CHAPTER 111 Pediatric Anesthesia and Critical Care
The management of congenital heart disease (CHD) has progressed significantly over the past 3 decades. Most congenital heart lesions are now amenable to either anatomic or physiologic repair early in infancy. Advances in diagnostic and interventional cardiology, the evolution of surgical techniques and conduct of cardiopulmonary bypass, and refinements in postoperative management have all contributed to a substantial decrease in morbidity and mortality associated with CHD. The approach to repairing CHD as early as possible, preferably in the neonatal period, has had significant implications for the anesthetic care of these critically ill infants during cardiac surgery. To meet this challenge, a clear understanding of neonatal respiratory and cardiac physiology, neonatal responses to anesthesia and surgery, and the pathophysiology of complex congenital heart defects is necessary.
Care of the critically ill neonate requires an appreciation of the special structural and functional features of immature organs. The neonate appears to respond more quickly and extremely to physiologically stressful circumstances; this may be expressed in terms of rapid changes in, for example, pH, lactic acid, glucose, and temperature.1
The physiology of the preterm and full-term neonate is characterized by a high metabolic rate and O2 demand (a twofold to threefold increase compared with adults), which may be compromised at times of stress because of limited cardiac and respiratory reserve. The myocardium in the neonate is immature, with only 30% of the myocardial mass made up of contractile tissue, compared with 60% in mature myocardium. In addition, neonates have a lower velocity of shortening, a diminished length–tension relationship, and a reduced ability to respond to afterload stress.2,3 Because the compliance of the myocardium is reduced, the stroke volume is relatively fixed and cardiac output is heart-rate dependent, so the Frank-Starling relationship is functional only within a narrow range of left ventricular end-diastolic pressure. The cytoplasmic reticulum and T-tubular system are underdeveloped and the neonatal heart is dependent on the trans-sarcolemmal flux of extracellular calcium both to initiate and sustain contraction.
Cardiorespiratory interactions are important in neonates and infants. In simple terms, ventricular interdependence refers to a relative increase in ventricular end-diastolic volume and pressure, causing a shift of the ventricular septum and diminished diastolic compliance of the opposing ventricle.4 This effect is particularly prominent in the immature myocardium. Therefore, a volume load from an intracardiac shunt or valve regurgitation, and a pressure load from ventricular outflow obstruction or increased vascular resistance, may lead to biventricular dysfunction. For example, in neonates with tetralogy of Fallot and severe outflow obstruction, hypertrophy of the ventricular septum may contribute to diastolic dysfunction of the left ventricle and an increase in end-diastolic pressure. This does not improve immediately after repair in the neonate, as it takes some weeks or months for the myocardium to remodel. Therefore, an elevated left atrial pressure is not an unexpected finding after neonatal tetralogy repair. This circumstance may be further exacerbated if there is a persistent volume load to the left ventricle after surgery, such as from residual ventricle septal defects (VSDs).
The mechanical disadvantage of an increased chest wall compliance and reliance on the diaphragm as the main muscle of respiration limits ventilatory capacity in the neonate. The diaphragm and intercostal muscles have fewer type I muscle fibers (i.e., slow contracting, high oxidative fibers for sustained activity), and this contributes to early fatigue when the work of breathing is increased. In the newborn, only 25% of fibers in the diaphragm are type I, reaching a mature proportion of 55% by 8 to 9 months of age.5,6 Diaphragmatic function may be significantly compromised by raised intra-abdominal pressure, such as from gastric distension, hepatic congestion, and ascites.
The tidal volume of full-term neonates is between 6 to 8 mL/kg and, because of the mechanical limitations just mentioned, minute ventilation is respiratory-rate dependent. The resting respiratory rate of the newborn infant is between 30 and 40 breaths per minute, which provides the optimal alveolar ventilation to overcome the work of breathing and match the compliance and resistance of the respiratory system. When the work of breathing increases, such as with parenchymal lung disease, airway obstruction, cardiac failure, or increased pulmonary blood flow, a larger proportion of total energy expenditure is required to maintain adequate ventilation. Infants therefore fatigue readily and fail to thrive.
The neonate has a reduced functional residual capacity (FRC) secondary to an increased chest wall compliance (FRC being determined by the balance between chest wall and lung compliance). Closing capacity is also increased in newborns, with airway closure occurring during normal tidal ventilation.7 Oxygen reserve is therefore reduced, and in conjunction with an increased basal metabolic rate and oxygen consumption two to three times adult levels, neonates and infants are at risk for hypoxemia. However, atelectasis and hypoxemia do not occur in the normal neonate because FRC is maintained by dynamic factors, including tachypnea, breath stacking (early inspiration), expiratory breaking (expiratory flow interrupted before zero flow occurs), and laryngeal breaking (auto–positive end-expiratory pressure [PEEP]).
Organ immaturity of the liver and kidney may be associated with reduced protein synthesis and glomerular filtration, such that drug metabolism is altered and synthetic function is reduced. These problems may be compounded by the normally increased total body water of the neonate compared with the older patient, along with the propensity of the neonatal capillary system to leak fluid out of the intravascular space.8 This is especially pronounced in the neonatal lung, in which the pulmonary vascular bed is almost fully recruited at rest and the lymphatic recruitment required to handle increased mean capillary pressures associated with increases in pulmonary blood flow may be unavailable.9
The caloric requirement for neonates, especially preterm neonates, is high (100 to 150 kcal/kg/24 hr) because of metabolic demand. The task of supplying nutrition for growth becomes even more difficult when necessary limits are placed on the total amount of fluid that may be administrated either parentally or by the enteral route. Hyperosmolar feedings have been associated with an increased risk for necrotizing enterocolitis (NEC) in the preterm neonate, or to the neonate born at term who has decreased splanchnic blood flow of any cause (e.g., left-sided obstructive lesions).10
Specific classification of congenital heart defects is difficult because of the complex nature of many lesions. Basing identification and classification on physiology brings an organized framework to the intraoperative anesthetic management and postoperative care of children with complex CHD.
Intra-atrial mixing of pulmonary and systemic venous return is essential for maintenance of cardiac output in patients with defects such as right or left atrioventricular valve atresia (e.g., tricuspid atresia or hypoplastic left heart syndrome), and in those with an anatomically parallel pulmonary and systemic circulation, such as D-transposition of the great vessels. If complete mixing occurs, the systemic arterial oxygen saturation (SaO2) should be approximately 85% in room air, although this is highly variable depending on the amount of pulmonary blood flow. Inadequate mixing across a restrictive atrial septal defect (ASD) can cause significant desaturation secondary to reduced pulmonary blood flow or pulmonary edema from pulmonary venous hypertension. The septal defect can be enlarged by catheter balloon septostomy or balloon dilation, or surgically by atrial septectomy.
Shunts causing an increase in pulmonary blood flow may be simple or complex, occurring between the ventricles, atria, or great arteries, and they are described by the ratio of pulmonary blood flow (Qp) to systemic blood flow (Qs), or Qp/Qs. Patients may be acyanotic or cyanotic, have one or two ventricles, or have a single outflow trunk, yet have a significant increase in Qp/Qs and be at risk for congestive heart failure (CHF) and pulmonary hypertension (Table 111-1).
|Type of Shunt||Acyanotic||Cyanotic|
|Aortopulmonary (AP) connection||PA/MAPCA|
ASD, atrial septal defect; BT, Blalock-Taussig; CAVC, complete atrioventricular canal; D-TGA, D-transposition of the great arteries; DORV, double-outlet right ventricle; HLHS, hypoplastic left heart syndrome; MA, mitral atresia; MAPCA, multiple aortopulmonary collateral arteries; PA, pulmonary atresia; PDA, patent ductus arteriosus; TA, tricuspid atresia; VSD, ventricular septal defect.
In patients with large left-to-right shunts and low pulmonary vascular resistance, a substantial increase in pulmonary blood flow can occur. If the increase in pulmonary blood flow and pressure continues, structural changes occur in the pulmonary vasculature, until eventually pulmonary vascular resistance (PVR) becomes persistently elevated.11,12 The time course for developing pulmonary vascular obstructive disease depends on the amount of shunting, but changes with some lesions may be evident by 4 to 6 months of age. The progression is more rapid when both the volume and pressure load to the pulmonary circulation is increased, such as with a large VSD. As PVR decreases in the first few months after birth, and the hematocrit falls to its lowest physiologic value, the increased left-to-right shunt, and therefore volume load on the systemic ventricle, can lead to congestive cardiac failure and failure to thrive.
The end-diastolic volume is increased in patients with an increased Qp/Qs ratio, but the time course over which irreversible ventricular dysfunction develops is variable. Generally, if surgical intervention to correct the volume overload is undertaken within the first 2 years of life, residual dysfunction is uncommon.13
The volume load on the systemic ventricle and increased end-diastolic pressure contribute to increased lung water and pulmonary edema by increasing pulmonary venous and lymphatic pressures. Compliance of the lung is therefore decreased, and airway resistance increased secondary to small airway compression by distended vessels.14–16 Lungs may feel stiff on hand ventilation and deflate slowly. Besides cardiomegaly on the chest radiograph, the lung fields are usually hyperinflated. Ventilation-perfusion mismatch contributes to an increased alveolar–arterial oxygen gradient, and dead-space ventilation.17 Minute ventilation is therefore increased, primarily by an increase in respiratory rate. Pulmonary artery and left atrial enlargement may compress main-stem bronchi, causing lobar collapse. Symptoms and signs of CHF to note in neonates and infants are shown in Box 111-1.
Manipulating PVR is an important means of limiting pulmonary blood flow and pressure. During anesthesia, PVR can be maintained or increased by using a low fraction of inspired oxygen (FiO2) and altering ventilation to achieve a normal pH and PaCO2.18 Care must be taken at induction of anesthesia, as patients may have a diminished contractile reserve. Preload, contractility, and heart rate must be maintained; afterload reduction is often well tolerated and will reduce pulmonary flow and myocardial work.
In complex shunts, there is additional pulmonary or systemic outflow obstruction, and the Qp/Qs is determined by the size of the orifice, the outflow gradient, and the resistance across the pulmonary or systemic vascular bed. The obstruction may be fixed as with valvular stenosis, or dynamic as in forms of tetralogy of Fallot (TOF).
Severe outflow obstruction in the newborn may be associated with ventricular hypertrophy and vessel hypoplasia distal to the level of obstruction. The increased pressure load may cause ventricular failure, with mixing or shunting at the atrial or ventricular level (or both) necessary to maintain cardiac output if there is complete outflow obstruction. Maintenance of preload, afterload, and normal sinus rhythm is important to prevent a fall in cardiac output or coronary hypoperfusion. As the time to develop significant ventricular dysfunction is longer in patients with a chronic pressure load than in those with a chronic volume load, symptoms of CHF are uncommon unless the obstruction is severe and prolonged.
Pulmonary hypertension may be idiopathic or secondary to increased pulmonary artery flow and pressure or pulmonary venous obstruction. Factors that increase PVR and pulmonary pressures include light anesthesia with a poorly attenuated stress response, hypoxemia, hypoventilation with a fall in FRC and respiratory acidosis, metabolic acidosis, hypothermia, prolonged bypass with associated inflammatory response and capillary leak, and administration of protamine or blood products (e.g., platelets) (Box 111-2).
After repair of defects with large left-to-right shunts, pulmonary artery pressures may remain elevated immediately after bypass, as the pulmonary arteries initially remain reactive to factors that increase PVR. While the patient is on bypass, factors contributing to this include compression and atelectasis of the lung, and pulmonary edema from inadequate venting of the left atrium or from the humoral and cellular response to bypass. Attenuation of the stress response with deep anesthesia using high-dose narcotics will prevent increases in PVR.19 A high FiO2 and hyperventilation to induce a respiratory alkalosis will reduce PVR, and boluses of bicarbonate may be necessary to maintain metabolic alkalosis.20–22 Ideally, the pH should be around 7.45 to 7.50 and the arterial CO2, 30 to 35 mm Hg. A strategy of hyperventilation to induce a respiratory alkalosis and lower PVR may have an adverse effect on central nervous system recovery by lowering cerebral blood flow. The pattern of ventilation and maintenance of lung volumes is important: atelectasis and decreases in lung compliance may cause a significant rise in PVR and pulmonary pressures. Changes in ventilation must be cautiously made and frequently reassessed.
Several intravenous vasodilators, including the nitric oxide (NO) donors nitroprusside and glycerol trinitrate, the phosphodiesterase (PDE) inhibitors amrinone and milrinone, the eicosanoids prostaglandin E1 and prostaglandin I2,23 tolazoline, and isoproterenol have been used to treat postoperative patients with elevated PVR.24,25 The chief limitation of these pharmacologic agents is that their vasodilatory effects are not specific to the pulmonary vasculature, so vasodilation of the systemic vasculature and systemic hypotension may accompany reduction of pulmonary hypertension.
Inhaled NO selectively dilates smooth muscle cells in small pulmonary vessels, and lowers PVR.26 The selective effect of inhaled NO on the pulmonary vasculature is a result of the rapid uptake and inactivation by hemoglobin as NO diffuses from alveoli to the lumen of lung capillaries. The usefulness of inhaled NO for congenital heart disease patients with pulmonary hypertension has been documented in several populations.27,28 After surgery, NO has been shown to reduce pulmonary artery pressure and PVR in patients with pulmonary venous obstruction, such as total anomalous pulmonary venous connection and mitral stenosis, to a lesser extent in patients with a large preexisting left-to-right shunt, and in those with cavopulmonary connections (Fontan physiology)29 or pulmonary hypertensive crises related to cardiopulmonary bypass (CPB). NO has also improved both pulmonary hypertension and impaired gas exchange in patients who have undergone lung transplantation. Patients with a variety of other pulmonary vascular or parenchymal diseases, including persistent pulmonary hypertension of the newborn,30–32 primary pulmonary hypertension, acute respiratory distress syndrome,33 and acute chest syndrome in sickle cell disease34 have also shown significant improvements in oxygenation from treatment with inhaled NO.
Recent therapeutic advances have significantly improved the prognosis for patients with pulmonary arterial hypertension.23,35,36 The role of newer pulmonary vasodilating drugs such as the PDE type V inhibitor sildenafil, and endothelin I blocking drugs, such as bosentan, have shown encouraging results.37–39 The value of these drugs in children with CHD is yet to be established.
Patients with complex defects require frequent evaluation and often repeat cardiac operations as a staged approach to surgical repair. Previous anesthetic, bypass, or surgical problems should be noted. In general, providing continuity of care in these patients, such as by a dedicated cardiac anesthesia service, is useful to ensure consistent management practices, and it enhances the long-term relationship with patients and families.
Failure to thrive is an important indicator of cardiopulmonary compromise. Symptoms as described in Box 111-1 should be noted. Murmurs and extra heart sounds may be difficult to interpret if tachycardic, but a palpable thrill usually indicates a significant murmur. In older children, failure to thrive, lethargy, and poor exercise tolerance are significant symptoms. Orthopnea, syncope, and palpitations may also be described. Recurrent respiratory infections and wheezing are common in patients with left-to-right shunts. Four-limb blood pressures should be compared, and room air baseline peripheral arterial saturations should be noted along with potential airway problems. The chest radiograph should be analyzed for cardiomegaly, pulmonary congestion, airway compression, and atelectasis. Echocardiographic assessment and cardiac catheterization results provide valuable information about anatomic structure, myocardial function, intracardiac pressures, shunting, and gradients across obstructions. They should be interpreted in conjunction with the cardiologist and surgeon. Patients with cardiac failure are often stabilized on digoxin, diuretics, and oral vasodilators such as captopril. Preoperative digoxin levels and hypokalemia must be checked.
The consequences of chronic hypoxemia also need special consideration. Polycythemia increases oxygen-carrying capacity, but when the hematocrit rises to greater than 65%, the increased blood viscosity causes stasis and potential thrombosis, and it exacerbates tissue hypoxia. Dehydration must be avoided, and intravenous (IV) maintenance fluids should be begun while the patient is fasting preoperatively. Bleeding disturbances, common in cyanotic patients,40 may result from thrombocytopenia, defective platelet aggregation, or clotting factor abnormalities.
The monitoring technique used for a patient should depend on the child’s condition and the magnitude of the planned procedure. For elective patients, noninvasive monitoring (electrocardiography, pulse oximetry, capnography, and a noninvasive blood pressure cuff) is placed before induction of anesthesia.
Monitoring by electrocardiogram (ECG) is essential, as significant rhythm disturbances may occur before and after bypass, particularly with VSD and outflow tract surgery. Myocardial ischemia occurs in pediatric patients mostly because of anatomic and shunt-related problems rather than coronary occlusive disease. Anomalous coronary arteries are associated with a number of complex defects such as transposition of the great vessels and pulmonary atresia. Ischemia also occurs when coronary perfusion pressure falls, such as in hypoplastic left heart syndrome, truncus arteriosus, and critical aortic stenosis. Ventricular fibrillation may occur in these settings,41 particularly on induction of anesthesia. Ischemia after bypass may result from air embolism or complications related to surgery, such as coronary reimplantation or coronary compression from conduits.
Pulse oximetry is an important monitor before and after bypass, as peripheral arterial saturation levels provide an indicator of pulmonary blood flow. The anesthesiologist needs to know the patient’s baseline, pre-bypass peripheral O2 saturation (SpO2) and the anticipated level after surgery. Causes for lower than expected SpO2, in patients with single-ventricle physiology, include pulmonary venous desaturation and intrapulmonary shunt, reduced pulmonary blood flow, and low cardiac output. For patients who have undergone a two-ventricle repair, a lower than expected SpO2 is usually secondary to intrapulmonary shunting, either because of parenchymal lung disease (e.g., atelectasis or edema) or restrictive pulmonary defects (e.g., pleural effusion or pneumothorax). After repair of a neonatal right ventricular outflow tract, such as tetralogy of Fallot or truncus arteriosus, a small atrial communication is an advantage as it provides a right-to-left atrial shunt. Although these patients may be cyanotic immediately after surgery, the right-to-left shunt will decrease and the SpO2 will rise as the compliance of the right ventricle improves.
Once the patient is anesthetized, a direct arterial line is placed percutaneously or via a cutdown. The site of the arterial line placement needs careful consideration. For example, patients undergoing placement of a modified Blalock-Taussig shunt from the subclavian or innominate artery should have the radial arterial line placed in the opposite extremity. Similarly, a right radial arterial line is necessary when repair of coarctation of the aorta is planned. The arch anatomy and possible aberrant arterial vessels are additional considerations when planning arterial access. Aortic root pressure monitoring may be necessary immediately after bypass if the peripheral arterial pressure is damped from hypothermia or low output state. Alternatively, a femoral artery catheter may provide a more reliable arterial waveform after CPB, particularly in newborns and infants, and is often preferable to a peripheral arterial catheter. Care must be taken to prevent thrombus and distal limb ischemia, and femoral lines are best removed early once the patient is in stable condition. Caution is necessary when flushing arterial catheters in neonates and infants, as retrograde flow into the carotid arteries is possible.42
Some centers routinely use central venous pressure monitoring for all cardiovascular surgery. Percutaneous central venous access enables titration of volume replacement and administration of vasoactive infusions before CPB, and during CPB it may provide a measure of the adequacy of cerebral venous drainage. Insertion of central venous catheters can be particularly difficult in pediatric patients, and central venous lines should be used with caution in neonates and infants because of the risk for infection and superior vena cava thrombosis, which can have significant sequelae if collateral veins are poorly developed. Transthoracic right and left atrial lines can be inserted by the surgeon for hemodynamic pressure monitoring and drug infusions after bypass.43 They have a low complication rate, and they may be left in situ for longer during postoperative recovery and are easily removed in the intensive care unit (ICU). Swan-Ganz catheters are rarely used in pediatric cardiac surgery because of anatomic limitations. Direct pulmonary artery catheters can be inserted by the surgeon to measure pulmonary saturations, to detect residual outflow tract gradients, and for thermodilution measurement of cardiac output.
Ultrasound-guided technique has been shown to increase the overall success rate and reduce the incidence of traumatic complications associated with central venous cannulation.44,45 The anatomy of the central venous drainage should be known before attempting percutaneous cannulation. Heterotaxy syndrome and possible vein occlusions after previous catheterization are considerations, and if in doubt, ultrasound evaluation of the position and size of a central vein before cannulation is useful.
Long-term neurodevelopmental impairment is common in newborns and infants undergoing repair for complex CHD. The etiologies of adverse neurologic sequelae in these patients are multifactorial and include prenatal, preoperative, intraoperative, and postoperative factors. Cerebral protection is a concern during bypass for congenital heart surgery, particularly if deep hypothermic arrest or low-flow bypass is used, and the importance of routine perioperative monitoring of the brain is increasingly recognized. Tympanic or nasopharyngeal temperature monitoring is used to assess the adequacy of cerebral cooling and rewarming. Continuous electroencephalographic monitoring,46 transcranial Doppler,47 and frontal lobe infrared spectroscopy48–50 or cerebral oximetry can be used to evaluate cerebral blood flow velocity and perfusion, and O2 delivery and extraction.
Intraoperative transesophageal echocardiography (TEE) has achieved a role in intraoperative monitoring of patients undergoing repair of CHD.51–53 The development of smaller probes has allowed transesophageal monitoring to replace epicardial echocardiographic imaging in many cases, and it is now routinely performed. Placement of a transesophageal probe after the induction of anesthesia in the operating room enables reevaluation of the anatomy before surgical intervention, but, more importantly, the adequacy of surgical repair can be evaluated as soon as the patient is weaned from CPB. Interference of the probe with the airway and the effect on unstable hemodynamics before and after CPB must be carefully evaluated to avoid the complications of this monitoring.
The frequency of anesthesia-related cardiac arrests during general pediatric procedures has been reported to be between 1.4 and 4.6 per 10,000 anesthesia events, which is higher than that reported in adults. An American Society of Anesthesiologists (ASA) Physical Status of greater than 3 and younger age are risk factors for cardiac arrest during pediatric anesthesia, and a recent study demonstrated that patients with CHD are also at increased risk for cardiac arrest during cardiac surgery.54 The incidence of anesthesia-related and procedure-related cardiac arrests was highest in neonates, and although it can be difficult to distinguish contributing factors in patients with underlying cardiac disease, there is a possible association between altered coronary perfusion and myocardial ischemia and cardiac arrest. Coronary perfusion may be reduced in patients who have uncontrolled or continuous runoff of blood flow from the systemic to pulmonary circulation and therefore low aortic root diastolic pressure (e.g., patients with a diagnosis of truncus arteriosus, and patients with a ductus-dependent systemic circulation such as hypoplastic left heart syndrome and interruption of the aortic arch or coarctation with VSD). Patients with altered coronary blood flow, such as those with pulmonary atresia, an intact ventricular septum, and a right ventricle–dependent coronary circulation from fistulas, are also at increased risk for ischemia. These patients also have a limited ability to increase coronary blood flow when myocardial oxygen demand is increased, such as occurs secondary to tachycardia, increased contractility, or wall stress in response to a surgical stimulus if there is an inadequate depth of anesthesia to blunt a stress response.19,41,55 The importance of maintaining diastolic pressure and coronary perfusion is also important in the setting of severe left ventricle hypertrophy (e.g., in Williams syndrome and hypertrophic cardiomyopathy).55a
Because of the potential for rapid and dramatic hemodynamic changes in young patients with CHD, especially infants, complete preparation of anesthetic and monitoring equipment and required drugs is essential. Adequate assistance should be immediately available during the induction of anesthesia in case problems develop.
The choice of induction technique is influenced by the response to premedications, the parent–child–anesthesiologist relationship, and the anesthetic management plan. In older patients who have minimal compromise of their cardiac reserve, the choice of induction techniques is large. Inhalation, intravenous, or intramuscular induction of anesthesia can be accomplished provided individual pathophysiologic limitations are understood. Cooperative children with an adequate cardiac reserve and difficult IV access or a morbid fear of needles can have anesthesia induced cautiously with inhaled anesthetics, even if the patients are cyanotic. An inhalation induction with sevoflurane is suitable for most infants and children, provided they have stable ventricular function and adequate hemodynamic reserve. This emphasizes the importance of preoperative evaluation when planning the induction technique. Inhalational induction can be used safely in patients with cyanotic heart disease, although uptake may be slower due to the right-to-left shunt.56 Saturations will generally increase, provided cardiac output is maintained and airway obstruction is avoided.
An IV induction should be used for all patients with severely limited hemodynamic reserve, particularly those with severe ventricular failure or pulmonary hypertension. When hemodynamic instability during induction is likely, starting an inotropic agent such as dobutamine or dopamine prior to induction should be considered. Although the stress of placing an IV line may be considerable for some patients, particularly those with difficult IV access after previous procedures, the IV line is preferable to the potential myocardial depression during an inhalation induction.
A combination of fentanyl (15 to 25 μg/kg) and pancuronium (0.2 mg/kg) provides hemodynamic stability and prompt airway control, and it attenuates the stress-induced increase in PVR associated with intubation. IV ketamine (1 to 3 mg/kg) is safe and reliable, providing hemodynamic stability and minimal increases in PVR. It is particularly useful in patients with severe CHF and ventricular outflow tract obstructions. Atropine (20 μg/kg) or glycopyrrolate (10 μg/kg) is traditionally given concurrently because of increased secretions. If IV access is difficult and stressful in infants, a combination 4 mg/kg of ketamine, 10 μg/kg of glycopyrrolate, and 2 mg/kg of suxamethonium intramuscularly allows prompt induction and airway control.
Etomidate is an anesthetic induction agent with minimal cardiovascular and respiratory depression,57 and it is frequently used to induce anesthesia in patients with limited hemodynamic reserve. An IV dosage of 0.2 to 0.3 mg/kg induces rapid loss of consciousness with a duration of action of 3 to 5 minutes. Etomidate may be used as an alternative to the synthetic opioids for induction of anesthesia in patients with limited myocardial reserve.
Barbiturates and propofol can be used in patients with normal ventricular function, The principal hemodynamic effect of propofol in children with CHD is a decrease in systemic vascular resistance (SVR) and direct myocardial depression. In children with an intracardiac left-to-right shunt, this can result in changes in the Qp/Qs ratio, and it can lead to a low cardiac output state.58 Patients with a right-to-left intracardiac shunt may experience a faster induction and loss of consciousness, and the dosage must be carefully titrated to effect in these circumstances. Titrated dosages are suitable for short procedures such as cardioversion or TEE. Midazolam (0.1 to 0.2 mg/kg) is also a useful adjunct during a narcotic induction, but it may cause hypotension in patients dependent on a high sympathetic drive.