Changes in serum potassium during reperfusion in liver transplantation.
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Biomedical subjects
Publications and source records attributed to T Sansano.
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During orthotopic liver transplantation (OLT) citrate accumulates and magnesium can be chelated, which can lead to ionized hypomagnesemia and cardiovascular dysfunction. Our aim was to study the serum ionized magnesium (Me2+) evolution and establish its relation to serum total Mg and citrate levels during OLT. We studied 58 adult patients undergoing OLT. The serum Me2+ level dropped significantly at the end of the preanhepatic phase, and remained low until the end of the procedure. Furthermore, the Me2+ levels remained below the range of reference from the beginning of the anhepatic phase onward. There was an inverse correlation between Me2+ and citrate for all patients. Me2+, like ionized calcium (Ca2+), is chelated by citrate and its evolution is a mirror image of that of citrate. In our patients, we did not observe any significant dysrhythmias that could be directly attributed to ionized hypomagnesemia. In conclusion, low preoperative levels, together with the massive transfusion of blood products and the increase in renal losses, cause progressive ionized hypomagnesemia in OLT patients. We propose that it he routinely monitored and treated accordingly, as is already done with Ca2+.
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Postreperfusion syndrome (PRS) is the most dramatic and acute hemodynamic alteration that occurs in OLT. Our aim was to determine heart function by hemodynamic monitoring and transesophageal echocardiography during PRS. We studied 24 nonconsecutive patients allocated to 2 groups: group A (n = 8), patients with PRS, and group B (n = 16), patients without PRS. Usual hemodynamic data were obtained simultaneously with transesophageal echocardiography recording of the left ventricular imaging in 4 different stages: after induction of anesthesia, 5 min before the end of the anhepatic phase, between 2 and 5 min after reperfusion, and 5 min after graft reperfusion. The hemodynamic and echocardiographic findings during reperfusion were (group A vs. group B patients): mean arterial pressure, 50.0 +/- 15.2 vs. 74.7 +/- 13.9 mmHg (P < 0.01); pulmonary capillary wedge pressure, 12.7 +/- 6.1 vs. 13.9 +/- 5.7 mmHg (NS); left ventricular ejection fraction, 79.6 +/- 9.3 vs. 83.4 +/- 9.4% (NS); left ventricular end diastolic volume index, 35.5 +/- 12.7 vs. 54.7 +/- 21.3 ml/m2 (P < 0.05); and stroke volume index, 27.9 +/- 8.9 vs. 45.5 +/- 15.9 ml/m2 (P < 0.01). There was a mild decrease in left ventricular compliance in group A. We found no alteration in left ventricular function that can justify PRS. The hemodynamic changes during PRS seemed to be caused by an insufficient increase in preload after unclamping.
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