Cardiac Output and Stroke Volume

Introduction

Cardiac output (CO) and stroke volume (SV) are central concepts in cardiovascular physiology, representing the heart’s ability to supply oxygenated blood to meet the body’s metabolic demands. Cardiac output is defined as the volume of blood ejected by the heart per minute, whereas stroke volume is the volume ejected per beat. Together, these parameters reflect the heart’s performance, influencing systemic blood pressure, tissue perfusion, and overall cardiovascular health.

An understanding of CO and SV is crucial for medical students, clinicians, cardiologists, and researchers, as alterations in these parameters are fundamental to conditions like heart failure, shock, valvular disease, and exercise physiology. This article provides a detailed discussion of CO and SV, including their physiological determinants, regulation, measurement techniques, clinical significance, and pathophysiological considerations.

1. Definitions

1.1 Cardiac Output (CO)

Formula:

CO=HR×SVCO = HR \times SVCO=HR×SV

where HR = heart rate (beats per minute) and SV = stroke volume (mL per beat).

Normal resting CO in adults: 4–8 L/min, varying with body size, metabolic demands, and activity level.
CO can increase up to 20–30 L/min during intense exercise.

1.2 Stroke Volume (SV)

Definition: The volume of blood pumped by a ventricle in one contraction.
Formula:

SV=EDV−ESVSV = EDV – ESVSV=EDV−ESV

where EDV = end-diastolic volume, ESV = end-systolic volume.

Normal resting SV: 60–100 mL/beat.
SV is influenced by preload, afterload, and contractility, the three primary determinants of cardiac performance.

2. Anatomy Relevant to CO and SV

2.1 Ventricles

Left ventricle (LV): Thick-walled, ellipsoid chamber responsible for systemic circulation.
Right ventricle (RV): Thin-walled, crescent-shaped chamber supplying pulmonary circulation.
Chordae tendineae and papillary muscles: Stabilize AV valves, ensuring unidirectional blood flow and optimizing stroke volume.

2.2 Atria

Atrial contraction (atrial systole) contributes to ventricular filling and preload, impacting SV.
Loss of atrial systole (e.g., atrial fibrillation) can reduce LV SV by 10–30%.

2.3 Valves

Atrioventricular valves (mitral, tricuspid): Open during diastole to allow filling; prevent regurgitation during systole.
Semilunar valves (aortic, pulmonary): Open during systole to allow ejection; prevent retrograde flow.

3. Determinants of Stroke Volume

Stroke volume is influenced by three major factors: preload, afterload, and contractility.

3.1 Preload

Preload refers to the initial stretching of ventricular myocardial fibers at end-diastole, determined largely by venous return.
Frank-Starling law: Increased preload → greater fiber stretch → stronger contraction → increased SV.
Clinical relevance: Hypovolemia reduces preload and SV; fluid resuscitation increases preload and SV.

3.2 Afterload

Afterload is the resistance the ventricle must overcome to eject blood, largely determined by arterial pressure and systemic vascular resistance (SVR).
Increased afterload (e.g., hypertension, aortic stenosis) → decreased SV.
Decreased afterload (e.g., vasodilation) → increased SV.

3.3 Contractility

Intrinsic myocardial contractile strength independent of preload and afterload.
Influenced by:
- Sympathetic stimulation (β1-adrenergic activation → increased Ca²⁺ influx).
- Inotropic drugs (digitalis, dobutamine).
Increased contractility → decreased ESV → increased SV.

3.4 Heart Rate

Indirectly affects SV via diastolic filling time:
- Tachycardia: Shortened diastole → reduced EDV → potential decrease in SV.
- Bradycardia: Increased filling time → potential increase in SV.

4. Determinants of Cardiac Output

4.1 Relationship to Stroke Volume and Heart Rate

CO=SV×HRCO = SV \times HRCO=SV×HR

Example: SV = 70 mL, HR = 75 bpm → CO = 5250 mL/min (~5.25 L/min).
Changes in SV or HR directly affect CO.

4.2 Autonomic Regulation

Sympathetic stimulation: Increases HR and contractility → increased CO.
Parasympathetic stimulation: Reduces HR (via vagus nerve) → decreased CO.
Baroreceptor reflex adjusts HR and SV in response to changes in blood pressure.

4.3 Hormonal Influence

Catecholamines (epinephrine, norepinephrine): Increase contractility and HR → increase CO.
Renin-angiotensin-aldosterone system: Increases preload by promoting sodium and water retention → indirectly increases SV and CO.
Thyroid hormones: Enhance heart rate and contractility → elevated CO.

5. Cardiac Cycle Phases and Their Contribution to CO

5.1 Ventricular Filling (Diastole)

Early rapid filling + diastasis + atrial systole → determines EDV → influences SV via Frank-Starling mechanism.

5.2 Isovolumetric Contraction

No blood ejected yet, but ventricular pressure rises, preparing to overcome afterload.

5.3 Ventricular Ejection (Systole)

SV = volume ejected during systole.
Ejection fraction (EF) = SV / EDV × 100%, a measure of ventricular performance.

5.4 Isovolumetric Relaxation

Ventricles relax; semilunar valves close; AV valves prepare to reopen for filling.

6. Measurement of Stroke Volume and Cardiac Output

6.1 Direct Methods

Fick principle: Based on oxygen consumption and arterial-venous O₂ difference.
Thermodilution: Measured via pulmonary artery catheter; indicator dilution technique.

6.2 Non-Invasive Methods

Echocardiography: SV = LVOT area × velocity-time integral (VTI).
Doppler ultrasound: Measures flow velocities in LV outflow tract.
MRI: Gold standard for volumetric measurement of SV and CO.
Impedance cardiography: Estimates SV based on thoracic electrical resistance changes.

6.3 Clinical Indices

Ejection fraction (EF): SV / EDV × 100%; normal LV EF ~55–70%.
Cardiac index (CI): CO normalized to body surface area (BSA); normal ~2.5–4 L/min/m².

7. Factors Affecting Cardiac Output

7.1 Physiological Factors

Exercise: ↑HR, ↑SV → CO can rise 5–6×.
Posture changes: Supine → standing decreases venous return → transient ↓CO.
Pregnancy: Increased blood volume → ↑preload → ↑SV and CO.

7.2 Pathological Factors

Heart failure: Reduced contractility → ↓SV → ↓CO.
Valvular heart disease: Stenosis ↑afterload; regurgitation reduces effective SV.
Arrhythmias: AF → loss of atrial systole → ↓EDV → ↓SV → ↓CO.

7.3 Drugs and Therapeutics

Inotropes: ↑contractility → ↑SV and CO.
Vasodilators: ↓afterload → ↑SV → ↑CO.
Beta-blockers: ↓HR and contractility → ↓CO in acute phase but beneficial in chronic heart failure.

8. Stroke Volume Variation and Preload-Dependence

SV is preload-dependent: the more the ventricle fills (within limits), the more it ejects.
Frank-Starling curve: Illustrates relationship between LVEDV and SV.
Clinical application: Fluid responsiveness in critically ill patients can be assessed by SV variation.

9. Cardiac Output Distribution

CO is distributed according to organ metabolic needs:
- Brain: 15%
- Heart: 4–5%
- Kidneys: 20–25%
- Skeletal muscle: 20% at rest (up to 85% during exercise)
- Liver and gut: 25–30%
Redistribution occurs during exercise, shock, and sympathetic activation.

10. Pressure-Volume Loops and Their Relation to SV

EDV: Volume at end-diastole (preload).
ESV: Volume at end-systole.
SV: EDV – ESV.
Loop interpretation:
- ↑Preload → rightward shift → ↑SV
- ↑Afterload → taller loop → ↓SV if contractility unchanged
- ↑Contractility → steeper slope → ↑SV, ↓ESV

11. Ejection Fraction and Its Clinical Relevance

EF = SV / EDV × 100%
Normal: 55–70%
Reduced EF: systolic heart failure (<40%)
Preserved EF: diastolic dysfunction (≥50%)
EF is load-dependent and should be interpreted in the context of preload, afterload, and HR.

12. Clinical Assessment of CO and SV

Physical signs: Pulse volume, blood pressure, jugular venous pressure.
Hemodynamic monitoring: Pulmonary artery catheter, arterial lines, central venous pressure.
Echocardiography: Most common non-invasive method for assessing SV and CO.
Stress testing: Evaluates CO reserve and SV augmentation during exercise.

13. Pathophysiology: Alterations in CO and SV

13.1 Heart Failure

↓Contractility → ↓SV → ↓CO
Compensatory mechanisms: ↑HR, vasoconstriction, RAAS activation.

13.2 Hypovolemia

↓Preload → ↓EDV → ↓SV → ↓CO
Corrected with fluid resuscitation.

13.3 Hypertension

↑Afterload → ↑ESV → ↓SV → initial ↓CO, compensatory ↑HR.

13.4 Valve Disease

Aortic stenosis: ↑afterload → ↓SV
Mitral regurgitation: ↓effective forward SV despite normal total SV
Tricuspid regurgitation: ↓effective RV SV → ↓pulmonary CO

14. Therapeutic Modulation of CO and SV

Inotropes: Enhance contractility (dobutamine, milrinone)
Vasodilators: Reduce afterload (ACE inhibitors, nitrates)
Beta-blockers: Improve efficiency in chronic HF by lowering HR
Volume management: Optimize preload (diuretics, fluid resuscitation)
Pacemakers: Improve AV synchrony → optimize SV

15. Summary Table: Determinants and Modifiers

Determinant	Effect on SV	Effect on CO	Clinical Notes
Preload	↑EDV → ↑SV	↑CO if HR stable	Hypovolemia ↓, Fluid therapy ↑
Afterload	↑Resistance → ↓SV	↓CO if contractility unchanged	HTN, Aortic stenosis
Contractility	↑Myocardial force → ↑SV	↑CO	Inotropes ↑, HF ↓
Heart Rate	↑HR → ↑CO (if filling adequate)	Shortened diastole ↓SV at high HR	Tachyarrhythmia reduces SV
Valve function	Regurgitation ↓effective SV	↓CO	MR, TR, AR, PR