NEET SS Cardiology (DM) Flashcards

24 sample cards from the Cardiology (DM) deck

Sampled from the end of the deck, so these are different cards from the ones shown on the syllabus page.

1. List the indications for cardiac resynchronization therapy (CRT) in heart failure.

   LVEF <=35%, sinus rhythm, NYHA II-IV on optimal GDMT, with QRS >=150 ms and LBBB morphology = strongest (Class I) benefit. Benefit is attenuated with QRS 120-149 ms or non-LBBB. CRT improves dyssynchrony, symptoms, and survival.

2. State the severity criteria and indications for intervention in severe aortic stenosis.

   Severe AS: aortic valve area <1.0 cm2, mean gradient >=40 mmHg, peak jet velocity >=4 m/s. Intervene (SAVR or TAVR) for symptomatic severe AS, or asymptomatic severe AS with LVEF <50%, undergoing other cardiac surgery, or very severe/abnormal stress test. TAVR favored in higher surgical risk/older patients.

3. Contrast acute vs chronic mitral regurgitation in presentation and management.

   Acute MR (e.g., papillary muscle rupture, endocarditis): sudden pulmonary edema/cardiogenic shock, normal-sized LA/LV, soft murmur - needs urgent surgery. Chronic primary MR: gradual LA/LV dilation, AF, holosystolic apical murmur radiating to axilla; operate when symptomatic or LVEF <=60% or LVESD >=40 mm. Mitral repair preferred over replacement.

4. What are the auscultatory and intervention features of mitral stenosis?

   Loud S1, opening snap, low-pitched mid-diastolic rumble at apex (best in left lateral decubitus); shorter S2-OS interval indicates more severe disease. Usually rheumatic. Severe: valve area <1.5 cm2. Percutaneous balloon mitral valvuloplasty preferred if favorable morphology, no significant MR, and no LA thrombus.

5. Describe Eisenmenger syndrome and its hemodynamic consequence in adult congenital heart disease.

   A long-standing large left-to-right shunt (VSD, ASD, PDA) causes progressive pulmonary vascular disease and pulmonary hypertension; PVR rises until the shunt reverses to right-to-left, producing cyanosis and erythrocytosis. It is then inoperable for shunt closure; management is supportive +/- pulmonary vasodilators and possible heart-lung transplant.

6. Differentiate the murmur and physiology of ASD vs VSD vs PDA.

   ASD: wide FIXED splitting of S2 with a pulmonary mid-systolic flow murmur (shunt itself silent). VSD: harsh holosystolic murmur at left lower sternal border (smaller defects are louder). PDA: continuous 'machinery' murmur at left infraclavicular area. All are left-to-right shunts that can lead to Eisenmenger if uncorrected.

7. State the modified Duke criteria framework for diagnosing infective endocarditis.

   Major: positive blood cultures with typical organisms (2 separate cultures) and evidence of endocardial involvement (echo vegetation, abscess, new valvular regurgitation). Minor: predisposing condition/IVDU, fever >=38C, vascular phenomena, immunologic phenomena, suggestive microbiology. Definite IE = 2 major, or 1 major + 3 minor, or 5 minor.

8. List surgical indications and the most common organisms in infective endocarditis.

   Surgery for: heart failure from valve dysfunction, uncontrolled infection/abscess/persistent bacteremia, and prevention of embolism (large mobile vegetations >10 mm with embolic events). Organisms: Staphylococcus aureus (most common overall, acute/IVDU), viridans streptococci (subacute, native valve), enterococci, and coagulase-negative staph (prosthetic valve).

9. Contrast acute pericarditis, cardiac tamponade, and constrictive pericarditis.

   Acute pericarditis: pleuritic chest pain relieved by sitting forward, friction rub, diffuse ST-elevation with PR depression. Tamponade: pericardial effusion causing Beck triad (hypotension, muffled heart sounds, raised JVP), pulsus paradoxus, electrical alternans - treat with pericardiocentesis. Constriction: thickened/calcified pericardium, Kussmaul sign, pericardial knock, square-root sign on cath.

10. Define pulsus paradoxus and Kussmaul sign and their associations.

    Pulsus paradoxus: exaggerated inspiratory fall in systolic BP >10 mmHg - classic in cardiac tamponade (also severe asthma/COPD). Kussmaul sign: paradoxical rise in JVP with inspiration - seen in constrictive pericarditis, restrictive cardiomyopathy, RV infarction, and tricuspid stenosis (typically absent in pure tamponade).

11. How is hypertension classified per current guidelines (ACC/AHA), and what is the BP treatment threshold/target?

    Normal <120/80; Elevated 120-129/<80; Stage 1: 130-139 or 80-89; Stage 2: >=140 or >=90. Treat with lifestyle +/- drugs; pharmacotherapy for stage 1 with ASCVD/high risk or stage 2. General target <130/80 mmHg. First-line agents: thiazides, ACEi/ARB, and CCBs.

12. Distinguish hypertensive urgency from emergency and outline emergency management principles.

    Urgency: severely elevated BP (often >180/120) WITHOUT acute target-organ damage - manage with oral agents, gradual reduction. Emergency: severe HTN WITH acute end-organ damage (encephalopathy, ACS, aortic dissection, pulmonary edema, AKI, eclampsia) - IV agents in ICU, lower MAP ~10-20% in first hour (except dissection/stroke have specific targets), avoid precipitous drops.

13. Give the hemodynamic definition and WHO clinical classification groups of pulmonary hypertension.

    PH = mean pulmonary arterial pressure >20 mmHg at rest (right heart catheterization). Groups: 1 = pulmonary arterial hypertension (PAH); 2 = due to left heart disease (most common); 3 = due to lung disease/hypoxia; 4 = chronic thromboembolic PH (CTEPH); 5 = multifactorial/unclear. Pre-capillary PAH: PAWP <=15 mmHg and PVR >2 Wood units.

14. Name the drug classes used to treat Group 1 pulmonary arterial hypertension by pathway.

    Nitric oxide pathway: PDE-5 inhibitors (sildenafil) and sGC stimulators (riociguat). Endothelin pathway: endothelin receptor antagonists (bosentan, ambrisentan, macitentan). Prostacyclin pathway: prostanoids (epoprostenol, treprostinil) and IP-receptor agonists (selexipag). Vasoreactive patients may respond to calcium channel blockers.

15. Contrast Stanford type A and type B aortic dissection and their management.

    Type A: involves the ascending aorta - surgical emergency (risk of tamponade, AR, coronary/cerebral malperfusion). Type B: confined to descending aorta (distal to left subclavian) - usually medical management with strict BP/heart-rate control (IV beta-blockers first to reduce dP/dt), with endovascular/surgical repair if complicated (malperfusion, rupture, refractory pain).

16. State thresholds for elective repair of thoracic and abdominal aortic aneurysms.

    Abdominal aortic aneurysm (AAA): repair at diameter >=5.5 cm, rapid growth (>0.5 cm/6 months or >1 cm/year), or symptomatic/ruptured. Ascending thoracic aortic aneurysm: repair at >=5.5 cm (lower, ~4.5-5.0 cm, in Marfan/bicuspid valve/Loeys-Dietz or family history of dissection). EVAR vs open repair depends on anatomy and risk.

17. Outline the Wells criteria use and diagnostic pathway for suspected pulmonary embolism.

    Wells score stratifies pretest probability. Low/unlikely PE: D-dimer (age-adjusted) - if negative, PE excluded. High/likely PE or positive D-dimer: CT pulmonary angiography (V/Q scan if contrast contraindicated). Hemodynamically unstable (massive PE): bedside echo/immediate CTPA then reperfusion. PERC rule can exclude PE in very low-risk patients.

18. Classify PE severity and indicate when thrombolysis vs anticoagulation is used.

    Massive (high-risk): hypotension/shock - systemic thrombolysis (or catheter-directed/embolectomy if contraindicated). Submassive (intermediate-risk): RV dysfunction/positive troponin but normotensive - anticoagulate, consider thrombolysis if deterioration. Low-risk: anticoagulation alone (DOAC preferred), often outpatient. Anticoagulation is the foundation for all unless contraindicated.

19. Give Virchow's triad and how it explains venous thromboembolism risk.

    Virchow's triad: (1) venous stasis (immobility, surgery, long travel), (2) endothelial injury (trauma, surgery, catheters), and (3) hypercoagulability (malignancy, pregnancy, estrogen, inherited thrombophilias like factor V Leiden, prothrombin mutation, antiphospholipid syndrome). VTE encompasses DVT and PE.

20. What is the universal definition of myocardial infarction (Type 1 vs Type 2)?

    MI = rise/fall of cardiac troponin with at least one value above the 99th percentile plus evidence of ischemia (symptoms, ECG changes, imaging, or angiographic thrombus). Type 1: due to atherothrombotic plaque rupture/erosion. Type 2: supply-demand mismatch without acute atherothrombosis (e.g., tachyarrhythmia, anemia, hypotension, spasm).

21. What are the mechanical complications of acute MI and their typical timing?

    Papillary muscle/chordae rupture (acute severe MR, days 2-7), ventricular septal rupture (new harsh holosystolic murmur, days 3-5), free wall rupture (tamponade/PEA, days 3-7), LV aneurysm (weeks-months, persistent ST-elevation), and pseudoaneurysm. Inferior MI with RV involvement causes hypotension; all warrant urgent echo and surgical/mechanical support.

22. Explain the wavefront phenomenon of myocardial infarction.

    After coronary occlusion, necrosis begins in the subendocardium (most vulnerable to ischemia) and progresses transmurally toward the epicardium over time as a 'wavefront.' This time-dependence is why rapid reperfusion salvages myocardium - 'time is muscle.'

23. Differentiate cardiac biomarkers: high-sensitivity troponin vs CK-MB in timing and reinfarction.

    hs-Troponin: rises 2-3h, peaks ~24h, stays elevated 7-14 days - most sensitive/specific for myonecrosis; serial 0/1h or 0/2h algorithms rapidly rule in/out. CK-MB: rises 3-6h, normalizes in 48-72h - useful for detecting REINFARCTION because it normalizes faster than troponin.

24. What is the dual antiplatelet therapy (DAPT) strategy after PCI for ACS?

    Aspirin plus a P2Y12 inhibitor (prasugrel or ticagrelor preferred over clopidogrel in ACS) for typically 12 months, balanced against bleeding risk (high bleeding risk may shorten to 1-6 months). Prasugrel contraindicated with prior stroke/TIA; thereafter continue lifelong aspirin (or P2Y12 monotherapy in selected patients).

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