USMLE Step 3 (Fach) / Cardiovascular (Lektion)

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• Congestive heart failure Defined as inability of the heart to pump adequate blood to meet the demands of the body. One categorization scheme includes:- Systolic heart failure (aka HFrEF)- Diastolic heart failure (aka HFpEF)- Heart failure related to vascular disease- Heart failure related to arrhythmias
• Systolic heart failure Weakened pumping function of the heart. Common causes include ischemic heart disease, long-standing hypertension, toxins (e.g., alcohol), and viral or idiopathic cardiomyopathy in younger patients. Symptoms:- Patients present with poor exercise tolerance, exertional dyspnea, and easy fatigability.- Volume-overloaded patients may present with orthopnea, paroxysmal nocturnal dyspnea, poor appetite, RUQ pain, and ankle swelling. Exam:- Exam often reveals inspiratory crackles (may be absent in chronic heart failure), a diffuse PMI that is displaced to the left (reflects cardiomegaly), an S3 gallop, ↑ JVP, and lower extremity edema. Cool extremities and/or confusion may suggest low cardiac output. Differential: Deconditioning, lung disease (e.g., COPD, chronic thromboembolic pulmonary hypertension, 1° pulmonary hypertension), other categories of heart failure (e.g., diastolic dysfunction), other causes of edema (e.g., cirrhosis, vascular incompetence, low albumin, nephrotic syndrome). Diagnosis:- The history and exam are suggestive, but determination of the EF via an imaging study (e.g., echocardiography, radionuclide imaging, cardiac MRI) confirms the diagnosis.- Look for the cause of the low EF:→ Perform a stress test or cardiac catheterization to look for CAD; evaluate for thyroid and renal disease.→ Look for a history of alcohol use or exposure to offending cardiotoxic medications such as doxorubicin.- Dilated cardiomyopathy can be seen in postpartum females.- A myocardial biopsy may be performed in selected cases to evaluate for infiltrative disease or other rare causes of heart failure when other evaluations are inconclusive. Treatment: Based on optimizing cardiac output via the following mechanisms:-  Preload reduction: Diuretics (furosemide, torasemide)-  ↓ Wall stress: β-blockers (metoprolol, bisprolol, carvedilol)- Optimization of contractility: Digoxin (may lower the frequency of hospitalizations and improve symptoms but does not ↓ mortality)- Afterload reduction: Renin-angiotensin-aldosterone antagonists (ACEIs/ARBs; spironolactone if potassium and creatinine are not ↑ and the patient is on optimal dosages of β-blockers and ACIs/ARBs). Hydralazine and nitrates may be useful additions to ACIs/ARBs in African American patients or an alternative to ACEIs/ARBs in patients with kidney disease/hyperkalemia. Spironolactone improves mortality in symptomatic systolic heart failure.- Exacerbations: Give loop diuretics such as furosemide when the patient is volume overloaded. These are generally given first in the IV form and then transitioned to oral form once the patient is closer to euvolemia. β-blockers and afterload reduction agents can be initiated once the patient is euvolemic.- Implantable cardiac defribillators (ICDs) are associated with ↓ mortality from ventricular tachycardia and ventricular fibrillation (VT/VF) in heart failure patients who are symptomatic and have a ↓ EF (< 35%).- Cardiac resynchronization therapy (CRT) is sometimes indicated in heart failure patients with both a ↓ EF and intraventricular conduction delay (QRS > 120 msec).- Treat the underlying cause of the systolic heart failure (e.g., CAD).
• Diastolic heart failure During diastole, the heart is stiff and does not relax well, resulting in ↑ diastolic filling pressure. However, the EF is often normal, so isolated diastolic heart failure is sometimes referred to "heart failure with preserved ejection fraction" (HFpEF). Hypertension with left ventricular hypertrophy (LVH) is the most common cause; other causes include hypertrophic cardiomyopathy and infiltrative diseases. Symptoms/Exam:- Signs and symptoms are the same as those of systolic heart failure.- Exam findings are similar to those of systolic failure. Listen for an S4 rather than an S3 (if rhythm is regular) or an irregular rhythm (AF is commonly associated with diastolic dysfunction). Diagnosis:- Presents with symptoms of heart failure with a preserved EF on echocardiogram.- Echocardiography often shows ventricular hypertrophy. Biopsy may be needed to establish the underlying diagnosis if infiltrative disease is suspected. Cardiac MRI is becoming an increasingly popular modality for this purpose. Treatment:- Control hypertension.- Give diuretics to control volume overload and symptoms, but avoid overdiuresis, which can ↓ preload and cardiac output.- Manage arrhythmias (e.g., AF) that are frequently associated with diastolic dysfunction.- Control renal and vascular disease, both of which are thought to be associated with diastolic heart disease.
• Mitral stenosis Etiology:- Most commonly due to rheumatic fever  - Autoimmune diseases: systemic lupus erythematosus, rheumatoid arthritis Clinical features:- Dyspnea, orthopnea, PND- Hemoptysis- Atrial fibrillation - Later stages: signs and symptoms of right-sided heart failure Exam: - Mid-diastolic murmur best heart at the apex- Loud first heart sound (S1)  - Opening snap: occurs when leaflet motion suddenly stops during diastole after the stenosed valve has reached its maximum opening- Mitral facies (pinkish-purple patches on cheeks) Treatment:- HR control- Endocarditis prophylaxis- High grade and/or symptomatic mitral stenosis → First-line: percutaneous balloon commissurotomy
• Mitral regurgitation Symptoms:- Has a long asymptomatic period- When severe or acute, presents with symptoms of heart failure Exam:- Blowing systolic murmur at the apex, radiating to the axilla- The posterior leaflet may lead to a murmur along the sternal border Treatment:- If acute, surgery is always required- For chronic mitral regurgitation, repare or replace the valve when symptomatic or if the ejection fraction (EF) is < 60%- Surgery is indicated in some patients with an EF > 60% (new AF, pulmonary hypertension). Comments: Long-standing regurgitation dilates the atrium, increasing the chance of AF.
• Mitral valve prolapse Symptoms: Asymptomatic Exam:- Midsystolic click- Also murmur if mitral regurgitation is present Treatment:- Endocarditis prophylaxis is not required Comments: Questionable association with palpitations and panic attacks. The most common cause of mitral regurgitation.
• Aortic regurgitation Symptoms:- Usually asymptomatic until advanced; then presents with symptoms of heart failure. Exam:- Wide pulse pressure- Soft, high-pitched diastolic murmur along the left sternal border- Radiates towards the apex Treatment:- Afterload reduction with ACEIs, hydralazine- Valve replacement if symptomatic or in the setting of a ↓ EF Comments:- Many cases are associated with aortic root disease, dissection, syphilis, ankylosing spondylitis, and Marfan's syndrome.
• Pericarditis Inflammation of the pericardial sac. May be acute (< 6 weeks; most common), subacute (6 weeks to 6 months), or chronic (> 6 months). Causes include bacterial or viral infection (especially enterovirus), mediastinal radiation, post-MI (Dressler's syndrome), cancer, rheumatologic diseases (SLE, RA), uremia, TB, and prior cardiac surgery. May also be idiopathic. Symptoms/Exam:- Presents with chest pain that is often improved with sitting up or leaning forward. The pain may radiate to the back and to the left trapezial ridge.- If large effusion is present, the patient may be short of breath.- Exam may reveal a pericardial friction rub (a leathery sound that can be present in multiple stages of the cardiac cycle). Differential: Myocardial ischemia, aortic dissection, pneumonia, pulmonary embolism, pneumothorax. Diagnosis:- Echocardiography may reveal an associated pericardial effusion.- Search for underlying cause – i.e., take a history for viral illness, radiation exposure, and malignancy. Check ANA, PPD, blood cultures if febrile, and renal function. Treatment:- Where possible, treat the underlying disorder (e.g., SLE, advanced renal failure)- For viral or idiopathic pericarditis, give NSAIDs, colchicine, or aspirin. Avoid NSAIDs or steroids in early post-MI pericarditis, as they may interfere with scar formation. Complications: Patients may develop a clinically significant pericardial effusion and tamponade.
• Pericarditis vs. Acute MI Pericarditis:- Clinical: Pain improves with sitting up or leaning forward; sometimes pleuritic.- ECG: Diffuse ST-segment elevation, often with upward concavity; PR-segment depression; ST-T changes tend to normalize more rapidly than those in MI. MI:- Clinical: Pain is not alleviated or exacerbated by position.- ECG: ST-segment elevation is localized to the distribution of coronary arteries, often with downward concavity.
• Pericardial effusion and cardiac tamponade Accumulation of fluid (usually chronic) or blood (usually acute and posttraumatic/postsurgical) in the pericardial cavity surrounding the heart. Symptoms/Exam:- Symptomatology often depends on the rate of fluid accumulation. If acute, patients may present with shock. If chronic, patients may present with shortness of breath and heart failure (if gradual, several liters of fluid may accumulate).- In patients with pericardial effusions and tamponade physiology, exam classically reveals distant or muffled heart sounds, ↑ JVP, and pulsus paradoxus (a drop of > 10 mmHg in systolic BP during inspiration). Differential: Pneumothorax, acute MI, heart failure Diagnosis:- Echocardiography is needed to confirm the diagnosis.- CXR may reveal an enlarged cardiac silhouette, and ECG may show low voltages and electrical alternans (beat-to-beat variation in R-wave amplitude). Treatment:- Consider emergent pericardiocentesis for patients with post-chest trauma shock as well as those whose echocardiogram shows evidence of tamponade physiology.- Also consider a pericardial window for those with recurrent or malignant effusions. While evaluation with echocardiography is being pursued, give IV fluids to maintain preload and systemic BP.
• Advanced cardiac evaluation - Indications for stress testing include diagnosis of CAD/evaluation of symptoms, preoperative evaluation, risk stratification in patients with known disease, and decision making about the need for revascularization. - Contraindications include severe aortic stenosis, acute coronary syndrome, acute pulmonary embolus, unstable arrhythmias, and decompensated heart failure. - Testing consists of a stressing modality and an evaluating modality. - Within available options for pharmacologic stressing modalities, dobutamine ↑ cardiac contractility, whereas adenosine and dipyridamole dilate the coronary arteries (the latter ↑ blood flow in healthy arteries but not in the already maximally dilated diseased arteries, creating a differential flow that can be detected on nuclear imaging). ECG: Cannot localize the lesion, cannot use with baseline ST-segment abnormalities or left bundle branch block (LBBB); cannot use if the patient is on digoxin.Echocardiography: Provider dependentRadionuclide tracer (Thallium or technetium): Localizes ischemia; localizes infarcted tissue. Usefulness can be limited in extensive, multivessel CAD with balanced ischemia in different regions.
• Hypertension A major contributor to cardiovascular disease; more common with increasing age and among African Americans. Symptoms:- Asymptomatic unless severe.- If severe without symptoms, it is termed hypertensive urgency. - If severe with symptoms or evidence of organ damage (dizziness, lightheadedness), it is termed hypertensive emergency. Exam:- BP > 140/90 mmHg.- A displace PMI or an S4 suggests LVH.- Listen for bruits, which indicate peripheral vascular disease.- Examine fundi, which can show AV nicking and "copper-wire" changes to the arterioles. In severe hypertension, look for papilledema and retinal hemorrhages.- Look for signs suggestive of 2° hypertension. Differential: The vast majority of cases are due to essential (1°) hypertension, but in the right clinical settings or in cases of refractory hypertension, consider 2° causes. Diagnosis:- Diagnosed in the setting of a BP > 140/90 on 3 separate occasions (elevation of either systolic or diastolic BP).- A systolic BP of 120-139 or a diastolic BP of 80-89 is considered "prehypertension" and predicts the future development of hypertension. Treatment:- Based on the most recent guidelines, the goal BP for almost all patients, including those with diabetes or CKD, is < 140/90 mmHg.- New guidelines also suggest that for patients > 60 years of age without diabetes or CKD, the goal BP should be < 150/90 mmHg.- Interventions include the following:→ Lifestyle modification: Weight loss, exercise, ↓ sodium intake, smoking cessation.→ Medications: First-line agents include thiazide diuretics, CCBs, ACEIs, or ARBs.→ Control other cardiovascular risk factors, such as diabetes, smoking, and hypercholesterolemia. Complications: Long-standing hypertension contributes to renal failure, heart failure (both systolic and diastolic), CAD, peripheral vascular disease, and stroke.
• Aortic dissection Aortic dissection most commonly occurs in patients with a history of long-standing hypertension, cocaine use, aortic aneurysm, or aortic root disease such as Marfan's syndrome or Takayasu's arteritis. Symptoms/Exam:- Presents with sudden onset of severe chest pain that sometimes radiates to the back, often described as a burning, searing, or tearing pain. May also present with neurologic symptoms resulting from occlusion of vessels supplying the brain or spinal cord.- On exam, evaluate for aortic regurgitation, asymmetric pulses and blood pressures, and neurologic findings. Differential: MI (aortic dissection can also cause MI if it exends into a coronary artery), pulmonary embolism, pneumothorax Diagnosis:- Requires a high index of suspicion.- CXR has low sensitivity but may show a widened mediastinum or a hazy aortic knob.- CT with IV contrast is diagnostic and shows the extent of dissection.- Transesophageal echocardiography (TEE) is highly sensitive and specific. - MRI may also be used, but is often time consuming and may not be optimal for unstable patients. Treatment:- Initial medical stabilization: Aggressive HR and BP control, first with β-blockers (typically IV esmolol) and then with IV nitroprusside if needed.- Ascending dissection – Stanford type A (involves the ascending aorta): Emergent surgical repair.- Descending dissection – Stanford type B (distal to the left subclavian artery): Medical management is indicated unless there is intractable pain, progressive dissection in patients with chest pain, or vascular occlusion of the aortic branches. Complications: Aortic rupture, acute aortic regurgitation, tamponade, MI, neurologic impairment, limb or mesenteric ischemia, renal ischemia.
• Peripheral vascular disease Atherosclerotic disease of vessels other than the coronary arteries. Risk factors are similar tot hose for CAD and include smoking, diabetes, hypercholesterolemia, hypertension, and increasing age. Symptoms:- Mesenteric ischemia: Postprandial abdominal pain and food avoidance ("food fear"), bloody diarrhea.- Lower extremities: Claudication, leg ulceration or nonhealing wounds, rest pain.- Kidneys: Usually asymptomatic, but may present with difficult-to-control hypertension.- CNS: Stroke and TIA. Exam:- Mesenteric disease: No specific findings. The patient may be thin because of weight loss from avoidance of food.- Abdomen: Palpate for a pulsatile mass (abdominal aortic aneurysm) in the abdominal midline.- Lower extremity disease: Exam reveals ulcers and nonhealing wounds, diminished pulses, ↓ ankle-brachial indices, skin atrophy and loss of hair, and bruits over affected vessels (abdominal, femoral, popliteal).- Renal artery stenosis: Listen for bruit during systole and diastole (highly specific). Differential:- Abdominal pain: Stable symptoms can mimic PUD or biliary colic. If the colon is predominantly involved, episodes of pain and bloody stool can look like infectious colitis.- Lower extremities: Spinal stenosis can produce lower extremity discomfort similar to claudication. Claudication improves with rest (except for severe peripheral arterial disease with rest claudication), but spinal stenosis classically improves with sitting forward (lumbar flexion improves spinal stenosis symptoms). Diagnosis:- Mesenteric disease: A diagnosis of exclusion. Angiography reveals lesions.- Lower extremity disease: Diagnosed via the ankle-brachial index (compares BP in the lower and upper extremities) and Doppler ultrasound. Angiography or MRA is used in preparation for revascularization but is generally not used for diagnosis.- Renal artery stenosis: CT angiography, MRA, conventional angiography, or ultrasound with Doppler flow (technically difficult). Treatment:- Control modifiable risk factors, especially smoking.- Mesenteric disease: Treat with surgical revascularization or angioplasty.- Lower extremity disease: Treat with exercise (to improve functional capacity), surgical revascularization, and sometimes angioplasty. Cilostazol is moderately useful (improves pain-free walking distance by 50%), whereas pentoxifylline is of marginal benefit. Antiplatelet therapy (aspirin, clopidogrel) is indicated to prevent cardiovascular events.- Renal artery stenosis: Surgery or angioplasty may be of benefit.
• Hypercholesterolemia One of the principal factors contributing to atherosclerotic vascular disease. ↑ LDL and ↓ HDL are the 1° contributors. Hypercholesterolemia can be idiopathic, genetic, or 2° to other diseases, such as diabetes, nephrotic syndrome, and hypothyroidism. Symptoms:- Generally asymptomatic unless the patient develops ischemia (e.g., angina, stroke, claudication) or unless severe hypertriglyceridemia leads to pancreatitis. In certain cases, patients may notice fat deposits (xanthomas) in certain body regions. Exam:- Look for evidence of atherosclerosis – e.g., carotid, subclavian, abdominal and other bruits; diminished or asymmetric pulses; or ischemic foot ulcers or other skin or hair changes.- Look for xanthomas over the tendons, above the upper eyelid, and on the palms. Diagnosis:- Diagnosis is based on a lipid panel. A full panel consists of total cholesterol, HDL, LDL, and triglycerides.- A nonfasting lipid profile can be obtained for ease of testing. Fasting and nonfasting LDL values vary very little. However triglyceride values ↑ following a meal. If triglyceride values are of concern, fasting levels should be obtained.- Look for other contributing conditions. Check glucose and TSH; check body weight, and consider nephrotic syndrome.- In patients with a family history of early heart disease, consider novel risk factors such as homocysteine, Lp(as), and CRP. These can be treated with folic acid supplementation, niacin, and statins, respectively. Treatment:- Treatment is aimed at preventing pancreatitis when triglycerides are very high (generally > 1000 mg/dL) and at preventing atherosclerotic disease.- Medications: HMG-CoA reductase inhibitors (statins), cholesterol absorption inhibitors (ezetimibe), fibrates (gemfribozil), bile acid-binding resins, niacin
• Endocarditis Inflammation of the heart valves. Can be infective or noninfective. Infective endocarditis (IE) is commonly seen in IV drug abusers, hemodialysis patients, and those with valvular lesions or prosthetic heart valves. Valvular thrombi are composed of bacteria and platelets and are devoid of WBCs. IE is further distinguished as follows:- Acute IE (days): Usually affects normal heart valves and is most often caused by S aureus, group A streptococci, or other β-hemolytic streptococci, such as Streptococcus pneumoniae. IV drug users typically have S aureus organisms and right heart involvement.- Subacute IE (weeks to months): Usually colonizes a previously damaged valve in the setting of bacteremia from oral surgery or poor dentition. It is most often caused by the viridans group of streptococci. The aortic and mitral valves are most commonly affected. Symptoms:- Acute IE: Presents with fever, rigors, heart failure from valve destruction, and symptoms related to systemic emboli (neurologic impairment, back pain, pulmonary symptoms).- Subacute IE: Characterized by weeks to months of fever, malaise, and weight loss. Also presents with symptoms of systemic emboli.- Noninfective endocarditis: Generally asymptomatic. Can cause heart failure by destroying valves. Exam:- Listen for a new murmur.- Neurologic: Focal neurologic deficits; tenderness to percussion or palpation of the spine.- Ophthalmologic: Retinal exudates (Roth's spots).- Extremities: Deep-seated painful hand/foot nodules (Osler's nodes); small skin infarctions (Janeway lesions) Differential:- Differential for a vegetation found on echocardiography: IE, nonbacterial thrombotic endocarditis (NBTE, also known as marantic endocarditis), verrucous endocarditis (Libman-Sacks endocarditis), valve degeneration.- Differential bacteremia: IE, infected hardware (e.g., from a central line, abscess, osteomyelitis). Diagnosis:- Noninfective endocarditis is usually an incidental finding on echocardiography. It may be found during the workup of systemic emboli.- IE is diagnosed by a combination of lab and clinical data. If suspicious, obtain at least 3 sets of blood cultures and an echocardiogram. If TEE is ⊕, proceed to TEE (more sensitive). ⊕ Blood cultures and echocardiogram findings together are strongly suggestive of IE. The modified Duke criteria are often used for diagnosis. Treatment:- Treat with prolonged antibiotic therapy, generally for 4-6 weeks (can be as short as 2 weeks for small subgroups of patients; > 6 weeks for patients with highly virulent organisms). Begin empiric therapy with gentamicin and antistaphylococcal penicillin (oxacillin or nafcillin). If there is a risk of MRSA, treat empirically with vancomycin instead of oxacillin/nafcillin.- Valve replacement is appropriate for fungal endocarditis, heart failure from valve destruction, valve ring abscess, cardiac conduction abnormalities, persistently ⊕ blood cultures despite antibiotic treatment, large or mobile vegetations, or systemic emboli despite adequate antibiotic therapy.- Following treatment for IE, patients should receive endocarditis prophylaxis.- For NBTE, treat the underlying disorder (often malignancy). Systemic anticoagulation (LMWH or UFH) is useful for preventing recurrent emboli. Surgery is rarely indicated.- For verrucous endocarditis, no treatment is required. Patients should receive endocarditis prophylaxis. Prevention:Endocarditis prophylaxis is indicated only in patients whose cardiac conditions are associated with the highest risk of an adverse outcome from endocarditis. These include:- Congenital cardiac disease:→ Unrepaired cyanotic disease, including those with palliative shunts and devies.→ Congenital cardiac defects that have been completely repaired during the first 6 months after the repair (endothelialization occurs after 6 months).→ Repaired congenital cardiac disease with residual defects that may inhibit endothelialization.- Other:→ Prosthetic heart valves (both homograft and bioprosthetic).→ A patient history of prior IE.→ Cardiac transplant patients with cardiac valvulopathy.- Guidelines for antibiotic prophylaxis:→ Dental procedures: All dental procedures that involve the manipulation of gingival tissue or the periapical region of the teeth, as well as procedures involving perforation of the oral mucosa (not for routine anesthetic infections through noninfected tissue, dental radiographs, bleeding from trauma, adjustment of orthodontic devices, or shedding of deciduous teeth).→ Respiratory tract procedures: Any of the above-mentioned cardiac patients who are undergoing an invasive procedure of the respiratory tract that involves incision (e.g., tonsillectomy) or biopsy of the respiratory mucosa (includes bronchoscopy with biopsy).→ Skin procedures: Any of the above-mentioned cardiac patients who are undergoing procedures involving infected skin or musculoskeletal tissue.→ GI and GU procedures: Prophylaxis is not recommended even for high-risk patients but may be considered in special scenarios involving the above-mentioned cardiac patients.- Prophylactic regimens: Amoxicillin (or clindamycin, azithromycin, or cephalexin for those with penicillin allergy) 30-60 minutes before the procedure. Complications: Spinal osteomyelitis, valve destruction and heart failure, stroke and renal damage (from septic emboli), metastatic abscesses, mycotic aneurysms.
• Acute decompensated heart failure Clinical presentation:- Acute dyspnea, orthopnea, paroxysmal nocturnal dyspnea- Hypertension common; hypotension suggests severe disease- Accessory muscle use, tachycardia, tachypnea- Diffuse crackles with possible wheezes (cardiac asthma)- Possible S3, jugular venous distention, peripheral edema Treatment:- Normal or elevated blood pressure with adequate end-organ perfusion:→ Supplemental oxygen→ Intravenous loop diuretic (e.g., furosemide)→ Consider intravenous vasodilator (e.g., nitroglycerin)- Hypotension or signs of shock→ Supplemental oxygen→ Intravenous loop diuretic (e.g., furosemide) as appropriate→ Intravenous vasopressor (e.g., norepinephrine)
• Vasovagal syncope Clinical presentation:- Inciting event (e.g., stress, prolonged standing)- Prodrome (e.g., palor, nausea, diaphoresis)- Consciousess regained rapidly (e.g., < 1 minute) Diagnosis:- Mainly clinical diagnosis- Upright tilt-table testing in uncertain cases Treatment:- Reassurance- Avoidance of triggers- Counterpressure techniques for recurrent episodes
• Atrial septal defect Epidemiology: Prevalence: ∼ 2/1000 live births Etiology:- Down syndrome- Fetal alchohol syndrome- Holt-Oram syndrome: Autosomal dominant disorder, which is also called hand-heart syndrome because affected children present with an ASD, a first degree heart block, and abnormalities of the upper limbs (e.g., absent radial bones). Clinical findings:- Small defects: usually asymptomatic- Large defects: Palpitations  - ASDs typically manifest with advancing age.   Auscultation:- Systolic ejection murmur over the left second ICS sternal border  - Widely split second heart sound (S2) over the left second ICS, which is fixed (does not change with respiration), normal S1- Soft mid-diastolic murmur over the lower left sternal border Diagnostics:- Echocardiography (confirmatory test): to visualize the defect, its extent, and shunt volume- ECG: vertical or right axis, P pulmonale, right bundle branch block (complete or incomplete), signs of right heart hypertrophy, PR prolongation- Chest x-ray: enlarged right atrium, ventricle, and pulmonary arch; increased pulmonary vasculature Treatment:- In childhood, spontaneous closure may occur.- Patch repair
• Paroxysmal supraventricular tachycardia Paroxysmal supraventricular tachycardia (PSVT) is a type of arrhythmia arising from a defect in atrioventricular conduction, which causes the heart to sporadically beat faster. Atrioventricular nodal reentrant tachycardia (AVNRT): tachycardia caused by a dysfunctional AV node that contains two electrical pathways Atrioventricular reciprocating tachycardia (AVRT): tachycardia caused by an accessory pathway between the atria and ventricles- Wolff-Parkinson-White syndrome (WPW): A congenital condition characterized by intermittent tachycardias and signs of ventricular pre-excitation on ECG, which both arise from an accessory pathway known as the “Bundle of Kent” (an accessory pathway that conducts impulses from the atriato the ventricles)→ The bundle of Kent connects the atria and ventricles, bypassing the AV node and leading to a pre-excitation of the ventricles.  → Up to one-third of patients may develop paroxysmal atrial fibrillation.→ May result in supraventricular tachycardia due to a reentry circuit ECG:- Supraventricular: narrow QRS complex (< 120 ms)- AVNRT: no P waves or atrial activity- AVRT: P wave in the ST segment Treatment:- Hemodynamically unstable patient: Cardioversion- Hemodynamically stable patient:→ First step: Vagal maneuvers→ AVNRT and orthodromic AVRT: First line: IV adenosine: briefly blocks the AV node (↑ refractoriness)→ For antidromic AVRT: procainamide→ For WPW patients with AF: generally rhythm control (e.g., procainamide)
• Ventricular septal defect Epidemiology: The most common congenital heart defect (4/1000 live births) Etiology:- Genetic syndromes: Down syndrome, Edward syndrome, Patau syndrome  - Fetal alcohol syndrome- Intrauterine infection (e.g., TORCH) Clinical findings:- Small defects: usually asymptomatic- Medium-sized or large defects→ Lead to cardiac failure in the first 2–3 months of life→ Some VSDs can present after the first weeks of life because pulmonary vascular resistance (PVR) is high at birth and decreases thereafter. ↓ PVR → ↓ right ventricular pressure → ↑ left-to-right shunt → presence of symptoms- Palpation: Hyperdynamic precordium may be detected in hemodynamically relevant defects.   Auscultatory findings:- Harsh holosystolic murmur over the left lower sternal border; typically louder in small defects  - Becomes louder with maneuvers that increase left ventricular afterload (e.g., handgrip) because of increased left-to-right shunting- Mid-diastolic murmur over cardiac apex  - Systolic thrill  - Loud pulmonic S2 (if pulmonary hypertension develops) Diagnostics:- Doppler echocardiography: confirms diagnosis; evaluation of defect size and shunt volume; exclusion of other anomalies- ECG: signs of right heart hypertrophy- Chest x-ray Treatment:- Small VSDs: rarely require surgical interventions → small to moderate defects often heal spontaneously; follow-up echocardiography recommended- Symptomatic and large VSDs: → Surgical (patch) repair in children < 1 year of age with signs of pulmonary hypertension and older children who did not improve with medical therapy→ Heart-lung transplant or lung transplant with concurrent VSD repair if Eisenmenger's reaction has occurred
• ECG changes diagnostic of STEMI New ST elevation at the J point in ≥ 2 anatomically contiguous leads with the following threshold:- > 1 mm (0.1 V) in all leads except V2 and V3- ≥ 1.5 mm in women, ≥ 2 mm in men age ≥ 40, and ≥ 2.5 mm in men age < 40 in leads V2 and V3 OR New left bundle branch block with clinical presentation consistent with acute coronary syndrome.
• Exercise stress testing Factors associated with increased risk of adverse cardiovascular events Clinical variables:- Poor exercise capacity- Exercise-induced angina at low workload- Fall in systolic blood pressure from baseline- Chronotropic incompetence ECG variables:- > 1 mm ST depression (flat or downsloping)- ST depression at low workload- ST elevation in leads without Q waves- Ventricular arrhythmias
• Exercise stress testing Factors associated with increased risk of adverse cardiovascular events Clinical variables:- Poor exercise capacity- Exercise-induced angina at low workload- Fall in systolic blood pressure from baseline- Chronotropic incompetence ECG variables:- > 1 mm ST depression (flat or downsloping)- ST depression at low workload- ST elevation in leads without Q waves- Ventricular arrhythmias
• Torsades de pointes Polymorphic ventricular tachycardia with QRS complexes that appear to twist around the isoelectric line Most severe complication: progression to life-threatening ventricular arrhythmia Cause: prolonged QT interval caused by congenital disease, electrolyte abnormalities, and drugs   Treatment:- If hemodynamically unstable → defibrillation- If hemodynamically stable → IV magnesium sulfate
• Long QT syndrome Etiology:- Congenital LQTS→ Jervell and Lange-Nielsen syndrome: Autosomal recessive, associated with congenital deafness→ Romano-Ward syndrome: Autosomal dominant, no associated deafness- Acquired LQTS→ Drugs: Diuretics (due to electrolyte imbalances), antiemetics (e.g., ondansetron), antipsychotics (e.g., haloperidol, quetiapine, risperidone), tricyclic antidepressants, SSRIs, antiarrhythmics (e.g., amiodarone, sotalol, flecainide), antibiotics (e.g., macrolides, fluoroquinolones)→ Metabolic disorders: Electrolyte imbalances (↓ K, ↓ Mg, ↓ Ca), starvation, hypothyroidism→ Bradyarrhythmias: Sinus node dysfunction, AV block Clinical features:- Often asymptomatic, especially if the QT interval is only minutely prolonged- Palpitations- Dizziness- Syncope- Cardiac arrest Diagnostics:- The primary finding in LQTS is a long QT interval corrected for heart rate (QTc) interval. Males: > 440 ms, Females: > 460 ms. Treatment:- Both congenital and acquired LQTS:→ Avoid activities that stress the heart→ Avoid cold temperatures (e.g., swimming, diving, skiing)- Congenital LQTS: First line: beta blockers (e.g., propranolol)- Acquired LQTS: treat cause (remove offending drug, fix electrolyte imbalances, etc.)
• Constrictive pericarditis Etiology:- Idiopathic or viral pericarditis- Cardiac surgery - Tuberculous pericarditis (in endemic areas)- Collagen vascular disease: systemic lupus erythematosus, rheumatoid arthritis- Other causes: renal failure (uremia), tumors (Hodgkin lymphoma), radiation Clinical features:- Fatigue & dyspnea on exertion- Peripheral edema & ascites- ↑ Jugular venous pressure- Pericardial knock may be heard- Pulsus paradoxus- Kussmaul's sign Diagnostics:- ECG may be nonspecific or show atrial fibrillation or low-voltage QRS complex- Imaging shows pericardial thickening & calcification- Jular venous pulse tracings show prominent x & y descents Treatment:- Treat underlying condition- Symptomatic therapy (manage fluid overload with diuretic therapy)- Pericardiectomy (complete removal of the pericardium)
• Acute pericarditis Etiology:- Viral, bacterial- Myocardial infarction: pericarditis may occur either within 1-3 days as an immediate reaction (i.e., post-infarction fibrinous pericarditis), or weeks to months following an acute myocardial infarction (Dressler syndrome).- Postoperative (post-pericardiotomy syndrome): blunt or sharp trauma to the pericardium- Collagen vascular disease: systemic lupus erythematosus, rheumatoid arthritis- Other causes: renal failure (uremia), tumors (Hodgkin lymphoma), radiation Clinical features:- Low-grade intermittent fever, tachypnea, dyspnea, nonproductive cough  - Pleuritic chest pain (↓ when sitting up) - Pericardial friction rub (highly specific) Diagnostics:- Blood tests: CBC (leukocytosis), ↑ troponin I, ↑ ESR, ↑ CRP, abnormal renal parameters (BUN, creatinine, electrolytes) if caused by underlying uremia- ECG: diffuse ST-segment elevation & PR-segment depression- Echocardiography: pericardial effusion Treatment:- Acute pericarditis is often self-limiting and resolves within approx. 2-6 weeks. - Restricted physical activity- NSAIDs plus colchicine for viral etiology- High-dose aspirin (e.g., 650 mg 3x a day) for peri-infarction pericarditis
• Risk factors for coronary heart disease CHD risk equivalents:- Noncoronary atherosclerotic disease (e.g., carotid, peripheral artery, abdominal aortic aneurysm)- Diabetes mellitus- Chronic kidney disease CHD established risk factirs:- Age (especially > 50 in men & postmenopausal women)- Male gender- Family history of CHD in first-degree relative age < 50 (men) or age < 60 (women)- Hypertension- Dyslipidemia- Cigarette smoking- Obesity
• Abdominal aortic aneurysm Risk factors:- Advanced age- Smoking (most important risk factor)  - Atherosclerosis- Hypercholesterolemia and arterial hypertension- Positive family history- Trauma Screening: Abdominal ultrasound in men age 65-75 who have ever smoked Clinical features:- Mostly asymptomatic- Lower back pain- Pulsatile abdominal mass at or above the level of the umbilicus- Bruit on auscultation  - Peripheral thrombosis and distal atheroembolic phenomena (e.g., blue toe syndrome and livedo reticularis)- Decreased ankle brachial index   Diagnostics:- Ultrasound: best initial and confirmatory test for AAAs Treatment:- Smoking cessation- Optimal blood pressure levels (< 120/80 mmHg)- Aspirin & statin therapy- Follow-up→ < 3 cm → no further follow-up→ 3-4 cm → Ultrasound every year→ 4-4.5 cm → Ultrasound every 6 months→ 4.5-5.5 cm → Ultrasound every month- Elective repair recommended for:→ Large (≥ 5.5 cm) aneurysms → Rapidly enlarging aneurysms (≥ 1 cm per year)
• Aortic stenosis Etiology:Congenital:- Bicuspid aortic valve: caused by a fusion of two of the three aortic-valve leaflets in utero- Most common congenital heart defect, 3:1 ♂ predominance- Predisposes the valve to dystrophic calcification and degenerationAcquired:- Calcific aortic stenosis: Characterized by calcification and fibrosis of aortic valve leaflets that occur at an increasing rate as patients age (prevalence is 65% in those aged 75-84 years) Clinical features:- Dyspnea- Angina pectoris- Dizziness and syncope- Small blood pressure amplitude, decreased pulse pressure   Cardiac exam: - Weak and delayed distal pulse (pulsus parvus et tardus)- Palpable systolic thrill over the bifurcation of the carotids and the aorta- Harsh crescendo-decrescendo (diamond-shaped), late systolic ejection murmur that radiates bilaterally to the carotids→ Best heard in the 2nd right intercostal space  → Hand grip decreases the intensity of the murmur.  → Valsalva and standing from squatting decreases or does not change the intensity of the murmur (in contrast to hypertrophic cardiomyopathy).- Soft S2  - S4 is best heard at the apex.  - Early systolic ejection click  - Frequently associated with aortic regurgitation  Conservative management: regular follow-ups indicated for asymptomatic patients with mild aortic stenosis Surgical - Indications: → Symptomatic patients  → Asymptomatic patients with severe AS and either significantly ↓ LV EF or those undergoing cardiac surgery- Aortic valve replacement (AVR): 3 possible approaches→ Surgical AVR: patients with low surgical risk.→ Transcatheter AVR (TAVR): patients with high surgical risk or contraindication→ Catheter balloon valvuloplasty: children without AV calcification
• Valve replacement in aortic stenosis Severe AS criteria:- Aortic jet velocity ≥ 4.0 m/s OR- Mean transvalvular pressure gradient ≥ 40 mmHg- Valve area usually ≤ 1.0 cm2 but not required Indications for valve replacement:- Severe AS & ≥ of the following:→ Onset of symptoms (e.g., angina, syncope)→ Left ventricular ejection fraction < 50%→ Undergoing other cardiac surgery (e.g., CABG)
• Preferred antiarrhythmic therapy in patients with atrial fibrillation No CAD or structural heart disease:- Flecainide- Propafenone Left ventricular hypertrophy:- Dronedarone- Amiodarone CAD without heart failure:- Sotalol- Dronedarone Heart failure:- Amiodarone- Dofetilide Recurrent AF symptoms refractory to medication:- Radiofrequency ablation
• Pulmonary hypertension Chronically elevated mean pulmonary arterial pressure (mPAP) at rest ≥ 20 mm Hg (normal: 10–14 mm Hg) due to chronic pulmonary and/or cardiac disease or unknown reasons Classification:- Group 1: Idiopathic- Group 2: Due to left-sided heart disease - Group 3: Due to chronic lung disease (eg, COPD, ILD)- Group 4: Due to chronic thromboembolic disease- Group 5: Other (e.g., sarcoidosis) Diagnostics:- Echocardiogram (best initial test)- Right heart catheterization (confirmatory test) Treatment:- Calcium channel blockers- Long-acting synthetic prostacyclin (epoprostenol) or prostacyclin analogs (e.g., iloprost, treprostinil): bind to prostacyclin receptors  - Endothelin receptor antagonists (e.g., bosentan, macitentan, and ambrisentan): inhibit endothelin-1 receptors  - Phosphodiesterase 5 inhibitors (e.g., sildenafil)
• Predictors of major cardiac complications with noncardiac surgery (Revised Cardiac Risk Index) Clinical risk factors:- High-risk surgery (e.g., vascular)- History of ischemic heart disease- Heart failure- History of stroke- Diabetes mellitus treated with insulin- Preoperative creatinine > 2 mg/dL Rate of cardiac death, nonfatal cardiac arrest, or nonfatal MI:- No risk factors: 0.4%- 1 risk factor: 1%- 2 risk factors: 2.4%- ≥ 3 risk factors: 5.4%
• Hypertension – Nonpharmacologic measures Weight loss: Reduction of BMI to < 25 kg/m2- Approximate ↓ systoplic BP (mmHg): 5-20 mmHg per 10-kg loss DASH diet: Diet high in fruits & vegetables & low in saturated & total fats- Approximate ↓ systoplic BP: 8-14 mmHg Exercise: 30 minutes/day for 5-6 days/week- Approximate ↓ systoplic BP: 4-9 mmHg Dietary sodium: < 3 g/day- Approximate ↓ systoplic BP: 2-8 mmHg Limit alcohol intake: ≤ 2 drinks/day in men, ≤ 1 drink/day in women- Approximate ↓ systoplic BP: 2-4 mmHg
• Cardiac myxoma Epidemiology:- Most common primary cardiac neoplasm (usually benign)  - Most common location: left atrium (∼ 75% of all cases)  - Sex: ♀ > ♂ (3:1)- Peak incidence: 40-60 years Etiology:- Most cases are sporadic.- Familial inheritance: ∼ 10% of all cases→ Autosomal dominant inheritance→ Carney syndrome Clinical features:- Production of IL-6 by tumor causes constitutional symptoms (e.g., weight loss, fever, pallor)- Clubbing of the fingers- Symptoms caused by obstruction→ Dyspnea on exertion, paroxysmal nocturnal dyspnea, and/or orthopnea→ Dizziness or syncope→ Palpitations- Auscultatory findings→ Low pitched, mid-diastolic rumbling murmur over apex (similar to mitral stenosis)→ “Tumor plop”: a sound related to movement of the tumor→ Potentially, an additional heart sound (audible just after S2)→ These sounds may change when the patient changes position.- Symptoms due to embolization Treatment: surgical resection
• Cardiovascular effects of cocaine intoxication Physiologic effects:- Hypertension & tachycardia- Coronary vasoconstriction- ↑ Platelet activity & thrombus formation Clinical features:- Myocardial ischemia or infarction- Aortic dissection- Neurologic ischemia or stroke Treatment:- Benzodiazepines & nitroglycerin- Beta blockers contraindicated- CCBs for persistent chest pain- Phentolamine for persistent hypertension- Same as STEMIs (percutaneous angioplasty or thrombolysis, aspirin, nitrates) 
• Bicuspid aortic valve Etiology:- Affects 1% of population- Predominant in male patients- Present in 30% of patients with Turner syndrome- Autosomal dominant with incomplete penetrance or sporadic Diagnosis: Screening echocardiogram for patient & first-degree relatives Complications:- Infective endocarditis- Severe regurgitation or stenosis- Aortic root or ascending aortic dilation- Dissection Management:- Follow-up echocardiogram every 1-2 years- Balloon valvuloplasty or surgery (valve & ascending aorta replacement)
• Cardiac tamponade Etiology:- Cardiac wall rupture (e.g., complication of myocardial infarction)- Chest trauma- Aortic dissection- Cardiac surgery (e.g., heart valve surgery, coronary bypass surgery)- Infection (e.g., viral, tuberculosis)- Connective tissue disease (e.g., SLE)- Malignancy or radiation therapy Clinical features:- Shortness of breath, especially while lying down (orthopnea)- Beck's triad1. Hypotension2. Muffled heart sounds3. Distended neck veins  - Tachycardia, pulsus paradoxus (SBP ↓ > 10 mmHg with inspiration)- Retrosternal chest pain- Apical impulse difficult to locate or nonpalpable- Pallor, cold sweats Diagnosis:- Echocardiography (gold standard): Right atrial & ventricular collapse, plethora of the IVC- ECG: Low voltage; Electric alternans- CXR: enlarged cardiac silhouette, in severe cases a globular "water bottle-shaped" heart contour (water bottle sign)   Treatment:- Hemodynamically unstable: Pericardial fluid drainage- Hemodynamically stable: Pericardial window
• Mitral valve prolapse Epidemiology:- Prevalance: 2-3 % (one of the most common valvular abnormalities in the US)- The most common cause of mitral regurgitation in developed countries Etiology:- Mostly idiopathic- Connective tissue disorders: Marfan syndrome, Ehlers-Danlos syndrome, osteogenesis imperfecta- Myocardial infarction  - Acute rheumatic heart disease- Infective endocarditis Clinical features:- Most patients are asymptomatic.- Rarely: atypical chest pain and anxiety- In case of complications: fatigue, dyspnea, syncope, and palpitations Auscultatory findings  - Mitral valve prolapse click: high-frequency, midsystolic click that is best heard at the mitral region  - High-frequency, mid-to-late systolic murmur that is best heard at the mitral region and may radiate to the axilla (squatting diminishes the murmur)  - Patients with severe MR: S3 may be heard as a result of left ventricular overload (especially in the left decubitus position) Diagnostics:- Transthoracic echocardiography (test of choice) to confirm diagnosis Treatment:- No treatment is required in most cases.- Patients with severe mitral regurgitation : mitral valve repair or replacement 
• Indications for implantable cardioverter-defibrillator placement Primary prevention:- Prior myocardial infarction & LVEF ≤ 30%- NYHA class II or III & LVEF ≤ 35% Secondary prevention:- Prior VF or unstable VT without reversible cause- Prior sustained VT with underlying cardiomyopathy
• Cardiac glycoside poisoning Etiology:- Digoxin overdose (iatrogenic, by nonadherence to prescribed dosages or by ingestion of plants containing cardiac glycosides)  - Ouabain poisoining  - Hypokalemia  - Renal failure- Treatment with verapamil, diltiazem, amiodarone, and/or quinidine  - Volume depletion (e.g., treatment with diuretics) Clinical features:- Nausea/vomiting, diarrhea, abdominal pain, and anorexia- Blurry vision with a yellow tint and halos, disorientation, weakness Diagnostics:- ECG: potentially severe cardiac arrhythmias→ Premature ventricular beats→ T-wave inversion or flattening→ Downsloping ST segment depression (“scooped” ST segments)→ ↓ QT interval→ ↑ PR interval→ Atrial tachycardia with AV block- Serum digoxin concentration (ideally, measure 6 hours after ingestion)- Serum electrolyte levels: hyperkalemia  - Creatinine and blood urea nitrogen to evaluate renal function Treatment:- Digoxin-specific antibodyfragments  - Atropine for symptomatic bradycardia- Slowly normalize serum K+ levels- Mg2+- Class IB antiarrhythmics- Temporary cardiac pacing
• Varicose veins Risk factors for chronic venous disease - Higher age and female sex - Family history of venous disease- Ligamentous laxity- Sedentary lifestyle and prolonged standing- Obesity- Pregnancy- Smoking- Prior thrombosis (postthrombotic syndrome)- Prior extremity trauma Clinical features:- Chief complaints: generalized or localized pain, lower extremity discomfort/cramping, and limb swelling→ Worsened by heat→ Worse while standing, relieved by walking and raising of legs  - Pruritus, tingling, and numbness- Edema formation (may be unilateral) that starts in the ankle and may involve the calf later in the disease course- Telangiectasias (esp. in women)- Lipodermatosclerosis: Localized chronic inflammation and fibrosis of skin and subcutaneous tissues of lower leg Diagnosis: Test of choice: duplex ultrasonography Treatment:- Conservative→ Compression therapy with compression stockings→ Frequent elevation of the legs→ Physical therapy, manual lymphatic drainage→ Avoid long periods of standing and sitting (with bent legs) and heat- Definite treatment: vein ablation therapies  → Interventional: First-line: endovenous thermal ablation (laser and radiofrequency)→ Alternative: chemical ablation (sclerotherapy)  → Open surgery with partial or complete removal of a vein: only for veins that are not accessible by interventional techniques  
• Antithrombotic therapy in patients with mechanical heart valves Aspirin:- 75-100 mg/day (in addition to warfarin) in all patients with aortic valve replacement or mitral valve replacement- 75-325 mg/day in patients who cannot take warfarin Warfarin goal INR 2.0-3.0: Aortic valve replacement if no risk factors are present* Warfarin goal INR 2.5-3.5:- Mitral valve replacement- Aortic valve replacement with presence of risk factors*- In the first 3 months after aortic valve replacement (weak recommendation) Risk factors include: Atrial fibrillation, severe left ventricular dysfunction (ejection fraction ≤ 30%), prior thromboembolism, or presence of hypercoagulable state
• Bacterial endocarditis prophylaxis High-risk cardiac conditions:- Prosthetic heart valve- Previous infective endocarditis- Structural valve abnormality in transplanted heart- Unrepaired cyanotic congenital heart disease- Repaired congenital heart disease with residual defect Indicated procedures & appropriate coverage:- Gingival manipulation or respiratory tract incision→ Viridans group Streptococcus coverage (eg, amoxicillin)- GU or GI tract procedure in setting of active infection→ Enterococcus coverage (eg, ampicillin)- Surgery on infected skin or muscle→ Staphylococcus coverage (eg, vancomycin)- Surgical placement of prosthetic cardiac material→ Staphylococcus coverage (eg, vancomycin)
• Treatment of symptomatic peripheral artery disease Step 1A- Risk factor management - Smoking cessation - Blood pressure & diabetes control - Antiplatelet & statin therapy Step 1B- Supervised exercise therapy Step 2 - Cilostazol (preferred over pentoxifylline) Step 3 - Revascularization for persistent symptoms Angioplasty ± stent placement - Autogenous or synthetic bypass graft
• Cardiac risk stratification for noncardiac surgical procedures Risk of cardiac death or nonfatal MI: High risk (>5%)Type of surgery:- Aortic or other major vascular- Peripheral vascular- Risk of cardiac death or nonfatal MI Risk of cardiac death or nonfatal MI: Intermediate risk (1%-5%)Type of surgery- Carotid endarterectomy- Head & neck- Intraperitoneal & intrathoracic- Orthopedic- Prostate Risk of cardiac death or nonfatal MI: Low risk (<1%)Type of surgery:- Ambulatory or superficial procedure- Endoscopic procedure- Cataract- Breast
• Brugada syndrome Rare autosomal dominant condition that affects sodium channels and disturbs repolarization Epidemiology: most common in Asian males Clinical features- Often an incidental finding, as patients are mostly asymptomatic- Syncope- Sudden cardiac death Diagnosis:- Brugada pattern on ECG: Pseudo-RBBB with ST elevation in leads V1-2- Rule out underlying heart disease (e.g., stress test and echocardiography) Treatment:- Implantable cardiac defibrillator (ICD) placement- Screen all 1st-degree relatives annually with clinical exam and ECG
• Cardiac injury Possible injuries- Cardiac contusion: Clinical features depend on the extent of the injury.→ Cardiac arrhythmia (palpitations, dizziness, syncope)→ Hypotension and tachycardia that do not respond to fluid resuscitation  - Myocardial rupture: hypotension, muffled heart sounds→ Most patients die before reaching the hospital.- Septal or valvular injury- Acute coronary syndrome Diagnostics:- Best initial test: ultrasound (FAST)  - ECG and echocardiography   Treatment- Cardiac monitoring- Cardiac rupture: immediate surgery

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