Chest Pain
Managment of acute STEMI -key medications -when should you not give beta blocker? what do you give instead? -when do you avoid nitrates?
-Cardiology consult -coronary angiography/cath lab -possibly thrombolytics -antiplatelet/anticoagulation therapy -IV metoprolol if patient is tachy Key medications: ASA, beta blockers, clopidogrel, morphine, nitrates, and O2 -if the patient is in heart failure or in cardiogenic shock, do not give beta blocker, instead, give ace provided that the patient is not hypotensive -if inferior wall MI, avoid nitrates due to risk of severe hypotension
Complications acute MI -examples -most common? which one most commonly causes death? -complications by time day 1 day 2-4 day5-10 weeks to months
-arrhythmias (bradyarrhythmias and tachyarrhythmias) -reduced ventricular function -cardiogenic shock -papillary muscle dysfunction with acute valvular dysfunction -ventricular free wall rupture -pericarditis -recurrent thrombosis -recurrent thrombosis Arrhythmia is the most common complication and most common cause of death following acute MI Timeline: first day- heart failure 2-4: arrhytmia, pericarditis 5-10: wall and papillary muscle rupture weeks to months: ventricular aneurysm
Angina
A patient who is male in his late 40's presenting with exertional substernal chest pain has pretest probability for coronary artery disease (including unstable angina and acute MI) at over 90%. Tobacco use increases the risk for coronary artery disease and thus for acute MI and unstable angina. Exertional chest pain makes a cardiac cause for chest pain more likely than PE, GERD, or really any of the other considerations except muscular strain. Dyspnea is the most common associated symptom in patients with angina or MI. Angina and MI are often associated with nausea, as well as other symptoms such as belching, indigestion, dizziness, and fatigue. A normal ECG in the presence of chest pain should not really change your opinion about unstable angina/ACS, and really only suggests that the patient has not had an MI in the past. Normal troponins this early in an MI may also be expected, since a rise does not usually occur until four to six hours after the infarct.
Systolic murmurs
Aortic stenosis: A harsh systolic ejeciton murmur that radiates to the carotids Mitral regurgitation: a holosystolic murmur that radiates to the axxila Mitral valve prolapse: a midsystolic or late systolic murmur witha preceding click Flow murmur: usually soft murmur that is position-dependent (very common and does not inply cardiac disease)
Discharge medicaitons following an MI and Stent placement
Aspirin therapy should be started promptly in all patients with a suspected acute coronary syndrome and should be continued indefinitely. Administer aspirin, 160 to 325 mg, immediately upon presentation with suspected acute coronary syndrome (ACS) and continue daily aspirin at a dose of 75 to 325 mg/day. Clopidogrel should be continued for a year after stent placement in addition to aspirin to prevent stent thrombosis. β-adrenoceptor blockers should be started early in all patients with suspected ACS unless there are significant contraindications. Begin with oral β-blockerswithin a few days of the event, if not begun acutely, and continue them indefinitely. Goal heart rate is <70 and blood pressure <130/80. HMG CoA reductase inhibitors (statins) should be started while in the hospital in patients with ACS. Sublingual nitroglycerin should be sent home with patients post-admission. Angiotensin Converting Enzyme (ACE) Inhibitor
Unstable angina admission orders
Bed rest PO metoprolol Continuous cardiac monitoring- is indicated to detect tachyarrhythmias and bradyarrhythmias that may occr in the stetting of an acute MI anticoagulation with a heparin drip or subcutaneous low molecular weight heparin Morphine is used in patients with ongoing chest pain for analgeisa, but is not needed if there is no current chest pain
Hypertension managment post MI
Beta-blockers, like metoprolol, are first-line agents for hypertension in the setting of coronary artery disease. Angiotensin-converting enzyme (ACE) inhibitors are recommended in the setting of new left-ventricular systolic dysfunction. Spironolactone can be used for hypertension, but is typically not a first-line agent; it has been shown to reduce mortality in patients with reduced ejection fraction. Similarly, hydralazine and nitrates may be added to a multidrug, antihypertensive regimen. The combination of both has been shown to decrease morbidity and mortality in select patients with heart failure with reduced ejection fraction.
Aortic dissection diagnosis -Gold standard? -Classification? type A vs Type B -managment? when is it a surgical emergency?
CT angiography is the gold standard of imaging. MRA can be used if contrast CT is contraindicated. TEE may also be used to visualize details of the proximal aorta and coronary vessles and can also evaluate for pericardial effusion The standford system classifies any disseciton proximal to the left sublavian artery as type A and all others as type B Treatment: monitor and medically manage BP and heart rate as necessary. Avoid thrombolytics, begin B-blockade before starting vasodilators to prevent reflex tachycardia. If the dissection involves the ascending aorta, it is surgical emergency; descending dissecitons can often be managed with BP and heart rate control
Causes of Chest pain
Cardiac Stable angina Unstable angina Acute MI Atypical or variant angina (coronary vasospasm, Prinzmetal's angina) Cocaine-induced chest pain Pericarditis Aortic dissection: tearing chest pain radiating to back Valvular heart disease, i.e., critical aortic stenosis Cardiac arrhythmia Gastrointestinal Esophageal disease (GERD, esophagitis, esophageal dysmotility) Biliary disease (cholecystitis, cholangitis): typically RUQ with radiation to shoulder, may be referred to chest Peptic ulcer disease Pancreatitis Pulmonary Pneumonia Spontaneous pneumothorax Pleurisy Pulmonary embolism Pulmonary hypertension/cor pulmonale Pleural effusion Musculoskeletal Costochondritis Rib fracture Myofascial pain syndromes Muscular strain Herpes zoster Psychogenic Panic disorders Hyperventilation Somatoform disorders
Pulmonary embolism -presenting symptoms -Findings on ECG
Chest pain and dyspnea are frequent presenting complaints Pain of PE is typically described as "sharp" and is usually pleuritic Smoking is an independent risk factor for pulmonary embolism in both men and women ECG is abnormal in 70% of patients with pulmonary thromboembolism. However, the two most common abnormalities - sinus tachycardia and nonspecific ST and T-wave changes, do not discriminate among diagnoses. - Findings more suggestive of pulmonary embolism are S1Q3T3 (S wave in lead one, Q wave in lead three and inverted T-wave in lead three), transient right bundle branch block, and T-wave inversions in V1-V4. These findings are relatively infrequent.
coronary artery disease risk factors
Clinical manifestations include: stable and unstable angina, shorness of breath, dyspnea on exertion, arrhythmias, MI, heart failure, and sudden death Risk factors include -Diabetes -Family history of premature CAD (males <55, females <65) -smoking -dyslipidemia -abdominal obesity -HTN -Age(males <45, females < 55) -
Pericardial effusions -what is it? -causes?
Collection of fluid surrounding the heart. Acute pericarditis (viral, bacterial, tuberculous, or idiopathic in origin) ●Autoimmune disease ●Postmyocardial infarction or cardiac surgery ●Sharp or blunt chest trauma, including a cardiac diagnostic or interventional procedure ●Malignancy, particularly metastatic spread of noncardiac primary tumors ●Mediastinal radiation ●Renal failure with uremia ●Myxedema ●Aortic dissection extending into the pericardium ●Selected drugs
Acute MI criteria and classification -Criteria -symptoms -what is the best predictor of patient survival?
Criteria for acute MI: Rise and fall of troponin or creatine kinase myocardial band (CK-MB) plus ONE of the following: -Symptoms consistent with myocardial ischemia -Electrocardiogram changes indicating myocardial ischemia (ST-segment elevation or depression) -New pathologic Q waves -Findings on percutaneous coronary intervention (PCI) Symptoms -acute onste of substernal chest pain associated with diaphoresis, shortness of breath, lightheadedness, anxiety, nause/vomiting, and syncope physical exam may show signs of arrhythmia, hypotension, CHF The best predictor of survival is LV EF
Diagnosis of angina Treatment of stable angina
ECG is the best initial test for any type of chest pain Stress testing: ST segment or wall motion changes with exercise or pharmacologic stress are diagnositic of CAD. ECG stress test is contraindicated for pateints with abnormal baseline ECGs. Treatment for stable angina includes aspirin, beta blockers, and nitroglycerine, as well as risk factor reduction
Diagnosing Stemi -ecg findings? -secquence of ecg changes
ECG will show ST segment elevaiton or new LBBB. ST segment depressions and dominatn R waves in leads V1-V2 can also be reciprocal change indicating posterior wall infarct sequence of ecg changes: peaked T waves -> St segment elevation -> q waves -> T wave inversion -> ST segment normalization -> T wave normalization over several hours
More pericarditis -physical exam findings? -pain is worse with what? -what is the hallmark sign? -what initial tests should be done? -findings on ecg
Examination: May reveal a pericardial friction rub. Elevated JVP and pulsus paradoxus (a decrease in systolic BP > 10 mmHg on inspiration) can be present with tampanade Typically worsened with inspiration and is constant Hallmark: alleviation of chest pain with position change from the supine to the sitting and leaning forward position. diagnosis -initial tests: CXR, ECG, and echocardiogram to rule out MI and pneumonia -pericardial thickening or effusion may be evident on echocardiography -Classic ECG findings are diffuse concave-upward ST segment elevations and a depressed PR segment. However, these findings are often transient and may not be present at all.
Stable vs Unstable angina vs MI -what is the underlying cause of angina? -what is classic angina symtpoms? -what is stable angina? -what is unstable angina? -what is an acute MI -how do you differentiate between unstable angina and MI
In general, angina is related to an imbalance between myocardial oxygen supply and demand that is related to atherosclerotic plaque. Classic angina is retrosternal chest pain that comes on with exertion and is relieved with rest or nitroglycerin. Stable angina describes symptoms that have been occurring chronically and are predictable with exertion. It is thought to be caused by a stable atherosclerotic plaque. Unstable angina is when the chest pain occurs at rest, is new, is increasing in frequency, or when its onset is triggered with a lower level of exertion. Unstable angina is caused by an unstable plaque that has ruptured and caused a non-occlusive thrombus. Acute MI results from rupture of an unstable plaque with subsequent occlusive coronary artery thrombosis and myocardial necrosis. Differentiating between unstable angina and Non-ST-elevation MI (NSTEMI) is based on whether the troponins increase, so determining whether a patient has unstable angina or NSTEMI may require serial measurements of troponins. Remember, No troponin increase = No MI.
Pericarditis -what is it? -causes?
Inflammation of the pericardial sac. It can compromise cardiac output via tamponade or constrictive pericarditis. Most commonly idiopathic, although known etiiologies include viral infection, TB, SLE, uremia, drugs, radiation, and neoplasms. May also occur after MI or open heart surgery CARDIAC RIND collagen vascular disease aoritc disection radiation drugs infections acute renal failure cardiac (MI) rheumatic fevery injury neoplasms dressler syndrome .
Juglar venous distension Hepato jugular reflux Kussmal sign
Juglar venous distension: -> 7 cm above the sternal angle: most typically from volume overload, stemming form conditions such as right heart failure or pulmonary hypertension Hepato jugular reflux -distension of neck veins upon applying pressure to the liver: seen in same conditions as JVD Kussmal sign -increase in jugular venous pressure with inspiration: often seen in cardiac tamponade and constrictie pericarditis.
Left and right ventricular hypertrophy
LVH: the amplitude of S in V1 + R in V5 or V6 > 35mm -alternative criteria= The amplitude of R in avl + S in V3 is > 28 mm in men or > 20 in women RVH: right axid deviation and an R wave in V1 > 7
ECG -what are we looking for on ECG in ACS -Can the first ECG be normal in MI? what should we do about it?
Most patients presenting with chest pain should have an ECG done immediately to look for ST segment abnormalities that indicate myocardial injury. ST segment elevations are present in a STEMI; in a NSTEMI, ST segment depressions may occur or the ST segments may be normal. It is important to recognize the initial ECG may be non-diagnostic in half of patients. For this reason, serial ECGs are recommended in patients suspected of angina, unstable angina, or MI. An ECG's ability to diagnose Acute Myocardial Infarction (AMI) is greater if performed during an episode of chest pain. In patients with ST elevation on the ECG, do not delay further management while awaiting laboratory results. An ECG may not be necessary when there is a clear non-cardiac etiology of the pain in low-risk patients. The ECG is clearly indicated in this patient who has exertional chest pain, nausea, and a family history of early CAD.
Acute ischemia on ECG -what is the progression of ischemic changes on ECG? -Q wave criteria? -What about R waves as a determination of ischemia?
Natural progression starts withT wave inversion, progresses to ST segment changes (either depression or elevation), and finally results in Q waves (> 40 msec or more than one-third of the QRS amplitude) on the ECG. Because of this, Q waves signify either acute or prior ischemic events and do not provide information on when an event took place. Poor R wave progression in precordial waves can also be a sign of ischemia, although it is not specific. In a normal ECG, R waves increase in size compared to the S wave between leads V1 and V5. Poor R wave progression refers to diminished R waves in these precordial leads
Pericardial effusion diagnosis -diagnosis done by what? -size -work up for underlying cause? -treatment
Once a pericardial effusion is suspected, the diagnostic approach consists of three steps: confirming the presence of a pericardial effusion; assessing its hemodynamic impact, if any; and, whenever possible, establishing the cause of the pericardial effusion. Echocardiography is both specific and sensitive for the detection of pericardial effusion and can also provide information regarding the hemodynamic significance of the effusion. -small: <10mm thick -medium: between 10 and 20mm -Large: > 20mm If etiology is not specific: -check a cbc, cmp, thyroid, CXR, ANA Treatment: pericardial centesis and in most cases fluid cytology, gram stain, AFB stain for TB
ECG intervals -PR interval -QRS interval: what can a Wide QRS be indicative of? -Normal QTc
PR interval: normally between 120-200 milliseconds QRS inteval: normall < 120 msec Wide QRS interval can be indicative of bundle branch block QT interval: normal QTc (the QT interval corrected for extremes in heart rate) is < 440 msec. In long QT syndrome, QTc > 440 msec. Long QT syndorme is an underdiagnosed congenital disorder that is one cause of long QT and predisposes to ventricular tachyarrhythmias
Physical exam findings and their associated conditions Pericardial rub on initial presentation Lung crackles combination of fever, crackles, and decreased breath sounds Unilateral leg swelling and/or tenderness RUQ tenderness epigastric discomfort on palpation. Chest wall tenderness Pulse and BP differential from side to side Diastolic heart murmur
Pericardial rub on initial presentation -pericarditis Lung crackles -heart failure combination of fever, crackles, and decreased breath sounds -pneumonia Unilateral leg swelling and/or tenderness -DVT/PE RUQ tenderness -acute cholecystitis epigastric discomfort on palpation. -GERD Chest wall tenderness -trauma, costochondritis, and other muscular causes of chest pain could also be ACS Pulse and BP differential from side to side -significant peripheral arterial obstruction - including aortic dissection* Diastolic heart murmur -aortic dissection
Edema -causes of pulmonary edema -causes of peripheral edema
Pulmonary: left heart failure (fluid back up into the lungs). Peripheral: right heart failure and biventricular failure. also nephrotic syndroem, hepatic disease, lymphedema, hypoalbuminemia, and drugs.
right and left bundle branch block
RBBB: QRS >120, RSR' complex (rabbit ears), qR or R morphology with a wide R wave in V1; QRS pattern wiht a wide S wave in 1, V5, and V6 LBBB: QRS duration > 120 msec; deep S wave and no R wave in V1; wide, tall R waves in 1, V5, and V6
ECG Rate Rhythm and Axis -what is normal rate? -how do you determine if rhythm is normal? -how do you determine axis?
Rate -normal is between 60-100 Sinus rhythm: normal rhythm that originates form the sinus node has a p before every QRS and a QRS after every p Axis: can be determined by examining the QRS in leads 1 and AVF -normal: up in lead 1 and up in AVF (-30 to 90) -left axis deviation lead 1 up and AVF down (<-30) -right axis deviation lead 1 down and AVF up (> 90)
Right atrial abnormality Left atrial abnormality
Right atrial abnormality: The p wave amplitude in lead 2 is > 2.5mm Left atrial abnormality: The P Wave width in lead 2 is > 120 msec, or terminal - defleciton in V1 is > 1mm in amplitude and > 40 msec in duration. Notched P waves can frequentl y be seen in lead 2
Gallops
S3 gallop: a sign of fluid overload (heart failure, mitral valve disease) often normal in younger patients and in high output states (pregnancy) S4 gallop: A sign of decreased compliance (hypertension, diastolic dysfunction), usually pathologic but can be normal in younger patients and in athletes
Stemi vs non stemi -what is stemi....what other ecg finding can be indicative of STEMI -Nstemi
ST elevation MI (STEMI) is an acute MI in which the ST segment on the ECG shows elevation typical of myocardial ischemia. Any patient who presents with a clinical history consistent with acute MI and has a new left-bundle branch block should be triaged as ST-elevation MI (STEMI). In some cases, acute MI can occur without those changes. This is known as non-ST elevation MI (non- STEMI).
Troponins -what are they? examples, which is most specific -how often should they be repeated -how long can they take to rise? when will they return to normal -when do you give oxygen to MI patients? and to what level?
Serum biomarkers of myocardial necrosis (i.e. Troponins, CK-MB) are elevated in MI and indicate death of cardiac myocytes. When considering cardiac causes of chest pain, these markers should be done along with the ECG as part of the initial workup. If initial markers are normal, repeat these measurements at 6 and 12 hours. Cardiac troponins are highly sensitive and specific for an MI within the last 24 hours. They will be elevated in both STEMI and NSTEMI. Toponin I is the most sensitive and specific cardiac enzyme Both CK-MB and troponin I can take up to 6 hours to rise following the onset of chest pain. They peak in 1-2 days and return to normal levels at 3 and 5 days respectively Sublingual nitroglycerin is not indicated if the patient is not currently experiencing chest pain because it is a vasodilator used to alleviate chest pain. It can also cause the side effect of headache and there is no data empiric use improves outcomes. While changes in guidelines (and clinical practice) are often delayed in response to new research, it may be reasonable (as suggested by the review article referenced below) to reserve supplemental oxygen use in ACS for hypoxemic patients and then to titrate to an oxygen saturation of 94-96%.
Acute managment of unstable angina
Sublingual nitroglycerin -improve symptoms but does not lead to clear mortality benefit Beta blocker -Early oral or intravenous administration of beta blockers is used to reduce myocardial oxygen demand by decreasing heart rate, blood pressure, and cardiac contractility. This should be avoided if the patient is hypotensive (in shock), has acute heart failure, or has evidence of high-grade (2nd or 3rd degree) heart block. Avoid pindolol and other beta blockers with intrinsic sympathomimetic activity. Active wheezing from asthma is a relative contraindication to beta blockers. Aspirin Heparin -Anticoagulation therapy (antithrombotic therapy) with either subcutaneous low molecular weight heparin or intravenous unfractionated heparin should be added to antiplatelet therapy in patients with likely or definite acute unstable angina. Angiography with percutaneous coronary intervention -Coronary angiography is usually indicated in patients with non-ST elevation acute coronary syndrome (NSTE-ACS) who have recurrent symptoms of ischemia despite adequate medical therapy or who are at high risk as categorized by clinical findings (HF, serious ventricular arrhythmias), noninvasive test findings (significant LV dysfunction with EF <0.40, large anterior or multiple perfusion defects or wall motion abnormalities on echocardiography, high-risk Duke treadmill score ≤−11), high-risk TIMI or GRACE scores, or markedly elevated troponin levels. In patients with NSTE-ACS, early angiography and revascularization results in lower rates of recurrent unstable angina, recurrent hospitalization, MI, and death. Please see Table 8 from Statin therapy -high intensity statin therapy is recommended for patients with acute coronary
Chest pain risk stratification scores -what are the two stratification scores? -what scores indicate high risk?
TIMI score for unstable angina/NSTEMI -each of the following receive 1 point > 65 three ormore CAD risk factors (DM, smoking, HTN, HLD) known CAD (stenosis > 50%) ASA use in the past 7 days severe angina ST deviation > .5mm + cardiac marker a score > or equal to three indicates high risk patient Heart Score -5 categories each scored 0-2 History ECG Age Risk factors Troponin 0-10 scoring -0-3 = low risk (discharge) -4-6= mediaum risk observation, ischemia detection -7-10= high risk, observation, treatment, CAG
Physical exam findings of acute coronary syndrome
Tachycardia or hypertension can be found with acute MI because of increased circulating levels of catecholamines. -A new murmur may be caused by papillary muscle rupture or dysfunction. -An S3 or S4 may be heard as a result of damage associated with heart failure or decreased diastolic relaxation. -The presence of bruits would suggest peripheral arterial disease. This finding would increase the pretest probability for coronary atherosclerosis and, thus, acute coronary syndrome.
Initial Managment of Actue coronary syndrome -what is included in ACS? -what medication should be given for those with ACS? how much -what tests should be run?
The American Heart Association defines ACS as an umbrella term to cover any group of clinical symptoms compatible with acute myocardial ischemia. This term therefore includes unstable angina as well as both ST segment elevation and non-ST segment elevation myocardial infarction (STEMI and NSTEMI). Aspirin should be given to all patients suspected of an acute coronary syndrome without contraindication. Aspirin reduces the risk of myocardial infarction (MI) in unstable angina and reduces mortality in patients with an MI by preventing platelet aggregation through irreversibly inhibiting platelet cyclooxyenase and the consequent formation of thromboxane A2. Patients should receive 160-325 mg on arrival and continue daily aspirin at 81 mg per day. Clopidogrel can be given to those with aspirin allergy. ECG Troponins
CABG (coronary artery bypass graft) vs Percutaneous transluminal angioplasty -do both procedures have similar results? what is the downside to PCI? -when would CABG be prefered?
The decision about coronary artery bypass graft (CABG) versus angioplasty is often complex. Percutaneous transluminal angioplasty (PTCA) with or without stenting produces a similar survival rate to CABG but is associated with a higher rate of recurrent symptoms and target vessel revascularization, although this may be changing with the use of drug-eluting stents. CABG may be preferred in left main lesions or in complex proximal LAD disease with other unfavorable lesions (three-vessel disease) or in patients with left ventricular dysfunction or diabetes mellitus.
Thrombolytic indications and contraindications -indicated for what conditions? -major complications -contraindicaitons
Thrombolytic agents, such as tissue plasminogen activator (tPA), activate plasminogen with lysis of fibrin (and fibrinogen), resulting in rapid lysis of clot with reperfusion of the infarct-related territory and improving survival. Thrombolytics are indicated in patients with acute STEMI or new LBBB MI when primary PCI is not performed. The major complications associated with these agents are bleeding and hemorrhagic stroke. -Strong suspicion of dissection of the aorta -Pericardial effusion -Active gastrointestinal or other internal bleeding -Brain tumor, arteriovenous malformation, or aneurysm -Ischemic stroke in preceding 6 months (a verified transient ischemic attack (TIA) is an exception) -Previous intracerebral hemorrhage or subarachnoid hemorrhage Intracranial procedure or recent head trauma -Severe known bleeding disorder: coagulation abnormality, thrombocytopenia, etc.
Features of ischeic chest pain -typical symptoms -who can present with atypical symptoms
Typical -squeezing, tightness, pressure -diffuse, difficult to localize, not one specific spot -radiation to shoulders, arms, wrist, fingers, neck and throat, lower jaw and teeth -releived by rest or nitroglycerin -associated with shortness of breath, diaphoresis, belching, nausea, indigestion, dizziness, weakness, and fatigue Remember that atypical symptoms are present in diabetics, women, and elderly
Chostochondritis -what is it? -Presentation?
Typically associated with a more persistent pain picture and areas of tenderness on exam. Although the costochondral pain syndrome is a frequent diagnosis in patients with noncardiac chest pain, the causes, natural history, and treatment of this condition are poorly documented. Most cases follow a self-limited course with occasional exacerbations.
Aortic Disection -what is it? most common cause? most common site of origin -age group, more common in males or females? -presentation? -Exam Bp, pulses, murmur?,
a transverse tear in the intima of a vessel that results in blood entering the media, creating a false lumen and leadingto a hematoma thata propagates longitudinally. Most commonly secondary to HTN. the most common sites of origin are above the aortic valve and distal to the left suclavian artery. Most often occurs at 40-60 years of age, with a greater frequency in males History and physical: -Presenation: sudden tearing/ripping pain in the anterior chest (ascending) or back (descending) -Examination: patients are typically hypertensive. if hypotensive, consider pericardial tamponade, hypovolemia from blood loss, or other cardiopulmonary etiologies -asymmetric pulses and BP measurements -a murmur of aortic regurgitation may be heard if the aortic valve is involved with a proximal dissection -neurologic deficits may be seen in fthe aortic arch or spinal arteries are involved
Pericarditis treatment -what is the treatment -what should you avoid in post MI pericarditis? why?
address the underlying cause (corticosteroids/immunosuppressants for SLE, dialysis for uremia) or symptoms (ASA for post MI pericarditis, ASA/NSAIDS for viral pericarditis). Treatment***** three months of colchicine + NSAIDS until assymptomatic and then tapered over a few weeks Avoid corticosteroids within a few days after MI, as they can predispose to ventricular wall rupture Pericardial effusions without symptoms can be monitored, but evidence of tamponade requires pericardiocentesis with continuous drainage as needed
Prinzmetal angina -aka -what is iit? -important lab findings?
aka variant angina -mimics angina pectoris but is caused by vasopspasm of coronary vessles. It classically affects young women at rest in the early morning and is associated with ST segment elevation in the absence of cardiac enzyme elevation
Diastolic murmurs
always abnormal aortic regurgitation: an early decrescendo murmur mitral stenosis: a mid to late low pitched murmur
What is dressler syndrome
an autoimmune process occuring 2-10 weeks post MI, presents iwth fever, pericarditis, pleural effusion, leukocytosis, and increased ESR
Peripheral pulses: -causes of increased pulses? -causes of decreased? -pulsus paradoxus -Pulsus alternans -Pulsus parvus et tardus
increased: compensated aortic regurgitation; coarctation; patent ductus arteriosus decreased: peripheral arterial disesease; late stage heart failure pulsus paradoxus (decreased systolic BP with inspiration: pericardail tamponade; also seen in obstructive lung diseases, tension pneumothorax, and foreign body in airway pulsus alternans (alternating weak and strong pulses: cardiac tamponade, impaired left ventricular systolic funciton. Poor prognosis pulsus parvus et tardus: weak and delayed pulse: aortic stenosis
ECG leads an the portion of the heart they correspond to -anterior -inferior -lateral Anatomy of coronary artery occlusions and infarction -inferior infarct -anterior infarct -lateral -both lateral and inferior
leads V1-V4 reflect the anterior wall leads II, III and AVF reflect the inferior portion of the heart leads I, AVL, V5 and V6 correspond to the lateral myocardial wall -Inferior infarction is typically associated with a right coronary artery lesion for approximately 90% of the population who possess a right-dominant coronary circulation. Approximately 10% of the population have atypical "left-dominant" or "co-dominant" coronary circulation, in which case the circumflex artery or the posterior descending artery supply the inferior portion of the heart. In such patients, occlusion of these vessels may lead to inferior MI. - -Anterior infarction is usually associated with left anterior descending artery (LAD) occlusions. -Lateral infarctions are generally associated with circumflex artery occlusions -Infarctions involving both the anterior and lateral portions of the heart most commonly represent a proximal occlusion of the left main coronary artery.
emergent angiography and PCI -how quickly should PCI be performed? -critera for thrombolysis? -what are the options for thrombolysis? -long term treatment of MI
should be performed if possible in STEMI. If PCI cannot be performed in 90 mins and there are no contraindicaitons to thrombolysis (history of hemorragic stroke, or recent ischemic stroke, severe heart failure, or cardiogenic shock), and the patient presents withing 3 hours of chest pain onset, thrombolysis with tpa, reteplase, streptokinase should be performed instead of PCI. Long term treatmetn includes ASA, ACEIs, beta blockers, high dose statins, and clopidigrel
Pericardial effusions -symptoms depend on what? -most common ecg findings? -CXR findings?
symptoms: Most patients without a hemodynamically significant pericardial effusion will have no symptoms specific to the effusion, but they may have symptoms related to the underlying cause (eg, fever in the setting of pericarditis, etc). Thus, pericardial effusions are often discovered incidentally during evaluation of other cardiopulmonary diseases. However, patients with a hemodynamically significant pericardial effusion leading to cardiac tamponade usually present with signs and symptoms related to impaired cardiac function (ie, fatigue, dyspnea, elevated jugular venous pressure, edema). The most common electrocardiographic (ECG) findings in patients with a pericardial effusion are sinus tachycardia, low QRS voltage, and electrical alternans. Chest radiograph — The findings on chest radiograph are variable, depending on the etiology and size of the effusion and underlying comorbidities. Small to moderate effusions (less than 200 to 300 mL) may not result in significant findings on the chest radiograph, while larger pericardial effusions typically present with an enlarged cardiac silhouette with clear lung fields (image 1). However, an enlarged cardiac silhouette on chest radiograph is not specific and cannot be considered diagnostic for the presence of a pericardial effusion.
