Side Effects and Contraindications

Induction of anesthesia with propofol is associated with several side effects, including pain on injection, myoclonus, apnea, decrease in arterial blood pressure, and rarely, thrombophlebitis of the vein into which propofol is injected. Pain on injection is less than or equal to that with etomidate, equal to that with methohexital, and greater than after thipental.^{[213] [241] [275]} Pain on injection is reduced by using a large vein, avoiding veins in the dorsum of the hand, and adding lidocaine to the propofol solution.^[213] Myoclonus occurs more frequently after propofol than after thiopental, but less frequently than after etomidate or methohexital.^[241] Apnea after induction with propofol is common. The incidence of apnea may be similar to that after thiopental or methohexital; however, propofol produces a greater incidence of apnea lasting longer than 30 seconds.^{[139] [145]} The addition of an opiate increases the incidence of apnea, especially prolonged apnea.^{[139] [141]}

The most significant side effect on induction is the decrease in systemic blood pressure. Addition of an opiate just before induction of anesthesia appears to augment the decrease in arterial blood pressure.^[168] Perhaps slow administration and smaller doses in adequately prehydrated patients may attenuate the decrease in arterial blood pressure. Conversely, the effects of laryngoscopy and endotracheal intubation and the increases in mean arterial pressure, heart rate, and systemic vascular resistance are less significant after propofol than after thiopental.^{[164] [168]}

Propofol infusion syndrome is a rare, but lethal syndrome associated with infusion of propofol at 5 mg/kg/hr or greater for 48 hours or longer. It was first described in children but has also subsequently been observed in critically ill adults. Clinical features include cardiomyopathy with acute cardiac failure, metabolic acidosis, skeletal myopathy, hyperkalemia, hepatomegaly, and lipemia.^{[81] [276]} Present evidence suggests that this syndrome occurs as a result of failure of free fatty acid metabolism because of inhibition of free fatty acid entry into mitochondria and failure of the mitochondrial respiratory chain.^[277]