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Other causes are side effects of topical decongestants such as oxymetazoline and phenylephrine. Both of these medications activate alpha-1 adrenergic receptors that result in smooth muscle constriction. Non-selective beta blockers are known to facilitate bronchospasm as well. Beta blockers bind to the β2 receptors and block the action of ...
People experiencing bronchospasm due to the β 2 receptor-blocking effects of nonselective beta blockers may be treated with anticholinergic drugs, such as ipratropium, which are safer than beta agonists in patients with cardiovascular disease. Other antidotes for beta blocker poisoning are salbutamol and isoprenaline.
These medications include short-acting muscarinic antagonists (SAMAs) such as ipratropium, and long-acting muscarinic antagonists (LAMA) such as tiotropium. Onset of action for SAMAs is typically between 30 and 60 minutes, making these drugs less efficacious in treating acute asthma attacks and bronchospasm. [9]
They bind to the receptor and cause depolarization by opening channels just like acetylcholine does. This causes repetitive excitation that lasts longer than a normal acetylcholine excitation and is most likely explained by the resistance of depolarizing agents to the enzyme acetylcholinesterase. The constant depolarization and triggering of ...
Nebulizers continuously deliver aerosolized drug and salbutamol delivered through nebulizer was found to be more effective than IV administration. [10] Salbutamol and terbutaline are also both available in oral forms. [11] In addition, several of these medications are available in intravenous forms, including both salbutamol and terbutaline.
Propafenone is more selective for cells with a high rate, but also blocks normal cells more than class Ia or Ib anti-arrhythmic medications. Propafenone differs from the prototypical class Ic antiarrhythmic in that it has additional activity as a beta-adrenergic blocker which can cause bradycardia and bronchospasm.
Salbutamol is typically used to treat bronchospasm (due to any cause—allergic asthma or exercise-induced), as well as chronic obstructive pulmonary disease. [8] It is also one of the most common medicines used in rescue inhalers (short-term bronchodilators to alleviate asthma attacks).
The issue of bronchospasm acquired prominence in the neuromuscular-blocking agents arena after the withdrawal from clinical use of rapacuronium (Raplon - a steroidal neuromuscular-blocking agent marketed by Organon) in 2001 [9] [10] after several serious events of bronchospasm, [11] [12] including five unexplained fatalities, [13] following its ...