Hemodynamic effects of inhaled terbutaline in congestive heart failure patients without lung disease: beneficial cardiotonic and vasodilator beta-agonist properties evaluated by ventricular catheterization and radionuclide angiography.
To evaluate the hemodynamic effects of the beta-adrenergic receptor agonist, terbutaline sulfate, when given by inhalation in ventricular dysfunction, 0.5 mg of the agent was given by nebulizer to 13 patients with congestive heart failure (nine coronary heart disease and four with idiopathic cardiomyopathy). Data were obtained before and 10 and 30 minutes post inhalation, by right heart catheterization and by gated equilibrium radionuclide ventriculography. All patients responded with increased cardiac output (3.5 to 4.3 L/min, p less than 0.01) and stroke volume (40 to 49 ml, p less than 0.01) without change in heart rate. Decreases occurred in peripheral vascular resistance (1924 to 1443 dsc-5, p less than 0.01), left ventricular filling pressure (21 to 15 mm Hg, p less than 0.01), and systemic arterial oxygen tension (81 to 72 mm Hg, p less than 0.05). both left and right ventricular ejection fractions rose (0.24 to 0.38 and 0.36 to 0.51, both p less than 0.01) with concomitant declines in biventricular end-diastolic volumes. All variables indicated changed rapidly at 10 minutes post inhalation and returned to control levels by 30 minutes after the agent. Thus moderate inhaled doses of terbutaline produce prompt, potent, and transient salutary hemodynamic effects due to its peripheral vasodilator and cardiotonic properties, without untoward arrhythmogenic or anginal provoking influences in the present study.[1]References
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