CMC – Cardiac Medicine Certification

Every cardiac condition on the exam is ultimately a disturbance of myocardial oxygen supply versus demand or of cardiac output. Cardiac output (CO) = heart rate × stroke volume, and stroke volume is governed by preload, afterload, and contractility. The Frank–Starling relationship states that, up to a point, greater end-diastolic stretch produces a more forceful contraction; a failing ventricle sits on a flattened curve, so additional volume raises filling pressures and congestion with little gain in output.

The left ventricle is perfused almost entirely during diastole, when intramyocardial pressure falls. This explains why tachycardia, diastolic hypotension, and a high LVEDP are each ischemic, and why therapies such as beta-blockade (slower rate) and IABP (diastolic augmentation) improve supply.

The SA node fires at 60–100 beats/min. The impulse spreads across the atria via internodal pathways to the AV node, which delays conduction so the atria can complete ventricular filling. The bundle of His divides into the right and left bundle branches (the left subdivides into anterior and posterior fascicles), and the Purkinje fibers depolarize the ventricles from endocardium to epicardium. Disease above the His bundle (nodal) tends to be vagally mediated and atropine-responsive; disease below it (infranodal) produces wide escape rhythms and requires pacing.

The left main coronary artery divides into the left anterior descending (LAD), which supplies the anterior wall, anterior two-thirds of the septum, and much of the bundle branches, and the circumflex (LCx), which supplies the lateral wall. The right coronary artery (RCA) supplies the RV, the inferior wall, the SA node in most people, and the AV node in right-dominant circulation. Dominance is defined by which artery gives rise to the posterior descending artery (PDA); most people are right-dominant.