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PY5.1-16 | Cardiovascular Physiology — Part 1
CLINICAL SCENARIO
Your heart pumps 7,000 litres of blood per day — enough to fill a small tanker truck. It beats about 100,000 times a day, 3 billion times in a lifetime, and it never takes a holiday. How does a fist-sized muscle do this? The answer lies in an elegant cycle of filling and emptying that repeats every 0.8 seconds — the cardiac cycle. By the end of this section, you'll understand every phase of that cycle, why you hear 'lub-dub' with a stethoscope, and how the heart adjusts its output from 5 L/min at rest to 25 L/min during a sprint.
WHY THIS MATTERS
As a doctor, the cardiac cycle is not abstract physiology — it's what you hear every time you place a stethoscope on a patient's chest. Understanding the cycle tells you what each heart sound means, why murmurs occur at specific times, what cardiac output means for tissue perfusion, and why heart failure is fundamentally a failure of the pump. Every decision in cardiology, anaesthesia, surgery, and emergency medicine depends on understanding how this pump works.
RECALL
From Anatomy (AN22), you know the heart has four chambers — two atria (receiving chambers) and two ventricles (pumping chambers). You know the AV valves (mitral and tricuspid) guard the AV orifices, and the semilunar valves (aortic and pulmonary) guard the outflow tracts. You know the coronary arteries supply the heart muscle itself. Now we ask: how do these structures work together as a coordinated pump?
Properties of Cardiac Muscle (PY5.1, PY5.5)
Five Properties of Cardiac Muscle
| Property | Definition | Key Feature | Clinical Significance |
|---|---|---|---|
| Automaticity | Self-generation of action potentials | SA node fires at 70-80/min without neural input | Transplanted (denervated) hearts keep beating |
| Rhythmicity | Regular, repetitive firing | SA node > AV node > Purkinje fibres (hierarchy) | Fastest pacemaker dominates; escape rhythms if SA fails |
| Conductivity | Cell-to-cell spread via gap junctions | Functional syncytium; AV bundle is sole atrial-ventricular bridge | Heart block if AV bundle damaged |
| Excitability | Response to stimuli with action potential | Long refractory period (~250 ms) prevents tetanus | Heart cannot sustain continuous contraction |
| Contractility | Force of contraction can be modulated | Positive inotropy: sympathetic, catecholamines, digoxin | Basis of inotropic drug therapy in heart failure |
Cardiac muscle is unique — it shares features with both skeletal and smooth muscle, yet has properties found in neither.
Five Properties of Cardiac Muscle
| Property | Definition | Mechanism | Clinical Significance |
|---|---|---|---|
| Automaticity | Self-generation of action potentials without neural input | SA node pacemaker potential (If current) | Denervated transplant hearts keep beating |
| Rhythmicity | Regular, repeating firing pattern | Hierarchy: SA node 70-80 > AV node 40-60 > Purkinje 15-40/min | Fastest pacemaker dominates; ectopic pacemakers if SA fails |
| Conductivity | Cell-to-cell spread of impulse via gap junctions | Intercalated discs form functional syncytium; fibrous skeleton insulates atria from ventricles | Bundle of His is the ONLY atrio-ventricular electrical bridge |
| Excitability | Response to stimuli with an action potential | Long refractory period (~250 ms) due to Phase 2 plateau | Prevents tetanus — sustained contraction would be fatal |
| Contractility | Adjustable force of contraction | Ca2+ influx and SR release; Frank-Starling mechanism | Positive inotropes (sympathetic, digoxin) increase force; negative inotropes decrease it |
Five special properties of cardiac muscle:
- Automaticity (self-excitation) — cardiac muscle can generate its own action potentials WITHOUT neural input. The SA node (sinoatrial node) is the 'pacemaker' — it fires spontaneously at ~70-80 beats/min. Even a denervated heart (after transplant) keeps beating.
- Rhythmicity — the SA node fires at a regular rhythm. Each part of the conduction system has an intrinsic rate: SA node ~70-80/min, AV node ~40-60/min, Purkinje fibres ~15-40/min. The fastest pacemaker controls the heart — normally the SA node.
- Conductivity — the action potential spreads from cell to cell through gap junctions (intercalated discs). This makes the entire atrium (or ventricle) contract as a single unit — a functional syncytium. The atria and ventricles are electrically insulated from each other by the fibrous skeleton of the heart; the ONLY electrical connection between them is the AV bundle (Bundle of His).
- Excitability — cardiac muscle responds to stimuli with an action potential. But unlike skeletal muscle, it has a long refractory period (~250 ms) because of the prolonged plateau phase (Phase 2) of the cardiac action potential. This prevents tetanus — the heart cannot sustain a continuous contraction, which would be fatal.
- Contractility — the force of contraction can be increased (positive inotropic effect) by sympathetic stimulation, catecholamines, digoxin, or increased calcium. Decreased contractility (negative inotropic effect) occurs with heart failure, acidosis, or beta-blockers.
The cardiac action potential has 5 phases (0-4), unlike the simple depolarization-repolarization of skeletal muscle. The key difference is Phase 2 (plateau) — a sustained inflow of Ca2+ through L-type calcium channels that maintains depolarization for ~200-300 ms. This plateau is responsible for the long refractory period and for triggering contraction via calcium-induced calcium release (CICR) from the sarcoplasmic reticulum.
The Cardiac Cycle (PY5.2)
The cardiac cycle is one complete sequence of contraction and relaxation of the heart. At a heart rate of 75 bpm, one cycle = 0.8 seconds.
Figure: The Cardiac Cycle (PY5.2)
The cycle has 7 phases — follow this sequence carefully:
1. Atrial systole (0.1 s) — The atria contract, pushing the final 20-30% of blood into the ventricles (the 'atrial kick'). The ventricles are already ~70% filled from passive filling during diastole. P wave on ECG precedes this.
2. Isovolumetric (isovolumic) ventricular contraction (0.05 s) — The ventricles begin contracting. Pressure rises rapidly. Both AV valves AND semilunar valves are CLOSED — so volume doesn't change. First heart sound (S1, 'lub') occurs here — caused by closure of the AV valves (mitral and tricuspid).
3. Rapid ventricular ejection (0.1 s) — When ventricular pressure exceeds aortic/pulmonary pressure, the semilunar valves open. Blood rushes out. About 70% of stroke volume is ejected in this phase.
4. Reduced ventricular ejection (0.15 s) — Ejection slows as the pressure gradient decreases. T wave on ECG occurs during this phase (ventricular repolarization).
5. Isovolumetric ventricular relaxation (0.08 s) — The ventricles relax. Pressure drops rapidly. Both semilunar AND AV valves are CLOSED — volume doesn't change again. Second heart sound (S2, 'dub') occurs here — caused by closure of the semilunar valves (aortic and pulmonary).
6. Rapid ventricular filling (0.1 s) — When ventricular pressure falls below atrial pressure, the AV valves open. Blood rushes in passively (no atrial contraction needed). Third heart sound (S3) may be heard here — caused by rapid filling stretching the ventricular wall. Normal in children, pathological in adults (indicates heart failure with a dilated, compliant ventricle).
7. Reduced ventricular filling (diastasis) (0.2 s) — Filling slows as atrial and ventricular pressures equalize. Then the P wave fires and the cycle repeats.
Key numbers: End-diastolic volume (EDV) = ~120 mL; End-systolic volume (ESV) = ~50 mL; Stroke volume (SV) = EDV - ESV = ~70 mL; Ejection fraction = SV/EDV = ~58-60%.
Heart Sounds and Cardiac Output (PY5.2, PY5.6)
Heart Sounds — Summary
| Sound | Cause | Best Heard At | Timing | Clinical Note |
|---|---|---|---|---|
| S1 ('lub') | AV valve closure (mitral + tricuspid) | Apex (mitral area) | Start of ventricular systole | Loud S1 in mitral stenosis |
| S2 ('dub') | Semilunar valve closure (aortic + pulmonary) | Base (aortic/pulmonary area) | End of ventricular systole | Physiological split on inspiration |
| S3 | Rapid ventricular filling | Apex, left lateral decubitus | Early diastole | Normal in young; pathological >40 yrs (heart failure) |
| S4 | Atrial contraction into stiff ventricle | Apex | Late diastole (presystolic) | Always pathological — LVH, diastolic dysfunction |
Heart sounds in clinical practice:
Figure: Heart Sounds and Cardiac Output (PY5.2, PY5.6)
Heart Sounds — Normal and Abnormal
| Sound | Cause | Best Heard At | Timing | Clinical Significance |
|---|---|---|---|---|
| S1 ('lub') | AV valve closure (mitral + tricuspid) | Apex (mitral area, 5th ICS MCL) | Start of ventricular systole | Loud S1 in mitral stenosis; soft S1 in mitral regurgitation |
| S2 ('dub') | Semilunar valve closure (aortic + pulmonary) | Base (aortic = R 2nd ICS; pulmonary = L 2nd ICS) | End of ventricular systole | Physiological splitting on inspiration (A2 before P2) |
| S3 | Rapid ventricular filling | Apex, left lateral decubitus | Early diastole | Normal in young adults; pathological >40 yrs (volume overload, HF) |
| S4 | Atrial contraction against stiff ventricle | Apex | Late diastole (presystolic) | Always pathological — indicates reduced ventricular compliance (LVH, HCM) |
Heart Sounds — Normal and Abnormal
| Sound | Cause | Best Heard At | Timing | Clinical Significance |
|---|---|---|---|---|
| S1 ('lub') | AV valve closure (mitral + tricuspid) | Apex (mitral area, 5th ICS MCL) | Start of ventricular systole | Loud S1 in mitral stenosis; soft S1 in mitral regurgitation |
| S2 ('dub') | Semilunar valve closure (aortic + pulmonary) | Base (aortic = R 2nd ICS; pulmonary = L 2nd ICS) | End of ventricular systole | Physiological splitting on inspiration (A2 before P2) |
| S3 | Rapid ventricular filling | Apex, left lateral decubitus | Early diastole | Normal in young adults; pathological >40 yrs (volume overload, HF) |
| S4 | Atrial contraction against stiff ventricle | Apex | Late diastole (presystolic) | Always pathological — indicates reduced ventricular compliance (LVH, HCM) |
- S1 ('lub') — AV valve closure. Best heard at the apex (mitral area, 5th intercostal space, mid-clavicular line). Marks the START of ventricular systole.
- S2 ('dub') — Semilunar valve closure. Best heard at the base (aortic area = right 2nd intercostal space; pulmonary area = left 2nd intercostal space). Marks the END of ventricular systole. S2 normally splits during inspiration (A2 before P2) because the right ventricle takes slightly longer to empty.
- S3 — Rapid ventricular filling. Low-pitched, best heard at the apex with the bell of the stethoscope. Normal in children and young adults; pathological in older adults (indicates volume overload, heart failure).
- S4 — Atrial contraction into a stiff ventricle. Occurs just before S1. Always pathological — indicates decreased ventricular compliance (hypertrophic cardiomyopathy, hypertensive heart disease).
Cardiac output (CO) = Heart Rate x Stroke Volume = ~75 x 70 mL = ~5.25 L/min at rest.
Regulation of cardiac output:
- Preload (Frank-Starling mechanism) — the more the heart is filled (increased venous return), the more it stretches, and the more forcefully it contracts. Within physiological limits, 'the heart pumps whatever comes to it.' This is the most important intrinsic mechanism.
- Afterload — the resistance the ventricle must overcome to eject blood (primarily arterial blood pressure). Increased afterload = decreased stroke volume (the heart works harder but pumps less).
- Contractility — the force of contraction independent of preload/afterload. Sympathetic stimulation increases contractility (positive inotropic effect). Heart failure decreases contractility.
- Heart rate — regulated by the autonomic nervous system. Sympathetic increases HR; parasympathetic (vagus) decreases HR. The vagus is dominant at rest (resting vagal tone).
Measurement of CO — Fick's principle: CO = O2 consumption / (arteriovenous O2 difference). If the body consumes 250 mL O2/min, and arterial blood carries 200 mL O2/L while venous blood carries 150 mL O2/L, then CO = 250 / (200-150) = 250/50 = 5 L/min.