Fourteenth Annual Meeting of the Society for Pediatric Anesthesia, San Francisco, California, October 13, 2000

The 14th Society of Pediatric Anesthesia annual meeting took place in beautiful San Francisco. The morning session included a series of lectures discussing the cardiorespiratory system. The first lecture, by Jeffrey Fineman, MD (University of California, San Francisco), discussed the effects of the transitional circulation. Dr. Fineman initially discussed the morphology of the pulmonary vasculature. He demonstrated how the pulmonary vasculature of the fetus and immediate newborn has a thicker medial smooth muscle coat compared with that of adults. This muscularity contributes to the vasoreactivity and high pulmonary vascular reactivity found in newborns and the late-term fetus. Within the first several weeks after birth, the medial smooth muscle involutes and the thickness of the media of the small pulmonary arteries decreases rapidly and progressively. In addition to the muscularity, the number and volume of small arterioles in the lung increase throughout gestation, and the increase in the cross-sectional area of the vasculature actually decreases the effective resistance in the pulmonary vasculature. The pulmonary arterial growth continues through the first 10 yr of life but is more rapid during the first 2 yr of life. Although anatomic changes contribute to pulmonary reactivity in the newborn, Dr. Fineman discussed the mechanical and molecular factors involved in the regulation of the transitional circulation. Mechanical factors, such as the expansion of the lung (even without changing the oxygen tension), increase fetal pulmonary blood flow and decrease pulmonary vascular resistance, but not to newborn values. Lung expansion allows unkinking of small pulmonary arteries, removes fluid from the alveolar space, and creates a negative intraalveolar pressure that maintains patency of the pulmonary vasculature. Prostaglandin (PG) I2 production increases in response to lung expansion, and the inhibition of PGI2 production impairs pulmonary vascular dilation. The addition of air or oxygen completes the pulmonary vasodilation that occurs after birth. Oxygen has a direct effect on pulmonary vascular relaxation and an indirect effect through nitric oxide. Other mediators such as PGE2, PGD2, histamine, and bradykinin appear to have minor roles, and their roles vary throughout gestation. Prostaglandin D2 is a vasodilator in the fetus and a constrictor in the newborn. Endogenous nitric oxide (NO) production increases from late gestation through the first 4 wk of life, and inhibition of endogenous NO production attenuates the decrease in pulmonary vasodilation. Therefore, basal NO production is an important factor in the in utero and postnatal regulation of pulmonary vascular resistance. Postnatal pulmonary vascular reactivity is also dependent on oxygen tension, pH, and, to a lesser degree, prostaglandins E1 and endothelin. The failure of the transition of the pulmonary circulation occurs because of underdevelopment of the lung as seen in diaphragmatic hernia, maladaptation of the lung as seen in sepsis or meconium aspiration, and maldevelopment of the lung as occurs with premature ductal closure and subsequent endothelial cell injury. Endothelial cell dysfunction results in impaired NO production, decreased endogenous nitric oxide synthesis production, and reduced gene expression. Increased production of endothelin A, a vasoconstrictor, and reduced production of endothelin B, a vasodilator, are demonstrated with endothelial cell dysfunction in utero. Dr. Fineman reviewed the role of NO as a therapeutic agent in the treatment of neonates with abnormal pulmonary reactivity. He reviewed the Ninos study on the slight improvement in pulmonary reactivity of patients with diaphragmatic hernia who received NO after extracorporeal membrane oxygenation (ECMO). He also discussed the benefits of NO in the neonate with primary pulmonary hypertension, which remains the only medically approved therapeutic use of NO. Dr. Fineman reviewed some of his own data which (in contrast to published data) suggest that doses of NO of 20 parts per million may improve Pao2 and decrease pulmonary artery pressure when compared to doses of 5–10 parts per million. In this select population, Dr. Fineman’s data would support at least a brief trial of doses of approximately 20 parts per million. The second morning lecture discussed a pathophysiologic directed approach to the management of right and left heart dysfunction. Dr. Jon Meliones (Duke University) began his discussion by reviewing the basic principles of ventricular function. In his review, Dr. Meliones highlighted the importance of optimizing heart rate and stroke volume to improve cardiac output in pediatric patients. Increasing heart rate is a particularly important strategy in the management of ventricular dysfunction in newborns and infants, especially when relative bradycardia exists. However, because coronary blood flow occurs during ventricular diastole, marked increases in heart rate generally in excess of 180–190 bpm can significantly reduce ventricular myocardial blood flow and therefore contribute to myocardial ischemia and decreased contractile forces. Further, excessive increases in heart rate may decrease ventricular fillings and result in a marked diminution in stroke volume and systemic cardiac output. Dr. Meliones used pressure volume diagrams to illustrate the contribution of preload, afterload, and contractility on optimizing ventricular stroke volume. Left ventricular stroke volume can be modulated by changes in preload or left ventricular end-diastolic volume. Neonates have a limit to the degree of recruitable stroke volume because of ventricular noncompliance. In general, left-sided filling pressures in excess of 15 mm Hg are less beneficial and may reduce stroke volume because of increases in end-systolic wall tension and secondary endocardial ischemia. Once preload is optimized, increasing the inotropic state of the left ventricle can be performed by altering plasma calcium levels and administering inotropic drugs. Calcium supplementation is essential in the neonate because of the underdevelopment of the sarcoplasmic reticulum. Intracellular calcium stores are not readily stored or released to the myocardium, and therefore extracellular calcium concentrations have a marked effect on myocardial cell function. Therefore, calcium supplementation and avoidance of wide fluctuations in ionized calcium levels are important factors in optimizing left ventricular stroke volume in neonates and infants. The use of inotropic drugs is also of great benefit. In neonates, the left ventricle responds to dopamine with a dose-dependent response similar to that seen in adults. Dobutamine is a pure β-agonist. In neonates, the peripheral β2 effects may predominate, resulting in mild peripheral vasodilation and little increase in ventricular contractility. The benefits of dobutamine are lessened in immature animals and it has an increased incidence of tachyarrhythmias resulting from its structural similarity to isoproterenol. This may limit its use in newborn and premature infants with heart rates of ≥180 bpm. Epinephrine infusions in the 0.05–0.1 μg · kg−1 · min−1 range have a potent β1 effect and increase left ventricular contractility with minimal α effects. Doses in the 0.1–0.2 μg · kg−1 · min−1 range have a mixed α/β effect. Doses larger than 0.2 μg · kg−1 · min−1 have a predominant α effect that may increase afterload and wall tension in patients with severe left ventricular dysfunction. These large doses must be used with caution, and measures of improved oxygen delivery should be sought. Evidence of increased urine output, increasing mixed venous saturation, or reductions in lactate should be demonstrated. Increased blood pressure alone may not correlate with improvements in oxygen delivery to tissue. Phosphodiesterase inhibitors increase inotropy by preventing the breakdown of cyclic adenosine monophosphate. Both cyclic adenosine monophosphate and increased calcium availability to the myocardium will enhance contractility. Milrinone, the most commonly used agent, affects cyclic guanosine monophosphate in a similar fashion and therefore has a role in reducing pulmonary vascular resistance and systemic vascular resistance as well. Milrinone will therefore not only increase contractility but will also further augment cardiac output by reducing the afterload of both the right and left ventricles. Reducing afterload is the next therapeutic intervention. Pure vasodilators, such as the NO donor sodium nitroprusside and the selective peripheral vasodilator nicardipine, effectively decrease systemic vascular resistance and have negligible effects on the myocardium. Drugs such as milrinone will decrease systemic vascular resistance as well as improve ventricular contractility. For the right ventricle, inhaled NO will decrease right ventricular afterload and augment right ventricular contractility. Dr. Wanda Miller-Hance (University of California, San Francisco) reviewed the natural history of repaired congenital hearts. Dr. Miller-Hance remarked on the dramatic improvement in survival for patients with complex congenital cardiac disease over the last 15 yr. She noted that an escalating number of children with palliated and repaired hearts will require operative interventions and in virtually all congenital cardiac patients (other than atrial septal defects and ductus ligation), a component of residual cardiac abnormalities remains and therefore an anesthetic risk exists. Dr. Miller-Hance discussed that right, left, or biventricular dysfunction may be evident and may be global or regional. The causes of ventricular dysfunction are multifactorial and relate to the age at operation, chronicity of abnormal cardiac workload (either volume or pressure), or may be due to the direct effects of surgery and cardiopulmonary bypass (CPB). Patients with tetralogy of Fallot can serve as a good example of these effects. Late repair (after 1–3 yr of age) results in prolonged exposure to right ventricular outlet obstruction and cyanosis. In response, the right ventricle becomes both pressure loaded and ischemic. Late follow-up has demonstrated an increased risk of right heart dysfunction and sudden death from ventricular tachycardia originating in the right ventricle in this patient population. Right heart dysfunction can occur even with earlier repair; factors include right ventriculotomy and right heart ischemia from prolonged exposure to CPB or circulatory arrest and impaired myocardial protection resulting from right ventricular hypertrophy and increased end-diastolic pressures. Other factors include residual disease created by the type of operative intervention. For example, the need for a transannular patch to open the pulmonary valve may leave the patient with significant pulmonary insufficiency, which over time may result in a volume-loaded right ventricle and a dilated cardiomyopathy. Therefore, a multitude of factors may result in differing pathophysiologic consequences for the anesthesiologist caring for adolescents or adults with previously repaired congenital cardiac disease. A careful evaluation of the current cardiac pathophysiology is required to plan a safe anesthetic. Other factors, such as chronic cyanosis, may result in polycythemia, neovascularization, coagulation abnormalities, an increased risk for stroke, and may contribute to hypoxic injuries to other organs such as the liver and kidneys. A careful evaluation of the renal, hepatic, and coagulation systems should be considered in the preoperative evaluation. Polycythemia increases blood viscosity and may lead to vascular sludging and stroke. Neovascularization can result in numerous collateral vessel formations, which can increase operative blood loss or contribute to vascular steal from cerebral vessels to supply additional blood to the lungs. This is a particular problem in children who may require operative interventions using CPB. Rhythm disturbances are present in a wide range of congenital cardiac patients, particularly in patients with single-ventricle physiology who have undergone a Fontan procedure. They are prone to atrial dysrhythmias such as atrial fibrillation or flutter. The absence of atrioventricular synchrony and the atrial “kick” may have severe consequences on systemic cardiac output. Ventricular dysrhythmias are more frequent in patients requiring a ventriculotomy or possessing ventricular hypertrophy. Heart block or significant conduction delays occur after ventricular septal defect closure and after atrioventricular septal defect repairs. Pressure overload is a common problem in children who require right ventricular outflow tract conduits such as in truncus arteriosus repair and tetralogy with pulmonary atresia. Over time the child may outgrow the conduit or the conduit may calcify and narrow causing significant right ventricular outflow obstruction. In response, the right ventricle hypertrophies to the pressure load. Similarly residual left ventricular obstruction may occur in children with arch hypoplasia, coarctation, or residual aortic valve stenosis. Volume overload occurs from prolonged exposure to shunt flow or valvular regurgitation. In response the ventricle dilates and if severe or prolonged, the patient will develop congestive heart failure or a dilated cardiomyopathy. Another factor to consider in the congenital cardiac patient is the presence of pulmonary hypertension. The presence of increased pulmonary blood flow resulting from, for instance, a ventricular septal defect, atrioventricular canal, or aortopulmonary shunt, will result in hypertrophy of the pulmonary vasculature and reactive or fixed pulmonary vascular resistance. Factors such as hypoxemia, acidosis, or hypercarbia can contribute to extreme life-threatening increases in pulmonary vascular resistance. Other factors discussed by Dr. Miller-Hance included bacterial endocarditis prophylaxis, placement of air filters in venous lines in children with residual intra- or extracardiac shunts, and noncardiac residual problems such as phrenic or recurrent laryngeal nerve injury after reoperative procedures. In the afternoon session, three lecturers were given discussing resource utilization. The first lecture was by Dr. Robert Nelson of the Children’s Hospital of Philadelphia. Dr. Nelson discussed the ethical issues of resource allocation by reframing the question of health care quality in terms of limited financial resources. Using this framework, Dr. Nelson offered that society is left with four choices of balancing the supply and demand for health care services. 1) Restrict access for all residents who fail to meet a selected means test (increase the uninsured population). 2) Ration health care, i.e., refuse to provide certain forms of medical care to all eligible residents. 3) Cut reimbursement rates to extend access to all residents. 4) Increase spending to provide all necessary care. Dr. Nelson focused on the second choice and asked the following questions: Is the rationing of health care morally justifiable, and if so, should health care be rationed by medical need or ability to pay? Should the level of health care that all persons have access to be uniform or nonuniform? If a nonuniform system is proposed, should the basic plan be set independent of economic factors or should it vary according to the available resources? The choices for the latter scenario are of a single-payer system with uniform benefits, similar to the Canadian system, which assures access but does not control costs, versus a two- or more-tiered system that rations health care and therefore may fail to meet a quality standard. Dr. Nelson discussed rationing using the following argument. According to the formal principle of justice, discrimination is plausible only when it is relevant to the resource being distributed. Therefore, rationing on the basis of medical necessity for a specific category of illness is ethical and does not violate fairness doctrine. Rationing on the ability to pay, however, does violate the principle of justice or equality. Therefore, the provision of a basic level of benefits seems appropriate. However, community resources are not limitless and providing the “appropriate” level of basic care is both a fiscal and moral decision. Providing an acceptable level of basic care is a duty of charity. 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