Iraqi Board Cardiology study materials
Iraqi Board Cardiology study resources

Iraqi Board Cardiology flashcards

Iraqi Board Cardiology · Build recall with a focused review session.

32 cards. Read the term and the definition here. The deck at the top of this page is optional.

Frank-Starling law
Increased preload stretches myocardial fibres, increasing stroke volume up to an optimal sarcomere length; beyond this, further stretch reduces contractility.
Laplace law
Wall stress = (pressure × radius) / (2 × wall thickness). Dilated ventricles have higher wall stress; hypertrophy reduces stress by increasing thickness.
Digoxin mechanism
Inhibits Na+/K+-ATPase, raising intracellular Na+ and thereby Ca2+ via the Na+/Ca2+ exchanger; also increases vagal tone, slowing AV conduction.
Marfan syndrome gene
FBN1 mutation causing fibrillin-1 deficiency; leads to aortic root dilation and dissection, mitral valve prolapse, and lens dislocation.
Jugular venous pressure
Assessed at 30–45° with sternal angle as reference; >3 cm above sternal angle is elevated, indicating right heart failure or volume overload.
Aortic stenosis murmur
Ejection systolic murmur at right upper sternum radiating to carotids, with slow-rising pulse, narrow pulse pressure, and soft S2.
Beck's triad
Hypotension, raised JVP, and muffled heart sounds-classic for cardiac tamponade; pulsus paradoxus and electrical alternans may also occur.
STEMI reperfusion
Primary PCI if available within 120 min of first medical contact; otherwise fibrinolysis within 12 h of symptom onset if no contraindications.
Troponin kinetics
Rises 3–6 h after myocardial injury, peaks at 12–24 h, and remains elevated for 7–14 days; high-sensitivity assays detect earlier.
Killip classification
In STEMI: I = no heart failure; II = crackles, S3, raised JVP; III = pulmonary oedema; IV = cardiogenic shock; higher class predicts higher mortality.
Wellens syndrome
Deep inverted or biphasic T waves in V2–V3 in a pain-free patient, indicating critical proximal LAD stenosis; stress testing is contraindicated.
HFrEF four pillars
ARNI/ACEi/ARB, evidence-based beta-blocker, mineralocorticoid receptor antagonist, and SGLT2 inhibitor-all reduce mortality in heart failure with reduced ejection fraction.
Hypertrophic cardiomyopathy
Asymmetric septal hypertrophy with dynamic LV outflow obstruction and systolic anterior motion of the mitral valve; beta-blockers are first-line; avoid vasodilators.
Cardiac amyloidosis ECG
Low voltage on ECG despite thick walls on echocardiography; 'sparkling' myocardium; AL or ATTR type; bone scintigraphy aids ATTR diagnosis.
Severe aortic stenosis
Peak velocity ≥4 m/s, mean gradient ≥40 mmHg, or valve area ≤1.0 cm²; symptomatic severe AS requires valve replacement (SAVR or TAVI).
Mitral stenosis severity
Valve area ≤1.5 cm² indicates severe mitral stenosis; percutaneous balloon mitral valvuloplasty is preferred if valve morphology is suitable and no LA thrombus.
Carcinoid heart disease
Right-sided valve fibrosis (tricuspid and pulmonary) due to serotonin; left side spared because serotonin is metabolised in the lungs.
Atrial fibrillation anticoagulation
Use CHA2DS2-VASc score: anticoagulate if ≥2 in men or ≥3 in women; consider if 1 in men or 2 in women; DOACs preferred over warfarin in most.
Ventricular tachycardia
Wide QRS (>120 ms), regular rhythm, AV dissociation, capture/fusion beats; unstable VT requires synchronised cardioversion; pulseless VT requires defibrillation.
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; ablation is curative.
Hypertension first-line drugs
ACE inhibitors/ARBs, calcium channel blockers, and thiazide-like diuretics; beta-blockers are not first-line unless a specific indication exists.
LDL 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, with ezetimibe or PCSK9 inhibitors added if needed.
Ventricular septal defect
Most common congenital heart defect; small defects may close spontaneously; large defects cause heart failure and pulmonary hypertension; surgical closure if significant.
Tetralogy of Fallot
VSD, overriding aorta, pulmonary stenosis, and right ventricular hypertrophy; cyanosis; 'boot-shaped' heart on X-ray; surgical repair is definitive.
Eisenmenger syndrome
Pulmonary vascular disease reverses a left-to-right shunt to right-to-left, causing cyanosis; avoid pregnancy and vasodilators that may worsen systemic hypotension.
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 effusion with right ventricular diastolic collapse; treat with pericardiocentesis.
Pulmonary hypertension definition
Mean pulmonary artery pressure >20 mmHg at rest; pre-capillary if pulmonary artery wedge pressure ≤15 mmHg and pulmonary vascular resistance >3 Wood units.
ECG intervals
At 25 mm/s: P wave <120 ms, PR 120–200 ms, QRS <120 ms, QTc <440 ms (men) or <460 ms (women).
Fractional flow reserve
Invasive pressure-derived index; FFR ≤0.80 indicates a haemodynamically significant coronary stenosis and justifies revascularisation.
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 versus PCI.
Cardiac arrest algorithm
Start CPR immediately; defibrillate shockable rhythms (VF/pulseless VT) as soon as possible; adrenaline 1 mg every 3–5 min; amiodarone after third shock.