Hemodynamic effects of salbutamol, an oral long-acting beta-stimulant, in patients with congestive heart failure

Should Acute Treatment with Inhaled Beta Agonists be Withheld from Patients with Dyspnea Who May Have Heart Failure?

“…Finally, the majority of studies found no significant change in blood pressure with treatment (8,17,(19)(20)(21)(22)(23)25,28,29). Of the three studies examining inhaled agents, one showed no change in blood pressure and two showed a slight decrease in diastolic blood pressure (4 -7 mm Hg), with no change in mean or systolic blood pressure (8 -10).…”

“…However, there is no evidence in the studies reviewed to suggest that acute beta-2 agonist administration increases or worsens myocardial ischemia, either from direct evidence in patients with ADHF or from indirect evidence in patients with chronic heart failure, and no electrocardiographic changes suggestive of ischemia were observed (8,9,15,18,20,22,23,25,26,28). In fact, Dawson et al showed that when albuterol was administered to 31 patients with myocardial infarction and cardiogenic shock, hemodynamics improved and no subject developed worsening ischemia (20).…”

Electrophysiologic Effects of Salbutamol, a β2‐Selective Agonist

“…Early studies on β 2 stimulation with oral and intravenous salbutamol in patients with chronic or acute heart failure showed significant hemodynamic changes with a decrease in systemic vascular resistance and increases in cardiac output, ejection fraction, and heart rate. These cardiovascular effects were explained as resulting from reduced afterload caused by vasodilation, which was considered to be the primary effect 3–5 …”

“…These cardiovascular effects were explained as resulting from reduced afterload caused by vasodilation, which was considered to be the primary effect. [3][4][5] In more recent studies, infusion of a low dosage of terbutaline, another β-adrenergic agonist with predominantly β 2receptor selectivity, caused a pronounced increase in heart rate and systolic blood pressure, which was not prevented by selective β 1 blockade with atenolol, given either alone or in combination with atropine. 6,7 These results are best explained by direct cardiac chronotropic and inotropic β 2 effects.…”

This patient is not breathing properly: is this COPD, heart failure, or neither?

“…Various treatments prescribed for COPD, alone or in combination, acutely improve lung function and symptoms, and might also have beneficial effect on cardiac haemodynamics (such as increasing the cardiac index, or lowering the end-diastolic ventricular pressure, and/or peripheral resistance) in patients with HF (72,73). The long term prescription of treatments for COPD has never been convincingly shown to reduce mortality (74)(75)(76).…”