Responses to High‐Dose Narcotic “Anesthesia” During Cardiac Surgery

Narcotics as Anesthetics. Production of profound analgesia (“narcotic anesthesia”) without hemodynamic deterioration is easily and reliably achieved in patients with compromised cardiovascular systems by intravenous administration of large doses of opioids. Even extremely high plasma levels of opioids alone often fail to prevent hypertensive responses to anesthetic and surgical stimulation. It has not been possible to define a blood level of the narcotic that is consistently associated with prevention of hemodynamic or hormonal responses. Since some of the interventions that are associated with hemodynamic and hormonal responses are probably not painful per se, the hemodynamic and hormonal responses may not represent inadequate “anesthesia,” as it is usually defined. Different narcotics have different systemic and neurally mediated effects upon muscle vascular resistance. Local infusion of morphine produces a decline in vascular resistance, whereas local infusion of sufentanil does not. Intravenous administration of morphine is associated with a transient neurally mediated, passive decline in muscle vascular resistance that appears to be due to central sympatholysis, and a persistent neurally mediated increase in muscle vascular resistance. Sufentanil actively dilates muscle vasculature by a neural mechanism. Since the latter may be blocked by local α 1 ‐adrenergic blockade or by the combination of local H1 and H2 blockers, we interpret these data to indicate that a local histaminergic system in the blood vessel walls is activated by withdrawal of α 1 ‐adrenergic activity, possibly related to an α 2 agonist action of sufentanil at central nervous system receptors.