Cardiac drugs beta blockers

Beta-blockers initially reduce cardiac output, but after a few days their action may include a decrease in vascular resistance as a contributing effect. The latter effect may result from reduced angiotensin levels (beta-blockers reduce renin release from the kidney). The beta-blockers are among the most heavily used antihypertensive drugs. Beta-blocker therapy is associated with slightly elevated LDL and triglyceride concentrations and diminished HDL levels in the blood other potential adverse effects are listed in Table 11-2. 

Other drugs that may interact with cardiac glycosides include the following Albuterol, amphotericin B, beta-blockers, calcium, disopyramide, loop diuretics, nondepolarizing muscle relaxants, potassium-sparing diuretics, succinylcholine, sympathomimetics, thiazide diuretics, thioamines, and thyroid hormones. 

Drugs that may be affected by brimonidine include CNS depressants, beta-blockers, antihypertensives, MAOIs, and cardiac glycosides. 

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-... 

Calcium channel blockers can also be given to treat stable angina, especially if beta blockers are not tolerated or are contraindicated in specific patients.13 These drugs decrease cardiac workload directly by limiting calcium entry into myocardial cells and indirectly by producing peripheral vasodilation, thus decreasing cardiac preload and afterload.47 Hence, cal-... 

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. 

Nonselective beta blockers affect beta-2 receptors on the lungs as well as beta-1 receptors on the heart, and these nonselective agents can increase bronchocon-striction in patients with asthma and chronic obstructive pulmonary disease. Hence, a drug that is more specific for beta-1 receptors is preferred in these patients. Beta blockers can also produce excessive slowing of cardiac conduction in some patients, resulting in an increase in arrhythmias. Severe adverse reactions are rare, however, and beta blockers are well-tolerated by most patients when used appropriately to treat arrhythmias. 

Problem/lnfluence of Medication. Propranolol and the other beta blockers are successful in reducing various supraventricular arrhythmias. These drugs, however, also attenuate the cardiac response to exercise. Heart rate and cardiac output are lower at any absolute workload, and maximal heart rate and cardiac output are attenuated by beta blockade. Consequently, the exercise response of a patient taking a beta blocker will be less than if the patient is not tak-... 

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. 

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