Iraqi Board Cardiology cheat sheet

Frank-Starling law: increased preload increases stroke volume up to a point; beyond optimal sarcomere length, contractility falls.

Action potential phases: phase 0 (rapid Na+ influx), 1 (transient K+ efflux), 2 (Ca2+ influx/K+ efflux plateau), 3 (K+ efflux repolarisation), 4 (resting potential; spontaneous depolarisation in pacemaker cells via If).

Wiggers diagram: a cardiac cycle has systole (isovolumetric contraction, ejection) and diastole (isovolumetric relaxation, filling). S1 = mitral/tricuspid closure; S2 = aortic/pulmonary closure.

Laplace law: wall stress = (pressure × radius) / (2 × wall thickness). This explains why dilated ventricles have higher wall stress and why hypertrophy normalises stress.

Coronary blood flow occurs predominantly in diastole; tachycardia shortens diastole and can cause subendocardial ischaemia.

Beta-1 receptors increase heart rate and contractility; beta-2 receptors cause vasodilation and bronchodilation; alpha-1 receptors cause vasoconstriction.

Digoxin inhibits Na+/K+-ATPase, raising intracellular Na+ and thereby intracellular Ca2+ via the Na+/Ca2+ exchanger; it also increases vagal tone.

Marfan syndrome: FBN1 mutation, fibrillin-1 deficiency; risk of aortic root dilation and dissection. Loeys-Dietz: TGFBR1/2 mutations, more aggressive vascular disease.

Familial hypercholesterolaemia: LDLR, APOB, or PCSK9 mutations; autosomal dominant; high LDL and premature atherosclerosis.

Chest pain: use SOCRATES (Site, Onset, Character, Radiation, Associated symptoms, Timing, Exacerbating/relieving factors, Severity). Cardiac pain is typically central, pressure-like, radiating to jaw/arm, provoked by exertion and relieved by rest.

Jugular venous pressure: measured with head at 30–45°, sternal angle as reference; >3 cm above sternal angle is elevated. Hepatojugular reflux supports right heart failure.

Aortic stenosis: ejection systolic murmur at right upper sternum, radiating to carotids, slow-rising pulse, narrow pulse pressure, soft S2.

Mitral regurgitation: pansystolic murmur at apex radiating to axilla; severity correlates with loudness (unlike AS).

Mitral stenosis: mid-diastolic rumble with opening snap; loud S1; associated with atrial fibrillation and pulmonary hypertension.

Aortic regurgitation: early diastolic decrescendo murmur at left sternal edge; wide pulse pressure, water-hammer pulse, head bobbing.

Heart failure signs: raised JVP, bibasal crackles, S3 gallop, peripheral oedema, hepatomegaly.

Pericardial tamponade: Beck's triad (hypotension, raised JVP, muffled heart sounds), pulsus paradoxus, electrical alternans.

Infective endocarditis: Osler nodes (tender, pulp), Janeway lesions (non-tender, palms/soles), Roth spots, splinter haemorrhages, new regurgitant murmur.

STEMI: ST elevation ≥1 mm in two contiguous limb leads or ≥2 mm in precordial leads (or new LBBB with symptoms). Reperfusion within 12 hours: primary PCI if available within 120 min, else fibrinolysis.

NSTEMI: elevated troponin with ischaemic symptoms/ECG changes; risk-stratify with GRACE score; early invasive strategy for high-risk features.

Troponin rises 3–6 h after injury, peaks at 12–24 h, remains elevated 7–14 days. High-sensitivity assays detect earlier.

Dual antiplatelet therapy (aspirin + P2Y12 inhibitor) is standard post-ACS; duration depends on bleeding risk and stent type.

Secondary prevention post-MI: aspirin, statin, beta-blocker, ACE inhibitor (especially with LV dysfunction), and aldosterone antagonist if EF ≤40% with heart failure/diabetes.

Absolute contraindications to fibrinolysis: prior intracranial haemorrhage, known cerebral vascular lesion, malignant intracranial neoplasm, ischaemic stroke within 3 months, suspected aortic dissection, active bleeding.

Killip class predicts mortality in STEMI: I (no heart failure), II (crackles, S3, raised JVP), III (pulmonary oedema), IV (cardiogenic shock).

Wellens syndrome: deep inverted or biphasic T waves in V2–V3 in a pain-free patient indicates critical proximal LAD stenosis; avoid stress testing.

HFrEF: EF ≤40%; HFmrEF: 41–49%; HFpEF: ≥50%. Diagnosis requires symptoms/signs plus objective evidence (elevated natriuretic peptides, imaging).

Four pillars of HFrEF therapy: ARNI/ACEi/ARB, evidence-based beta-blocker, MRA, and SGLT2 inhibitor. Add diuretics for congestion.

Ejection fraction = (EDV − ESV) / EDV × 100%.

Hypertrophic cardiomyopathy: asymmetric septal hypertrophy, dynamic LV outflow obstruction, systolic anterior motion of mitral valve; avoid vasodilators and diuretics that worsen obstruction; beta-blockers first-line.

Dilated cardiomyopathy: dilated LV with reduced EF; causes include idiopathic, familial, alcohol, viral, postpartum, chemotherapy (doxorubicin).

Restrictive cardiomyopathy: impaired filling with normal or reduced cavity size; associated with amyloidosis, sarcoidosis, haemochromatosis, endomyocardial fibrosis.

Cardiac amyloidosis: low voltage on ECG despite thick walls on echo; 'sparkling' myocardium; AL or ATTR type; bone scintigraphy helps diagnose ATTR.

Arrhythmogenic right ventricular cardiomyopathy: fibrofatty replacement of RV; epsilon wave, T-wave inversion V1–V3; risk of ventricular arrhythmias; genetic (desmosomal).

Myocarditis: often viral; presents with chest pain, heart failure, arrhythmia; troponin may be elevated; MRI shows late gadolinium enhancement; avoid strenuous exercise.

Aortic stenosis severity: peak velocity ≥4 m/s, mean gradient ≥40 mmHg, valve area ≤1.0 cm² (severe). Symptomatic severe AS requires valve replacement (SAVR or TAVI).

Mitral stenosis: valve area ≤1.5 cm² is severe; percutaneous balloon mitral valvuloplasty is preferred if valve morphology is suitable and no LA thrombus.

Mitral regurgitation: severe if effective regurgitant orifice ≥0.4 cm², regurgitant volume ≥60 mL, or vena contracta ≥0.7 cm. Surgery if symptomatic or LV dysfunction (EF <60% or LVESD >40 mm).

Aortic regurgitation: severe if jet width/LVOT >65%, vena contracta >0.6 cm, or holodiastolic flow reversal. Surgery if symptomatic or LVEF ≤50% or LVESD >50 mm.

Prosthetic valves: mechanical valves require lifelong warfarin; bioprosthetic valves have lower thrombogenicity but degenerate over time. Target INR depends on valve type and position.

Antibiotic prophylaxis for infective endocarditis is recommended for prosthetic valves, prior IE, and certain congenital heart disease, before dental procedures.

Rheumatic heart disease: most commonly affects mitral valve; results in stenosis and/or regurgitation; prevention with penicillin prophylaxis.

Carcinoid heart disease: right-sided valve fibrosis (tricuspid and pulmonary) due to serotonin; left side spared because serotonin is metabolised in lungs.

Atrial fibrillation: irregularly irregular rhythm, absent P waves. Anticoagulate based on CHA2DS2-VASc score (≥2 in men, ≥3 in women); rate control with beta-blocker or calcium channel blocker; rhythm control for symptoms.

Ventricular tachycardia: wide QRS (>120 ms), regular, AV dissociation, capture/fusion beats. Unstable VT requires synchronised cardioversion; pulseless VT requires defibrillation.

Supraventricular tachycardia: narrow QRS, regular, no visible P waves; vagal manoeuvres then adenosine. Avoid adenosine in asthma.

Complete heart block: P waves and QRS complexes independent; indication for pacing if symptomatic, or if wide QRS or high-grade block.

Long QT syndrome: QTc >440 ms (men) or >460 ms (women); risk of torsades de pointes; avoid QT-prolonging drugs; beta-blockers and sometimes ICD.

Brugada syndrome: ST elevation in V1–V3 with right bundle branch block pattern; risk of ventricular fibrillation; ICD for survivors of cardiac arrest.

Wolff-Parkinson-White: short PR, delta wave, wide QRS; risk of pre-excited AF; avoid AV nodal blockers (adenosine, digoxin, verapamil) in pre-excited AF; catheter ablation is curative.

Radiofrequency ablation is curative for many SVTs (AVNRT, AVRT, focal atrial tachycardia) and typical atrial flutter.

Hypertension diagnosis: office BP ≥140/90 mmHg confirmed by ambulatory or home monitoring; home BP ≥135/85 mmHg. Stage 1: 140–159/90–99; Stage 2: ≥160/100.

First-line antihypertensives: ACEi/ARB, calcium channel blockers, thiazide-like diuretics. Beta-blockers not first-line unless specific indication.

Hypertensive emergency: severe BP elevation with target organ damage (encephalopathy, aortic dissection, pulmonary oedema); reduce BP gradually (except aortic dissection where rapid control is needed).

LDL cholesterol targets: very high risk <1.4 mmol/L (55 mg/dL) and ≥50% reduction; high risk <1.8 mmol/L (70 mg/dL).

Statins are first-line for dyslipidaemia; ezetimibe or PCSK9 inhibitors added if targets not met.

ASCVD risk assessment: use validated risk scores (e.g., SCORE2, pooled cohort equations); consider risk enhancers (family history, inflammatory disease, ethnicity).

Smoking cessation is the single most effective preventive measure; offer pharmacotherapy (nicotine replacement, varenicline, bupropion) and behavioural support.

Secondary prevention after ASCVD: aspirin, high-intensity statin, BP control, smoking cessation, diabetes management, and regular exercise.

Ventricular septal defect: most common congenital heart defect; small defects may close spontaneously; large defects cause heart failure and pulmonary hypertension; treat with surgical closure if significant.

Atrial septal defect: fixed split S2; left-to-right shunt; closure if significant shunt and pulmonary vascular resistance not too high.

Patent ductus arteriosus: continuous machinery murmur; closure with indomethacin in preterm infants or device/surgery in older patients.

Tetralogy of Fallot: VSD, overriding aorta, pulmonary stenosis, right ventricular hypertrophy; cyanosis; 'boot-shaped' heart on X-ray; surgical repair.

Transposition of the great arteries: aorta from RV, pulmonary artery from LV; requires prostaglandin E1 to maintain ductus, then arterial switch operation.

Coarctation of the aorta: upper limb hypertension, weak femoral pulses, radio-femoral delay; associated with bicuspid aortic valve; treat with stenting or surgery.

Eisenmenger syndrome: pulmonary vascular disease reverses shunt to right-to-left; cyanosis; avoid pregnancy and vasodilators that may worsen systemic hypotension.

Fontan circulation: single ventricle palliation; risk of arrhythmias, protein-losing enteropathy, liver disease; requires lifelong specialist follow-up.

Acute pericarditis: chest pain worse on inspiration, pericardial friction rub, diffuse ST elevation and PR depression; treat with NSAIDs and colchicine.

Cardiac tamponade: hypotension, raised JVP, muffled heart sounds, pulsus paradoxus; echo shows pericardial effusion with right ventricular diastolic collapse; treat with pericardiocentesis.

Constrictive pericarditis: thickened pericardium, impaired filling; echo shows septal bounce, 'square root' sign on ventricular pressure tracing; treat with pericardiectomy.

Pulmonary hypertension definition: mean pulmonary artery pressure >20 mmHg at rest; pre-capillary if pulmonary artery wedge pressure ≤15 mmHg and PVR >3 Wood units.

Pulmonary arterial hypertension (Group 1) treatment: calcium channel blockers if vasoreactive; endothelin receptor antagonists, PDE5 inhibitors, prostacyclins, soluble guanylate cyclase stimulators.

Cor pulmonale: right heart failure due to lung disease; treat underlying cause, diuretics, oxygen; avoid systemic vasodilators that worsen gas exchange.

Right ventricular infarction: suspect with inferior MI, raised JVP, hypotension; treat with fluids (cautious), avoid nitrates and diuretics.

ECG: 25 mm/s paper speed, 10 mm/mV calibration. P wave <120 ms, PR 120–200 ms, QRS <120 ms, QTc <440 ms (men) / <460 ms (women).

Transthoracic echocardiography: first-line for ventricular function, valves, pericardium. Transoesophageal echo better for posterior structures, thrombi, endocarditis.

Stress testing: exercise ECG for diagnosis of stable angina if interpretable; stress echo or myocardial perfusion imaging if baseline ECG abnormal.

Cardiac CT: high negative predictive value for coronary artery disease; CT coronary angiography for low-intermediate risk; calcium scoring for risk stratification.

Cardiac MRI: gold standard for myocardial tissue characterisation (scar, inflammation, infiltration); late gadolinium enhancement patterns help diagnose cardiomyopathy.

Coronary angiography: invasive gold standard for coronary anatomy; fractional flow reserve (FFR) ≤0.80 indicates haemodynamically significant stenosis.

Nuclear cardiology: myocardial perfusion imaging with SPECT or PET; useful for ischaemia detection and viability assessment.

Right heart catheterisation: measures pulmonary pressures, cardiac output, and vascular resistance; essential for pulmonary hypertension diagnosis.

Primary PCI for STEMI: door-to-balloon time <90 min (or <120 min if transfer).

CABG indications: left main stenosis, three-vessel disease (especially with diabetes or reduced EF), or two-vessel disease involving proximal LAD; SYNTAX score guides choice.

TAVI is preferred for severe symptomatic aortic stenosis in patients at high or intermediate surgical risk; SAVR for low-risk or younger patients.

Mitral valve repair is preferred over replacement for severe degenerative mitral regurgitation when feasible.

Drug-eluting stents reduce restenosis compared with bare-metal stents; require dual antiplatelet therapy for at least 1–6 months depending on bleeding risk.

Intravascular ultrasound (IVUS) and optical coherence tomography (OCT) guide complex PCI and assess stent optimisation.

Cardiac transplantation is indicated for end-stage heart failure refractory to medical therapy, with no contraindications.

Left ventricular assist devices (LVAD) are used as bridge to transplant or destination therapy in advanced heart failure.

Cardiac arrest: start CPR immediately, defibrillate shockable rhythms (VF/pulseless VT) as soon as possible; adrenaline 1 mg every 3–5 min; amiodarone after third shock.

Post-cardiac arrest care: targeted temperature management (32–36°C), avoid hyperoxia, treat hypotension, coronary angiography if STEMI.

Cardiogenic shock: hypotension (SBP <90 mmHg) with hypoperfusion despite fluid resuscitation; treat cause (e.g., revascularisation for MI), use inotropes/vasopressors, mechanical support if needed.

Acute pulmonary oedema: sit upright, oxygen, IV diuretics, nitrates if BP allows, non-invasive ventilation for respiratory distress.

Hypertensive emergency: controlled BP reduction (except aortic dissection where rapid control is needed); avoid rapid drops that cause organ ischaemia.

Informed consent: must be obtained before invasive procedures; include risks, benefits, alternatives; document capacity assessment.

Patient safety: use checklists for procedures, verify patient identity and site, follow sterile technique, and report adverse events.

Ethical principles: beneficence, non-maleficence, autonomy, justice. Advance directives and do-not-resuscitate orders should be respected.

Withdrawal of life-sustaining therapy: consider patient wishes, prognosis, and involve family and palliative care team.