TextbookClinical SciencesCardiovascular Physiology

Cardiovascular Physiology

Cardiovascular physiology encompasses cardiac electrophysiology, the cardiac cycle, regulation of cardiac output, and vascular haemodynamics essential for understanding heart disease.

Key Facts

Cardiac output (CO) = stroke volume (SV) × heart rate (HR); normal CO approximately 5 L/min at rest Stroke volume is determined by preload (Frank-Starling mechanism), afterload, and contractility SA node intrinsic rate ~100 bpm (vagal tone reduces to ~70 bpm); AV node ~40-60 bpm; Purkinje fibres ~20-40 bpm Starling's law: Increased venous return → increased end-diastolic volume → increased stroke volume (up to a point) Mean arterial pressure (MAP) = diastolic BP + ⅓(systolic − diastolic); normal ≥65 mmHg Baroreceptor reflex: Carotid sinus and aortic arch detect BP changes → adjust HR and SVR via autonomic nervous system Coronary blood flow occurs predominantly in diastole (left ventricle); autoregulation maintains flow between MAP 60-140 mmHg Ejection fraction = (SV/EDV) × 100; normal 55-70%; HFrEF defined as EF ≤40%

Overview

Key Facts

The cardiovascular system delivers oxygen and nutrients to tissues while removing metabolic waste. Understanding cardiac physiology is fundamental to interpreting cardiovascular disease, pharmacology, and haemodynamic management.

Epidemiology

Cardiovascular disease is the second leading cause of death in the UK, responsible for approximately 27% of all deaths (~160,000/year). Heart failure affects approximately 900,000 people in the UK, with an incidence of 2-3 per 1,000/year.

Aetiology

Cardiovascular function depends on:

  • Cardiac electrophysiology: Generation and conduction of action potentials
  • Cardiac mechanics: Systolic contraction and diastolic relaxation
  • Vascular function: Arterial resistance, venous capacitance, endothelial regulation
  • Neurohumoral control: Sympathetic/parasympathetic, RAAS, natriuretic peptides

Pathophysiology

Cardiac action potentials:

  • Pacemaker cells (SA/AV node): Phase 4 spontaneous depolarisation (funny current, If); phase 0 slow upstroke (Ca²⁺ channels); no true resting potential
  • Cardiomyocytes: Phase 0 rapid depolarisation (Na⁺); phase 1 partial repolarisation (K⁺); phase 2 plateau (Ca²⁺ influx balanced by K⁺ efflux); phase 3 repolarisation (K⁺); phase 4 resting potential (−90mV)

Cardiac cycle:

  • Isovolumetric contraction → ejection → isovolumetric relaxation → rapid filling → diastasis → atrial systole
  • S1 (mitral/tricuspid closure) and S2 (aortic/pulmonary closure) heart sounds correspond to valve events

Pressure-volume loops demonstrate the relationship between preload, afterload, contractility and stroke volume

Clinical Presentation

Heart Failure (Reduced Cardiac Output)

  • Dyspnoea, orthopnoea, PND, fatigue
  • Peripheral oedema, raised JVP, bibasal crackles
  • S3 gallop (rapid ventricular filling), displaced apex beat

Shock States

  • Cardiogenic: Low CO, high SVR, raised JVP
  • Hypovolaemic: Low CO, high SVR, flat JVP
  • Distributive (septic): High CO, low SVR, warm peripheries initially

Arrhythmias

  • Palpitations, syncope/pre-syncope, dyspnoea
  • Haemodynamic compromise if rate too fast or too slow

Red Flags

  • MAP <65 mmHg — organ hypoperfusion, requires urgent intervention
  • New-onset S3 gallop with dyspnoea — acute heart failure
  • Syncope with exercise — consider aortic stenosis, HOCM, arrhythmia

Differential Diagnosis

DiagnosisKey FeaturesInvestigation
Heart failure with reduced EFDyspnoea, oedema, EF ≤40%BNP, echocardiogram
Heart failure with preserved EFDyspnoea, oedema, EF ≥50%, diastolic dysfunctionBNP, echocardiogram, E/e' ratio
Valvular heart diseaseMurmur, exercise intoleranceEchocardiogram
Pericardial effusion/tamponadeMuffled heart sounds, raised JVP, hypotension (Beck's triad)Echocardiogram, pulsus paradoxus
Hypovolaemic shockTachycardia, hypotension, flat JVP, cool peripheriesClinical assessment, lactate
Septic shockPyrexia, warm peripheries, low SVRBlood cultures, lactate, qSOFA

Diagnosis / Investigation

Bedside

  • ECG: Heart rate, rhythm, conduction, ischaemia
  • Blood pressure: Systolic, diastolic, MAP calculation
  • JVP assessment: Reflects right atrial pressure
  • Pulse oximetry: Oxygen delivery assessment

Bloods

  • BNP/NT-proBNP: Heart failure screening — BNP >100 pg/mL or NT-proBNP >300 pg/mL suggest HF
  • Troponin: Myocardial injury marker
  • Lactate: Tissue hypoperfusion indicator
  • FBC, U&Es, LFTs, TFTs: Baseline cardiac assessment

Imaging

  • Echocardiogram: EF, wall motion, valvular function, diastolic function
  • CXR: Cardiomegaly (CTR >50%), pulmonary oedema, pleural effusions

Special Tests

  • Cardiac catheterisation: Invasive haemodynamic assessment — wedge pressure, CO measurement
  • Cardiac MRI: Gold standard for EF, tissue characterisation, infiltrative cardiomyopathy
  • Exercise testing: Functional capacity, chronotropic response, ischaemia assessment

Management

Non-pharmacological

  • Fluid restriction (1.5L/day) and salt restriction (<6g/day) in heart failure
  • Cardiac rehabilitation
  • Lifestyle modification: exercise, weight management, smoking cessation

Pharmacological

Heart failure (NICE NG106):

  • First-line: ACE inhibitor (ramipril 1.25-10mg OD) + beta-blocker (bisoprolol 1.25-10mg OD)
  • Add: Mineralocorticoid receptor antagonist (spironolactone 25-50mg OD) if EF ≤35% and symptomatic
  • Add: SGLT2 inhibitor (dapagliflozin 10mg OD) — DAPA-HF trial showed 26% reduction in CV death/HF hospitalisation
  • Add: Sacubitril/valsartan (PARADIGM-HF trial) — replace ACEi if EF ≤35% and symptomatic despite optimal therapy
  • Diuretics: Furosemide 20-80mg OD for congestion (symptom relief, no mortality benefit)

Shock:

  • Cardiogenic: Dobutamine 2.5-10mcg/kg/min (inotrope); noradrenaline for MAP support
  • Hypovolaemic: IV fluid resuscitation (250-500mL crystalloid bolus)
  • Septic: Noradrenaline first-line vasopressor, target MAP ≥65 mmHg

Referral Criteria

  • New heart failure diagnosis — cardiology
  • Cardiogenic shock — critical care
  • Consideration for CRT/ICD if EF ≤35%

Prognosis

  • Heart failure: 5-year survival approximately 50% (worse than many cancers)
  • NYHA class IV: 1-year mortality approximately 50%
  • ACEi + beta-blocker + MRA therapy reduces HF mortality by approximately 50% combined
  • CRT improves survival in selected patients (LBBB, QRS >150ms, EF ≤35%)
  • Heart transplant: 1-year survival ~85%, 5-year ~75%

Other Relevant Information

Cardiac Output Determinants

FactorDefinitionClinical Relevance
PreloadEnd-diastolic volume (venous return)Increased by IV fluids, decreased by diuretics
AfterloadResistance to ventricular ejectionIncreased by vasoconstriction, aortic stenosis
ContractilityForce of contraction (inotropy)Increased by digoxin, dobutamine; decreased by beta-blockers
Heart rateBeats per minuteChronotropy; affected by autonomic tone, drugs

Landmark Heart Failure Trials

TrialInterventionKey Finding
CONSENSUSEnalapril in severe HF40% mortality reduction at 6 months
CIBIS-IIBisoprolol34% mortality reduction
RALESSpironolactone30% mortality reduction
PARADIGM-HFSacubitril/valsartan vs enalapril20% reduction in CV death/HF hospitalisation
DAPA-HFDapagliflozin26% reduction in CV death/HF hospitalisation