The Cardiac Cycle

• Why is the SA node the heart’s pacemaker?

  The SA node sets the heart rate because it has the fastest spontaneous depolarisation rate due to:

  • Unstable phase 4 depolarisation (If "funny" current).
  • No resting membrane potential (continuously depolarising).
  • Inherent firing rate (~60-100 bpm), faster than the AV node or Purkinje fibres.

  Other pacemakers (AV node, Purkinje fibres) have slower rates and only take over if the SA node fails.
• When do S3 and S4 heart sounds occur, and what do they indicate?

  • S3 (early diastolic filling sound) → Can be normal in young people but indicates heart failure in older adults.
  • S4 (atrial contraction sound) → Associated with left ventricular hypertrophy or stiff ventricle.
• What is the Wiggers diagram and why is it important?

  • The Wiggers diagram shows simultaneous changes in pressure, volume, ECG, and heart sounds during the cardiac cycle.
  • Helps visualise the timing of mechanical and electrical events.
• What is the role of the SA node in the conduction system?

  • The SA node generates spontaneous action potentials at a rate of 60–100 beats per minute (bpm).
  • It is the primary pacemaker of the heart due to its fastest intrinsic rhythm.
  • Located in the right atrium, near the superior vena cava opening.
  • Depolarisation spreads across both atria, causing atrial contraction (atrial systole).
• What is the role of calcium in the cardiac action potential?

  • In ventricular myocytes, Ca²⁺ influx (Phase 2) triggers contraction via calcium-induced calcium release (CICR) from the sarcoplasmic reticulum.
  • In pacemaker cells, Ca²⁺ (L-type) drives depolarisation (Phase 0) instead of Na⁺.

  Clinical Relevance:

  • Calcium channel blockers (e.g., verapamil, diltiazem) slow conduction through the AV node, reducing heart rate.
• What is the refractory period, and why is it important?

  The refractory period prevents tetanic contraction and ensures proper heart function.

  • Absolute Refractory Period (ARP): No new action potential can be triggered (Na⁺ channels inactivated).
  • Relative Refractory Period (RRP): A stronger stimulus can trigger a weak action potential.

  Clinical Relevance:

  • Prolonged refractory periods (e.g., due to drugs or genetic mutations) can cause arrhythmias like Torsades de Pointes.
• What is the normal sequence of electrical conduction in the heart?

  1. SA node fires → atrial depolarisation → atria contract.
  2. AV node delays impulse (~0.1 sec) → allows atrial contraction.
  3. Bundle of His transmits impulse to ventricles.
  4. Right & Left Bundle Branches spread impulses through septum.
  5. Purkinje fibres distribute impulse → ventricles contract (ventricular systole).

  Mnemonic: "Start A Big Pulse"(SA node → AV node → Bundle of His → Purkinje fibres)
• What is the function of the AV node in cardiac conduction?

  • The AV node receives impulses from the SA node.
  • It delays conduction (approx. 0.1 sec) to allow complete atrial contraction before ventricular contraction.
  • Can act as a secondary pacemaker (40–60 bpm) if the SA node fails.
• What is the function of Purkinje fibres in cardiac conduction?

  • Purkinje fibres distribute impulses throughout the ventricular myocardium, ensuring a rapid and coordinated contraction.
  • Essential for efficient ejection of blood from the heart.
  • Conduct at 2–4 m/s, the fastest in the cardiac conduction system.
  • Ventricular depolarisation leads to ventricular systole (contraction).
• What is the ejection fraction (EF) and its normal range?

  • EF (%) = (Stroke Volume / EDV) × 100.
  • Normal EF = 50-70%.
  • Measures heart efficiency (low EF suggests heart failure).
• What is the difference between rapid and reduced ejection?

  • Rapid ejection: The first part of ventricular ejection, when blood flows quickly into arteries due to high pressure.
  • Reduced ejection: The later part, as ventricular pressure falls and blood flow slows.
• What is the cardiac action potential?

  The cardiac action potential is the rapid change in membrane potential in cardiac cells that initiates and propagates electrical impulses, leading to coordinated contraction of the heart. It occurs in two types of cells
• What is the Bundle of His and its role in conduction?

  • The Bundle of His (AV bundle) is a collection of specialised fibres that transmits electrical impulses from the AV node to the ventricles.
  • Located in the interventricular septum.
  • Divides into right and left bundle branches to ensure coordinated contraction of the ventricles.
• What is stroke work, and how is it calculated?


  Stroke work is the amount of work done by the ventricle to pump blood into the aorta. It is calculated as: Stroke Work = Stroke Volume x Mean Aortic Pressure. On average, stroke work = 70 mL × 100 mmHg = 7000 mmHg·mL.
• What is stroke volume, and how is it calculated?

  Stroke volume (SV) is the amount of blood ejected from the left ventricle per beat. It is calculated as:SV = EDV - ESVOn average, SV is 70 mL (120 mL - 50 mL).
• What is end-diastolic volume (EDV) and end-systolic volume (ESV)?

  • EDV (~120 mL): The volume of blood in the ventricles at the end of diastole (before contraction).
  • ESV (~50 mL): The volume of blood left in the ventricles after systole (after contraction).
• What happens to left ventricular pressure when the aortic valve opens?

  • The pressure continues to rise as blood is ejected into the aorta (~80 → 120 mmHg).
  • Once ejection slows, pressure decreases (~120 → 80 mmHg).
• What happens to atrial pressure during atrial systole?

  • Atrial pressure increases due to contraction.
  • The pressure gradient drives blood into the ventricles.
  • Atrial pressure then decreases as blood moves into the ventricles.
• What happens if the SA node fails?

  • The AV node takes over as the pacemaker (40–60 bpm).
  • If the AV node fails, the Purkinje fibres can generate impulses (20–40 bpm), but this is too slow to sustain life.
  • This condition may require an artificial pacemaker.
• What happens during ventricular filling?

  • AV valves open as ventricular pressure falls below atrial pressure.
  • Blood flows passively from the atria into the ventricles (first rapidly, then slower).
  • Accounts for ~70-80% of ventricular filling before atrial systole.
  • Corresponds to the T-P interval on ECG.
• What happens during ventricular ejection?

  • Ventricular pressure exceeds aortic & pulmonary artery pressures, opening the semilunar valves (aortic & pulmonary valves).
  • Blood is ejected into the aorta & pulmonary artery.
  • Aortic pressure rises (~120 mmHg in systole).
  • Ventricular volume decreases.
• What happens during isovolumetric relaxation?

  • Ventricles relax (beginning of diastole).
  • Semilunar valves close, producing the second heart sound (S₂).
  • AV valves remain closed.
  • No blood enters or leaves the ventricles (isovolumetric).
  • Ventricular pressure falls rapidly, but volume remains the same.
• What happens during isovolumetric contraction?

  • Ventricles begin to contract (QRS complex on ECG).
  • AV valves close due to increased ventricular pressure (producing the first heart sound, S₁).
  • Semilunar valves remain closed (no blood ejection).
  • Ventricular volume remains constant (hence "isovolumetric").
  • Pressure rises sharply.
• What happens during atrial systole?

  • Atria contract (P wave on ECG).
  • Increased atrial pressure pushes final 20-30% of blood into ventricles.
  • Ventricular volume reaches end-diastolic volume (EDV) (~120 mL).
  • Atrioventricular (AV) valves (tricuspid & mitral) remain open, semilunar valves closed.
• What drugs affect cardiac action potentials?

  • Class I (Na⁺ blockers): Slow Phase 0 depolarisation (e.g., Lidocaine).
  • Class II (β-blockers): Reduce If current, slowing HR (e.g., Metoprolol).
  • Class III (K⁺ blockers): Prolong repolarisation (e.g., Amiodarone).
  • Class IV (Ca²⁺ blockers): Slow conduction, especially at AV node (e.g., Verapamil).
• What determines the stroke work of the left ventricle?

  • Preload (end-diastolic volume)
  • Afterload (aortic pressure)
  • Contractility (strength of ventricular contraction)
• What causes the second heart sound (S₂)?

  Closure of the semilunar valves (aortic & pulmonary valves) due to falling ventricular pressure in early diastole.
• What causes the rapid pressure drop during isovolumetric relaxation?

  The ventricular myocardium relaxes, but the aortic and mitral valves remain closed, leading to a sudden decrease in pressure.
• What causes the large pressure rise during isovolumetric contraction?

  The ventricular myocardium contracts, but since the aortic valve is closed, the volume remains constant, causing a sharp increase in pressure.
• What causes the first heart sound (S₁)?

  Closure of the AV valves (tricuspid and mitral valves) due to rising ventricular pressure in isovolumetric contraction.
• What are the two types of cells that a cardiac action potential occurs in?

  • Pacemaker cells (SA node, AV node) – generate spontaneous action potentials.
  • Cardiomyocytes (Atrial and Ventricular muscle) – contract in response to action potentials.
• What are the two phases of ventricular filling?

  1. Rapid filling – Blood flows quickly into the ventricles due to the pressure gradient.
  2. Reduced filling (diastasis) – Blood flow slows as ventricular pressure rises.
• What are the phases of an ECG (electrocardiogram) related to conduction?

  • P wave → Atrial depolarisation (SA node activation).
  • PR interval → AV node delay (0.12–0.2 sec).
  • QRS complex → Ventricular depolarisation (Bundle of His, Purkinje fibres).
  • T wave → Ventricular repolarisation.
  • QT interval → Time for ventricular depolarisation & repolarisation.
• What are the main phases of the pacemaker action potential?

  • Phase 4 (Slow Depolarisation): Funny Na⁺ (If) and T-type Ca²⁺ channels gradually depolarise the cell.
  • Phase 0 (Depolarisation): L-type Ca²⁺ influx instead of Na⁺ influx.
  • Phase 3 (Repolarisation): K⁺ efflux via delayed rectifier K⁺ channels.
• What are the main phases of the ventricular (non-pacemaker) action potential?

  The ventricular action potential has five phases (0-4):

  • Phase 0 (Depolarisation): Rapid Na⁺ influx via voltage-gated Na⁺ channels.
  • Phase 1 (Initial Repolarisation): Na⁺ channels inactivate, transient K⁺ efflux.
  • Phase 2 (Plateau): L-type Ca²⁺ channels open, Ca²⁺ influx balances K⁺ efflux.
  • Phase 3 (Repolarisation): K⁺ efflux via delayed rectifier K⁺ channels.
  • Phase 4 (Resting Membrane Potential): Na⁺/K⁺ ATPase and K⁺ leak channels maintain resting potential (~ -90mV).
• What are the main phases of the cardiac cycle?

  1. Atrial systole (Phase 1) – Atria contract, pushing blood into ventricles.
  2. Isovolumetric contraction (Phase 2) – Ventricles contract with closed valves, increasing pressure.
  3. Ventricular ejection (Phase 3) – Blood is ejected into the aorta and pulmonary artery.
  4. Isovolumetric relaxation (Phase 4) – Ventricles relax with closed valves, decreasing pressure.
  5. Ventricular filling (Phase 5) – Blood flows passively from atria to ventricles.
• What are the key structures involved in the conduction pathway of the heart?

  1. Sinoatrial (SA) node – The pacemaker of the heart, located in the right atrium.
  2. Atrioventricular (AV) node – Delays the impulse to allow atrial contraction before ventricular contraction.
  3. Bundle of His – Conducts impulses from the AV node to the ventricles.
  4. Right and Left Bundle Branches – Carry the impulse down the interventricular septum.
  5. Purkinje Fibres – Spread the impulse through the ventricles for coordinated contraction.
• What are the key ionic movements in each phase of the ventricular action potential?

  • Phase 0: Na⁺ influx (via fast voltage-gated Na⁺ channels).
  • Phase 1: K⁺ efflux (transient outward K⁺ current, Ito).
  • Phase 2: Ca²⁺ influx (via L-type Ca²⁺ channels) & K⁺ efflux (slow rectifier K⁺ channels).
  • Phase 3: K⁺ efflux (via delayed rectifier K⁺ channels).
  • Phase 4: K⁺ equilibrium (maintained by K⁺ leak channels and Na⁺/K⁺ ATPase).
• What are common conduction abnormalities?

  • Bradycardia – Slow HR (<60 bpm), due to SA node dysfunction or AV block.
  • Tachycardia – Fast HR (>100 bpm), can be atrial or ventricular in origin.
  • Heart block – Impaired AV node conduction, classified as:
  • 1st-degree → Prolonged PR interval.
  • 2nd-degree → Some impulses fail to pass to ventricles.
  • 3rd-degree → Complete AV dissociation; ventricles rely on Purkinje fibres.
  • Atrial fibrillation (AF) – Disorganised atrial impulses; no clear P waves.
  • Ventricular fibrillation (VF) – Life-threatening, uncoordinated ventricular contractions.
• How does the pacemaker (SA node) action potential differ from the ventricular action potential?

  • SA node cells lack Phase 1 & 2 (plateau).
  • Depolarisation is slower (Ca²⁺-dependent, not Na⁺-dependent).
  • Phase 4 is unstable, allowing automaticity (spontaneous firing).