1. Definition
Cardiac output (CO) is the volume of blood the heart pumps into the circulatory system per minute, calculated as the product of heart rate and stroke volume.
2. Calculation
Cardiac output (CO) is calculated as the product of heart rate (HR) and stroke volume (SV):
[math] CO = HR \times SV[/math]
3. Influencing Factors
The normal physiological value of cardiac output in a healthy adult at rest is typically around 4.5 to 5 liters per minute. This value can increase significantly during physical exertion, sometimes up to four times. Cardiac output increases through the Frank-Starling mechanism, where greater venous return stretches the heart muscle more, leading to a stronger contraction and increased stroke volume. This allows the heart to pump more blood without changing the heart rate.
In general cardiac output is influenced by heart rate, stroke volume, which is determined by preload (venous return), afterload (arterial resistance), myocardial contractility, and the Frank-Starling mechanism.
4. Measurement
Stroke volume is defined as the product of end-diastolic ventricular volume and the ejection fraction. Determining stroke volume is complex and involves various methods for measuring cardiac output:
Cardiac output can be measured using several methods, including:
4.1. Thermodilution: A Swan-Ganz catheter is used to inject cold saline into the bloodstream, and the change in blood temperature is measured to calculate cardiac output.
4.2. Echocardiography: Stroke volume is estimated by assessing ventricular volume and ejection fraction, then multiplied by heart rate to determine cardiac output.
4.3. Fick Principle: This method calculates cardiac output by measuring oxygen consumption and the difference in oxygen content between arterial and venous blood.
4.4. Doppler Ultrasound: Measures blood flow velocity and cross-sectional area of the vessels to estimate stroke volume and, consequently, cardiac output.
Each method varies in precision and is chosen based on clinical requirements
5. Decrease in Cardiac Output
- Bradycardia: A slower heart rate reduces the number of beats per minute, lowering cardiac output.
- Tachycardia: Extremely high heart rates can reduce diastolic filling time and worsen coronary perfusion.
- Decreased contractility: Conditions like myocardial infarction or heart failure weaken the heart muscle, reducing its ability to pump blood effectively.
- Increased afterload: Higher arterial resistance (e.g., due to hypertension) makes it harder for the heart to eject blood, decreasing stroke volume.
- Reduced preload: Insufficient venous return or low blood volume (e.g., due to dehydration or hemorrhage) decreases stroke volume.
- Valvular heart disease: Dysfunctional heart valves can impair the efficient flow of blood through the heart, reducing cardiac output.
6. Increase in Cardiac Output
- Increased heart rate: Sympathetic nervous system activation, stress, or physical activity can increase heart rate, raising cardiac output.
- Increased stroke volume: Enhanced by mechanisms like the Frank-Starling mechanism, where increased venous return stretches the heart muscle, leading to stronger contractions.
- Improved contractility: Sympathetic stimulation or the use of positive inotropic drugs (e.g., adrenaline) can strengthen heart contractions.
- Decreased afterload: Lower arterial resistance (e.g., through vasodilation) makes it easier for the heart to pump blood, increasing stroke volume.
- Physical conditioning: In athletes, cardiac output can increase due to a more efficient cardiovascular system and greater stroke volume from myocardial hypertrophy.