Cardiovascular Physiology

The heart is a muscular pump about the size of your fist, sitting slightly left of centre in your chest. Its sole job is to move blood — continuously, for your entire life, without rest. The heart has four chambers: - Right atrium — receives deoxygenated blood from the body (via the vena cava) - Right ventricle — pumps this blood to the lungs (via the pulmonary artery) - Left atrium — receives oxygenated blood returning from the lungs (via the pulmonary veins) - Left ventricle — pumps this blood to the entire body (via the aorta) The left ventricle has much thicker walls than the right — because it must generate far more pressure to push blood to the toes, the brain, and everywhere else. The right ventricle only needs to push blood a short distance to the lungs. Two circulations work in parallel: 1. Pulmonary circulation — right heart → lungs → left heart (short loop for gas exchange) 2. Systemic circulation — left heart → body → right heart (long loop delivering oxygen everywhere) Four valves prevent backflow: - Tricuspid (right atrium → right ventricle) - Pulmonary (right ventricle → pulmonary artery) - Mitral (bicuspid) (left atrium → left ventricle) - Aortic (left ventricle → aorta) The familiar "lub-dub" of the heartbeat is the sound of these valves snapping shut — "lub" is the mitral and tricuspid closing, "dub" is the aortic and pulmonary closing.

Every heartbeat is a carefully coordinated sequence called the cardiac cycle. One complete cycle — one heartbeat — takes about 0.8 seconds at rest (heart rate ~75 beats per minute). The cycle has two phases: Systole (contraction): - The ventricles contract, squeezing blood out - Left ventricle → aorta (to the body) - Right ventricle → pulmonary artery (to the lungs) - The aortic and pulmonary valves are OPEN; the mitral and tricuspid valves are CLOSED (preventing backflow into the atria) - Blood pressure in the arteries rises — this is the systolic blood pressure (the top number, e.g. 120 mmHg) Diastole (relaxation): - The ventricles relax and refill with blood from the atria - The mitral and tricuspid valves are OPEN; the aortic and pulmonary valves are CLOSED - Pressure in the arteries falls — this is the diastolic blood pressure (the bottom number, e.g. 80 mmHg) - The coronary arteries (which supply blood to the heart muscle itself) fill predominantly during diastole — this is why a fast heart rate can reduce coronary filling time and cause angina (heart pain) Cardiac output = how much blood the heart pumps per minute: Cardiac output = Heart rate × Stroke volume - Heart rate: beats per minute (normally ~70 bpm at rest) - Stroke volume: volume ejected per beat (~70 mL at rest) - Normal cardiac output: ~5 L/min — approximately the entire blood volume every minute During exercise, cardiac output can increase to 20–25 L/min as both heart rate and stroke volume increase.

The heart doesn't wait for the nervous system to tell it when to beat — it generates its own electrical signals. This is called automaticity (or autorhythmicity). How the heartbeat is initiated: 1. Sinoatrial (SA) node — the heart's natural pacemaker Located in the right atrium. Spontaneously generates an electrical impulse about 70 times per minute. This impulse spreads across both atria, causing them to contract and push blood into the ventricles. 2. Atrioventricular (AV) node — the gatekeeper The impulse reaches the AV node (at the junction of atria and ventricles) and is *deliberately delayed* for about 0.1 seconds. This delay gives the atria time to finish contracting before the ventricles start — ensuring efficient filling. 3. Bundle of His and Purkinje fibres — the ventricles' wiring After the AV node delay, the impulse travels rapidly down specialised conducting fibres (bundle of His → left and right bundle branches → Purkinje fibres) to the ventricular muscle. The ventricles contract almost simultaneously — pushing blood out efficiently. The ECG (Electrocardiogram) records these electrical events from electrodes on the skin: - P wave — atrial depolarisation (atria contracting) - QRS complex — ventricular depolarisation (ventricles contracting) — this is the biggest spike - T wave — ventricular repolarisation (ventricles resetting for next beat) Clinical relevance: - An absent P wave suggests AF (atrial fibrillation) — the most common heart rhythm disorder - A widened QRS suggests a bundle branch block — one side of the ventricles is contracting late - A raised ST segment (the flat line between QRS and T wave) is the classic ECG sign of a heart attack

Blood travels through a network of vessels, each with a specific structure suited to its function: Arteries — carry blood AWAY from the heart - Thick elastic walls to withstand high pressure from ventricular contraction - Larger arteries (aorta, pulmonary) have most elasticity — they stretch during systole and recoil during diastole, smoothing out the pulsatile flow - Arterioles (small arteries) have muscular walls — they can constrict or dilate to regulate flow to individual organs and control blood pressure Capillaries — the site of exchange - Just one cell thick — the thinnest possible barrier - Oxygen, nutrients, and hormones diffuse FROM blood INTO tissues - Carbon dioxide and waste products diffuse FROM tissues INTO blood - Surface area is enormous — estimated 500–700 m² total in the body - Blood moves slowly through capillaries — giving time for exchange Veins — carry blood BACK to the heart - Low-pressure, thin walls - Have valves to prevent backflow (blood must travel against gravity returning from the legs) - Act as a blood reservoir — about 60% of the blood volume is in the veins at any given time - Muscle contraction around veins (e.g. walking) helps push blood back — this is why prolonged sitting raises the risk of clots (deep vein thrombosis) Clinical connections: - Varicose veins — valves in leg veins become incompetent → blood pools → veins dilate and become visible - Deep vein thrombosis (DVT) — clot forms in a leg vein, often from prolonged immobility → risk of it breaking off and travelling to the lungs (pulmonary embolism) - Shock — inadequate blood flow to tissues, despite the heart pumping. Can be from low blood volume (haemorrhage), heart failure, or widespread vasodilation (sepsis)

Exercise is one of the greatest tests of cardiovascular physiology — and the body's response demonstrates multiple regulatory systems working together. What happens during exercise: Immediate (seconds): - Muscles demand more oxygen - Sympathetic nervous system activates → heart rate increases, stroke volume increases → cardiac output rises dramatically (up to 5× resting) - Blood vessels in active muscles dilate (via local metabolites like CO₂, lactic acid, adenosine) → more blood delivered where needed - Blood vessels in non-essential areas (gut, kidneys, skin) constrict → blood redirected to muscles Within minutes: - Core temperature rises → skin blood vessels dilate → sweating begins → heat lost - Chemoreceptors detect rising CO₂ and falling O₂ → breathing rate and depth increase - Blood pressure rises moderately (systolic increases; diastolic stays roughly stable or falls because muscle vasodilation reduces total resistance) Long-term adaptation (weeks of training): Regular aerobic exercise causes the heart to remodel: - Increased stroke volume — the ventricle becomes larger and stronger, pumping more blood per beat - Lower resting heart rate — athletes often have resting heart rates of 40–50 bpm (compared to 70 for untrained individuals) because each beat delivers more blood - Increased capillary density in trained muscles — better oxygen delivery - Reduced blood pressure — regular exercise is one of the most effective non-drug treatments for hypertension This is why a trained athlete's heart looks different on an ECG and echocardiogram — larger ventricles and slower electrical conduction. It is called "athlete's heart" and is completely normal.