Arrhythmias Following Congenital Heart Disease Surgery Arrhythmias occurring after open-heart surgery for congenital heart disease contribute greatly to the morbidity and mortality of surgery Arrhythmias that might be tolerated in the normal heart result in hemodynamic instability when they occur within the first several days after surgery A lack of AV synchrony and rapid heart rates that prevent diastolic filling result in low cardiac output and mandate early recognition and therapy JET is the most frequent hemodynamically significant tachycardia occurring postoperatively (Fig 22.40) This narrow QRS tachycardia can have AV dissociation with a slower atrial than ventricular rate, although 1 : 1 retrograde conduction can occur Hemodynamic compromise occurs, likely as a result of the lack of atrial contribution to cardiac output Risk factors associated with JET after congenital heart surgery include younger age, longer cardiopulmonary bypass times, and longer cross-clamp times.86,88,205 FIG 22.40 Postoperative management algorithm for high-grade atrioventricular (AV) block EPS, Electrophysiologic study; LAD, left anterior descending coronary artery; PVARP, postventricular atrial refractory period; RBBB, right-bundle-branch block Although the precise mechanisms are not known, the setting of the arrhythmia gives clues to its etiology Several surgical and nonsurgical risk factors have emerged The surgical risk factors include resection of muscle bundles, correction of RVOT obstruction, and correction of VSDs.206,207 The reported incidence of JET varies depending on patient selection and study location In a nationwide study in Finland, the incidence of JET in the congenital cardiac surgery population was 5%.88 This study identified many of the previously reported risk factors showing that the JET population is overall sicker as compared with their age- and procedure-matched controls However, in the logistic regression model, only longer cardiopulmonary bypass time and higher postoperative troponin T were identified as independent risk factors, probably a result of more difficult surgical correction and larger surgical trauma Further, higher body temperature at the onset of arrhythmia was found to be nearly significant (P = 050) Treating JET in this critically ill population remains a challenge Therapy should start with general measures such as correcting fever, anemia, hypovolemia, and electrolyte abnormalities, and optimizing sedation.86,208 Some institutions use intravenous amiodarone as a primary treatment because of the good response in patients who failed to respond to conventional therapies or are hemodynamically unstable.88 There are recent reports on the role of dexmedetomidine for control of JET A prospective randomized double-blind control study followed 230 consecutive patients who underwent correction surgery for tetralogy of Fallot.209 One group received an initial bolus of dexmedetomidine (0.5 µg/kg) over 10 minutes followed by a continuous infusion of 0.5 µg/kg per hour The infusion continued throughout the operation and until the child was weaned from ventilator In the control group a similar volume of normal saline was given JET occurred more often in the group not treated with dexmedetomidine If JET occurred in the dexmedetomidine-treated group, it was later in onset and of shorter duration The time to extubation was also shorter in the dexmedetomidine-treated group Cooling has long been considered as a general measure in the treatment of JET In 1997 Walsh et al found that of the multiple treatment stages they employed, only correction of fever and combined procainamide and hypothermia appeared to be efficacious.208 Others have advocated the use of supplemental magnesium sulfate during the rewarming phase of cardiopulmonary bypass,210 and normalization of the serum magnesium is an important general measure The addition of intravenous amiodarone to the pharmacologic armamentarium has improved the landscape in this problematic arrhythmia Amiodarone is a class III antiarrhythmic drug that prolongs repolarization and refractory period of atrial, nodal, and ventricular tissues, with effects similar to those of both βblockers and potassium channel blockers Its action in JET may be due to its