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Short Note: Cardiac Output, Stroke Volume, Cardiac Index, and Stroke Volume Index — Factors Affecting Cardiac Output

(From Guyton and Hall Textbook of Medical Physiology, 4th South Asia Edition)

Definitions

1. Cardiac Output (CO)

Cardiac output is the quantity of blood pumped into the aorta each minute by the heart. It is also the quantity of blood that flows through the circulation per minute. It equals the sum of blood flows to all tissues of the body, making it one of the most important parameters of cardiovascular function.

CO = Stroke Volume (SV) × Heart Rate (HR)

Normal resting value in adults: approximately 5 L/min (5.6 L/min in young men; ~15% lower in women).

CO is always equal to venous return, except for transient beats when blood is temporarily stored in or removed from the heart and lungs.

2. Stroke Volume (SV)

Stroke volume is the volume of blood ejected by one ventricle per single contraction (heartbeat). It is the difference between end-diastolic volume (EDV) and end-systolic volume (ESV).

SV = EDV - ESV

Normal resting SV ≈ 70 mL/beat. Stroke volume is influenced by preload, afterload, and myocardial contractility (governed by the Frank-Starling mechanism).

3. Cardiac Index (CI)

Because cardiac output increases approximately in proportion to body surface area (BSA), it is standardized as the cardiac index — the cardiac output per square meter of body surface area.

CI = CO ÷ BSA (m²)

A person weighing 70 kg has a BSA of ~1.7 m², giving a normal cardiac index of:

~3 L/min/m² at rest

The cardiac index rises to >4 L/min/m² at age 10 years and declines to ~2.4 L/min/m² at age 80 years, reflecting declining metabolic activity and muscle mass with aging. In people with obesity, commonly used BSA equations slightly overestimate surface area, so CI may not accurately reflect metabolic demands in this group.

4. Stroke Volume Index (SVI)

Stroke volume index is the stroke volume normalized to body surface area, allowing comparison across individuals of different sizes.

SVI = SV ÷ BSA (m²)

Normal SVI ≈ 40-60 mL/beat/m². It provides a more accurate indicator of ventricular performance than SV alone.

Factors Affecting Cardiac Output

Cardiac output is controlled mainly by peripheral factors (venous return) under normal resting conditions, with the heart automatically adjusting via the Frank-Starling mechanism. The key factors are:

A. Venous Return (Primary Controller)

The heart pumps automatically whatever blood flows into the right atrium. Venous return - which is the sum of all local tissue blood flows - is therefore the primary determinant of cardiac output under normal conditions. When more blood enters the heart, the stretching of cardiac muscle walls causes stronger contraction (Frank-Starling law), increasing SV and CO.

B. Frank-Starling Mechanism

Increased ventricular filling (preload) stretches myocardial fibers, increasing contractile force and thus SV. Stretching the sinus node also directly increases heart rate by 10-15%, and the Bainbridge reflex (via the right atrial stretch → vasomotor center → sympathetic nerves and vagi) further raises heart rate.

C. Total Peripheral Resistance (TPR)

CO varies inversely with TPR when arterial pressure remains unchanged:

CO = Arterial Pressure ÷ TPR

Increased TPR → decreased CO
Decreased TPR (e.g., AV fistula, hyperthyroidism, anemia, beriberi) → increased CO

D. Metabolic Needs of Tissues (Local Blood Flow Control)

Local tissue metabolism is the most fundamental driver. When O₂ consumption increases (as in exercise), local arterioles dilate, decreasing peripheral resistance, increasing venous return, and raising CO proportionally. CO and O₂ consumption rise in parallel with increasing exercise.

E. Autonomic Nervous System

Sympathetic stimulation: Increases heart rate, myocardial contractility (positive inotrope), and arterial pressure - can raise CO to as high as 25-30 L/min during intense exercise
Parasympathetic stimulation: Decreases heart rate and CO
During exercise, the autonomic system also prevents the fall in arterial pressure caused by peripheral vasodilation, preserving the driving pressure for blood flow

F. Heart Rate

CO = SV × HR; increased heart rate raises CO, but very high rates reduce diastolic filling time and therefore SV (SV reaches its maximum before HR is maximal during exercise)

G. Factors Causing Abnormally High CO (High-Output States)

All characterized by chronically reduced TPR:

Beriberi (thiamine deficiency) - CO may double
Arteriovenous fistula
Hyperthyroidism - CO up to 40-80% above normal
Anemia - reduced viscosity + vasodilation

H. Factors Causing Low CO

Myocardial infarction, cardiac failure
Severe valvular disease (e.g., aortic stenosis)
Cardiac tamponade, severe arrhythmias

Summary Table

Parameter	Formula	Normal Value
Stroke Volume (SV)	EDV - ESV	~70 mL/beat
Cardiac Output (CO)	SV × HR	~5 L/min
Cardiac Index (CI)	CO ÷ BSA	~3 L/min/m²
Stroke Volume Index (SVI)	SV ÷ BSA	~40-60 mL/beat/m²

Source: Guyton and Hall Textbook of Medical Physiology (ISBN 9780443111013), Chapter 20 - Cardiac Output, Venous Return, and Their Regulation, pp. 249-255.

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