Are beta-blockers contraindicated for Asthma or COPD with heart failure patients?
There are 3 types of β receptors. β1-Adrenoceptors are situated in the cardiac sarcolemma. If activated, they lead to an increase in the rate and force of myocardial contraction (positive inotropic effect) by opening the calcium channels. On the other hand, β2-Adrenoceptors are found mainly in bronchial and vascular smooth muscles. If activated, they cause broncho- and vaso-dilatation. There are, however, sizable populations of β2-Adrenoceptors in the myocardium, of about 20%–25%, which leads to the cardiac effects of any β2-Adrenoceptors stimulation. There is a relative up-regulation of these receptors to about 50% in heart failure. The role of β3-Adrenoceptors in the heart is not yet fully identified and accepted .
Beta-blockers are classified into three generations. The first generation agents (such as Propranolol, Sotalol, Timolol, and Nadolol), are nonselective and block β1 and β2 receptors. Blocking β1-receptors affects the heart rate, conduction and contractility, while blocking β2-receptors, tends to cause smooth muscle contraction, therefore, bronchospasm in predisposed individuals. The second-generation agents or the cardioselective agents (such as Atenolol, Bisoprolol, Celiprolol, and Metoprolol) block β1-receptors in low doses but are capable of blocking β2-receptors in higher doses. This selective mode of action makes the use of these agents more suitable in patients with chronic lung disease or those with insulin-requiring diabetes mellitus. Cardioselectivity varies between agents with the Bisoprolol among the most selective. The third generation agents have vasodilatory properties. There action is either selective (Nebivolol) or nonselective (Carvidolol and Labetolol). The vasodilatory properties are mediated either by nitric oxide release as for Nebivolol or Carvidolol or by added alpha-adrenergic blockade as in Labetolol and Carvidolol. A third vasodilatory mechanism, as in Pindolol and Acebutolol, acts via β2-intrinsic sympathomimetic activity (ISA).
These beta-blockers therefore have the capacity to stimulate as well as to block adrenergic receptors and tend to cause less bradycardia than the other beta-blockers and may cause less coldness of the extremities.
Because of the bradyarrhythmic and hypotensive effects of beta-blockers, the major heart failure trials excluded patients with a heart rate of <50 to 68 beats per minute (BPm) or systolic blood pressure <80 to 100 mm hg (the ranges cited reflect the variation in cut points from one study to another) and in clinical practice, physicians often withhold beta-blocker therapy from heart failure patients who also have chronic obstructive pulmonary disease (coPd) or asthma, hypotension, or metabolic risk factors for diabetes.
Some avoid prescribing beta-blockers because they believe that the drugs adversely affect patients’ quality of life, despite evidence to the contrary.In all these cases, there is little justification for doing so.
Although beta-blockers can worsen and precipitate bronchospasm, recent evidence suggests that patients with coPd and asthma can tolerate them.In fact, there is reason to believe that bronchospasm is aggravated by excessive stimulation and sensitization of the beta-2 receptors, and that blocking them may even be of therapeutic value. nonetheless, the danger of worsening bronchospasm with a nonselective beta-blocker such as carvedilol remains—particularly for patients with asthma, who tend to have a higher degree of bronchial sensitivity and reactivity. So, while beta-blockers are not contraindicated for patients with coPd, their use in this patient population requires caution.