Beta blockers cardiac effects

Drugs that block beta-1 receptors on the myocardium are one of the mainstays in arrhythmia treatment. Beta blockers are effective because they decrease the excitatory effects of the sympathetic nervous system and related catecholamines (norepinephrine and epinephrine) on the heart.5,28 This effect typically decreases cardiac automaticity and prolongs the effective refractory period, thus slowing heart rate.5 Beta blockers also slow down conduction through the myocardium, and are especially useful in controlling function of the atrioventricular node.21 Hence, these drugs are most effective in treating atrial tachycardias such as atrial fibrillation.23 Some ventricular arrhythmias may also respond to treatment with beta blockers. 

Because of their reflex cardiac effect, vasodilators, if used alone in the treatment of hypertension, have not been a successful therapeutic tool. However, the reflex tachycardia and increase in cardiac output can be effectively blocked by the therapeutic association with a sympathetic blocker guanethidine, reserpine, methyldopa, or clonidine. More specifically, blockade of the cardiac beta-adrenergic receptors will also prevent the cardiac response to hydralazine. Thus, the therapeutic combination of hydralazine and propranolol can be successfully employed for effective blood pressure reduction(11). 

Concomitant use of calcium channel blockers (atenolol) Bradycardia and heart block can occur and the left ventricular end diastolic pressure can rise when beta-blockers are administered with verapamil or diltiazem. Patients with preexisting conduction abnormalities or left ventricular dysfunction are particularly susceptible. Recent acute Ml (sotalol) Sotalol can be used safely and effectively in the long-term treatment of life-threatening ventricular arrhythmias following an Ml. However, experience in the use of sotalol to treat cardiac arrhythmias in the early phase of recovery from acute Ml is limited and at least at high initial doses is not reassuring. 

Mecfianism of Action A nonselective beta-blocker that blocks beta - and betaj-ad-renergic receptors. Large doses increase airway resistance. Therapeutic Effect Slows sinus heart rate, decreases cardiac output and BP. Decreases myocardial ischemia severity by decreasing oxygen requirements. 

Beta-blockers interact with a large number of other medications. The combination of beta-blockers with calcium antagonists should be avoided, given the risk for hypotension and cardiac arrhythmias. Cimetidine, hydralazine, and alcohol all increase blood levels of beta-blockers, whereas rifampicin decreases their concentrations. Beta-blockers may increase blood levels of phenothiazines and other neuroleptics, clonidine, phen-ytoin, anesthetics, lidocaine, epinephrine, monoamine oxidase inhibitors and other antidepressants, benzodiazepines, and thyroxine. Beta-blockers decrease the effects of insulin and oral hypoglycemic agents. Smoking, oral contraceptives, carbamazepine, and nonsteroidal anti-inflammatory analgesics decrease the effects of beta-blockers (Coffey, 1990). 

Beta antagonists are generally administered for their effect on the beta-1 receptors that are located on the heart.31 When stimulated, these receptors mediate an increase in cardiac contractility and rate of contraction. By blocking these receptors, beta antagonists reduce the rate and force of myocardial contractions. Consequently, beta antagonists are frequently used to decrease cardiac workload in conditions such as hypertension and certain types of angina pectoris. Beta blockers may also be used to normalize heart rate in certain forms of cardiac arrhythmias. Specific clinical applications of individual beta blockers are summarized in Table 20-2. 

Currently, a number of beta blockers are used clinically the selection of a specific agent depends on factors such as cardioselectivity, duration of action (half-life), and several other ancillary properties of each drug.110 Certain beta blockers, for instance, produce added effects such as mild peripheral vasodilation or stabilization of cardiac membranes that can be beneficial in treating certain cardiovascular condi-... 

Beta-adrenergic blockers have been used extensively to decrease blood pressure and are a mainstay of antihypertensive therapy in many patients.4,81 Beta blockers exert their primary effect on the heart, where they decrease heart rate and force myocardial contraction. In hypertensive patients, these drugs lower blood pressure by slowing down the heart and reducing cardiac output. This statement, however, is probably an oversimplification of how beta blockers produce an antihypertensive effect. In addition to their direct effect on the myocardium, beta blockers also produce a general decrease in sympathetic tone.19,39 Although their exact effects on sympathetic activity remain to be determined, beta blockers may decrease sympathetic activi-... 

Beta blockers bind to beta-1 receptors on the myocardium and block the effects of norepinephrine and epinephrine (see Chapter 20). These drugs therefore normalize sympathetic stimulation of the heart and help reduce heart rate (negative chronotropic effect) and myocardial contraction force (negative inotropic effect). Beta blockers may also prevent angina by stabilizing cardiac workload, and they may prevent certain arrhythmias by stabilizing heart rate.40 These additional properties can be useful to patients with heart failure who also have other cardiac symptoms. 

Acute intoxication with amphetamine is associated with tremor, confusion, irritability, hallucinations and paranoid behaviour, hypertension, sweating and occasionally cardiac arrhythmias convulsions and death may occur. The cardiovascular effects of the stimulants may be treated by beta-blockers, or by the combined alpha- and beta-blocker labetalol calcium channel antagonists such as nifedipine may correct the arrhythmias, while intravenous diazepam is of value in attenuating seizures. 

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