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Cardiology IM Board Review

Diagnostic Studies and Imaging

  • Chest X-Ray (CXR): Recognize key findings:

    • Aortic dissection: Widened mediastinum (prominent aortic knob).
    • Heart failure: Cardiomegaly, cephalization of flow, Kerley B lines, costophrenic angle blunting.
    • Pericardial effusion: “Water bottle” cardiac silhouette (globular enlarged heart): often due to uremia (e.g. missed dialysis).
    • Constrictive pericarditis: Pericardial calcification on CXR; may see a “skull around the heart” (heart encased by calcified pericardium).
    • Pacemaker lead displacement: Abnormal lead position on CXR with pacing symptoms (e.g. diaphragmatic pacing causing hiccups). Rib notching on CXR suggests coarctation of aorta (enlarged intercostals eroding ribs).

  • Transthoracic Echocardiography (TTE): First-line cardiac imaging for structure and function:

    • Indications: Wall-motion abnormalities (e.g. RV dyskinesis in PE: McConnell’s sign, apical ballooning in stress cardiomyopathy), suspected valve lesions (murmur grade ≥II/VI), new arrhythmia, unexplained embolic stroke (looking for cardiac thrombus), aortic root disease (e.g. Marfan aneurysm), evaluation of fixed split S2 (e.g. atrial septal defect on echo).
    • Avoid unnecessary TTE in low-risk scenarios: Innocent murmurs (soft, mid-systolic flow murmurs), benign postpartum mammary souffle (changes with chest pressure), stable mild valve disease or chronic HF without change. (Follow mild valve lesions clinically and echo only every ~3 years; moderate/severe yearly).

  • Transesophageal Echocardiography (TEE): High-resolution imaging of small structures:

    • Use for suspected endocarditis (detect vegetations, abscess): e.g. Staph aureus bacteremia, prosthetic valves.
    • Use intraoperatively in valve surgeries and to guide transcatheter interventions (e.g. TAVR, ASD closure).
    • Ideal in critical ill when TTE windows are poor (intubated, obese, chest trauma). Example: TEE visualizing large mitral valve vegetation and abscess in endocarditis with heart block.

  • Cardiac Stress Testing: Choose modality based on patient’s exercise ability and ECG:

    • Exercise Treadmill ECG (no imaging): Appropriate if patient can exercise to >85% max HR and has a normal baseline ECG (no LBBB, LVH strain, WPW, or paced rhythm). Avoid in acute MI, unstable angina, aortic dissection, PE, or pericarditis.

      • Positive findings: ST depression ≥1 mm (especially at low workload or early in test), drop in BP, ventricular arrhythmias, or slow recovery of heart rate indicate high-risk ischemia. These should prompt angiography.
      • A normal exercise stress test confers a “1-year warranty” (low event rate for ~12 months).

    • Stress Imaging (Perfusion scan or Stress Echo): Indicated if baseline ECG is not interpretable (e.g. LBBB, ventricular pacing, WPW, or >1 mm ST depression at rest). In these cases, use exercise or pharmacologic stress with imaging (nuclear or echo) to detect ischemia.

      • Nuclear (MPI): Uses vasodilators (adenosine/regadenoson) or dobutamine. Perfusion defects: at rest, tracer uptake is uniform; with vasodilator, healthy arteries hyper-dilate while stenotic arteries maximally dilated at baseline can’t further increase flow → relative cold spots (perfusion defects). Reversible defect = ischemia; fixed defect = scar.
      • Stress Echocardiography: Uses exercise or dobutamine. Wall-motion abnormality with stress (new akinesis or dyskinesis) indicates ischemia; a resting wall-motion abnormality that persists = infarct scar.
    • Pharmacologic stress: Use adenosine or regadenoson for vasodilation (contraindicated in bronchospastic disease) and dobutamine for patients who cannot exercise (increases HR/contractility).
    • High-risk stress test findings: e.g. ischemia at low workload or in multiple territories, warrant prompt cardiac catheterization.

  • Cardiac Catheterization (Angiography):

    • Indications: Acute STEMI (primary PCI within 90 minutes); unstable NSTEMI/high-risk ACS (TIMI ≥3) for early invasive management; persistent angina despite medical therapy or high-risk stress test findings.
    • Timing: Door-to-balloon goal <90 min="" pci="" hospital="" or="" 120="" min="" transfer="" for="" stemi="" if="" pci="" delay="">120 min and presentation <12 hours of symptom onset, give fibrinolysis first.
    • Complications (≈6% morbidity): Vascular injury (hematoma, retroperitoneal bleed: Grey Turner sign: flank bruising), pseudoaneurysm or AV fistula at access site, stroke, acute MI, emergency CABG, arrhythmia, allergic contrast reaction, cholesterol embolization (blue toe syndrome, livedo reticularis, renal failure, eosinophilia). Monitor for back pain or hypotension (suspect RP hemorrhage).
    • Cholesterol Embolization Syndrome: Presents days post-cath with fever, blue/purple toes, livedo reticularis, renal failure, and eosinophils in blood/urine. No specific treatment; manage supportively and avoid further invasive procedures if possible.

  • Coronary CT Angiography (CCTA): Noninvasive coronary visualization (high sensitivity ~95-99%). Requires careful patient selection: Heart rate <60 in sinus rhythm, IV contrast (need adequate renal function), and ability to hold breath ~15s. Use: R/O CAD in low-to-intermediate risk chest pain in ED or to identify anomalous coronaries. Not suitable in active AF, very high calcium burden, or renal failure.

    • Coronary Calcium Score: CT without contrast to detect calcified plaque. Agatston score 0 = very low CAD risk (excludes significant CAD as cause of symptoms). Higher scores correlate with atherosclerosis (e.g. >400 indicates severe disease).

  • Cardiac MRI (CMR): Best for tissue characterization and congenital anatomy. Identifies infiltrative cardiomyopathy (e.g. amyloidosis vs. sarcoid by late gadolinium enhancement patterns). Gold standard for volumes and ventricular function; can assess perfusion and viability too. Example: Clearly identified an atrial myxoma when echo images were suboptimal. Not first-line for CAD diagnosis (limited role in detecting coronary stenoses).

 

Physical Exam Clues in Cardiology

  • Jugular Venous Pressure (JVP): Elevated JVP reflects right atrial pressure. Differential for an elevated JVP includes right HF, pulmonary embolism, tamponade or constrictive pericarditis, severe TR, SVC obstruction.

    • Kussmaul’s sign (JVP rise on inspiration) suggests constrictive pericarditis or RV infarction; absent y-descent suggests tamponade.

  • Pulsus Paradoxus: An exaggerated >10 mmHg drop in systolic BP on inspiration, causing a weaker radial pulse during inspiration. Causes: Cardiac Tamponade, Constrictive pericarditis, severe asthma/COPD, and tension pneumothorax. (Mnemonic: C.A.R.D.: Cardiac tamponade, Asthma/COPD, Restrictive pericarditis, D (tension) pneumothorax: the “car driving cat”). In tamponade, look for Beck’s triad: Hypotension, JVD, muffled heart sounds.

  • Heart Sounds: S2 Splitting:

    • Physiologic Split S2: Normal: Inspiration delays P2 (more RV filling) and hastens A2 (less LV filling), causing A2…P2 with inspiration (audible “lub–da–dub”).
    • Wide Splitting: Persistent split that widens on inspiration: e.g. RBBB or Pulmonic Stenosis (P2 delay), or severe MR (early A2) combined with pulmonary HTN (late P2). Example: Chronic severe MR with pulmonary hypertension causes a wide, variable split S2 (A2 early from MR, P2 late from high RV pressure).
    • Fixed Split S2: Atrial Septal Defect (ASD): Fixed A2--P2 interval unaffected by respiration. Often with a systolic flow murmur at left upper sternal border and RBBB on ECG. Secundum ASD: RAE, Right axis deviation & RSR′ pattern (incomplete RBBB) on ECG. Indication to close ASD: Left-to-right shunt with Qp\:Qs >1.5:1 (and no severe pulmonary HTN).
    • Paradoxical Split S2: Left bundle branch block, severe aortic stenosis: delayed A2 causes P2 to occur before A2 (split on expiration, single on inspiration). LBBB causes A2 delay; on inspiration P2 moves later and “catches up” to the delayed A2, eliminating the split.

  • Extra Heart Sounds:

    • S3 Gallop: Early diastolic “ventricular gallop” after S2. Indicates volume overload or floppy ventricle (inrush of blood decelerating). Heard best with bell at apex in left lateral decubitus, during expiration. Causes: HFrEF (systolic dysfunction), severe MR or AR, high-output states (VSD, PDA). Can be physiologic in young (<40) or high-output (fever, anemia, pregnancy, thyrotoxicosis).
    • S4 Gallop: Late diastolic “atrial kick” sound before S1. Due to atrial contraction against a stiff ventricle. Seen in LVH (hypertension, AS) or acute MI. Absent in AF (needs atrial contraction).
    • Opening Snap (OS): High-pitched sound after S2 in mitral stenosis (MS). The shorter the S2–OS interval, the more severe the MS (higher LA pressure snaps valve sooner). MS also has a low-pitched rumbling diastolic murmur with presystolic accentuation.

  • Murmur Maneuvers (Preload dependency):

    • Valsalva strain & Standing (↓venous return): Increases intensity of mitral valve prolapse (click moves earlier) and hypertrophic obstructive cardiomyopathy (HOCM) murmurs, while decreasing most others (AS, MR, etc).
    • Squatting or Leg Raise (↑venous return/afterload): Decreases HOCM and MVP murmurs (more volume reduces obstruction/prolapse), increases regurgitant and VSD murmurs (more flow).
    • Handgrip (↑afterload): Diminishes forward-flow murmurs (AS, HOCM), intensifies backward-flow murmurs (MR, VSD, AR).
    • Inspiration: Increases right-sided murmurs (e.g. tricuspid regurg) by increasing venous return to RV. Expiration accentuates left-sided murmurs.

 

Coronary Artery Disease (CAD) and Acute Coronary Syndromes

  • Coronary Risk Factors: Classic: HTN, hyperlipidemia, smoking, diabetes, age, family history. Newly recognized risk enhancers (especially in women): history of preeclampsia, gestational HTN or diabetes, premature menopause, chronic inflammatory diseases (RA, SLE, psoriasis), HIV infection, and CKD. These factors further heighten CAD risk beyond traditional factors.

  • Stable Ischemic Angina: Usually exertional chest pressure relieved by rest or nitroglycerin. Initial evaluation with stress testing (see above) if intermediate pre-test probability. Medical management is first-line: beta-blockers, nitrates, +/- calcium blockers for symptom control; high-intensity statin and risk factor control for prevention.

    • PCI vs. CABG vs. Medical Therapy: Revascularization is indicated for symptom relief if meds fail, or for prognosis if high-risk anatomy. CABG improves survival in left main disease, 3-vessel disease (or 2-vessel with proximal LAD) especially in diabetics or low EF. Otherwise, PCI can relieve angina but generally does not extend life in stable CAD.
    • Microvascular Angina (Cardiac X Syndrome): Angina with positive stress test but normal coronaries on cath. Due to small arteriole dysfunction. Treat same as CAD (beta-blockers, etc.): improves symptoms, though no stenting needed.

  • Acute Coronary Syndromes (ACS): Encompasses Unstable Angina (UA), NSTEMI, STEMI. Typically caused by plaque rupture and thrombosis. May present classically with crushing chest pain radiating to arm or jaw, or atypically with dyspnea, fatigue, nausea (more common in women, diabetics, elderly).

    • Initial Management (ACS): Within minutes of arrival: chew aspirin 325 mg (reduces mortality), obtain ECG and cardiac markers, brief targeted history & exam, and begin MONA-B (Morphine for pain, Oxygen if sat <90%, Nitrates for pain, Anticoagulation with heparin, Beta-blocker if no contraindication). Start high-intensity statin early. Assess risk (e.g. TIMI score) to guide further therapy.

    • ECG Changes:

      • NSTEMI/UA: ST depressions and/or T-wave inversions (transient). No ST elevation or Q-waves.
      • STEMI: Initially may see hyperacute peaked T-waves, then ST elevations in contiguous leads, followed hours later by Q-waves and T-wave inversions. Evolution: ST elev → Q waves (within 6-24h).
      • Localizing STEMI: Elevations in V1-V4 = anterior (LAD); I, aVL, V5-V6 = lateral (circumflex); II, III, aVF = inferior (RCA in 80%). Example: ST elevation in I, aVL, V5-6 and V1-4 indicates left main occlusion (anterolateral MI).
      • LBBB and STEMI: A new LBBB with hemodynamic instability or heart failure is a STEMI-equivalent (emergent cath). For known old LBBB, use Sgarbossa criteria: concordant ST elevation ≥1 mm or excessively discordant ≥5 mm suggests infarct.
    • Cardiac Biomarkers: Troponin-I/T rise by ~4-6 hours, peak ~24 hours, remain elevated ~7-14 days. Troponin is sensitive but not specific (can elevate in CHF, sepsis, myocarditis): interpret with clinical context.

  • NSTEMI/Unstable Angina Management:

    • Antithrombotic Therapy: Dual antiplatelet (ASA + P2Y₁₂ inhibitor like clopidogrel or ticagrelor): give clopidogrel loading dose unless high bleeding risk or immediate surgery planned. Anticoagulate with IV heparin (or enoxaparin/bivalirudin). Consider IV GP IIb/IIIa inhibitors (eptifibatide, tirofiban) for very high-risk or if urgent PCI is planned: these act immediately to block platelet aggregation.
    • Anti-ischemic meds: Oxygen if hypoxic; beta-blockers (oral or IV) within 24h (reduces arrhythmia and recurrent MI): avoid if acute HF, low output, or high-degree AV block. Nitrates for pain (avoid if RV infarct or hypotension). High-intensity statin (stabilizes plaque).

    • Risk Stratification: Calculate TIMI Risk Score (AMERICA mnemonic: Age ≥65, Markers (elevated troponin), ECG ST deviation, Risk factors ≥3, Ischemic episodes ≥2 in 24h, CAD known (≥50% stenosis), ASA use in last 7d). TIMI ≥3 → benefit from early invasive strategy. Low TIMI (0–1) → consider conservative management with stress test (ischemia-guided strategy).

      • Other high-risk features favoring early cath: new heart failure or EF <40%, recurrent angina or arrhythmias despite therapy, hemodynamic instability, or recent PCI/CABG.
    • Early Invasive vs Conservative: For high-risk NSTEMI (TIMI ≥3 or features above), proceed to angiography + PCI within 24–48 hours. In lower-risk, can treat medically and perform stress test later (“ischemia-guided”). Persistent chest pain or ST changes despite treatment also mandates urgent cath. Example: Ongoing pain and dynamic ST depressions in a 41F NSTEMI despite meds: requires urgent cath (not stress test or fibrinolysis).

  • STEMI Reperfusion Therapy:

    • Primary PCI (preferred): If available within 90 min (up to 120 min if transfer needed). Stenting restores patency and treats underlying lesion (improves outcomes vs fibrinolysis). Door-to-balloon goal: 90 min.

      • If initial fibrinolysis was given (e.g. due to delay), arrange rescue PCI as soon as possible; even if lytic successful, plan angiography during hospitalization (within 24 hours).
      • Bare-metal vs Drug-eluting stents: DES are standard (reduce restenosis). Bare-metal stents reserved if patient has very high bleeding risk or imminent surgery so cannot take prolonged dual antiplatelet therapy.

    • Fibrinolysis: Indicated if PCI unavailable within 120 min and symptom onset <12h (can consider up to 24h if ongoing pain and large area at risk). Give tPA (alteplase), TNK-tPA, or reteplase: fibrin-specific agents preferred over streptokinase.

      • Contraindications (absolute): Any prior intracranial hemorrhage, known cerebral AVM or tumor, ischemic stroke in past 3 months (except acute stroke under 4.5h for which tPA is indicated), active bleeding, aortic dissection, significant closed head or facial trauma within 3 months, intracranial or spinal surgery <2 months, severe uncontrolled HTN, or recent streptokinase use (<6 months, due to antibodies).
      • After lysis, initiate heparin and transfer to PCI-capable center: up to 50% re-occlude if no stent, so plan definitive therapy once stable.

    • Adjunct meds in STEMI: Same DAPT and anticoagulation as NSTEMI. Start beta-blocker early (if no contraindications): reduces ventricular arrhythmias and mortality (especially important in large MIs). Begin ACE inhibitor by 24h, especially if anterior MI, low EF, or CHF, to limit remodeling (prevent ventricle dilation and fibrosis via RAAS blockade). Aldosterone antagonists (eplerenone) improve outcomes post-MI in EF ≤40% with HF or diabetes.

      • Avoid beta-blockers acutely if signs of cardiogenic shock, severe HF, or high-grade AV block. Contraindicated if acute cocaine intoxication (unopposed alpha can worsen vasospasm): use benzodiazepines and nitrates for cocaine-related ACS.
    • Monitoring: Watch for reperfusion arrhythmias (accelerated idioventricular rhythm is common and benign after reperfusion). Initiate cardiac rehab and aggressive risk factor management on discharge.

  • ACS Complications:

    • Arrhythmias: Ventricular fibrillation is the leading cause of early death: most episodes occur in first 48 hours (why continuous telemetry is required). Primary VF within 48h doesn’t mandate an ICD if EF recovers; VF after 48h (secondary to scar) indicates high risk: consider ICD before discharge. Sustained VT >48h post-MI also warrants ICD for secondary prevention. Temporary arrhythmias like non-sustained VT can be managed with IV amiodarone and electrolytes.
    • Bradyarrhythmias: Inferior MI may cause AV node ischemia (transient block); anterior MI causing new bundle branch block is more ominous. High-degree AV block in MI may require temporary pacing.

    • Mechanical: Occur 2–7 days post-MI (when necrotic tissue weakens):

      • Papillary muscle rupture (often inferior MI: RCA supplies posteromedial pap muscle): acute severe mitral regurgitation → pulmonary edema, shock. Look for new holosystolic murmur and rapid decline. Surgical emergency (repair/replace valve).
      • Ventricular septal rupture (usually large anterior MI: LAD): acute VSD causes biventricular failure and a new harsh murmur with thrill. Requires urgent surgical repair; can stabilize with afterload reduction and mechanical support if available.
      • Free wall rupture (usually anterior MI, older hypertensive females, or those on NSAIDs/delayed reperfusion): leads to cardiac tamponade (PEA arrest, hypotension, JVD). Often fatal; emergent pericardiocentesis and surgical repair needed if caught early.
      • All these often present as acute deterioration a few days after MI (recurrent chest pain, shock). If suspect mechanical complication, get emergent echo to diagnose (VSD vs regurg vs effusion) while calling surgical team.
    • Cardiogenic Shock: Large infarcts (≥40% LV) can cause pump failure. Presents with persistent hypotension, cool extremities, pulmonary edema. Treat with inotropes (dobutamine) and urgent revascularization. Intra-aortic balloon pump (IABP) can support temporarily (especially for acute MR or VSD) by reducing afterload and improving coronary perfusion.
    • Pericarditis: Acute pericarditis can occur 2–4 days post-MI (inflammation over necrotic area). Presents with pleuritic chest pain and pericardial rub; treat with high-dose aspirin (avoid NSAIDs/steroids early post-MI to not impair healing). Dressler syndrome is an autoimmune pericarditis weeks after MI, treated with NSAIDs.
    • Ventricular aneurysm: Late complication (weeks) of a transmural MI: persistent ST elevations on ECG, and LV apical dyskinesis on imaging. Can lead to thrombus formation (requires anticoagulation) or arrhythmias.

 

Hyperlipidemia Management

  • Statin Therapy: Key Groups: (Remember “Choose A Statin”: Clinical ASCVD, Above 190 LDL, Sugar (diabetes) or high Score)

    1. Clinical ASCVD (CAD, stroke, PAD): High-intensity statin for age ≤75; moderate if >75. Aim LDL reduction ≥50%.
    2. Severe hyperlipidemia (LDL ≥ 190): High-intensity statin (likely familial hypercholesterolemia).
    3. Diabetes (age 40–75, LDL 70–189): At least moderate-intensity statin (even if 10-yr risk <7.5%). If diabetic + ASCVD risk ≥7.5%, consider high-intensity.

    4. Intermediate Risk (10-year ASCVD ≥7.5%): Moderate-intensity statin if age 40–75 (consider risk enhancers). Borderline risk (5–7.4%) may also benefit if multiple risk enhancers present.

    5. Risk Enhancers: Family history premature ASCVD, high lifetime risk, South Asian ethnicity, inflammatory diseases, CKD, metabolic syndrome, Lp(a) elevation, high coronary calcium, etc. These favor statin use even if risk slightly below threshold.

  • Statin Intensity: High: atorvastatin 40–80 mg, rosuvastatin 20–40 mg. Moderate: atorva 10–20, rosuva 5–10, simva 20–40, pravastatin 40, etc.

    • Statin Adverse Effects: Monitor LFTs and CK. Discontinue if ALT >3× ULN or CK >10× ULN (rhabdomyolysis). Manage mild myalgias by lowering dose or switching statin (e.g. to pravastatin, which is hydrophilic and often better tolerated).

  • Non-Statin Therapy:

    • Ezetimibe: First add-on if LDL above goal or statin not tolerated. Lowers LDL ~20% by reducing intestinal cholesterol absorption.
    • PCSK9 Inhibitors: (e.g. evolocumab, alirocumab): Injectable antibodies that drastically lower LDL. High-cost; reserved for familial hypercholesterolemia or very high-risk patients not at goal on max therapy.
    • Fibrates: Not first-line unless triglycerides >500 mg/dL (to prevent pancreatitis). Outcome data for CHD prevention is poor.
    • Niacin: No longer routinely recommended: no additional ASCVD benefit and causes side effects.
  • Hypertriglyceridemia: If TG ≥500, consider fibrates or high-dose omega-3 to prevent pancreatitis, but focus on lifestyle (diet, glycemic control). Statins primarily target LDL but also modestly reduce TG.

 

Arrhythmias and Conduction Disorders

  • Atrial Fibrillation (AF): Irregularly irregular rhythm with no distinct P waves. Often from ectopic foci (usually near pulmonary veins in left atrium). Classified as: Paroxysmal (self-terminates in <7 days), Persistent (>7 days or needs cardioversion), Long-standing (>12 months), or Permanent (accepted). May be asymptomatic or cause palpitations, fatigue, dyspnea, dizziness. Common precipitants: hypertension, HF, valvular disease, hyperthyroid, alcohol (“holiday heart”).

    • Rate vs Rhythm Control: Large trials (e.g. AFFIRM) show rate control with AV nodal blockers is usually as effective as attempting sinus rhythm, except in those who remain very symptomatic in AF. Thus, for most patients, control ventricular rate and anticoagulate. Pursue rhythm control (antiarrhythmics or ablation) in patients who have intolerable symptoms or heart failure exacerbated by AF.
    • Rate Control Meds: Target resting HR <80–110 (lenient control <110 is often acceptable if symptoms controlled). Use beta-blockers (metoprolol, atenolol) or non-dihydropyridine CCB (diltiazem, verapamil) as first-line. Add digoxin in HFrEF or sedentary patients if needed (especially helpful for rate control at rest). In acute AF with RVR, IV metoprolol or diltiazem are typical; IV amiodarone if refractory or if AF + acute HF hypotension. Avoid CCB in decompensated HFrEF.
    • Rhythm Control: Options include electrical cardioversion (synchronized DC shock) and antiarrhythmic drugs (Class IC like flecainide/propafenone for structurally normal hearts, or Class III like sotalol, dofetilide, amiodarone for structural heart disease). Catheter ablation (pulmonary vein isolation) is effective in paroxysmal AF or if drug therapy fails. Ensure proper anticoagulation for several weeks before elective cardioversion if AF >48h (to avoid stroke from atrial thrombus).
    • Unstable AF (AF with hypotension, acute HF, or angina): immediate synchronized cardioversion is indicated.

    • Anticoagulation in AF: Determined by CHA₂DS₂-VASc score for non-valvular AF. Calculate: CHF (1), HTN (1), A₂ge ≥75 (2), Diabetes (1), S₂ Stroke/TIA history (2), Vascular disease (1), Age 65–74 (1), Sc = Sex category female (1 if ≥1 other factor).

      • Score 0 (men) or 0–1 (women) → low risk, no anticoagulation needed.
      • Score 1 (men) or 2 (women) → consider anticoagulation (oral anticoagulation is favored over aspirin as monotherapy since aspirin is weak in AF).
      • Score ≥2 (men) or ≥3 (women) → Anticoagulate (DOAC preferred).
      • DOACs (direct oral anticoagulants) are first-line in non-valvular AF: e.g. dabigatran (direct thrombin inhibitor) 150 mg BID if normal renal function (reduce to 75 mg BID if CrCl 15–30), rivaroxaban, apixaban, edoxaban. They have equal or better stroke prevention and less intracranial bleeding vs warfarin. Avoid DOAC if mechanical valve or moderate-to-severe mitral stenosis: those “valvular AF” cases require warfarin (goal INR 2–3).
      • In AF + mechanical heart valve or rheumatic MS: Warfarin is indicated (target INR 2.5–3.5 for mechanical mitral, 2.0–3.0 for mechanical aortic): DOACs are not used in these patients.
      • Left Atrial Appendage Occlusion (Watchman device) is an option if high stroke risk but contraindication to anticoagulation.
      • Note: Aspirin (± clopidogrel) is insufficient for stroke prevention in most AF patients and is only considered if CHA₂DS₂-VASc is 1 and bleeding risk is very high.
    • Valvular AF: AF in the setting of mechanical valves or rheumatic mitral stenosis is high risk: always anticoagulate with warfarin (target per valve type).
    • Hypertrophic Cardiomyopathy AF: Treat as non-valvular: DOAC now recommended first-line, because HCM AF carries high stroke risk.
    • Rate vs Rhythm Outcomes: If rate-controlled and symptom-free, staying in AF is acceptable. If patients have heart failure due to AF or cannot tolerate AF, aim for rhythm control (e.g. AF ablation can improve EF in tachycardia-induced cardiomyopathy).

  • Atrial Flutter: Typically a regular narrow complex tachycardia, atrial rate ~300 with “sawtooth” flutter waves (usually 2:1 AV block → ~150 bpm). Type I (typical) is a cavotricuspid isthmus-dependent circuit in right atrium (counterclockwise around tricuspid annulus).

    • Patients may have palpitations, fatigue, or hemodynamic compromise if rate is very fast. Treat similar to AF: rate control (beta-blocker/CCB), anticoagulation (flutter often progresses to AF, so stroke risk is considered the same). If unstable, cardiovert.
    • Catheter ablation of the flutter circuit is the definitive treatment: ~95% success in curing typical atrial flutter. It is indicated in symptomatic recurrent flutter, as patients often relapse quickly after cardioversion alone.

  • Supraventricular Tachycardias (SVT): Reentrant tachycardias originating above ventricles → narrow QRS (unless aberrant conduction). AV Nodal Reentrant Tachycardia (AVNRT) is most common: dual pathways in AV node form a loop (typically presents as sudden palpitations in young women). AV Reentrant Tachycardia (AVRT) involves an accessory pathway (e.g. WPW: anterograde conduction via AV node, retrograde via accessory Kent bundle, causing orthodromic SVT).

    • SVT usually has abrupt onset/termination (“paroxysmal SVT”) and heart rate 160–220 bpm. P waves may be hidden in QRS or shortly after.
    • Acute management: If unstable (hypotension, angina, acute HF), do immediate synchronized cardioversion. If stable, start with vagal maneuvers (Valsalva, carotid sinus massage) to slow AV node. If unsuccessful, give IV adenosine (6 mg rapid push, then 12 mg): transient AV block often terminates AVNRT/AVRT. Alternatively, IV diltiazem or beta-blocker can be used.
    • Long-term: For recurrent symptomatic SVT, catheter ablation is highly effective (especially for WPW or AVNRT). Note: In WPW patients, avoid AV nodal blocking agents (beta-blocker, CCB, digoxin) if they develop AF with WPW: blocking the AV node can cause preferential conduction down the accessory pathway → very rapid ventricular rates or torsades/VFib. Instead, use IV procainamide for AF in WPW.
    • WPW Pattern: Short PR interval <120 ms and delta wave (slurred QRS upstroke) on resting ECG. WPW syndrome = WPW + symptomatic tachyarrhythmias (AVRT or AF). Treat WPW tachycardias with ablation of accessory pathway for cure.

  • Ventricular Tachycardia (VT): Wide QRS (>120ms) tachycardia originating in ventricles. Monomorphic VT: consistent QRS morphology, usually due to a scar reentry (post-MI). Polymorphic VT: varying QRS, typically from acute ischemia or long QT (Torsades de Pointes).

    • Sustained VT (>30s or requiring intervention) can cause hypotension, syncope, or degenerate to VF. Pulseless VT or VF → immediate unsynchronized defibrillation (ACLS protocol). Unstable VT with a pulse → synchronized cardioversion. Stable VT → try IV antiarrhythmics (amiodarone or lidocaine) and arrange expert consultation.
    • Torsades de Pointes: A form of polymorphic VT in the setting of QT prolongation (congenital or drug-induced). ECG shows twisting QRS axis around baseline (“party streamer” appearance). Causes include antiarrhythmics (class Ia, III), certain antidepressants/antipsychotics, electrolyte disturbances (low K, Mg, Ca). Treat acute torsades with IV magnesium sulfate (even if Mg level normal) and remove offending cause. Temporary pacing to increase heart rate can also shorten QT and terminate torsades. Defibrillate if torsades persists and causes hemodynamic collapse.
    • Primary VT Prevention: Implantable cardioverter-defibrillator (ICD) indicated in: survivors of VF or sustained VT (secondary prevention), and in EF ≤35% due to prior MI or nonischemic cardiomyopathy after ≥3 months of optimal medical therapy (primary prevention). ICD improves survival by aborting lethal arrhythmias. Example: Patient with EF 29% 1 year post-MI on GDMT should get an ICD: waiting or meds alone is insufficient, as risk of sudden death is high.
    • VT Storm: ≥3 episodes of sustained VT/VF in 24h: requires aggressive management (IV antiarrhythmics, sedation, ablation).

  • Bradyarrhythmias & Heart Block:

    • AV Block Mobitz II or 3° (Complete) Heart Block often necessitates a permanent pacemaker. Look for cannon A waves in JVP in complete heart block (atria and ventricles dissociated). In acute setting (e.g. inferior MI causing AV block), may use temporary pacing.
    • Sick Sinus Syndrome: Symptomatic sinus bradycardia or sinus pauses, often alternating with paroxysmal AF (“tachy-brady syndrome”). Treatment is pacemaker implantation (for brady) plus rate control or antiarrhythmic for tachy episodes as needed.

  • Sudden Cardiac Death (SCD) in Young Athletes: Usually due to lethal arrhythmia (VF) during exercise. Key causes (often autosomal dominant hereditary conditions):

    • Hypertrophic Cardiomyopathy (HCM): #1 cause in US. Often asymptomatic or with exertional syncope. Pre-participation sports screens look for murmur that increases with Valsalva (HOCM) and family history. ICD indicated in high-risk HCM (see below).
    • Congenital Coronary Artery Anomalies: #2 cause in US. Anomalous origin of left coronary from the right sinus (or vice versa) can cause compression of artery between great vessels → ischemia or SCD during exercise. Any symptomatic coronary anomaly, or origin from pulmonary artery, warrants surgical repair.
    • Myocarditis: (often due to Coxsackie virus) can cause acute DCM and fatal arrhythmias in athletes. Suspect if recent viral illness.
    • Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC): Fibrofatty infiltration of RV → VT (especially in young males, can present as exercise syncope/SCD). Epsilon wave on ECG. Requires ICD and activity restriction.

    • Primary Electrical Diseases:

      • Long QT Syndrome: Congenital (e.g. Jervell, Romano-Ward) or acquired long QT leads to torsades. Triggered by exercise or acoustic stimuli in certain subtypes. Treat with beta-blockers; ICD if history of syncope or sustained arrhythmia.
      • Brugada Syndrome: Sodium channelopathy in Asian males; ECG: persistent ST elevation V1–V3 with RBBB-like pattern. High risk of polymorphic VT/v-fib: managed with ICD.
      • Catecholaminergic Polymorphic VT (CPVT): Stress/exercise-induced polymorphic VT/VF in a structurally normal heart (often in children). Treat with beta-blockers and ICD.
      • WPW Syndrome: Can rarely cause SCD if AF conducts rapidly via accessory pathway → VF. (See WPW, treat accessory pathway).
      • Commotio Cordis: Sudden VF from blunt chest trauma in ventricular repolarization phase (e.g. baseball to chest). Prevention with chest protectors; treatment is defib.
    • Valvular/Aortic: Bicuspid Aortic Valve (can lead to early severe AS), Marfan Syndrome (risk of aortic dissection/rupture), Severe PS, Coarctation of Aorta. These structural issues can also cause exertional sudden death (e.g. rupture of aorta in Marfan).

 

Cardiomyopathies

  • Hypertrophic Cardiomyopathy (HCM): Usually autosomal dominant sarcomere gene mutations (β-myosin heavy chain, etc) leading to asymmetric septal hypertrophy. Causes LV outflow tract (LVOT) obstruction from septal wall and systolic anterior motion (SAM) of mitral valve. Key findings: harsh crescendo-decrescendo systolic murmur (similar to AS but ↑ with Valsalva/standing, ↓ with squatting/handgrip), may have bifid carotid pulse. Apical beat is forceful and sustained. Can cause exertional angina, syncope, or SCD.

    • Echo: Septal wall thickness ≥15 mm, systolic anterior mitral motion, and Doppler gradient. ECG: LVH signs (tall R in V₅/V₆, deep S in V₁), often with giant Q waves in inferolateral leads from septal hypertrophy. If TTE is equivocal and suspicion high, get cardiac MRI for detail. Screen first-degree relatives (echo +/- genetic testing): HCM is familial.
    • Treatment: First-line: β-blockers (non-vasodilating) to slow HR and prolong diastole. Can use verapamil or diltiazem if beta-blockers inadequate. Goal resting HR <60 to improve filling and coronary perfusion. Advise hydration and avoid excessive vasodilation (no nitrates or ACEi: they worsen obstruction by reducing afterload).
    • If significant LVOT gradient (≥50 mmHg) and symptoms persist despite meds: consider septal reduction. Options: Surgical myectomy (gold standard, especially if other cardiac surgery needed) or Alcohol septal ablation via catheter to create controlled infarction in septum. Both reduce obstruction and improve symptoms, but do not eliminate arrhythmia risk. Mitral valve surgery may be needed if obstruction due to abnormal mitral apparatus.
    • Risk of SCD: HCM is a leading cause of SCD in young. ICD indicated for: survivors of cardiac arrest or sustained VT/VF, or high-risk features (e.g. syncope with VT, family history of sudden death, massive septal thickness ≥30 mm, nonsustained VT on Holter, abnormal BP response to exercise). Discuss ICD for primary prevention if multiple risk factors. Note: Septal ablation/surgery does not reduce arrhythmogenic risk: risk comes from diffuse myocardial disarray (histology) predisposing to reentry.
    • Activity: HCM patients should avoid high-intensity competitive sports due to SCD risk.
    • Special: If AF develops in HCM, anticoagulate (increased stroke risk) and consider rhythm control (AF poorly tolerated).

  • Dilated Cardiomyopathy (DCM): Systolic dysfunction leading to enlarged ventricle(s) and reduced EF. Causes: Ischemic heart disease (post-MI remodeling), long-standing uncontrolled HTN, valvular disease; Non-ischemic causes include myocarditis (viral), alcohol abuse, chemotherapy (e.g. doxorubicin), tachycardia-mediated (chronic high-rate like rapid AF), peripartum cardiomyopathy, genetic mutations, and infiltrative diseases (late stage).

    • Presents with signs of heart failure: dyspnea, fatigue, edema. Treat HFrEF per guidelines (see Heart Failure section): ACEi/ARNI, beta-blocker, diuretics, spironolactone, ICD if EF ≤35%. Address reversible causes (revascularize CAD, abstain from alcohol, control rate in AF, etc.). Consider transplant or LVAD if end-stage (Stage D).
    • Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC): A subtype of DCM affecting RV (fibrofatty replacement). Presents with VT or SCD in young; treat with ICD and avoid exercise.

  • Restrictive Cardiomyopathy (RCM): Diastolic dysfunction: heart muscle is stiff, limiting filling, with usually preserved EF. Causes: Amyloidosis (most common; look for speckled myocardium on echo, apple-green birefringence with Congo Red stain), Sarcoidosis (noncaseating granulomas, can also cause arrhythmias/AV block), Hemochromatosis (iron deposition, often also causes dilated features), Fabry disease, endomyocardial fibrosis, radiation heart disease.

    • Signs: Right-sided HF > left (JVP, edema, ascites) with a relatively normal-sized heart. Distinguish from constrictive pericarditis: RCM will have elevated BNP (released from stressed myocardium), and no pericardial knock or calcifications. Constriction (pericardial disease) often has equalization of diastolic pressures and interventricular interaction (Kussmaul’s, etc.), whereas RCM is myocardial.
    • Treatment: Treat the underlying cause if possible (chelation for hemochromatosis, steroids for sarcoid, etc). Diuretics for symptom relief of congestion. In amyloid, avoid digoxin (binds to amyloid fibers and can cause toxicity). Prognosis varies by cause; amyloid and idiopathic RCM often have poor outcomes unless transplant.

  • Stress Cardiomyopathy (Takotsubo): Acute, transient apical ballooning (dilated apex) with hypercontractile base, often triggered by severe emotional or physical stress (“broken heart syndrome”). Mimics MI (chest pain, ST elevations, troponin rise) but no obstructive CAD on angiogram. Recovers in days to weeks. Treat supportively (like HF) and follow-up imaging to confirm recovery.

 

Heart Failure (CHF)

  • Definitions: HFrEF (Heart Failure with Reduced EF): LVEF ≤40% (systolic dysfunction). HFpEF (Preserved EF): EF ≥50% (diastolic dysfunction). Intermediate EF 41–49% sometimes termed HFmrEF. Stage vs NYHA Class: ACC/AHA Stages A–D (based on disease progression) and NYHA Classes I–IV (based on symptoms with activity).

    • HFpEF (Diastolic HF): Often due to long-standing HTN (LVH) or aging, also infiltrative disease. EF normal but heart can’t relax. Treat contributing factors: manage BP, control rate in AF (they are very preload-sensitive), diuretics for edema. No therapies yet proven to improve mortality specifically in HFpEF, though newer trials with SGLT2 inhibitors show promise. Clues: HF symptoms with normal EF, often elevated BP, LVH on echo.
    • HFrEF (Systolic HF): Many causes (ischemic, myocarditis, valvular, etc.). EF low, dilated LV. Clues: displaced apical impulse, S3 gallop, functional MR/TR due to dilation. This has many proven therapies (see below).

  • Signs/Symptoms: Left HF: dyspnea, orthopnea, PND, crackles, S3 (if systolic). Right HF: JVD, hepatic congestion, ascites, edema. Chronic HF may have cachexia. BNP is a helpful marker: <100 pg="" ml="" makes="" hf="" unlikely="" cause="" of="" dyspnea="" while="">500 is more suggestive (intermediate values gray zone).

  • ACC/AHA Stages of HF:

    • Stage A: High risk with no structural disease (e.g. HTN, CAD, DM). Manage risk factors: ACE inhibitor or ARB for vascular protection (especially in DM or post-MI), Statin if indicated.
    • Stage B: Structural heart disease but no symptoms (e.g. low EF, LVH, prior MI, asymptomatic valve disease). Interventions: Beta blockers and ACEi/ARNI to prevent progression. If prior MI or LVEF ≤35%, this patient qualifies for ICD for primary prevention of sudden death. Revascularize if appropriate (e.g. CABG for ischemic cardiomyopathy). Our case patient with EF 29% post-MI is Stage B and needed ICD.
    • Stage C: Structural disease with past or current symptoms (most diagnosed HF patients). Manage: Dietary sodium restriction, daily weights, and GDMT medications (see below) to improve symptoms & survival. Diuretics (loop diuretics like furosemide) for volume overload: improve symptoms but do not prolong survival (symptom control only). Titrate beta-blockers and ACEi/ARNI to target doses as tolerated. Add aldosterone antagonist and hydralazine–nitrate as indicated. Many Stage C patients will be NYHA II or III. Consider CRT (biventricular pacing) if LBBB with QRS ≥150 ms and EF ≤35% (improves symptoms and mortality).
    • Stage D: Refractory end-stage HF (symptoms at rest, frequent hospitalizations). Options: Advanced therapies: inotropes (dobutamine infusion) or mechanical circulatory support (LVAD), cardiac transplant evaluation. Focus on palliative care: discuss ICD deactivation, hospice for poor candidates of advanced therapies.

  • Heart Failure Medications (HFrEF): “The Fantastic Four”: These improve survival in HFrEF (NYHA class II–IV unless contraindicated):

    • ACE Inhibitors (or ARBs): e.g. lisinopril, enalapril (or valsartan, etc.). Reduce afterload and preload, limit remodeling via RAAS blockade: improve symptoms and mortality. Indicated for all patients with HFrEF or Stage B with low EF. Side effects: cough (ACEi), hyperkalemia, renal impairment, angioedema.
    • ARNI (Angiotensin Receptor-Neprilysin Inhibitor): Sacubitril/valsartan (Entresto) has replaced ACEi/ARB in NYHA II–III HFrEF for further mortality reduction. Initiation: If transitioning from ACEi, allow a 36-hour washout to avoid angioedema. Start 49/51 mg BID and titrate to 97/103 mg BID over 2–4 weeks as tolerated. Improves outcomes beyond ACEi.
    • Beta-Blockers: Proven ones: Carvedilol, Metoprolol succinate, Bisoprolol. Start low dose after patient is stabilized (not in acute decompensation). Titrate every 2 weeks toward target (e.g. carvedilol ~25 mg BID, metoprolol XL 200 mg daily) or until heart rate ~60 or symptomatic hypotension. Beta-blockers reduce arrhythmia risk, improve EF over time, and reduce mortality. Do not start if patient is wet and cold (decompensated): wait until IV diuretics/off pressors.
    • Mineralocorticoid Receptor Antagonists: Spironolactone or eplerenone. Indicated in HFrEF (EF ≤35%) NYHA II–IV after ACEi (or ARNI) + beta-blocker, provided K+ <5.0 and GFR >30. Reduce mortality and hospitalizations (RALES, EPHESUS trials). Start 12.5–25 mg, target 25–50 mg daily (aim for 50 mg if tolerated, as trials showed dose-dependent benefit). Monitor K and renal function for hyperkalemia.
    • Hydralazine + Isosorbide Dinitrate: Adds survival benefit in African American patients with HFrEF NYHA III–IV on above therapy. Also indicated in any patient who cannot tolerate ACEi/ARB (e.g. due to renal failure or hyperkalemia). Improves outcomes in A-HeFT trial. Typical dosing: hydralazine 75 mg TID + isosorbide dinitrate 40 mg TID. Side effects: headache, hypotension.

  • Devices:

    • ICD: Prevents sudden death from arrhythmias. Indicated in EF ≤35% (ischemic or nonischemic) after ≥3–6 months of optimized therapy, NYHA II–III (Class I indication). Also secondary prevention if survived VT/VF arrest (unless within 48h of MI).
    • CRT (Biventricular Pacing): Indicated if EF ≤35%, LBBB with QRS ≥150 ms, NYHA II–IV symptoms on meds. Improves synchronization and cardiac output, reduces mortality. Often combined with ICD (CRT-D).
    • Advanced Support: LVADs (implantable pumps) can bridge to transplant or destination therapy in end-stage HF. Heart transplant for eligible Stage D patients (improves survival and quality of life). Palliative inotropes (e.g. home milrinone) sometimes used for symptom control in those not transplant candidates, but long-term inotropes increase mortality.

  • Acute Decompensated HF (Pulmonary Edema): Presenting with severe dyspnea, rales, often hypertension, +/- pink frothy sputum. Treat with LMNO: Lasix (IV loop diuretic), Morphine (venodilator, use sparingly), Nitrates (reduce afterload/preload if BP allows), Oxygen/ventilatory support (CPAP/BiPAP for acute pulmonary edema can reduce need for intubation). If in cardiogenic shock, use IV inotrope (dobutamine) and possibly mechanical support (IABP or impella).

  • Other HF Therapies:

    • Loop Diuretics: Symptom relief only. Use to treat congestion (edema, JVD, pulmonary edema). Furosemide, torsemide, bumetanide are mainstay for volume control. If diuretic resistance, increase dose, switch to bumetanide, or add metolazone. Monitor renal function and electrolytes.
    • Digoxin: In HFrEF, decreases symptoms and hospitalizations but does not improve survival. Consider in patients with persistent symptoms despite GDMT, especially if they also have AF with rapid rate. Keep level <1.0 ng/mL to avoid toxicity (risk higher in renal failure, low K). Signs of toxicity: GI upset, confusion, visual changes, arrhythmias (PVCs or AV block).
    • Ivabradine: Sinus node If channel inhibitor: slows heart rate without lowering BP. Indicated in NYHA II–III HFrEF with EF ≤35% who are in sinus rhythm with resting HR ≥70 bpm despite max beta-blocker (or if beta-blocker contraindicated). Shown to reduce HF hospitalizations (SHIFT trial). Do not use if AF or sick sinus (needs sinus rhythm to work).
    • Vasopressin Antagonists: (Tolvaptan) can be used short-term in hospitalized HF patients with severe hyponatremia (helps raise Na by causing free water excretion).
    • Acute inotropes: (dobutamine, milrinone) are IV only: used in acute cardiogenic shock or as a bridge in advanced HF. Chronic outpatient inotrope infusions may palliate symptoms in stage D but increase arrhythmia risk.
    • Neprilysin inhibitors (ARNI) are now preferred over ACEi if possible, as noted above.
    • Iron supplementation: IV iron has been shown to improve exercise capacity in HF patients with iron deficiency (ferritin <100 or iron sat <20%).

 

Valvular Heart Disease

  • Aortic Stenosis (AS): Usually due to calcific degeneration (age >70) or congenital bicuspid aortic valve (younger patients; ~1% pop.). Causes a harsh crescendo-decrescendo systolic murmur (best at right upper sternal border, radiating to carotids). Pulses parvus et tardus (weak and delayed carotid upstroke) if severe. Symptoms: Angina, Syncope, HF (triad of severe AS). Once symptomatic, prognosis is poor without intervention (~2–5 years).

    • Severity: Severe AS criteria: Valve area <1.0 cm², jet velocity ≥4 m/s, or mean gradient ≥40 mmHg. On exam, severe AS murmur peaks late in systole and S2 is soft (or single as A2 soft).

    • Indications for AVR (Aortic Valve Replacement):

      • Symptomatic severe AS (any symptoms: angina, syncope, dyspnea): Class I indication for valve replacement.
      • Asymptomatic severe AS with LVEF <50% or if undergoing other cardiac surgery: also intervene.
      • Severe AS with abnormal exercise test or very high gradient (>60 mmHg) may also warrant early intervention.
    • “5–4–1 Rule” (mnemonic): Severe AS if Aortic jet >4 m/s, Mean gradient >40 mmHg, and critical valve area ~1.0 cm²; if EF <50% (the “5” part, i.e. <0.5 or <50%) even without symptoms, operate.
    • Low-Flow, Low-Gradient AS: In patients with low EF, AS may appear less severe (low gradient) due to low flow. Use dobutamine stress echo to distinguish true severe AS from pseudo-stenosis: if with increased contractility the calculated gradient jumps to severe range (≥40 mmHg or velocity ≥4 m/s) then AS is truly severe. If gradient stays low despite output rise, valve is not the primary issue (more likely dilated cardiomyopathy).

    • Treatment: Surgical AVR or Transcatheter AVR (TAVR). Surgical AVR is preferred in younger, low-surgical-risk patients (and often if concurrent CABG needed). TAVR is indicated in older (>65–70) or high surgical risk patients: catheter valve deployed within the old valve. TAVR has become alternative even in moderate-risk patients.

      • Bicuspid valves and very young patients still generally surgical (and bicuspid often have aortopathy that might need repair).
    • Heyde’s Syndrome: Severe AS can cause angiodysplasia in colon and bleeding (acquired vWF deficiency). Remarkably, aortic valve replacement can stop the GI bleeding.

  • Aortic Regurgitation (AR): Causes: Valve leaflet disease (bicuspid valve, endocarditis, rheumatic) or aortic root dilation (Marfan, aneurysm, dissection, syphilis). Acute AR (e.g. aortic dissection or valve infection) causes flash pulmonary edema and cardiogenic shock: a surgical emergency. Chronic AR leads to volume overload of LV → eccentric hypertrophy.

    • Murmur: High-pitched blowing decrescendo diastolic murmur at left sternal border, intensified by patient sitting up, leaning forward, end-expiration. Wide pulse pressure is hallmark (e.g. BP 160/60). Bounding “water-hammer” pulse (Corrigan pulse), head bobbing (De Musset sign), capillary pulsations in nail beds (Quincke sign) are classic peripheral signs of AR from high stroke volume and rapid runoff. In acute AR, these signs may be absent (no time for compensation).
    • Acute AR: (e.g. post-endocarditis or aortic root tear): presents with acute pulmonary edema, hypotension. Treat emergently: vasodilators + inotropes (e.g. IV nitroprusside + dobutamine) to stabilize, avoid beta-blockers. Urgent surgery is definitive.

    • Chronic AR: Often asymptomatic for years due to compensation. When advanced, causes DOE, pounding heartbeat sensations.

      • Indications for surgery (chronic AR): Symptomatic severe AR (regardless of EF): Class I. Asymptomatic severe AR if LVEF <55% or LV end-systolic diameter >50 mm (the “55 rule”: operate when EF <55% or LVESD >55). These thresholds indicate beginning LV dysfunction: intervene to prevent irreversible damage. Also consider if end-diastolic diameter >65 mm.
      • Medical therapy: While waiting for surgery or if not a candidate, use vasodilators (ACEi, nifedipine) to reduce afterload and improve forward flow. Treat systolic hypertension aggressively. Avoid bradycardia (long diastole worsens regurgitant volume).
      • Follow-up: In asymptomatic AR not yet at criteria, monitor with serial echocardiograms every 6–12 months for EF and diameter changes.

  • Mitral Stenosis (MS): Almost all cases due to rheumatic fever (years/decades after infection) causing thickening and fusion of mitral valve leaflets. Predominantly affects females. Leads to high left atrial pressure → pulmonary HTN and AF. Presents with dyspnea, fatigue, and often hemoptysis or hoarseness (Ortner’s syndrome from LA compressing laryngeal nerve). Pregnancy or AF onset may precipitate symptoms.

    • Exam: Opening snap after S2, followed by a low-pitched rumbling mid-diastolic murmur best heard at apex with patient in left lateral decubitus. A shorter S2–OS interval = more severe MS (higher LA pressure snaps valve open sooner). Signs of pulmonary HTN (loud P2, RV heave) often present in advanced MS.
    • Severity: Normal MV area ~4–6 cm². Severe MS if area ≤1.5 cm². LA enlarges on CXR (straightened left heart border, double density). Enlarged LA can cause AFib (very common in MS) and dysphagia (esophageal compression).
    • Treatment: If symptomatic severe MS (≤1.5 cm²), and valve morphology is favorable (pliable, non-calcified, no significant MR or thrombus), do Percutaneous Balloon Mitral Valvuloplasty (PBMV): preferred over surgery if anatomy suitable. Suitability is graded by Wilkins score (leaflet thickening, mobility, calcification, subvalvular fusion: score ≤8 is ideal for balloon). If not a candidate for balloon, perform surgical repair or replacement.
    • Medical: Beta-blockers or nondihydropyridine CCBs can slow heart rate to prolong diastolic filling time, improving symptoms. Diuretics for congestion. Anticoagulate if AF is present (MS + AF carries high stroke risk). Infective endocarditis prophylaxis for dental work if MS is rheumatic?: guidelines usually only for prosthetic valves or history of endocarditis, but some older practice did for rheumatic MS with prior interventions.

  • Mitral Regurgitation (MR): Etiologies: Primary (valve): MVP (myxomatous degeneration) is most common cause in developed countries, also rheumatic, endocarditis, flail leaflet/chordae rupture (myxomatous or post-MI pap muscle rupture). Secondary (functional): LV dilation (ischemic or non-ischemic cardiomyopathy) causing annular stretch and papillary displacement.

    • Murmur: Holosystolic “blowing” murmur best heard at apex radiating to axilla. Intensity increases with handgrip (↑afterload) and in left lateral decubitus. Severe MR: S3 often present (high volume flow back into LA). Acute severe MR (papillary rupture) can present with soft or minimal murmur but acute pulmonary edema and shock.
    • Acute MR: (e.g. papillary muscle rupture in inferior MI, chordae tendineae rupture in MVP, or acute endocarditis): causes abrupt volume overload. Presents as flash pulmonary edema and hypotension. Emergent stabilization with vasodilators (nitroprusside) and IABP can help reduce regurgitation while awaiting urgent surgical repair. An Intra-aortic balloon pump in acute MR can reduce afterload and improve forward output. Definitive: urgent valve surgery.

    • Chronic MR: The LV and LA enlarge to compensate, so patient may be asymptomatic for long period. Eventually causes volume-overload HF (fatigue, dyspnea) and often AF due to LA dilation.

      • Indications: Surgery (repair preferred): Symptomatic severe MR (EF >30%): Class I for surgery. Asymptomatic severe MR if EF <60% or LV end-systolic diameter ≥40 mm (even without symptoms, LV is starting to fail: “60/40 rule” for MR). Note EF >60% in MR is actually “normal-plus” due to forward/backward flow; once EF drops <60, systolic dysfunction is present. Also consider surgery if new onset AF or pulmonary HTN in setting of severe MR. If EF <30% or advanced HF, surgery is high risk and outcomes are poorer: may consider if refractory symptoms, otherwise manage medically or consider transplant if applicable.
      • Preferred Intervention: Mitral valve repair (annuloplasty) is favored over replacement for degenerative MR if feasible, as it preserves LV function and has lower mortality. Repair is highly successful especially for posterior leaflet prolapse.
      • Transcatheter option: For high-surgical-risk patients with significant MR, MitraClip (edge-to-edge percutaneous repair) can reduce MR and improve symptoms. It essentially clips anterior and posterior leaflets together at mid-point (creating a double-orifice valve) to reduce regurgitation.
      • If MR is secondary (functional) due to LV dysfunction, address the HF (often CRT can reduce MR if LBBB present). Sometimes MitraClip is used for secondary MR if persistent despite GDMT.
    • Mitral Valve Prolapse (MVP): Redundant myxomatous valve bows into LA in systole; mid-systolic click ± late systolic murmur. Often asymptomatic; may cause palpitations or atypical chest pain. MVP murmur/click occur earlier and louder with maneuvers that decrease LV volume (standing, Valsalva). Most cases mild; severe MVP can cause MR (flail leaflet). Endocarditis prophylaxis not indicated unless prior endocarditis.

  • Tricuspid Regurgitation (TR): Most commonly functional (due to RV enlargement from left HF or cor pulmonale). Holosystolic murmur ↑ with inspiration (Carvallo’s sign). Treat underlying cause; consider tricuspid annuloplasty if severe during left heart valve surgery. IV drug use causes tricuspid endocarditis: septic emboli to lung.

  • Prosthetic Heart Valves:

    • Mechanical Valves: Durable (last decades) but require lifelong anticoagulation. Warfarin + low-dose aspirin is now recommended for all mechanical valve patients: this combination lowers thromboembolism risk. INR targets: Mitral mechanical: target INR 3.0; Aortic mechanical: target 2.5 (if standard bileaflet). (Older guidelines gave ranges 2.5–3.5 and 2.0–3.0 respectively, but current emphasize specific targets). Mechanical valves are favored in younger patients (<50–60) due to longevity.
    • Bioprosthetic Valves: (Porcine or bovine): No long-term anticoagulation (just aspirin after 3–6 months). Less durable (degenerate in ~10–15 years). Often chosen in age >70. After surgical bioprosthesis, give warfarin for first 3 months (INR ~2.5) until endothelialization occurs. Transcatheter aortic valve replacements (TAVR) typically require dual antiplatelet for 3–6 months then single antiplatelet.
    • Valve Replacement Peri-op Management: Minor procedures (dental, skin): continue warfarin if INR in range; for major surgery, hold warfarin ~5 days prior. Bridge with heparin if mechanical mitral or older caged-ball valves, as these are higher risk. (Mechanical aortic valves without risk factors can often be managed by simply restarting warfarin soon after surgery without bridging).
    • Prosthetic Valve Thrombosis: Suspect if new murmur or HF in prosthetic patient: urgent fluoro or TEE can confirm. Treat with thrombolysis for stuck right-sided valves or small thrombus; surgery for large thrombus or left-sided valves if high risk embolization.

 

Infective Endocarditis

  • Epidemiology & Organisms: Staphylococcus aureus is now the most common cause of endocarditis (acute presentations, often attacks normal valves). Viridans streptococci (e.g. S. mutans) classically cause subacute endocarditis on abnormal valves (e.g. after dental work). Enterococci: common in older men after GU manipulation. Staph epidermidis (coag-neg staph): common in prosthetic valve endocarditis (and devices). Culture-negative causes include HACEK organisms and Coxiella, Bartonella.

    • Valve involvement: Mitral valve is most often affected in native valve endocarditis. Tricuspid valve endocarditis is common in IV drug users (S. aureus, often MRSA): look for septic pulmonary emboli. Prosthetic valves and cardiac devices are often S. epidermidis or S. aureus.
  • Clinical Features: Fever, chills, night sweats, malaise are common. New or changing murmur in ~50%. Can present as acute sepsis (especially S. aureus) or indolent. Look for embolic phenomena: Janeway lesions: small, painless erythematous lesions on palms/soles (microemboli); Osler nodes: tender nodules on finger/toe pads (immune complex deposits); Roth spots: oval hemorrhages with pale center on retina (immune complex); splinter hemorrhages under nails; petechiae on conjunctiva or mucosa. Also possible: Septic emboli to brain (stroke/abscess), lung (if right-sided), kidney or spleen (infarcts). Glomerulonephritis and RF positive may occur (immune complex deposition).

  • Diagnosis: Use Modified Duke criteria: requires either 2 major, 1 major + 3 minor, or 5 minor for definitive diagnosis.

    • Major criteria: (1) Positive blood cultures for typical organisms (S. aureus, viridans strep, Strep gallolyticus (bovis), Enterococcus, HACEK) or persistent bacteremia; (2) Evidence of endocardial involvement (vegetation or abscess on echo, or new valve regurgitation).
    • Minor criteria: Fever ≥38°C, predisposition (IVDU, abnormal valve), vascular phenomena (emboli, Janeway lesions), immunologic phenomena (Osler nodes, Roth spots, GN, RF+), positive blood culture not meeting major criteria.
    • Workup: Draw 3 sets of blood cultures from different sites (before antibiotics if possible). Do TTE initially: if positive (vegetation seen) that’s usually sufficient. If TTE negative but suspicion remains high (especially if prosthetic valve or persistent bacteremia), proceed to TEE (much higher sensitivity ~90%). If TEE is also negative and no major criteria, reconsider diagnosis: could be culture-negative endocarditis (e.g. Coxiella, Bartonella: use serologies).
  • Management: IV antibiotics tailored to organism (4–6 weeks). Empiric for acute native valve: e.g. vancomycin + gentamicin while cultures pending (covers MRSA, strep, Enterococcus). Surgery (valve replacement) indications include: acute heart failure from valve destruction (e.g. acute MR), abscess or fistula on echo, difficult-to-treat organisms (fungi, multi-resistant), persistent bacteremia or enlarging vegetation despite antibiotics, or very large vegetations (>1 cm, especially if embolizing).
  • Endocarditis Prophylaxis: Antibiotic prophylaxis indicated for high-risk cardiac conditions before high-risk dental or invasive procedures. High-risk patients: prosthetic heart valve, prior infective endocarditis, certain congenital heart diseases (unrepaired cyanotic CHD, or repaired CHD with prosthetic material in first 6 months, or repaired CHD with residual defect), and cardiac transplant with valve regurgitation. Give Amoxicillin 2 g 30–60 min before dental procedures that involve gingival manipulation (if penicillin-allergic, use clindamycin 600 mg or azithromycin 500 mg). No prophylaxis needed for routine GI/GU procedures unless active infection present.

 

Peripheral Vascular Disease and Aortic Disease

  • Peripheral Arterial Disease (PAD): Atherosclerosis of arteries to legs (and arms). Risk factors: diabetes, smoking, HTN, hyperlipidemia. Often coexists with CAD (PAD patients “die from CAD”), so aggressive risk factor management is key.

    • Claudication: Exertional calf or thigh pain relieved with rest. Exam: diminished pulses, cool extremity, shiny skin, hair loss. Ankle-Brachial Index (ABI) is first-line diagnostic: ABI <0.9 = PAD (normal 1.0–1.4). Calculate ABI as highest ankle systolic pressure divided by highest brachial pressure. ABI 0.91–0.99 is borderline; <0.8 moderate="" 0="" 4="" severe="" if="" abi="">1.40* (noncompressible vessels from calcification, e.g. diabetes), do toe-brachial index or arterial ultrasound.
    • Claudication vs Pseudoclaudication: Lumbar spinal stenosis (neurogenic claudication) causes bilateral leg pain/numbness when standing or downhill walking, relieved by flexion (e.g. leaning on shopping cart). Vascular claudication is exercise-induced and relieved just by rest (position doesn’t matter). Our case: pain worse walking downhill and relief leaning forward = spinal stenosis, confirmed by MRI of lumbar spine.
    • Management: Exercise therapy is first-line for claudication: supervised exercise training 30–45 min ≥3 days/week for ≥12 weeks improves walking distance. Smoking cessation is crucial: encourage and assist by any means (it markedly accelerates PAD). Antiplatelet therapy (aspirin or clopidogrel) recommended to reduce CV events. Control BP and lipids (PAD patients benefit from statin). Cilostazol (PDE-3 inhibitor) can improve claudication symptoms and walking distance: use only if EF is normal (contraindicated in heart failure due to increased mortality in HF patients). Mnemonic: Cilostazol for Claudication in patients with Competent Cardiac output (no HF).
    • Revascularization: Indicated if lifestyle-limiting claudication refractory to medical therapy or if critical limb ischemia (rest pain, nonhealing ulcers). Options: endovascular angioplasty/stenting for focal lesions or surgical bypass for extensive disease. Obtain arterial imaging (e.g. arterial Doppler ultrasound, CT/MR angiography) to map disease when intervention is considered.
    • Critical Limb Ischemia: Rest pain, ulcers, or gangrene: urgent vascular consultation for possible revascularization to save limb. Acute limb ischemia (6 Ps: pain, pallor, pulseless, poikilothermia, paresthesia, paralysis) is an emergency: usually due to embolus or thrombosis; manage with immediate heparin and surgical or catheter thrombolysis/embolectomy.

  • Abdominal Aortic Aneurysm (AAA): Focal aortic dilation ≥3.0 cm (usually infrarenal). Risk: older males, smoking history (most important risk factor), HTN, family history. Often asymptomatic until large or ruptured. Palpable pulsatile abdominal mass or seen on imaging.

    • Screening: One-time abdominal ultrasound is recommended for men 65–75 who have ever smoked. (Some extend to men ≥65 with family history of AAA). This has high yield: our lecturer keeps it on his template and has found several.
    • Management: Elective repair indicated for diameter ≥5.5 cm in men (≥5.0 cm in women), or if growing >0.5 cm in 6 months. Between 4.0–5.4 cm, monitor periodically with imaging (frequency depends on size). Repair can be open surgical or endovascular stent graft (EVAR). Ruptured AAA presents with acute back/abd pain, hypotension: surgical emergency (50% die before reaching hospital).

  • Aortic Dissection: Tear in intima creates a false lumen. Risk: HTN, connective tissue disorders (Marfan, Ehlers-Danlos), bicuspid aortic valve, cocaine use. Presents with sudden sharp “tearing” chest or back pain, asymmetric BP in arms. CXR may show widened mediastinum. Diagnose with CT angiography (TEE if unstable). Stanford Type A (ascending aorta) requires emergent surgery; Type B (descending only) managed medically (aggressive BP and HR control with IV beta-blocker, nitroprusside as needed).

  • Renal Artery Stenosis: Consider in resistant HTN, flash pulmonary edema, diffuse atherosclerosis, or onset of HTN <30 fibromuscular="" dysplasia="" in="" young="" females:="" string="" of="" beads="" appearance="" clue:="" rise="" in="" creatinine="">30% when starting ACE inhibitor (suggests bilateral RAS). Diagnosis by renal Doppler U/S or MR/CT angio. Treat atherosclerotic RAS with BP control (ACEi/ARB careful in unilateral) and statin; fibromuscular dysplasia can be cured with angioplasty.

  • Carotid Artery Disease: Carotid bruit may indicate stenosis. Carotid endarterectomy (CEA) indicated for symptomatic carotid stenosis ≥70%, or ≥50% in certain cases, to prevent stroke. In asymptomatic, consider CEA if stenosis >70–80% and low surgical risk. Otherwise manage with intensive medical therapy (statin, BP control, antiplatelet). Carotid stenting is alternative if high surgical risk.

 

Pulmonary Circulation & Heart-Lung Interactions

  • Pulmonary Hypertension (PH): Mean pulmonary artery pressure ≥25 mmHg at rest by right heart cath (updated guidelines now say ≥20 mmHg, but boards often use 25). Presents with exertional dyspnea, fatigue, and maybe signs of RV failure (edema, JVD, loud P2). Exam: loud S2 (P2), RV heave, possibly TR murmur.

    • WHO Groups: Group 1: Pulmonary arterial hypertension (PAH): idiopathic (primary), heritable (BMPR2 mutation), connective tissue diseases (scleroderma), HIV, portal HTN, drugs (e.g. anorexigens, methamphetamines), schistosomiasis. This is pre-capillary PH (normal LV). Group 2: PH due to left heart disease (e.g. HF, valvular disease): post-capillary PH (elevated PCWP). Group 3: PH due to lung diseases or hypoxemia (COPD, interstitial lung disease, sleep apnea, high altitude). Group 4: Chronic thromboembolic PH (CTEPH): recurrent or unresolved PE (treatable with pulmonary endarterectomy or balloon angioplasty, and anticoagulation). Group 5: PH with unclear/multifactorial mechanisms (e.g. sarcoidosis, hemoglobinopathies).
    • General Measures: Treat the underlying cause (e.g. oxygen for COPD, left HF therapy, anticoagulation for CTEPH). All PH patients: O₂ to keep sats >90% (hypoxia causes vasoconstriction). Diuretics (loop ± spironolactone) for right HF symptoms. Avoid excessive volume depletion though (preload dependent). Exercise training as tolerated.

    • Pulmonary Arterial Hypertension (Group 1): Often young women with idiopathic PAH. Poor prognosis if untreated (median survival ~7–10 years). All patients should undergo vasoreactivity testing during RHC: give inhaled NO or IV epoprostenol and see if mean PAP falls ≥10 mmHg to ≤40 mmHg with normal output. If positive responder, treat with high-dose calcium channel blocker (e.g. nifedipine or diltiazem): these patients can do very well long-term on CCB alone. Only ~10% of idiopathic PAH are responders.

      • If non-responsive or fails CCB: use targeted PAH therapy. Current strategy often initial combination therapy (per AMBITION trial): Endothelin receptor antagonists (e.g. ambrisentan, bosentan) to vasodilate and reduce remodeling + PDE-5 inhibitor (e.g. tadalafil, sildenafil) to augment NO: improves exercise capacity and delays progression. Other agents: Prostacyclin analogs (IV epoprostenol, SQ treprostinil, inhaled iloprost) for advanced cases: improve symptoms and survival in idiopathic PAH. Soluble guanylate cyclase stimulators (riociguat) for CTEPH or PAH.
      • PAH patients are at risk of in-situ pulmonary artery thrombosis: many experts anticoagulate idiopathic PAH with warfarin (unless contraindicated).
      • Eventually, lung transplant (or heart-lung transplant if concomitant HF) is the definitive option for eligible patients once medical therapy fails.
    • Cor Pulmonale: Refers to right ventricular enlargement/failure due to lung disease (Group 3 PH). Chronic COPD is a common cause. Manifests as edema, hepatomegaly, JVD, with signs of lung disease (barrel chest, hypoxia). Treat the lung disease (O₂ for COPD), diuretics for RV edema (cautiously), and in some cases vasodilators if appropriate. Acute cor pulmonale from massive PE can cause acute RHF and cardiovascular collapse.

  • Eisenmenger Syndrome: The final stage of an uncorrected large left-to-right shunt (usually VSD, PDA, or AV canal). Chronic high-flow, high-pressure pulmonary blood flow → pulmonary arterial hypertension → shunt reversal to right-to-left. Causes cyanosis, clubbing, polycythemia after reversal (often in adolescence/early adulthood). Example: A large VSD or AVSD present from birth, unrepaired: initially causes CHF in childhood, then as pulmonary resistance rises, the shunt reverses and patient develops cyanosis and clubbing. Once Eisenmenger develops, the pulmonary vascular changes are irreversible: the only cure is heart-lung transplant. Do NOT close the shunt at this point, as it’s a safety valve for the RV: closing it can precipitate RV failure. Management is supportive (oxygen, phlebotomy for hyperviscosity) and advanced PH therapy if applicable. Pregnancy is very high risk (50% mortality) in Eisenmenger: contraindicated.