High Yield Cardiology

❤️ Cardiology

• 📌 STEMI = ST elevation in contiguous leads ± reciprocal depression → urgent reperfusion (PCI first-line if available).
• 📌 Inferior MI (II, III, aVF) + hypotension + clear lungs → think right ventricular infarction → give IV fluids, avoid nitrates.
• 📌 Aortic stenosis triad = syncope + angina + dyspnoea.
• 📌 Aortic dissection = tearing chest pain radiating to the back + pulse/BP differential.
• 📌 Cardiac tamponade = hypotension + raised JVP + muffled heart sounds (Beck triad).
• 📌 Acute pericarditis = pleuritic chest pain relieved by sitting forward + diffuse ST elevation + PR depression.
• 📌 Mitral stenosis predisposes to atrial fibrillation and embolic stroke.
• 📌 Infective endocarditis → always get blood cultures before antibiotics if the patient is stable.
• 📌 Atrial fibrillation management = assess hemodynamic stability first; unstable → synchronized cardioversion.
• 📌 HOCM murmur gets louder with Valsalva/standing and quieter with squatting.

❤️ Cardiology

• 📌 Acute coronary syndrome (ACS) = think plaque rupture → platelet aggregation → thrombosis. STEMI usually reflects complete coronary occlusion; NSTEMI/unstable angina usually reflect partial occlusion.
• 📌 STEMI = ST elevation in contiguous leads ± reciprocal ST depression → urgent reperfusion (primary PCI first-line if available). Do not delay reperfusion for troponin if the ECG is diagnostic.
• 📌 Inferior MI = ST elevation in II, III, aVF. If there is hypotension + raised JVP + clear lungs, suspect right ventricular infarction → do right-sided leads, give IV fluids, and avoid nitrates because these patients are preload dependent.
• 📌 Anterior MI (V1–V4) usually reflects LAD occlusion and carries a high risk of pump failure, cardiogenic shock, and ventricular arrhythmias.
• 📌 Posterior MI = horizontal ST depression + tall R waves in V1–V3. Think of it as a “mirror image” STEMI; posterior leads can confirm it.
• 📌 Troponin is sensitive for myocardial injury, but the exam question often hinges on the ECG pattern + clinical timing. A normal early troponin does not exclude acute MI.
• 📌 Aortic dissection = sudden tearing chest pain radiating to the back + pulse or blood pressure differential. Major risk factors include hypertension, connective tissue disease, bicuspid aortic valve, and pregnancy.
• 📌 Stanford type A dissection involves the ascending aorta and is a surgical emergency; type B usually starts distal to the left subclavian artery and is often managed medically first with blood pressure control.
• 📌 Cardiac tamponade = hypotension + raised JVP + muffled heart sounds (Beck triad). Other clues: tachycardia, pulsus paradoxus, and electrical alternans.
• 📌 Pulsus paradoxus = exaggerated fall in systolic BP during inspiration. Think of tamponade, severe asthma, and constrictive physiology.
• 📌 Acute pericarditis = pleuritic chest pain relieved by sitting forward + diffuse ST elevation + PR depression. Unlike STEMI, the ST elevation is usually widespread rather than confined to one coronary territory.
• 📌 Pericardial effusion may complicate pericarditis; large or rapidly accumulating effusions can cause tamponade.
• 📌 Aortic stenosis = classic triad of syncope, angina, and dyspnoea. Exam clues include a slow-rising pulse, ejection systolic murmur, and radiation to the carotids.
• 📌 Severe aortic stenosis causes a fixed outflow obstruction, so patients cannot appropriately increase cardiac output during exertion → this explains exertional syncope.
• 📌 Aortic regurgitation = collapsing pulse, wide pulse pressure, and an early diastolic murmur. Acute severe AR can present with pulmonary oedema and shock.
• 📌 Mitral stenosis usually results from rheumatic heart disease. It causes left atrial enlargement, predisposing to atrial fibrillation, pulmonary congestion, and embolic stroke.
• 📌 Mitral regurgitation = pansystolic murmur radiating to the axilla. Acute MR after MI suggests papillary muscle dysfunction or rupture, which is a life-threatening complication.
• 📌 Mitral valve prolapse classically causes a mid-systolic click. The murmur becomes earlier/louder when LV volume falls, such as with Valsalva.
• 📌 HOCM = hypertrophic obstructive cardiomyopathy with dynamic LV outflow obstruction. The murmur gets louder with Valsalva or standing and quieter with squatting or handgrip.
• 📌 Why HOCM changes with manoeuvres: reduced preload makes the LV cavity smaller, worsening obstruction; increased preload enlarges the cavity and reduces obstruction.
• 📌 Atrial fibrillation management always starts with hemodynamic stability. If the patient is unstable (shock, chest pain, pulmonary oedema, syncope), perform synchronized cardioversion.
• 📌 Stable atrial fibrillation: think rate control, rhythm strategy where appropriate, and anticoagulation. The stroke risk arises because blood stagnates in the left atrial appendage.
• 📌 Atrial flutter classically gives a saw-tooth pattern, often with 2:1 block and a ventricular rate around 150/min.
• 📌 Supraventricular tachycardia (SVT) = regular narrow-complex tachycardia. If stable, start with vagal manoeuvres, then adenosine if appropriate.
• 📌 Ventricular tachycardia should be assumed in any broad-complex tachycardia until proven otherwise, especially with structural heart disease or prior MI.
• 📌 Unstable tachyarrhythmia → synchronized cardioversion. Pulseless VT/VF → defibrillation.
• 📌 Bradycardia + hypotension, syncope, or shock → think unstable bradycardia; exam answers often involve atropine followed by pacing if needed.
• 📌 AV block patterns:
• 1st degree = prolonged PR only
• Mobitz I = progressive PR prolongation then dropped beat
• Mobitz II = dropped beats without progressive PR prolongation
• 3rd degree = AV dissociation
• 📌 Mobitz II and complete heart block are more concerning because they can progress to severe bradycardia and often need pacing.
• 📌 Infective endocarditis = fever + murmur + vascular/immunologic phenomena. If the patient is stable, always get multiple blood cultures before antibiotics.
• 📌 Native valve endocarditis after dental work suggests viridans streptococci; in IV drug users, think Staphylococcus aureus, often affecting the tricuspid valve.
• 📌 Endocarditis complications include heart failure, abscess, stroke, glomerulonephritis, and septic emboli. A new conduction abnormality may suggest a peri-annular abscess.
• 📌 Heart failure with reduced EF (HFrEF) is driven by maladaptive neurohormonal activation: RAAS + sympathetic nervous system worsen remodelling over time.
• 📌 Left-sided heart failure causes pulmonary oedema, orthopnoea, PND, and bibasal crackles; right-sided failure causes peripheral oedema, raised JVP, hepatomegaly, and ascites.
• 📌 Acute pulmonary oedema = severe dyspnoea, hypoxia, crackles, pink frothy sputum. This is a medical emergency: think oxygen/ventilatory support + diuresis + treat precipitant.
• 📌 BNP/NT-proBNP is released in response to myocardial stretch and helps support the diagnosis of heart failure, though it can also be raised in other states.
• 📌 Restrictive cardiomyopathy causes impaired filling with relatively preserved systolic function; dilated cardiomyopathy causes systolic failure; hypertrophic cardiomyopathy causes diastolic dysfunction ± obstruction.
• 📌 Stable angina = predictable exertional chest pain relieved by rest or nitrates. It reflects a fixed atherosclerotic narrowing rather than acute plaque rupture.
• 📌 Unstable angina = angina at rest or worsening frequency/severity, but without troponin rise. It still represents ACS and requires urgent risk stratification.
• 📌 Coronary territories frequently tested:
• LAD → anterior wall / septum
• RCA → inferior wall, SA/AV node in many patients
• LCx → lateral wall
• 📌 Mechanical complications after MI usually occur days later:
• Papillary muscle rupture → acute severe MR
• Ventricular septal rupture → new harsh murmur + heart failure
• Free wall rupture → tamponade / sudden collapse
• 📌 Dressler syndrome = autoimmune pericarditis occurring weeks after MI.
• 📌 Syncope red flags in cardiology include exertional syncope, family history of sudden cardiac death, structural heart disease, and ECG abnormalities.
• 📌 Marfan syndrome is linked to aortic root dilatation, aortic regurgitation, and aortic dissection.
• 📌 Acute limb ischaemia and stroke in a patient with AF often reflect cardioembolism.
• 📌 USMLE-style “next best step” cardiology triggers:
• ⚡ STEMI → urgent reperfusion
• ⚡ Unstable AF / SVT / VT with pulse → synchronized cardioversion
• ⚡ Pulseless VT/VF → defibrillation
• ⚡ Tamponade → urgent pericardiocentesis
• ⚡ Type A dissection → urgent surgery
• ⚡ Hyperkalaemia with ECG changes → IV calcium first

❤️ Acute Coronary Syndromes (ACS)

⚡ STEMI Territories (ECG Leads)

🫀 ACS “Next Best Step” Triggers

🧠 Cardiology Exam Tips

• 📌 First decide whether the problem is electrical, ischaemic, valvular, structural, or hemodynamic.
• 📌 In chest pain questions, use the pain quality + ECG + hemodynamics to separate MI, pericarditis, dissection, and PE.
• 📌 In murmur questions, always think about timing, radiation, and manoeuvres.
• 📌 In arrhythmia questions, the first branch point is almost always stable vs unstable.
• 📌 In shock questions, raised JVP helps narrow the differential: think tamponade, RV infarct, massive PE, or severe heart failure.