Cardiac failure beta-blockers

Cardiac failure Beta blockers depress myocardial contractility and may precipitate cardiac failure bradycardia. 

Liggett, S. B., Mialet-Perez, J., Thaneemit-Chen, S., et al. (2006) A polymorphism within a conserved beta(l)-adrenergic receptor motif alters cardiac function and beta-blocker response in human heart failure. Proc. Natl. Acad. Sci. U. S. A. 103,11288-11293. 

VERAPAMIL HYDROCHLORIDE Avo d verapamil in patients with severe left ventricular dysfunction (eg, ejection fractions less than 30%) or moderate to severe symptoms of cardiac failure and in patients with any degree of ventricular dysfunction if they are receiving a beta-adrenergic blocker. 

Carteolol (Cartrol/ Ocupress Ophthalmic) [Beta Blocker/ Glaucoma Agent] Uses HTN, T lOP, chronic open-angle glaucoma Action Blocks [3-adrenergic receptors (p, 2)1 ISA Dose Ophth 1 gt in eye(s) bid Caution [C (1st tri) D (2nd 3rd tri), /-] Cardiac failure, asthma Contra Sinus bradycardia heart block >lst-degree bronchospasm Disp Ophth soln SE Drowsiness, sexual dysfxn, bradycardia, edema, CHF, ocular conjunctival... 

Reiken, S., Wehrens, X. H., Vest, J. A., Barbone, A., Klotz, S., Mancini, D., Burkhoff, D., and Marks, A. R. (2003). Beta-Blockers Restore Calcium Release Channel Function and Improve Cardiac Muscle Performance in Human Heart Failure. Circulation 107(19) 2459-66. 

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. 

Abbreviations-. BEST, beta-blocker evaluation survival trial CAPRICORN, caiveclilol postinfarct suivival control in left ventricular dysfunction C1B1S II, Cardiac Insufficiency Bisoprolol Study II COMET, Carvedilol or Metoprolol European Trial COPERNICUS, carvedilol prospective randomized cumulative survival HF, heart failure LVEF, left ventricular ejection fraction MDC, metoprolol in dilated cardiomyopathy MERIT-HF, metoprolol controlled-release randomized intervention trial in congestive heart failure fJYHA, New York Heart Association. 

BETA-BLOCKERS LIDOCAINE 1. Risk of bradycardia (occasionally severe), 1 BP and heart failure with intravenous lidocaine 2. Risk of lidocaine toxicity due to t plasma concentrations of lidocaine, particularly with propranolol and nadolol 3. t plasma concentrations of propranolol and possibly some other beta-blockers 1. Additive negative inotropic and chronotropic effects 2. Uncertain, but possibly a combination of beta-blocker-induced reduction in hepatic blood flow (due to 1 cardiac output) and inhibition of metabolism of lidocaine 3. Attributed to inhibition of metabolism by lidocaine 1. Monitor PR, BP and ECG closely watch for development of heart failure when intravenous lidocaine is administered to patients on beta-blockers 2. Watch for lidocaine toxicity 3. Be aware. Regional anaesthetics should be used cautiously in patients with bradycardia. Beta-blockers could cause dangerous hypertension due to stimulation of alpha-receptors if epinephrine is used with focal anaesthetic... 

The adverse effects of beta-blockers are usually mild, with occurrence rates of 10-20% for the most common in most studies. Most are predictable from the pharmacological and physicochemical properties of these drugs. Examples include fatigue, cold peripheries, bradycardia, heart failure, sleep disturbances, bronchospasm, and altered glucose tolerance. Gastrointestinal upsets are also relatively common. Serious adverse cardiac effects and even sudden death can follow abrupt withdrawal of therapy in patients with ischemic heart disease. Most severe adverse reactions can be avoided by careful selection of patients and consideration of individual beta-blockers. Hjrpersensitivity reactions have been relatively rare since the withdrawal of practolol. Tumor-inducing effects have not been estabhshed in man. 

Beta-blockade reduces mortality in patients with heart failure by at least a third when initiated carefully, with gradual dose titration, in those with stable heart failure (34,35). Similarly, beta-blocker prescribing should be encouraged in people with diabetes, since they have a worse outcome after cardiac events and beta-blockade has an independent secondary protective effect (36,37). The small risk of masking metabohc and autonomic responses to hypoglycemia, which was only a problem with non-selective agents in type I diabetes, is a very small price worth paying in diabetics with coronary heart disease. 

In the Randomized Aldactone Evaluation Study (RALES) in 1663 patients with New York Heart Association (NYHA) class III (70%) or IV (30%) symptoms and an ejection fraction less than 35%, the addition of spironolactone 25 mg/day to conventional treatment (an ACE inhibitor, a loop diuretic, in most cases digoxin, and in 11% a beta-blocker) for an average of 24 months lowered the risk of all-cause mortality by 30% (from 46% to 35%), death from progressive heart failure, and sudden death (28). There were similar reductions in hospital admissions for worsening heart failure and for all cardiac causes. The magnitude of the overall effect was similar and additional to the proven benefit from ACE inhibition in severe heart failure. 

Aortic and mitral valvular fibrosis can lead to congestive cardiac failure fibrosis rarely affects the endocardium more extensively (extending into the myocardium) or the pericardium (resulting in constrictive pericarditis). Vasospastic effects can occasionally be as severe in susceptible subjects as with ergotamine especially dangerous are combinations with ergotamine tartrate, as are combinations of ergot alkaloids with beta-blockers (SEDA-9,128). 

Beta-blockers with intrinsic sympathomimetic (ISA) properties are not pure antagonists. These agents partially stimulate the beta-receptors as well. Theoretically, these agents are less likely to cause bradycardia and bronchospasm, increase lipids, decrease cardiac output, and cause peripheral vasoconstriction. However, these agents can still cause bronchospasm or exacerbate heart failure. 

Cardiovascular agents Drugs that have their action on the heart or peripheral blood vessels for the treatment of hypertension (high blood pressure), angina, heart failure, or cardiac arrhythmia (e.g., beta-blockers,... 

Acebutolol is indicated in the management of hypertension and premature ventricular contractions. It is contraindicated in hypersensitivity to beta-blockers persistently sever bradycardia greater than first-degree heart block congestive heart failure, unless secondary to tachyarrhythmia treatable with beta-blockers overt cardiac failure sinus bradycardia cardiogenic shock. The side effects reported for acebutolol include hypotension, bradycardia, CHF, cold extremities, heart block, insomnia, fatigue, dizziness. 

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