Introduction to Cardiovascular Hemodynamics and Cardiac Electrophysiology

Cardiovascular hemodynamics is the study of blood flow, pressure, and resistance within the heart and blood vessels. Blood flows from higher to lower pressure, and blood flow is determined by the pressure gradient and vascular resistance. A key relationship is Blood Flow (Q) = Pressure Gradient (ΔP) / Resistance (R). Arterioles are the major resistance vessels, while veins act as capacitance vessels and store a large proportion of circulating blood. Cardiac output (CO) is the amount of blood pumped by the heart per minute and is calculated as CO = Heart Rate × Stroke Volume.

Cardiovascular Clinical Correlation

Alterations in hemodynamics have important clinical consequences. Increased vascular resistance can raise blood pressure, while reduced cardiac output may lead to inadequate tissue perfusion. Preload is related to ventricular filling, whereas afterload is the load against which the ventricle ejects blood. According to the Frank–Starling law, increased ventricular filling generally increases the force of contraction and stroke volume within physiological limits. Understanding these relationships helps explain conditions such as hypertension, heart failure, and circulatory shock.

Cardiac Action Potential Phases

Cardiac electrophysiology deals with the electrical activity responsible for cardiac contraction. In ventricular myocytes, the action potential has five phases:

Phase 0 – Rapid depolarisation: mainly due to rapid Na⁺ influx.
Phase 1 – Initial repolarisation: mainly due to transient K⁺ efflux.
Phase 2 – Plateau: caused by Ca²⁺ influx through L-type calcium channels, balanced by K⁺ efflux.
Phase 3 – Repolarisation: mainly due to continued K⁺ efflux.
Phase 4 – Resting phase: maintenance of the resting membrane potential, approximately −90 mV in ventricular myocytes.

The prolonged cardiac action potential and refractory period prevent tetanic contraction, allowing the heart to contract and relax rhythmically. Pacemaker cells, particularly those in the SA node, differ because they undergo spontaneous Phase 4 depolarisation and have a Ca²⁺-dependent Phase 0.

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