Cardiovascular

hypertriglyceridemia

- >150 mg triglycerides per dL of blood - triglycerides are the most abundant fatty molecule in an organism; they can be found in subcutaneous tissue or surrounding organs; can function as energy source; gathered from diet (exogenous, absorbed in small intestine; go into circulation in chylomicrons which are broke down by lipases and ultimately leads to free fatty acids being store/used for energy in skeletal muscle cells or adipocytes) or made from liver (endogenous; fatty acids made from carbs or released from adipose tissue and released in form of VLDL into circulation to skeletal muscle or adipocytes; lipases break it down further into IDL [or VLDL remnants] which is further metabolized into LDL which is taken up by LDL receptors throughout the body including the liver) - Complications: atherosclerosis (endothelial vessel damage allows triglyceride remnants to go into intimal layer of vessel; macrophages eat it and become foam cells which leads to fatty streaks which are precursors for atherosclerotic plaque) and pancreatitis (chylomicrons build up blocks flow in capillaries leading to pancreatic ischemia) - Secondary cause pathophys: obesity (increased creation of VLDL but decreased breakdown of circulating triglycerides); diabetes (decreased function of lipoprotein lipase); high carb diet (>60% of diet; leads to more production of free fatty acids); hypothyroidsim (decreased hepatic lipase activity so decrease breakdown of IDL); alcohol (decreases lipid break down) - Primary = genetic - Sx: asymptomatic until 1000-2000 triglyceride levels; hepatosplenomegaly, lipemia retinalis (creamy colored retinal vessels); xanthomas; SOB and CP with atherosclerosis; N/V and epigastric pain with pancreatitis - cholesterol to build cell walls and hormones, triglycerides for fat storage and energy

Wolff-Parkinson White Syndrome

- An extra electrical pathway (bundle of Kent) that connects the atria and ventricles bypasses the AV node and its delay. The result is premature ventricular contraction. The PR interval is shorted as a result (less that 120ms [normal = 12-200]) and QRS is widened (over 110ms [normal = 80-100ms]). A delta wave is formed at the beginning of the QRS complex - This pattern turns into a syndrome when it facilitates other arrhythmias, like atria arrhythmias that are fast because there is another pathway without delays that move on to the ventricles (not enough filling time so not enough stroke volume so cardiogenic shock). Symptoms can include palpitations , lightheadedness, chest pain, or sudden cardiac death - Reentry circuits can also occur since most bundles of Kent are bidirectional, called atrioventricular reentrant tachycardia (AVRT). This is the most common cause of symptoms. Electrical currents can move from the ventricles back up through the bundle of Kent (orthodromic conduction) or from the bundle of Kent back up the bundle of His (antidromic conduction). - Treatment: radiofrequency catheter ablation or surgical ablation can destroy that extra pathway; medications like procainamide or quinidine; Avoid medications that block AV node delays, like digoxin, adenosine, calcium channel blockers, as they can increase the risk of developing ventricular fibrillation

long QT syndrome

- Congenital: due to gene abnormality (LQT1 and 2 have QT lengthening in response to stress and catecholamines; 3 shortens with tachycardia); defined by QT interval >440 ms; Sx = presyncope, syncope, Torsades, cardiac arrest; Tx = beta blockers (nadolol or propanolol; counteracts response to catecholamines, more for types 1 and 2; not as effective for type 3 which benefits from cardiac pacing and AICDs) - Acquired: electrolyte abnormalities (low K, Ca), medication (some macrolides and antidepressants, etc.); Tx = stop med, fix electrolyte abnormalities; IV magnesium or pacing for torsades

Heart Failure

- Most common cause: ischemic heart disease - Systolic dysfunction (HFrEF):↓ EF, Cardiac output (CO) dependent on afterload - Diastolic dysfunction (HFpEF): Impaired myocardial relaxation → abnormal LV filling; CO dependent on preload - Left heart failure: ↑ LVEDV + ↑ LVEDP → blood backup into lungs → pulmonary edema; Dyspnea, orthopnea, paroxysmal nocturnal dyspnea; Crackles - Right heart failure: Most common cause = left heart failure; JVD, peripheral edema, ascites - S3 - BNP: distinguishes between CHF and dyspnea of pulmonary etiology - Most useful study: echocardiogram

STEMI

- ST elevation myocardial infarction - CP, positive troponin, ST elevation > 1mm in contiguous leads - Leads II, III, aVF = Inferior infarction - Leads I, aVL, V5, V6 = Lateral infarction - Leads V1-V4 = anterior, septal (V3-V4 just anterior i think) - V7-9 ST elevation or ST depression in V1-V2 (PAILS; for examples if there is a posterior infarct then the next letter [A] will have depression; another way to look at it is if you see depressions in contiguous leads, then the letter before PAILS will be where the infarction is) - - Tx: MONA and BASH: Morphine (only if pain severe and unmanageable; CI = inferior, posterior MI), Oxygen if <90%, Nitrates (if no pain improvement after 3 sublinguals [cut off with stable angina] can give IV; decrease preload and afterload and decrease cardiac demand, increase bloodflow to myocardium; CIs = hypotension [<90 systolic or if decreases more than 30mmHg], inferior/posterior MI with right ventricular involvement bc it's dependent on preload, and if taken PDE5 inhibitor in last 24 hours), Aspirin (give to everyone unless allergy or if taken/given prior to hospital arrival; 160-325 mg); Beta blockers (decrease O2 demand of heart, decrease BP, decrease remodeling with happens when heart dies, decrease infarct size, decrease mortality early on, improve LV hemodynamic function, reduce ventricular arrhythmias which are big causes of death in MIs; CIs = hypotension, 2nd or 3rd degree heart block, be careful with reactive air disease, cardiogenic shock risk), ACE inhibitors (more for longterm use; start with 16 days; improve LV ejection fraction, reduce remodeling), Statins (high intensity like Atorvastatin 80mg or rosuvastatin 20-40mg [RA in charge]), Heparin (prevent more clots from forming but doesn't break up existing ones); can also use meds like clopidogrel (Plavix) and glycoprotein IIb and IIIa inhibitors like integrilin and abciximab -- Reperfusion Therapy: PCI (percutaneous coronoary intervention: stent, angioplasty; do within 90 mins) or TPA (if can't get catheterization within 90 minutes)

Angina/ACS Treatment

- Stable Angina: Beta blocker (BEAM, angiosleective), Aspirin, Nitrates, treat underlying conditions (HTN, Smoking, Diabetes, HLD) - Unstable Angina: MOAN (morphine, oxygen if below 90%, aspirin, nitrates [long term too as need I believe]); Beta blocker, Add heparin for 2-5 days and clopidogrel at hospital (alternatives to heparain include direct thrombin inhibitor and just clopidogrel or GPIIb/IIIa instead [tirofiban and eptifibatide]) - NSTEMI: MOAN (morphine, oxygen if below 90%, aspirin, nitrates [long term too as need I believe]); Beta blocker, Aspirin, (add heparin for 2-5 days and clopidogrel at hospital; alternatives to heparain include direct thrombin inhibitor and just clopidogrel or GPIIb/IIIa instead [tirofiban and eptifibatide]), Statins - STEMI: MOAN (morphine, oxygen if below 90%, aspirin, nitrates [long term too as need I believe]: NO if inferior MI bc depends on preload); Beta blocker, Aspirin, (add heparin for 2-5 days and clopidogrel at hospital; alternatives to heparain include direct thrombin inhibitor and just clopidogrel or GPIIb/IIIa instead [tirofiban and eptifibatide]; ROSH is saying only heparin for acute MI), Statins, Reperfusion (90 mins to cath lab), ACE inhibitors - Cocaine-induced and Prinzmetals = CCBs first line; Nitrates 2nd line; NO beta blockers (risk of unopposed alpha agonism) - No nitrates if using PDE-5 inhibitors or inferior MI - Use HEART (6 months) and TIMI (2 weeks) score - Do CABG if >50% LAD stenosis, >70% stenosis in 3 vessel disease, or EF < 40% (percutaneous transluminal coronary angioplasty [PTCA], for patients with coronary artery disease and resultant angina involving one or two vessels but not involving the left main coronary artery and in those with normal ventricular function) - BTW: contraindications to thombolytics = Hx if hemorrhagic stroke, ischemic stroke within 6 months, head traums in past 3 months, intracranial mass/AVM/aneurysm, suspected aortic dissection, internal bleeding

Treatments for heart failure

- Treatments that decrease mortality: BASH - beta blockers, ace inhibitors, spironolactone, hydralazine with nitrates - Symptom relief: Loop diuretics

deep vein thrombosis

- a thrombus that affects a deep vein, such as the femoral, popliteal, tibial, fibular, and gastrocnemius veins - a constellation of diseases known as venous thromboembolism (VTE). Classically, the pathogenesis is thought to be related to three risk categories (i.e., venous stasis, endothelial injury, and hypercoagulability [Virchow triad]). Other important risk factors include age greater than 60 years, malignancy, personal history of venous thromboembolism, prolonged immobilization, recent surgery, and pregnancy. Clinical presentation usually includes unilateral lower extremity edema, tenderness, warmth, and erythema along the deep venous system and a palpable cord. Calf pain with passive ankle dorsiflexion (also known as Homans sign) may also indicate DVT. The Wells criteria for DVT can help risk-stratify patients who present with symptoms that indicate DVT. A D-dimer test can be used for patients with low to intermediate pretest probability for DVT. The D-dimer test has a high sensitivity but low specificity for VTE. Therefore, a negative D-dimer rules out DVT but is nondiagnostic if it is positive. If the D-dimer is positive, duplex ultrasound should be used to confirm or rule out DVT. For patients with high pretest probability for DVT, a duplex ultrasound is recommended as the initial diagnostic test. Venography is the most accurate diagnostic test for DVT, however, it is rarely used due to the invasive nature of the exam. Anticoagulation is the mainstay treatment for DVT. Low-molecular-weight heparin, unfractionated heparin, warfarin, indirect factor Xa inhibitors, and direct oral anticoagulants can be used to obtain anticoagulation. Unfractionated heparin with a bridge to warfarin is used in patients with a creatinine clearance of < 30 mL/min. It is, therefore, the most appropriate therapy in this patient. - treat with anticoagulation for 45 days

infective endocarditis

- an acute or subacute bacterial infection of the endocardium and heart valves (mitral valve most common unless drug user then it's the tricuspid valve). - Risk Factors: over 60 years of age, male, IV drug use, poor dentition/dental infections, history of infective endocarditis or structural heart disease including valves, prosthetic heart valves - Acute infective endocarditis (about a few weeks) is most commonly caused by Staphylococcus aureus bacteremia and is most prevalent in patients with a history of IV drug use. Group B strep also common but not as much as staph. Acute Staphylococcus aureus bacteremia (especially MRSA) causing endocarditis in those who use IV drugs typically affects tricuspid valve. Bacteria more virulent bc attacking usually healthy tissue. Staph Aureus = think A means acute and addiction - Subacute infective endocarditis (weeks to months) is associated with bacteremia caused by the following organisms: HACEK group bacteria (small, fastidious gram-negative bacilli), Streptococcus viridians (most common; part of normal mouth flora; V = vulnerable valves), and Enterococcus species (common with recent GI, GU exam; ENT = Enema N' Turp). Attacks vulnerable valves, so not as aggressive/virulent bacteria can cause problems - Early prosthetic valve infection = less than 60 days, most common is staph, especially staph epidermis (EPI = enters prosthetic implants) - Late prosthetic valve infection = staph also seen - Strep Bovis usually seen with colon cancer or ulcerative colitis (think Bo in Bovis and Bowel) - Most common sx: fever - FROM JANE: Fever, Roth spots (retinal hemorrhages), Osler nodes (tender, at tips of finger/toes), Murmur, Janeway lesions (nontender, on palms, soles), Anemia, Nailbed hemorrhages or splinter hemorrhages, Emboli - The Duke criteria are used to diagnose infective endocarditis. It uses known risk factors, signs, symptoms, laboratory data, and diagnostic studies to predict the probability of bacterial endocarditis. Major Duke criteria include blood cultures showing a bacteria that is common in infective endocarditis and evidence of endocardial involvement seen on either echocardiogram or heard as a new heart murmur on physical exam. Minor Duke criteria include predisposition condition (e.g., history of IV drug use, cardiac catheter, etc.), fever, immunologic phenomenon (e.g., Osler nodes, Roth spots, glomerulonephritis, positive rheumatoid factor), vascular phenomena (e.g., Janeway lesions, septic emboli, mycotic aneurysms, intracranial hemorrhage), microbiological evidence of bacteremia from an organism that is not typically associated with infectious endocarditis, and positive echocardiogram not meeting major criteria. (Minor criteria is basically FROM JANE, risk factors, and less convincing major criteria). The Duke criteria indicate infective endocarditis in the following cases: two major clinical criteria are met, one major and three minor clinical criteria are met, or when five minor criteria are met. In the case of this patient, three minor Duke criteria features are met (i.e., history of IV drug use, fever, and Janeway lesions). Thus, an additional major criterion is needed in order to diagnose infective endocarditis. Gram-positive cocci seen in the patient's blood culture is indicative of Staphylococcus aureus bacteremia and, therefore, an example of a major Duke criterion. Parts vegetations breaking off from valves can cause emboli - Treatment of infective endocarditis is achieved by treating the underlying bacteremia with IV antibiotics. Empiric antimicrobial therapy (usually for acute bc you want to treat them quickly; can wait for lab results for subacute) should include coverage for staphylococci, streptococci, and enterococci. Gentamicin plus ceftriaxone or vancomycin is an appropriate initial therapy for patients with suspected bacterial endocarditis. For acutely ill patients with heart failure, gentamicin, vancomycin, plus cefepime is warranted. - Cram the Pance says: -- Native valves = treat with antistaphylococcus penicillin (like Nafcillin, Oxacillin) and Gram - coverage (Ceftriaxone or Gentamicin) with 4-6 weeks. Think: Only Native Cardiac Gears (choose one for each side of coverage; use Vancomycin if MRSA present [use for IV drug users]) -- For prosthetic valves (want to cover staph enterococci and gram negative bacilli): Gentamicin + Vancomycin (synergistic effect between the two) + Rifampin (helps penetrate biofilm; start after 2-3 days not right away bc potential for mutation/resistance); Treat for 4-6 weeks; Think = Valves Generally Recreated -- If fungal treat with amphotericin B - Okay so I'm also seeing... -- Native valves acute = vancomycin + cefepime -- Native valves subacute = vancomycin + augmentin -- Prosthetic valves < 12 monts = Vanc + gentamicin + ceftriaxone + rifampin -- Prosthetic valves > 12 months = Vanc + ceftriaxone - Prophylactic antibiotic therapy (using amoxicillin 2g or clindamycin 600mg if penicillin allergy) is recommended before an invasive dental procedure (tooth extractions, etc.; not for routine exam) or surgical procedure (like respiratory tract procedure that involved incision/biopsy or if it involves infected tissue) in patients with prosthetic valves or other heart parts/devices, previous endocarditis, congenital heart disease (particularly cyanotic, starts with a T), acquired valvular disease, hypertrophic cardiomyopathy, or cardiac transplant with valvulopathy. For persistent cases of endocarditis despite antibiotic therapy, valve replacement may be necessary. Anticoagulation therapy is not beneficial in patients with native valves, and it is controversial in those with prosthetic valves. -- Tx usually mutlidisciplinary

valvular disorders sounds and treatment overview

- aortic stenosis = crescendo decrescendo systolic murmur at right upper sternal border; Tx = valve replacement (mechanical lasts longer but requires anticoagulants, bovine last less but doesn't require thinners); bridges to valve replacement include percutaneous valvuloplasty and intraaortic ballon pump); avoid physical exertion and drugs that reduce preload [bc condition is preload dependent] like nitrates or that decrease inotropic function like CCBs or beta blockers); can have S4 gallop - mitral regurgitation = holosystolic systolic murmur @ apex of heart (mid clavicular at 5th intercostal space, radiates to axilla; MVP most common cause in US and rheumatic fever most common cause worldwide; also commonly due to papillary muscle or chordae tendinae rupture due to MI); Tx = decrease afterload (ACE inhibitors, ARBs, hydralazine, nitrates, diuretics) and surgery if refractory to medical treatments or EF < 60% - MVP = mid-late systolic murmur with click at apex (mid clavicular at 5th intercostal space; murmur increases with decreased preload and resulting smaller left ventricle size), most common cause of mitral regurgitation in the US; Tx = good prognosis, monitor; no BBs unless autonomic dysfunction; avoid alcohol, caffeine, diuretics, and amphetamines - pulmonic stenosis = crescendo decrescendo mid-systolic murmur with ejection click at left upper sternal border; usually congenital or in the young; Tx = balloon valvuloplasty - aortic regurgitation (aka insufficiency) = diastolic decrescendo blowing murmur at LEFT upper sternal border; bounding pulses, can get Austin-Flint murmur (mid-late diastolic at apex of heart due to mix of retrograde flow with anterograde flow from left atrium and aorta); Tx = reduce afterload (surgery if symptomatic of EF < 55% bc EF usually high in this condition) - Mitral stenosis = mid-diastolic rumbling murmur heard most at apex of the heart (rheumatic fever the most common cause); Tx = percutaneous balloon valvuloplasty (best treatment), mitral valve replacement (if valvuloplasty CI or poor valve morphology); medical tx = diuretics and sodium restriction, treat a fib if it emerges (rate limiting drug, anticoagulants) - Helpful factoids: -- harsh/rumbling sounds = stenosis -- blowing soungd = regurgitation ("regurg" and "that blows" sounds like slang) -- sitting up and leaning forwards accentuates aortic murmurs -- lying on left side accentuates mitral murmurs -- increased afterload increases regurgitation murmurs but decreases outflow murmurs -- AS and HOCM both decrease with increased afterload and increased with decreased afterload; but they go in opposite directions for preload -- inspiration increases ALL murmurs at right side of heart and decreases ALL murmurs at left side of heart; expiration decreases ALL murmurs at right side of heart and increases ALL murmurs at left side of the heart

aortic aneurysm

- at least a 50% increase in the diameter of a full-thickness segment of a blood vessel - most common cause of thoracic aortic aneurysm (TAA) is degenerative (mechanical factors and protein degradation are believed to result in medial degeneration), and patients with or at-risk for atherosclerosis (including patients with dyslipidemia, hypertension, male sex, and smoking) - tobacco is the greatest risk factor for abdominal aortic aneurysm and most common location for AAA is infrarenal - other risk factors: over 60 years old, Marfan syndrome, Ehlers-Danlos syndrome, family history - most patients are asymptomatic and can be found incidentally; radiologic findings include displacement of the trachea from midline, enlarged aortic knob, and a widened mediastinum; pulsatile abdominal mass; hypotension and syncope if ruptured - acute onset of chest pain; upper back, abdominal, flank, or groin pain; nerve dysfunction related to compression of structures surrounding the aneurysm; if symptomatic then usually very large, at high-risk for rupture, and are associated with high mortality rates (triad = chest pain, pulsatile abdominal mass, hypotension) - monitor 4 - 4.9 cm annually, 5 - 5.4 every 6 months (MRI or CT); one-time screening by ultrasonography (standard imaging for AAA) in men aged 65-75 who have ever smoked - elective surgery if > 5.5 cm or aneurysms with rapid expansion rate (> 0.5 cm in 6 months or > 1 cm per year); surgical repair (laparotomy) if symptomatic

venous insufficiency

- elevated venous pressure which leads to vein dilation, interstitial fluid accumulation, skin changes, or skin ulceration; underlying issues leading to venous hypertension include inadequate muscle pump function, incompetent venous valves (reflux), and venous thrombosis or obstruction - chronic venous insufficiency can lead to inflammation, which can lead to fibrosis and ulcers - Risk factors = arteriovenous shunt, family history, high estrogen states, increasing age, ligament laxity, lower extremity trauma, obesity, pregnancy, sedentary lifestyle, smoking, prior venous thrombosis, and some genetic conditions - Sx: leg aches and pain, heaviness, swelling, muscle cramps, and dry, tight, itching, irritated skin; worsens at the end of the day and when sitting - you can diagnose clinically but duplex ultrasound is definitive - most appropriate first-line management plan includes conservative treatment which focuses on compression therapy, exercise, and leg elevation, which compress dilated veins, decrease edema, improve oxygen transportation, and reduce inflammation; ablation therapy if the problem persists - ulcer treatment = wet-to-dry saline dressings and unna venous boot - Klippel-Trenaunay syndrome = genetic condition predisposes individuals to developing chronic venous insufficiency and is also a contraindication for ablation therapy

ACE inhibitors

- end in pril; MOA = inhibit ACE (angiotensin converting enzyme) to stop conversion of angiotension I to angiotensin II (which is responsible for vasoconstriction, so you get vasodilation and an decrease in preload and afterload; ACE also breaks down bradykinin, a vasodilater) - ADRs: CHAD = Cough, Hyperkalemia, Hyperuricemia, Angioedema, Dose 1 Hypotension

varicose veins

- enlarged, tortuous superficial veins resulting from venous hypertension; valvular insufficiency the most common cause, although decreased function of the venous pump, venous wall deformities, and venous thrombosis are also causative factors - risk factors: pregnancy, obesity, sedentary lifestyle, prolonged standing, family history of varicosities, genetic syndromes, smoking (damages vein walls and valves), advanced age, trauma, and previous superficial or deep vein thrombosis - can be diagnosed clinically, although Doppler ultrasound of the affected extremity is useful to rule out thrombosis and to guide treatment decisions - First-line therapy: compression stockings and lifestyle modifications, such as smoking cessation, exercise, and elevation of the affected limb - after three months of conservative therapy, more invasive therapy can be considered, especially for patients who continue to have pain or are troubled by the cosmetic appearance of the varicosities; Sclerotherapy of superficial veins involves injecting a sclerosing agent directly into the varicose vein. Thermal vein ablation uses laser or radiofrequency energy to destroy the vein walls. Surgical excision of the varicose veins can also be performed (but more invasive with more risks). In patients with superficial varicosities that are the result of deep vein insufficiency and reflux, ablation of the deep vein should be performed first (or may be performed concomitantly) before superficial veins are treated. This treatment will result in a lower incidence of recurrence of the superficial varicose veins

PR interval

- from beginning of P ways to beginning of Q wave - .12 -.2 seconds (half to one full big box)

atrial septal defect

- hole in the atrial septum; most commonly due to incomplete closure of ostium secondum (other causes include incomplete closure of ostium primum, sinus venosus, coronary sinus); left to right shunt (bc higher pressure on left side; acyanotic heart defect); most common heart defect in adults; about 10-15% of all congenital defects; associated with fetal alcohol syndrome and present in about 25% patient with down syndrome - Sx:usually asymptomatic and resolves on its own; symptoms in children = dyspnea on exertion, failure to thrive, frequent respiratory infections; sx in adults = dyspnea on exertion, arrhythmias, syncope, heart failure, fatigue; also risk of developing paradoxical emboli (stroke from venous clots bc can travel from RA to LA and bypass lungs and go to systemic circulation including the brain) - Physical Exam: systolic ejection crescendo-decrescendo murmur best heard at the pulmonic area with wide, fixed split S2 -- the letter "A" looks like its doing a wide split; also A for anchor as in fixed - Dx: Echocardiogram the go to; Cardiac cath gold standard but rarely used; CXR can show cardiomegaly and increased CV markings; EKG can show incomplete RBBB or Corchetage sign (notch at R wave peak in inferior leads) - Tx: observe if less than 5mm and asymptomatic (most resolve on their own); surgically correct (percutaneous transcatheter closure vs surgical intervention) if >1cm or symptomatic (usually ages 2-4)

superficial vein thrombosis

- in the lower legs it involves occlusion of an axial vein, either the great saphenous vein or small saphenous vein; more common in women. - risk factors = varicose veins, obesity, injury, intravenous drug use, and hypercoagulability due to pregnancy, malignancy, or other condition - signs/sx: superficial vein thrombosis includes erythema and pain along the inner medial thigh following the course of the vein

Atrial fibrillation

- instead of one coordinated contraction of the atria, the many muscle fibers contract at different times, leading to quivering of the atria and loss of the atrial kick (when a small amount of blood is pushed into ventricles during systole) - Risk factors include conditions that can cause an inflammatory state or physically stretch out the atria and damage the cells there leading to them having different properties (tissue heterogeneity), including CAD, hypertension, heart failure, and valvular disease. Other risk factors include obesity, diabetes, and excessive alcohol consumption; there may also be a genetic component - AF that comes and goes and lasts less than 1 week is paroxysmal AF. Repeated paroxysmal events stress the atrial cells even more leading to progressive fibrosis that leads to persistent AF (lasts more than a week without self-termination). Repeated paroxysmal events stress the atrial cells even more leading to progressive fibrosis that leads to persistent AF (more than 1 week but not more than 12 months). Long-standing persistent AF is more than 12 months and permanent AF is when there are no more attempts to stop it - Symptoms: General fatigue, shortness of breath, dizziness, weakness, palpitations - Diagnosis: Holter monitor for paroxysmal AF (monitors rhythm and records episodes); ECG for persistent AF Transthoracic echocardiography can evaluate cardiac function and structure, while transesophageal echocardiography is essential for evaluating the presence of thrombi, which is indicated before performing cardioversion or invasive procedures that can cause embolization. Laboratory studies, including metabolic, cardiac, and thyroid profiles, should be obtained to exclude or rule in other cardiovascular diseases. Ambulatory rhythm monitoring is necessary for patients with intermittent atrial fibrillation. Treatment of atrial fibrillation includes rate control and rhythm control strategies. The main goal of rate control strategy involves symptom management and prevention of tachycardia-mediated cardiomyopathy, with the resting heart rate maintained at 80 beats/min and the exertional heart rate maintained at or below 100 beats/min. Rate control can be achieved by administering atrioventricular nodal blockers such as beta-adrenergic blockers (most effective) and nondihydropyridine calcium channel blockers (such as verapamil and digoxin). Rhythm control is indicated in patients with continuing symptoms despite rate control, whose rate is difficult to control, or who develop tachycardia-mediated cardiomyopathy or in younger patients with the first onset of the disease or whose symptoms are precipitated by an acute illness. Cardioversion, antidysrhythmic medications, and catheter ablation can be used for rhythm control. Electrical cardioversion is often successful at reversing atrial fibrillation but is associated with recurrence. Patients who present with atrial fibrillation for > 48 hours should be anticoagulated for 21 days prior to cardioversion. Catheter ablation involves ablating the pulmonary veins (the most common sites of atrial fibrillation electrical triggers) using radiofrequency or cryotherapy. It is indicated in patients with symptomatic atrial fibrillation who are taking at least one antidysrhythmic medication. Patients with atrial fibrillation have a fivefold risk of developing stroke. Thus, the need for anticoagulation should be determined using the CHA2DS2-Vasc score. Patients with a score of 2 or above should be started on anticoagulation such as rivaroxaban, dabigatran, or apixaban. Since anticoagulation can also increase the risk of gastrointestinal and intracranial bleeding, patients' risk of bleeding should be stratified using the HAS-BLED score. Patients who score 3 or above should be monitored more closely, or therapy should not be initiated if the risk outweighs the benefit. - pacemaker (for atria or for ventricles if AV node ablation done bc no more communication between atria and ventricles)

restrictive cardiomyopathy

- most common cause is amyloidosis - Other causes: sarcoidosis and hemochromatosis (Amy HAS [Amyloidosis, hemochromatosis, amyloidsos again bc most common, sarcoidosis]) restrictive cardiomyopathy), chemo, radiation, metastatic disease - causes stiffening of ventricles so decreased amount of blood in heart and can cause diastolic heart failure (right sided more common) - Kussmaul sign = breathing in (which decreases intrathoracic pressure and pulls blood including fron the jugular vein into right atrium) will cause JVD (bc blood backing up bc can't all fit into heart like it used to) - atrial dilation bc blood backing up there - endomyocardial biopsy will stain Apple green for Amyloidosis - Tx: treat underlying cause steroids, phlebotomy/iron chelation for hemochromatosis; beta blocks, diuretics, etc.

tetralogy of fallot

- mots common cyanotic congenital defect; consists of four structural defects: right ventricle outflow obstruction (from valve or infundibulum narrowing [area below valve]), right ventricular hypertrophy (bc of aforementioned outflow obstruction), large unrestrictive VSD, overriding aorta the VSD (exact location variable); although blood usually move from left to right in VSH, the RVH is so great that is causes blood to move from right to left (causing cyanosis bc deoxygenated blood pumped to rest of body); associated with chromosome 22 deletion and digeorge syndrome - Clinical presentation: usually cyanotic at birth (cyanosis when SpO2 < 80%); old patients with get more cyanotic with time and with exertion (aka tet spell; ways to decrease cyanosis include squatting or bring knees to chest [latter use for babies] bc kinks femoral arteries, increase peripheral vascular resistance, increases afterload and increase pressure on left side of heart for a change and switching it to a left to right shunt temporarily), digital clubbing, harsh systolic murmur at left upper or middle sternal border, right ventricular heave (palpable/visible chest movement) - Dx: echocardiogram preferred; CXR shows boot shape (bc right ventricle enlargement); EKG shows RVH, right atrial enlargement - Tx: surgery by 4-12 months (patch VSD and decrease outflow obstruction); prostaglandin infusion before surgery to keep ductus arteriosus open to improve circulation; prophylaxis for bacterial endocarditis

Wandering Atrial Pacemaker

- multiple ectopic atrial foci that generate impulses that are conducted to the ventricles - Criteria = 3 or more morphologically different P waves with QRS that is within 3 little boxes and HR < 100 - multifocal atrial tachycardia is the same but HR is 100 or greater

acute limb ischemia

- sudden decrease in limb perfusion that threatens its viability; almost exclusively associated with arterial occlusion (common femoral artery is the most common site of occlusion); most commonly occurs in the setting of a previously patent but atherosclerotic artery, however, it may be due to acute thrombosis of a stent or graft, dissection of an artery, or the result of an embolus from a proximal source (most commonly heart due to atrial fibrillation) lodging in a more distal vessel - common risk factor = prior history of peripheral arterial disease (PAD) - chronic limb ischemia typically have a less drastic presentation due to the development of collateral circulation that develops over time in patients with chronic ischemia - Sx: 6 P's = pain, pallor, pulselessness, poikilothermia, paresthesia, paralysis (really bad, later finding) - diagnosis can often be made clinically; CTA or catheter-based angiography done for viable or marginally threatened limbs - anticoagulation with a heparin drip and intravenous fluid therapy should be immediately initiated prior to making plans for intervention (open embolectomy, thrombolysis, and transcatheter thrombectomy); once the acute limb issues have been attended to, the subsequent diagnostic evaluation is focused on identifying the suspected embolic source, typically using echocardiography or additional vascular imaging.

hypertrophic cardiomyopathy

- thickening of heart wall, including the septum, which leads to outflow obstruction - diastolic heart failure - left sternal border harsh systolic murmur that worsens with decreased preload (like Valsalva maneuver or standing up bc the blood helps open the obstruction) and improves with increase venous return (raising legs, squatting) - can be autosomal dominant genetic disorder, can be deadly in young men - Diagnose with echo (15mm or more ventricular thickness, 13mm if family history) - Tx: beta blocks, non-dihydropyridine Ca channel blockers increase filling - Avoid: Nitrates and diuretics (decrease left ventricular volume, preload) and meds/activities (sports) that increase contractility of heart which worsen obstruction

syncope

- think lack of perfusion to the brain - Reflex (neurally mediated): Vasovagal (most common cause; present with bradycardia or vasodilation, feeling warm; associated emotion or standing for a long period of time), carotid sinus pressure - Cardiac causes: Valvular (aortic stenosis), heart failure, cardiomyopathy (HOCM), arrhythmia (think syncope at rest; btw also think seizure if at rest), pericardial effusion - Vascular: basilar artery (vertigo, perioral numbness, vision changes), subclavian steal (subclavian stenosis so vertebral artery steal blood flow in opposite direction away from the brain; worse with left arm exertion, numbness, ischemia which occurs bc blood supply from vertebral artery not enough), hypotension (dehydrated, bleeding, sepsis, vasodilators, alcohol), brain bleed - Heme: anemia, bleeding - Pulmonary: PE, pneumonia? - Endocrine: hypoglycemic - Trauma - Drugs? - Tests: CBC, EKG, dry CT head, BMP, quick glucose test, chest x-ray; BNP, echo, tilt table (for vasovagal), D dimer; don't forget to look at SpO2 and do neuro exam, utox? - shortcut to thinking about causes: CHESS = CHF, Hematocrit, EKG, Shortness of breath, Systolic BP < 90)

HF rEF

< 55%; Left-sided heart failure is caused by coronary artery disease (most common cause) and hypertension, while right-sided heart failure is most commonly caused by left-sided heart failure or pulmonary disease. Systolic heart failure is associated with a reduced ejection fraction and is the most common form of heart failure. It is caused by myocardial infarctions and dilated cardiomyopathy. Patients with left-sided failure will present with dyspnea (e.g., orthopnea, dyspnea at rest, and paroxysmal nocturnal dyspnea) and complaints of pulmonary congestion (e.g., cough with pink frothy sputum and wheezing). Patients with right-sided failure will present with complaints of peripheral edema, anorexia, and nausea. Physical exam will reveal hypertension, bibasilar rales on auscultation, laterally displaced point of maximal impulse, S3 gallop, peripheral edema, jugular venous distention, and hepatojugular reflux. The S3 gallop is caused by the sudden deceleration of blood entering the left ventricle. Heart failure is diagnosed with echocardiogram. The echocardiogram shows reduced ventricular function and reduced ejection fraction. A chest X-ray is useful during acute exacerbations of heart failure to assess for pulmonary effusions. With regards to lab tests, B-type natriuretic peptide is elevated during periods of volume overload and is therefore also useful at identifying acute exacerbations, where usually it is greater than 400 pg/mL. Lifestyle management includes limiting sodium to < 2 g per day, restricting fluids to < 2 L per day, and ceasing smoking. Medical management of heart failure includes an angiotensin-converting enzyme (ACE) inhibitor, a diuretic, and a beta-blocker. ACE inhibitors, beta-blockers, and spironolactone decrease mortality for patients with heart failure. An implantable cardioverter-defibrillator device should be considered for patients with ejection fraction less than 35% due to poor tolerance of cardiac dysrhythmias.

Long-standing persistent Atrial Fibrillation

AF lasting more than 12 months

Paroxysmal Atrial Fibrillation

AF that comes and goes and lasts less than 1 week. Repeated paroxysmal events stress the atrial cells even more leading to progressive fibrosis that leads to persistent AF

AV blocks

AV blocks occur when the conduction through the AV node is delayed. This delay can be the result of Lyme carditis, infiltrative cardiomyopathy, medication, or myocardial ischemia. There are four types of AV block: first-degree, second-degree Mobitz type I, second-degree Mobitz type II, and third-degree block. First-degree AV block is described as a consistently prolonged PR interval greater than 0.2 seconds with a QRS complex associated with every P wave. Second-degree Mobitz type I AV block, also known as Wenckebach, is a progressively prolonged PR interval with occasional dropped QRS complexes, which indicates the electrical conduction did not make it to the ventricles. A second-degree Mobitz type II AV block occurs when the PR interval is consistently greater than 200 milliseconds with occasional dropped QRS complexes. A third-degree AV block, also known as complete atrioventricular block, occurs when there is no association between the P waves and QRS complexes. Treatment is typically only indicated if the patient has second-degree Mobitz type II or complete atrioventricular block. If the patient is hemodynamically unstable, atropine and transcutaneous pacing are typically utilized first in the ED. Reversible causes of AV block should be addressed or permanent pacemaker placement is the next step. Some patients will need a temporary pacemaker in place while underlying conditions are resolved.

Treatments after an MI

BASH: beta blocker, ace inhibitors, statins, heparin (an anticoagulant meaning it prevents more clots from emerging or growing)

cardioselective beta blockers

BEAM = Bisoprolol, Esmolol, Atenolol, Metoprolol - target beta 1 receptors, focused like a BEAM of light

Persistent Atrial Fibrillation

Lasts more than 1 week but not more than 12 months without self-terminating

MI Treatments

Morphine, Oxygen (if patient not over 90%), Aspirin (add ticagrelor or prasugrel for dual antiplatelet therapy; reduces mortality and decreases stent thrombosis), Nitrates (.4 mcg every 5 minutes for a total of 3 doses)

mitral stenosis

a common heart condition caused by a structural abnormality of the mitral valve that results in obstruction of left ventricular inflow. The most common cause of mitral stenosis is rheumatic heart disease. While at rest, patients are often asymptomatic, however, in instances of increased heart rate, patients may develop dyspnea. Hoarseness may also be present due to compression of the left recurrent laryngeal nerve against the pulmonary artery by the enlarged left atrium. In cases of severe mitral stenosis, patients may present with pink-purple patches on the cheeks, called mitral facies

third degree heart block

a complete dissociation between the atria and the ventricles. It is caused by a lesion that is distal to the bundle of His. Some risk factors for third-degree atrioventricular block are ischemic heart disease, cardiomyopathy, viral myocarditis, Lyme carditis, hyperkalemia, and AV nodal blockers. Patients with a third-degree AV block may present with syncope, dizziness, confusion, palpitations, or symptoms of heart failure. Diagnosis is made by observing a complete disassociation between the atrial depolarization (P wave) and ventricular depolarization (QRS complex) on an ECG. Treatment for a third-degree AV block is transcutaneous or transvenous pacing in the acute setting and an implanted cardiac pacemaker for long-term treatment and is based on the patient's clinical stability. Patients who present with third-degree AV block but do not have signs of hypoperfusion (hypotension, confusion, cool diaphoretic extremities, chest pain, shortness of breath, or unresponsiveness) can be managed medically until an implantable pacemaker can be inserted. Patients who have signs of hypoperfusion are considered unstable and should be treated with transcutaneous or transvenous pacing to improve perfusion until an implantable defibrillator can be placed.

hyperlipidemia

a condition characterized by elevated levels of fat (lipids) in the bloodstream. Primary causes are usually a result of genetic mutations. Secondary causes are much more common and include alcohol use, diabetes mellitus, hypothyroidism, obesity, renal disease, liver disease, and a sedentary lifestyle. Clinical manifestations are not always present but may include xanthomas (fatty subcutaneous deposits) and xanthelasmas (xanthomas found around the eyelids). The 2016 U.S. Preventive Service Task Force guidelines recommend screening for lipid disorders in men ≥ 35 years old (class A), men 20-35 years old at increased risk for coronary heart disease (class B), women ≥ 45 years old at increased risk for coronary heart disease (class A), and women 20-45 years old at increased risk for coronary heart disease (class B). The 2018 AHA/ACC guidelines recommend screening all adults ≥ 20 years old for high blood cholesterol. Screening for hyperlipidemia should be done with a fasting lipid profile. Elevated cholesterol, elevated LDL, elevated triglycerides, and decreased HDL are consistent with hyperlipidemia and increase the risk of coronary heart disease, atherosclerosis, and pancreatitis. Lifestyle modifications are first line and include smoking cessation, weight loss, exercise, and a heart-healthy diet low in simple carbohydrates and high in fruits, vegetables, and fiber. The AHA/ACC recommends the coronary artery calcium score as the best method for risk stratification to aid in guiding treatment. Statins are considered first-line therapy. (Statin drugs are indicated for patients with established cardiovascular disease or with a ten-year cardiovascular risk assessment [using an online risk calculator which takes into account age, race, total cholesterol, high-density lipid cholesterol, smoking status, and comorbidities such as hypertension and diabetes] which is greater than 7.5 percent.) For patients on statins who are at the maximally tolerated dosage, the ODYSSEY OUTCOMES and IMPROVE-IT clinical trials demonstrated the efficacy of PCSK9 inhibitors and ezetimibe, respectively, in improving cardiovascular outcomes when added to statins. The ISIS-2 clinical trial demonstrated the efficacy of aspirin in decreasing all-cause mortality in patients with established cardiovascular disease. If a patient is unable to obtain a total cholesterol under 200 mg/dL on high dose rosuvastatin or atorvastatin therapy, adjunctive medications can be added. The only non-statin lipid-lowering agent that has proven to have additive effects on the prevention of cardiovascular adverse events is ezetimibe, which inhibits intestinal absorption of cholesterol. Ezetimibe is administered in an oral daily dose of 10 mg. Common side effects include diarrhea and cough. - nicotinic acid or niacin is the most effective medication to increase HDL levels; side effect = flushing due to increased prostaglandins which can be prevented by taking NSAIDs beforehand - ASCVD risk score calculates 10-year risk of having a cardiovascular event incorporating age, sex, race, BP, cholesterol level, diabetes, smoking, meds - Primary prevention of CVD with statin therapy (2019 AHA/ACC guidelines) -- Age 0-19 and familial hypercholesterolemia (individuals with very significantly elevated low-density lipoprotein (LDL) cholesterol (LDL-C) or "bad cholesterol" and an increased risk of early onset of coronary artery disease if not sufficiently treated): statin -- Age 20-39, LDL ≥ 160 mg/dL, FH of premature CVD: consider statin -- Age 40-75: LDL ≥ 190: high-intensity statin (for any age); Diabetes: moderate-intensity statin; Intermediate risk (score ≥ 7.5%): moderate-intensity statin may be indicated; consider risk enhancers, coronary artery calcium score; High risk (score ≥ 20%): initiate statin to reduce LDL by ≥ 50% -- Age ≥ 75: risk discussion with patient - AACE guidelines for goal LDL level: Extreme ASCVD risk: LDL < 55 mg/dL; Very high risk: LDL < 70 mg/dL; Moderate and high risk: LDL < 100 mg/dL; Low risk: LDL < 130 mg/dL; Goal triglyceride level: < 150 mg/dL - Screening guidelines (nonfasting first, if abnormalities then fasting): -- every 9-11 yo and 17-21 yo -- low CV risk: 35 for men and 45 for women -- high CV risk (HTN, smoking hx, family hx): 25-30 for men and 30-35 for women

Chronic venous insufficiency

a disease of variable severity caused by venous hypertension and incompetent valves leading to dilated veins, discoloration, swelling, pain, skin changes, and ulceration. Chronic venous insufficiency affects 2.5 million people in the United States. Chronic venous insufficiency involves both superficial and deep venous systems. In order for venous return to function appropriately, a series of bicuspid valves within the veins and muscle pumps in the foot, calf, and thigh must prevent backflow toward the feet. Chronic venous insufficiency results from an interruption of this blood flow within the system. The interruption can be caused by a number of factors, including valvular reflux, thrombotic obstruction of the valves, or a combination of the two. As a result, there is an increase in inflammation that leads to endothelial damage. Over time, this inflammation may result in dilated and tortuous capillaries, increased edema, decreased oxygenation to surrounding tissue, stasis changes of the overlying skin, thromboses, and ulceration. Risk factors for chronic venous insufficiency include prolonged standing, pregnancy, prior deep vein thrombosis, obesity, advancing age, and previous leg injury. Women are three times more likely to develop chronic venous insufficiency than men, most likely due to pregnancy. The most common physical exam findings in patients with chronic venous insufficiency are edema, pain, overlying skin changes, and leg heaviness. Telangiectasias and reticular veins are less severe manifestations of venous disease. Telangiectasias are dilated intradermal veins and reticular veins are subdermal. Both can be present in the absence of more severe findings of chronic venous insufficiency. Varicose veins are dilated, elongated, tortuous, subcutaneous veins 3 mm or greater in diameter. They are a more severe representation of venous disease. The visible signs of chronic venous disorders are categorized depending on the severity of venous signs, which include dilated veins, leg edema, skin changes, and ulceration. Other categorical factors include etiology (congenital, primary, or post-thrombotic), anatomy (superficial, perforator, or deep veins), and pathophysiology (reflux, obstruction, or both). Correct classification will dictate the appropriate therapy. The differential diagnosis for chronic venous insufficiency should include heart failure, nephrotic syndrome, endocrine disorders, liver disease, Achilles tendon tear, deep vein thrombosis, or medication side effects. If chronic venous insufficiency is suspected, duplex ultrasound scanning is the diagnostic modality of choice. Duplex ultrasound will show venous anatomy, venous flow pattern, and whether reflux is present. Duplex ultrasound cannot indicate disease severity. Initial conservative measures are recommended for most patients with chronic venous disease. Leg elevation, exercise, and compression therapy will improve oxygen transport to the skin and subcutaneous tissues, decrease edema, reduce inflammation, and compress dilated veins. Overlying stasis skin changes may respond to topical steroids. Conservative measures may improve symptoms, but they are not curative. Historically, high ligation and stripping of the saphenous vein was the preferred surgical treatment. Currently, this technique has been replaced by percutaneous endovenous thermal ablation. This procedure is performed on an ambulatory basis with local anesthesia. Patients are typically completely ambulatory following treatment, and the recovery time is short. Two types of thermal ablation procedures exist: endovenous laser ablation and radiofrequency ablation. Significant reflux, defined as reflux greater than 1000 ms in deep veins (such as the great saphenous vein described in the above vignette), documented on Doppler ultrasound examination is an indication for endovenous laser ablation. Chronic venous insufficiency is associated with significant morbidity and mortality and may indicate the presence of other serious vascular conditions. One serious complication of chronic venous insufficiency is venous ulcers (bc skin being stretched bc of swelling). Due to the low rate of healing and high rate of recurrence, venous ulcers can be debilitating and cause a significant decrease in quality of life.

sinus sick syndrome

a dysrhythmia characterized by periods of sinus arrest, persistent bradycardia, or chronotropic incompetence, indicating that the heart is not reacting appropriately to increased metabolic demands. Sinoatrial node disease and previous corrective cardiac surgery are risk factors for developing sick sinus syndrome. Patients may present with a variety of complaints related to sick sinus syndrome, including syncope, palpitations, fatigue, lightheadedness, dyspnea, and exercise intolerance. Diagnosis is confirmed by electrocardiogram, which shows bradycardia alternating with tachycardia as well as extended periods of sinus inactivity. If the initial ECG is not diagnostic, ambulatory ECG monitoring is required for diagnosis. A permanent pacemaker is indicated for symptomatic patients. If patients are hemodynamically unstable, dopamine, epinephrine, or atropine should be administered and transcutaneous pacing may be required. Asymptomatic patients typically do not require intervention but should be routinely evaluated for deterioration.

Multifocal Atrial Tachycardia

a dysrhythmia commonly seen in patients with COPD or other hypoxic states (e.g., congestive heart failure, pneumonia, lung cancer, pulmonary embolism). The patient's binge drinking episode increases the chance that he was not properly managing his COPD over the weekend. An ECG will show an irregular rhythm, tachycardia usually between 100-140 beats/minute, and three or more P wave morphologies (same as wandering atrial pacemaker but more than 100 BPM). MAT is occasionally mistaken for atrial fibrillation, as it is an irregularly irregular rhythm, but a careful analysis of the P wave morphology will aid in a correct diagnosis. First-line treatment for MAT is aimed at addressing underlying conditions, such as COPD management and correction of hypoxia. For certain patients, verapamil 240-480 mg orally daily in divided doses is effective in treating MAT.

aortic dissection

a medical emergency in which a tear in the aortic intima occurs and blood collects in the aortic media, creating a false lumen. The most common underlying pathology implicated in aortic dissection is hypertension, which results in increased stress on the aortic wall. Other conditions that increase the risk for dissection include smoking, cocaine use, pregnancy, pheochromocytoma, prior cardiac surgery, Takayasu arteritis, giant cell arteritis, and Behcet disease. Acute trauma in motor vehicle collisions, falls, or weightlifting can also cause dissection. Genetic disorders that weaken the lining of the aorta are associated with an increased risk of dissection and include Marfan syndrome, Loeys-Deitz syndrome, Turner syndrome, and familial thoracic aortic aneurysm and dissection syndrome. The classic presentation of aortic dissection is a sudden onset of severe and tearing pain radiating to the back. Signs of dissection may include diminished or unequal pulses, hemiplegia, or paralysis of the lower extremities. Untreated dissection may lead to valvular regurgitation, heart failure, cardiac tamponade, and ischemia of the brain, intestines, kidneys, or extremities. A CT scan is the diagnostic test of choice and is indicated in any hypertensive patient with chest pain and nonspecific ECG findings. The Stanford and DeBakey systems are the most commonly used classification systems for aortic dissection. Stanford A dissections (equivalent to DeBakey I and II) involve the ascending aorta, and Stanford B (equivalent to DeBakey III) dissections involve the descending aorta. DeBakey I dissections originate in the ascending aorta and propagate to the aortic arch. DeBakey II dissections are confined to the aortic arch. DeBakey III dissections originate in the descending aorta and may or may not extend distally. Immediate management of aortic dissection includes aggressive reduction of blood pressure with beta-blockers to a goal of 100-120 mm Hg and a surgical consult. Morphine is often given for pain control. All Stanford A dissections require emergency surgical repair. Stanford B dissections should be repaired if there is evidence of a major vascular occlusion or aortic rupture. The prognosis for aortic dissections is poor, with the mortality rate for untreated Stanford A dissection increasing by 1% every hour for the first 72 hours. Annual CT scans are recommended to monitor for aneurysmal enlargement near the site of dissection. - can have different BP between the arms (by about 20 mmHg)

Prinzmetal (or variant) angina

a rare form of angina that occurs due to coronary vasospasm and often occurs late at night or early in the morning. This condition most frequently occurs in women under 50 years of age. Chest pain symptoms may be identical to the chest pain experienced during a myocardial infarction. Risk factors for Prinzmetal angina include hypertension, smoking, cocaine use, diabetes, obesity, emotional stress, and certain medications (e.g., beta-blockers and triptan medications). Vasospasm at rest with preservation of exercise capacity is associated with Prinzmetal angina. The right main coronary artery (associated with the inferior ECG leads) is most commonly affected in Prinzmetal angina. Transient ST elevations during angina with return to baseline upon resolution of symptoms is characteristic. Cardiac biomarkers will be normal. Patients with angina and ST elevation should undergo coronary angiography to identify the presence of stenotic lesions. Percutaneous coronary intervention or aggressive pharmacologic therapy is indicated in the presence of coronary stenosis. In the absence of coronary stenosis, lifestyle modifications (e.g., avoidance of smoking and cocaine), calcium channel blockers (first line med), and nitrates are indicated. A 2016 trial concluded that chronic renin-angiotensin system inhibitor therapy (e.g., angiotensin-converting enzyme inhibitors and angiotensin receptor blockers) was associated with improved cardiovascular outcomes in patients with coronary vasospasm. On the other hand, beta-blockers (e.g., propranolol, nadolol, sotalol, timolol; especially non selective BBs bc of alpha blockage) exacerbate coronary vasospasm and should be avoided in patients with Prinzmetal angina in the absence of coronary stenosis. Calcium channel blockers and nitrates (2nd choice) for cocaine induced infarction to stop vasospasm of the coronary arteries

NSTEMI

a subset of acute coronary syndromes that involves elevation in cardiac biomarkers (such as troponin) but not ST segment elevation on ECG. NSTEMI and unstable angina share similar ECG features (lack of elevation in the ST segment) but can be differentiated by the elevation in troponin, which is seen in NSTEMI and not unstable angina. The difference between NSTEMI and STEMI is the elevation in ST segment of an ECG, which is only seen in STEMI. Patients typically present with substernal chest pain or discomfort that may radiate to the jaw, left shoulder, or arm. Dyspnea, nausea, diaphoresis, or syncope may accompany chest pain but can also be the only presenting symptom. Atypical manifestations are seen in older patients, women, and diabetic patients and may include nausea, vomiting, back pain, and no chest pain. Initially, depending on the time of symptom onset to presentation, laboratory studies may be normal. As time passes, CK-MB or troponin levels become elevated, indicating myocyte necrosis and diagnosis of myocardial infarction. The universal definition of myocardial infarction is a rise of cardiac biomarker (> 99th percentile of the upper limit of normal) and one of the following: symptoms of ischemia, ECG changes of new ischemia, new Q waves, or imaging evidence of new loss of viable myocardium or new wall abnormality. ECG shows ST depression without elevation. Patients with NSTEMI should be hospitalized, maintained on bed rest or at a very limited activity for the first 24 hours, monitored, and given supplemental oxygen. Benzodiazepines may be administered if anxiety is present. As outlined in the ACC/AHA management guidelines, patients diagnosed with NSTEMI with high-risk features should undergo an early invasive strategy with catheterization and revascularization. For patients without high-risk features, either invasive or noninvasive approaches can be used. The noninvasive approach involves the administration of antiplatelet and anticoagulant agents upon presentation with NSTEMI. For antiplatelet therapy, aspirin (162 to 325 mg) should be initiated immediately and continued for one month thereafter. P2Y12 inhibitors (clopidogrel, prasugrel, or ticagrelor) should be added to aspirin therapy. Clopidogrel, when added to aspirin, reduces the composite endpoint of cardiovascular death, myocardial infarction, and stroke in patients with NSTEMI. Glycoprotein IIB or IIIA inhibitors (tirofiban, eptifibatide) can be added in high-risk patients (positive biomarkers or presence of fluctuating ST segment depression), especially when undergoing percutaneous coronary intervention. For anticoagulant therapy, enoxaparin is more effective than unfractionated heparin in preventing recurrent ischemic events. Fondaparinux has similar effectiveness as enoxaparin but has a 50% reduction in major bleeding, which translates to a significant reduction in mortality, death, and myocardial infarction in 30 days. Direct thrombin inhibitors (bivalirudin) are an alternative to heparin plus a glycoprotein IIB or IIIA antagonist in patients undergoing early coronary intervention. High-dose statins (atorvastatin) are recommended in all patients with NSTEMI as they improve outcomes and delay death or major cardiovascular events by up to three months.

Acute Rheumatic Fever

a systemic immune response that may occur 1 to 5 weeks following group A Streptococcus pharyngeal infection. Patients between 5 and 15 years old are most commonly affected, and symptoms of acute rheumatic fever typically occur 2 to 3 weeks after the initial infection. The underlying pathophysiology is believed to be due to antibody cross-reactivity and most commonly affects the heart, joints, skin, and central nervous system. The Jones criteria is a diagnostic tool for rheumatic fever. In patients with a recent streptococcal infection, an initial diagnosis of acute rheumatic fever can be made in the presence of two major criteria or one major and two minor criteria. Recurrent episodes of acute rheumatic fever with group A Streptococcus infection can be diagnosed with two major criteria, one major and two minor criteria, or three minor criteria. The patient in the vignette above had a positive rapid strep test 2 weeks ago. Chorea (major criteria) with a 102°F fever (minor criteria) and a reversible prolonged PR interval (minor criteria) would be sufficient to make the initial diagnosis of acute rheumatic fever. Other major criteria include carditis, erythema marginatum (red circular rash with raised, darker edges), subcutaneous nodules, and polyarthritis. (Carly Caught Strep Easter Afternoon = Carditis, Chorea, Subcutaneous nodules, Erythema marginatum, Arthritis). Polyarthralgias, elevated erythrocyte sedimentation rate (ESR), and elevated C-reactive protein (CRP) are minor criteria. Rheumatic heart disease is a concerning complication of acute rheumatic fever. The mitral valve is most commonly affected, though the aortic or tricuspid valve may also be affected along with the mitral valve. The typical lesion seen on histology is a perivascular granuloma with vasculitis. Initial treatment includes strict bed rest until the fever, ESR, and heart rate have returned to normal and the patient is stable. Salicylates may be used for fever, joint pain, and swelling but have no effect on the disease course. Benzathine penicillin 1.2 million units IM once may be used to treat a current streptococcal infection and may be given once every 4 weeks for prophylactic prevention of recurrent acute rheumatic fever episodes. Corticosteroids may be used if joint pain persists after salicylate administration. Prognosis is worse with untreated streptococcal infection and recurrent acute rheumatic fever, both of which are more prevalent in resource-limited countries. An estimated 250,000 young people die from acute rheumatic fever worldwide each year.

atrial flutter

a tachydysrhythmia caused by a single excitable electrical focus in the left or right atrium. Heart failure, obstructive sleep apnea, thyrotoxicosis, and COPD are risk factors for developing atrial flutter. Patients may present with new-onset palpitations, lightheadedness, fatigue, and shortness of breath. ECG will show characteristic sawtooth wave patterns (best seen in leads II, III, and aVF) and a heart rate of 240-340 beats per minute. The treatment algorithm for atrial flutter is the same as it is for atrial fibrillation. In a hemodynamically stable patient, rate control and anticoagulation are the initial treatments of choice, followed by chemical or electrical cardioversion. Rate control is typically achieved with a nondihydropyridine calcium channel blocker such as diltiazem or a beta-blocker such as metoprolol. The CHA2DS2-VASc tool should be employed to stratify risk before initiating anticoagulation. In a hemodynamically unstable patient, immediate electrical cardioversion is the necessary treatment.

constrictive pericarditis

a thickened, fibrotic pericardium that restricts ventricular diastolic filling. This presentation may be the result of chronic inflammation of the pericardium, connective tissue disorders, uremia, cardiac surgery, or radiation therapy. Patients with constrictive pericarditis present with dyspnea, fatigue, and signs of right-sided heart failure, such as peripheral edema. Physical exam will reveal elevated regular venous distention, hepatojugular reflux, and a pericardial knock. The pericardial knock is heard when ventricular filling suddenly ceases due to the thickened and noncompliant pericardium. Atrial fibrillation is a common complication of constrictive pericarditis that may also be noted on physical exam. It can also lead to cardiac tamponade (Beck's Triad) An echocardiogram may reveal a thickened pericardium, abnormal septal motion, variation of ventricular filling with respiration, and dilated inferior vena cava and hepatic veins. If the echocardiogram is nondiagnostic, a right-sided heart catheterization may be done. Treatment of hemodynamically stable patients is similar to pericarditis treatment and includes nonsteroidal anti-inflammatory agent and colchicine can be added. Diuretics are also commonly utilized in the management of constrictive pericarditis. Treatment of hemodynamically unstable patients or patients with persistent symptoms involves a pericardiectomy. This procedure has high morbidity and mortality associated with it, so the patient should be medically optimized as best as possible prior to the procedure. - diffuse ST elevation and PR depression, but no depressions in reciprocal leads (like in a STEMI)

tricuspid regurgitation

a valvular disorder that occurs when there is retrograde blood flow from the right ventricle to the right atrium during systole. The underlying pathophysiology is a right-sided pressure overload leading to right-sided heart failure. Common causes of tricuspid regurgitation include congenital abnormalities of the tricuspid valve, structural abnormalities resulting from infection, and chronic pulmonary hypertension. Pacemaker lead placement is an increasingly common iatrogenic cause of tricuspid regurgitation. As tricuspid regurgitation persists, right-sided cardiomegaly, systemic venous congestion, and eventually right-sided heart failure ensue. Signs of severe tricuspid regurgitation are associated with systemic venous congestion and include distended, pulsating neck veins, a pulsatile enlarged liver, and anasarca. On cardiac auscultation, tricuspid regurgitation is a pansystolic murmur that becomes louder with inspiration and reduced with expiration or Valsalva maneuver. It is best heard at the left lower sternal border and radiates to the right lower sternal border. Chest radiography may show an enlarged right heart border. ECG findings include right-axis deviation, P wave changes indicating right atrial enlargement, and R and S wave changes indicating right ventricular hypertrophy. Definitive diagnostic methods for tricuspid regurgitation include echocardiography and cardiac catheterization. Valvular regurgitations are classified as mild, moderate, or severe based on a variety of measurements obtained from diagnostic measures. Since most cases of tricuspid regurgitation are secondary, treatment of the underlying cause should be considered first. Patients with mild or moderate tricuspid regurgitation may be managed with oral diuretics (e.g., furosemide). Moderate tricuspid regurgitation warrants a cardiology consult. Severe tricuspid regurgitation may require IV diuretics such as torsemide. Spironolactone may be used if ascites is present along with severe tricuspid regurgitation. Severe cases require regular monitoring by a cardiologist. Valvular repair may be indicated in patients with tricuspid valve endocarditis. Patients with refractory symptoms due to inherent defects may need a tricuspid valve replacement.

unstable angina

aka acute coronary syndrome; typically caused by unstable atherosclerotic plaque or a thrombus and is associated with progressively worsening angina. Patients with unstable angina may experience symptoms at rest, new onset of angina symptoms, angina brought on with less exertion than before, and an increase in frequency and duration of symptoms. Chest pain lasting for more than 10 minutes is a typical characteristic of unstable angina. Unstable angina is less responsive to sublingual nitrogen. Unstable angina is a clinical emergency and may result in cardiac dysrhythmias, cardiac arrest, or death. The American Heart Association views unstable angina and non-ST segment elevation myocardial infarction (NSTEMI) as a single entity. Patients experiencing acute chest pain should take sublingual nitroglycerin, chew 325 mg of aspirin, and go to the nearest emergency department for evaluation. A 12-lead ECG is essential in determining the treatment path. Positive cardiac biomarkers (e.g., troponin, CK-MB) with serial ECGs that do not show ST elevations of ≥ 1 mm in two contiguous leads are indicative of NSTEMI, unstable angina will not have a change in cardiac biomarkers. Risk stratification using tools such as the thrombolysis in myocardial infarction (TIMI) score aid in determining treatment. Conservative measures for unstable angina include dual antiplatelet therapy, careful monitoring with serial ECGs, echocardiography, and stress testing. Long-term pharmacologic therapy includes aspirin, nitrates, beta-blockers, statins, calcium channel blockers, angiotensin-converting enzyme (ACE) inhibitors, and ranolazine. Invasive measures for higher-risk patients include cardiac catheterization, angioplasty, and cardiac stenting. High-risk indicators that favor early invasive treatment strategies include hemodynamic instability, elevated troponin 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%

Dressler syndrome

aka postmyocardial infarction syndrome; a pericarditis usually seen one to two weeks after an acute myocardial infarction or cardiac procedure. Patients must be evaluated carefully to distinguish Dressler syndrome from acute myocardial infarction. Dressler syndrome is most likely due to an autoimmune inflammatory response following transmural myocardial necrosis and may be recurrent even when treated. Typical signs and symptoms associated with Dressler syndrome include pleuritic chest pain relieved when leaning forward, a pericardial friction rub, and tachycardia. Fever and leukocytosis are associated with the inflammatory response seen in Dressler syndrome. A pericardial or pleural effusion is more common with postoperative patients and may lead to cardiac tamponade. Diffuse concave ST segment elevation in all leads except aVR, PR segment depression in precordial leads, and ST segment depression and PR segment elevation in aVR are initially seen on ECG in Dressler syndrome. These initial ECG changes are followed by a return to baseline and T wave inversion. Electrical alternans and a low voltage QRS may be seen if a large effusion is present. An echocardiogram should be ordered if an effusion is suspected. Laboratory values commonly seen in Dressler syndrome include an elevated WBC, CRP, and ESR. First-line treatment for Dressler syndrome includes aspirin and colchicine (don't use other NSAIDs as they can thin infarction zone of MI and interfere with scar formation). Steroids may be used in refractory patients but are not first line in Dressler syndrome, as they may impair myocardial healing.

orthostatic hypotension

aka postural hypotension; a type of low blood pressure that occurs upon standing or 15-90 minutes after eating (termed postprandial hypotension). Many disorders can cause orthostatic hypotension, including acute or chronic volume depletion and certain pharmacotherapeutics, particularly antihypertensives. The pathophysiology of orthostatic hypotension involves inappropriately functioning compensatory mechanisms when changing postural stances. In patients without orthostatic hypotension, upon standing, 500-1,000 mL of blood begins to pool in the lower extremities. This pooling initiates a sequence of events. First, a rapid decrease in venous return to the heart results in decreased cardiac output and blood pressure. This fall in blood pressure initiates a compensatory baroreceptor reflex that raises the peripheral vascular resistance, venous return, and cardiac output, which results in a limit in the fall of blood pressure. In patients without orthostatic hypotension, upon standing, there is a small fall in systolic blood pressure of 5-10 mm Hg, a slight increase in diastolic blood pressure of 5-10 mm Hg, and an increase in pulse rate of 10-25 bpm. In patients with orthostatic hypotension, one or more of these compensatory mechanisms fail, resulting in a more dramatic change in heart rate and blood pressure upon standing. The prevalence of orthostatic hypotension varies from 5-20% and increases with age. Postprandial hypotension is also common in elderly patients. Orthostatic hypotension may also be found in younger patients, however, it is less common. Risk factors for orthostatic hypotension include advancing age, certain antihypertensive medications, vasodilators (calcium channel blockers), antidepressants, opiates, and alcohol use. In younger patient populations, orthostatic hypotension is often the result of volume depletion due to diuretics, hemorrhage, or vomiting. Patients with orthostatic hypotension often do not have symptoms at rest and only experience symptoms upon standing. These symptoms result from cerebral hypoperfusion and include generalized weakness, dizziness or lightheadedness, visual blurring or darkening of the visual fields, and syncope. Symptoms can range in severity from mild to incapacitating, with some patients completely unable to stand without experiencing presyncope or syncope. Over 50% of patients presenting with orthostatic hypotension present with systolic hypertension while seated. Orthostatic hypotension may be accurately diagnosed by measuring changes in blood pressure with changes in posture. Orthostatic hypotension is diagnosed when, within two to five minutes of quiet standing after a five-minute period of supine rest, at least a 20 mm Hg fall in systolic pressure or at least a 10 mm Hg fall in diastolic pressure is witnessed. Both of these falls in blood pressure may occur in some patients. Additionally, if the patient does not exhibit an expected increase in heart rate upon standing, orthostatic hypotension may be suspected. However, the presence of a heart rate increase does not exclude autonomic failure (including autoimmune autonomic neuropathy and multiple system atrophy). An increase in heart rate of more than 30 bpm suggests a different condition called postural tachycardia syndrome, which typically does not include orthostatic hypotension. A tilt-table test may also be performed but is not as readily available as a simple measuring of blood pressure while sitting and standing. Additional tests to consider include laboratory testing (hematocrit, electrolytes, blood urea nitrogen, creatinine, glucose) and a 12-lead electrocardiogram to evaluate for underlying anemia, dehydration, or heart disease. Treatment for orthostatic hypotension should be tailored to the patient's symptomatology and should focus on improving daily life more than strict adherence to specific blood pressures. The first step in management is identifying and discontinuing any causative medications. Pharmacotherapeutics that can cause or exacerbate orthostatic hypotension include terazosin, antidepressant drugs, antihypertensive drugs, beta-blockers (specifically propranolol), diuretics (specifically hydrochlorothiazide and furosemide), vasodilators (specifically hydralazine and calcium channel blockers), narcotics, and alcohol. Once the offending drug has been eliminated or changed, treatment should then focus on nonpharmacologic measures such as increasing salt intake, initiating use of compression stockings, introducing physical maneuvers, and exercising. If nonpharmacologic measures are ineffective at appropriately managing orthostatic hypotension, pharmacotherapeutics, such as low-dose fludrocortisone for patients with volume depletion, or a sympathomimetic pressor, such as midodrine, may be considered. In the vignette presented above, the initial step should be to discontinue hydrochlorothiazide. The prognosis for orthostatic hypotension is typically very good, and patients are able to manage this condition without issue.

aortoenteric fistula

an abnormal communication between the aorta and the gastrointestinal tract. Primary aortoenteric fistulas are caused by compression of gastrointestinal structures by an aortic aneurysm. Secondary aortoenteric fistulas result from erosion of an aortic prosthetic graft into an adjacent gastrointestinal structure. As such, abdominal aortic aneurysm and a history of aortic surgery are the most common risk factors for aortoenteric fistula formation. Other causes include reflux esophagitis, peptic ulcer disease, non-aneurysmal aortitis, and penetrating aortic ulcers. The duodenum is the most common site of fistula formation. The classic triad of gastrointestinal bleeding, abdominal pain, and a palpable mass is rarely present and a known history of aortic aneurysm is often lacking. Gastrointestinal bleeding, including hematemesis, hematochezia, and melena, is often the presenting symptom. Although massive hemorrhage is common, many patients will have a small "herald bleed," a seemingly self-limited episode of gastrointestinal bleeding, prior to a larger bleed. Complications include hemorrhage and sepsis from seeding of the blood with gastrointestinal flora. While uncommon, aortoenteric fistula should be on the differential diagnosis for gastrointestinal bleeds, especially in patients with a history of aneurysm or aortic surgery, as the condition is life-threatening. Management of aortoenteric fistulas is surgical repair.

pulsus paradoxus

an exaggerated drop in blood pressure when you breathe in; can see in problems like constrictive pericarditis

pericardial effusion

an increase in fluid in the pericardial sac, which can be due to multiple factors, including pericarditis, infection, malignancy, autoimmune disease, and chronic renal failure. The initial symptoms of a patient with pericardial effusion are nonspecific. As the effusion progresses, the patient may develop symptoms such as dyspnea, orthopnea, chest tightness, and chest pain. On physical exam, this patient would have distant or muffled heart sounds secondary to the accumulation of fluid in the pericardial sac. Diagnosis is made by an echocardiogram, which would visualize the fluid within the pericardial sac. For pericardial effusion, the diastolic function of the heart is not affected. An effusion may show sinus tachycardia or electrical alternans on ECG. If the effusion is large, an ECG would show low voltage QRS complexes. Treatment is dependent on the size and cause of the pericardial effusion. If it is small, observation is the treatment of choice. However, if it is moderate to large in size, treatment involves either a pericardiocentesis or open thoracotomy with a pericardial window

myocarditis

an infection of the heart muscle that leads to myocardial necrosis and dysfunction. The most common etiology is viral, especially enteroviruses, such as the coxsackievirus. Other causes include Ebstein-Barr virus, hepatitis C, toxoplasmosis, Churg-Strauss syndrome, Kawasaki disease, and amphetamine use, among many others. Patients will present after an acute respiratory infection with pleuritic chest pain or nonspecific signs of heart failure, such as peripheral edema, dyspnea, or coughing. Physical exam will reveal tachycardia, tachypnea, and an S3 gallop. Lab work may reveal leukocytosis, an elevated erythrocyte sedimentation rate, and an elevated C-reactive protein. Troponin levels may be elevated as well. ECG may show tachycardia, nonspecific ST changes, or other nonspecific dysrhythmias. A chest X-ray will show cardiomegaly. An echocardiogram will also show cardiomegaly, as well as changes in contractile function. An MRI with gadolinium will reveal various areas of injury within the myocardium. Echocardiogram will show decreased ventricular ejection fraction with hypokinesis and wall motion abnormalities Ultimately, an endomyocardial biopsy is required to confirm the diagnosis. The biopsy will show infiltration of lymphocytes and myocardial necrosis. Treatment is similar to heart failure therapy and includes diuretics such as furosemide for fluid overload, angiotensin-converting enzyme inhibitors to help with remodeling, and beta-blockers if the ejection fraction is less than 40%. Antibiotics should be initiated if appropriate, any causative medications should be stopped, and the underlying cause should be addressed. Prognosis is variable. Acute myocarditis has a high death rate, however, if patients recover, there is minimal residual cardiomyopathy. Clozapine, methyldopa, isoniazid, and phenytoin are drugs that can cause noninfectious myocarditis

dilated cardiomyopathy

broad category of conditions in which the heart muscle enlarges, causing left ventricular systolic dysfunction defined as an ejection fraction of less than 50%. There is no wall hypertrophy. Dilated cardiomyopathy is the third most common cause of heart failure and the most frequent reason for heart transplantation. The onset of dilated cardiomyopathy typically occurs during adulthood and is responsible for roughly 30% of all cases of heart failure in the United States. It occurs more often in men than women, with increased frequency in patients of African American ethnicity. There are three types of cardiomyopathies: dilated, hypertrophic, and restrictive, although these classes continue to evolve and expand with advancing medicine. The etiology of dilated cardiomyopathy is variable, but all etiologies cause deficits in the normal muscular function of the myocardium. This deficit results in varying degrees of physiologic compensation, which include increases in stroke volume, heart rate, and peripheral vascular tone. As a result of heart stress, there are numerous neurohormonal compensatory mechanisms that may worsen dilated cardiomyopathy, including stimulation of the adrenergic nervous system, stimulation of the renin-angiotensin-aldosterone system, the release of arginine vasopressin from the hypothalamus, and elevation of natriuretic peptide levels. Often, the most successful pharmacotherapies for cardiomyopathies are directed at altering these neurohormonal responses. Once the compensatory mechanisms can no longer maintain cardiac output, the disease progresses to chronic heart failure. Risk factors for dilated cardiomyopathy include advancing age, diabetes, obesity, hypertension, alcohol use, substance use, infections, and exposure to different toxins. The etiology of dilated cardiomyopathy is variable and includes inherited disease, infections, and toxins. Toxins are a significant cause, and nearly 30% of cases result from alcohol use. Additional common causes of dilated cardiomyopathy include viral myocarditis, familial cardiomyopathy, cardiomyopathy associated with collagen vascular disease, hypertensive cardiomyopathy, and peripartum cardiomyopathy. The clinical presentation of dilated cardiomyopathy is variable. In instances of dysrhythmias, patients may present with palpitations, dizziness, or syncope. When concomitant with heart failure, patients may present with dyspnea, orthopnea, edema, fatigue, jugular venous distention, or rales. In patients who present with fatigue and dyspnea on exertion, reduced cardiac output in dilated cardiomyopathy should be considered. Additionally, patients presenting with thromboembolic disease and dilated cardiomyopathy may present with stroke or chest pain. The diagnosis of dilated cardiomyopathy can be established in several ways. Echocardiography is helpful for determining left ventricular dilation and systolic dysfunction. This diagnostic tool also rules out congenital heart disease or valvulopathies as potential causes of dilated cardiomyopathy. An electrocardiogram is helpful in determining if there are any underlying dysrhythmias contributing to dilated cardiomyopathy. A chest radiography will identify cardiomegaly and will help in determining the presence of pulmonary vascular congestion. There are many different laboratory tests that can help to rule out other etiologies. Cultures can rule out infectious diseases, CBC can evaluate for beta-thalassemia, and brain natriuretic peptide levels can help identify fluid overload in heart failure. In some cases, dilated cardiomyopathy may reverse with appropriate treatment of the underlying disease, however, most cases of dilated cardiomyopathy ultimately progress to heart failure. Additionally, progressive dilation can lead to mitral and tricuspid regurgitation, which often leads to further dilation and myocardial dysfunction. Once the underlying cause of dilated cardiomyopathy has been determined, directed therapy should be initiated. Lifestyle changes that could benefit patients with dilated hypertrophic cardiomyopathy include sodium restriction, fluid restriction, and regular exercise. Appropriate pharmacotherapy includes angiotensin-converting enzyme (ACE) inhibitors, beta-blockers, aldosterone antagonists, and diuretics. Unless dysrhythmias are present, calcium channel blockers should be avoided. For patients with severe symptoms, a left ventricular assist device may prolong life until cardiac transplantation is possible. - Causes = 6 D's: Don't know (idiopathic), Drinking, Drugs (cocaine), Doxorubicin, Disease (espeically viral like coxsackie virus), Deficiency of vitamin B1

J or Osborn wave

camel-hump at the J point of the EKG; most common cause is hypothermia

cardiac tamponade

caused by the collection of fluid in the pericardium resulting in decreased diastolic filling and a subsequent decline in cardiac output. Common etiologies include penetrating trauma, pericarditis, iatrogenesis (e.g., central line placement, pericardiocentesis, and pacemaker placement) and post-myocardial infarction with free wall rupture. Clinical manifestations common in cardiac tamponade include tachypnea, tachycardia, hypotension, increased jugular venous distension, distant (muffled) heart sounds, narrowed pulse pressure, and pulsus paradoxus. Pulsus paradoxus is defined as a > 10 mm Hg decrease in systolic blood pressure during inhalation. Cardiac tamponade restricts the degree to which the myocardium can expand, thus, the increased diastolic pressure causes the ventricular septum to bow outwards into the left ventricle. This bowing of the ventricular septum leads to a decreased cardiac output of the left ventricle and a subsequent drop in systemic systolic blood pressure during inhalation. ECG findings common in cardiac tamponade include tachycardia, low voltage, and electrical alternans. Echocardiography is the most sensitive and specific exam for cardiac tamponade and will show a pericardial effusion. Pericardiocentesis is the definitive treatment for cardiac tamponade. - Beck's triad = hypotension, muffled heart sounds, JVD; Beck Hates MJ Period (Beck, Hypotenstion, Muffled heart sounds, Jugular vein distension, and period makes me think of Tamponade; quinten Beck is mysterio)

left anterior fascicular block

characterized by left axis deviation; small Q waves with tall R waves in I and aVL; small R with deep S waves in II, III, and aVF; prolonged R wave peak time in aVL > 45 ms; and increased QRS voltage in the limb leads

left posterior fascicular block

characterized by right axis deviation; small R waves with deep S waves in I and aVL; small Q with tall R waves in II, III, and aVF; prolonged R wave peak time in aVF; no evidence of right ventricular hypertrophy; and no evidence of other etiologies for right axis deviation.

acute severe hypertension

defined as a blood pressure greater than 180/110-120 mm Hg; has two different clinical presentations: hypertensive emergency and hypertensive urgency. The most common risk factor for acute severe hypertension is noncompliance with an established antihypertensive regimen. Other possible precipitants of acute severe hypertension include drugs (e.g., NSAIDs, cocaine, corticosteroids), anxiety, stroke, heart attack, preeclampsia or eclampsia, pheochromocytoma crisis, or iatrogenesis (e.g., stopping antihypertensives and IV normal saline infusions). Hypertensive urgency is defined as blood pressure of greater than 180/110-120 mm Hg with no signs of acute target organ damage. Patients with hypertensive urgency may present with symptoms such as headache, atypical chest pain, epistaxis, and dizziness. Because hypertensive urgency likely represents moderate acute or chronic elevated blood pressure, the risk of morbidity and mortality is relatively low in the acute context. Hence, treatment in the ambulatory setting with oral agents, such as captopril, labetalol, clonidine, or prazosin, is recommended for hypertensive urgency. Recommendations indicate that follow-up in one to seven days is reasonable for these patients. Hypertensive emergency is defined as blood pressure greater than 180/110-120 mm Hg with evidence of acute target organ damage. Acute target organ damage includes hemorrhagic or ischemic stroke, acute coronary syndrome, aortic dissection, diffuse microvascular injury (i.e., malignant hypertension), and hypertensive encephalopathy. The presence of anemia, thrombocytopenia, acute kidney injury, or new-onset retinopathy is indicative of acute microvascular disease, which is the case with the patient in the vignette above. All patients who meet clinical criteria for hypertensive emergency should be admitted to the ICU for blood pressure stabilization with IV antihypertensives due to the risk of significant morbidity and mortality associated with this syndrome. The rate in which blood pressure is lowered in patients with hypertensive emergency depends on concomitant end-organ damage. In general, current guidelines recommend lowering blood pressure by no more than 20-25% over one hour, then to 160/100 mm Hg within six hours, and then to target blood pressure in 48 hours in most patients. Another source said 10-20% in first hour, 5-15% over next 23 hours. Judicious treatment of severe hypertension is recommended due to evidence of increased morbidity and mortality associated with rapidly lowering blood pressure. Patients with aortic dissection, pheochromocytoma, intracerebral hemorrhage, and eclampsia or preeclampsia require more aggressive treatment (i.e., reduction to systolic blood pressure to less than 140 mm Hg in the first hour and to less than 120 mm Hg in the case of aortic dissection). If they have ischemic stroke and will treat with tPA, can allow up to 185/110 before treating BP. If not a candidate for reperfusion, cal allow to go up to 220/120 before lowering it allow perfusion tot he brain. Choice of antihypertensive agents also depends on the etiology of acute end-organ damage. Dihydropyridine calcium channel blockers (e.g., nicardipine) and labetalol have been shown to be the most effective at lowering blood pressure in most clinical scenarios, especially with neurologic problems. Other agents, including beta-blockers (esmolol and metoprolol), nitroglycerine, nitroprusside, and hydralazine, are also appropriate in the correct clinical setting and have fast onset. The beta blockers good for cardiovascular issues. After initial stabilization of blood pressure in hypertensive urgency, it is recommended to start chronic oral antihypertensives in an attempt to transition the patient to long-term blood pressure control.

hypertension

defined by two levels: elevated blood pressure with systolic pressure between 120 and 129 mm Hg and diastolic pressure less than 80 mm Hg, and stage I hypertension, which is defined as a systolic BP of 130 to 139 mm Hg or a diastolic BP of 80 to 89 mm Hg. Hypertension is the most common diagnosis in the United States and a major risk factor for stroke, myocardial infarction, vascular disease, and chronic kidney disease. Primary (essential) hypertension is the most common cause of elevated BP. It has no specific identifiable cause, and the pathogenesis is multifactorial, including genetic disposition, increasing age and African American race, environmental factors (excessive salt intake, obesity), alcohol use, metabolic syndrome, imbalance in the renin-angiotensin system, lack of exercise, low potassium intake, and sympathetic nervous system hyperactivity. Secondary hypertension indicates an underlying, potentially reversible cause, with the prevalence and etiologies varying by age. In children, the most common causes of secondary hypertension are renal parenchymal disease and coarctation of the aorta. In adults 65 years and older, renal artery stenosis due to atherosclerosis is the most common cause of secondary hypertension. Renal artery stenosis causes a decrease in blood flow to the juxtaglomerular apparatus, thereby leading to the activation of the renin-angiotensin-aldosterone system, which in turn causes hypertension. Patients with renal artery stenosis often present with sudden onset of hypertension that is refractory to more than three antihypertensive drugs. A physical exam may reveal abdominal bruits (heard best at the left upper quadrant, right upper quadrant, and the epigastrium). Pulmonary edema and atherosclerosis of the aorta and peripheral vessels are usually present. Laboratory studies may demonstrate hypokalemia, decreased renal function, and an abrupt increase in serum creatinine after the use of angiotensin-converting enzyme (ACE) inhibitors. Duplex Doppler ultrasound of the renal arteries can be obtained initially. MRA can be performed in the setting of renal failure. The definitive diagnosis of renal artery stenosis is made by renal arteriogram, although contrast media is nephrotoxic. Other causes of secondary hypertension include Cushing syndrome, pheochromocytoma, hyperthyroidism, primary hyperaldosteronism, chronic steroid therapy, NSAID use, and sleep apnea. Once the diagnosis of hypertension is made, the treatment goal should be to achieve a BP reading of < 140/90 mm Hg (in otherwise healthy individuals) and < 130/80 mm Hg (in those with chronic kidney disease or diabetes). Treatment of hypertension includes lifestyle modification (including a low-fat diet [DASH diet including high in fruits/veggies and fibers and lean proteins and low in red meats, sugars and refined carbs; increase potassium as they are associated with lower BP], regular exercise, weight loss, cessation of smoking, limitation of alcohol [2 per day for men and 1 for women] , low-sodium diet) and pharmacotherapy (diuretics, beta-adrenergic antagonists, angiotensin-converting enzyme inhibitors, angiotensin II receptor blocking agents, calcium channel blockers, aldosterone receptor antagonists, and alpha-adrenergic antagonists). Diuretics treat hypertension by reducing plasma volume and peripheral resistance and are considered first-line therapy for hypertension. Treatment of secondary hypertension targets the underlying cause. For renal artery stenosis, revascularization with percutaneous transluminal renal angioplasty can be performed initially. ACE inhibitors or calcium-channel blockers can be initiated either as monotherapy or in combination. Beta blockers if concomitant heart disease, heart failure. If not getting to goal, adding another med better than just increasing dose. Also look for secondary causes - Tests to get: fasting blood gluocse, urinalysis (include creatine: albumin ratio to see if any proteinuria which can be a sign of early kidney issues), TSH, lipid profile, EKG, electrolytes and serum creatinine, ASCVD score, and fundoscopy to check for retinopathy)

aortic regurgitation

inability of the aortic valve leaflets to remain closed during diastole, resulting in a portion of the left ventricular volume leaking back from the aorta into the left ventricle. Symptoms of aortic regurgitation are similar to aortic stenosis and include exertional dyspnea, angina, and other symptoms of heart failure. Physical exam may reveal a Corrigan pulse (a "water hammer" or "collapsing" pulse characterized by a rapidly rising and falling arterial pulse with a wide pulse pressure palpated at the carotid, radial, or brachial arteries) and de Musset sign (a head bob occurring with each heartbeat). The heart murmur associated with aortic regurgitation, called an Austin Flint murmur, is described as a soft, high-pitched, early diastolic decrescendo murmur heard at the third intercostal space - Quincke is pinky pulsation found in this

right ventricular infarction triad

increase JVP, clear lungs (no left sided failure), and positive Kussmaul sign (paradoxical increase in JVP with inspiration)

right bundle branch block

indicates slowed conduction through the right ventricle. RBBB may be caused by pulmonary embolism, chronic obstructive pulmonary disease, cor pulmonale, cardiomyopathy, or pulmonary hypertension, or it may be idiopathic. ECG findings associated with RBBB include a wide QRS complex (> 120 ms), QRS complex with sR′ or rsR′ in V1 and V2, and S waves that are slurred in V6 and I. There is no specific treatment for RBBB other than treating the underlying condition. Prognosis is good if the RBBB is not associated with acute coronary syndrome or a pulmonary embolism.

J point

the junction between the termination of the QRS complex and the beginning of the ST segment

Permanent Atrial Fibrillation

patient and clinician make joint decision to stop further attempts to restore and/or maintain normal sinus rhythm

stable angina pectoris

precordial chest pain typically precipitated by stress or exertion and rapidly relieved by rest or nitrates. It is often due to atherosclerotic heart disease but can also be caused by coronary vasospasm, congenital anomalies, emboli, arteritis, or dissection. Additionally, angina can occur in the absence of coronary artery obstruction as a result of severe myocardial cardiomyopathy, severe aortic stenosis or regurgitation, hyperthyroidism, or severe anemia. Patients present with chest discomfort that most commonly occurs during activity and is relieved by rest or nitrate. Angina is often described as a sensation of tightness, squeezing, burning, pressing, choking, aching, or bursting or an ill-characterized discomfort. Pain radiates most often to the left shoulder and upper arm but can also radiate to the right shoulder, lower jaw, neck, or even back. The duration of the pain is typically less than 30 minutes. Pain lasting more than 30 minutes is suggestive of an acute coronary syndrome (unstable angina or myocardial infarction) or an alternative diagnosis. Hypertension or hypotension may be noted on physical exam, with the latter reflecting the presence of severe ischemia or inferior ischemia (especially with bradycardia). A systolic murmur of mitral regurgitation and a gallop rhythm may be present during pain only. Laboratory studies such as CBC, CMP, troponin, and CK-MB are often obtained but are not helpful in diagnosing stable angina. Resting ECG is often normal in patients with stable angina but can also reveal old myocardial infarction, nonspecific ST-T changes, and changes of left ventricular hypertrophy. Exercise ECG is the most commonly used noninvasive procedure for evaluating inducible ischemia in patients with stable angina. Exercise ECG can be combined with imaging (nuclear or echocardiography). The usual ECG criterion for a positive test is 1 mm horizontal or downsloping ST segment depression measured 80 msec after the J point. Exercise ECG remains the preferred initial procedure because it is cost-effective, convenient, and has longstanding prognostic data. Selective coronary arteriography is the definitive procedure for coronary artery disease, but due to the invasive nature and cost, it is only indicated in patients with a high pretest probability of coronary artery disease. Sublingual nitroglycerin is the treatment of choice for acute stable angina. The use of nitroglycerin can be repeated in three minutes if angina does not improve. Angina that is not relieved or improving after five minutes of nitroglycerin is likely evolving to unstable angina. Pain that is not responding to three nitroglycerin tablets or lasts more than 20 minutes may represent an evolving infarction.

heart failure

results from the heart's inability to supply sufficient blood to meet the body's need. Heart failure affects more than 23 million people worldwide, and in the United States, more than 550,000 new patients are diagnosed each year. Heart failure is often precipitated by cardiac injury or dysfunction. Such events include ischemic heart disease, chronic hypertension, and valvular disorders. Additional causes of heart failure include diabetes, anemia, alcohol use, and congenital heart defects. The American College of Cardiology/American Heart Association (ACC/AHA) describes the severity of heart failure in four stages. Stage A represents a high risk of heart failure but no structural heart disease or symptoms of heart failure. Stage B represents structural heart disease but no symptoms of heart failure. Stage C represents structural heart disease and symptoms of heart failure. Stage D represents refractory heart failure requiring specialized interventions. These stages emphasize the disease development and progression. The pathophysiology of heart failure is multifactorial and involves compensatory mechanisms. As a result of cardiac injury or dysfunction, cardiac output decreases and triggers compensatory mechanisms, beginning with stimulation of baroreceptors and the sympathetic nervous system. As renal perfusion declines (due to decreased cardiac output), the renin-angiotensin-aldosterone system is activated in order to increase cardiac output and restore tissue perfusion. Therapies that block activation of these responses can improve myocardial function and slow down disease progression. Risk factors for heart failure include hypertension, coronary artery disease, myocardial infarction, diabetes, obstructive sleep apnea, congenital heart defects, valvular heart disease, cardiac dysrhythmias, obesity, and alcohol and tobacco use. The primary symptoms of heart failure are variable and include dyspnea, orthopnea, and fatigue. Presenting signs and symptoms of fluid retention include tachycardia, pleural effusions, basilar crackles, an S3 gallop, jugular venous distension, ascites, hepatomegaly, and pitting edema. Diagnosing heart failure is multifactorial. The initial diagnosis of heart failure includes measuring a blood cell count, urinalysis, serum electrolytes, serum glucose, liver function tests, lipid panel, blood urea nitrogen, and serum creatinine and evaluating thyroid-stimulating hormone levels. A 12-lead electrocardiogram is often recommended, although two-dimensional echocardiography is the diagnostic test of choice. Radiologic imaging with anterior-posterior chest X-ray may be helpful in identifying certain aspects of heart failure, including cardiomegaly and pulmonary congestion. In addition to appropriately diagnosing heart failure, identifying and managing comorbidities can significantly improve outcomes for patients with heart failure. There are two biomarkers specific to heart failure. Brain natriuretic peptide (BNP) and N-terminal pro-B-type natriuretic peptide (NT-proBNP) are helpful in not only diagnosing heart failure but also differentiating pulmonary from cardiac causes in patients with shortness of breath. The prognosis for heart failure is highly variable and worsens with disease progression. Mortality is greater than 50% for patients with ACC/AHA stage D heart failure. Heart failure associated with acute myocardial infarction has an inpatient mortality of 20-40% and approaches 80% in patients who are also hypotensive. The treatment for patients with heart failure first involves nonpharmacologic management and then varies based on disease severity. Nonpharmacologic management includes patient education, sodium intake restriction, exercise training, and cardiac rehabilitation. Sodium intake restriction helps to reduce congestive symptoms and minimize the development of hypertension, left ventricular hypertrophy, and cardiovascular disease. The general population consumes more than 4 g of sodium per day, which is well over the recommended daily intake for patients diagnosed with any stage of heart failure. The current maximum sodium intake is 2.0 g per day for most patients with stage C or D heart failure and less than 3 g per day for patients with stage A or B heart failure. If nonpharmacologic measures are not sufficient, medical therapy may be initiated. Heart failure pharmacotherapy consists of angiotensin-converting enzyme (ACE) inhibitors, or angiotensin II receptor blockers (ARBs) for patients who cannot tolerate ACE inhibitors, and bisoprolol, carvedilol, or metoprolol succinate as the recommended beta-blocker. Loop diuretics, aldosterone receptor antagonists, anticoagulants, and digoxin may also be considered.

DVT

results when a clot forms in large veins, most commonly the legs. Virchow triad describes the three biggest risk factors for a DVT: venous stasis, endothelial damage, and hypercoagulability. Other risk factors include increased age, malignancy, pregnancy, oral contraceptives, and stroke. Patients will present with complaints of unilateral extremity swelling and tenderness, and physical exam will reveal swelling, tenderness, warmth, and erythema. A D-dimer test is highly sensitive but not specific. A normal D-dimer (< 0.50 mg/L) rules out a DVT in low- to moderate-risk patients. A venous duplex ultrasound is the first-line imaging choice and shows decreased blood flow or a noncompressible vein. Computed tomography venography is the definitive imaging modality if the ultrasound imaging is indeterminate. Anticoagulation therapy is the mainstay of treatment for DVT. Patients traditionally were started on heparin and then transitioned to warfarin, however, there is now the option to begin patients on novel anticoagulants (e.g., rivaroxaban or apixaban). Patients should be continued on anticoagulation therapy for at least three months or longer, depending on what triggered the DVT. Pregnant patients should be anticoagulated with low-molecular-weight heparin. Inferior vena cava filters are an option for patients who have absolute contraindications to anticoagulation or have failed anticoagulation therapy. Prognosis is good for patients with DVT. Complications include chronic venous insufficiency, and if untreated, approximately 50% of DVTs become pulmonary embolisms.

stable angina

reversible myocardial ischemia and is commonly associated with atherosclerotic plaque that obstructs the flow of the coronary vasculature. Patients with stable angina often report chest pain with crushing or pressure-like quality. This pain may be accompanied by radiation to the upper extremity or jaw. In stable angina, the chest pain occurs episodically and the is relieved by immediate-release nitrates or rest. A cardiac stress test (either exercise or pharmacologic) is used in the initial evaluation for patients with suspected coronary artery disease (CAD) causing stable angina. If stress testing indicates coronary pathology, an angiogram is needed to confirm the diagnosis of CAD and to assess the degree of the disease. All individuals with CAD should be treated with a lifestyle modification (such as improved diet, weight loss, exercise, and smoking cessation), statin, antiplatelet therapy (e.g., low-dose aspirin or clopidogrel), and antianginal medications. Individuals with stable angina should be treated until symptoms are controlled with antianginal medications such as beta-blockers, calcium channel blockers, nitrates, and ranolazine. As-needed sublingual nitroglycerin is usually initiated first for stable angina for immediate symptomatic relief. Beta-blockers (atenolol and metoprolol) are first-line long-term antianginal agents, especially in patients who have a personal history of myocardial infarction. This is because beta-blockers are associated with decreased recurrence of myocardial infarction, and therefore, they have mortality benefits in patients with previous myocardial infarction. If beta-blockers cannot be tolerated or if they do not sufficiently treat the patient's symptoms, then calcium channel blockers (such as amlodipine), long-acting nitrates (such as isosorbide mononitrate), or ranolazine can be added to the treatment regimen or used as monotherapy. Importantly, aspirin and beta-blockers are the only known medications that lower mortality in patients with stable angina. In this patient, beta-blockers cannot be used because they can worsen underlying COPD, and ranolazine is contraindicated due to hepatic impairment. Therefore, the calcium channel blocker (amlodipine) is the best first-line therapy in this patient. For patients with multiple affected coronary arteries, who are severely symptomatic, or who have a high degree of coronary obstruction, invasive procedures such as coronary artery bypass grafting or coronary stent placement may be indicated.

cardiac arrest

sudden loss of cardiac output and is most commonly caused by an acute dysrhythmia. The two most common dysrhythmias associated with cardiac arrest are pulseless ventricular tachycardia (pVT) and ventricular fibrillation (VFib), both of which are caused by an abnormal electrical focus or foci in the ventricular myocardium. The most common etiology of ventricular dysrhythmia that results in cardiac arrest is acute coronary syndrome. Pulseless electrical activity (PEA) and asystole are much less common, but they are associated with a worse prognosis. PEA and asystole cause complete systemic hemostasis, and so the prompt initiation of cardiopulmonary resuscitation (CPR) is paramount in their management. It is also important to treat the underlying cause of PEA, which often includes cardiac tamponade, tension pneumothorax, massive pulmonary embolism, acidosis, hypovolemia, hypokalemia, or hypoxia. When managing care for a patient with cardiac arrest, the American Heart Association's algorithmic guidelines aid in a rapid and organized response. Any individual who is unresponsive and has no palpable carotid pulse (checked for no more than 10 seconds) should receive CPR, be started on oxygen, and be attached to a defibrillator. For patients with pVT or VFib (as is the case with this patient), early defibrillation should be performed followed by continued CPR for two minutes. If return of spontaneous circulation (ROSC) is not achieved after the first cycle of CPR and defibrillation, epinephrine 1 mg intravenous is indicated and can be administered every three to five minutes or until ROSC is achieved. If ROSC is still not achieved after the third shock, administration of amiodarone can be considered. PEA and asystole are known as nonshockable rhythms. Therefore, if at any time, a shockable rhythm converts to a nonshockable rhythm or the patient initially presents with one of these rhythms, no defibrillation is indicated. Continuous cycles of CPR and rhythm revaluation every two minutes with administration of epinephrine every three to five minutes is the appropriate treatment for PEA or asystole. In both shockable and nonshockable rhythms, intubation should be considered.

peripheral artery disease

the atherosclerotic or thromboembolic obstruction of the peripheral arteries. Atherosclerotic plaques can form at various different locations in the peripheral arterial network. However, the most common sites of obstruction occur in the superficial femoral artery, aortoiliac bifurcation, and popliteal artery. Primary risk factors for developing PAD include hyperlipidemia, hypertension, diabetes, and tobacco use. Patients will typically present with exertional pain that improves with rest in the muscles distal to the arterial obstruction. This kind of pain is also known as claudication. Patients may also present with nonhealing ulcers (usually located on the lateral malleolus), muscle atrophy, diminished hair growth in the distal extremities, vascular bruits, thick toenails, and decreased peripheral pulses. Physical exam may also reveal pallor with lower extremity elevation and reperfusion when the extremity is lowered. In patients with suspected PAD, ankle-brachial index (ABI) testing is the initial test of choice. ABI is the ratio of systolic blood pressure in the dorsalis pedis artery to systolic blood pressure in the brachial artery. This measurement is a surrogate for the degree of arterial obstruction. ABI of 0.9-1.3 is normal while ABI of less than 0.9 is indicative of mild to moderate PAD. ABI of less than 0.4 is suggestive of critical limb ischemia. ABI of > 1.3 may represent severe disease since this may indicate arteries that are calcified and noncompressible. All patients with PAD should be treated with a statin agent, an antiplatelet agent, and lifestyle modification encouragement (e.g., smoking cessation, exercise, and appropriate diet). Additional treatment depends on the degree of arterial obstruction. In general, patients with mild to moderate arterial obstruction benefit the most from cilostazol and structured exercise therapy. Cilostazol is a PDE3 inhibitor, antiplatelet, and vasodilator that can be used to improve walking distances in patients with PAD. In patients with severe PAD, arterial bypass using a venous graft is needed.

mitral regurgitation

the most prevalent valvular disorder in the United States. It refers to the abnormal reversal of blood flow from the left ventricle to the left atrium. Mitral regurgitation can lead to increased intracardiac pressure, left ventricular dysfunction, and the inability of the mitral valve leaflets to close appropriately. The prevalence of mitral regurgitation increases with age, and prevalence in adults over 75 years of age approaches 10%. Mitral regurgitation is classified based on the cause. Primary mitral regurgitation is most commonly caused by mitral valve prolapse. Other causes for primary mitral regurgitation include rheumatic heart disease, radiation, chronic annular calcification, and congenital causes. Secondary mitral regurgitation is caused by ischemic heart disease or heart failure. Additional risk factors for mitral regurgitation include lower body mass index, renal dysfunction, previous myocardial infarction, and previous mitral stenosis. Mitral regurgitation has no relation to other cardiovascular disorders such as diabetes or hypercholesterolemia. Most patients with chronic mitral regurgitation present asymptomatically. As the disease develops, patients may develop fatigue, exercise intolerance, and dyspnea on exertion. More severe cases of mitral regurgitation may also be associated with pulmonary hypertension, orthopnea, and peripheral edema. In patients with acute mitral regurgitation, sudden onset of dyspnea as a result of acute mitral regurgitation can be caused by ruptured chordae tendineae, which is considered a medical emergency. As seen in the vignette above, patients may present with hypotension, tachycardia, weakness, dizziness, and altered mental status. The diagnosis of mitral regurgitation is most often made by auscultation of the heart. The murmur associated with mitral regurgitation is most commonly described as a systolic, soft, low-pitched decrescendo with or without thrill radiating to the axilla and best heard at the apex of the heart. Transthoracic echocardiogram is often used to confirm diagnosis and to evaluate the mechanism and severity of mitral regurgitation. Transesophageal echocardiogram may also be used to provide a more detailed picture of mitral regurgitation but is not often used for diagnostic purposes. Treatment of both types of mitral regurgitation is highly patient-specific. Pharmacologic treatment should be considered in patients with an ejection fraction of less than 60%. Therapy includes beta-blockers, angiotensin-converting enzyme (ACE) inhibitors, and angiotensin II receptor blockers (ARBs). Patients who are symptomatic with an ejection fraction of less than 30% should be considered for valve repair or replacement. Patients with mitral regurgitation should be closely monitored due to the strong association of mitral regurgitation with heart failure. Patients with a low to moderate asymptomatic mitral regurgitation have a very good prognosis.

aortic stenosis

thickened, stiff leaflets that result in a narrowing of the aortic valve. This narrowing results in left ventricular outflow obstruction. The most common causes of aortic stenosis vary by geographic location. Worldwide, rheumatic heart disease is the most common cause of aortic valve disease, and in North America, calcification is the most common cause. Aortic stenosis is a common heart condition and is the most common type of valvular heart disease in adults that leads to sudden death. The disease prevalence increases with age, and it is found equally in men and women. Risk factors for aortic stenosis include advancing age, congenital heart disease, acquired infections affecting the heart, hypertension, hypercholesterolemia, and diabetes. The clinical presentation of aortic stenosis varies based on disease severity. In cases of mild or moderate disease, the patient may present without symptoms and aortic stenosis may be an incidental finding. In severe aortic stenosis, the patient presents with syncope, angina, and dyspnea. The most common presenting symptoms include dyspnea on exertion, decreased exercise tolerance, exertional dizziness, and exertional angina. The murmur associated with aortic stenosis is described as a harsh, crescendo-decrescendo systolic ejection murmur heard at the aorta and radiating to the carotid arteries. Patients with aortic stenosis may also present with a delayed carotid upstroke. When aortic stenosis is suspected, an echocardiogram is the diagnostic modality of choice. Other available tests may include electrocardiography, which may reveal left ventricular hypertrophy or left bundle branch block, or chest radiography, which may show aortic valve calcification or left ventricle prominence. Once symptomatic, the average survival is two to three years without appropriate treatment. Medical treatment may not prevent or delay disease progression, therefore, the only definitive treatment is aortic valve replacement. Symptomatic aortic stenosis may be treated with antihypertensives, diuretics, or digoxin, but ultimately, surgical intervention is required. For patients who are not good surgical candidates, balloon valvuloplasty provides temporary relief of symptoms. The gold standard of therapy for aortic stenosis is aortic valve replacement. Regular follow-up is recommended in all patients with aortic stenosis. Medical treatment may stabilize patients in heart failure, but intervention is required in all patients with symptomatic severe aortic stenosis. Additionally, intervention is indicated in asymptomatic patients with severe aortic stenosis in the following instances: when they are undergoing other cardiac surgery, a reduced left ventricular ejection fraction < 50%, mean gradient > 55 mm Hg, failure of blood pressure to rise > 20 mm Hg with exercise, severe valvular calcium, and a rapid increase in peak aortic gradient. Interventions for aortic stenosis include aortic valve replacement, aortic root replacement, transcatheter aortic valve replacement, and percutaneous balloon valvuloplasty. Aortic valve replacement with bioprosthetic valves is acceptable for patients at any age for whom anticoagulant therapy is contraindicated, not desired, or cannot be managed and is preferred in patients older than 70 years of age. Percutaneous balloon valvuloplasty can be used in young and adolescent patients but is associated with early restenosis in the elderly population and, hence, is used as a temporizing measure.

mitral valve prolapse

when one or both leaflets of the mitral valve (located in the left atrium) are displaced. This prolapse may be due to a disruption or elongation of leaflets, chordae, or papillary muscles. The hallmark murmur of mitral valve prolapse is a midsystolic click. a valvular condition that occurs when the mitral leaflets bulge upward (prolapse) into the left atrium during systole. These "floppy" valves are most commonly a result of degenerative processes, but they can also be a normal anatomic variant most often seen in healthy, thin, young women. MVP can be associated with systemic collagen disorders (e.g., Marfan or Ehler-Danlos syndrome) and skeletal changes such as scoliosis and pectus excavatum. MVP is a common cause of mitral regurgitation. Isolated MVP and MVP with mild mitral regurgitation are commonly asymptomatic, though some patients may have mild symptoms such as nonspecific angina, dyspnea, and fatigue. Chronic MVP that results in moderate to severe mitral valve regurgitation can lead to an increased left atrial pressure, pulmonary edema, and progressive exertional dyspnea with fatigue. A midsystolic click on cardiac auscultation is heard when the mitral valve leaflets prolapse into the left atrium. A holosystolic murmur best heard at the apex is consistent with mitral regurgitation. A transthoracic echocardiogram is the best initial diagnostic tool to evaluate valvular conditions. CT or MRI angiography is indicated in patients with MVP who may have aortic root disease or aortic dilation. In patients with isolated MVP, such as the patient in this case, no treatment or follow-up is needed unless they become symptomatic. Therefore, reassurance and clearance for sports participation are appropriate. In the presence of dysrhythmias or hyperadrenergic states, a low-dose beta-blocker may be indicated. Patients with orthostatic hypotension or anxiety secondary to MVP may be treated with a selective serotonin reuptake inhibitor. If mitral regurgitation is heard on auscultation, patients should be referred to a cardiologist for serial echocardiography and further evaluation. Early surgery is associated with improved mortality and morbidity in patients with MVP and severe mitral regurgitation. Mitral valve repair is preferred over valve replacement and can be done using a variety of techniques. Valve replacement may be done with either a mechanical or bioprosthetic valve.