In our case series, TER-ASD repair under hyperkalemic arrest was performed with no episodes of fatal hyperkalemia and arrhythmia or organ dysfunction during the postoperative period. This procedure was performed safely with good clinical results and excellent cosmetic outcomes.
Recently, robotic technology has progressed to provide cardiac surgeons with assistance that improves precision and accuracy. Moreover, as robotic-assisted cardiac surgery is ultra-minimally invasive, cosmetic concerns in ASD patients, especially those who are young and female, are resolved .
In terms of anesthetic management, robotic-assisted cardiac surgery has several concerns. One important concern is respiratory care during general anesthesia. Utilization of thoracoscopic ports requires the initiation of one-lung ventilation for adequate visualization of the cardiac structures. Moreover, insufflation of the left hemithorax with carbon dioxide is performed during robotic cardiac surgical procedures for adequate exposure of the heart and great vessels. In these condition, patients may experience arterial oxygen desaturation and hypercapnia because of one-lung ventilation and left artificial pneumothorax due to carbon dioxide. As hypoxemia and hypercapnia induce increased pulmonary artery vasoconstriction, right ventricular dysfunction may be caused by volumetric and pressure overload in patients with ASD. However, despite these concerns, in our series, there were no cases of desaturation as SPO2 below 90% and hypercarbia as ETCO2 above 50 mmHg, and no cases of right ventricular dysfunction.
There are several approaches to achieve myocardial protection without aortic clamping and cardioplegia, such as deep hypothermic cardiac arrest and hyperkalemic arrest [4,5,6]. Hyperkalemic cardiac arrest has been reported in reoperation for aortic valve replacement in a patient with a previous left internal thoracic artery to left arterial descending coronary artery bypass graft . Compared to hypothermic cardiac arrest, hyperkalemia cardiac arrest is associated with decreased myocardial adenosine triphosphate levels . In our series, serum CK-MB at ICU admission was slightly increased compared with the normal level. In all cases, 1 day after operation, serum CK-MB was decreased within normal levels which indicated that our hyperkalemia cardiac arrest technique provided efficient myocardial protection.
In our method, potassium was infused for cardiac arrest after inducing hypothermia. Hypokalemia caused by influx of extracellular potassium to intracellular compartments is frequently observed during hypothermia after cardiac arrest [8, 9]. In turn, intracellular potassium is moved to the extracellular compartment during rewarming, suggesting that hyperkalemia is caused by administered potassium as well as by transport from the intracellular compartment and its effective removal is crucially important.
To prevent postoperative fatal arrhythmia due to hyperkalemia, the most important procedure is to remove excessive serum potassium during CPB. In our series, the methods of reducing serum potassium levels included a dialyzer instead of a hemoconcentrator during CPB. The surface area of the dialyzer is 2.5 m2 compared with that of the hemoconcentrator, which is 1.2 m2. Serum potassium levels can be lowered more quickly using the dialyzer. However, compared with hyperkalemic arrest time, CPB time was much longer, due to the longer time required to reduce the potassium level below 5 mEq/L.
If potassium levels exceed 5 mEq/L after CPB weaning, calcium gluconate and sodium bicarbonate (1 mEq/kg) are administered. Indeed, two patients showed potassium concentration > 6.0 mEq/L and required calcium gluconate and sodium bicarbonate. If potassium levels remain above 5 mEq/L, a glucose-insulin solution (glucose 5 g/insulin 1U) is administered. Although calcium gluconate stabilizes the cardiac cell membrane against undesirable depolarization and sodium bicarbonate and glucose-insulin solution induce potassium shift back into the intracellular component, these effects are transient and the potassium cannot be removed in vivo. Thus, we routinely administer loop diuretics at a dose of 20 mg at CPB weaning. In our series, urine output has been sufficient after CPB weaning and there were no cases with hyperkalemia exceeding 6 mEq/L from ICU admission onward.
This study has some limitations. The patients were carefully selected to meet specific criteria. Patients did not have reduced cardiac function, coronary artery disease, peripheral artery disease, lung disease, renal dysfunction, or previous cardiac surgery. Another limitation is that this study was a retrospective analysis at a single institution. It would be difficult to generalize the results of this study to the general patient population.