ABSTRACT
BACKGROUND: Dopamine plays an important role in the regulation of respiration and low-dose dopamine infusion is associated with a decreased respiratory drive response to hypoxia in animals and humans. The effects of dopamine on ventilation in patients with chronic obstructive pulmonary disease (COPD) is unknown. We tested the hypothesis that dopamine inhibits ventilation in patients with COPD. MATERIALS AND METHODS: In a double-blinded, cross-over, placebo-controlled, randomized study we studied nine patients with decompensated COPD, ventilated in the pressure support mode in the intensive care unit (ICU) and five ambulatory patients with stable COPD. All patients received 5 micro g kg(-1) min(-1) of dopamine or an equivalent volume of 5% glucose solution. RESULTS: In the mechanically ventilated COPD patients, there was no difference in the effects of dopamine compared with placebo on blood pressure, heart rate, minute ventilation (-0.5 +/- 1.1 vs. -0.2 +/- 0.9 L min(-1), P = 0.46, respectively), respiratory rate (-0.4 +/- 2.7 vs. -0.3 +/- 2.1 min(-1), P = 0.96), PaO(2) (-5 +/- 4 vs. -5 +/- 10 mmHg, P = 0.90, respectively), or PaCO(2) (-0.7 +/- 1.4 vs. -1.0 +/- 3.4 mmHg, P = 0.83, respectively). In spontaneously breathing stable patients, dopamine increased systolic blood pressure (P = 0.02) but did not influence other haemodynamic and respiratory variables. CONCLUSION: Although low-dose dopamine has been shown to depress ventilation in a variety of conditions, it does not compromise ventilation in COPD patients either breathing spontaneously or when weaned using pressure support ventilation.
Subject(s)
Dopamine/administration & dosage , Pulmonary Disease, Chronic Obstructive/drug therapy , Aged , Cross-Over Studies , Double-Blind Method , Female , Forced Expiratory Volume/physiology , Humans , Male , Pulmonary Disease, Chronic Obstructive/physiopathology , Vital Capacity/physiologyABSTRACT
A 34-year-old woman collapsed secondary to ventricular fibrillation 3 hours following the ingestion of ergotamine tartrate for migraine. She underwent defibrillation and recovered rapidly without any subsequent consequences. The mechanism of action and the side effects of ergotamine and other antimigraine drugs are discussed. We hypothesize that a coronary spasm induced by ergotamine could be the aetiologic factor leading to ischaemic ventricular fibrillation.
