--- module: 007-01 language: en chapter: 7 title: "Cardiac Electrophysiology and the Cardiac Cycle" module_title: "Foundations" source_sha256: 7553fbbb3c6c47c9cf4b25a70b38c39520180dabeac8df9c7ee40a4a384db00e --- # Cardiac electrophysiology and the cardiac cycle ## Pacemaker activity ### No stable resting voltage #### Hyperpolarisation-activated inward current #### Reduced potassium efflux #### Calcium entry toward threshold ### Calcium current drives the nodal upstroke ### Slope of diastolic depolarisation sets rate ### Autonomic control #### Beta one raises cyclic adenosine monophosphate #### Steeper pacemaker slope, faster conduction #### Muscarinic acetylcholine slows node and conduction ## Conduction sequence ### Sinoatrial node to atrial myocardium ### Slow atrioventricular node lets atria fill the ventricle ### His bundle, bundle branches, Purkinje fibres ### Septum and apex before the free wall ## Working myocyte action potential ### Fast sodium entry depolarises ### Early potassium currents begin repolarisation ### Plateau: L-type calcium against potassium efflux ### Delayed potassium currents complete repolarisation ### Long refractory period prevents tetany ## Excitation-contraction coupling ### L-type channels in transverse tubules open ### Calcium-induced calcium release through ryanodine receptors ### Calcium binds troponin C, tropomyosin moves ### Actin-myosin cross-bridge cycling ### Relaxation removes calcium #### Sarcoplasmic-reticulum pumps #### Sodium-calcium exchange #### Membrane calcium pumps ## The electrocardiogram ### P wave: atrial depolarisation ### P R interval: atrial conduction plus nodal delay ### Q R S: ventricular depolarisation ### S T segment: ventricular plateau ### T wave: ventricular repolarisation ### It does not show contraction, output or coronary anatomy ### Prolonged corrected Q T #### Early afterdepolarisations #### Torsades de pointes #### Bradycardia, low potassium, low magnesium, drugs ## Mechanical events ### Diastole: atrioventricular valves open, passive filling ### End-diastolic volume is maximal ### First heart sound closes mitral and tricuspid valves ### Isovolumetric contraction: constant volume, rising pressure ### Ejection when ventricular pressure exceeds arterial ### Stroke volume equals end-diastolic minus end-systolic volume ### Ejection fraction is stroke volume over end-diastolic volume ### Second heart sound, then isovolumetric relaxation ### Tachycardia costs diastolic time first ## Mitral regurgitation as a worked route ### Backward flow into the atrium during systole ### Ejection fraction can look reassuring ### Acute: unadapted atrium transmits pressure to the lungs ### Chronic: enlargement and compliance delay symptoms ## Preload, afterload, contractility ### Preload is fibre stretch before contraction ### Frank-Starling matches output to venous return ### Afterload: arterial pressure, obstruction, impedance, geometry ### Pressure load gives concentric hypertrophy ### Volume load gives dilation and eccentric remodelling ### Contractility at fixed load; lusitropy is relaxation ### Cardiac output equals rate times stroke volume ## Coronary supply and demand ### High oxygen extraction at rest, so flow must rise ### Left-ventricular flow is mainly diastolic ### Demand: rate, contractility, wall stress, muscle mass ### Supply: oxygen content, perfusion pressure, patency, diastolic time ## Rhythm disturbance ### Abnormal impulse formation or conduction ### Enhanced automaticity and triggered activity ### Re-entry needs circuit, unidirectional block, timing ### Atrial fibrillation: lost atrial contraction, thrombus risk ### Ventricular tachycardia can degenerate to fibrillation ### Electrolytes #### Hyperkalaemia slows conduction and widens Q R S #### Hypokalaemia increases ectopy and delays repolarisation #### Magnesium deficiency and calcium change the plateau and Q T