Electrocardiographic, Cardiac Enzymes, and Magnesium in Patients With Severe Acute Pancreatitis

Abstract

Severe acute pancreatitis (SAP) can lead to multiple-organ dysfunction syndrome (MODS). Electrocardiographic (ECG), cardiac enzyme, and serum magnesium abnormalities occur after SAP. Electrocardiographic and cardiac enzyme abnormalities are described as variables in SAP patients, which contribute to the effects of MODS. Hypomagnesium is also closely associated with ECG abnormalities; therefore, hypomagnesium was also considered to be a variable in this study. A consecutive series of 54 patients admitted within 72 hours after SAP occurred was studied. A standard 12-lead ECG, cardiac enzyme, and serum magnesium measurement were routinely performed at admission. Linear correlation was used to analyze the relationship between hypomagnesemia and sinus tachycardia. The nonparametic binomial test was used to analyze dichotomized dependent variables (premature beat, atrial fibrillation, ST-segment depression, abnormal T wave, and long QT interval). Hypomagnesemia was present in 15 patients (28%), who subsequently had sinus tachycardia. There was a significant negative relationship (-1 < r <0) between hypomagnesemia and sinus tachycardia (p < .05). There were 14 (17%) premature beat, 7 (8%) atrial fibrillation, 21 (25%) ST-segment depression, 18 (21%) abnormal T wave, and 17 (31%) long QT-interval events in 54 SAP patients. Hypomagnesemia is a reason for ECG abnormalities. Electrocardiographic and cardiac enzyme abnormalities are considered to be transitory variables that are present in patients with SAP.

Electrocardiogram Heart Rate as a Predictor of Severity in Acute Alcohol-Related Pancreatitis With Alcohol Withdrawal Syndrome

“…In another study of 54 patients with severe acute pancreatitis and ECG findings, hypomagnesemia (n=15) was an important negative correlate of sinus tachycardia (n=15). A third of their patients had elevated CK-MB [25]. The ECG was not directly correlated with the severity scoring system.…”

Serum Magnesium Levels in Pediatric Inpatients: A Study in Laboratory Overuse

“…Over the 2-year study period, 823 696 non-ICU inpatient cases were identifi ed; 16 There were 13 cases of hypermagnesemia (range: 2.3-2.8 mg/dL) that led to interventions; 11 were associated with TPN, and 10 were in 1 of the 4 major diagnosis categories de scribed earlier. The remaining 3 cases were as follows: (1) a 9-year-old with chronic pancreatitis who had Mg levels in TPN adjusted after a level of 2.6 mg/dL was recorded; (2) a 16-year-old with infl ammatory bowel disease who received Mg citrate for bowel preparation before a colonoscopy and had Mg levels in TPN adjusted after a level of 2.4 mg/dL was recorded; and (3) a 14-yearold with status asthmaticus and aortic stenosis who received intravenous furosemide after a dose of intravenous Mg sulfate (peak level: 2.7 mg/dL).…”

Cardiac depression in severe acute pancreatitis: development mechanisms and possible treatment approaches. Review

“…Снижение трансмембранного потока ионов кальция при гипокальциемии вызывает снижение сократимости миокарда [53]. Потенциальный механизм развития гипомагниемии при ОП -реакция омыления между свободным магнием плазмы и липидами некротизированной мезентериальной клетчатки, в результате чего свободный магний оказывается связанным [54]. Механизмы повреждения миокарда при гипомагниемии множественны.…”

“…Кроме того, синусовая тахикардия, вызванная этим электролитным нарушением, способна усугублять ишемию миокарда, вызванную иными причинами [19,55]. Увеличение интервала QT на электрокардиограмме, характерное для гипомагниемии, может косвенно свидетельствовать о нарушении диастолического расслабления миокарда, что характерно для МД при ОП, однако это утверждение требует дальнейших исследований [54,56]. Гипофосфатемия может угнетать сократимость миокарда при помощи ряда механизмов, и в первую очередь -за счет замедления синтеза аденозинтрифосфата [57].…”