General care . Successful postoperative management requires accurate monitoring and documentation of the patient’s vital signs, medication administration, and laboratory results. Vital signs including heart rate, arterial or noninvasive blood pressure (BP), oxygen saturation, and respiratory rate are monitored closely (e.g., every 15 to 60 min). Urine and chest tube outputs, end-tidal or transcutaneous CO ₂ , central venous pressure, and, at times, right and left atrial and pulmonary arterial pressures are recorded meticulously. All administered medications, enteral or parenteral fluids, and blood products are documented. Fluid balance is monitored continuously. Laboratory results and their trends are charted for review electronically.

Pulmonary system

• a.
  

  Arterial blood gases are in the acceptable normal range.

  
  
• b.
  

  Chest radiography shows no evidence of pneumothorax, atelectasis, pleural effusion, or elevation of hemidiaphragm.

Cardiovascular system

• a.
  

  Warm skin, full peripheral pulses with brisk capillary refill, normal BP, and an adequate urine output (at least 1 mL/kg/hr) are clinical evidence of good cardiac output. Decrease in expected systemic venous saturation is a sensitive predictor of low cardiac output. A normal systemic arterial-to-venous oxygen saturation difference of less than 30% is indicative of good cardiac output.

  
  
• b.
  

  Mild arterial hypertension is present in the early postoperative period following CPB (due to increased levels of catecholamines, plasma renin, or angiotensin II).

  
  
• c.
  

  Cardiac rhythm should be sinus and the heart rate relatively high. Ranges of heart rates in normally convalescing postoperative patients are shown in Table 28.1 .

  
  
  
  

  Table 28.1

  
  

  Heart Rate Ranges in Normally Convalescing Postoperative Patients

  
  

  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  

  Age	Heart rate (beats/min)
  Less than 6 months	110 to 190
  6 to 12 months	100 to 170
  1 to 3 years	90 to 160
  Over 3 years	80 to 150

   
  
  

Renal system . Adequate urine output (i.e., >1 mL/kg/hr) and evidence of adequate solute excretion (e.g., serum K ⁺ <5 mEq/L; BUN <40 mg/dL; creatinine <1 mg/dL) are signs of normal renal function.

Metabolic system

• a.
  

  Retention of water and sodium and depletion of whole-body potassium are commonly seen following open heart surgeries. They result in mild hyponatremia and hypokalemia, and a 5% weight gain. In anticipation of fluid overload, mechanical ultrafiltration is performed in selected cases intraoperatively.

  
  
• b.
  

  Mild metabolic acidosis (with a base deficit of −4 mEq/L) associated with mild lactic acidemia is common in the first few hours after CPB and does not usually require treatment.

  
  
• c.
  

  Varying degrees of fever are nearly always present during the first few days, and extensive workup for infection is not indicated. Causes of fever include reaction to CPB, reaction to allogenic blood, atelectasis, pleural effusion, low cardiac output, infection, and brainstem damage.

Gastrointestinal (GI) system . As the splanchnic circulation receives over 25% of total cardiac output, avoidance of low cardiac output syndrome is the principal strategy to avoid GI dysfunction. Feedings are started after the patient becomes hemodynamically stable and are advanced as tolerated. Daily caloric count and its adjustment are crucial. H ₂ -receptor antagonists (famotidine, 0.25 mg/kg/dose every 12 hours, maximum pediatric dose of 40 mg/day) or protein pump inhibitors (e.g., esomeprazole 0.5–1 mg/kg/dose IV every 24 hours, maximum pediatric dose 20 mg/day) are initiated for gastric protection.

Hematologic system . Results of clotting studies should be normal, and hemoglobin should be at least 9.5 g/dL or higher depending on the patient’s age, cardiac anatomy, and surgical procedure.

Neurologic system . The patient should respond appropriately for the level of sedation without evidence of neurologic defects (e.g., hemiplegia, visual field defects) or seizures. Near-infrared spectroscopy (NIRS) for transcranial cerebral oximetry is a noninvasive method to monitor frontal lobe oxygen metabolism. Cerebral oxygen saturation, measured by NIRS, is a composite of the oxygen saturation in combined cerebral arterial and venous vascular bed (arterial and venous blood flow ratio of ≈25:75, with negligible capillary blood). It is a helpful method to detect cerebral hypoxia during low cardiac output states.

General care

• a.
  

  Fluid replacement: Because of the tendency to retain sodium and water, a minimal amount of dextrose in water without (D ₁₀ W in infants, D ₅ W in children) or with only a small amount of sodium (D ₁₀ {1/4}NS, D ₅ {1/4}NS) is administered for approximately 48 hours after surgery. A modest amount of potassium (e.g., KCl, 4 mEq/100 mL IV fluids) is given on the first day of surgery. Recommended fluid volume in the first 24 hours after open procedures is 50% of maintenance volume with gradual increase over the following postoperative days to 60% and then to 75%.

  
  
• b.
  

  The patient should receive medications for adequate analgesia and sedation. For pain relief fentanyl (IV drip at 1 to 3 μg/kg/hr or 1 to 2 μg/kg/dose IV every 30 to 60 min) or morphine sulfate (IV drip at 0.01 to 0.05 mg/kg/hr or 0.1 to 0.2 mg/kg/dose IV every 2 to 4 hours, maximum dose 15 mg/dose) are commonly used. Sedation is achieved by administration of midazolam (0.05 to 0.15 mg/kg/dose IV every 1 to 2 hours or IV drip at 1 to 2 μg/kg/min) or other benzodiazepams. Another medication used for sedation and/or analgesia includes dexmedetomidine a selective α ₂ -adrenergic receptor agonist with minimal risk of respiratory depression, which is infused continuously at a rate of 0.2 to 1.5 μg/kg/hr after a loading dose of 0.1 to 1 μg/kg IV over 10 min.

Pulmonary system

• a.
  

  Extubated patients should show no signs of respiratory distress (grunting, nasal flaring, and retraction). Good chest expansion and evidence of good air exchange to both lungs should be present. Depending on the hemodynamics or cardiopulmonary pathophysiology, patients may be administered supplemental oxygen via nasal cannula or face mask. Pulmonary physiotherapy (consisting of incentive spirometry, coughing and deep breathing exercise, and chest percussion with postural drainage) is administered as necessary.

  
  
• b.
  

  In intubated patients, chest radiographs are obtained to check the position of chest tubes and central and arterial lines and to check for evidence of pneumothorax, atelectasis, pleural effusion, or main-stem bronchus intubation. Significant degrees of pneumothorax or pleural effusion may require treatment. Widening of the mediastinal shadow suggests accumulation of blood and requires investigation of the function of the mediastinal chest tube.

  
  
• c.
  

  In the first postoperative days, the goal of ventilation is to maintain adequate arterial partial pressure of oxygen (Pa o ₂ ) and mild respiratory alkalosis along with an arterial partial pressure of carbon dioxide (Pa co ₂ ) between 28 and 35 mm Hg (all to decrease PVR). Hyperventilation (Pa co ₂ <28 mm Hg) is corrected by decreasing the ventilator rate, decreasing the tidal volume, and adding dead space (5 to 10 mL at a time) to the airway. Hypoventilation is corrected by the opposite maneuvers. Low Pa o ₂ is corrected by raising the F io ₂ , adding positive-end expiratory pressure (PEEP), or increasing tidal volume. Physiologic PEEP of 3 to 5 cm H ₂ O is used in children. The use of high mean airway pressure or high levels of PEEP may increase PVR and decrease cardiac output; both should be avoided in a patient who has had atrial switch operation (i.e., Senning, Mustard procedure) or cavopulmonary anastomosis (i.e., Glenn or Fontan operation).

  
  
• d.
  

  Tracheal toilet is carried out through the endotracheal tube every 2 hours, or more often if necessary. It consists of instillation of 0.5 to 5 mL of saline solution and suctioning of both main-stem bronchi and bag ventilation for 1 to 2 min with oxygen (F io ₂ 1) immediately before and after suctioning.

  
  
• e.
  

  Extubation is performed as soon as possible, usually in the operating room in children undergoing closed procedures, within 4 to 8 hours after uncomplicated open heart procedures, and the day after complex open procedures. Criteria for extubation include the following:

  
  
  
  
  • (1)
    

    The patient should be awake and alert, and should have a favorable nutritional status.

    
    
  • (2)
    

    The patient should be breathing well, with a satisfactory spontaneous respiratory rate for age and no use of accessory respiratory muscles. Ideally, vital capacity should be more than 15 mL/kg. On minimal ventilatory support (Fi o ₂ no more than 0.4, tidal volume at 8 to 10 mL/kg, and PEEP no more than 5 cm H ₂ O), there should be adequate Pa o ₂ and no evidence of acidosis or hypercapnia.

    
    
  • (3)
    

    The patient should be in a reasonable and stable hemodynamic state (normal BP, adequate cardiac output, no significant arrhythmias). There should be no significant pneumothoraces or pleural effusions. The patient should not have important bleeding and should have minimal chest tube drainage.

    
    
  • (4)
    

    Postextubation laryngeal edema is treated with racemic epinephrine (2.25% solution; 0.125 to 0.5 mL diluted with 3 mL of water or normal saline solution given via nebulizer).

  
  
  
  
• f.
  

  Postoperative pulmonary hypertensive crisis leads to decreased cardiac output and, if untreated, may be fatal. The best strategy is prevention. Measures to prevent pulmonary hypertensive crisis are important for patients who had severe pulmonary arterial hypertension preoperatively. The following are recommended:

  
  
  
  
  • (1)
    

    Adequate analgesia and sedation.

    
    
  • (2)
    

    Paralysis by vecuronium bromide (continuous IV drip at 0.05 to 0.15 mg/kg/hr or intermittent IV infusion of 0.05 to 0.1 mg/kg/dose every 60 min) or pancuronium bromide (continuous IV drip at 0.02 to 0.1 mg/kg/hr or intermittent IV infusion of 0.05 to 0.1 mg/kg/dose every 30 to 60 min).

    
    
  • (3)
    

    Supplemental oxygen.

    
    
  • (4)
    

    Avoidance of hypercapnia.

    
    
  • (5)
    

    Low PEEP.

    
    
  • (6)
    

    Maintaining alkalotic pH.

    
    
  • (7)
    

    Avoidance of deep and vigorous tracheal aspiration.

    
    
  • (8)
    

    Administration of inhaled nitric oxide (selective pulmonary vasodilator) at 5 to 40 ppm (usual range 5 to 20 ppm).

    
    
  • (9)
    

    Intravenous vasodilators (α-adrenergic antagonists, phosphodiesterase inhibitors, nitrovasodilators, and prostaglandins) may be considered. However, it should be noted that essentially all these agents dilate the systemic vasculature as well, leading to systemic hypotension.

  
  

Cardiovascular system . Complete correction of the intracardiac defect and adequate intraoperative myocardial protection generally will result in good cardiac function. Signs of reduced cardiac output, abnormal BPs, abnormal heart rate, and abnormal rhythm should be monitored continually.

• a.
  

  Low cardiac output syndrome (LCOS) is the most serious condition of abnormal convalescence. Signs of LCOS include systemic vasoconstriction (poor perfusion, cold extremities, weak pulses), resting tachycardia, oliguria, pulmonary venous congestion (rales, rhonchi), and systemic venous congestion (hepatomegaly, anasarca, ascites). Systemic hypotension may be a late result of LCOS and is an ominous sign. Means to evaluate for LCOS include mixed venous oximetry, NIRS, serial lactate levels, and transthoracic or transesophageal echocardiography. Laboratory findings of LCOS may include metabolic acidosis, lactic acidemia, azotemia, reduced creatinine clearance, rising serum K ⁺ , decreased partial central venous pressure of oxygen (Pv o ₂ ) below 30 mm Hg from RA or central venous line, and increased arterial-to-venous oxygen saturation difference of more than 40%.

  
  
• b.
  

  Inadequate cardiac output may be caused by (1) low preload, (2) high afterload, (3) depressed myocardial contractility, (4) cardiac tamponade, (5) arrhythmias including sinus bradycardia or sinus tachycardia, (6) inadequate surgical repair, (7) pulmonary hypertension, and (8) insufficient ventilation. Treatment is directed at the cause.

  
  
  
  
  • (1)
    

    Low preload may be due to intravascular volume depletion (manifested by decreased RA and LA pressures) or due to diminished blood flow to LV (e.g., pulmonary venous obstruction, PA hypertension, PS, or RV failure in the absence of adequate intraarterial shunting; evident by elevated RA and decreased LA pressure). In the case of MS, which also decreases LV preload, RA and LA pressures are both elevated. Although all these conditions ultimately reduce the LV preload and subsequently the cardiac output, treatment is specific to each condition. Low intravascular volume is treated with IV crystalloid or colloid to increase the intravascular volume to raise central venous pressure to 10 to 15 mm Hg. Other conditions are treated by eliminating the cause.

    
    
  • (2)
    

    High afterload (with increased SVR) may be caused by hypoxia, acidosis, hypothermia, or pain. In addition to the correction of the cause, the elevated SVR is treated with afterload reduction.

    
    
    
    
    • (a)
      

      Phosphodiesterase inhibitors (e.g., milrinone) play a crucial role in treatment of LCOS. They not only have a vasodilatory effect, but also lusitropic and inotropic effects without being significantly arrhythmogenic. These effects occur without an increase in myocardial oxygen consumption. Milrinone is usually initiated in the operating room and is continued as an IV drip at a rate of 0.1 to 1 μg/kg/min (usual range 0.25 to 0.75 μg/kg/min) postoperatively.

      
      
    • (b)
      

      Nitroprusside (IV drip at 0.3 to 10 μg/kg/min) or nitroglycerin (IV drip at 0.5 to 6 μg/kg/min) can be used to further reduce elevated SVR. Both agents have a favorable effect on PVR. In addition, nitroglycerin is a potent coronary vasodilator, which may be beneficial after arterial switch operation.

      
      
    • (c)
      

      Phenoxybenzamine, a long-acting α-adrenergic blocking agent, is used in selected postoperative patients.

    
    
    
    
  • (3)
    

    Depressed myocardial contractility (demonstrated by echo) may be treated by optimizing arterial oxygen saturation; by addressing anemia, hypocalcemia, and/or acidemia; and by administration of inotropic agents. The optimal oxygenation is achieved by maintaining a patent airway with good respiratory care, adjusting F io ₂ if necessary, reducing pulmonary shunting by the use of PEEP, and reducing pulmonary edema by the use of diuretics. The following inotropic agents among others may be used:

    
    
    
    
    • (a)
      

      Epinephrine (continuous IV drip at a rate of 0.01–0.05 μg/kg/min; low dose to minimize undesirable α-agonist effects).

      
      
    • (b)
      

      Dopamine (continuous IV drip, starting at 2.5 μg/kg/min and increasing up to 10 μg/kg/min if necessary).

      
      
    • (c)
      

      Milrinone (by inhibition of type III phosphodiesterase increases intracellular cyclic adenosine monophosphate [ cAMP], which ultimately augments myocardial contractility) is started with or without a loading dose of 50 μg/kg and is maintained at an infusion rate of 0.1 to 1 μg/kg/min.

    
    
    
    
  • (4)
    

    Cardiac tamponade is treated with urgent decompression of the pericardial space. Early cardiac tamponade results from persistent surgical bleeding not properly drained by the chest tubes; it may even occur when the pericardium is removed or left widely open. It must be suspected when the chest tube drainage abruptly decreases or stops in a patient with previously significant bleeding. Characteristically, the patient is tachycardic and hypotensive with narrowed pulse pressure. Atrial pressures are elevated. Response to volume administration and inotropic agents is minimal. Chest radiographs show widening of the cardiac silhouette. Echo demonstrates pericardial effusion and diastolic collapse of the RA and RV, sensitive indicators of tamponade. Cardiac tamponade requires prompt pericardiocentesis or surgical exploration for evacuation of the pericardial hematoma or control of bleeding by urgent opening of the sternotomy, often in the intensive care unit.

    
    
  • (5)
    

    Sinus bradycardia or tachycardia may be detrimental in a postoperative patient with limited cardiac reserve.

    
    
    
    
    • (a)
      

      Attention to detail is necessary to unmask secondary causes of sinus bradycardia, such as medication interaction, hypoxia, hypoglycemia, electrolyte imbalance, increased intracranial pressure, and hypothyroidism. Injury to the sinus node or its artery, particularly during Fontan procedure or atrial switch operations (Senning and Mustard), may occur and result in persistent sinus bradycardia. If necessary, patients are treated with atrial and/or ventricular pacing, or chronotropic agents. Atrial and ventricular pacing wires are usually placed at the time of open heart procedures and are left postoperatively until the desired heart rate and AV synchrony are returned, maintained, and verified.

      
      
    • (b)
      

      Extreme sinus tachycardia is treated by eliminating causes (e.g., pain, anemia, fever, volume depletion, chronotropic agents). Administration of catecholamines should be minimized, as excessive tachycardia increases myocardial oxygen consumption. Furthermore, tachycardia shortens the diastolic period and consequently reduces coronary blood flow.

      
      
    • (c)
      

      Treatments of other arrhythmias are described in a section to follow.

    
    
    
    
  • (6)
    

    Revision of surgical repair is occasionally indicated when an inadequate repair (such as a large residual L-R shunt or significant residual COA) is the cause of low cardiac output. Echo and, if necessary, cardiac catheterization may reveal a residual defect and its significance.

    
    
  • (7)
    

    Pulmonary hypertensive crisis is characterized by an acute rise in PA pressure followed by a reduction in cardiac output and a fall in arterial oxygen saturation. It occurs in neonates and infants who had CHDs with pulmonary hypertension (e.g., complete ECD, persistent truncus arteriosus), often after vigorous suctioning of the endotracheal tube. It is difficult to treat and may be fatal; prevention is critically important (see “General care” earlier in this chapter). Treatment includes sedation, paralysis, supplemental oxygen, and inhaled nitric oxide.

    
    
  • (8)
    

    Inadequate ventilation secondary to hemothorax, pleural effusion, or pneumothorax should be searched for and if necessary treated, such as with replacement of chest tube or even return to the operation room to manage possible hemorrhage.

  
  
  
  
• c.
  

  Hypotension and hypertension

  
  
  
  
  • (1)
    

    Hypotension due to low intravascular volume, recognized by low RA (central venous) and LA pressure, is treated as follows:

    
    
    
    
    • (a)
      

      Volume expanders or PRBCs are given as an IV bolus (initially 5 to 10 mL/kg, up to 20 mL/kg). As transfused citrated blood binds ionized calcium, replacement of calcium is necessary in maintaining BP and cardiac output.

      
      
    • (b)
      

      Inotropic agents are used if volume expansion fails to raise BP.

      
      
    • (c)
      

      Vasopressin (IV drip at 0.0003 to 0.01 U/kg/min) may be considered in patients with adequate myocardial function but with severe vasodilatory hypotension.

    
    
    
    
  • (2)
    

    Severe hypertension is treated with vasodilators (see “Low cardiac output syndrome” earlier in this chapter).

  
  
  
  
• d.
  

  Rhythm disorders . Sinus rhythm and maintenance of AV synchrony are optimal. Junctional rhythm may reduce cardiac output by 10% to 15%. In addition to the specific treatment for arrhythmias, possible causes should be investigated and corrected (e.g., oxygenation status, acid-base status, electrolyte imbalance, arrhythmogenic medications). If the patient is hemodynamically unstable, defibrillation or synchronized cardioversion should not be delayed.

  
  
  
  
  • (1)
    

    Infrequent and isolated PACs or PVCs are followed without intervention.

    
    
  • (2)
    

    Paroxysmal SVT (AV node and accessory pathway re-entry tachycardia) is treated with the drug of choice, adenosine (rapid IV bolus of 0.1 mg/kg/dose followed by rapid saline flush; if unsuccessful subsequent doses can be increased to 0.2 mg/kg). Intermittent episodes of SVT are treated with IV amiodarone (loading dose: 5 to 10 mg/kg over 20 to 60 minutes, followed by IV drip at a rate of 5 to 15 μg/kg/min or IV boluses of 2.5 mg/kg every 6 hours). Persistent SVT may also be treated with overdrive suppression or synchronized cardioversion. In more resistant cases, other medications, such as IV β-receptor blockers, verapamil, procainamide, and digoxin, may be used with caution (taking into account myocardial function, BP stability, ventricular preexcitation, etc.). Oral β-receptor blockers, flecainide, or sotalol can be used in more chronic and stable patients.

    
    
  • (3)
    

    Other SVTs (multifocal atrial tachycardia or ectopic atrial tachycardia) are treated by ventricular rate control with medications such as amiodarone, β-receptor blockers, calcium channel blockers, or digoxin.

    
    
  • (4)
    

    Atrial flutter is treating with overdrive atrial pacing (through esophageal or intraoperatively placed temporary atrial leads) or synchronized cardioversion. Procainamide (loading dose: 2 to 6 mg/kg, maximum dose 100 mg/dose followed by IV continuous drip at 20 to 80 μg/kg/min, maximum 2 g/day) and/or digoxin is the pharmacologic approach for this condition.

    
    
  • (5)
    

    Atrial fibrillation is a rare condition in the acute postoperative pediatric cardiac population; nevertheless, it is treated with amiodarone, sotalol, or flecainide (in stable patients) or cardioversion (in hemodynamically compromised patients). If unsuccessful, ventricular rate control is the management of choice.

    
    
  • (6)
    

    Postoperative junctional ectopic tachycardia (JET), the most common significant postoperative tachycardia, is discussed in detail in Chapter 29.

    
    
  • (7)
    

    Frequent PVCs, if hemodynamically significant, are managed with avoidance of arrhythmogenic drugs, optimizing homodynamic status, or correction of electrolyte imbalance (especially magnesium), hypoxia, and acidemia, and are suppressed with lidocaine (IV bolus 1 mg/kg followed by continuous drip at 20 to 50 μg/kg/min).

    
    
  • (8)
    

    Monomorphic VT with adequate perfusion is treated with amiodarone (loading dose: 5 mg/kg over 20 minutes, followed by IV drip at a rate of 5 to 15 μg/kg/min or IV boluses of 2.5 mg/kg every 6 hours), lidocaine (IV bolus of 1 mg/kg, followed by IV drip at 20 to 50 μg/kg/min), procainamide (loading dose: 2 to 6 mg/kg, maximum dose 100 mg/dose, followed by IV continuous drip at 20 to 80 μg/kg/min, maximum 2 g/day), esmolol (loading dose of 100 to 500 μg/kg IV over 1 min followed by 50 to 500 μg/kg/min continuous drip), or electrical cardioversion.

    
    
  • (9)
    

    Torsades de pointes (uncommon variant of polymorphic VT), which occurs mostly in the setting of prolonged QT, requires a special approach. Amiodarone and procainamide may have a disastrous effect on this type of VT with further prolongation of the QT. Torsades often responds to IV magnesium sulfate (25 to 50 mg/kg, maximum dose 2 g), even when the magnesium level is normal. Esmolol and lidocaine may also be effective.

    
    
  • (10)
    

    Postoperative advanced second- or third-degree heart block is treated by temporary pacing and/or isoproterenol (IV drip at 0.05–2 μg/kg/min). Permanent pacemaker implantation may be indicated if advanced AV block persists at least 7 days after the surgery.

  
  

Renal system . Anuria or oliguria (<1 mL/kg/hr) and evidence of solute accumulation (serum K ⁺ >5 mEq/L, BUN >40 mg/dL, creatinine >1 mg/dL) indicate acute kidney injury. Acute reduction of cardiac output is the most common cause of renal failure. Initial treatment is directed at improving cardiac output and inducing diuresis.

• a.
  

  Preload and afterload should be optimized.

  
  
• b.
  

  Furosemide, 0.5 to 2 mg/kg/dose every 6 to 12 hours IV or as a continuous IV drip at 0.05 to 0.4 mg/kg/hr, is given if the patient is oliguric.

  
  
• c.
  

  If serum K ⁺ rises above 6.0 mEq/L, calcium chloride (10 mg/kg/dose, slow central IV push), bicarbonate (1 mEq/kg/dose IV), D ₂₅ W (2 mL/kg IV; 0.5 g glucose/kg) plus regular insulin (0.1 U/kg IV) solution, and sodium polystyrene sulfonate (Kayexalate; 1 g/kg per rectum or nasogastric tube) are used.

  
  
• d.
  

  Peritoneal dialysis may be necessary if the above measures are ineffective. Indications for peritoneal dialysis include hypervolemia, azotemia (BUN over 150 mg/dL or lower if rising rapidly), life-threatening hyperkalemia, intractable metabolic acidosis, neurologic complications (secondary to uremia or electrolyte imbalance), calcium-phosphate imbalance, pulmonary compromise, or fluid restrictions limiting caloric intake.

Metabolic system

• a.
  

  Abnormalities of electrolytes and acid-base balance:

  
  
  
  
  • (1)
    

    Metabolic acidosis is treated if the base deficit is >5 mEq/L. Total extracellular base deficit = base deficit (mEq/L) × 0.3 × body weight (kg). The dosage of sodium bicarbonate is half the total extracellular base deficit.

    
    
  • (2)
    

    Lactic acidemia may be caused by LCOS and ensuing poor cerebral and intestinal tissue perfusion. Treatment is directed at improvement of cardiac output.

    
    
  • (3)
    

    Mild hyponatremia does not require treatment except for fluid restriction and diuresis. Serum Na ⁺ <125 mEq/L requires treatment to elevate sodium levels.

    
    
  • (4)
    

    Hypernatremia with the serum Na ⁺ >155 mEq/L requires treatment with sodium restriction and liberalization of fluids.

    
    
  • (5)
    

    Hypocalcemia may cause hypotension secondary to decreased myocardial function. It should be followed closely, especially in neonates and patients with DiGeorge syndrome. Ionized calcium level below 1.2 mEq/L should be treated. Central line administration is the ideal route of IV calcium, as extravasation will lead to tissue necrosis.

    
    
  • (6)
    

    Hypomagnesemia may lead to arrhythmia and subsequently to low cardiac output. A magnesium level of more than 0.7 mmol/L (1.4 mEq/L) is desirable.

  
  
  
  
• b.
  

  Postoperative hypoglycemia (<5 mmol/L or 90 mg/dL) or hyperglycemia (>7.8 mmol/L or 140 mg/dL) has been associated with increased mortality and morbidity. It seems prudent to avoid these conditions. Hypoglycemia is managed with a bolus of dextrose or administration of higher-concentrated glucose in water. Hyperglycemia is treated with restriction of glucose and/or infusion of insulin.

  
  
• c.
  

  Postoperative hypothermia could interfere with hemostasis and exacerbate coagulopathy, necessitating gradual rewarming to control hemorrhage. Shivering should be avoided, as it increases the oxygen consumption. However, management of junctional ectopic tachycardia may include core temperature cooling. Unlike hypothermia, treatment of postoperative fever (>38.5°C) is more urgent. LCOS is one of the causes of postoperative hyperthermia so that management of postoperative fever not only includes antipyretics or cooling, but also optimizing cardiac output with afterload reduction.

GI system . Adequate caloric intake (120 to 150 kcal/kg/day) is essential in infants recovering from congenital cardiac surgery. Enteral feeding is individualized. When stable hemodynamically, several hours after extubation, oral feeding can be started with clear liquids (e.g., oral rehydration solutions). It is then advanced to an appropriate formula. Nasogastric tube feeding should be used in infants who are too weak to suck. Children with prolonged intubation require gavage feeding or total parenteral nutrition. Gastric protection is achieved with H ₂ -receptor blockade (e.g., famotidine, 0.25 mg/kg/dose every 12 hours, maximum pediatric dose of 40 mg/day) or protein pump inhibitors (e.g., esomeprazole, 0.5 to 1 mg/kg/dose IV every 24 hours, maximum pediatric dose 20 mg/day). The ranitidine dose needs to be adjusted in patients with renal failure, or alternatively protein pump inhibitors could be used. Enterally fed patients should be examined frequently for any signs of intestinal dysfunction. Evidence of abdominal distention, absence of peristalsis, hyperperistalsis, or hematochezia is sought routinely. If one of these develops, enteral feeding is discontinued, nasogastric suction is applied, and parenteral nutrition is considered. GI dysfunction may be caused by LCOS, acute pancreatitis, hepatic or intestinal necrosis, ileus, and others.

Hematologic system . Different thresholds are established for transfusion of PRBCs, fresh frozen plasma, or platelets at different institutions. Transfusion of blood products depends on hemodynamic status and coagulation status of individual patients.

• a.
  

  Maintain adequate hemoglobin (Hgb) and a desirable filling pressure (e.g., LA pressure 10 to 15 mm Hg) by infusion of PRBCs or albumin, depending on the patient’s Hgb or hematocrit (Hct). Patients with cyanotic CHD or myocardial dysfunction are given PRBCs to maintain Hct above 40%.

  
  
• b.
  

  Coagulation abnormalities may result from inadequate heparin neutralization (causing prolongation of aPTT), thrombocytopenia (<50,000 platelets/mm ³ ), or disseminated intravascular coagulation (DIC; secondary to sepsis, low cardiac output, acidosis, hypoxia, or tissue necrosis or as a reaction to blood transfusion).

  
  
  
  
  • (1)
    

    Unneutralized heparin is corrected by administration of additional protamine.

    
    
  • (2)
    

    Thrombocytopenia is treated with slow infusion of platelet concentrates with an infusion pump, given over 20 to 30 min; rapid infusion may cause pulmonary hypertension and RV failure.

    
    
  • (3)
    

    DIC (characterized by hemorrhage, tissue necrosis, hemolytic anemia, positive d -dimer test, low platelets and serum fibrinogen, and prolonged PT and aPTT) is managed by prompt and vigorous treatment of the underlying cause. Management may include transfusion of platelets, cryoprecipitates, and/or fresh frozen plasma as well as administration of heparin.

  
  
  
  
• c.
  

  Excessive postoperative bleeding occurs more frequently in severely cyanotic patients, polycythemic patients, and patients who had a reoperation. The necessity to infuse more than 10 to 15 mL/kg of volume requires investigation for excessive blood loss and for a possible surgical exploration. Surgical exploration is indicated (1) if the chest tube drainage in the absence of clotting abnormalities exceeds 3 mL/kg/hr for 3 hours or (2) if there is a sudden marked increase in chest tube drainage of 5 mL/kg/hr in any 1 hour.

  
  
• d.
  

  Long-term anticoagulation with aspirin or warfarin is indicated in selected patients. Patients with cavopulmonary anastomosis (e.g., Glenn or Fontan procedure) or systemic-to-pulmonary shunts (e.g., modified B-T shunt) are bridged to oral anticoagulation by continuous heparin drip and its dose is adjusted for aPTT of 60 to 85 seconds. Aspirin (3 to 5 mg/kg PO once daily) is started when chest is closed, all major intracardiac lines are removed, and patients are hemodynamically stable and have adequate platelet count without evidence of active bleeding. Alternatively or additionally, warfarin is given if the patient is in a hypercoagulable state (e.g., factor V Leiden mutation, protein S or C deficiency). Patients with mechanical valve prostheses will require warfarin; the dose is adjusted to maintain adequate anticoagulation (international normalized ratio [INR] 2.5 to 3.5 for mitral valve and INR 2.0 to 3.0 for aortic valve). While patients are maintained on aspirin, cyclooxygenase (COX)-2 inhibitors (e.g., ibuprofen, naproxen) should be avoided as they inhibit the antiplatelet effect of aspirin.

Neurologic system . The incidence of central nervous system anomalies including brain dysmorphology or neurobehavioral abnormalities is increased in patients with congenital cardiac defects. These may be multifactorial, isolated findings, or in association with particular genetic defects. In addition, pre- and perioperative neurologic events complicate establishing the accurate cause of the neurologic insult.

• a.
  

  Localized neurologic defects such as hemiplegia and visual field defects are abnormal and may be due to air or particulate emboli.

  
  
• b.
  

  Seizures may be caused by hypoxia, metabolic abnormalities, infections, cerebral edema, embolism or hemorrhage, or decreased cerebral perfusion. Early postoperative clinical seizures occur at an incidence rate of 3% to 6%; however, EEG and video monitoring may reveal an incidence of 20% of subclinical seizures. Seizures documented by electroencephalography have been associated with worse neurodevelopmental outcome. Management of seizures includes the following:

  
  
  
  
  • (1)
    

    Determine arterial blood gases, serum glucose, calcium, electrolytes, cardiac output, and temperature. Correct any abnormalities.

    
    
  • (2)
    

    Anticonvulsant therapy.

    
    
    
    
    • (a)
      

      Lorazepam, 0.05 to 0.1 mg/kg/dose IV over 2 to 5 min (maximum single dose 2 mg; may cause respiratory depression).

      
      
    • (b)
      

      Fosphenytoin, 15 to 20 mg phenytoin equivalent (PE)/kg IV (maximum infusion rate of 150 mg PE/min due to risk of hypotension), followed by a maintenance dose of 5 mg PE/kg/day IV or IM. Therapeutic levels are 10 to 20 mg/L (free and bound phenytoin) or 1 to 2 mg/L (free phenytoin). Fosphenytoin causes less hypotension than traditional phenytoin; however, both medications are contraindicated in patients with heart block or sinus bradycardia.

      
      
    • (c)
      

      Phenobarbital, 10 to 20 mg/kg IV over 5 to 10 min. The full effect may take several hours. Phenobarbital maintenance dose is 5 mg/kg/day given in 1 or 2 daily doses. Therapeutic level is 10 to 40 mg/L. Side effects of phenobarbital include myocardial depression with hypotension, particularly after large and rapid infusion.

    
    

  
  
  
  
• c.
  

  Choreiform movement and grossly inadequate behavior are major neurologic complications. Pharmacologic control is difficult. These complications usually but not always clear without demonstrable sequelae.