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20.10
The Heart and Homeostasis
    Learning Outcomes

    After reading this section, you should be able to:

  1. Describe how changes in blood pressure, pH, carbon dioxide, and oxygen affect the function of the heart.
  2. Explain how extracellular ion concentration and body temperature affect the function of the heart.

The pumping efficiency of the heart plays an important role in maintaining homeostasis. Blood pressure in the systemic vessels must be high enough to allow nutrient and waste product exchange across the walls of the capillaries and to meet metabolic demands. In addition, the heart's activity must be regulated because the metabolic activities of the tissues change under such conditions as exercise and rest. Baroreceptor reflexes regulate blood pressure, and chemoreceptor reflexes help regulate the heart's activity.

Effect of Blood Pressure

Baroreceptor (bar'ō-rē-sep'ter, bar'ō-rē-sep'tōr) reflexes detect changes in blood pressure and lead to changes in heart rate and force of contraction. Stretch receptors, the sensory receptors of the baroreceptor reflexes, are in the walls of certain large arteries, such as the internal carotid arteries and the aorta. These stretch receptors measure blood pressure (figure 20.22). The anatomy of these sensory structures and their afferent pathways are described in Chapter 21.

Afferent neurons project primarily through the glossopharyngeal (cranial nerve IX) and vagus (cranial nerve X) nerves from the baroreceptors to an area in the medulla oblongata called the cardioregulatory center, where sensory action potentials are integrated (figure 20.22). The part of the cardioregulatory center that increases heart rate is called the cardioacceleratory center, and the part that decreases heart rate is called the cardioinhibitory center. Efferent action potentials then travel from the cardioregulatory center to the heart through both the sympathetic and the parasympathetic divisions of the autonomic nervous system.

Elevated blood pressure within the internal carotid arteries and aorta causes their walls to stretch, thereby stimulating an increase in action potential frequency in the baroreceptors (figure 20.23). At normal blood pressures (80–120 mm Hg), afferent action potentials are sent from the baroreceptors to the medulla oblongata at a relatively constant frequency. When blood pressure rises, the arterial walls are stretched farther, and the afferent action potential frequency increases. When blood pressure decreases, the arterial walls are stretched to a lesser extent, and the afferent action potential frequency decreases. In response to elevated blood pressure, the baroreceptor reflexes reduce sympathetic stimulation and increase parasympathetic stimulation of the heart, causing the heart rate to slow. Decreased blood pressure causes decreased parasympathetic and increased sympathetic stimulation of the heart, resulting in an increased heart rate and force of contraction. Withdrawal of parasympathetic stimulation is primarily responsible for increases in heart rate up to approximately 100 bpm. Larger increases in heart rate, especially during exercise, result from sympathetic stimulation. The baroreceptor reflexes are homeostatic because they keep the blood pressure within a narrow range of values that is adequate to maintain blood flow to the tissues.

 
HOMEOSTASIS FIGURE 20.23
Summary of the Baroreceptor ReflexThe baroreceptor reflex maintains homeostasis in response to changes in blood pressure.
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Effect of pH, Carbon Dioxide, and Oxygen

Chemoreceptor (kē'mō-rē-sep'tor) reflexes help regulate the heart's activity. Chemoreceptors sensitive to changes in pH and carbon dioxide levels exist within the medulla oblongata. A drop in pH and a rise in carbon dioxide decrease parasympathetic and increase sympathetic stimulation of the heart, resulting in increased heart rate and force of contraction (figure 20.24).

HOMEOSTASIS FIGURE 20.24
Summary of the Chemoreceptor ReflexThe chemoreceptor reflex maintains homeostasis in response to changes in blood CO2 and H+ concentrations.

Chemoreceptor Reflex Control of Blood Pressure

The increased cardiac output causes greater blood flow through the lungs, where carbon dioxide is eliminated from the body. This helps lower the blood carbon dioxide level to within its normal range and helps increase blood pH.

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Chemoreceptors primarily sensitive to blood oxygen levels are found in the carotid and aortic bodies. These small structures are located near large arteries close to the brain and heart, and they monitor blood flowing to the brain and the rest of the body. A dramatic decrease in blood oxygen levels, as occurs during asphyxiation, activates the carotid and aortic body chemoreceptor reflexes. In carefully controlled experiments, it is possible to isolate the effects of the carotid and aortic body chemoreceptor reflexes from other reflexes, such as the medullary chemoreceptor reflexes. These experiments indicate that a reduction in blood oxygen results in decreased heart rate and increased vasoconstriction. The vasoconstriction causes blood pressure to rise, which promotes blood delivery despite the decrease in heart rate. The carotid and aortic body chemoreceptor reflexes may protect the heart for a short time by slowing the heart rate, thereby reducing its need for oxygen. The carotid and aortic body chemoreceptor reflexes normally do not function independently of other regulatory mechanisms. When all the regulatory mechanisms function together, large, prolonged decreases in blood oxygen levels increase the heart rate. Low blood oxygen levels also increase stimulation of respiratory movements (see Chapter 23). Increased inflation of the lungs stimulates stretch receptors in the lungs. Afferent action potentials from these stretch receptors influence the cardioregulatory center, which causes the heart rate to increase. The reduced oxygen levels that exist at high altitudes can cause an increase in heart rate even when blood carbon dioxide levels remain low. However, the carotid and aortic body chemoreceptor reflexes are more important in regulating respiration (see Chapter 23) and blood vessel constriction (see Chapter 21) than heart rate.

Effect of Extracellular Ion Concentration

The ions that affect cardiac muscle function are the same ions (K+, Ca2+, and Na+) that influence membrane potentials in other electrically excitable tissues. However, cardiac muscle responds to these ions differently than nerve or skeletal muscle tissue does. For example, the extracellular levels of Na+ rarely deviate enough from normal to significantly affect cardiac muscle function.

Excess K+ in cardiac tissue cause the heart rate and stroke volume to decrease. A twofold increase in extracellular K+ results in heart block, which is the loss of action potential conduction through the heart. The excess K+ in the extracellular fluid cause partial depolarization of the resting membrane potential, resulting in a reduced amplitude of action potentials and, because of the reduced amplitude, a decreased rate at which action potentials are conducted along cardiac muscle cells. As the conduction rates decrease, ectopic action potentials can occur. In many cases, partially depolarized cardiac muscle cells spontaneously produce action potentials because the membrane potential reaches threshold. Elevated blood levels of K+ can produce enough ectopic action potentials to cause fibrillation. The reduced action potential amplitude also results in less Ca2+ entering the sarcoplasm of the cell; thus, the strength of cardiac muscle contraction lessens.

Although the extracellular concentration of K+ is normally small, a reduction in extracellular K+ causes the resting membrane potential to become hyperpolarized; as a consequence, it takes longer for the membrane to depolarize to threshold. Ultimately, the reduction in extracellular K+ results in a decrease in heart rate. The force of contraction is not affected, however.

A rise in the extracellular concentration of Ca2+ produces a greater force of cardiac contraction because of a higher influx of Ca2+ into the sarcoplasm during action potential generation. Elevated plasma Ca2+ levels have an indirect effect on heart rate because they reduce the frequency of action potentials in nerve fibers, thus reducing sympathetic and parasympathetic stimulation of the heart (see Chapter 11). Generally, elevated blood Ca2+ levels lower the heart rate.

A low blood Ca2+ level increases the heart rate, although the effect is imperceptible until blood Ca2+ levels are reduced to approximately one-tenth of their normal value. The reduced extracellular Ca2+ levels cause Na+ channels to open, which allows Na+ to diffuse more readily into the cell, resulting in depolarization and action potential generation. However, reduced Ca2+ levels usually cause death due to tetany of skeletal muscles before they decrease enough to markedly influence the heart's function.

Effect of Body Temperature

Under resting conditions, the temperature of cardiac muscle normally does not change dramatically, although alterations in temperature influence the heart rate. Small increases in cardiac muscle temperature cause the heart rate to speed up, and decreases in temperature cause the heart rate to slow. For example, during exercise or fever, increased heart rate and force of contraction accompany temperature elevations, but the heart rate drops under conditions of hypothermia. During heart surgery, body temperature is sometimes reduced dramatically on purpose to slow the heart rate and other metabolic functions.

ASSESS YOUR PROGRESS
  1. Explain how the nervous system detects and responds to each of the following:

    1. a decrease in blood pressure.

    2. an increase in blood carbon dioxide level.

    3. a decrease in blood pH.

    4. a decrease in blood oxygen level.

  2. Describe the baroreceptor reflex and the heart's response to an increase in venous return.

  3. What effect does an increase or a decrease in extracellular potassium, calcium, and sodium ions have on the heart's rate and force of contraction?

  4. What effect does temperature have on heart rate?