What is Cardiac Output?
Cardiac output (CO) is the amount of blood ejected from the left ventricle, into the aorta of your heart, then out to the rest of the body in one minute. Normally, an average person has about five liters of blood circulating throughout the body’s systems.
Cardiac Output Equation
This CO equation helps you determine a patient’s cardiac output by calculating the amount of blood pumped by the heart in one minute. Here’s the equation (where CO = cardiac output (liters/min), HR = heart rate (beats/min), and SV = stroke volume (milliliters)):
Heart rate (beats/min.) x Stroke volume (mL) = Cardiac output (l/min.)
What is Stroke Volume?
Stroke volume is the amount of blood in one clean pump – in other words, what your heart pumps with each beat. It’s a measurement of how much blood goes through your body every minute. Results depend on the size of the heart and how fast it contracts.
Normal stroke volume will depend on each individual patient, but it’s typically between 50 to 100 mL.
Backing up of traffic (too much blood) causes the left ventricle to swell or inflate because it’s trying its hardest to push blood out, going against the resistance of high blood pressure.
Decreased stroke volume = compromised cardiac output = left ventricular hypertrophy
Many of the same factors that regulate HR also impact cardiac function by altering SV. While a number of variables are involved, SV is ultimately dependent upon the difference between EDV and ESV. The three primary factors to consider are preload, or the stretch on the ventricles prior to contraction; the contractility, or the force or strength of the contraction itself; and afterload, the force the ventricles must generate to pump blood against the resistance in the vessels.
1.Preload:
Definition:
The initial stretching of the cardiac myocytes prior to contraction.
Determinants:
- Ventricular volume (end-diastolic volume)
- Venous return
- Blood volume
- Cardiac compliance
Factors affecting preload:
- Volume status (hypovolemia/hypervolemia)
- Venous tone
- Cardiac function (heart failure)
- Medications (diuretics, vasodilators)
2.Afterload:
Definition:
The resistance against which the heart must pump blood.
Determinants:
- Systemic vascular resistance (SVR)
- Arterial blood pressure
- Cardiac output
- Vascular compliance
Factors affecting afterload:
- Blood pressure (hypertension/hypotension)
- Vascular tone
- Cardiac function (heart failure)
- Medications (vasodilators, vasoconstrictors)
Relationship between Preload and Afterload:
- Increased preload → Increased stroke volume (Frank-Starling mechanism)
- Increased afterload → Decreased stroke volume
- Decreased preload → Decreased stroke volume
- Decreased afterload → Increased stroke volume
Clinical Implications:
- Heart failure: Decreased preload, increased afterload
- Hypovolemia: Decreased preload
- Hypertension: Increased afterload
- Septic shock: Decreased afterload, increased preload
3.Cardiac contractility
Cardiac contractility or myocardial contractility refers to the ability of the ventricles to contract during the systolic phase.
In other words, the force with which ventricular ejection occurs is called contractility of the heart.
Factors affecting cardiac contractility
Several factors affect the contractility of the heart.
Factors that increase cardiac contractility are:
- Hormonal changes. For example, adrenaline, glucagon, and thyroxine increase cardiac contractility.
- Activation of the parasympathetic nervous system also increases the heart’s contractility due to noradrenaline release.
Factors that decrease cardiac contractility are:
- Increased hydrogen ion concentration in the blood (known as acidemia).
- Increased potassium level in the blood (known as hyperkalemia)
Measurement:
- Preload: Central venous pressure (CVP), pulmonary capillary wedge pressure (PCWP)
- Afterload: Systemic vascular resistance (SVR), arterial blood pressure
Manipulation:
- Preload: Fluid administration, diuretics
- Afterload: Vasodilators, vasoconstrictors
Other Factors Influencing Heart Rate and Force of Contraction
| Major Factors Increasing Heart Rate and Force of Contraction | |
|---|---|
| Factor | Effect |
| Cardioaccelerator nerves | Release of norepinephrine |
| Proprioreceptors | Increased rates of firing during exercise |
| Chemoreceptors | Decreased levels of O2; increased levels of H+, CO2, and lactic acid |
| Baroreceptors | Decreased rates of firing, indicating falling blood volume/pressure |
| Limbic system | Anticipation of physical exercise or strong emotions |
| Catecholamines | Increased epinephrine and norepinephrine |
| Thyroid hormones | Increased T3 and T4 |
| Calcium | Increased Ca2+ |
| Potassium | Decreased K+ |
| Sodium | Decreased Na+ |
| Body temperature | Increased body temperature |
| Nicotine and caffeine | Stimulants, increasing heart rate |
| Factors Decreasing Heart Rate and Force of Contraction | |
|---|---|
| Factor | Effect |
| Cardioinhibitor nerves (vagus) | Release of acetylcholine |
| Proprioreceptors | Decreased rates of firing following exercise |
| Chemoreceptors | Increased levels of O2; decreased levels of H+ and CO2 |
| Baroreceptors | Increased rates of firing, indicating higher blood volume/pressure |
| Limbic system | Anticipation of relaxation |
| Catecholamines | Decreased epinephrine and norepinephrine |
| Thyroid hormones | Decreased T3 and T4 |
| Calcium | Decreased Ca2+ |
| Potassium | Increased K+ |
| Sodium | Increased Na+ |
| Body temperature | Decrease in body temperature |
Many factors affect HR and SV, and together, they contribute to cardiac function. HR is largely determined and regulated by autonomic stimulation and hormones. There are several feedback loops that contribute to maintaining homeostasis dependent upon activity levels, such as the atrial reflex, which is determined by venous return.

SV is regulated by autonomic innervation and hormones, but also by filling time and venous return. Venous return is determined by activity of the skeletal muscles, blood volume, and changes in peripheral circulation. Venous return determines preload and the atrial reflex. Filling time directly related to HR also determines preload. Preload then impacts both EDV and ESV. Autonomic innervation and hormones largely regulate contractility. Contractility impacts EDV as does afterload. CO is the product of HR multiplied by SV. SV is the difference between EDV and ESV.
REFERENCES
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