Syncope antagonists

If the patient is started on an a-adrenergic antagonist, monitor the patient for hypotension, dizziness, or syncope. If present, assess the severity of each symptom. Reduce the drug dose or discontinue the drug, as necessary. If the patient has malaise or rhinitis, reassure the patient that these are usual, but bothersome, adverse effect, that often improve with continued therapy. 

The systemic effects exerted by eye-drops are most pronounced in the case of agonists and antagonists in the autonomic nervous system. For example, beta-blockers in eye-drops can cause bronchospasm, heart failure, syncope, and psychiatric disorders (4-6), especially at high doses and with non-selective beta-blockers, although these adverse reactions are usually related to failure to observe prescribing precautions (1). 

Approximately 10% to 12% of patients discontinue second-generation a 1 -adrenergic antagonists because of adverse effects, especially those affecting the cardiovascular system (e.g., syncope, dizziness, and hypotension). ... 

The cardiovascular effects of muscarinic receptor antagonists are of limited clinical application. Atropine may be considered in the initial treatment of patients with acute myocardial infarction in whom excessive vagal tone causes sinus or nodal bradycardia. Dosing must be judicious doses that are too low can cause a paradoxical bradycardia excessive doses will cause tachycardia that may extend the infarct by increasing demand. Atropine occasiormlly is useful in reducing the severe bradycardia and syncope associated with a hyperactive carotid sinus reflex. Atropine will protect the SA and AV nodes from the effects of excessive ACh in instances of poisoning with anticholinesterase pesticides. 

In patients with BPH, the most common adverse effects for ai-adrenergic antagonists are related to vasodilation, including dizziness, orthostatic hypotension, headache, and tachycardia, which occurred during the first 2 weeks of treatment (46). Therefore, a dose titration usually is required, especially in patients older than 60 years. These cardiovascular side effects are attributed to a nonselective blockade of ai-adrenoceptors present in vascular smooth muscle in addition to the required blockade of ai-adrenoceptors in prostate. No first-dose effect and fewer vasodilatory adverse events have been reported with the sustained-release formulations, which occur more frequently with the immediate-release formulation At higher doses, orthostatic hypotension occurs more frequently. The first-dose phenomenon of orthostatic hypotension and syncope has been reported occasionally in elderly patients and in those concurrently receiving calcium antagonists, diuretics, and p-blockers. 

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