General Principles

The principles underlying anesthetic management of children with congenital heart disease are based on an understanding of each disease process, pathophysiology, and a working knowledge of anesthetic effects and other pharmacologic interventions on a specific patient’s condition. Cardiac and great vessel structural abnormalities may result in shunt, outflow obstruction, regurgitation, common mixing, or a combination of lesions. Interactions between those lesions determine the clinical presentation and anesthetic considerations. Anesthesia and surgery will impact patient physiology, setting the stage for potential cardiovascular instability. Without being overly simplistic, once the defect characteristics, predominant physiology, and impact of surgery and anesthesia are understood, anesthesia for cardiac and noncardiac operations can be competently performed using a physiologic approach ( Table 20.1 ).

Critical to understanding congenital cardiac physiology and anesthesia is the concept of shunting. A shunt is defined as an abnormal connection between two chambers or vessels that allows passage of blood. The direction and magnitude of shunting depends on defect size and pressure gradient between the chambers connected to that defect. Shunting is typically fixed in a restrictive defect, whereas it varies with the relative vascular resistances of the connected structures in a nonrestrictive defect.

Cyanotic patients with right-to-left (R-L) shunt have too little pulmonary blood flow. This makes them less tolerant of airway obstruction or apnea during sedation or anesthesia. Systemic vasodilation may worsen a R-L shunt and cyanosis. R-L shunts slow the rate of inhalation induction by delaying the equilibration of partial pressure of alveolar-to-inspired anesthetic. This delay is more pronounced with the less soluble inhalation agents.

Depending on the type and size of defect, lesions with L-R shunt are generally better tolerated under anesthesia. Nevertheless, depending on location of shunt, increasing L-R shunt by maneuvers that decrease pulmonary vascular resistance (PVR) may lead to some degree of systemic hypotension with reduction of coronary perfusion. Uncorrected L-R shunting and pulmonary overcirculation over the long term may produce changes that increase pulmonary vasculature reactivity, especially when weaning from bypass. The onset of intravenous (IV) anesthetic is slower in L-R shunting, whereas inhalational anesthetic pharmacokinetics remain unchanged.

Right heart obstructive lesions are either dynamic or fixed and may create R-L shunt where pulmonary to systemic defect is present. The degree of cyanosis will depend on the degree of right-sided obstruction, PVR, and systemic vascular resistance (SVR). It is advantageous to avoid systemic vasodilation. Reducing dynamic obstruction (by decreasing contractility) is helpful by reducing R-L shunting and improving cyanosis during anesthesia.

Patients with left heart obstructive lesions have decreased cardiac output and systemic perfusion. Consequently, they can rapidly decompensate with anesthesia and surgical manipulation. For the ductile-dependent left heart obstructive lesions, maintenance of prostaglandin infusion is necessary. An increase in the fraction of inspired oxygen (FiO ₂ ) with concomitant decrease in PVR leads to steal from systemic circulation, which could be detrimental.

Management of regurgitant lesions (e.g., atrial-ventricular canal, Ebstein anomaly) includes reduction of regurgitant fraction by decreasing afterload (PVR for right-sided lesions, SVR for left-sided lesions), improvement in ventricular contractility, and heart rate increase.

Mixing lesions (e.g., single ventricle, total anomalous pulmonary venous return, tricuspid atresia, truncus arteriosus) are characterized by complete mixing of deoxygenated systemic venous blood and fully oxygenated pulmonary venous blood. Balance between systemic and pulmonary vascular resistances determines arterial blood desaturation. In a patient with single-ventricle physiology, PVR and SVR are the key determinants of hemodynamic stability. The desirable ratio of pulmonary blood flow to systemic perfusion (Q _p :Q _s ) of approximately 1 (balanced) leads to an oxygen saturation as measured by pulse oximetry (SpO ₂ ) of approximately 80%. This delicate balance of PVR/SVR will place a patient with single-ventricle physiology at a higher risk of myocardial ischemia during induction of anesthesia and surgical manipulation. Factors affecting the balance of PVR/SVR are listed in Table 20.2 .

The anesthesiologist will work toward hemodynamic goals by manipulating factors affecting cardiac output, systemic and pulmonary flow, and oxygen delivery with consideration of the specific anatomy and physiology as well as factors affecting the arterial O ₂ content, especially the hemoglobin level (see Table 20.1 ). Specific anesthetic strategies will be further discussed later in the chapter.

Physiologic Monitoring

Noninvasive monitors are placed before anesthesia induction. They include a five-lead electrocardiography system (one lead for each extremity and one precordial lead in V ₅ position), two pulse oximetry probes (preductal and postductal), and an appropriately sized blood pressure cuff. A nasopharyngeal temperature probe is inserted after intubation and is most closely reflective of brain temperature. Depending on the child’s condition and planned procedure, additional monitoring is necessary: an indwelling arterial catheter, a central line, and a urinary catheter. A second temperature monitor is added (often rectal to reflect core temperature) when planning to go on bypass.

SpO ₂ and capnography (end-tidal carbon dioxide [ETCO ₂ ]) provide instantaneous feedback concerning adequacy of oxygenation and ventilation. Capnography is of great value and remains the gold standard to confirm tracheal intubation. SpO ₂ and ETCO ₂ direct ventilatory and hemodynamic adjustments to optimize Q _p :Q _s in patients with shunts and pulmonary artery bands. Differences in preductal and postductal SpO ₂ values indicate shunting through a patent ductus arteriosus (PDA). SpO ₂ and ETCO ₂ can also be used to assess the adequacy of cardiac output. Low systemic arterial saturation or inability of the oximeter probe to register a pulse wave may be a sign of a very low cardiac output and high systemic resistances. SpO ₂ values less than 80% often overestimate arterial oxygen saturation, which make other means of tissue oxygenation measurement necessary.

Near-infrared spectroscopy (NIRS) measures regional oxygen saturation. Whereas the oxygen saturation displayed by the pulse oximeter represents only the pulsatile component of light transmitted to tissues, signal received by the NIRS represents the nonpulsatile blood (75%) as well as pulsatile blood (20%). Normal range of regional cerebral oxygen saturation (cerebral rSO ₂ ) for a noncyanotic patient is 60% to 85%. The somatic rSO ₂ is generally 10% higher than the cerebral. Any fall of rSO ₂ 20% or more below the baseline obtained before induction warrants interventions aimed at improving oxygen delivery and/or decreasing oxygen consumption to restore rSO ₂ ( Table 20.3 ). Numerous studies have indicated good correlation between rSO ₂ and central venous oxygen saturation (SvO ₂ ).

Continuous monitoring of arterial pressure is possible only through an indwelling intraarterial catheter. Previous procedures or currently planned procedure, such as radial artery cut-down, Blalock-Taussig shunt, or a subclavian flap for coarctation of the aorta repair, can impact the arterial pressure monitoring site. Other sites available for cannulation include ulnar, femoral, axillary, or umbilical arteries. Posterior tibial or the dorsalis pedis arterial catheters function poorly after CPB and do not reflect central aortic pressure when the temperature of the distal extremities remains low. The optimal position of the umbilical artery catheter tip is just above the aortic bifurcation between L3 and L4 or preferably, high above the diaphragm between T6 and T9. To decrease the risk of thrombosis of the renal and mesenteric arteries, the tip should not be left in the area of T12 to L2.

Major cardiovascular surgeries require some type of central venous pressure (CVP) monitoring. The CVP catheter is also used for administration of fluid, drugs, and blood products. Alternatively, directly placed transthoracic atrial lines may be used to deliver medications and to evaluate filling pressures during the separation from CPB and the postoperative period. Most often the right internal jugular is accessed. The left internal jugular is avoided in case of persistent left superior vena cava. Other percutaneous options include cannulation of subclavian, femoral, external jugular, or axillary veins. The use of real-time ultrasound guidance reduces the time and number of needle insertions required for successful venous cannulation and decreases the rate of complication compared to the use of anatomic landmarks. The greatest benefit was found for internal jugular cannulation. In case of preexisting peripherally inserted central catheters anesthesiologists should ascertain that the catheter is at least 3 French for rapid fluid and blood infusion, and that the tip is positioned centrally for infusion of vasoactive agents. For patients with single-ventricle physiology, superior vena cava thrombosis could be catastrophic, and femoral or atrial lines are sometimes the preferred options.

Another reliable source of central venous access is the umbilical vein. It is cannulated within the first week after birth. To use it as a central line, the optimal position of the tip should be in the right atrium or high in the inferior vena cava.

The utility of intraoperative echocardiographic assessment with Doppler color flow imaging in predicting outcome after repair of congenital heart defect was first demonstrated in 1989 by Ungerleider and associates, using an epicardial echocardiography probe. Since then, many authors have published strong evidence supporting transesophageal echocardiography (TEE) use for all cardiac defects requiring repair under CPB. Advances in probe technology make multiplane TEE use routine to confirm or revise the initial diagnosis and assess the heart function during the prebypass period, even in small neonates. In the postbypass period, TEE assesses repair adequacy, presence of residual defects, and ventricular filling and function. Bettex et al., in a series of 865 intraoperative TEE examinations for congenital heart defect surgeries, found that alteration in surgical management occurred in 12.7% of cases, including 7.3% repeat bypass run; alteration in medical management occurred in 19.4% of cases. The occurrence of airway compression or hemodynamic instability after insertion should prompt the removal of the TEE probe; using an intraoperative epicardial probe should be considered instead.

Preoperative Medication

For infants less than 6 month of age, no premedication is necessary. Children older than 9 months may require a dose of midazolam given orally 0.3 to 0.7 mg/kg to a maximum of 20 mg, 10 to 20 minutes before induction, to provide effective anxiolysis. If an IV access is available, then midazolam 0.05 mg/kg up to 4 mg may be given a few minutes before operating room transfer. On occasion, a child or adult with developmental delay and without IV access is given ketamine 4 to 5 mg/kg with glycopyrrolate 20 mcg/kg and midazolam 0.1 mg/kg via the intramuscular route; oral ketamine (5 mg/kg) and midazolam (0.5 mg/kg) is also an option for an older child with developmental delay or a patient who requires denser preoperative sedation.

Induction and Maintenance of Anesthesia

Although it is important to comprehend the complexities of shunt and vascular resistance changes, airway and ventilation effects on the cardiovascular system are of equal importance during induction and maintenance of anesthesia. Selection of an induction technique depends on the cardiac defect, the degree of cardiac dysfunction, and the level of preinduction sedation. Anesthetic agent titration is more important than specific anesthetic technique in patients with reasonable cardiac reserve. Successful and safe induction is possible with volatile agents such as sevoflurane and nitrous oxide or IV agents such as etomidate, fentanyl, midazolam, and ketamine.

Induction method choices include IV (when an IV catheter is present) and inhalational. Skillful airway management and adequacy of ventilation are essential during induction no matter what induction method is used.

The use of inhalation induction should be reserved for children with reasonable cardiac reserve. Sevoflurane is currently the only halogenated anesthetic used for induction in the United States. Sevoflurane may be combined with up to 50% of nitrous oxide during initial induction to speed induction and decrease patient response to pungent Sevoflurane odor. Sevoflurane increases the heart rate slightly, mildly depresses myocardial contractility, and lowers SVR and PVR. Depression of myocardial contractility and blood pressure with volatile agent use is more pronounced in neonates compared to older children and adults due to the effect of volatile agents on calcium channels in the immature cardiovascular system. Pronounced bradycardia is frequent during sevoflurane induction of patients with trisomy 21 with and without heart defects. Inhalation induction is generally well tolerated by most children, including some with cyanotic defects such as tetralogy of Fallot (TOF).

In situations in which a higher minimum alveolar concentration (MAC) is used during prolonged sevoflurane induction, cardiovascular compromise or collapse can occur, in particular when positive pressure ventilation is applied indiscriminately with excessive depth of anesthesia. Careful titration of anesthetic agent and depth is required.

After anesthetic induction, IV access is established or augmented as appropriate. A nondepolarizing muscle relaxant is usually administered, and an IV opioid and/or inhalation agent is chosen for maintenance of anesthesia. The child is preoxygenated before intubation, and a nasal or oral endotracheal tube is carefully positioned. Some degree of alveolar preoxygenation is recommended, even in an infant whose systemic perfusion might be jeopardized by PVR decrease. This maneuver delays desaturation during intubation. If the child arrives in the operating room with an endotracheal tube in place, it should be changed if the benefit of a new tube outweighs the reintubation risk.

Intravenous induction is preferable when a child arrives with a well-functioning preexisting IV catheter. For neonates and sick children, IV opioid plus relaxant induction is most prevalent. In patients with limited cardiac reserve, inhalation agents are less well tolerated as a primary anesthetic, especially after a CPB. Titrated doses of fentanyl or sufentanil are excellent induction and maintenance anesthetics for this group of patients because these opioids generally have a low impact on hemodynamics. After repair of a congenital heart defect, the hemodynamic effects of fentanyl at a dose of 25 mcg/kg with pancuronium given to infants in the postoperative period show no change in left atrial pressure, PVR, and cardiac index. There is only a small decrease in SVR and mean arterial pressure (MAP). Higher doses of fentanyl at 50 to 75 mcg/kg with pancuronium result in a slightly greater fall in arterial pressure and heart rate. Fentanyl has also been shown to block stimulus-induced pulmonary vasoconstriction and contributes to pulmonary circulation stability in neonatal congenital diaphragmatic hernia repair. Thus fentanyl use may be extrapolated post CPB in newborns with pulmonary vascular responsiveness. The ultra–short-acting opioid remifentanil has not shown any significant advantage over fentanyl. It is often possible to titrate low-dose inhalational agents with opioids and maintain hemodynamic stability. The combination of fentanyl/midazolam as an alternative to fentanyl/low-dose volatile agents is frequently used for maintenance of anesthesia. But this results in lower cardiac output due to a decrease in heart rate. Despite a widespread safety margin exhibited by opioids, it should be noted that patients with marginally compensated hemodynamic function sustained by endogenous catecholamines may decompensate with higher-dose opioids.

Isoflurane or sevoflurane may be used for maintenance of anesthesia. Inhalation agents can provide both anesthesia and vasodilation when a vaporizer is connected to the circuit during CPB. Some studies have found volatile agents to be neuroprotectors on CPB. Isoflurane and sevoflurane maintain the ratio Q _p :Q _s when the controlled ventilation is adequate.

Dexmedetomidine is a highly selective alpha-2 adrenergic receptor agonist that produces sedation. It is useful as an adjunct to a volatile agent or narcotic-based anesthetic to decrease surgical stress response. The reduction in central sympathetic outflow can lead to bradycardia and hypotension. Dexmedetomidine bolus of 0.5 mcg/kg over 10 minutes, followed by an infusion of 0.5 mcg/kg/h attenuates hemodynamic and neuroendocrine response to surgery and CPB. Dexmedetomidine is associated with a reduction in the incidence of postbypass ventricular and supraventricular tachyarrythmias. Because of its antiarrhythmic effects, it is not an ideal sedative for electrophysiologic studies.

Ketamine used to be popular for anesthetic induction in patients with cyanotic conditions because it increases SVR and diminishes the magnitude of R-L shunting. Administration of ketamine can be IV or intramuscular. Ketamine also increases salivation. It exerts a central nervous system–mediated sympathetic activation and catecholamine release, which makes ketamine an attractive anesthetic for patients with decreased function. However, it is a direct myocardial depressant and should be used with caution in very sick patients with exhausted sympathetic responses.

Another option for induction in hemodynamically unstable patients is etomidate. This imidazole derivative does not change the hemodynamic parameters at clinical doses. Etomidate has the undesirable effect of possible adrenal suppression, particularly when repeated doses are used.

Cardiopulmonary Bypass

For cardiac anesthesiologists, CPB is not a passive time. It can test the quality of interteam communication, even during a routine case. This is especially true when monitors or laboratory test results show anomalies (e.g., decreased cerebral and/or somatic NIRS, abnormal arterial blood gas values, worsening of lactic acidosis, elevated central venous pressure) and when problems occur as a result of poor myocardial protection or residual defects. Good communication is essential during separation from CPB and the decision-making process regarding mechanical circulatory support when things do not go according to plan (e.g., native cardiac output not sufficient to terminate CPB, difficult to control arrhythmia).

The major advances in pediatric CPB are improved circuitry, technology, and management strategies to reduce systemic inflammatory response and improve organ protection. Oxygenators specifically designed for neonates were developed and combined with an integrated arterial filter. There has been a wider adoption of mast-mounted pumps that are closer to the patient to shorten the length of the tubing line. These improvements provided significant reduction in prime volume and foreign surface area.

Hemodilution

Hemodilution to a hematocrit value of 24% or higher is associated with reduced lactate levels and better neurologic outcomes. Hemodilution to a hematocrit value of 25% versus a value of 35% during hypothermic CPB in infant surgery for two-ventricle repair shows no difference in hemodynamics during the procedure.

Temperature

The three ranges of hypothermia used are mild (30°C to 35°C), moderate (22°C to 30°C), and deep (<22°C). No proven benefit has been associated with normothermic CPB. Hypothermic CPB is used to preserve organ function during cardiac surgery. The scientific rationale for the use of hypothermia rests primarily on temperature-mediated reduction of metabolism. Whole body oxygen consumption metabolic rate, including cerebral, decreases by a factor of 2 to 2.5 for every 10°C reduction. Hypothermia significantly decreases excitatory amino acids release, suggesting an additional mechanism for protective effect.

Deep hypothermia is generally reserved for neonates, infants, and children requiring complex cardiac repair. Deep hypothermic circulatory arrest (DHCA) allows removal of atrial and/or aortic cannula. Using this technique increases precision and ease of surgical repair through a bloodless and cannula-free operative field. Duration of DHCA should be under 41 minutes to reduce permanent neurologic damage, according to the Boston Circulatory Arrest Trial. During DHCA it is recommended to cool evenly and slowly over at least 20 minutes to reduce risk of neurologic injury. The head must be covered with ice packs to avoid brain rewarming during DHCA.

Antegrade Cerebral Perfusion

Also known as regional cerebral perfusion, antegrade cerebral perfusion (ACP) may be used in lieu of DHCA. An arterial cannula flows into the innominate artery after direct insertion or via a prosthetic graft. Only the brain is actively perfused. To prevent the risk of cerebral hypoperfusion and hypoxemia, an ACP flow rate of at least 40 mL/kg/min is necessary for adequate flow to reach the left hemisphere via the circle of Willis. Furthermore, ACP times are frequently longer than DHCA, so adequate cerebral flow, deep hypothermia, and monitoring of NIRS are essential for brain protection.

pH-Stat Strategy

pH-stat blood gas management is preferred for deep hypothermic CPB, particularly during cooling. Hypothermia-induced alkalosis is corrected by adding CO ₂ to the circuit or by reducing CO ₂ removal. This strategy provides cerebral vasodilation and a more even cerebral cooling. Review of published data suggests better neurodevelopmental outcomes for pH-stat compared to alpha-stat management in pediatric cardiac surgery and possibly a reduction in intensive care unit (ICU) stay.

Perfusion Flow

Full bypass perfusion flow rate for a 2- to 7-kg patient is 120 to 200 mL/kg/min. For patients above 20 kg, it is 50 to 75 mL/kg/min. Monitors of adequate CPB flow include MAP, SVO ₂ , NIRS, lactate, and acid-base status. Vasodilators such as phentolamine, nitroprusside, or nitroglycerine may be used during hypothermic bypass to promote even organ perfusion, prevent hypertension on bypass, improve oxygen delivery, minimize acidosis, and improve patient outcome. During separation from bypass, excessive vasodilation may be reversed with low-dose vasopressin infusion if necessary.

Discontinuation of Cardiopulmonary Bypass

When weaning from CPB, blood volume is assessed by direct cardiac visualization and monitoring right and/or left atrial filling pressures. When filling pressures are adequate, patient fully warm, acid-base status normalized, and heart rate adequate and in sinus rhythm, CPB venous drainage is decreased, and the patient is weaned from bypass. The arterial cannula is temporarily left in place so that infusion of residual pump blood can be used to optimize filling pressures. Myocardial function is assessed by direct cardiac visualization, left and/or right atrial pressures, percutaneous jugular venous pressure, or echocardiography. After complex congenital heart defect repair the anesthesiologist and surgeon may have difficulty separating a patient from CPB. Under these circumstances the differential diagnosis may include an inadequate surgical result with a residual defect, pulmonary artery hypertension, right or left ventricular dysfunction, arrhythmia, bleeding, or any of these combined. TEE may be used to provide an intraoperative image of structural or functional abnormalities and to assist in the evaluation of the postoperative cardiac repair. Strategies will involve identification and correction of reason for failure to wean, including consideration of return to hypothermia and repair of residual defect. Leaving the operating room with a significant residual structural defect adversely affects survival and increases patient morbidity.

If the patient is unable to come off bypass due to early postoperative cardiac failure and has severe metabolic acidosis and high inotropic and/or pressor requirement, postoperative mechanical support with extracorporeal membrane oxygenation (ECMO) may be considered. Typically the same aortic and right atrial cannulae are used for conversion from bypass to ECMO.

Ultrafiltration

Conventional ultrafiltration or modified ultrafiltration (MUF) is used to remove excess total body water and reduce proinflammatory factors in almost all pediatric cardiac surgical centers in the United States. Conventional ultrafiltration is performed during bypass, whereas MUF is performed for 10 to 15 minutes after the discontinuation of bypass ( Figs. 20.1 and 20.2 ). MUF filters the patient’s blood volume and improves hemodynamic and pulmonary performance. After the patient is weaned from CPB, blood is removed from the patient via aortic cannula, fed through an ultrafilter, and then returned via venous cannula to the right atrium. A constant left or right atrial pressure is maintained for hemodynamic stability. Ultrafiltration is carried out with end points being either time of 15 to 20 minutes or hematocrit value of approximately 40%.

Conventional ultrafiltration throughout cardiopulmonary bypass.

After the patient is weaned from bypass, the circuit tubing is clamped at A to perform arteriovenous modified ultrafiltration. Blood from the venous reservoir can undergo ultrafiltration and be transfused as needed.

Anticoagulation and Hemostasis

CPB is a significant thrombogenic stimulus, requiring anticoagulation with heparin. The effect of heparin is followed by activated clotting time (ACT) monitoring. The effect of heparin is primarily due to antithrombin III coupling; because there are age-related and quantitative differences in procoagulants and inhibitors, heparin dosing may be variable. Maintaining an ACT above 400 seconds is recommended. Heparin is neutralized by protamine after CPB and MUF, but protamine excess may actually contribute to postoperative bleeding.

Bleeding after CPB is not an unusual occurrence. Neonates and young infants with congenital heart disease have low circulating levels of procoagulants and inhibitors. Thrombogenic and dilutional effects of CPB further contribute to hemostatic abnormalities. Furthermore, DHCA causes increased clotting and fibrinolytic activities. There are pharmacologic interventions aimed at reducing bleeding after CPB. Desmopressin acetate and antifibrinolytics aminocaproic acid or tranexamic acid have been tried with variable success. However, the most impressive results have been demonstrated with the use of aprotinin. It is a proteinase inhibitor with antifibrinolytic properties at low concentrations and a kallikrein inhibitor at higher levels. Aprotinin is not available in the United States at the time of this writing due to studies associating it with renal failure in adults.

When postoperative bleeding occurs, the surgeon should first attempt to identify any source of surgical bleeding. Next, adequate protamine reversal of heparin is assessed by ACT and laboratory evaluation. In general, standard coagulation tests show prolongation of prothrombin time, partial thromboplastin time, hypofibrinogenemia, and dilution of other procoagulants, as well as prolonged bleeding time in patients with and without bleeding. The most common reason for persistent bleeding is platelet dysfunction. Administration of platelets is warranted in those bleeding situations. Routine administration of blood products to correct laboratory coagulation abnormalities in the absence of bleeding is not indicated. If bleeding persists after platelets have been given, reassessment and a repeat of platelet infusion or cryoprecipitate administration may be beneficial, whereas fresh frozen plasma has not been found to be effective. When facing persistent bleeding despite repeated previously described interventions, recombinant activated factor VII may be used as a last resort.

Patient Transport and Handover to Intensive Care Unit

After surgery, when the patient is deemed stable for transport, report should be given to the ICU staff before departing from the operating room. All transport equipment is checked beforehand to confirm proper functioning. The patient is carefully transferred to the transport bed. The trip to the ICU requires full, continuous monitoring without any interruption of vasoactive medication infusion. The patient is manually ventilated at the appropriate FiO ₂ . If there is pulmonary hypertension that requires the use of nitric oxide post bypass, nitric oxide should not be interrupted during transport.

The complex nature of pediatric cardiac defects and procedures necessitates a structured and efficient handover process to ensure patient safety and continuity of care ( Box 20.1 , Fig. 20.3 ). A systematic review by Segall et al. offers the following recommendations: “(1) standardize processes (e.g., using checklists and protocols); (2) complete urgent clinical tasks before information transfer; (3) allow only patient-specific discussions during verbal handovers; (4) require that all relevant team members be present; and (5) provide training in team skills and communication.” It is imperative that each institution develops a handover process tailored to its setting. The sequence of events during a routine cardiac surgery done under CPB is listed in Box 20.2 .

Pediatric Heart Center Handoff Tool.

(Courtesy Jenny Montgomery, RN MSN CPNP-AC, Driscoll Children’s Hospital, Corpus Christi, TX.)

Anesthesia for Simple Open-Heart Procedures

“Simple” open-heart procedures include those defects that involve relatively straightforward surgical repair, uncomplicated hemodynamics, minimal to moderate postoperative intensive care, and mechanical ventilation or no mechanical ventilation. Simple is a relative term. A case that may be classified as simple may unexpectedly become more complicated ( Table 20.4 , Box 20.3 ). Examples of simple open-heart procedures include repairs of atrial septal defect (ASD), ventricular septal defect (VSD), TOF, and atrioventricular (AV) canal defect in otherwise healthy children with good cardiopulmonary reserve. ASD closure is often performed in the cardiac catheterization laboratory, so it is less often repaired surgically. Patients may present with a range of symptoms from no medical management, minimal management with afterload reduction or diuretic, to congestive heart failure with minimal reserve. The latter will require a different level of care, despite the relatively simple surgical procedure.

TABLE 20.4

Risk Stratification for Patients With Congenital Heart Disease

Cardiac Lesion	Low Risk	Moderate Risk	High Risk
Structural lesions	• Repaired atrial or ventricular septal defect (ASD, VSD) • Mild valvular stenosis or regurgitation	• Simple unrepaired lesions such as ASD or VSD • Fully repaired complex cardiac lesions • Single ventricle with Glenn or Fontan palliation	• Unrepaired complex cardiac lesions • Systemic arterial to pulmonary arterial shunts • Severe valvular disease
Pulmonary hypertension		• New York Heart Association functional class I • Normal cardiac index	• New York Heart Association functional class III or IV • Pulmonary artery pressures equal or higher than systemic pressures • Decreased cardiac index
Miscellaneous		• Post heart transplant	• Severe heart failure • Ventricular assist devices • Williams syndrome • Hypertrophic obstructive cardiomyopathy

Only gold members can continue reading. Log In or Register to continue

Share this:

• Click to share on Twitter (Opens in new window)
• Click to share on Facebook (Opens in new window)

Related

Related posts:

1. Organ System Response to Cardiac Function—Neurology
2. Cardiovascular Physiology for Intensivists
3. Ventricular Septal Defects
4. Palliative Procedures: Deciding on Clinical Pathway; One Versus Two Ventricles

Stay updated, free articles. Join our Telegram channel

Join