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Using a combination of autorhythmicity and innervation, the cardiovascular center is 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 ( [link] and [link] ). After reading this section, the importance of maintaining homeostasis should become even more apparent.
| Major Factors Increasing Heart Rate and Force of Contraction | |
|---|---|
| Factor | Effect |
| Cardioaccelerator nerves | Release of norepinephrine |
| Proprioreceptors | Increased rates of firing during exercise |
| Chemoreceptors | Decreased levels of O 2 ; increased levels of H + , CO 2 , and lactic acid |
| Baroreceptors | Decreased rates of firing, indicating falling blood volume/pressure |
| Limbic system | Anticipation of physical exercise or strong emotions |
| Catecholamines | Increased epinephrine and norepinephrine |
| Thyroid hormones | Increased T 3 and T 4 |
| Calcium | Increased Ca 2+ |
| Potassium | Decreased K + |
| Sodium | Decreased Na + |
| Body temperature | Increased body temperature |
| Nicotine and caffeine | Stimulants, increasing heart rate |
| Factors Decreasing Heart Rate and Force of Contraction | |
|---|---|
| Factor | Effect |
| Cardioinhibitor nerves (vagus) | Release of acetylcholine |
| Proprioreceptors | Decreased rates of firing following exercise |
| Chemoreceptors | Increased levels of O 2 ; decreased levels of H + and CO 2 |
| Baroreceptors | Increased rates of firing, indicating higher blood volume/pressure |
| Limbic system | Anticipation of relaxation |
| Catecholamines | Decreased epinephrine and norepinephrine |
| Thyroid hormones | Decreased T 3 and T 4 |
| Calcium | Decreased Ca 2+ |
| Potassium | Increased K + |
| Sodium | Increased Na + |
| Body temperature | Decrease in body temperature |
The catecholamines, epinephrine and NE, secreted by the adrenal medulla form one component of the extended fight-or-flight mechanism. The other component is sympathetic stimulation. Epinephrine and NE have similar effects: binding to the beta-1 receptors, and opening sodium and calcium ion chemical- or ligand-gated channels. The rate of depolarization is increased by this additional influx of positively charged ions, so the threshold is reached more quickly and the period of repolarization is shortened. However, massive releases of these hormones coupled with sympathetic stimulation may actually lead to arrhythmias. There is no parasympathetic stimulation to the adrenal medulla.
In general, increased levels of thyroid hormone, or thyroxin, increase cardiac rate and contractility. The impact of thyroid hormone is typically of a much longer duration than that of the catecholamines. The physiologically active form of thyroid hormone, T 3 or triiodothyronine, has been shown to directly enter cardiomyocytes and alter activity at the level of the genome. It also impacts the beta adrenergic response similar to epinephrine and NE described above. Excessive levels of thyroxin may trigger tachycardia.
Calcium ion levels have great impacts upon both HR and contractility; as the levels of calcium ions increase, so do HR and contractility. High levels of calcium ions (hypercalcemia) may be implicated in a short QT interval and a widened T wave in the ECG. The QT interval represents the time from the start of depolarization to repolarization of the ventricles, and includes the period of ventricular systole. Extremely high levels of calcium may induce cardiac arrest. Drugs known as calcium channel blockers slow HR by binding to these channels and blocking or slowing the inward movement of calcium ions.
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