Cardiac Physiology and Pathophysiology
Cardiac physiology and pathophysiology is the study of how the heart works as a pump and how that function fails. It links the cellular events of excitation and contraction to the chamber-level mechanics that determine cardiac output, and it traces the path by which injury, pressure or volume overload, and neurohormonal activation convert a normal heart into a failing one. For the cardiothoracic surgeon this body of knowledge is the physiological substrate on which operative decisions and perioperative haemodynamic management rest.
Definition
Cardiac physiology describes the mechanical, electrical, and metabolic functions by which the heart generates output to meet the body's demands; cardiac pathophysiology describes the cellular and integrative mechanisms by which those functions become impaired in disease.
Scope
This area orients the reader to the normal determinants of cardiac performance — preload, afterload, contractility, and heart rate — and to the principal ways they are deranged in disease. Its child topics develop myocardial contractility, the electrophysiological basis of arrhythmia, the pathophysiology of heart failure, valvular pressure- and volume-loading lesions, and cardiogenic shock. It is a reference and educational overview, not a manual of clinical or surgical management.
Sub-topics
Core questions
- What cellular and chamber-level determinants set cardiac output, and how are they integrated?
- How do excitation–contraction coupling and the force–length relationship govern myocardial performance?
- By what pathways does pressure overload, volume overload, ischaemia, or neurohormonal activation lead to heart failure?
- How do structural and electrical remodelling explain the transition from compensated to decompensated states?
Key concepts
- Preload, afterload, and contractility
- Cardiac output and stroke volume
- Pressure–volume loop
- Systolic versus diastolic dysfunction
- Myocardial remodelling and hypertrophy
- Neurohormonal activation
Key theories
- Frank–Starling mechanism
- The intrinsic relationship by which increased end-diastolic fibre length (preload) raises stroke volume on a beat-to-beat basis, allowing the heart to match output to venous return; its operating curve is depressed in the failing ventricle.
- Excitation–contraction coupling
- The sequence linking sarcolemmal depolarisation to calcium-induced calcium release from the sarcoplasmic reticulum and cross-bridge cycling, providing the cellular basis of contractility and a locus of dysfunction in disease.
- Neurohormonal model of heart failure
- The framework in which chronic activation of the sympathetic nervous system and renin–angiotensin–aldosterone axis, initially compensatory, drives maladaptive remodelling and progressive pump failure.
Mechanisms
Cardiac output is the product of stroke volume and heart rate, and stroke volume is governed by preload, afterload, and contractility. At the cellular level, membrane depolarisation triggers calcium entry that releases stored calcium and drives actin–myosin cross-bridge cycling (excitation–contraction coupling); the Frank–Starling mechanism then matches output to filling. Disease perturbs these layers: ischaemia and metabolic stress impair contraction, pressure or volume overload imposes wall stress that provokes hypertrophic or dilated remodelling, and sustained neurohormonal activation — sympathetic and renin–angiotensin–aldosterone — promotes fibrosis, apoptosis, and chamber dilatation. The integrated result is a downward-shifted pump function relationship that defines the failing heart.
Clinical relevance
Understanding these determinants underlies how clinicians and cardiothoracic surgeons reason about haemodynamics — for example, why an overloaded ventricle behaves differently under anaesthesia, or why valve lesions impose characteristic loading patterns. The material describes physiological principles that frame perioperative and surgical reasoning and is not itself a source of individualised diagnostic or treatment recommendations.
Evidence & guidelines
The physiological framework summarised here is consolidated in standard texts such as Katz's Physiology of the Heart and in integrative reviews of cardiac plasticity and the heart-failure syndrome; clinical translation of these principles is addressed in society guidelines covered by the child topics.
History
Modern cardiac physiology grew from the late-nineteenth- and early-twentieth-century work of Otto Frank and Ernest Starling on the length–tension behaviour of cardiac muscle, was extended through the twentieth century by the elucidation of excitation–contraction coupling and calcium handling, and was reframed in the late twentieth century around the neurohormonal model that now organises understanding of heart failure.
Key figures
- Otto Frank
- Ernest Starling
- Donald Bers
- Eugene Braunwald
- Arnold Katz
Related topics
Seminal works
- bers-2002
- hill-olson-2008
- braunwald-2015
Frequently asked questions
- What are the four determinants of cardiac output?
- Stroke volume is set by preload, afterload, and contractility, and cardiac output is stroke volume multiplied by heart rate; these are the four variables that integrate to determine the heart's output.
- How does this area relate to cardiothoracic surgery?
- It provides the physiological reasoning behind perioperative haemodynamics and the loading consequences of valvular and ischaemic disease, which inform how surgeons and intensivists interpret a patient's circulatory state.