Induction and Maintenance of Anesthesia

Communication with the surgical team is essential before starting induction of anesthesia in order to decrease ischemic time of the organ. The timing should take into consideration the longer surgical time needed in patients undergoing reoperation.

Frequently, the induction and maintenance of anesthesia does not differ much from the techniques used in other patients with poor cardiac function undergoing cardiac anesthesia. However, cricoid pressure is usually applied to prevent aspiration of gastric contents. A combination of narcotics (e.g., fentanyl, sufentanil) and muscle relaxants (e.g., pancuronium, rocuronium, cisatracurium) is administered, and their hemodynamic effects are followed carefully. Narcotics are administered until loss of consciousness. The choice of muscle relaxants depends mainly on the desired change in heart rate. Alternatively, a hypnotic agent that is devoid of myocardial depressant effects (etomidate) has been used with succinylcholine to provide rapid intubating conditions.

Although the anesthetic agents that are used have no significant direct hemo-dynamic effects, the loss of consciousness by itself may lead to a reduction in sympathetic output from the brain stem and circulating catecholamines, leading to hypotension as a result of systemic vasodilation and possibly a further decrease in myocardial contractility. In addition, venous dilatation may exacerbate the mildly hypovolemia that is frequently present as a result of aggressive diuretic therapy. Therapy of hypotension during induction of anesthesia is usually guided by the hemodynamic monitoring: vasodilation may be treated with volume administration and small amounts of vasoconstrictors (e.g., phenylephrine 50-100 |ig boluses), while reductions in myocardial contractility can be treated with inotropic agents (e.g., dopamine or dobutamine 3-5 ^g/kg/min). More accurate monitoring and therefore also more directed treatment can be initiated once the TEE probe has been placed after tracheal intubation. It has to be recognized that volume therapy can exacerbate congestive heart failure, and that vasoconstrictors can increase left ventricular afterload and therefore decrease cardiac output. Also, catecholamines can lead to arrhythmias which are frequently poorly tolerated in these patients. Reaction to intubation or surgical stimulation can be different from that seen in other patients: light anesthesia may not be reflected as hypertension and tachycardia, but merely as a decrease in cardiac output, an increase in pulmonary capillary wedge pressure and systemic vascular resistance, and a decrease in SvO2. This requires additional anesthetics or the use of vasodilators (nitroglycerine or nitroprusside).

Anesthesia is maintained with a combination of narcotics (e.g., fentanyl 50-100 |ig/kg followed by 5-10 |ig/kg/h, or sufentanil 10-15 |ig/kg followed by 1-2 |ig/kg/h), muscle relaxants, and amnestic agents (e.g., midazolam 5-10 mg, lorazepam 2-4 mg). However, the addition of benzodiazepines to high-dose narcotics may be associated with mild reductions in cardiac output and systemic vascular resistance, resulting in hypotension. Low-dose dopamine, mannitol and diuretics (furosemide) are frequently used intraoperatively, especially in patients

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