BackgroundA prolonged QT interval can lead to malignant ventricular arrhythmias and sudden cardiac death, and has frequently been found in end-stage liver disease (ESLD). However, myocardial repolarization lability has not yet been fully investigated. We evaluated the QT variability index (QTVI), a marker of temporal inhomogeneity in ventricular repolarization and an abnormality associated with re-entrant malignant ventricular arrhythmias. We determined whether QTVI is affected by the head-up tilt test in ESLD.MethodsWe assessed 36 ESLD patients and 12 control subjects without overt heart disease before and after the 70-degree head-up tilt test. The electrocardiography signal (lead II) was recorded on a computer with an analog-to-digital converter. The RR interval (RRI) and QT interval were measured after recording 5 min of the digitized electrocardiography. Then, the QT intervals were corrected with Bazett's formula (QTc). QTVI was calculated through the following formula: QTVI = log10 [(QTv/QTm2)/(RRIv/RRIm2)], QTv/RRIv: variance of QTI/RRI, QTm/RRIm: mean of QT interval/RRI.ResultsCirrhotic patients exhibited an elevated QTVI. In particular, Child class C patients had a significantly increased QTVI compared to Child class A patients and the control subjects in the supine position. However, the head-up tilt test did not cause a significant difference in QTVI in relation to the severity of ESLD.ConclusionsMyocardial repolarization lability was significantly altered in end-stage liver disease. Our data suggest that the severity of ESLD is associated with the degree of the alteration in the QT variability index.

Neurogenic pulmonary edema (NPE) in brain dead organ donors occurring after an acute central nervous system insult threatens organ preservation of potential organ donors and the outcome of organ donation. Hence the active and immediate management of NPE is critical. In this case, a 50-year-old male was admitted to the intensive care unit (ICU) for organ donation. He was hypoxic due to NPE induced by spontaneous intracerebral hemorrhage and intraventricular hemorrhage. Protective ventilatory management, intermittent recruitment maneuvers, and supportive treatment were maintained in the ICU and the operating room (OR). Despite this management, the hypoxemia worsened after the OR admission. So inhaled nitric oxide (NO) therapy was performed during the operation, and the hypoxic phenomena showed remarkable improvement. The organ retrieval was successfully completed. Therefore, NO inhalation can be helpful in the improvement of hypoxemia caused by NPE in brain dead organ donors during anesthesia for the organ donation.

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