Anesthetic management

The presence of CHF in a patient with CHD should raise concern, especially if the patient has pulmonary hypertension or an obstructive outflow lesion, because these patients are at increased risk for experiencing serious perioperative morbidity and death. In some patients, the stress of surgery may be enough to lead to acute cardiac decompensation, typically reflected by a respiratory, as well as metabolic, acidosis. There is no single anesthetic technique that has been identified as “ideal” for these patients. Anesthetic management must include knowledge of the individual physiologic aspects of the cardiac anatomy (shunt flow) and a plan to minimize myocardial depression and maintain baseline hemodynamic parameters.

Central to the anesthetic management of patients with CHF secondary to L-to-R shunting is to avoid increasing the shunt and pulmonary overcirculation. Repeated cardiopulmonary evaluations are important to identify influences on the patient that would increase systemic vascular resistance or decrease PVR (Table 202-1). One of the foremost responsibilities of the anesthesia team is to consider factors that may adversely affect shunt flow. However, the team must be cautious about the degree to which the L-to R-shunt is manipulated to reduce pulmonary overcirculation. Efforts to aggressively reduce systemic vascular resistance or increase PVR to reduce pulmonary overcirculation and, hence, improve CHF will lessen the L-to-R shunt; however, the ensuing hypotension or pulmonary hypertension, respectively, reduces coronary perfusion and stresses a poorly functioning right ventricle, leading to hemodynamic deterioration. In contrast, cyanotic CHD with R-to-L shunts can be improved dramatically with aggressive measures to increase systemic vascular resistance or decrease PVR, often in association with immediate hemodynamic improvement.

Altering ventilation or oxygenation or both are important ways to influence either L-to-R or R-to-L shunts. The pulmonary vasculature is very sensitive to changes in PaCO₂. Values of PaCO₂ between 28 and 32 mm Hg are associated with pulmonary vasodilation that will worsen CHF in patients with L-to-R shunts. A PaCO₂ above 55 mm Hg raises PVR and lessens pulmonary overcirculation in these patients. However, the patient will tolerate hypercarbia only until the associated respiratory acidosis results in worsening myocardial function and compromised hemodynamics, overcoming any benefit from reduced L-to-R shunt. The effect of O₂ as a potent pulmonary vasodilator often goes unnoticed in patients with shunts. The patient’s inspired O₂ concentration (FIO₂) should be lowered incrementally after induction of anesthesia to avoid hyperoxia, which decreases PVR and could worsen pulmonary overcirculation.

Patients with CHF secondary to L-to-R shunts or obstructive lesions will benefit from anesthetic medications that do not change or only minimally decrease myocardial contractility. Administering appropriate doses of synthetic opioids, ketamine, or both (which have minimal to no negative inotropic effects) provides excellent hemodynamic stability for these patients. Ketamine is widely used for neonates and infants with CHF because it maintains cardiac output and perfusion pressures by enhanced sympathetic stimulation. Propofol has been used infrequently in this patient population, but even with careful dose adjustments, the use of these drugs poses risks to hemodynamic stability. The use of propofol has been associated with significant vasodilation and hypotension in adults. Preservation of baseline heart rate is essential in the neonate or infant because neonates and infants, unlike adults, are unable to augment cardiac output with increases in stroke volume. Ketamine preserves the heart rate better than does any other anesthetic agent and prevents the bradycardia often associated with the administration of fentanyl alone. A benefit to the use of synthetic opioids in patients with CHD and CHF is the ability of these drugs to attenuate increases in PVR. Though these patients with CHD and CHF may have hypertrophied pulmonary vasculature, the vasculature can be very reactive. Any insult that increases PVR may cause severe systemic hypotension by decreasing left ventricular preload and hypoxemia by decreasing perfusion of the lungs.

If the intravenous route is not an option for induction of anesthesia, intramuscular or inhalation techniques may be used. For intramuscular induction, ketamine is the drug of choice for use when obtaining venous access by causing dissociative anesthesia. A major advantage of ketamine over other medications for intramuscular induction is the limited respiratory depression and maintenance of airway reflexes caused by ketamine, which increases safety until venous access is obtained. Halogenated inhalation agents have been used for induction for years in pediatric patients with CHD and CHF. In the past, the nonirritating airway effects of halothane made it a popular choice for induction, but the associated significant myocardial depression, bradyarrhythmia, and prolonged time to induction were particularly disadvantageous for neonates and infants with CHD, who responded with a greater degree of hypotension to the use of inhalation agents than do older children and adults. Hypotension occurs with the use of inhalation agents (see Chapter 66) as a result of a combination of reduced myocardial contractility, increased vasodilation, lower heart rate, and inhibition of compensatory reflex mechanisms.

The development of inhalation agents with low solubility and less myocardial depression (desflurane and sevoflurane) since the 1990s has been very beneficial, creating an opportunity to use these inhalation agents in managing the care of neonates and infants with CHF. The lower solubility of these inhalation agents results in more rapid induction and emergence. Unlike desflurane, sevoflurane has been evaluated repeatedly in neonates and infants with either cyanotic or acyanotic CHD and has been found to be acceptable in terms of cardiopulmonary side effects when used appropriately for induction and maintenance of anesthesia. It has replaced halothane as the agent of choice for inhalation induction because it results in more rapid inductions, reasonably well maintained hemodynamics, fewer arrhythmias, better contractility, and more rapid emergence and possesses the nonirritating airway effects of halothane. Furthermore, the use of sevoflurane has been shown to be associated with less breath holding, coughing, and laryngospasm, as compared with halothane.

Anesthesia can be induced by sevoflurane in patients with obstructive lesions, but at the concentration often used for an inhalation induction, the negative inotropic effect and risk of hypotension present a risk of hemodynamic collapse, a phenomenon not seen when ketamine is used to induce anesthesia. However, compared with the hypotension associated with the use of other inhalation agents, hypotension from sevoflurane can be quickly corrected by decreasing the concentration of inhaled drug. When inhalation induction with sevoflurane is used, an intravenously administered induction agent should be substituted to complete induction as soon as intravenous access is obtained because, irrespective of the inhalation agent used, a ketamine-based or an opioid-based anesthetic induction is more likely to provide greater hemodynamic stability in this population of patients.