Summary
Highlights
A patient presenting with myopericarditis is discussed, highlighted by a triphasic rub, recent viral URI, diffuse ST elevations, and elevated troponin, indicating myocardial involvement. The rapid clinical deterioration in this case distinguishes it from typical pericarditis. Myocarditis, inflammation of the heart muscle, can range from asymptomatic to fulminant, with common causes including Coxsackie virus and, more recently, coronavirus. Giant cell myocarditis is discussed as a rapidly progressive and often fatal form requiring immunosuppression and close monitoring.
A patient with QT prolongation induced by haloperidol is presented, leading to Torsades de Pointes. The characteristic sine wave pattern of Torsades is shown, and treatment with electricity (defibrillation) and magnesium is discussed. The role of bradycardia in precipitating Torsades and the use of pacing or isoproterenol to shorten the RR interval are explained. Monomorphic VT is also briefly shown for recognition.
An ECG showing Wenckebach phenomena (Mobitz Type 1 second-degree AV block) is analyzed. This rhythm is characterized by progressive PR prolongation followed by a dropped QRS, and is generally considered benign, requiring only reassurance and avoidance of nodal blocking agents. The different types of AV block (first-degree, Mobitz I, Mobitz II, and third-degree) are explained with their ECG characteristics, emphasizing prognosis and management differences.
A case of a hemodynamically unstable patient with rapid atrial fibrillation (irregularly irregular narrow complex tachycardia) highlights the need for immediate synchronized cardioversion. The limitations of various rate-controlling medications in unstable patients (hypotension, contraindications) are discussed. The overall strategy for AFib/AFlutter management involves rate control, rhythm control (electrical or pharmacological cardioversion), and anticoagulation based on CHADS-VASc score. Atrial flutter ECG recognition with sawtooth waves is also demonstrated.
An ECG showing scooped ST segments, a classic sign of digoxin toxicity, is presented. Symptoms of digoxin toxicity (nausea, vomiting, anorexia, yellow halos) and ECG findings (heightened vagal tone, increased automaticity, regularized AFib, scooped ST depressions, bi-directional VT) are reviewed. Digoxin's narrow therapeutic window makes toxicity a relevant board's topic.
A patient with stable angina, hypertension, and a normal EKG is presented. The optimal initial diagnostic step for boards is an exercise stress test without imaging, given the normal EKG and intermediate pretest probability. The rationale for choosing an exercise test over pharmacological stress tests or angiography in this stable setting is explained, focusing on assessing physiological response.
A patient with NSTEMI (chest pain, elevated troponin, ST depression, known CAD) receiving initial medical therapy is discussed. The crucial intervention among the options is high-intensity statin administration, which has mortality benefit, alongside aspirin, antiplatelet agents, beta-blockers, and anticoagulants. The 'MOANA' acronym is critically reviewed, emphasizing which components truly offer mortality benefits.
A patient with a late-presenting MI (2 days of pain) develops acute shortness of breath and hypotension, suggesting a mechanical complication. An echocardiogram is the essential diagnostic test. Mechanical complications include acute mitral regurgitation (papillary muscle rupture or tethering), ventricular septal rupture (VSR), and free wall rupture. Timing and hemodynamic consequences of each are detailed, emphasizing surgical intervention and temporizing measures.
A patient with inferior STEMI and symptoms of shock (hypotension, bradycardia) prompts suspicion for a right ventricular infarct. The diagnostic hallmark is ST elevation in V4R (right-sided ECG leads). RV infarcts cause preload dependence, require fluid resuscitation, inotropes, timely reperfusion, and often temporary pacing for bradyarrhythmias. The concept of an accelerated idioventricular rhythm (AIVR) as a 'reperfusion rhythm' is introduced, signifying successful reperfusion and generally not requiring antiarrhythmic treatment.
A patient with anterior STEMI complicated by cardiogenic shock (low cardiac index, elevated filling pressures, cold extremities) is presented. The choice of inotropic support (dobutamine pure inodilator) is discussed, contrasting it with vasopressors or vasodilators not indicated in this scenario. Hemodynamic parameters (nickels, quarters, dimes) are reviewed. The importance of differentiating cardiogenic shock from septic shock, especially with post-MI inflammatory response, is highlighted.
A patient with peripheral vascular disease and claudication has multiple risk factors and is on appropriate medications. The single most effective intervention for improving symptoms is an exercise program, which promotes collateral circulation. Risk factors for PAD (smoking, diabetes, hypertension) are reviewed, emphasizing atherosclerosis as a systemic illness. Aspirin is the mainstay of antiplatelet therapy in PAD, unless other indications dictate different therapy.
A 70-year-old gentleman with a smoking history requires a one-time abdominal ultrasound screening for AAA, as recommended by USPSTF for males aged 65-75 with any smoking history. Management criteria (diameter >5.5 cm or rapid growth) for surgical referral are also discussed.
A patient with a systolic ejection murmur decreasing with Valsalva and increasing with leg raise, plus a diastolic murmur, points to a bicuspid aortic valve with both aortic stenosis (AS) and aortic insufficiency (AI). The specific physical exam maneuvers differentiate AS from HOCM. Progression of AS symptoms (angina, syncope, dyspnea) indicates worsening prognosis. Replacement is indicated for symptomatic severe AS or if LV function declines. For chronic severe AI, replacement is indicated if symptoms appear or LV EF drops to <50%, or LV diameter >50mm.
Anticoagulation for mechanical heart valves requires warfarin, with specific INR goals: 2.0-3.0 for aortic valves (high-flow, less thrombosis risk) and 2.5-3.5 for mitral valves (low-flow, higher thrombosis risk). NOACs/DOACs are contraindicated. The complex management of mechanical valves during pregnancy, especially concerning warfarin dosage and switching to heparin, is highlighted.
A pregnant woman from Ghana with volume overload and a diastolic low-pitch rumble at the apex, consistent with mitral stenosis, is discussed. Treatment focuses on slowing heart rate (beta-blockers) to prolong diastole and improve LV filling, and diuretics for volume overload. Mitral balloon valvuloplasty is often a definitive treatment during pregnancy. Classic physical exam findings for mitral stenosis include opening snap and loud S1. Indications for intervention (symptomatic, severe MS, elevated pulmonary pressures) are reviewed.
A patient with multiple cardiac risk factors undergoing surgery is able to climb one flight of stairs without dyspnea or chest pain (functional capacity of ~4 METs). This indicates no need for stress testing prior to surgery, as good functional capacity predicts good outcomes. The current guidelines for perioperative cardiac assessment, emphasizing functional status over routine stress testing, are explained. Revascularization for stable CAD does not improve perioperative prognosis.
A patient with Marfan's syndrome presenting with acute chest and back pain, and a CT scan showing an aortic dissection flap, is a classic board's scenario. The genetic mutation (fibrillin-1) associated with Marfan's is relevant. Type A dissections (involving ascending aorta) are surgical emergencies, while Type B (descending aorta) are usually managed medically initially. IV labetalol is the agent of choice for blood pressure and heart rate control to reduce stress on the aortic wall. Avoidance of vasodilators is also emphasized.
The specific patient groups requiring antibiotic prophylaxis for dental procedures are reviewed: prosthetic cardiac valves, indwelling prosthetic material in the heart, previous endocarditis, and specific congenital heart diseases (unrepaired cyanotic, repaired within 6 months, or repaired with residual defects near a device/patch). Mitral valve prolapse is no longer an indication for prophylaxis.
A fixed split S2 on cardiac auscultation is pathognomonic for an atrial septal defect (ASD). The most common type is ostium secundum ASD, which often presents with increased right-sided volume due to left-to-right shunting.
Differentiation between venous stasis ulcers and arterial insufficiency ulcers is discussed. Venous stasis ulcers present with characteristic skin changes (diluted epithelium) and are often located over the medial malleolus, whereas arterial ulcers are typically distal, painful, and associated with hair loss and shiny skin. Normal ABI (ankle-brachial index) of 1.1 helps rule out arterial insufficiency.
Different classifications of hypertension in pregnancy are defined: chronic hypertension (diagnosed <20 weeks), preeclampsia/eclampsia (>20 weeks with proteinuria), gestational hypertension (>20 weeks without proteinuria), and preeclampsia superimposed on chronic hypertension. Management involves treating blood pressures >160 mmHg, with labetalol, nifedipine, or methyldopa as preferred agents. ACE inhibitors and ARBs are contraindicated due to fetal renal abnormalities. The lecture concludes by encouraging continued practice and critical thinking for board preparation.
The pathognomonic physical exam finding of an early systolic ejection murmur that accentuates with Valsalva and decreases with handgrip is linked to HOCM. The genetic basis (autosomal dominant, beta-myosin heavy chain mutation) and its association with sudden cardiac death in athletes are discussed. The dynamic nature of LV outflow obstruction and how different maneuvers affect the murmur are detailed. Treatment options include beta-blockers/verapamil, septal myectomy, or alcohol septal ablation, and ICD placement for high-risk features.
Dr. Lorrel Brown introduces a cardiology review designed for internal medicine boards, emphasizing that cardiovascular disease is the highest represented discipline on the ABIM exam. The lecture will use board-style multiple-choice questions to prompt discussion across major categories like cardiomyopathy, arrhythmia, ischemia, and valvular disease, encouraging viewers to pause and select an answer before listening to the explanation.
The first question discusses a patient with incidentally discovered systolic heart failure (EF 25%) on lisinopril and carvedilol. The best option is switching lisinopril to an ARNI (sacubitril/valsartan), due to superior mortality benefit per 2017 guidelines. Other common heart failure medications and their roles are also reviewed, including diuretics for symptom relief, aldosterone antagonists, and the role of isosorbide dinitrate/hydralazine in African American patients. The new algorithm for heart failure treatment is presented, emphasizing ARNI as a preferred first-line therapy. Device therapies like ICDs and CRT for specific patient profiles are also discussed, including criteria for EF, QRS width, and LBBB.
A case of new cardiomyopathy with regional wall motion abnormality in a patient with risk factors (diabetes, hypertension, tobacco abuse) is presented. The discussion highlights the importance of evaluating for ischemic cardiomyopathy in such patients. Given the patient's risk factors, a coronary angiogram is chosen as the gold standard diagnostic test, over stress tests which might yield false negatives.
A classic presentation of Takotsubo (stress) cardiomyopathy, often triggered by emotional or physical stress, is reviewed. Key diagnostic features include mild troponin elevation disproportionate to LV dysfunction, diffuse T-wave inversions/QT prolongation on ECG, apical akinesis on echocardiogram, and non-obstructive coronary artery disease. Three classic ballooning patterns (apical, mid-ventricular, basal) are explained. The condition is reversible.
A patient with cancer and chemotherapy-induced pericardial effusion presenting with hypotension, elevated JVD, clear lungs, low-voltage ECG, and an enlarged cardiac silhouette suggests cardiac tamponade. The most expedient bedside test is pulsus paradoxus evaluation. Tamponade is a clinical diagnosis where increased intrapericardial pressure impairs ventricular filling, leading to decreased cardiac output. The physiologic basis of pulsus paradoxus is explained, alongside other signs like electrical alternans on ECG.