--- module: 007-02 language: en chapter: 7 title: "Cardiac Electrophysiology and the Cardiac Cycle" module_title: "Pressure-volume loops, arrhythmia mechanisms, and pump efficiency" source_sha256: ef0c2bca30fe9b5ed2ace52369b9df1c67ab111c7c753aa2524b2737e35eacb8 --- # Pressure-volume loops and arrhythmia mechanisms ## Reading the pressure-volume loop ### Filling adds volume at low pressure ### Isovolumetric contraction raises pressure alone ### Ejection reduces volume ### Isovolumetric relaxation at constant end-systolic volume ### Width is stroke volume ### Enclosed area approximates stroke work ### End-diastolic relation reflects passive compliance ### End-systolic relation reflects contractile state ## Loading changes the loop ### More preload widens it through Frank-Starling ### More afterload raises end-systolic volume ### More contractility lowers end-systolic volume ### Mitral regurgitation: volume escapes to a low-pressure atrium ### Aortic stenosis: pressure work and wall stress rise ## Wall stress and remodelling ### Rises with pressure and radius, falls with thickness ### Pressure overload thickens the wall ### Volume overload adds sarcomeres in series ### Adaptation fails with fibrosis and capillary mismatch ### Hypertrophy is not stronger effective pumping ### Preserved ejection fraction with high filling pressure ## Oxygen demand without occlusion ### Demand tracks wall stress, rate, contractile activity ### Dilated ventricle faces greater wall stress ### Hypertrophied ventricle has lower capillary density per mass ### Tachycardia adds demand and shortens diastole ## Diastole and ventricular interaction ### Relaxation is energy-dependent ### Ischaemia impairs diastole before systole ### A stiff ventricle depends on atrial contraction ### Shared septum inside the pericardium #### Right dilation shifts the septum leftward #### Tamponade and high airway pressure limit both chambers ### Positive-pressure ventilation #### Reduces venous return when volume is low #### Reduces left transmural afterload ## Arrhythmia initiation ### Abnormal automaticity outside the sinoatrial node ### Triggered activity depends on a preceding beat #### Early afterdepolarisations during prolonged repolarisation #### Delayed afterdepolarisations after calcium overload ### Re-entry needs substrate and trigger #### Scar, fibrosis, unequal refractoriness, accessory pathway #### A premature impulse supplies the trigger ### Antiarrhythmics can be proarrhythmic #### Sodium block promotes another circuit #### Potassium block permits early afterdepolarisations #### Nodal blockers can worsen accessory-pathway rhythms ## Electrocardiography as spatial sampling ### Each lead projects the cardiac vector onto an axis ### Biphasic signal when the vector is perpendicular ### Axis deviation is a clue, not a diagnosis ### Broad Q R S: block, ventricular origin, pre-excitation, pacing, drugs ### S T and T changes are not specific to occlusion ### Corrected Q T formulae fail at rate extremes ## Haemodynamic consequence and priorities ### Danger comes from rate, lost synchrony, or degeneration ### Adverse features #### Hypotension or shock #### Ongoing ischaemic chest discomfort #### Acute pulmonary oedema or altered consciousness ### Then find substrate and trigger #### Ischaemia, infection, electrolytes, endocrine, drugs #### A transient trigger does not exclude a substrate ### Serial assessment, because loading and tone change fast