Resting Cardiac Output

Cardiac output (CO) is a measurement of the amount of blood pumped by each ventricle in one minute. To calculate this value, multiply stroke volume (SV), the amount of blood pumped by each ventricle, by heart rate (HR), in contractions per minute (or beats per minute, bpm). It can be represented mathematically by the following equation:

CO = HR × SV

SV is normally measured using an echocardiogram to record EDV and 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.  This is because typical EDV and ESV values are approximately 120 mL and 50 mL, respectively and 70 mL = 120 mL – 50 mL. 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. There are several important variables, including size of the heart, physical and mental condition (via hormones and the ANS) of the individual, gender, contractility, duration of contraction, preload or EDV, and afterload or resistance that can affect SV and HR.

Using these numbers, the mean resting CO is 5.25 L/min, with a range of 4.0–8.0 L/min.  The CO of 5.25 L/min, was calculated using the following values.

CO L/min = 75 beats/min x 0.070 L/beat (where 0.070 L is equal to 70 mL).

Remember, however, that these numbers refer to CO from each ventricle separately, not the total for the heart. In a healthy heart the CO from each ventricle is the same. CO is influenced by HR and by SV. If SV decreases, CO can be maintained by increasing HR. Factors that influence HR are referred to as chronotropic factors. Chrono- refers to time. Positive chronotropic factors increase HR and negative chronotropic factors decrease HR. HR is influenced by the autonomic nervous system, chemicals, and other factors. The factors influencing CO are summarized in Figure 19.4.1.

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 percent, with a mean of 58 percent.  For example, if the average EDV is 120 mL and the SV is 70 mL, the ejection fraction of 58% is calculated as follows:

Ejection fraction (%) = (70 mL/120 mL) x 100

Exercise and Maximum Cardiac Output

In healthy young individuals, HR may increase to 150 bpm or higher 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.

Heart Rate and its Control

HRs vary considerably, not only with exercise and fitness levels, but also with age. Newborn resting HRs may be 120 bpm. 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 reach a maximum rate of approximately 180, and a 60-year-old person would achieve a HR of 160. Refer to the example below.

HR_Max = 220 – 60 yr

HR_Max = 160 bpm

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, there is less time spent in diastole and consequently less time for the ventricles to fill with blood. Even though there is less filling time, SV will initially remain high. However, as HR continues to increase, SV gradually decreases due to decreased filling time. 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.  It is also important to note that the coronary circulation nourishes the heart during diastole so as the HR increases the ability of the coronary circulation to nourish the myocardium decreases. 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.

Cardiovascular Centers

Nervous control over HR is centralized within the two paired cardiovascular centers of the medulla oblongata (Figure 19.4.2). The cardioaccelerator regions stimulate activity via sympathetic stimulation of the cardioacceleratory nerves, and the cardioinhibitory centers decrease heart activity via parasympathetic stimulation as one component of the vagus nerve, cranial nerve X. Both sympathetic and parasympathetic stimulations flow through a paired complex network of nerve fibers known as the cardiac plexus near the base of the heart. The cardioacceleratory center also sends additional fibers, forming the cardiac nerves via sympathetic ganglia (the cervical ganglia plus superior thoracic ganglia T1–T4) to both the SA and AV nodes to increase heart rate, plus additional fibers to the atrial and ventricular myocardium to increase force of contraction (see section on Contractility). The ventricles are more richly innervated by sympathetic fibers than parasympathetic fibers. During rest, both centers provide slight stimulation to the heart, contributing to autonomic tone. This is a similar concept to tone in skeletal muscles. Normally, vagal stimulation predominates as, left unregulated, the SA node would initiate a sinus rhythm of approximately 100 bpm.

At the nodes sympathetic stimulation causes the release of the neurotransmitter norepinephrine (NE) at the neuromuscular junction of the cardiac nerves. NE binds to the beta-1 receptors and opens chemical- or ligand-gated sodium and calcium ion channels, allowing an influx of positively charged ions. NE shortens the repolarization period, thus speeding the rate of depolarization and contraction, which results in an increase in HR. Some cardiac medications (for example, beta blockers) work by blocking these receptors, thereby slowing HR and are one possible treatment for hypertension. Overprescription of these drugs may lead to bradycardia and even stoppage of the heart.

Parasympathetic stimulation originates from the cardioinhibitory region with impulses traveling via the vagus nerve (cranial nerve X). The vagus nerve sends branches to both the SA and AV nodes to decrease HR. Parasympathetic stimulation releases the neurotransmitter acetylcholine (ACh) at the neuromuscular junction. ACh slows HR by opening chemical- or ligand-gated potassium ion channels to slow the rate of spontaneous depolarization and increase the time before the next spontaneous depolarization occurs. Without any nervous stimulation, the SA node would establish a sinus rhythm of approximately 100 bpm. Since resting rates are considerably less than this, it becomes evident that parasympathetic stimulation normally slows HR. This is similar to an individual driving a car with one foot on the brake pedal. To speed up, one need merely remove one’s foot from the break and let the engine increase speed. In the case of the heart, decreasing parasympathetic stimulation decreases the release of ACh, which allows HR to increase up to approximately 100 bpm. Any increases beyond this rate would require sympathetic stimulation. Figure 19.4.3 illustrates the effects of parasympathetic and sympathetic stimulation on the normal sinus rhythm.

Input to the Cardiovascular Centers

The cardiovascular center receives input from the limbic system as well as a series of visceral receptors with impulses traveling through visceral sensory fibers within the vagus and sympathetic nerves via the cardiac plexus. Among these receptors are various proprioreceptors, baroreceptors, and chemoreceptors. Collectively, these inputs normally enable the cardiovascular centers to regulate heart function precisely, a process known as cardiac reflexes. Increased physical activity results in increased rates of firing by various proprioreceptors located in muscles, joint capsules, and tendons. Any such increase in physical activity would logically warrant increased blood flow. The cardiac centers monitor these increased rates of firing, and suppress parasympathetic stimulation and increase sympathetic stimulation as needed in order to increase blood flow.

Similarly, baroreceptors are stretch receptors located in the aortic sinus, carotid bodies, the venae cavae, and other locations, including pulmonary vessels and the rightatrium. Rates of firing from the baroreceptors represent blood pressure, level of physical activity, and the relative distribution of blood. The cardiac centers monitor baroreceptor firing to maintain cardiac homeostasis, a mechanism called the baroreceptor reflex. With increased pressure and stretch, the rate of baroreceptor firing increases, and the cardiac centers decrease sympathetic stimulation and increase parasympathetic stimulation. As pressure and stretch decrease, the rate of baroreceptor firing decreases, and the cardiac centers increase sympathetic stimulation and decrease parasympathetic stimulation.

There is a similar reflex, called the atrial reflex or Bainbridge reflex, associated with varying rates of blood flow to the atria. Increased venous return stretches the walls of the atria where specialized baroreceptors are located. However, as the atrial baroreceptors increase their rate of firing and as they stretch due to the increased blood pressure, the cardiac center responds by increasing sympathetic stimulation and inhibiting parasympathetic stimulation to increase HR.

Increased metabolic byproducts associated with increased activity, such as carbon dioxide, hydrogen ions, and lactic acid, plus falling oxygen levels, are detected by a suite of chemoreceptors innervated by the glossopharyngeal and vagus nerves. These chemoreceptors provide feedback to the cardiovascular centers about the need for increased or decreased blood flow, based on the relative levels of these substances.

The limbic system can also significantly impact HR related to emotional state. During periods of stress, it is not unusual to identify higher than normal HRs, often accompanied by a surge in the stress hormone cortisol. Individuals experiencing extreme anxiety may manifest panic attacks with symptoms that resemble those of heart attacks. These events are typically transient and treatable. Meditation techniques have been developed to ease anxiety and have been shown to lower HR effectively. Doing simple deep and slow breathing exercises with one’s eyes closed can also significantly reduce this anxiety and HR.

Other Factors Influencing Heart Rate and Force of Contraction

Using a combination of autorhythmicity and innervation, the cardiovascular centers are able to provide relatively precise control over HR. However, there are a number of other factors that have an impact on HR as well, including epinephrine, NE, and thyroid hormones; levels of various ions including calcium, potassium, and sodium; body temperature; hypoxia; and pH balance (Table 19.1 and Table 19.2). Many of these factors also influence contractility which refers to the force of contraction of the heart muscle.  After reading this section, the importance of maintaining homeostasis should become even more apparent.

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. These factors are summarized in Table 19.1 and Table 19.2.

Afterload

Afterload refers to the tension or force that the ventricles must develop to pump blood effectively against the resistance in the vascular system. Any condition that increases resistance such as vasoconstriction or the disease atherosclerosis 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 as with vasodilation, decreases the afterload. Figure 19.4.4 summarizes the major factors influencing SV, Figure 19.4.5 summarizes the major factors influencing CO, and Table 19.3 and Table 19.4 summarize cardiac responses to increased and decreased blood flow and pressure in order to restore homeostasis.

Summary of Cardiac Response to Decreasing Blood Flow and Pressure Due to Decreasing Cardiac Output (Table 19.3)
	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
Action	Parasympathetic stimulation suppressed	Sympathetic stimulation increased
Effect on 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

Summary of Cardiac Response to Increasing Blood Flow and Pressure Due to Increasing Cardiac Output (Table 19.4)
	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
Action	Parasympathetic stimulation increased	Sympathetic stimulation suppressed
Effect on 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