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
§ norepinephrine (levarterenol)
§ isoproterenol hydrochloride and isoproterenol
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
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
asystole (no electrical activity in theheart)
Catecholamines that exert beta2 activity are used to treat:
§ acute or chronic bronchial asthma
§ acute hypersensitivity (allergic) reactions
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
· 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.
antidepressants taken with a catecholamine can lead to hypertension. (See Adverse reactions to catecholamines.)