Propofol Respiratory Depression

Propofol at common clinical concentrations-is potent ventilatory depressant and therefore it is sometimes common with the name propofol respiratory depression .

The Propofol respiratory depression of ventilation is dose dependent. After induction of anesthesia with propofol apnoea occurs in 25% to 35% of patients which may persist till 3 minutes. It reduces tidal volume (by 40—45%) and minute ventilation.

The ventilatory response to carbon dioxide is decreased by about 40%. Opioids administered with the preoperative medication may enhance this ventilatory depressant effect. Propofol decreases the acute hypoxic ventilatory response in humans and depresses in vivo carotid body chemosensitivity.

The magnitude of propofol respiratory depression being dependent on the severity of Po2 reduction, and that propofol causes a concentration-dependent block of cholinergic chemotransduction via the carotid sinus nerve. A maintenance infusion-of propofol decreases tidal volume and frequency of breathing.

Sedative concentrations of propofol depress the ventilatory response to hypercapnia. The propofol respiratory depression is attributed to an exclusive effect within the central chemoreflex loop at the central chemoreceptors.

However, propofol respiratory depression preserves the peripheral chemoreflex response to carbon dioxide.

Compared with thiopental, propofol decreases the prevalence of wheezing after induction of anesthesia and trachea intubation in healthy and asthmatic patients. Propofol has vagolytic effects on the airway and thus may inhibit vagal nerve stimulation induced bronchoconstriction.

However, recently introduced, a newer formulation of propofol with metabisulfite dose not have any effect on vagal nerve stimulation-induced bronchoconstriction. Metabisulfite itself causes airway narrowing in asthmatics. Following tracheal intubation, in patients with a history of smoking, airway resistance was increased more following the administration of propofol containing metabisulfite than propofol containing EDTA.

Therefore, preservative used for propofol can have a dramatic effect on its ability to attenuate bronchoconstriction. Propofol showed about 3 times higher potency in producing tracheal relaxation when solubilized with hydroxypropyl-betacyclodextrin compared with an oil-in-water emulsion of the drug.

Propofol respiratory depression resistance after tracheal intubation is lower after induction with propofol than after induction with thiopental or with high-dose etomidate.

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