Mechanisms by which systemic salbutamol increases ventilation

Salbutamol (SAL) has systemic effects that may adversely influence ventilation in asthmatic patients. The authors sought to determine the magnitude of this effect and mechanisms by which i.v. SAL affects ventilation.

A prospective study of nine healthy subjects (eight men, one woman; age 23 +/- 1.4 years (SD)) was undertaken. Each subject received i.v. SAL at 5, 10 and 20 microg/min each for 30 min at each dose and was observed for 1 h post infusion. Minute ventilation ((VE)), oxygen consumption (VO(2)), CO(2) production (VCO(2)), occlusion pressure (P(0.1)), heart rate, blood pressure, respiratory rate, glucose, arterial blood gases, lactate and potassium (K(+)) were recorded at baseline and at 30-min intervals. The effect of 100% oxygen on (VE) and P(0.1) during SAL infusion at 20 microg/min was observed. Results are expressed as mean +/- SEM.

V(E) was significantly increased at 20 microg/min SAL (37.8 +/- 12.1%, P = 0.01), as were VO(2) (22.5 +/- 5.1%, P < 0.01) and VCO(2) (40.9 +/- 10.6%, P < 0.01). Ventilation was in excess of metabolic needs as demonstrated by a rise in the respiratory exchange ratio (0.87 +/- 0.03 to 0.99 +/- 0.04, P < 0.05). Serum lactate rose by 124 +/- 30.4% from baseline to 20 microg/min (1.1 +/- 0.1 to 2.3 +/- 0.25 mmol/L, P < 0.01) and base excess decreased (0.89 +/- 0.56 to vs. -1.75 +/- 0.52 mmol/L, P < 0.01) consistent with a lactic acidosis contributing to the excess ventilation. There was no significant differences in (VE) or P(0.1) with F(I)O(2) = 1.0, suggesting peripheral chemoreceptor stimulation was not responsible for the rise in (VE). At 20 microg/min SAL, K(+) fell significantly from baseline (3.8 +/- 0.06 to 2.8 +/- 0.09 mmol/L, P < 0.001).

Systemic SAL imposes ventilatory demands by increasing metabolic rate and serum lactate. This may adversely affect patients with severe asthma with limited ventilatory reserve.