarization begins in the right atrium's sinoatrial node and passes through the right atrium's internodal tracts to activate the atrioventricular node. The AV node then sends the electrical impulse to the Bundle of His, which then passes current through the left and right bundle branches to the ventricular Purkinje fibers. Atrioventricular (AV) block is characterized as a delay in processing the electrical impulse within the atrioventricular node. This ultimately results in a delay in ventricular depolarization and contraction. There are three main types: first, second and third degree AV block. First-degree AV block is characterized as a prolonged PR interval > 0.2 sec, beginning at the start of the P wave and ending at the start of the QRS complex. Common causes of this type of block include electrolyte abnormalities, enhanced vagal tone (as in athletes), myocarditis or infarction and medications. Common medications which slow cardiac conduction through the AV node and produce a prolonged PR interval include beta and calcium-channel blockers, anticholinesterases and digitalis. Current passes normally from the SA to the AV node (A). Normal conduction is from the AV node to the Bundle of His (B), not the reverse. The left bundle does not normally propagate current to the right bundle (C).

Which of the following best describes the finding seen in the ECG above? Left bundle branch block Right bundle branch block Third-degree AV block Type I second-second degree AV block

Right bundle branch block Bundle branch blocks are abnormal conduction abnormalities (not rhythm disturbances) in which the ventricles depolarize in sequence, rather than simultaneously, thus producing a wide QRS complex (> 120 msec) and a ST segment with a slope opposite that of the terminal half of the QRS complex. A right bundle branch block (RBBB) is a unifascicular block in which ventricular activation is by way of the left bundle branch. The impulse travels down the left bundle, thus activating the septum from the left side (as it normally does in the absence of RBBB). This is followed by activation of the free wall of the left ventricle and finally the free wall of the right ventricle. Because of the two changes in direction, there is a tendency toward triphasic complexes in a RBBB (RSR'). The ECG in a RBBB will show a wide S wave in lead I and a RSR' pattern in lead V1. In left bundle branch block (A), lead I has a large R wave and in lead V1 there is a negative QS or rS complex. Third-degree AV block (C) presents with unmatched ratios of P waves to QRS complexes. Type I second-second degree AV block (D) has prolonged PR intervals.

What vessel is responsible for the majority of inferior myocardial infarctions?

Right coronary artery (80%) with the remainder due to occlusion of a dominant left circumflex artery.

A woman presents with dyspnea on exertion. Cardiac examination reveals an apical late diastolic murmur. You also notice pitting edema in both her legs. She undergoes echocardiographic testing. Which of the following abnormalities would you most expect to see on the echocardiogram? Decreased trans-mitral mean pressure gradient Increased opening of the mitral valve leaflets Left atrial hypertrophy Right ventricular hypertrophy

Right ventricular hypertrophy One of the diastolic murmurs is mitral stenosis, which is associated with rheumatic heart disease and endocarditis. This murmur is best appreciated at the apex with the bell, especially when the patient is placed in the left lateral decubitus position. It is characterized as a late diastolic, low frequency rumble which does not radiate. It is commonly associated with a left sternal border thrill. The intracardiac narrowing of this condition hampers outward flow from the left atrium, causing a "pressure back-up" into the pulmonary circulation and ultimately the right heart. Subsequently, right ventricular hypertrophy, and possibly right heart failure, are frequent associated findings. Symptoms of mitral stenosis include fatigue, weakness, dyspnea on exertion, orthopnea, palpitations and chest pain. If the condition is chronic, and right heart failure is present, peripheral edema, ascites and hepatomegaly may be present. Pregnancy and exercise can exacerbate the fatigue and weakness encountered in someone with mitral valve stenosis. An increased, not decreased, trans-mitral mean pressure gradient (A) is seen during Doppler echocardiography of mitral stenosis. It is the gold standard in diagnosing the severity of this valve disease. Decreased, not increased, mitral valve opening (B) is seen with mitral stenosis, whereas, increased mitral valve motion may be present in mitral valve prolapse. Left atrial dilation, not hypertrophy (C), is commonly found with mitral stenosis.

Arterial Thromboembolism

Risk factors: recent MI, atrial fibrillation • Sudden onset • 5 Ps: pain, pallor, paresthesias, pulselessness, paralysis, poikilothermia • Most common source: left heart • Most common site: femoral artery bifurcation

What is the Sokolow-Lyon electrocardiographic definition of left ventricular hypertrophy?

S wave in V1 + R wave in V5 or V6 ≥ 35 mm.

Heart Sounds

S1: mitral and tricuspid valve closure • S2: aortic and pulmonary valve closure • S3: in early diastole . During rapid ventricular filling phase . Large amount of blood striking a very compliant left ventricle (LV) . Normal in children, pregnant women • S4 ("atrial kick"): . Late diastole . Blood flowing against noncompliant LV

What is the abnormal heart sound heard in the above audio recording? Holosystolic murmur S3 S4 Systolic ejection murmur

S3 The S3 heart sound, also referred to as a protodiastolic gallop or ventricular gallop, is generally associated with acute heart failure. The sound is associated with early diastolic filling and is heard in such pathologic states as volume overload and left ventricular systolic dysfunction. It occurs at the beginning of diastole and produces a rhythm classically compared to the cadence of the word Kentucky (S1 = Ken; S2 = tuck; S3 = y). The S3 may be normal in people under 40 years of age, may sometimes be heard in pregnancy, and in some athletes but should disappear before middle age. S3 is a dull, low-pitched sound best heard with the bell placed over the cardiac apex with the patient lying in the left lateral decubitus position. Holosystolic murmurs (A) start at S1 and extend up to S2. They are usually due to regurgitation such as in mitral regurgitation, tricuspid regurgitation, or ventricular septal defect. S4 (C) occurs just after atrial contraction and immediately before the systolic S1. It produces a rhythm classically compared to the cadence of the word Tennessee (S4 = Tenn; S1 = ess; S2 = ee). S4 is caused by the atria contracting forcefully in an effort to overcome a hypertrophic ventricle. Systolic murmurs (D) are classified as ejection or regurgitant murmurs. Ejection murmurs emanate from the pulmonic or aortic valves or their surrounding structures. There are many causes of systolic ejection murmurs, including valvular aortic stenosis, atrial septal defect, acute mitral regurgitation, and ventricular septal defect.

Cardiac Electrical Conduction System

SA node → AV node → bundle of his → bundle branches → purkinje fibers

A woman presents with nausea and vomiting, chest pain at rest and altered mental status. Her past medical history is significant for poorly controlled diabetes mellitus and hypertension, as well as tobacco abuse. Which of the following would you most expect to see on an electrocardiogram? Absent P waves Prolonged QT interval R wave greater than S wave in lead V1 ST segment elevation

ST segment elevation Myocardial ischemia is usually due to atherosclerosis, whereas myocardial infarction results from ruptured and dislodged atherosclerotic plaques. This is the underlying pathology in the acute coronary syndromes, which encompass unstable angina, non-ST-elevation myocardial infarction and ST-elevation myocardial infarction (STEMI). Symptoms indicative of myocardial infarction include severe and usually progressive substernal chest pain with radiation to the neck, jaw or left upper extremity, diaphoresis, dyspnea and nausea and vomiting. STEMI angina also commonly occurs during rest and lasts > 30 minutes. The presence of ST-elevations on ECG suggests a high likelihood of coronary artery occlusion. Causes of ST-elevation include acute MI, pulmonary embolism, coronary spasm and myopericarditis. Treatment necessitates prompt percutaneous coronary intervention and revascularization. Absent P waves (A) are present in atrial fibrillation, junctional rhythm and sinoatrial blocks, conditions which typically do not present with angina. Prolonged QT interval (B) is associated with electrolyte abnormalities, antiarrhythmic, antiemetics, antibiotics and antipsychotics, but not typically myocardial infarction. Right ventricular hypertrophy (C), as may occur in cor pulmonale, mitral stenosis and tricuspid regurgitation, can be seen on ECG as R>S wave in V1, or R ≥7 mm in V1 or S ≥7 mm in V5 or V6.

A 34-year-old man presents to the emergency department with complaints of worsening chest pain, fever, and malaise. The pain is pleuritic, worsens when he lies down and improves when he leans forward. On exam, he appears unwell, but is not in acute distress. Auscultation over the precordium reveals a scratchy, grating sound with a normal S1 and S2. Which of the following is the most likely electrocardiogram finding in this patient? Shortened PR interval and slurring of the QRS complex ST segment depression in leads V2-V4 ST segment elevation with reciprocal ST depression in leads aVR and V1 U waves and flat T waves

ST segment elevation with reciprocal ST depression in leads aVR and V1 This patient with pericarditis will most likely have diffuse ST segment elevation with reciprocal ST depression in leads aVR and V1. Pericarditis is an inflammation of the pericardial sac. The pericardium is composed of a visceral layer, which forms the epicardium, and the parietal layer. These layers are separated by a space that normally contains 15-50 mL of serous fluid. During acute pericarditis, changes in the ECG reflect inflammation of the epicardium, since the parietal layer of the pericardium is electrically inert. The ECG evolves through as many as four stages during acute pericarditis. Lasting hours to days, stage 1 involves generalized ST segment elevations and PR segment depression. ST and PR segments normalize during stage 2. Stage 3 development is variable in some patients. Stage 3 is characterized by diffuse T wave inversions. Stage 4 represents normalization of the ECG. However, not all causes of pericarditis cause alterations in the ECG. Uremic pericarditis rarely causes epicardium inflammation and therefore, the ECG will show none of the changes described above. Chest pain is the most consistent finding associated with pericarditis. The pain is typically described as sharp and pleuritic. The tendency for the pain to decrease in intensity when the patient leans forward is a distinctive characteristic. Sitting up and leaning forward reduces the pressure on the parietal pericardium and allows for diaphragm splinting. In addition to an ECG, echocardiography should be performed to evaluate for pericardial effusions and to rule out cardiac tamponade. Unless contraindicated, nonsteroidal anti-inflammatory drugs (NSAIDs) are considered first line treatment for acute pericarditis. NSAIDs should not be used to treat pericarditis after myocardial infarction or uremic pericarditis. The typical ECG of Wolff-Parkinson-White syndrome ECG has a shortened PR segment and slurring of the initial QRS segment (A). Wolff-Parkinson-White syndrome is a congenital condition, characterized by abnormal conduction pathways between the atria and ventricles. ST segment depression in leads V2-V4 (B) is characteristic of myocardial ischemia. While both myocardial infarction and pericarditis can cause ST segment elevation, pericarditis differs from myocardial infarction in several ways. The morphology of the ST segment in pericarditis usually remains concave. The ST segment seen with an MI is typically convex. Additionally, ST segments in MI are limited to the corresponding affected artery, and reciprocal changes are usually noted in opposite leads. Pericarditis produces generalized ST segment elevation. Q waves may also be noted in MI. Pericarditis does not result in Q waves unless there is concomitant myocarditis. U waves and flattened T waves (D) are caused by hypokalemia. In severe hypokalemia, the T wave becomes completely flat. Prolonged vomiting and diarrhea, eating disorders, drugs, hyperaldosteronism, and renal disease are potential causes of hypokalemia.

What is the most common significant dysrhythmia in pediatrics?

SVT.

Atrial Flutter

Sawtooth pattern Atrial rate: 250-300/minute Ventricular rate: 150- +/-30 AV node conducts every 2 or 3 atrial impulses

List some causes of left bundle branch block?

Senile fibrosis of the conduction system, chronic hypertension, chronic cardiac ischemia, chronic congestive heart disease and valvular disease.

Which of the following is correct regarding cardiac markers in regards to myocardial infarction? Creatinine phosphokinase (CK) is specific to cardiac tissue Myocardial infarction can be ruled out with a single serum myoglobin Serum troponin is more sensitive than creatinine phosphokinase (CK-MB) Troponin levels return to normal in 2-3 days

Serum troponin is more sensitive than creatinine phosphokinase (CK-MB) Serum troponin is a more sensitive marker of myocardial infarction than creatinine phosphokinase (CK-MB). Biochemical markers (troponin, CK-MB, myoglobin) are essential in the diagnosis and risk stratification of myocardial infarction. Troponin I and T are myocardium specific proteins that are released from myocardial cells after cell damage occurs. Both have been found to be highly specific and sensitive for the early detection of myocardial injury and have supplanted the use of other biomarkers. The presence of serially negative troponins also predicts a low risk for an event. Troponin levels may not be detectable for up to 12 hours after symptoms onset in some patients with acute myocardial infarction. However, with highly sensitive troponin assays, detection may be possible as early as 3 hours. CK (A) is a protein that is found in large quantities in cardiac and skeletal muscle and is thus nonspecific. Myoglobin (B) is found in all muscle tissue and rises earlier in myocardial infarction than troponin. However, a single normal level does not rule out a myocardial infarction. While CK levels return to normal within 48-72 hours, troponin levels take up to 5-14 days (D) to return to baseline.

You see a one-year-old girl in your office. The girl was brought by her parents to the clinic for a well child examination. The girl has been doing well and has gained weight appropriately. The parents deny respiratory difficulties or diaphoresis. On physical exam, you note a murmur. Which of the following features is usually associated with an innocent murmur? Blowing quality Grade 3 intensity Increased intensity with upright position Short systolic duration

Short systolic duration Heart murmurs are common in infants and children. While the prevalence of congenital heart disease is approximately 1 percent, a majority of children have innocent murmurs at some time. Being able to distinguish a murmur associated with heart disease from a benign etiology is important for diagnosis and management. When evaluating an infant or child with a cardiac murmur, it is important to assess whether there are any symptoms concerning for heart disease. Concerning symptoms at any age include respiratory difficulties, diaphoresis (especially with exertion), and poor growth. In infants, symptoms may include poor feeding or excessive irritability. In older children, chest pain and syncope are important symptoms. The physical examination should include careful review of the vital signs, assessment of heart rate and rhythm, assessment of pulses, and a detailed cardiovascular exam. Features associated with innocent murmurs include the following: grade ≤ 2 intensity (flow murmurs and innocent Still's murmur are usually grade I or grade II in intensity), softer intensity when the patient is sitting compared with when the patient is supine, short systolic duration, minimal radiation, musical or vibratory quality. Blowing quality (A) is a feature of a pathologic murmur that is associated with regurgitant valves. Grade 3 intensity (B) is associated with a pathologic murmur. This is because lesions associated with increased turbulence are associated with a louder murmur. Increased intensity with upright position (C) is a usual feature of a pathologic murmur. Most innocent murmurs (with the exception of cervical venous hum) typically become softer in the upright position. An exception to this is mitral valve prolapse.

A 65-year-old man presents to the ED with sudden onset of chest pain that began two hours prior to arrival. He has a history of hypertension treated with hydrochlorothiazide, hyperlipidemia treated with simvastatin, erectile dysfunction treated with sildenafil, and takes a daily aspirin. An ECG demonstrates an anterior wall myocardial infarction. Which of the patient's home medications serves as a contraindication for the use of nitroglycerin to treat this his chest pain? Aspirin Hydrochlorothiazide Sildenafil Simvastatin

Sildenafil Sildenafil is an inhibitor of cyclic guanosine monophosphate (cGMP) specific phosphodiesterase type 5. It leads to an increased release of nitric oxide resulting in smooth muscle relaxation and vasodilation. Sildenafil is a commonly used medication in men for erectile dysfunction. The combination of sildenafil and nitroglycerin can result in profound hypotension. Therefore, the use of nitrates is contraindicated in patients who also take sildenafil. The use of aspirin (A), hydrochlorothiazide (B), and simvastatin (D) are not contraindications to the use of nitroglycerin.

Which of the following cardiac auscultation findings is most consistent with mitral valve regurgitation? Harsh, crescendo-decrescendo systolic murmur Loud S1, opening snap, and a diastolic rumble Mid-systolic click and late systolic murmur Soft S1 and a loud, blowing holosystolic murmur

Soft S1 and a loud, blowing holosystolic murmur A soft S1 and a loud, blowing holosystolic murmur are typical findings of mitral valve regurgitation. Mitral regurgitation is defined as abnormal reversal of blood flow from the left ventricle back into the left atrium. This results in an increased preload and reduced afterload. In chronic MR, the left atrium and ventricle dilate to maintain stroke volume. Mitral regurgitation (MR) is a common cardiac valvular disorder due to a primary abnormality of the valve apparatus or secondary to another cardiac disease. In the developed world, degenerative causes and coronary heart disease are the most common etiologies of MR. The most common presenting symptoms of mild to moderate, chronic MR are exertional dyspnea, fatigue, and paroxysmal to persistent atrial fibrillation. Severe, acute MR can present with heart failure and pulmonary edema. Physical exam findings may include a diminished S1, a pansystolic murmur that radiates to the axilla, and a hyperdynamic left ventricular impulse. The murmur of MR typically increases with leg raise, decreases with Valsalva maneuver, and has little respiratory variation. The findings of MR on chest radiography may include cardiomegaly and straightening of the left heart border. Electrocardiography, while not required for MR diagnosis, can be used to evaluate for concurrent conditions, such as left ventricular hypertrophy and atrial fibrillation. The diagnosis of MR is confirmed with transthoracic echocardiography (TTE). TTE is also used to determine the severity of regurgitation and for identifying the cause of MR. Medical therapy involves afterload reducing agents, diuretics, and beta blockers. Anticoagulation may be required for patients with atrial fibrillation. Surgical repair is indicated for patients with moderate to severe MR. All patients with MR should be referred to a cardiologist. A harsh crescendo-decrescendo murmur (A) that radiates to the neck is typical of aortic stenosis. Aortic stenosis can be caused by a congenital bicuspid valve or calcification of the valve. Angina pectoris, symptoms of heart failure, and syncope are the classic triad of aortic stenosis symptoms. The murmur of mitral stenosis is characterized by a loud S1, opening snap, and a diastolic rumble (B). Rheumatic disease is a common cause of mitral stenosis. Symptoms of mitral stenosis include exertional dyspnea, orthopnea, and paroxysmal nocturnal dyspnea. A mid-systolic click and late systolic murmur (C) is characteristic of mitral valve prolapse. Mitral valve prolapse is commonly seen in healthy, young women. The majority of patients with mitral valve prolapse have some degree of mitral regurgitation. Mitral valve prolapse is generally asymptomatic, but can be associated with palpitations, dyspnea, fatigue, atypical chest pain, and anxiety.

A 44-year-old man with a history of intravenous opioid use presents to the Emergency Department with fever, cough, and hemoptysis. Vital signs include BP 110/65 mm Hg, HR 120 beats per minute, RR 20 breaths per minute, and T 103.4°F. On auscultation of the chest, you hear a faint systolic ejection murmur. Which of the following would you expect to see on physical examination? Diffuse erythroderma Palpable purpura Positive Nikolsky sign Splinter hemorrhages

Splinter hemorrhages This patient is presenting with signs and symptoms of infectious endocarditis. Dermatologic and ocular manifestations of endocarditis are important indicators of the diagnosis. Roth spots are retinal hemorrhages with central clearing seen on funduscopic examination. Osler nodes are painful nodules on fingers and toes. Janeway lesions are painless erythematous plaques on the palms and soles. Splinter hemorrhages occur beneath the nails due to septic emboli. Risk factors for infectious endocarditis include rheumatic heart disease, congenital or acquired valvular disease, and intravenous drug use. Left-sided endocarditis involves either the aortic or mitral valve. It is more common than right-sided endocarditis. Organisms often implicated in left-sided endocarditis include Streptococcus viridans, Staphylococcus aureus, and those in the Enterococcus family. Complications include systemic infarcts from septic emboli. Right-sided endocarditis involves either the pulmonic or tricuspid valve. It is classically seen in intravenous drug users. Organisms implicated in right-sided endocarditis include Staphylococcus aureus, Streptococcus pneumoniae, and gram negative bacteria. Presenting symptoms often include fever, cough, hemoptysis, chest pain, and dyspnea. Diagnosis is made by having either both major criteria, 1 major and 3 minor criteria, or 5 minor criteria. Major criteria include 2 positive blood cultures with at least 3 sets sent one hour apart of organisms common to infectious endocarditis or abnormal echocardiography with either visible vegetation, new valvular regurgitation, prosthetic valve dehiscence, or myocardial abscess. Echocardiography is the hallmark of imaging for endocarditis and is preferably done via the transesophageal route. Minor criteria include predisposing risk factors or IV drug use, fever, vascular events such as septic emboli and Janeway lesions, immunologic events such as Osler nodes or Roth spots, echocardiographic findings consistent with endocarditis not meeting major criteria, and positive blood cultures not meeting major criteria. Management includes antibiotics for the suspected organism based on the clinical situation. Diffuse erythroderma (A) is the characteristic rash of toxic shock syndrome. Palpable purpura (B) is seen with Henoch-Schonlein purpura and disseminated intravascular coagulation. Positive Nikolsky sign (C) is characteristic of diseases that cause the top layers of skin to slough off with minimal pressure. This is seen in pemphigus vulgaris, staphylococcal scalded skin syndrome, and toxic epidermal necrolysis.

Which of the following statements is correct regarding the classification of heart failure? Stage A refers to patients with symptoms at rest Stage B refers to patients with valvular dysfunction who are symptomatic Stage C refers to patients with left ventricular dysfunction who are symptomatic with exertion Stage D refers to patients who are at risk of congestive heart failure but have no left ventricular dysfunction

Stage C refers to patients with left ventricular dysfunction who are symptomatic with exertion Stage C describes patients with left ventricular dysfunction who are symptomatic with exertion. This is equivalent to the NYHC Class II and Class III. This includes about five million people in the United States. The most recent ACC/AHA classification for heart failure takes into account risk factors in addition to the presence of left ventricular dysfunction and symptoms. This classification complements the New York Heart Classification and considers recent advances in pharmacologic and non-pharmacologic approaches to evaluate and treat heart failure. This classification reliably allows the physician to follow patients as their heart failure progresses from one stage to the next, and offers a unique set of treatments appropriate to each stage. Stage A (A) describes patients who are at risk of heart failure but are asymptomatic and have no left ventricular dysfunction. More than 60 million people fall into this category and include those with coronary artery disease, hypertension, diabetes mellitus, and a family history of cardiomyopathy. Stage A is an additional classification that was not present in the prior NYHC. Stage B (B) describes patients with left ventricular dysfunction who are asymptomatic. This is equivalent to Class I of the NYHC and includes approximately ten million people in the United States. Stage D (D) describes patients with symptoms at rest. This is equivalent to Class IV of the NYHC. This includes approximately 200,000 people in the United States.

What is the most common bacteria responsible for infective endocarditis?

Staphylococcus aureus.

What is the most common etiology of healthcare-associated infective endocarditis?

Staphylococcus aureus.

What is stasis dermatitis?

Stasis dermatitis occurs with venous insufficiency and valvular incompetency. The proximal skin appears thin and brown, and may occur with distal macules, papules, red irritation, skin thickening and edema.

What organism is classically associated with infectious endocarditis seen in patients with colon cancer?

Streptococcus bovis.

A 65-year-old woman presented to the emergency department with sub-sternal chest pain and dyspnea. Her cardiac biomarkers were mildly elevated and there was ST-segment elevation in the anterior leads. Apical ballooning was seen on echocardiography and coronary angiography revealed normal coronary arteries. She has no past medical history and takes no medications. Recently the patient lost her husband of 40 years. What is the most likely diagnosis? Non-ST-elevation myocardial infarction Pericarditis ST-elevation myocardial infarction Stress-induced cardiomyopathy

Stress-induced cardiomyopathy Stress-induced cardiomyopathy, also called Takotsubo cardiomyopathy and "broken heart" syndrome, is an increasingly reported syndrome characterized by transient cardiac dysfunction with ventricular apical ballooning, usually triggered by intense emotional or physical stress. This syndrome mimics acute myocardial infarction, but in the absence of obstructive coronary artery disease. It is approximated that stress cardiomyopathy accounts for approximately 2% of suspected acute coronary syndromes. Stress cardiomyopathy was historically called Takotsubo cardiomyopathy. Takotsubo is a Japanese word for octopus trap which resembles the characteristic apical ballooning seen on ventriculogram or echocardiography. It has also been referred to as apical ballooning syndrome or broken heart syndrome. The pathophysiology remains unknown, but catecholamine-mediated myocardial stunning is thought to be the most likely mechanism. This disorder is more common in women, specifically postmenopausal women. Patients typically present following physical stress or a stressful emotional event such as a loss of a loved one, natural disaster, or devastating financial losses; however, a triggering event is not always present. Common presenting features include electrocardiographic changes (often anterior ST-segment elevations), mildly elevated cardiac biomarkers, sub-sternal chest pain, and dyspnea. Accepted criteria for the diagnosis are (1) ST segment elevation, (2) transient regional wall motion abnormalities of apex and mid ventricle, (3) the absence of coronary artery disease, and (4) absence of other causes of left ventricular dysfunction such as pheochromocytoma or myocarditis. In-hospital mortality is approximately 2% and patients who survive the acute episode typically recover in several weeks. Treatment is largely supportive care with hydration and efforts to alleviate physical or emotional stressor. Distinguishing stress cardiomyopathy from a non-ST-elevation myocardial infarction (A) and ST-elevation myocardial infarction (C) is often difficult. Patients in both groups present with electrocardiographic changes and elevated cardiac biomarkers. The normal coronary arteries by coronary angiography suggest that this patient does not have either a non-ST-elevation myocardial infarction or ST-elevation myocardial infarction. Patients with pericarditis (B) usually present with pleuritic chest pain and different findings on electrocardiogram, including PR-segment depression and global ST-segment elevation. Additionally, wall motion abnormalities on imaging is not typical of acute pericarditis.

Hypertrophic cardiomyopathy in a young athlete can commonly lead to which disastrous result?

Sudden cardiac arrest and death.

On which side of the valve is the vegetation typically located in infectious endocarditis?

Superior.

What treatment can be curative in constrictive pericarditis?

Surgical pericardectomy.

Which of the following is used to measure the pulmonary artery wedge pressure? Arterial catheter Flexible bronchoscope Foley catheter Swan-Ganz catheter

Swan-Ganz catheter A Swan-Ganz catheter, or pulmonary artery catheter, can be used to obtain the pulmonary artery wedge pressure, which is an estimate of left atrial pressure. The Swan-Ganz catheter permits the clinician to directly measure pressures and sample blood from the right atrium, right ventricle, and pulmonary artery. It can also indirectly measure left atrial pressure. This involves inflating a balloon around the tip of the catheter which occludes a branch of the pulmonary artery, using the artery as an extension of the catheter. Assuming a normal pulmonary artery this technique estimates pressures in the left atrium. Pulmonary artery catheterization can be used for a variety of clinical purposes. It can differentiate among the types of shock, identify etiologies of respiratory and cardiac failure, and diagnose and manage a range of conditions in critically ill patients as well as measure the cardiac output or detect a left-to-right intracardiac shunt. An arterial catheter (A) is a thin, hollow, tube which is placed into an artery, most commonly the wrist or groin, and is indicated when blood pressure must be monitored on a moment-to-moment basis or frequent arterial blood gases are necessary. A flexible bronchoscope (B) is an instrument that is inserted through the mouth or a nasal orifice used to visualize the vocal cords or tracheobronchial tree. It can also be used to sample lesions within the airways. A foley catheter (C), or urinary bladder catheter, is used for urinary drainage or as a means to collect urine for measurement.

A 39-year-old man presents to the ED complaining of general weakness. He has signs of an upper respiratory infection on exam. His rhythm strip is seen above. Which of the following is the most appropriate next step in management? Administer 325 mg aspirin and send for a troponin Apply transcutaneous pacemakers and admit Consult cardiology Symptomatic care and discharge

Symptomatic care and discharge The ECG denotes first degree AV heart block. This is due to prolonged conduction of atrial impulses without the loss of any single impulse. On the ECG, the PR interval will be >200 ms. This type of block is often a normal variant without clinical significance, occurring in close to 2% of healthy young adults and does not require specific treatment. Although the block is benign, in some patients it may be associated with beta-adrenergic blocker therapy, endocarditis, myocarditis, inferior wall myocardial infarction, hyperkalemia, and hypothermia. Treatment for the patient in this case is supportive, and he can be sent home. Aspirin (A) is administered to patients with suspected acute coronary syndrome and is not necessary in this patient. First degree heart block does not progress to more advanced blocks that would require application of a transcutaneous pacemaker (B). Since this block is benign, cardiology (C) does not need to be consulted.

A 55-year-old man presents to the emergency department complaining of palpitations, nausea, and dizziness for 30 minutes. He is afebrile, his pulse is 140 beats per minute, and his blood pressure is 78/50 mm Hg. As the nurse attaches him to the cardiac monitor, you see the rhythm strip seen above. What is the most appropriate treatment? Adenosine 6 mg IV push Defibrillation at 360 joules Procainamide 18 mg/kg infused over 30 minutes Synchronized cardioversion at 200 joules

Synchronized cardioversion at 200 joules The monitor shows a wide complex tachycardia. Clinically, he is hypotensive and unstable, which necessitates the use of electrical rather than pharmacologic treatment. Synchronized cardioversion is indicated for the treatment of unstable tachydysrhythmias, including certain supraventricular dysrhythmias as well as monomorphic ventricular tachycardia. For treatment of ventricular fibrillation or polymorphic ventricular tachycardia, defibrillation (not synchronized cardioversion) is indicated. Adenosine (A) is a short-acting AV-nodal blocker used frequently in supraventricular dysrhythmias. Its use is not recommended in hypotensive patients with a wide-complex tachycardia. Defibrillating a patient who has a pulse (B) is dangerous and can result in the R-on-T phenomenon. This occurs when a depolarizing impulse (endogenous or exogenous) is delivered during ventricular repolarization (T wave). This can result in polymorphic ventricular tachycardia or ventricular fibrillation. To avoid this complication, synchronized cardioversion coordinates delivery of an electrical impulse so that it occurs with initiation of ventricular contraction (i.e., at the beginning of the QRS complex), thereby avoiding a shock during the relative refractory period of the cardiac cycle. Procainamide (C) is an option for patients with stable ventricular tachycardia, but it is not appropriate treatment of a hypotensive patient with an undifferentiated wide complex tachycardia. Procainamide may also worsen hypotension.

What primary disease process is associated with sterile vegetation endocarditis on both sides of the involved valve?

Systemic lupus erythematosus.

What is the equation for the target heart rate used for an exercise stress test?

Target heat rate = 85 % (220 - age (in years)).

Vasculitis

Temporal arteritis: PMR, carotid artery branches affected, vision loss, Rx: immediate steroids • Takayasu's arteritis: Asian, decreased pulses • PAN: generalized without lung involvement, HBV • Buerger's disease: smokers, claudication of hands/feet • Granulomatosis with polyangiitis (GPA): Upper and lower respiratory sx + renal sx, c-anca • Microscopic polyangitis: similar to GPA but without nasopharyngeal involvement, p-ANCA • Churg-Strauss syndrome: vasculitis + eosinophilia + asthma • Cryoglobulinemia: HCV, malaise, skin lesions, joint pain • Behçet's disease: oral and genital ulcers, hyperreactivity to needle sticks

What is the estimated mortality rate in undiagnosed Brugada syndrome?

Ten percent per year.

What is the most common cardiac cause for cyanosis of children (of any age)?

Tetralogy of Fallot.

What is the INR range in a patient taking warfarin for atrial fibrillation?

The INR range is 2-3.

While AV block is first examined by determining the length of the PR interval, bundle branch blocks are first examined by determining the length of which electrocardiographic entity?

The QRS complex.

What is the most common site of aortic dissection?

The ascending aorta.

An S3 extra heart sound is heard best with which end of a stethoscope?

The bell.

What is the most frequent site of arterial embolism?

The bifurcation of the common femoral artery.

What is the name of the accessory bundle in WPW syndrome?

The bundle of Kent.

When is the greatest risk of sudden death after a myocardial infarction?

The first few hours after secondary to ventricular tachycardia, ventricular fibrillation or cardiogenic shock.

What is the significance of an elevated creatinine kinase- MB and normal troponin value?

The injury is likely due to release from non-cardiac tissue.

Patients with aortic dissection may present with hoarseness due to compression of which nerve?

The recurrent laryngeal nerve.

What coronary artery supplies the AV node?

The right coronary artery.

Which coronary artery most commonly supplies the inferior wall with blood?

The right coronary artery.

Peripheral arterial disease most commonly affects which vessels?

The superficial femoral artery (calf pain) and aortoiliac system (thigh/buttock pain).

What blood pressure defines a hypertensive emergency?

There is no defining blood pressure; all that is needed is an elevated pressure in the setting of acute end-organ damage.

What is the most commonly used first line agent to treat hypertension?

Thiazide diuretics, such as hydrochlorothiazide or chlorthalidone.

What class of diabetes medications are contraindicated in the setting of heart failure?

Thiazolidinediones, such as pioglitazone and rosiglitazone. Metformin should also be avoided in patients with decompensated heart failure due to the risk of lactic acidosis.

What is the classic echocardiographic finding in constrictive pericarditis?

Thickened pericardium.

Which pericarditis cases are most prone to develop tamponade?

Those which are idiopathic or due to malignancy or uremia.

Atrial-based pacemakers are recommended in all patients with symptomatic bradycardia except for which subclass?

Those who also have chronic atrial fibrillation.

Aspirin is the first-line antiplatelet used in managing stable angina in all cases except for which patients?

Those with a recent MI or coronary stent, in which case, clopidogrel is the recommended first-line antiplatelet agent.

What dysrhythmia are patients with prolonged QT interval at risk for?

Torsades de pointes.

What diagnostic test is most sensitive in detecting valvular vegetations?

Transesophageal echocardiogram (TEE).

What is the study of choice in an unstable patient to confirm the diagnosis of aortic dissection?

Transesophageal echocardiogram.

A 24-year-old woman with no past medical history presents with left wrist pain after a fall. The left extremity is grossly deformed and the patient complains of severe pain. The patient has a blood pressure of 183/100 mm Hg. While awaiting X-rays, what management is indicated for the patients elevated blood pressure? Arrange admission for blood pressure control Start an oral beta-blocker and monitor for response Start intravenous beta-blocker and admit to the intensive care unit Treat the patient's pain and reassess the blood pressure

Treat the patient's pain and reassess the blood pressure The patient presents with a markedly elevated blood pressure in the setting of pain from a trauma and should have pain control initiated and her blood pressure rechecked. Hypertension is defined as a persistent SBP >140 mm Hg or DBP >90 mm Hg. Pain and anxiety are common causes of elevated blood pressure and heart rate in the outpatient setting. Historically, patients with elevated blood pressure and nonspecific symptoms were referred to as hypertensive urgency but this term has fallen out of use. In a patient presenting with elevated blood pressure who does not have signs or symptoms of end-organ damage, the clinician's focus should be on identifying external reasons for the elevated pressure and treating or addressing these. In this case, the reduction or relief of pain will likely lead to decreased blood pressure. Patients with elevated blood pressure and an absence of end-organ damage (e.g. acute coronary syndrome, aortic dissection, encephalopathy, change in renal function) do not require admission (A) for management. A primary care physician in the outpatient setting best manages these patients. Starting a beta-blocker (B) will not be beneficial in a patient with acute pain as the cause of elevated blood pressure. Similarly, administration of an intravenous beta-blocker and admission to the intensive care unit (C) is not indicated as the patient exhibits no end-organ damage.

A 40-year-old woman, who actively uses intravenous drugs, presents to the ED with fever and fatigue for the past 3 days. In the ED, her vital signs are BP 126/82, HR 90, RR 16, oxygen saturation 99% on room air, and temperature 101.6°F. On exam, a murmur is noted. A transesophageal echocardiography is ordered for suspected endocarditis. Which of the following valves is most likely to be affected? Aortic Mitral Pulmonic Tricuspid

Tricuspid This patient most likely has bacterial endocarditis. Endocarditis is more common in patients with valvular abnormalities, prosthetic valves, and IV drug users. Common pathogens include Staphylococcus aureus and viridans group streptococci. Of note, viridans streptococcus endocarditis commonly presents after dental work. Endocarditis presents most commonly with fever and malaise, although other signs and symptoms may be present. Although the classic triad is fever, anemia, and a heart murmur, this rarely presents clinically. IV drug users usually have right-sided endocarditis, most commonly affecting the tricuspid valve. The murmur noted on exam is usually tricuspid regurgitation. Labs should be ordered for those with suspected endocarditis, as one would expect leukocytosis, anemia, increased ESR, and increased CRP. Three blood cultures from three separate venipuncture sites should be taken, with the first and last draw occurring at least one hour apart. The most useful diagnostic imaging is an echocardiogram, especially a TEE, demonstrating vegetations. The Duke criteria are the most widely used and accepted criteria to clinically diagnose bacterial endocarditis. Empiric antibiotics should be initiated in those with suspected or confirmed endocarditis once cultures have been drawn, with antibiotics being altered as needed once the pathogen and susceptibility return. Left side valves (aortic, mitral) are most commonly involved in endocarditis outside of intravenous drug abusers and prosthetic valves. The mitral valve (B) is the most commonly affected valve in infective endocarditis, although the aortic valve (A) may also be affected. The pulmonic valve (C) is much less commonly affected.

You discover a blowing, holosystolic murmur in a newborn boy, heard loudest at the left sternal border. A pediatric cardiologist diagnoses Ebstein's anomaly. In addition to a malformed right atrium and ventricle, which of the following abnormalities would you most expect to see on this patient's echocardiogram? Left ventricular hypertrophy Overriding aorta Tricuspid insufficiency Tricuspid stenosis

Tricuspid insufficiency Tricuspid regurgitation (or incompetence, or insufficiency) manifests as a blowing, pansystolic murmur. It is commonly associated with a thrill. It is most intense in the left, fourth intercostal space, however, it can radiate to the apex, making it difficult to differentiate from a mitral regurgitation murmur. Like tricuspid stenosis, it is quite rare, affecting only 1% of the US population. Causes include rheumatic heart disease, right ventricular dilation, myxomatous degeneration and varied connective tissue disorders. It is part of Ebstein's anomaly, a congenital heart defect in which the tricuspid leaflets attach to the right ventricular wall, leading to a larger than normal right atrium and smaller than normal right ventricle. Ebstein's anomaly is also commonly associated with an atrial septal defect, patent foramen ovale and the pre-excitation, re-entrant conduction defect of Wolff-Parkinson-White syndrome. Diuretics are the mainstay of treatment, and valvuloplasty or valve repair, if necessary, is far more common than valve replacement. Left ventricular hypertrophy (A) is not associated with Ebstein's anomaly. It is commonly due to chronic systemic hypertension. An overriding aorta (B) is one of the four congenital cardiac malformations of Tetralogy of Fallot, not Ebstein's anomaly. Tricuspid stenosis (D) does not produce a systolic murmur.

Which of the following murmurs is associated with an increase in right atrial pressure? Aortic regurgitation Mitral regurgitation Mitral stenosis Tricuspid regurgitation

Tricuspid regurgitation Valve disorders are often characterized in terms of stenosis (incomplete opening of the valve, thereby increasing the resistance in blood flow) or regurgitation (an incomplete closure of a valve, resulting in a backflow of blood). The tricuspid valve is 1 of 2 atrioventricular (AV) valves and lies between the right atrium and right ventricle. In tricuspid regurgitation, there is incomplete forward flow from the right atrium into the right ventricle and blood flows from the right ventricle into the right atrium during systole. This backflow of blood results in increased right atrial pressure. Tricuspid regurgitation is caused by right ventricular dilation secondary to pulmonary hypertension, rheumatic heart disease, and infective endocarditis. Patients may complain of fatigue and dyspnea on exertion. On exam, there may be a holosystolic murmur best heard at the xiphoid area adjacent to the left sternal border. The aortic valve is one of 2 semilunar valves (the other being the pulmonary valve) and is positioned between the left ventricle and aortic trunk. Aortic regurgitation (A) results in a backflow of blood and an increase in pressure of left ventricle during diastole. The mitral valve is the 2nd AV valve and is situated between the left atria and left ventricle. Mitral regurgitation (B) causes a backflow into the left atria during systole, increasing left atrial pressure. In mitral stenosis (C), the mitral valve cannot fully open during diastole, resulting in an increase in resistance in blood flow through the valve and increasing the left atrial pressure while decreasing the filling of the left ventricle.

You are concerned with hearing a new diastolic, rumbling murmur in one of your patients. This murmur is best heard with the bell over the left sternal border at the fourth intercostal space and is louder during inspiration. Which of the following is the most likely diagnosis? Aortic regurgitation Aortic stenosis Tricuspid regurgitation Tricuspid stenosis

Tricuspid stenosis Tricuspid stenosis is a murmur that is heard best with the bell over the left sternal border at the fourth intercostal space. It can be caused by myxomatous degeneration, rheumatic heart disease, congenital malformations and endocardial fibroelastosis. It rarely occurs alone, and almost always occurs with mitral stenosis. It is usually described as a diastolic rumble, which is louder than mitral stenosis during inspiration. There may be an associated thrill. Overall, it is a relatively rare murmur, and when it is an isolated finding, it usually does not require treatment. However, as it commonly occurs with mitral stenosis, surgical valve replacement or balloon valvuloplasty may be necessary. Murmurs of the aortic valve (A and B) are most intense at the right, second intercostal space. Aortic regurgitation is a type of diastolic murmur but has no association wth Carvallo's sign. It is, however, associated with de Musset's sign (head nodding in time with the heart beat) and Quincke's sign (pulsation of the capillary bed in the nail). Tricuspid regurgitation (C) is a systolic, not diastolic, murmur.

Cardiac Biomarkers

Troponin Highest sensitivity and specificity Time detectable from onset: 3-12 hours Peak: 24-48 hours Return to baseline: 5-14 days CK-MB Time detectable from onset: 3-12 hours Peak: 24 hours Return to baseline: 48-72 hrs Useful for dx of reinfarction Myoglobin First to appear, first to peak, first to decline Lacks specificity

The risk of death in unstable angina is four-fold increased if which three biomarkers are elevated?

Troponin I or T, high-sensitivity C-reactive protein and B-type natriuretic peptide.

The risk for congenital heart disease is higher if a parent or sibling has a structural congenital heart defect, true or false?

True.

Which antibiotic is first line for endocarditis prophylaxis prior to a dental procedure?

Two grams of Amoxicillin 1 hour prior to procedure.

A man who presents with syncope is placed on the cardiac monitor. On the monitor you note a repeating trend of 6 P waves, 5 of which are followed by a narrow QRS complex and 1 of which is not followed by a QRS complex. The PR interval during this trend progressively increases. Which of the following is the most likely diagnosis? First-degree AV block Third-degree AV block Type I second-degree AV block Type II second-degree AV block

Type I second-degree AV block A key distinction between first-degree and second-degree heart block is that in first-degree block the P wave is always followed by a QRS complex. In other words, the ratio of P waves to QRS complexes is 1:1, or, the electrical signal from the atria always passes to the ventricles. In second-degree AV block, the electrical impulse sometimes gets to the ventricles. There are two main types of second-degree AV block. In Mobitz type I, or Wenckebach, second-degree block, there is a progressive beat-to-beat lengthening of the PR interval until a P wave does not conduct through the AV node. The absent conduction and resultant "missing" QRS complex is called a "dropped" QRS, which represents an absent beat of ventricular contraction. First-degree AV block (A) has a 1:1 ratio of P waves to QRS complexes. Mobitz type II second-degree heart block (D) is characterized by a nonconducted P wave which is not preceded by progressive PR interval prolongation. AV dissociation, or third-degree AV block (B), occurs when none of the P waves conduct through the AV node. This complete AV block occurs with separate atrial and ventricular rates. There is no discrete correlation or trend between P waves and QRS complexes.

Which is more serious, type I (Mobitz I/Wenckebach) or type II (Mobitz II) second-degree AV block?

Type II, which is more associated with complete heart block and cardiac arrest.

How long after cessation of alcohol intake do alcohol withdrawal seizures occur?

Typically, they occur between 6 and 48 hours after stopping alcohol intake but they can occur up to 5 days later.

Deep Vein Thrombosis

Unilateral leg swelling • Phlegmasia cerulean dolens (painful blue leg) = massive iliofemoral thrombosis with venous insufficiency • Phlegmasia alba dolens (painful white leg) = massive iliofemoral thrombosis → arterial spasm • Risk stratification: Well's criteria • Modality of choice: ultrasound • Treatment: . ​Proximal DVT: heparin, warfarin . Massive DVT: thrombectomy . Isolated calf vein thrombosis: aspirin, ultrasound in 2 - 5 days . Recurrent DVT on warfarin: heparin, IVC filter . Propagation of DVT on warfarin + heparin: IVC filter

Deep Vein Thrombosis

Unilateral leg swelling • Phlegmasia cerulean dolens (painful blue leg) = massive iliofemoral thrombosis with extensive vascular congestion and venous ischemia • Phlegmasia alba dolens (painful white leg) = massive iliofemoral thrombosis → arterial spasm • Risk stratification: Well's criteria • Modality of choice: ultrasound • Treatment: . ​Proximal DVT: heparin, warfarin . Massive DVT: thrombectomy . Isolated calf vein thrombosis: aspirin, ultrasound in 2-5 days . Recurrent DVT on warfarin: heparin, IVC filter . Propagation of DVT on warfarin + heparin: IVC filter

Which of the following statements is most accurate regarding acute ischemic heart disease? Elderly patients more often present with typical chest pain than atypical chest pain Reproducible chest wall tenderness excludes ischemia as a cause of chest pain Up to 33% of patients diagnosed with acute myocardial infarction do not have chest pain on presentation Women rarely present with atypical features of acute coronary syndrome

Up to 33% of patients diagnosed with acute myocardial infarction do not have chest pain on presentation A typical feature of acute coronary syndrome is crushing retrosternal chest pain or pressure. Often this is lacking, and patients present with atypical features of the pain or the presence of angina equivalent symptoms (e.g., dyspnea, nausea, vomiting, dizziness). Many patients with a diagnosis of ACS have pain that is pleuritic, positional, or reproduced by palpation. One large study showed that up to 33% of patients diagnosed with acute myocardial infarction did not have chest pain on presentation. Atypical complaints include dyspnea; nausea; diaphoresis; syncope; and pain in the arms, epigastrium, shoulder, or neck. Atypical features of ACS are present with increasing frequency in older populations. In patients older than 85 years (A), atypical symptoms are more common than typical chest pain, with dyspnea being the most common. Isolated physical exam findings are rarely diagnostic of the origin of chest pain. Palpation of the chest wall (B) may reveal localized tenderness, but 5%-10% of patients with ACS have chest pain and associated palpable chest wall tenderness. Being female (D) is a risk factor for an atypical presentation of ACS.

A detailed history and examination does not aid in the evaluation of new-onset hypertension in a 47-year-old man. In an attempt to search for an underlying cause, you order a basic metabolic panel, complete blood count, lipid panel and ECG. Which of the following tests should also be added to this standard diagnostic screen of secondary hypertension? Aortic ultrasound Echocardiogram Renal angiogram Urinalysis

Urinalysis The evaluation of hypertension involves specific history questions, exam findings and laboratory testing. A standard history should include questions about the presence of comorbidities (coronary artery disease, atherosclerosis, congestive heart failure, previous myocardial infarction, peripheral arterial disease, hypercholesterolemia, transient ischemic attacks and strokes, diabetes, renal insufficiency, endocrinopathies, retinal disease, connective tissue disease and obstructive sleep apnea), medications (oral contraceptives, corticosteroids, NSAIDs and cyclosporine), social history (salt intake, tobacco use, alcohol use, cocaine and methamphetamine use, dietary intake, and exercise trends) and family history of hypertension. The physical examination must include serial bilateral arm BP measurements, cardiac exam (murmurs, evidence of left ventricular hypertrophy), peripheral vascular and skin exam (edema, bruits, capillary refill, striae, moon fascies), thyroid exam, abdominal exam (masses, bruits), fundoscopic exam and neurologic exam. Baseline laboratory-diagnostic testing should include a basic metabolic panel, complete blood count, urinalysis, lipid panel and ECG. Aortic coarctation or aneurysm are rare causes of secondary hypertension. They are associated with abdominal, cardiac and peripheral vascular findings, which are missing in the above patient. Ultrasound (A) is the diagnostic test of choice when evaluating such abnormalities. Echocardiography (B) may be warranted if the clinician suspects left ventricular hypertrophy, valvulopathy, coronary artery disease or prior myocardial infarction as a cause of secondary hypertension, all of which would be suggested by abnormalities found during history and physical examination. Renal angiogram (C) offers great sensitivity and specificity in determining renovascular disease as a cause of secondary hypertension. However, it is not considered part of an initial evaluation, and should be considered if the initial tests above are noncontributory.

What is the leading cause of secondary healthcare-associated bacteremia?

Urinary tract infection associated with urinary catheters.

An obese 45-year-old man works for the local electric company as a utility-pole lineman. He presents with painful, tortuous superficial veins on his lower legs. These areas are not associated with erythema, warmth or skin breaks. Which of the following initial plans is most appropriate at this time? Dangle your legs at night over the side of your bed for 30 minutes Increase your daily exercise routine Schedule an appointment with a vascular surgeon Use compressive stockings during the day

Use compressive stockings during the day Venous insufficiency is mainly a chronic condition in which the "musculovenous pump" of the distal extremities does not properly return deoxygenated blood the heart, resulting in retrograde flow and distal blood back-up. A major cause of this is venous valvular incompetence, in which the vein leaflets do not operate properly. There are many causes of valvular incompetence, the most common of which is repeated vein injury, which can occur in utility pole lineman, or prior deep vein thrombosis. Two complications of valvular incompetence are varicose veins (with or without symptoms) and thrombophlebitis (inflamed superficial and/or deep vein inflammation due to a blood clot). Varicose veins are enlarged and twisted veins which have been dilated due to incompetent valves, retrograde blood flow and back-up of venous blood. Varicose veins most commonly occur in the superficial veins of the legs, especially when standing. They can be asymptomatic but have unsightly cosmesis, or they can be painful and be associated with distal edema, venous eczema, lipodermatosclerosis (skin thickening) and ulceration. They are more common in women, and are associated with pregnancy, obesity, aging, menopause, abdominal straining and prolonged standing. A complication is progression into thrombophlebitis. Treatment includes leg elevation, graduated compression stockings with or without intermittent pneumatic compression, aspirin or NSAIDs and topical anti-inflammatory gels. Leg elevation (A), especially at night, is recommended. Although somewhat counterintuitive, there is no supporting evidence to recommend regular exercise (B) as a viable treatment of symptomatic varicose veins. There are several surgical methods used in treating symptomatic varicose veins. However, this patient has not tried any conservative measures yet, and as such, referral to a surgeon (C) is not recommended at this time.

A 46-year-old woman with a past history of a DVT was recently diagnosed with Burkitt's lymphoma. Recent blood work revealed a creatinine of 2.3. She is currently hospitalized to receive chemotherapy when she suddenly develops tachycardia to a rate of 130 and oxygen saturation of 91%. Which of the following is the most appropriate test to confirm the diagnosis of pulmonary embolism? Chest X-ray CT angiogram of the chest with intravenous contrast D-dimer V/Q scan

V/Q scan According to the modified Wells Criteria this patient has a high clinical probability for a pulmonary embolism (PE). This patient has multiple risk factors for a PE including cancer, previous DVT, and immobilization secondary to hospitalization. She also has a heart rate greater than 100 and a decreased oxygen saturation, which are associated with PE. The elevated creatinine is a contraindication to receiving intravenous contrast and therefore a she cannot undergo CT angiography, which is the usual test of choice. Therefore, the most appropriate test for this patient is a V/Q scan. CT angiogram of the chest (B) is the preferred diagnostic modality in patients with suspected PE. However, the test requires that IV contrast is administered, which is contraindicated in patients with elevated creatinine. D-dimer (C) is useful in risk stratification of patients suspected of having a PE. A negative D-dimer rules out PE in patients with low or moderate risk established from Well's scoring. A chest X-ray (A) has poor sensitivity for PE.

A 23-year-old woman presents with acute onset dizziness and palpitations. Her ECG reveals evidence of AV nodal reentrant tachycardia with a rate of 170. Her blood pressure is 140/70 mm Hg. Which of the following is the most appropriate initial treatment? Atropine Cardioversion Valsalva maneuver Verapamil

Valsalva maneuver Supraventricular tachycardias (SVT) include paroxysmal, reentry or preexcitation tachycardias. Reentry SVTs include AV nodal reentry (AVNRT), atrioventricular reentry, or atrial reentry. Reentry circuits require the presence of at least two different conduction pathways with differential refractory times. It is characterized by an abrupt onset and termination of tachycardia, that distinguishes it from sinus tachycardia, which has gradual changes in rate. It is precipitated by a premature atrial or ventricular contraction or hyperadrenergic state. The ECG shows a regular, fast rhythm with absent P waves and narrow QRS complex. Unstable patients require immediate synchronized cardioversion. Stable patients, such as the patient above, should first undergo vagal maneuvers. Some common vagal maneuvers include holding your breath and bearing down (Valsalva maneuver), coughing, gagging, and immersing your face in ice-cold water. If vagal maneuvers are unsuccessful, adenosine is used both diagnostically and therapeutically. Adenosine transiently blocks the AV-node and allows the circuit to "reset." Atropine (A) is used to treat bradydysrhythmias. It inhibits vagal activity to the heart which leads to an increase in heart rate. Cardioversion (B) is not indicated in hemodynamically stable patients with PSVT. However, if unstable, the patient should undergo cardioversion. If vagal maneuvers are unsuccessful, intravenous adenosine or calcium-channel blockers, such as verapamil (D), are first-line pharmacologic options, which block the AV-node.

What is the definitive treatment for aortic stenosis?

Valve replacement.

A 46-year-old woman presents to the Emergency Department with fever, cough, and hemoptysis. She has a history of intravenous opioid use. Vital signs are BP 110/65 mm Hg, HR 120 beats per minute, RR 20 breaths per minute, and T 103.4°F. On auscultation of the chest, you hear a faint systolic ejection murmur. Which of the following is the most appropriate initial therapy? Ampicillin and gentamicin Ceftriaxone Oxacillin and rifampin Vancomycin and ceftriaxone

Vancomycin and ceftriaxone This patient is presenting with signs and symptoms of infectious endocarditis. Risk factors for infectious endocarditis include rheumatic heart disease, congenital or acquired valvular disease, and intravenous drug use. Right-sided endocarditis involves either the pulmonic or tricuspid valve. It is classically seen in intravenous drug users. Organisms implicated in right-sided endocarditis include Staphylococcus aureus, Streptococcus pneumoniae, and gram negative bacteria. Presenting symptoms often include fever, cough, hemoptysis, chest pain, and dyspnea. Right-sided endocarditis is frequently misdiagnosed initially as pneumonia. Management includes antibiotics for the suspected organism based on the clinical situation. In an IV drug user, coverage should include methicillin-resistant Staphylococcus aureus, staphylococci, streptococci and enterocci. The most appropriate antibiotic choice for this patient would be vancomycin and ceftriaxone. Ampicillin and gentamicin (A) would be an appropriate antibiotic regimen for resistant Streptococcus viridans and non-resistant enterococci. It does not adequately cover MRSA, which should be covered. Ceftriaxone (B) does not cover the typical infecting organisms. Oxacillin and rifampin (C) would be partially appropriate for a patient with prosthetic valve endocarditis as it covers for Staphylococcus aureus and adds rifampin to penetrate the biofilm on prosthetic valves; however, gentamicin should be added in order to cover for Pseudomonas aeruginosa. This would also not be an adequate regimen for MRSA as oxacillin would need to be substituted with vancomycin.

A 23-year-old man with a history of intravenous heroin abuse presents with fever of 38.5°C and mild cough. His HR is 133 bpm and BP is 114/72 mm Hg. On examination, he is ill-appearing, and you note a III/VI diastolic murmur. A chest radiograph is unremarkable. The patient states that he was hospitalized two weeks ago for arm cellulitis. Which of the following antibiotic regimens is appropriate for this patient? Ceftriaxone and azithromycin Nafcillin and vancomycin Pencillin and nafcillin Vancomycin and gentamicin

Vancomycin and gentamicin The combination of intravenous drug abuse, fever, and murmur is highly suspicious for infective endocarditis. The most common causative organism in this population is Staphylococcus aureus. The initial antibiotic regimen selected should reflect the susceptibilities of the suspected organism, the acuteness of the presentation, and local resistance patterns. Given the prevalence of methicillin-resistant Staphylococcus aureus (MRSA) in both the community and hospital setting, vancomycin, in addition to gentamicin (for its synergistic effects and coverage of gram-negative organisms), should be used for IV drug users with native valves. Ceftriaxone and azithromycin (A) would be an appropriate antibiotic choice if the patient had community-acquired pneumonia. But they will not provide sufficient coverage for suspected infective endocarditis. Nafcillin (B) is an excellent antibiotic to treat staph and strep infections. However, it is not effective for MRSA. This regimen also has poor gram-negative coverage (patients who abuse IV drugs are at risk for gram-negative endocarditis). Penicillin and nafcillin (C) are both effective for staph and strep species but ineffective against MRSA and do not cover gram-negative organisms well enough.

A 76-year-old man with a history of hypertension presents after a syncopal event. He also reports decreased exercise tolerance over the last two months. He is currently asymptomatic. His ECG is normal sinus rhythm with no changes. On examination, he has a harsh systolic murmur that radiates to the carotid arteries. Which of the following is true about the most likely cause of his syncope? Critical disease is defined by heart valve area less than 2 cm2 It typically results from rupture of the chordae tendinae The murmur increases with valsalva Vasodilators and diuretics should be used with caution

Vasodilators and diuretics should be used with caution Aortic stenosis is an abnormality of the heart valve that prevents left ventricular outflow. This results in left ventricular hypertrophy which eventually impairs diastolic filling and results in increased myocardial oxygen demand. The most common cause is degenerative calcification associated with diabetes, hypertension, and advanced age. Exam findings include a harsh systolic murmur that radiates to the carotids as well as an S4 gallop. Carotid pulses may be delayed and diminished and a narrowed pulse pressure is typically present. Classic symptoms start with dyspnea and chest pain and progress to syncope and congestive heart failure. Although patients may be asymptomatic for a long period of time, once symptoms develop mortality increases significantly. Because patients with critical aortic stenosis are preload dependent, vasodilators and diuretics should be avoided as they can cause significant hypotension. Definitive treatment is aortic valve replacement. A normal aortic valve area is greater than 3 cm2. Critical aortic stenosis (A) is defined by a heart valve area of less than 0.8 cm2. Mitral regurgitation is most commonly caused by post-myocardial infarction rupture of the chordae tendinae (B) or papillary muscle dysfunction and presents with acute onset of pulmonary edema and midsystolic apical murmur. The murmur of aortic stenosis decreases with valsalva (C).

A 20-year-old woman fainted while standing in line at the grocery store. The patient admits to feeling nauseated and diaphoretic before the episode. She denies bowel or bladder incontinence and did not experience a post-ictal state. The woman in line behind her observed jerking motions of her face and fingers. She has no past medical history and does not take any medications. What is the most likely diagnosis? Hypertrophic cardiomyopathy Orthostatic hypotension Seizure Vasovagal syncope

Vasovagal syncope Vasovagal, also called neurocardiogenic syncope, is often called the "common faint" and is the most common cause of syncope. Vasovagal syncope is a transient loss of consciousness caused by systemic hypotension and cerebral hypoperfusion. It is a neurally mediated reflex response characterized by bradycardia or peripheral vasodilation. Patients with vasovagal syncope are usually young and healthy. The clinical presentation of "classic" vasovagal refers to syncope triggered by provoking factors such as noxious stimuli, pain, blood draw, intense emotion, fear of bodily injury, prolonged standing, or heat exposure. Prodromal symptoms include feeling warm, sweating, nausea, and pallor. In addition, some patients present with myoclonic or other involuntary movements that are suggestive of a seizure but are actually due to cerebral hypoxia secondary to hypotension. This seizure like activity, historically, has been referred to as a "fainting fit." Vasovagal syncope is not dangerous; however, it is important that other more serious causes of syncope be ruled out. Hypertrophic cardiomyopathy (A) is also a cause of syncope in young and heathy individuals. However, it is usually related to exercise and associated with angina secondary to an exertion induced left ventricular outflow tract obstruction. Orthostatic hypotension (B) causes syncope upon assuming an upright position from supine or sitting. It is often caused by hypovolemia, medications or autonomic nervous system disorders. Seizure (C) causes a loss of consciousness, but it is associated with tonic-clonic jerking of extremities. Additionally, seizures often cause bowel or bladder incontinence as well as a post-ictal state. Syncopal events are not associated with incontinence and usually have a rapid and complete recovery.

What diagnostic test has the highest sensitivity for diagnosing a DVT?

Venography.

What are the common cardiac catheterization findings associated with restrictive cardiomyopathy?

Ventricular "dip and plateau" pressures, and atrial M and W waves.

An 81-year-old man with 10 years of coronary artery disease presents with chest pain and altered mental status. His ECG shows consecutive, large and wide QRS complexes. P waves cannot be appreciated. His pulse is 188 bpm. Which of the following is the most likely diagnosis? Atrial fibrillation Atrial flutter Ventricular fibrillation Ventricular tachycardia

Ventricular tachycardia Ventricular tachycardia is described electrocardiographically as "continuous PVCs", or more specifically, consecutive, fast, large and wide QRS complexes. A wide QRS complex clues one in that the underlying electrical problem is in the ventricles. Ventricular tachycardia can be further defined as monomorphic (QRSs are the same form) versus polymorphic (differing appearance of the QRSs), or sustained (>30 seconds) versus non-sustained (<30 seconds, self-terminates). In this tachydysrhythmia, the ventricles depolarize and contract so fast that cardiac output decreases, especially in the elderly or those with diseased myocardium or coronaries. This perpetuates ventricular ischemia leading to a precipitous decline if the dysrhythmia is not treated. Atrial fibrillation (A) and atrial flutter (B) both have narrow QRS complexes, either irregular or regular respectively. Ventricular fibrilation (C) is identified by a totally erratic appearance of unidentifiable waves. Discrete QRS complexes are absent.

A 60-year-old man presents with the ECG seen above. His blood pressure is 80/60 mm Hg. Which of the following is the most likely diagnosis? Atrial flutter Atrioventricular reentry tachycardia Supraventricular tachycardia Ventricular tachycardia

Ventricular tachycardia Ventricular tachycardia (VT) is present when there are >3 consecutive premature ventricular contractions occurring at a rate > 100. P waves are usually absent and the QRS complexes are wide (> 120 msec) and may be bizarre appearing. Ventricular tachycardia is classified as "monomorphic" (QRS complexes look the same) or "polymorphic" (QRS complexes have varying morphology). Sometimes it is difficult to distinguish ventricular tachycardia from supraventricular tachycardia (SVT) with aberrancy (presence of a bundle branch block). Nonetheless, any patient with a wide complex tachycardia who is hemodynamically unstable should undergo immediate electrical cardioversion. Atrioventricular reentry tachycardia (A) is a type of SVT. It is more commonly associated with regular pulse and monomorphic narrow QRS complexes. Atrial flutter (B) is more commonly associated with regular tachycardia and sawtooth appearance of P waves. It is sometimes difficult to distinguish ventricular tachycardia from supraventricular tachycardia with aberrancy. Any patient with a wide complex tachycardia who is hemodynamically unstable should be treated as having ventricular tachycardia. Some electrocardiographic characteristics that support VT over SVT (C) are extreme left axis deviation, QRS concordance (all QRS complexes from V1 to V6 are either all positive or all negative), and fusion or capture beats, which indicates AV dissociation.

The presence of coronary disease or infarcted myocardium is more closely associated with supraventricular tachycardia or ventricular tachycardia?

Ventricular tachycardia.

Which calcium channel blocker has the greatest effect on the AV node?

Verapamil

Which of the following treatments is contraindicated in the treatment of a 5-month-old with supraventricular tachycardia? Adenosine Ice bag to face Propranolol Verapamil

Verapamil Due to poor calcium reserves in the sarcoplasmic reticulum in infants, verapamil (calcium channel blocker) use in infants can cause profound hypotension and cardiovascular collapse. Therefore, it should be avoided in patients younger than 12-months-old. Adenosine (A) is the first-line agent to treat supraventricular tachycardia. Applying ice to the face (B) or other vagal maneuvers can be attempted before administration of adenosine. Propranolol (C) is a nonselective beta-blocker used in supraventricular tachycardia, but it is less effective than adenosine.

A 68-year-old man is being managed on a multi-drug antihypertensive regimen for essential hypertension. His blood pressure is at goal, but he notes persistent constipation and bilateral pedal edema. Which of the following medications is most likely responsible for these side effects? Enalapril Losartan Metoprolol Verapamil

Verapamil Verapamil, along with most other calcium channel blockers, is known to cause pedal edema and constipation, particularly in elderly patients. Other adverse effects of calcium channel blockers include headaches, flushing, and bradycardia, especially with the dihydropyridine calcium channel blockers (such as nifedipine, amlodipine, or nicardipine). Edema development can usually be lessened by adding an ACE inhibitor or angiotensin receptor blocker to the patient's regimen. Calcium channel blockers are generally well tolerated and valuable components of an antihypertensive regimen that work by causing peripheral vasodilation while minimizing the reflex tachycardia common with other vasodilating agents. Hypertension is diagnosed when a patient's systolic blood pressure exceeds 140 mm Hg, or their diastolic blood pressure exceeds 90 mm Hg on two separate occasions. If a work-up for secondary causes of hypertension proves fruitless, a patient is presumed to have essential hypertension and should be managed with diet, exercise, and medications to reach their goal blood pressure (acceptable goals range from <120 - <140/<90 depending on patient circumstances). Proper control is vital to reducing complications such as cardiovascular disease, cerebrovascular disease, hypertensive nephropathy, and hypertensive retinopathy. A medication regimen must be tailored for each patient, but will generally include some combination of diuretics, ACE-inhibitors, angiotensin receptor blockers, beta-blockers, calcium channel blockers, or centrally-acting sympatholytics. Enalapril (A), an ACE-inhibitor, is a common initial medication for treating hypertension. However, it is more likely to cause a chronic, dry cough and hyperkalemia rather than pedal edema or constipation. Losartan (B) is an angiotensin receptor blocker. This class of antihypertensive medications has similar utility to an ACE-inhibitor, and it also is likely to contribute to the development of hyperkalemia. It is unlikely to cause the edema and constipation seen with calcium channel blockers. Metoprolol (C), a beta-blocker, is also used for managing hypertension by decreasing the heart rate and cardiac output. Beta-blocker side effects normally include fatigue, lethargy, bronchospasm, and bradycardia, but do not commonly cause constipation or pedal edema.

What is the most common etiology of myocarditis in children?

Viral infections.

A 50-year-old woman with a history of mitral stenosis secondary to rheumatic fever presents with atrial fibrillation. She does not have a history of heart failure, hypertension, diabetes mellitus or previous stroke or transient ischemic attack. What is the most appropriate management for this patient? Aspirin Dabigatran No anticoagulation Warfarin

Warfarin Warfarin is the most appropriate management. This patient has mitral stenosis and requires anticoagulation with warfarin regardless of CHA2DS2 - VASc score. Validated risk factors for thromboembolism in patients with atrial fibrillation include mitral stenosis, previous thromboembolism, heart failure, systolic dysfunction, diabetes, hypertension, presence of a mechanical heart valve and older age. In patients without significant valvular disease, the mostly commonly used method to determine choice of thromboprophylaxis is the CHA2DS2 - VASc score. Those with a score of 0 are at low risk and anticoagulation is a clinical decision. A score of 1 is low to moderate risk and antiplatelet or anticoagulation therapy should be considered. A score of 2 or more is considered moderate to high risk and anticoagulation is recommended. Patients with mitral stenosis who have chronic atrial fibrillation have a stroke risk that may be as high as 7-15 % per year. It is recommended that patients with mitral stenosis and atrial fibrillation be started on warfarin, and it should be continued indefinitely to decrease the risk of systemic thromboembolism. The goal INR is between 2.0 to 3.0. Aspirin (A) is not appropriate because the presence of mitral stenosis necessitates anticoagulation with warfarin. No anticoagulation (C) is not appropriate as this patient has a risk factor that require further therapy. Newer oral anticoagulants, such as dabigatran (B), are now approved for prevention of systemic embolism in adults with nonvalvular atrial fibrillation. However, the use of warfarin in patients with mitral stenosis is recommended because patients with significant mitral valve disease were excluded from the trials of these newer agents.

What formula is used to calculate the average weight in a child?

Weight (kg) = (2 x age in years) + 8.

What is antidromic conduction?

When the impulse is conducted anterograde through the accessory pathway and retrograde through the AV node. The QRS complex is wide.

Ventricular tachycardia is most difficult to distinguish from which other dysrhythmia?

Wide-complex supraventricular tachycardia (SVT with aberrancy such as a bundle-branch block).

A 37-year-old man presents to the emergency department with chest pain and shortness of breath. His medical history is significant for uncontrolled type I diabetes and end-stage renal disease on hemodialysis. His last dialysis was four days ago and he missed his appointment this morning. His labs are notable for a fingerstick blood glucose 300 mg/dL, potassium 7.0 mmol/L, magnesium 2.0 mEq/L, and phosphorus 4.0 mmol/L. Which of the following findings is most likely to be seen on this patient's ECG? Osborn waves QT interval prolongation U waves Widened QRS complex

Widened QRS complex Symptomatic hyperkalemia is a life-threatening electrolyte abnormality typically seen in patients with underlying acute or chronic kidney disease. It can also be seen in conditions that cause increased tissue breakdown such as tumor lysis syndrome, rhabdomyolysis, and crush injuries. Muscle weakness and paralysis, cardiac conduction abnormalities and cardiac dysrhythmias are the most serious manifestations of hyperkalemia. Symmetrical peaked T waves with a shortened QT interval and ST-T segment depression are the earliest ECG changes seen in patients with hyperkalemia. Worsening hyperkalemia results in progressive lengthening of the PR interval and QRS duration, disappearance of the P wave, and ultimately widening of the QRS complex into a sinusoidal pattern. Treatment of hyperkalemia includes antagonizing the membrane effects of potassium, driving extracellular potassium into cells, and removing potassium from the body. Osborn waves (A), also known as J-waves, are positive deflections in the junction of the QRS complex and the ST segment. They are most commonly seen in patients with hypothermia. QT interval prolongation (B) is seen in hypokalemia, hypomagnesemia, and hypocalcemia. QT interval shortening is seen in hyperkalemia. U waves (C) are small deflections that follow the T wave and are typically seen in hypokalemia, rather than hyperkalemia.

Which of the following is most commonly seen on chest radiography in a patient with an aortic dissection? Abnormal aortic contour Calcification of the aorta Pleural effusion Widened mediastinum

Widened mediastinum The chest radiograph can be normal in 10%-20% of patients with known aortic dissection. Therefore, it cannot be used to rule out the diagnosis. In cases where there is an abnormality, a widened mediastinum is most commonly seen, occurring in approximately 62% of cases, according to the International Registry for Aortic Dissection (IRAD) study. A tortuous aorta, common in hypertensive patients, may be hard to distinguish from a widened mediastinum. In the elderly, a mildly or moderately enlarged (i.e., tortuous) aorta can be a normal finding. However, a markedly enlarged aorta is abnormal. In younger individuals (age <40 years), chest radiography is potentially more useful because any degree of aortic dilation is abnormal and indicates an increased risk of aortic dissection. Other radiologic abnormalities seen on chest radiography include a pleural effusion, left apical cap, tracheal deviation to the right, depression of left main stem bronchus, esophageal deviation, and loss of the paratracheal stripe. The IRAD study revealed an abnormal aortic contour (A) in 50% of cases, calcification of the aorta in 60% of cases (B), and pleural effusion (C) in 19% of cases.

Which of the following diseases is characterized by the presence of a delta wave on an electrocardiogram? Charcot-Marie-Tooth disease Parkinsonism Parkinson's disease Wolff-Parkinson-White syndrome

Wolff-Parkinson-White syndrome Wolff-Parkinson-White (WPW) syndrome is a congenital cardiac condition in which there is an abnormal conduction pathway (accessory bundle) between the atria and ventricles other than the atrioventricular node. This pathway provides the basis for a reentrant circuit which bypasses the typical delay thru the AV node, typically resulting in premature ventricular depolarization and supraventricular tachyarrhythmia. The premature depolarization of some of the ventricle produces a "slurring" of the normal depolarization wave thru the AV node. This is seen as a gradual upsloping of the QR segment, called a delta wave, which creates an illusion of PR interval shortening and QRS lengthening. Charcot-Marie-Tooth disease (A) is a hereditary sensorimotor neuropathy which commonly leads to peroneal muscular atrophy. Parkinson's disease (C) is a degenerative disorder of the dopamine-generating cells in the substantia nigra, which causes parkinsonism symptoms. Parkinsonism (B) is a term used to describe the typical parkinsonian symptoms which arise from a variety of diseases, with Parkinson's Disease being one of these causes. Parkinsonism generally refers to tremor, rigidity, slowed movements and balance impairment.

Which of the following is associated with a shortened PR interval? Brugada Syndrome Mobitz 2° AV Block Wellens Syndrome Wolff-Parkinson-White syndrome

Wolff-Parkinson-White syndrome Wolff-Parkinson-White syndrome (WPW) is a congenital condition in which there is an abnormal accessory conduction pathway called the bundle of Kent. This accessory conduction pathway causes a premature depolarization of the ventricles by bypassing the AV node. The AV node typically acts to delay depolarization (the PR interval) to the ventricles to allow them to fill before contracting (QRS complex). The accessory pathway causes early depolarization of the ventricles resulting in an early QRS complex, thereby shortening the PR interval. On an ECG, this is represented by an upslope of the QRS complex (delta wave) that causes a widened QRS complex (>120 msec). The primary significance of WPW syndrome is that it predisposes patients to the development of tachydysrhythmias, particularly atrial fibrillation. Brugada Syndrome (A) is a hereditary condition characterized by a right bundle branch block-like pattern with ST elevation in Leads V1 to V3. Wellens Syndrome (C) is described by a large inverted T wave in Leads V2 and V3 and is associated with critical stenosis of the proximal left anterior descending coronary artery. Both Brugada and Wellens syndromes have normal PR intervals. Mobitz 2° AV Block (B) occurs at the level of AV node. Depolarizations from the atria are blocked and do not reach the ventricles, resulting in some P waves not being followed by a QRS complex (thereby, having no PR interval). The P waves that are followed by QRS complexes have normal PR intervals.

Normal Pediatric Heart Rates

• <1: 100-160 bpm • 1-2: 90-150 bpm • 2-5: 80-140 bpm • 6-12: 70-120 bpm • >12: 60-100 bpm

Ventricular Tachycardia

• > 3 consecutive ectopic ventricular beats • Monomorphic, polymorphic • Bidirectional: digoxin toxicity • Wide complexes • Pulseless: immediate defibrillation • Unstable: synchronized cardioversion • Stable: procainamide, amiodarone, synchronized cardioversion (refractory) • If unsure, manage all wide complex tachycardias as ventricular tachycardia

Myocardial Infarction ECG Patterns

• Anterior: ST elevations in V3, V4 • Septal: ST elevations in V1, V2 • Lateral: ST elevations in V5, V6, I, aVL • Inferior: ST elevations in II, III, aVF • Right ventricular: ST elevations in V4R, V5R • Posterior: ST depressions in V1, V2, large R waves

PDE-5 Inhibitors

• Mechanism: inhibits PDE-5 → corpus cavernosum smooth muscle relaxation + ↑ blood flow → erection • Headache, dyspepsia ("Hot and heavy, but then headache, heartburn, hypotension") • Nitrates + PDE-5 inhibitor use → refractory hypotension

Rheumatic Fever

• Patient with a history of GAS infection • Complaining of fever, red skin lesions on the trunk and proximal extremities, and small, non-tender lumps located over the joints • PE will show JONES criteria: Joints, Oh, no carditis!, Nodules, Erythema marginatum, Sydenham's chorea • Labs will show anti-streptolysin O, anti-DNase B, positive throat culture, or positive rapid antigen test • Treatment is antibiotics, NSAIDs • Comments: Modified Jones Criteria for a first episode of acute rheumatic fever: need 2 major or 1 major and 2 minor

Heart Block: Second Degree Type I (Wenckebach/Mobitz I)

• Progressive PR interval prolongation until QRS dropped • Block within AV node • Usually benign

Sick Sinus Syndrome (SSS)

• SA node dysfunction • Tachycardia-bradycardia syndrome: sinus rate varies from fast to slow and back again • Syncope, palpitations • Definitive rx: pacemaker placement + rate control medication • Untreated SSS → sinus block or sinus arrest

Calcium Channel Blocker Toxicity

• SA/AV node slowing, vasodilation • Bradycardia, hypotension, hyperglycemia

Low-Output Heart Failure

• Systolic dysfunction • More common than high-output heart failure • Causes: ischemic heart disease (most common), hypertension, cardiomyopathy, valvular heart disease • Decreased CO, increased LVEDP and increased systemic oxygen extraction ratio • Rx: oxygen, BiPAP, nitrates, furosemide

ACE Inhibitors

• Use: HTN, DM II • MOA: block the conversion of angiotensin I to angiotensin II • ADR: cough, angioedema • Comments: Names end in "pril"

Brain Natriuretic Peptide (BNP)

• ↑ Ventricular myocyte stretch → release • ↓ In obese • BNP < 100 pg/mL: heart failure unlikely • Level does not correlate with heart failure severity