The effects of dopamine on the respiratory system: Friend or foe?

Abstract

Dopamine (DA) is an immediate precursor of noradrenaline that has stimulatory or inhibitory effects on a variety of adrenergic receptors. DA is primarily used in the management of circulatory shock for its combined vasopressor and inotropic effects, but it may also exert significant effects on the respiratory system Although the respiratory effects of intravenous DA attract less attention than its hemodynamic effects, there is evidence that DA affects ventilation, pulmonary circulation, bronchial diameter, neuromodulation of sensory pulmonary nerves and lung water clearance. Through these complex mechanisms, DA may exert beneficial as well as detrimental effects on respiration. DA may have beneficial effects on the respiratory system by decreasing oedema formation and improving respiratory muscle function, but can also have deleterious effects, by inhibiting ventilation. Hence, DA may be beneficial in lung oedema, but harmful in cases of difficult weaning from mechanical ventilation. DA should be used with caution in patients with heart failure during weaning from mechanical respiration; however, critically ill patients with chronic obstructive pulmonary disease (COPD) do not show this negative effect of DA on ventilatory drive.

Efficacy and safety of high dose versus low dose furosemide with or without dopamine infusion: The Dopamine in Acute Decompensated Heart Failure II (DAD-HF II) Trial

“…The findings of DAD-HF II not observed in DAD-HF are 1) higher heart rate at 4 and 8 h after treatment initiation and 2) longer time to oxygen saturation ≥96% in the LDFD compared with HDF and the LDF groups. These findings are in accordance with the reported cardiac [12,13] and pulmonary [14] adverse effects of dopamine. Aziz et al retrospectively evaluated 116 HF patients treated with furosemide infusion (0.2-0.4 mg/kg/h) combined with low-dose dopamine (1-2 μg/kg/min) or intermittent boluses of furosemide [15], and reported that continuous infusion in addition to low-dose dopamine was less nephrotoxic and associated with a shorter hospital stay and lower readmission rates at 30 days.…”

Brainstem Ventilatory Dysfunction: A Plausible Mechanism for Dyspnea in Parkinson's Disease?

“…The carotid body is also known to be strongly dopaminergic . Dopamine contributes to the peripheral and central control of breathing in mammals and has been shown to have inhibitory effects on ventilation at rest and to suppress responsiveness to hypoxia . Conversely, the opposite physiological response was demonstrated in a human study in which the D2‐receptor blocker haloperidol was administered .…”

“…50,51 Dopamine contributes to the peripheral and central control of breathing in mammals and has been shown to have inhibitory effects on ventilation at rest and to suppress responsiveness to hypoxia. 52,53 Conversely, the opposite physiological response was demonstrated in a human study in which the D2-receptor blocker haloperidol was administered. 54 In the model of PD, where there is degeneration of dopaminergic neurons, it could therefore be envisaged that there is enhanced ventilatory drive at rest and in hypoxic conditions, and these effects have in fact been confirmed in the 6-hydroxydopamine rat model of PD.…”

The carotid chemoreceptor contributes to the elevated arterial stiffness and vasoconstrictor outflow in chronic obstructive pulmonary disease

“…At moderate-to-high doses (i.e. 5-20 μg kg −1 min −1 ), dopamine can stimulate αand β-receptors (Hoffman & Lefkowitz, 1990;Ciarka et al 2007). β-receptor stimulation would be expected to increase heart rate; however, heart rate was unaffected in both groups with 2 μg kg −1 min −1 dopamine infusion, suggesting an absence of β-adrenergic stimulation.…”