Cardiac Physiology

Related Subjects: |Pulmonary Physiology |Pancreas Physiology |Renal Physiology |Pulmonary Physiology |Cardiac Anatomy and Physiology |Coronary Anatomy and Physiology |Cardiac Electrophysiology |Cardiac Embryology |Cardiac Physiology |Cardiac Physiology |Gastrointestinal tract Physiology |Autonomic Nervous System

🫀 Cardiac physiology explores how the heart generates, regulates, and coordinates mechanical and electrical activity to maintain blood flow. The heart is a four-chambered muscular pump that operates as two pumps in series — the right heart (pulmonary circulation) and left heart (systemic circulation). Its function depends on intricate interactions between electrical excitation, muscle contraction, valvular mechanics, and haemodynamic control systems that ensure continuous perfusion of tissues.

🧠 Key Concepts

• Anatomy and Functional Organisation
  • Four chambers: right atrium → right ventricle → lungs → left atrium → left ventricle → systemic circulation.
  • Valves maintain unidirectional flow: Tricuspid (RA–RV), Pulmonary, Mitral (LA–LV), and Aortic.
  • The coronary circulation arises from the aortic root and returns via the coronary sinus. Coronary flow occurs mainly during diastole due to compression of intramyocardial vessels during systole.
• Cardiac Muscle and Cellular Physiology
  • Cardiac muscle fibres are striated, branched, and interconnected by intercalated discs containing gap junctions that enable electrical synchrony (functional syncytium).
  • Excitation–contraction coupling:
    • An action potential travels along the sarcolemma and T-tubules.
    • Voltage-gated L-type calcium channels open, allowing Ca²⁺ influx.
    • This triggers Ca²⁺ release from the sarcoplasmic reticulum (SR) via ryanodine receptors — the “calcium-induced calcium release” mechanism.
    • Calcium binds to troponin C, causing tropomyosin to move, exposing actin-binding sites for myosin.
    • ATP-driven cross-bridge cycling follows the sliding filament theory.
    • Relaxation occurs when Ca²⁺ is pumped back into the SR by SERCA and extruded via the Na⁺/Ca²⁺ exchanger.
  • Unlike skeletal muscle, cardiac contraction is graded — the more Ca²⁺ that enters, the stronger the contraction.

⚡ Electrical Conduction and Action Potentials

• Conduction System: SA node → atria → AV node → Bundle of His → bundle branches → Purkinje fibres → ventricular myocardium.
• SA Node (pacemaker): Generates spontaneous depolarisation via slow inward Na⁺ (“funny current”) and Ca²⁺ influx, setting the heart rate (~60–100 bpm).
• AV Node: Provides a conduction delay (~0.1 s) to ensure atrial emptying before ventricular contraction.
• Purkinje fibres: Conduct impulses rapidly (~4 m/s) for synchronised ventricular activation.
• Action Potentials:
  • Ventricular Myocytes:
    1. Phase 0: Rapid Na⁺ influx → depolarisation.
    2. Phase 1: Transient K⁺ efflux.
    3. Phase 2: Plateau phase — Ca²⁺ influx via L-type channels balances K⁺ efflux.
    4. Phase 3: Repolarisation via K⁺ channels.
    5. Phase 4: Resting potential restored (~–90 mV).
  • Pacemaker Cells: No true resting potential; exhibit spontaneous diastolic depolarisation due to funny Na⁺ current.

💓 The Cardiac Cycle

• Phases:
  1. Atrial Systole: Completes ventricular filling (“atrial kick,” ~10–20% of end-diastolic volume).
  2. Isovolumetric Ventricular Contraction: Pressure rises with closed valves — S₁ (“lub”).
  3. Ventricular Ejection: Aortic and pulmonary valves open — blood expelled; pressure peaks (120 mmHg in LV).
  4. Isovolumetric Relaxation: Valves close (S₂, “dub”); volume constant as pressure falls.
  5. Ventricular Filling: Passive filling during early diastole → rapid and slow filling phases.
• Pressure–Volume Loop: Illustrates LV function — the area within the loop represents stroke work. The slope of the end-systolic pressure–volume relation reflects contractility, while the end-diastolic curve reflects compliance/preload.
• Heart Sounds:
  • S₁: Closure of mitral and tricuspid valves.
  • S₂: Closure of aortic and pulmonary valves.
  • S₃: Rapid filling in early diastole (normal in youth; pathological in heart failure).
  • S₄: Atrial contraction against stiff ventricle (hypertrophy or ischaemia).

📈 Regulation of Cardiac Output

• Cardiac Output (CO) = Heart Rate (HR) × Stroke Volume (SV)
• Stroke Volume depends on:
  • Preload: Ventricular end-diastolic volume; governed by venous return. ↑ Preload → ↑ stretch → ↑ force of contraction (Frank–Starling law).
  • Afterload: Resistance against which the ventricle ejects blood (aortic pressure). ↑ Afterload → ↓ stroke volume if contractility unchanged.
  • Contractility: Intrinsic strength of contraction independent of preload; increased by sympathetic stimulation and catecholamines.
• Heart Rate Regulation:
  • Sympathetic (β₁ receptors): Increases rate and contractility via cAMP-mediated Ca²⁺ influx.
  • Parasympathetic (vagus, M₂ receptors): Slows SA nodal depolarisation and AV conduction.
• Baroreceptor Reflex: Detects arterial pressure changes via carotid sinus and aortic arch → modulates autonomic output to maintain homeostasis.
• Hormonal Influences: Adrenaline, thyroid hormones, and renin–angiotensin–aldosterone system (RAAS) modify long-term output and vascular tone.

🩺 Clinical Integration

• Arrhythmias:
  • Atrial fibrillation: Chaotic atrial activity; loss of atrial kick → ↓ cardiac output.
  • Ventricular tachycardia/fibrillation: Rapid, ineffective ventricular depolarisations → cardiac arrest if untreated.
  • Clinical Case: Post-MI patient with scarred myocardium develops VT → requires defibrillation and β-blockers for suppression.
• Heart Failure:
  • Reduced cardiac output despite adequate filling pressures.
  • Systolic failure: Impaired contractility (e.g. post-infarction cardiomyopathy).
  • Diastolic failure: Impaired relaxation (e.g. hypertensive LV hypertrophy).
  • Case: 78-year-old with ischaemic heart disease and ankle oedema; echo shows EF 35%. Managed with ACE inhibitor, β-blocker, and loop diuretic.
• Myocardial Infarction:
  • Coronary artery occlusion → ischaemia → necrosis of myocardium.
  • Loss of contractile tissue decreases stroke volume → compensatory tachycardia via sympathetic drive.
• Valvular Disorders:
  • Aortic stenosis: ↑ afterload → concentric hypertrophy.
  • Mitral regurgitation: Volume overload → eccentric hypertrophy and left atrial dilation.
  • Case: 65-year-old with exertional dyspnoea and ejection systolic murmur; echo confirms calcific aortic stenosis with valve area 0.8 cm².
• Hypertension: Chronic elevation of afterload → LV hypertrophy → diastolic dysfunction and eventual heart failure.
• Cardiac Output and Shock:
  • Hypovolaemic: ↓ preload → ↓ CO (e.g. haemorrhage).
  • Cardiogenic: Pump failure (e.g. MI).
  • Distributive: Loss of vascular tone (e.g. sepsis → low afterload).

📊 Integrative Summary

Cardiac physiology unites electrical conduction, mechanical function, and autonomic control into a synchronised cycle that sustains circulation. Understanding preload, afterload, contractility, and heart rate provides the framework for managing virtually all cardiac disorders — from shock and arrhythmia to valvular and ischaemic disease. Modern therapies — β-blockers, calcium channel blockers, ACE inhibitors, and devices like pacemakers — all target specific physiological mechanisms uncovered through centuries of cardiovascular research.

💡 Teaching Tip: Think of the heart as an orchestra: the SA node is the conductor, the myocytes are the musicians,