The Cardiovascular System

The cardiovascular system is a closed circulatory network that delivers oxygen and nutrients to every cell in the body and removes metabolic waste. It consists of the heart, approximately 100,000 km of blood vessels, and roughly 5 litres of blood.

The heart is a four-chambered muscular pump. The right side receives deoxygenated blood from the systemic circulation via the superior and inferior venae cavae, and pumps it through the pulmonary circulation to the lungs for gas exchange. The left side receives oxygenated blood from the pulmonary veins and pumps it into the aorta for systemic distribution. The two sides are separated by the interventricular septum.

The cardiac cycle consists of diastole (ventricular filling) and systole (ventricular ejection). During isovolumetric contraction, both valves are closed and ventricular pressure rises sharply. The aortic valve opens once left ventricular pressure exceeds aortic pressure (~80 mmHg). At the end of ejection the aortic valve closes, producing the second heart sound (S2). The mitral valve opens when ventricular pressure falls below atrial pressure, allowing passive filling.

Cardiac output (CO) is the volume of blood pumped per minute: CO = Heart Rate × Stroke Volume. At rest, CO is approximately 5 L/min (HR 70 bpm × SV 70 mL). During maximal exercise, CO can reach 20–25 L/min in trained individuals. Stroke volume is determined by three factors. Preload is the degree of ventricular filling before contraction, reflected by end-diastolic volume (EDV). Afterload is the resistance the ventricle must overcome to eject blood, principally determined by systemic vascular resistance and aortic pressure. Contractility is the intrinsic force-generating capacity of the myocardium, regulated by sympathetic stimulation and intracellular calcium.

The Frank-Starling law states that stroke volume increases as preload (EDV) increases, up to an optimum. The cellular basis is length-dependent activation: stretching sarcomeres toward their optimal length (~2.2 µm) increases actin-myosin cross-bridge overlap and enhances troponin C sensitivity for calcium. This mechanism automatically balances the output of the right and left ventricles without neural input.

Preload is increased by increased venous return (exercise, fluid loading), whereas afterload is increased by hypertension or aortic stenosis. When afterload rises chronically, the left ventricle undergoes concentric hypertrophy (thicker walls, same chamber size) to normalise wall stress (Laplace's law: wall stress = Pr/2h).

Heart rate is regulated by the autonomic nervous system acting on the sinoatrial (SA) node. Sympathetic stimulation (noradrenaline, β1 receptors) steepens the pacemaker potential slope via the "funny" (If) current, increasing rate and contractility. Parasympathetic stimulation (acetylcholine, M2 receptors) activates IKACh, hyperpolarising the SA node and slowing rate. Resting heart rate is ~70 bpm due to dominant vagal tone; the intrinsic rate is ~100 bpm.

Blood pressure (BP = CO × Total Peripheral Resistance) is regulated short-term by arterial baroreceptors in the carotid sinus and aortic arch. Stretch-sensitive baroreceptors fire in proportion to arterial pressure; increased firing inhibits sympathetic outflow and augments vagal tone, lowering HR and causing arteriolar vasodilation. This reflex acts within seconds. Long-term blood pressure control is dominated by the renin-angiotensin-aldosterone system (RAAS) and pressure natriuresis.

The coronary arteries — the left anterior descending (LAD), left circumflex (LCx), and right coronary artery (RCA) — supply the myocardium. Coronary blood flow occurs predominantly during diastole because systolic compression impedes flow. Coronary vasodilation is driven by local metabolic factors including adenosine, CO2, and H+, which increase blood flow proportional to myocardial oxygen demand. Atherosclerotic plaque rupture with superimposed thrombosis causes acute myocardial infarction.