McKenna's Pharmacology for Nursing, 2e - page 495

C H A P T E R 3 1 Adrenergic blocking antagonists 483
reinfarction after an MI by decreasing cardiac workload
and oxygen consumption.
Beta1-selective adrenergic blocking agents in oph-
thalmic form are used to decrease intraocular pressure
and to treat open-angle glaucoma. The beta1 -selective
blocker of choice depends on the condition or combina-
tion of conditions being treated and personal experience
with the drugs. See Table 31.5 for usual indications for
each drug.
Pharmacokinetics
The beta1-selective adrenergic blockers are absorbed
from the GI tract after oral administration, reach peak
levels directly with IV infusion and are not usually
absorbed when given in ophthalmic form. The bio-
availability of metoprolol is increased if it is taken
in the presence of food. These drugs are metabolised
in the liver and excreted in the urine. Metoprolol
readily crosses the blood–brain barrier and may cause
more CNS effects than atenolol, which does not cross
the barrier.
Contraindications and cautions
The beta1-selective adrenergic blockers are contrain-
dicated in the presence of allergy to the drug or any
components of the drug to avoid hypersensitivity
reactions; with sinus bradycardia, heart block, cardio-
genic shock, HF or hypotension, all of which could
be exacerbated by the cardiac-depressing and blood
pressure-lowering effects of these drugs ; and with
breastfeeding because of the potential adverse effects on
the neonate. They should be used with caution in indi-
viduals with diabetes, thyroid disease or COPD because
of the potential for adverse effects on these diseases with
sympathetic blockade; and in pregnancy because of the
potential for adverse effects on the fetus . The safety and
efficacy of the use of these drugs in children have not
been established.
Adverse effects
People receiving these drugs often experience adverse
effects related to the blocking of beta1-receptors in the
SNS. CNS effects include headache, fatigue, dizziness,
depression, paraesthesias, sleep disturbances, memory
loss and disorientation. CV effects can include brady­
cardia, heart block, HF, hypotension and peripheral
vascular insufficiency. Pulmonary effects ranging from
rhinitis to bronchospasm and dyspnoea can occur; these
effects are not as likely to occur with these drugs as
with the non-selective beta-blockers. GI upset, nausea,
vomiting, diarrhoea, gastric pain and even colitis
can occur as a result of unchecked parasympathetic
activity and the blocking of the sympathetic receptors.
Genitourinary effects can include decreased libido,
impotence, dysuria and Peyronie’s disease. Other
effects that can occur include decreased exercise tol-
erance (people often report that their “get up and go”
is gone), hypoglycaemia or hyperglycaemia, and liver
changes that are reflected in increased concentrations
of liver enzymes. If these drugs are stopped abruptly
after long-term use, there is a risk of severe hyperten-
sion, angina, MI and stroke because the receptor sites
become hypersensitive to catecholamines after being
blocked by the drug.
Clinically important drug–drug interactions
A decreased hypertensive effect occurs if these drugs
are given with clonidine, NSAIDs, rifampicin or
barbiturates. If such a combination is used, the person
should be monitored closely and dose adjustment made.
There is an initial hypertensive episode followed by
bradycardia if these drugs are given with adrenaline.
Increased serum levels and increased toxicity of
intravenous lignocaine will occur if it is given with these
drugs.
An increased risk for orthostatic hypotension occurs
if these drugs are taken with prazosin. If this combina-
tion is used, the person must be monitored closely and
safety precautions taken.
The selective beta1-blockers have increased effects if
they are taken with verapamil, cimetidine or propylth-
iouracil. The person should be monitored closely and
appropriate dose adjustment made.
Prototype summary: Atenolol
Indications: Treatment of angina pectoris,
hypertension, myocardial infarction; off-label uses
are prevention of migraine headaches, alcohol
withdrawal syndrome and supraventricular
tachycardias.
Actions: Blocks beta1 -adrenergic receptors,
decreasing the excitability of the heart, cardiac
output and oxygen consumption; decreases renin
release, which lowers blood pressure.
Pharmacokinetics:
Route Onset Peak Duration
Oral Varies 2–4 hours 24 hours
IV Immediate 5 mins 24 hours
T1/2: 6 to 7 hours, with excretion in the bile, faeces
and urine.
Adverse effects: Allergic reaction, dizziness,
bradycardia, HF, arrhythmias, gastric pain,
flatulence, impotence, bronchospasm, decreased
exercise tolerance.