Cardiac Output

before you start

The autorhythmicity inherent in cardiac cells keeps the heart beating at a regular pace. However, the heart is regulated by and responds to outside influences as well. Neural and endocrine controls are vital to the regulation of cardiac function. In addition, the heart is sensitive to several environmental factors, including electrolytes.

1. Cardiac Output

key concept

Cardiac output (CO) is a measurement of the amount of blood pumped by each ventricle in one minute. This measurement is inherently dependent on the number of contractions the heart undergoes in a minute (or beats per minute, bpm), known as your heart rate (HR), and the amount of blood ejected by each ventricle with each contraction, known as your stroke volume (SV). This relationship can be represented mathematically by the following equation:

CO = HR × SV

SV is normally measured using an echocardiogram (an image of the heart using an ultrasound image) to record end diastolic volume (EDV) and end systolic volume (ESV), and calculating the difference: SV = EDV – ESV. SV can also be measured using a specialized catheter, but this is an invasive procedure and far more dangerous to the patient. A mean SV for a resting 70 kg (150 lb) individual would be approximately 70 mL. There are several important variables, including size of the heart, physical and mental condition of the individual, sex, contractility, duration of contraction, preload or EDV, and afterload or resistance. A normal range for SV would be 55–100 mL. An average resting HR would be approximately 75 bpm but could range from 60–100 in some individuals.

Using these numbers, the mean CO is 5.25 L/min, with a range of 4.0–8.0 L/min. Remember, however, that these numbers refer to CO from each ventricle separately, not the total for the heart.

SVs are also used to calculate ejection fraction, which is the portion of the blood that is pumped or ejected from the heart with each contraction. To calculate ejection fraction, SV is divided by EDV. Despite the name, the ejection fraction is normally expressed as a percentage. Ejection fractions range from approximately 55–70%, with a mean of 58%.

terms to know

Cardiac Output (CO)

A measurement of the amount of blood pumped by each ventricle in one minute.

Heart Rate (HR)

The number of contractions the heart undergoes in a minute.

Stroke Volume (SV)

The amount of blood ejected by each ventricle with each contraction.

Ejection Fraction

The portion of the blood that is pumped or ejected from the heart with each contraction.

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2. Exercise and Maximum Cardiac Output

Increased physical activity causes the total body demand for nutrients and waste removal to increase. To meet this demand, the body increases cardiac output. In healthy young individuals, HR may increase to 150 bpm during exercise. SV can also increase from 70 to approximately 130 mL due to increased strength of contraction. This would increase CO to approximately 19.5 L/min, 4–5 times the resting rate. Top cardiovascular athletes can achieve even higher levels. At their peak performance, they may increase resting CO by 7–8 times.

Since the heart is a muscle, exercising it increases its efficiency. The difference between maximum and resting CO is known as the cardiac reserve. It measures the residual capacity of the heart to pump blood.

term to know

Cardiac Reserve

The difference between an individual’s maximum and resting cardiac output.

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3. Heart Rates

think about it

Are heart rates the same for everyone?

HRs vary considerably, not only with exercise and fitness levels but also with age. Newborn resting HRs may be 120 bpm. As the body develops and grows, HR gradually decreases until young adulthood and then gradually increases again with age.

Maximum HRs are normally in the range of 200–220 bpm, although there are some extreme cases in which they may reach higher levels. As one ages, the ability to generate maximum rates decreases. This may be estimated by taking the maximal value of 220 bpm and subtracting the individual’s age. So a 40-year-old individual would be expected to hit a maximum rate of approximately 180 bpm, and a 60-year-old person would achieve an HR of 160 bpm.

For an adult, normal resting HR will be in the range of 60–100 bpm. Bradycardia is the condition in which resting rate drops abnormally low (i.e., below 60 bpm), and tachycardia is the condition in which the resting rate is abnormally high (i.e., above 100 bpm).

EXAMPLE

Trained athletes typically have very low HRs. If the patient is not exhibiting other symptoms, such as weakness, fatigue, dizziness, fainting, chest discomfort, palpitations, or respiratory distress, bradycardia is not considered clinically significant. However, if any of these symptoms are present, they may indicate that the heart is not providing sufficient oxygenated blood to the tissues. The term relative bradycardia may be used with a patient who has an HR in the normal range but is still suffering from these symptoms. Most patients remain asymptomatic as long as the HR remains above 50 bpm.

Bradycardia may be caused by either inherent factors or causes external to the heart. While the condition may be inherited, typically it is acquired in older individuals. Inherent causes include abnormalities in either the SA or AV node. If the condition is serious, a pacemaker may be required. Other causes include ischemia (restriction of blood supply) to the heart muscle or diseases of the heart vessels or valves. External causes include metabolic disorders, pathologies of the endocrine system, electrolyte imbalances, neurological disorders including inappropriate autonomic responses, autoimmune pathologies, over-prescription of beta blocker drugs that reduce HR, recreational drug use, or even prolonged bed rest. Treatment relies upon establishing the underlying cause of the disorder and may necessitate supplemental oxygen.

Tachycardia is not normal in a resting patient but may be detected in pregnant people or individuals experiencing extreme stress. In the latter case, it would likely be triggered by stimulation from the limbic system or disorders of the autonomic nervous system. In some cases, tachycardia may involve only the atria. Some individuals may remain asymptomatic, but when present, symptoms may include dizziness, shortness of breath, lightheadedness, rapid pulse, heart palpitations, chest pain, or fainting (syncope). While tachycardia is defined as an HR above 100 bpm, there is considerable variation among people. As noted above, the normal resting HRs of children are often above 100 bpm, but this is not considered to be tachycardia. Many causes of tachycardia may be benign, but the condition may also be correlated with fever, anemia, hypoxia, hyperthyroidism, hypersecretion of catecholamines, some cardiomyopathies, some disorders of the valves, and acute exposure to radiation. Elevated rates in an exercising or resting patient are normal and expected. The resting rate should always be taken after recovery from exercise. Treatment depends upon the underlying cause but may include medications, implantable cardioverter defibrillators, ablation, or surgery.

Term	Pronunciation	Audio File
Bradycardia	bra·dy·car·dia
Tachycardia	tachy·car·dia

terms to know

Bradycardia

A condition in which resting rate drops abnormally low (i.e., below 60 bpm).

Tachycardia

A condition in which resting rate drops abnormally high (i.e., above 100 bpm).

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4. Correlation Between Heart Rates and Cardiac Output

Initially, physiological conditions that cause HR to increase also trigger an increase in SV. During exercise, the rate of blood returning to the heart increases. However, as the HR rises, the heart spends less time in diastole and consequently there is less time for the ventricles to fill with blood. Even though there is less filling time, SV will initially remain high. However, later on, as HR continues to increase, filling time continues to decrease, leading to a gradual decrease in SV. Consequently, CO will initially stabilize as the increasing HR compensates for the decreasing SV, but at very high rates, CO will eventually decrease as increasing rates are no longer able to compensate for the decreasing SV.

Consider this phenomenon in a healthy young individual. Initially, as HR increases from resting to approximately 120 bpm, CO will rise. As HR increases from 120 to 160 bpm, CO remains stable, since the increase in rate is offset by decreasing ventricular filling time and, consequently, SV. As HR continues to rise above 160 bpm, CO actually decreases as SV falls faster than HR increases. So although aerobic exercises are critical to maintain the health of the heart, individuals are cautioned to monitor their HR to ensure they stay within the target heart rate range of between 120 and 160 bpm, so CO is maintained. The target HR is loosely defined as the range in which both the heart and lungs receive the maximum benefit from the aerobic workout and is dependent upon age.

term to know

Target Heart Rate

The range of heart beats per minute in which both the heart and lungs receive the maximum benefit from the aerobic workout.

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5. Stroke Volume

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.

5a. Preload

Preload is another way of expressing EDV. One of the primary factors to consider is the duration of ventricular diastole during which filling occurs. The more rapidly the heart goes through the cardiac cycle, the shorter the filling time becomes. If the ventricles spend less time filling, then the amount of stretch they will undergo—the preload or EDV—is limited. This effect can be partially overcome by increasing contractility and raising SV, but over time, the heart is unable to compensate for decreased filling time, and preload decreases.

With increasing ventricular filling, preload increases, and the cardiac muscle itself is stretched to a greater degree. At rest, there is little stretch of the ventricular muscle, and the sarcomeres remain short. As the sarcomeres reach their optimal lengths, they will contract more powerfully. If this process were to continue and the sarcomeres stretched beyond their optimal lengths, the force of contraction would decrease. However, due to the physical constraints of the location of the heart, this excessive stretch is not a concern.

The relationship between ventricular stretch and contraction has been stated in the well-known Frank-Starling mechanism or simply Starling’s Law of the Heart. This principle states that, within physiological limits, the force of heart contraction is directly proportional to the initial length of the muscle fiber. This means that the greater the stretch of the ventricular muscle (within limits), the more powerful the contraction is, which in turn increases SV. Therefore, by increasing preload, you increase the second variable, contractility.

Any sympathetic stimulation to the venous system will increase venous return to the heart, which contributes to ventricular filling, EDV, and preload. While much of the ventricular filling occurs while both atria and ventricles are in diastole, the contraction of the atria, the atrial kick, plays a crucial role by providing the last 20–30% of ventricular filling.

5b. Contractility

Contractility refers to the force of the contraction of the heart muscle, which controls SV, and is the primary parameter for impacting ESV. The more forceful the contraction is, the greater the SV and smaller the ESV are. Less forceful contractions result in smaller SVs and larger ESVs.

5c. Afterload

Afterload refers to the tension that the ventricles must develop to pump blood effectively against the resistance in the vascular system. Any condition that increases resistance requires a greater afterload to force open the semilunar valves and pump the blood. Damage to the valves, such as stenosis, which makes them harder to open will also increase afterload. Any decrease in resistance decreases the afterload.

	Factors Affecting Stroke Volume (SV)
	Preload	Contractility	Afterload
Raised due to:	increased filling time increased venous return, Increases end diastolic volume, Increases stroke volume.	sympathetic stimulation epinephrine and norepinephrine high intracellular calcium ions high blood calcium level thyroid hormones glucagon Decreases end systolic volume, Increases stroke volume.	increased vascular resistance semilunar valve damage Increases end systolic volume, Decreases stroke volume.
Lowered due to:	decreased thyroid hormones decreased calcium ions high or low potassium ions high or low sodium low body temperature hypoxia abnormal pH balance drugs (i.e., calcium channel blockers) Decreases end diastolic volume, Decreases stroke volume.	parasympathetic stimulation acetylcholine hypoxia hyperkalemia Increases end systolic volume, Decreases stroke volume.	decreased vascular resistance Decreases end systolic volume, Increases stroke volume.

	Baroreceptors (aorta, carotid arteries, venae cavae, and atria)	Chemoreceptors (both central nervous system and in proximity to baroreceptors)
Sensitive to	Decreasing stretch	Decreasing O₂ and increasing CO₂, H⁺, and lactic acid
Target	Parasympathetic stimulation suppressed	Sympathetic stimulation increased
Response of heart	Increasing heart rate and increasing stroke volume	Increasing heart rate and increasing stroke volume
Overall effect	Increasing blood flow and pressure due to increasing cardiac output; homeostasis restored	Increasing blood flow and pressure due to increasing cardiac output; homeostasis restored

	Baroreceptors (aorta, carotid arteries, venae cavae, and atria)	Chemoreceptors (both central nervous system and in proximity to baroreceptors)
Sensitive to	Increasing stretch	Increasing O₂ and decreasing CO₂, H⁺, and lactic acid
Target	Parasympathetic stimulation increased	Sympathetic stimulation suppressed
Response of heart	Decreasing heart rate and decreasing stroke volume	Decreasing heart rate and decreasing stroke volume
Overall effect	Decreasing blood flow and pressure due to decreasing cardiac output; homeostasis restored	Decreasing blood flow and pressure due to decreasing cardiac output; homeostasis restored

make the connection

If you're taking the Anatomy & Physiology II Lab course simultaneously with this lecture, it's a good time to try the Lab Cardiovascular Function During Exercise: Learn how your body reacts to exercise in Unit 2 of the Lab course. Review the lab-to-lecture crosswalk if you need more information. Good luck!

terms to know

Preload

The stretch on the ventricles prior to contraction.

Contractility

The force of the contraction of the heart muscle.

Afterload

The tension that the ventricles must develop to pump blood effectively against the resistance in the vascular system.