CARDIOVASCULAR EFFECTS OF OPIOIDS

Numerous reports have demonstrated that large doses of opioids, administered as the sole or primary anesthetic, result in hemodynamic stability throughout the operative period.

The choice of opioid can affect the perioperative hemodynamic profile. For example, alfentanil is less reliable than fentanyl and sufentanil in blocking increases in heart rate and blood pressure during anesthetic induction, sternotomy, sternal spread, and aortotomy in patients with ischemic heart disease who undergo coronary artery surgery.^{[175] [176]}

Neurologic Mechanisms

Key areas of the brainstem that integrate cardiovascular responses and maintain cardiovascular homeostasis are the nucleus solitarius, the dorsal vagal nucleus, the nucleus ambiguus, and the parabrachial nucleus. The nucleus solitarius and parabrachial nucleus play an important role in the hemodynamic control of vasopressin secretion. Enkephalin-containing neurons and opioid receptors are distributed in these regions. The direct administration of μ-agonists into the CNS of animals most commonly, but not always, produces hypotension and bradycardia.^[177] The ventrolateral periaqueductal gray region, a key central site mediating analgesia, also affects hemodynamic control.^[178] Opioids also can modulate the stress response through receptor-mediated actions on the hypothalamic-pituitary-adrenal axis. Most opioids reduce sympathetic and enhance vagal and parasympathetic tone. Patients who are volume-depleted, or individuals depending on high sympathetic tone or exogenous catecholamines to maintain cardiovascular function, are predisposed to hypotension after opioid administration.

Occasionally, opioids produce paradoxic effects. A hyperdynamic cardiovascular response was reported during anesthetic induction with high-dose fentanyl in 10% of one series of patients. It was attributed to central sympathetic activation. ^[179] Fentanyl increases norepinephrine release from some sympathetic nerve endings, and may also inhibit the neuronal uptake of norepinephrine in dogs.

The predominant and usual effect of opioids on heart rate is to produce bradycardia resulting from stimulation of the central vagal nucleus. Blockade of sympathetic actions may also play a role in opioid-induced bradycardia. Meperidine, in contrast to other opioids, rarely results in bradycardia, but may cause tachycardia. Tachycardia after meperidine may be related to its structural similarity to atropine, to normeperidine (its principal metabolite), or to early manifestations of its toxic CNS effects.