Cardiac Pathophysiology Foundations
Classification: A mechanism-based overview of cardiac output, ventricular loading, electrical activation, neurohormonal control, and remodeling.
Key diagnostic discriminator: Most cardiac disorders can be understood by asking what changed in rate/rhythm, preload, afterload, contractility, compliance, or coronary oxygen balance.
Clinical priority: Connect the structural or electrical abnormality to its effect on filling, ejection, perfusion, and congestion before memorizing disease-specific findings.
Cardiac Output and Stroke Volume
Cardiac output (CO) is the volume of blood ejected by the heart per minute and is determined by heart rate (HR) and stroke volume (SV): CO = HR × SV. Stroke volume is governed primarily by preload, afterload, contractility, and ventricular compliance. Disturbance in any of these variables can reduce forward flow or raise filling pressures even when another variable remains normal (Kusumoto, 2019; Norris, 2020).
Preload reflects ventricular filling at end diastole. Afterload is the resistance the ventricle must overcome to eject blood. Contractility is the myocardium’s intrinsic force-generating capacity. Compliance describes how readily the ventricle expands during filling (Kusumoto, 2019; Norris, 2020).
Frank-Starling Relationship
Within a physiologic range, increased end-diastolic stretch increases the force of contraction. This allows the heart to match output to venous return. Once myocardial fibers are excessively stretched or ventricular function is severely impaired, additional preload produces little improvement in stroke volume and mainly increases filling pressure and congestion (Kusumoto, 2019; Norris, 2020).
Pressure Versus Volume Overload
Pressure overload requires the ventricle to generate higher systolic pressure and tends to promote concentric hypertrophy. Volume overload increases end-diastolic volume and tends to promote chamber dilation and eccentric remodeling. These patterns recur across hypertension, valvular stenosis, valvular regurgitation, and heart failure (Kusumoto, 2019; Norris, 2020).
| Load | Typical adaptation | Examples |
| Pressure overload | Wall thickening / concentric hypertrophy | Hypertension, aortic stenosis |
| Volume overload | Chamber dilation / eccentric remodeling | Aortic or mitral regurgitation, shunts |
Electrical Activation and Mechanical Performance
Normal cardiac performance depends on coordinated sinoatrial initiation, atrial depolarization, atrioventricular conduction, and ventricular activation. Rhythm abnormalities can lower output by making the rate too fast or too slow, eliminating atrial contraction, or producing ineffective ventricular activation. Electrical instability can therefore become a primary hemodynamic problem rather than merely an ECG abnormality (Kusumoto, 2019; Norris, 2020).
Neurohormonal Control
The sympathetic nervous system and renin-angiotensin-aldosterone system can preserve blood pressure and perfusion when cardiac output falls. Sympathetic activity raises heart rate, contractility, and vascular tone. RAAS increases vasoconstriction and sodium-water retention. These responses are adaptive in the short term but increase myocardial workload, filling pressure, oxygen demand, fibrosis, and remodeling when chronically activated (Kusumoto, 2019; Norris, 2020).
Natriuretic peptides counter these systems by promoting natriuresis, diuresis, and vasodilation. Endothelins exert potent vasoconstrictor and hypertrophic effects. The balance among these pathways becomes especially important in heart failure (Ng & Yeung, 2026; Norris, 2020).
Myocardial Oxygen Supply and Demand
Myocardial ischemia develops when oxygen supply cannot meet myocardial demand. Demand rises with heart rate, contractility, and ventricular wall stress; supply depends on coronary blood flow, diastolic perfusion time, coronary vascular patency, and arterial oxygen content. Tachycardia can worsen both sides of the equation by increasing demand while shortening diastole, when most left-ventricular coronary perfusion occurs. This supply-demand framework links anemia, hypoxemia, hypotension, tachyarrhythmia, pressure overload, and obstructive coronary disease to myocardial ischemia (Kusumoto, 2019; Norris, 2020).
High-Yield Distinctions
- Low output can result from too little filling, excessive resistance to ejection, impaired contraction, abnormal relaxation, or a rate/rhythm problem.
- A normal ejection fraction does not guarantee normal filling pressure or normal cardiac function.
- Pressure overload favors hypertrophy; volume overload favors dilation.
- Compensation is not synonymous with recovery: mechanisms that preserve perfusion acutely may accelerate disease chronically.
Related YourDNP Resources
- Arrhythmias
- Heart Failure
- Valvular Heart Disease
- Coronary Artery Disease and Acute Coronary Syndromes
- Pericardial Disease
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References
Kusumoto, F. M. (2019). Cardiovascular disorders: Heart disease. In G. D. Hammer & S. J. McPhee (Eds.), Pathophysiology of disease: An introduction to clinical medicine (8th ed., pp. 289–328). McGraw-Hill Education.
Ng, T. M. H., & Yeung, S. L. (2026). Heart failure. In M. A. Chisholm-Burns, P. M. Malone, J. M. Kolesar, K. C. Lee, P. B. Bookstaver, & K. R. Matthias (Eds.), Pharmacotherapy principles & practice (7th ed.). McGraw Hill.
Norris, T. L. (2020). Porth’s essentials of pathophysiology (5th ed.). Wolters Kluwer.