CONTROL OF THE HEARTBEAT

A GOOD EXAMPLE OF AUTONOMIC CONTROL

The nervous control of heart rate provides a good example of autonomic control in which the effector, heart muscle in this case, is not under conscious control. (We may alter its rate of contraction indirectly by deliberately working into an emotional or excited state, or by consciously relaxing.)

Interestingly enough, nervous impulses are not necessary to make the heart beat; beats are initiated automatically by the S-A (sino-atrial) node in the wall of the right atrium. But the innate rhythm of the S-A node can be modified by impulses coming to it from sympathetic nerves, which excite the S-A node, and parasympathetic nerves, which inhibit it. Though the sympathetic nerves to the heart emanate from the CNS in the thoracic region of the spinal cord, the impulses they carry originate in the cardiac accelerating center in the medulla of the brain. Similarly, the impulses carried by the parasympathetic nerves to the heart originate in a cardiac-decelerating center in the medulla. The cardiac centers receive input from higher centers, particularly from the sympathetic and parasympathetic headquarters in the hypothalamus. The cardiac centers monitor pressure receptors and chemoreceptors in various places throughout the body and respond appropriately.

If the blood pressure is high, pressure receptors in the carotid artery of the neck and in the arch of the aorta (and to a lesser extent in other arteries) are stimulated. Impulses travel from them to the medulla, where the sympathetic pathways from the cardiac-accelerating center are inhibited, while the parasympathetic pathways from the cardiac-decelerating center are activated. The result is that the heart rate is slowed. As blood pressure falls, however, there is less stimulation of the pressure receptors, which consequently send fewer impulses to the medulla. The sympathetic pathways, freed from inhibition, begin carrying more impulses from the cardiac-accelerating center to the S-A node, while the parasympathetic ones carry fewer, and homeostasis is restored.

The chemoreceptor reflexes respond to changes in the carbon dioxide, oxygen, or pH levels in the blood. The chemoreceptors involved are sensory neurons located in the base of the carotid arteries and the arch of the aorta. When the chemoreceptors in the carotids or aorta detect a rise in carbon dioxide or a decrease in pH in the blood, the cardiac-accelerator centers are stimulated and cardiac-inhibitory centers are inhibited, with the result that vasoconstriction occurs and blood pressure rises. A drop in blood oxygen levels has the same effect on the chemoreceptors in the aorta, though it does not affect those in the carotids. Strong stimulation of these receptors causes an increase in heart rate and cardiac output.

The actual rate of heartbeat thus depends in part on the relative activity of the accelerating and decelerating centers in the medulla; the activity of these centers in turn reflects the amount of excitation they receive from the stretch receptors and the chemoreceptors in the arteries. These automatic reflex circuits serve to fine-tune heart rate with a negative feedback loop. The two centers in the medulla are also significantly influenced by signals from other parts of the brain. For example, when a person sees something frightening, impulses from the processing centers in the brain send signals to the medulla to quicken the pulse. Thus there are two classes of control, one a feedback-regulated system that maintains bodily processes on an even keel, and the other an emergency system to take over in emergency situations.