Page 122 - Small Animal Internal Medicine, 6th Edition

94 PART I Cardiovascular System Disorders

TABLE 4.3
VetBooks.ir Characteristics of Selected β-Blockers

DRUG ADRENERGIC RECEPTOR LIPID SOLUBILITY MAIN ROUTE OF
ELIMINATION
SELECTIVITY
Atenolol β 1 0 RE
Carvedilol β 1 , β 2 , α 1 + HM
Esmolol β 1 0 BE
Labetalol β 1 , β 2 , α 1 ++ HM
Metoprolol β 1 ++ HM
Nadolol β 1 , β 2 0 RE
Pindolol* β 1 , β 2 ++ B
Propranolol β 1, β 2 ++ HM
Sotalol † β 1 , β 2 0 RE
Timolol β 1 , β 2 0 RE

B, Both renal excretion and hepatic metabolism are important; BE, blood esterases; HM, hepatic metabolism; RE, renal excretion.
*Has intrinsic sympathomimetic activity.
† Also has class III antiarrhythmic activity.

β-blockers enhance the depression of AV conduction pro- blood flow for their metabolism (such as lidocaine). Feeding
++
duced by Ca -blockers, class I antiarrhythmic drugs, and delays oral absorption and increases drug clearance after IV
++
digoxin. Use of a β-blocker and a Ca -blocker simultane- dosing (by increasing hepatic blood flow). The half-life of
ously can markedly decrease heart rate and myocardial con- propranolol in the dog is only about 1.5 hours (0.5-4.2 hours
tractility. Because of possible β-receptor upregulation in cats); active metabolites exist. Dosing every 8 hours
(increased number or affinity of receptors) associated with appears to be adequate in both species. IV propranolol is
long-term β-blockade, therapy should not be discontinued used mainly for refractory ventricular tachycardia (in con-
abruptly. Chronic β-blocker therapy might increase risk for junction with a class I drug) and for emergency treatment of
hypotension and bradycardia during anesthesia. atrial or junctional tachycardia.
Toxicity most often is related to excessive β-blockade; this
Atenolol can develop at relatively low doses in some animals. Brady-
Atenolol is a selective β 1 -blocker. It is used commonly to cardia, heart failure, hypotension, bronchospasm, and hypo-
slow sinus rate and AV conduction and to suppress sympa- glycemia can occur. Infusion of a catecholamine (dopamine
thetically mediated ventricular premature beats. The half-life or dobutamine) will help reverse these effects. Propranolol
of atenolol is slightly more than 3 hours in dogs and about and other lipophilic β-blockers can cause CNS effects such
3.5 hours in cats. Its oral bioavailability in both species is as depressed attitude and disorientation.
high (≈90%). Atenolol is excreted in the urine; renal dys-
function delays its clearance. Atenolol’s β-blocking effect Esmolol
lasts more than 12 hours but less than 24 hours in normal Esmolol HCl is an ultra-short-acting β 1 -selective agent. It is
cats. This drug is hydrophilic. Adverse CNS effects are metabolized rapidly by blood esterases and has a half-life of
unlikely because atenolol does not readily cross the blood- less than 10 minutes. Steady state occurs in 5 minutes after
brain barrier. As with other β-blockers, weakness or exacer- a loading dose, or 30 minutes without. Esmolol’s effects end
bation of heart failure can occur. within 10 to 20 minutes after infusion is stopped. This drug
is used for acute therapy of tachyarrhythmias and feline
Propranolol hypertrophic obstructive cardiomyopathy.
Propranolol HCl is a nonselective β-blocker. It is not recom-
mended for patients with pulmonary edema, asthma, or Other β-Blockers
chronic small airway disease because of the potential for Many other β-blocking drugs are available. Their receptor
bronchoconstriction caused by β 2 -receptor antagonism. selectivity and pharmacologic characteristics vary. Sotalol is
Propranolol undergoes extensive first-pass hepatic a β-blocker that also prolongs action potential duration at
metabolism, and oral bioavailability is low; however, bio- higher doses; therefore it is usually considered a class III
availability increases with hepatic enzyme saturation. Pro- agent (see later). Certain β-blockers have been useful in
pranolol reduces hepatic blood flow, which prolongs its people with chronic, stable myocardial failure by reducing
elimination as well as that of other drugs dependent on liver the cardiotoxic effects of excessive sympathetic stimulation,