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Because of their common basic chemical structure, all catechol-amines share certain properties—they stimulate the nervous sys-tem, constrict peripheral blood vessels, increase heart rate, and dilate the bronchi. They can be manufactured in the body or in a laboratory. Common catecholamines include:
§ epinephrine, epinephrine bitartrate, and epinephrine hydrochlo-ride
§ norepinephrine (levarterenol)
§ isoproterenol hydrochloride and isoproterenol sulfate.
Catecholamines can’t be taken orally because they’re destroyed by digestive enzymes. In contrast, when these drugs are given sublin-gually (under the tongue), they’re absorbed rapidly through the mucous membranes. Any sublingual drug not completely ab-sorbed is rapidly metabolized by swallowed saliva.
SubQ absorption is slowed because catecholamines cause the blood vessels around the injection site to constrict.
Catecholamines are widely distributed in the body. They’re metab-olized and inactivated predominantly in the liver but can also be metabolized in the:
§ GI tract
§ other tissues.
Catecholamines are excreted primarily in urine; however, a small amount of isoproterenol is excreted in feces and some epineph-rine is excreted in breast milk.
Catecholamines are primarily direct-acting. When catecholamines combine with alpha receptors or beta receptors, they cause either an excitatory or an inhibitory effect. Typically, activation of alpha receptors generates an excitatory response, except for intestinal relaxation. Activation of beta receptors typically produces an in-hibitory response, except in heart cells, where norepinephrine produces excitatory effects.
The clinical effects of catecholamines depend on the dosage and administration route. Catecholamines are potent inotropes—they make the heart contract more forcefully. As a result, the ventricles empty more completely with each heartbeat, increasing the heart’s workload and the amount of oxygen it needs to do this harder work.
Catecholamines also produce a positive chronotropic effect, which means that they cause the heart to beat faster. That happens because the pacemaker cells in the heart’s sinoatrial (SA) node depolarize at a faster rate. As catecholamines cause blood vessels to con-strict and blood pressure to rise, the heart rate can fall as the body tries to compensate for an excessive rise in blood pressure.
Catecholamines can cause the Purkinje fibers (an intricate web of fibers that carry electrical impulses into the ventricles) to fire spontaneously, possibly producing abnormal heart rhythms, such as premature ventricular contractions and fibrillation. Epineph-rine is more likely than norepinephrine to produce this sponta-neous firing.
The therapeutic uses of catecholamines depend on the particular receptor that’s activated.
· Norepinephrine stimulates alpha receptors almost exclusively.
· Dobutamine and isoproterenol stimulate only beta receptors.
· Epinephrine stimulates both alpha and beta receptors.
· Dopamine activates primarily dopamine receptors.
Catecholamines that stimulate alpha receptors are used to treat low blood pressure (hypotension). They generally work best when used to treat hypotension caused by:
· relaxation of the blood vessel (also called a loss of vasomotortone)
· blood loss (such as from hemorrhage).
Catecholamines that stimulate beta1 receptors are used to treat:
· heart block (a delay or interruption in the conduction of electri-cal impulses between the atria and ventricles)
· low cardiac output.
Because they’re believed to make the heart more responsive to de-fibrillation (using an electrical current to terminate a deadly ar-rhythmia), beta1-adrenergic drugs are used to treat:
· ventricular fibrillation (quivering of the ventricles, resulting in no pulse)
· asystole (no electrical activity in theheart)
· cardiac arrest.
Catecholamines that exert beta2 activity are used to treat:
§ acute or chronic bronchial asthma
§ acute hypersensitivity (allergic) reactions to drugs.
Dopamine, which stimulates the dopamine receptors, is used in low doses to improve blood flow to the kidneys by dilating the re-nal blood vessels.
The effects of natural catecholamines (those produced by the body) differ somewhat from the effects of manufactured cate-cholamines. Manufactured catecholamines have a short duration of action, which can limit their therapeutic usefulness.
Drug interactions involving catecholamines can be serious, result-ing in hypotension, hypertension, arrhythmias, seizures, and high blood glucose levels in diabetic patients.
· Alpha-adrenergic blockers, such as phentolamine, can produce hypotension when taken with a catecholamine.
· Beta-adrenergic blockers, such as propranolol, taken with a cat-echolamine can lead to bronchial constriction.
· Epinephrine may cause hyperglycemia in diabetic patients re-ceiving the drug. These patients may require an increased dose of insulin or oral antidiabetic agents.
· Other adrenergics taken with a catecholamine can produce ad-ditive, or double, effects, such as hypertension and arrhythmias, as well as enhance other adverse effects. Increased risk of adverse effects, such as hypertension, may occur when adrenergic drugs are given with other drugs that can cause hypertension.
· Tricyclic antidepressants taken with a catecholamine can lead to hypertension. (See Adverse reactions to catecholamines.)
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