Since each beat of the heart produces a surge of pressure in the arteries, the easiest way to measure heart rate is to palpate the pulse in a superficial artery and count beats per minute. In newborn infants, the resting heart rate is commonly 120 bpm or greater. It declines steadily with age, averaging 72 to 80 bpm in young adult females and 64 to 72 bpm in young adult males. It rises again in the elderly.
Tachycardia28 is a persistent, resting adult heart rate above 100 bpm. It can be caused by stress, anxiety, drugs, heart disease, or fever. Heart rate also rises to compensate to some extent for a drop in stroke volume. Thus, the heart races when the body has lost a significant quantity of blood or when there is damage to the myocardium.
Bradycardia29 is a persistent, resting adult heart rate below 60 bpm. It is common during sleep and in endurance-trained athletes. Endurance training enlarges the heart and increases its stroke volume. Thus, it can maintain the same cardiac output with fewer beats. Hypothermia (low body temperature) also slows the heart rate and may be deliberately induced in preparation for cardiac surgery. Diving mammals such as whales and seals exhibit bradycardia during the dive, as do humans to some extent when the face is immersed in cool water.
Factors that raise the heart rate are called positive chronotropic30 agents, and factors that lower it are negative chronotropic agents. We next consider some chronotropic effects of the autonomic nervous system, hormones, electrolytes, and blood gases.
Chronotropic Effects of the Autonomic Nervous System
Although the nervous system does not initiate the heartbeat, it does modulate its rhythm and force. The cardiac center of the medulla oblongata consists of two neuronal pools, a cardioacceleratory center and cardioinhibitory center. The cardioacceleratory center sends signals by way of sympathetic cardiac accelerator nerves to the SA node, AV node, and myocardium. These nerves secrete norepinephrine, which binds to ^-adrenergic receptors in
28tachy = speed, fast + card = heart + ia = condition
2abrady = slow
30chrono = time + trop = turn, change, influence the heart and increases the heart rate. Cardiac output peaks when the heart rate is 160 to 180 bpm, although the sympathetic nervous system can get the heart rate up to as much as 230 bpm. This limit is set mainly by the refractory period of the SA node; it cannot fire any more frequently. At such a high rate, however, the ventricles beat so rapidly that they have little time to fill between beats; therefore, the stroke volume and cardiac output are less than they are at rest. At a heart rate of 65 bpm, ventricular diastole lasts about 0.62 seconds, but at 200 bpm, it lasts only 0.14 seconds. At that high rate, there is less time available for refilling between beats.
The cardioinhibitory center sends signals by way of parasympathetic fibers in the vagus nerves to the SA and AV nodes. The right vagus nerve innervates mainly the SA node, and the left vagus nerve innervates the AV node. The vagus nerves secrete acetylcholine, which binds to muscarinic receptors and opens K+ channels in the nodal cells. As K+ leaves the cells, the cells become hyperpolarized and fire less frequently, so the heart slows down.
The vagus nerves maintain a background firing rate called vagal tone that inhibits the nodes. If the vagus nerves to the heart are severed, the SA node fires at its own intrinsic frequency of about 100 times per minute. With the vagus nerve intact, however, vagal tone holds the heart rate down to the usual 70 to 80 bpm. Maximum vagal stimulation can reduce the heart rate to as low as 20 bpm.
The cardiac center receives and integrates input from multiple sources. Sensory and emotional stimuli can act on the cardiac center by way of the cerebral cortex, limbic system, and hypothalamus; therefore, heart rate can climb even as you anticipate taking the first plunge on a roller coaster, and it is influenced by emotions such as love and anger. The cardiac center also receives input from receptors in the muscles, joints, arteries, and brainstem:
• Proprioceptors in the muscles and joints quickly inform the cardiac center of changes in physical activity. Thus, the heart can increase its output even before the metabolic demands of the muscles rise.
• Baroreceptors (pressoreceptors) are pressure sensors in the aorta and internal carotid arteries (see fig. 15.1, p. 565). They send a continual stream of signals to the cardiac center. If blood pressure drops, the signaling rate drops and the cardiac center increases the heart rate and raises the blood pressure. If blood pressure rises too high, the signaling rate from the baro-receptors rises and the cardiac center reduces the heart rate.
• Chemoreceptors sensitive to blood pH, carbon dioxide, and oxygen are found in the aortic arch, carotid arteries, and medulla oblongata. They are more important in respiratory control than in cardiovascular
Saladin: Anatomy & Physiology: The Unity of Form and Function, Third Edition
Chapter 19 The Circulatory System: The Heart 739
control but do influence the heart rate. If circulation to the tissues is too slow to remove CO2 as fast as the tissues produce it, then CO2 accumulates in the blood and cerebrospinal fluid (CSF) and produces a state of hypercapnia (CO2 excess). Furthermore, CO2 generates hydrogen ions by reacting with water: CO2 + H2O ^ HCO3— + H+. The hydrogen ions lower the pH of the blood and CSF and may create a state of acidosis (pH < 7.35). Hypercapnia and acidosis stimulate the cardiac center to increase the heart rate, thus improving perfusion of the tissues and restoring homeostasis. The chemoreceptors also respond to extreme hypoxemia (oxygen deficiency), such as in suffocation, but the effect is usually to slow down the heart, perhaps so the heart does not compete with the brain for the limited oxygen supply.
Such responses to fluctuations in blood chemistry and blood pressure, called chemoreflexes and baroreflexes, are good examples of negative feedback loops. They are discussed more fully in chapter 20.
Epinephrine and norepinephrine are potent cardiac stimulants. They are secreted by the cardiac accelerator nerves and the adrenal medulla in response to arousal, stress, and exercise. These catecholamines act through cAMP. Caffeine and the related stimulants in coffee, tea, and chocolate produce positive chronotropic effects by inhibiting cAMP breakdown. Nicotine also accelerates the heart by stimulating catecholamine secretion. Thyroid hormone increases the number of adrenergic receptors in the cardiac muscle, making the heart more responsive to sympathetic stimulation and thus increasing the heart rate. Hyperthyroidism causes tachycardia, which in the long run can weaken the heart and cause heart failure.
The ion with the greatest chronotropic effect is potassium (K+). Hyperkalemia,31 a K+ excess, is especially dangerous. A rapid rise in K+ concentration makes the myocardium unusually excitable and subject to systolic arrest (in which the ventricles contract and fail to relax and refill). A slow rise in K+ makes it less excitable than normal; the heartbeat becomes slow and irregular, and may arrest in diastole. In hypokalemia, a K+ deficiency, myocytes become hyperpolarized—their membrane voltage is lower than normal and it is more difficult to stimulate the cells to threshold. These potassium imbalances are very dangerous and require emergency medical treatment. Chapter 24 further explains the causes and effects of these electrolyte imbalances.
Hypercalcemia (a calcium excess) reduces the heart rate and hypocalcemia (a calcium deficiency) increases it. These calcium imbalances are relatively rare, however, and when they do occur, their primary effect is on contraction strength.
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