Beta-receptor blockade depresses myocardial contractility and excitability. In patients with abnormal myocardial function, cardiac output may be dependent on sympathetic drive. If this stimulus is removed by β blockade, cardiac decompensation may ensue. Thus, caution must be exercised in starting a β-receptor antagonist in patients with compensated heart failure even though long-term use of these drugs in these patients may prolong life. A life-threatening adverse cardiac effect of a β antagonist may be overcome directly with isoproterenol or with glucagon (glucagon stimulates the heart via glucagon receptors, which are not blocked by β antagonists), but neither of these methods is without hazard. A very small dose of a β antagonist (eg, 10 mg of propranolol) may provoke severe cardiac failure in a susceptible individual. Beta blockers may interact with the calcium antagonist verapamil; severe hypotension, bradycardia, heart failure, and cardiac conduction abnormalities have all been described. These adverse effects may even arise in susceptible patients taking a topical (ophthalmic) β blocker and oral verapamil.
Patients with ischemic heart disease or renovascular hypertension may be at increased risk if β blockade is suddenly interrupted. The mechanism of this effect might involve up-regulation of the number of β receptors. Until better evidence is available regarding the magnitude of the risk, prudence dictates the gradual tapering rather than abrupt cessation of dosage when these drugs are discontinued, especially drugs with short half-lives, such as propranolol and metoprolol.
The incidence of hypoglycemic episodes exacerbated by β-blocking agents in diabetics is unknown. Nevertheless, it is inadvisable to use β antagonists in insulin-dependent diabetic patients who are sub-compared with that in diabetics receiving nonselective β-adrenoceptor ject to frequent hypoglycemic reactions if alternative therapies are antagonists. There is considerable potential benefit from these drugs available. Beta1-selective antagonists offer some advantage in these in diabetics after a myocardial infarction, so the balance of risk versus patients, since the rate of recovery from hypoglycemia may be faster benefit must be evaluated in individual patients.
•Propranolol•Nadolol•TimololBlock β1 and β2 LowerHRandBP•reducerenin Hypertension•anginapectoris•arrhythmias•migraine•hyperthyroidism•glaucoma(topical timolol) Oral,parenteral•Toxicity: Bradycardia•worsenedasthma•fatigue•vividdreams•coldhands•Metoprolol•Atenolol•Betaxolol•NebivololBlock β1 > β2 LowerHRandBP•reducerenin•maybesaferinasthma Anginapectoris•hypertension•arrhythmias•glaucoma(topicalbetaxolol) Toxicity: Bradycardia•fatigue•vividdreams•coldhands•Butoxamine1 Blocks β2 > β1 Increases peripheral resistance No clinical indication Toxicity: Asthma provocation •Pindolol•Acebutolol•Carteolol•Bopindolol1 •Oxprenolol1 •Celiprolol1 •Penbutololβ1, β2, with intrinsic sympathomimetic (partial agonist) effect LowerBP•modestlylowerHR Hypertension•arrhythmias•migraine•mayavoidworseningof bradycardia Oral•Toxicity: Fatigue•vividdreams•coldhands•Carvedilol•Medroxalol1 •Bucindolol1 (see labetalol above) β > α1 block Heart failure Oral,longhalf-life•Toxicity: Fatigue 1Not available in the USA.