The heart

The mammalian heart is a four-chambered, double pump made of cardiac muscle (myocardium) enclosed by a tough fibrous pericardium.

Chambers and septum. The heart has two atria (R and L) and two ventricles (R and L). A muscular septum separates the left side (oxygenated blood) from the right side (deoxygenated blood) so the two never mix. The atria are thin-walled (they only push blood a short distance into the ventricles); the ventricles are thick-walled (they pump blood out at higher pressure).

Left vs right ventricle. The left ventricle wall is about three times thicker than the right ventricle wall. The left ventricle pumps blood at ~120 mmHg around the systemic circulation, which requires far more force than the ~25 mmHg required to push blood through the short pulmonary circuit. Higher pressure in the pulmonary circuit would damage the thin-walled alveolar capillaries.

Valves. Four valves ensure one-way flow:

• Tricuspid valve — the right atrioventricular (AV) valve; between R atrium and R ventricle. Three cusps.
• Bicuspid (mitral) valve — the left AV valve; between L atrium and L ventricle. Two cusps.
• Pulmonary semilunar valve — at the exit of the R ventricle into the pulmonary artery.
• Aortic semilunar valve — at the exit of the L ventricle into the aorta.

The AV valves are anchored by tough fibrous chordae tendineae to papillary muscles projecting from the ventricle wall. The chordae tendineae do NOT open or close the valves; they prevent the cusps from being pushed back (everting) into the atria when ventricular pressure rises during systole.

Major vessels.

• Vena cavae (sup. and inf.) bring deoxygenated blood into the R atrium.
• Pulmonary artery leaves the R ventricle carrying deoxygenated blood to the lungs.
• Pulmonary vein enters the L atrium carrying oxygenated blood from the lungs.
• Aorta leaves the L ventricle carrying oxygenated blood to the body.

Coronary arteries. Branch from the aorta just above the aortic valve and supply the cardiac muscle itself with oxygenated blood. Coronary blockage (atherosclerosis) → myocardial infarction (heart attack), because cardiac muscle quickly dies if deprived of O₂.

The cardiac cycle is one complete sequence of events from the start of one heartbeat to the start of the next. At a resting heart rate of 75 beats per minute, one cycle lasts ~0.8 s, made up of:

• Atrial systole ~0.1 s
• Ventricular systole ~0.3 s
• Diastole ~0.4 s

The cycle is driven by pressure changes in the four chambers and the aorta/pulmonary artery. Valves open and close passively when the pressure on one side exceeds the pressure on the other.

1. Late diastole and atrial filling. Blood returns from the body to the R atrium (via the vena cavae) and from the lungs to the L atrium (via the pulmonary veins). As atrial pressure rises above ventricular pressure, the AV valves open and blood flows passively into the ventricles. About 70-80% of ventricular filling happens here. Semilunar valves remain closed (aortic/pulmonary artery pressure > ventricular pressure).

2. Atrial systole. Stimulated by the SAN, the atria contract simultaneously and push the remaining 20-30% of blood into the ventricles, topping them up to end-diastolic volume (~130 ml in an adult). AV valves remain open; semilunar valves still closed.

3. Ventricular systole — closure of AV valves. After the AVN delay, the Purkinje fibres trigger ventricular contraction from the apex upwards. Ventricular pressure rises rapidly above atrial pressure, closing the AV valves — this produces the first heart sound ('LUB', S1). The chordae tendineae prevent the valves from everting into the atria.

4. Isovolumetric contraction. All four valves are momentarily closed. Ventricular pressure climbs further but volume is constant.

5. Ventricular systole — ejection. When ventricular pressure exceeds aortic pressure (~80 mmHg, the diastolic pressure) and pulmonary arterial pressure, the semilunar valves open and blood is ejected. Each ventricle pumps about 70 ml (the stroke volume). Ventricular pressure peaks at ~120 mmHg in the LV and ~25 mmHg in the RV.

6. Early diastole — closure of semilunar valves. Ventricles begin to relax; ventricular pressure falls. When ventricular pressure drops below aortic/pulmonary arterial pressure, the semilunar valves close — second heart sound ('DUB', S2). A small dicrotic notch in the aortic pressure trace marks this.

7. Isovolumetric relaxation. All valves closed; ventricles relax further; pressure falls below atrial pressure.

8. Cycle repeats. AV valves open and the ventricles refill — back to phase 1.

Pressure traces. A standard 9700 graph shows three curves: aortic pressure (high, with a small dip — the dicrotic notch — at semilunar valve closure), ventricular pressure (rises sharply during ventricular systole, then falls steeply during diastole) and atrial pressure (low; small bump during atrial systole). You should be able to identify each phase from the graph and indicate where valves open and close.

The mammalian heart is myogenic — it contracts and relaxes rhythmically without nerve impulses from outside. A transplanted heart, with its nerves cut, still beats. External nerves and hormones (sympathetic, parasympathetic vagus, adrenaline) only adjust the rate set by the heart's own pacemaker.

1. Sino-atrial node (SAN) — the pacemaker. A patch of specialised cardiac muscle in the wall of the right atrium, near where the superior vena cava enters. SAN cells depolarise spontaneously at intervals (~70 times per minute at rest) due to leaky Na⁺/Ca²⁺ ion channels. Each depolarisation launches a wave of electrical excitation.

2. Wave through atria → atrial systole. The wave spreads through the muscle of both atria via gap junctions in the intercalated discs. Atrial muscle depolarises and contracts simultaneously — atrial systole.

3. Atrio-ventricular node (AVN) — the delay. The wave reaches the AVN, located in the septum between the atria and ventricles. The AVN imposes a delay of ~0.1 s before passing the signal on. This is essential: it ensures the atria have finished contracting and emptied into the ventricles before the ventricles themselves begin to contract.

4. Bundle of His. From the AVN, the wave travels rapidly down a band of conducting tissue — the Bundle of His — through the interventricular septum to the apex of the heart.

5. Purkinje fibres. At the apex, the Bundle of His divides into Purkinje fibres that fan UP through the walls of the ventricles. These fibres conduct very rapidly, so the ventricular muscle depolarises almost simultaneously throughout.

6. Ventricular systole — apex upwards. The ventricles contract from the apex upwards, pushing blood UP towards the semilunar valves and out into the aorta and pulmonary artery. The 'apex to base' direction is essential — contracting top-down would push blood back towards the atria.

Rate modulation. The SAN's intrinsic rate of ~70-100/min is modulated by:

• Sympathetic nerves (and adrenaline) — increase SAN firing rate.
• Parasympathetic vagus nerve — decreases SAN firing rate.
• Stretch receptors in atria and aorta feed back to the medulla.

If the SAN fails, the AVN can act as a back-up pacemaker, but at a slower rate (~50/min). Artificial pacemakers replace this function.

An electrocardiogram (ECG) is a surface recording of the changing voltages produced by the heart's electrical activity. Electrodes placed on the skin detect the wave of depolarisation as it travels through the cardiac muscle.

A normal ECG trace shows a repeating pattern of three components per heartbeat:

• P wave — a small upward deflection corresponding to depolarisation of the atria. Immediately precedes atrial systole.
• PR interval — the flat segment between the end of the P wave and the start of the QRS complex. Corresponds to the delay at the AVN.
• QRS complex — a large spike corresponding to depolarisation of the ventricles. Immediately precedes ventricular systole. The QRS is much larger than the P wave because the ventricular muscle has a far greater mass than the atrial muscle. (Atrial repolarisation is hidden inside the QRS.)
• ST segment — flat plateau corresponding to the plateau of the ventricular action potential during ventricular ejection.
• T wave — a rounded deflection corresponding to repolarisation of the ventricles. Coincides with the start of ventricular diastole.

A typical resting heart rate (~70-75 bpm) gives ~70-75 P-QRS-T cycles per minute.

Abnormal ECGs are diagnostic:

• Tachycardia — heart rate >100 bpm at rest (could be due to fever, anxiety, exercise, hyperthyroidism).
• Bradycardia — heart rate <60 bpm at rest (could be normal in athletes; abnormal if symptomatic).
• Atrial fibrillation — no clear P waves; irregular QRS; atrial contractions uncoordinated.
• Heart block — atrial activity (P) and ventricular activity (QRS) become dissociated.
• Myocardial infarction — raised ST segment, inverted T wave; pathological Q wave develops later.
• Ventricular fibrillation — chaotic QRS; cardiac arrest if untreated; treated by defibrillation.

For 9700 you should be able to (a) label P, QRS and T on a normal trace, (b) relate each to events in the cardiac cycle, and (c) calculate heart rate from time markings on the trace.

Two simple measures describe heart function:

• Stroke volume (SV) — the volume ejected by one ventricle per heartbeat. At rest in an adult, SV ≈ 70 ml (0.07 dm³).
• Heart rate (HR) — number of beats per minute. At rest, HR ≈ 70-75 bpm.

$\text{Cardiac output (Q)} = \text{stroke volume} \times \text{heart rate}$

At rest: Q ≈ 0.07 × 75 ≈ 5 dm³ min⁻¹ — the entire blood volume (~5 L) passes through the heart every minute.

During exercise, Q can rise to >20 dm³ min⁻¹ through:

• Increased heart rate (sympathetic stimulation, less vagal inhibition, raised adrenaline).
• Increased stroke volume (greater venous return ⇒ greater ventricular filling ⇒ stretched myocardium contracts more forcefully — Starling's law of the heart).

Heart rate regulation. The medulla oblongata contains a cardiovascular control centre. It receives input from:

• Stretch receptors (baroreceptors) in the aorta and carotid arteries — signal high BP.
• Chemoreceptors in the aorta and carotid bodies — signal high CO₂ / low O₂ / low pH.
• Higher brain centres (anticipation, emotion).

Output runs via the autonomic nervous system:

• Sympathetic (cardiac accelerator nerves) — release noradrenaline at the SAN → increase rate.
• Parasympathetic (vagus nerve) — release acetylcholine at the SAN → decrease rate.

Adrenaline from the adrenal medulla amplifies the sympathetic effect during stress or exercise. The result is moment-by-moment matching of cardiac output to metabolic demand.