Cardiac Cycle

Understanding the cardiac cycle is fundamental for interpreting nearly all cardiovascular pathology in finals. It's the rhythmic sequence of events that ensures efficient blood flow, and its disruption underpins conditions from heart failure to valvular disease. The cycle is divided into systole (contraction) and diastole (relaxation), with precise timing of valve openings and closings. You need to grasp how electrical activity (ECG) translates into mechanical events (pressure/volume changes) and how these manifest as heart sounds and murmurs. This knowledge is critical for diagnosing and managing common cardiac conditions.

The cardiac cycle is initiated by the SA node, generating an action potential that spreads through the atria (P wave on ECG), causing atrial systole. The impulse then pauses at the AV node (PR segment), allowing ventricular filling, before rapidly propagating through the Bundle of His and Purkinje fibres to the ventricles (QRS complex), initiating ventricular systole. Repolarisation of the ventricles is the T wave. Mechanically, ventricular systole begins with isovolumetric contraction (all valves closed, pressure rising), followed by ejection as aortic/pulmonary valves open. Diastole starts with isovolumetric relaxation (all valves closed, pressure falling), followed by rapid and then reduced ventricular filling as AV valves open. The Frank-Starling mechanism states that increased venous return (preload) stretches the cardiac muscle, leading to a more forceful contraction and increased stroke volume, up to a point. This is due to optimal actin-myosin filament overlap.

Auscultation is a core OSCE skill. You must differentiate S1 and S2, and time murmurs correctly: systolic murmurs occur between S1 and S2 (e.g., aortic stenosis, mitral regurgitation), while diastolic murmurs occur between S2 and S1 (e.g., aortic regurgitation, mitral stenosis). Abnormal heart sounds like S3 (ventricular gallop, often in heart failure due to rapid filling of a dilated ventricle) or S4 (atrial gallop, in stiff ventricles like hypertension or aortic stenosis) are high-yield. Conditions like cardiac tamponade (Beck's triad: muffled heart sounds, raised JVP, hypotension) represent acute disruptions of the cycle. Atrial fibrillation leads to loss of the 'atrial kick', reducing cardiac output, especially in patients with pre-existing ventricular dysfunction.

The ECG provides electrical timing (P, QRS, T waves) for the cycle. Echocardiography is the cornerstone investigation: it directly visualises valve function, chamber sizes, wall motion, and allows calculation of ejection fraction and stroke volume. Doppler echocardiography assesses blood flow velocities and pressure gradients across valves. Pressure-volume loops derived from invasive catheterisation (e.g., Swan-Ganz) provide detailed insights into ventricular function, preload, afterload, and contractility, but are rarely used solely for cycle assessment in routine practice. Chest X-ray can show cardiomegaly or pulmonary oedema, indirect signs of cardiac cycle dysfunction.

Management of cardiac cycle dysfunction often targets preload, afterload, and contractility. Diuretics reduce preload in heart failure. ACE inhibitors and ARBs reduce afterload. Beta-blockers improve ventricular filling time and reduce myocardial oxygen demand. In valvular heart disease, surgical repair or replacement may be necessary to restore normal flow. For arrhythmias like atrial fibrillation, rate control (e.g., beta-blockers, calcium channel blockers) or rhythm control (e.g., amiodarone, cardioversion) are crucial, alongside anticoagulation to prevent stroke due to stasis in the left atrium.