📌 Professor’s Notes: Quick Revision
High-yield revision notes for rapid review before university examinations.
- Cardiac output (CO) is the volume of blood pumped by each ventricle per minute. It is the product of stroke volume × heart rate. Normal resting cardiac output is 5–6 L/min. Stroke volume is about 70 mL/beat, end-diastolic volume (EDV) is 120–130 mL, end-systolic volume (ESV) is 50 mL, ejection fraction (EF) is 55–70%, and cardiac index is 2.5–4.0 L/min/m². Cardiac reserve is the extra cardiac output available during increased demand.
- Cardiac output increases during exercise, emotional stress, pregnancy, after meals, and heat exposure. It decreases on standing suddenly and after excessive fluid loss. It declines with advancing age and is slightly lower in females because of smaller body size.
- Measurement of cardiac output:
- Fick method: Based on oxygen consumption and the arteriovenous oxygen difference. It is accurate but invasive and requires pulmonary artery catheterization.
- Indicator dilution method: Uses dilution of a known quantity of dye or tracer to calculate cardiac output.
- Thermodilution method: Uses cold saline as an indicator and is widely used in intensive care units.
- Echocardiography is the common noninvasive clinical method. Other methods include ballistocardiography, X-ray, and pulse-pressure estimation.
- Cardiac output depends on stroke volume and heart rate. Stroke volume is determined by preload, myocardial contractility, and afterload.
- Preload represents ventricular filling (EDV). According to the Frank–Starling mechanism, increased ventricular filling stretches myocardial fibers, producing a stronger contraction and increasing stroke volume (heterometric autoregulation). Venous return is increased by the skeletal muscle pump, thoracic pump, abdominal pump, increased blood volume, sympathetic venoconstriction, atrial contraction, and normal ventricular compliance. Cardiac tamponade and reduced ventricular compliance decrease preload and cardiac output.
- Myocardial contractility is increased by sympathetic stimulation, catecholamines, glucagon, thyroxine, caffeine, and digitalis. It is reduced by hypoxia, hypercapnia, acidosis, myocardial infarction, anesthetics, and negative inotropic drugs.
- Afterload is the resistance against which the ventricle ejects blood. Increased peripheral resistance or blood viscosity increases afterload and reduces stroke volume, whereas vasodilation decreases afterload (homometric autoregulation).
- Heart rate is regulated mainly by the autonomic nervous system. Moderate increases in heart rate increase cardiac output, but severe tachycardia shortens diastole, reduces ventricular filling, and may decrease cardiac output. Bradycardia prolongs filling time and may maintain cardiac output by increasing stroke volume.
- Regulation of cardiac output occurs through:
- Intrinsic mechanisms: Frank–Starling mechanism and force–frequency relationship.
📝 Practice MCQs
🎙️ Frequently Asked Viva Questions
High-yield viva questions with concise answers for rapid university examination preparation.
Q1. Why does severe tachycardia sometimes decrease cardiac output despite a faster heart rate?
Answer: Severe tachycardia markedly shortens diastole, reducing ventricular filling and stroke volume. The fall in stroke volume may outweigh the increase in heart rate, decreasing cardiac output.
Q2. Explain the Frank–Starling mechanism.
Answer: Increased ventricular filling stretches myocardial fibers, producing a stronger contraction and increasing stroke volume. This intrinsic regulation is called heterometric autoregulation.
Q3. What is preload, and how does it affect cardiac output?
Answer: Preload is ventricular filling at the end of diastole (end-diastolic volume). Increased preload increases stroke volume and cardiac output within physiological limits.
Q4. What is afterload, and what happens when it increases?
Answer: Afterload is the resistance the ventricle must overcome to eject blood. Increased afterload reduces stroke volume and cardiac output by making ventricular ejection more difficult.
Q5. How does the skeletal muscle pump increase cardiac output?
Answer: Skeletal muscle contraction compresses veins and pushes blood toward the heart. Venous valves prevent backflow, increasing venous return, preload, and cardiac output.
Q6. How does inspiration increase venous return?
Answer: Inspiration lowers intrathoracic pressure and increases intra-abdominal pressure, creating thoracic and abdominal pump effects that promote venous return to the heart.
Q7. Why does sympathetic stimulation increase cardiac output?
Answer: Sympathetic stimulation increases heart rate, myocardial contractility, and venous return, thereby increasing stroke volume and cardiac output.
Q8. Why does ventricular compliance affect cardiac output?
Answer: A compliant ventricle fills easily during diastole. Reduced compliance limits ventricular filling, decreases end-diastolic volume, lowers stroke volume, and reduces cardiac output.
Q9. What is the principle of the Fick method for measuring cardiac output?
Answer: Cardiac output equals oxygen consumption divided by the arteriovenous oxygen content difference. Oxygen is used as the indicator.
Q10. What is the basic principle of the indicator dilution method?
Answer: A known amount of indicator is injected into the circulation. Cardiac output is calculated from the degree of dilution of the indicator during its first passage.
Q11. Why is thermodilution preferred for repeated cardiac output measurements?
Answer: It uses cold saline, which is safe and rapidly dissipates, allowing repeated measurements with minimal error from recirculation.
Q12. How does digitalis increase myocardial contractility?
Answer: Digitalis inhibits Na⁺–K⁺ ATPase, increasing intracellular calcium availability and producing stronger cardiac contractions.
Q13. What is the Anrep effect?
Answer: The Anrep effect is an intrinsic increase in myocardial contractility that helps maintain cardiac output when afterload or arterial pressure increases, without changing myocardial fiber length.
Q14. Why do trained athletes have greater cardiac reserve?
Answer: Endurance training increases stroke volume and improves myocardial efficiency. Athletes can achieve much higher cardiac output during exercise while maintaining a lower resting heart rate.
Q15. How does severe hypoxia reduce cardiac output?
Answer: Severe hypoxia depresses myocardial contractility, reducing stroke volume and cardiac output despite reflex stimulation of heart rate.
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