Hyperkalemia Accompanies Hemorrhagic Shock and Correlates with Mortality

Abstract

OBJECTIVE:This study was designed to evaluate the effects of terlipressin versus fluid resuscitation with normal saline, hypertonic saline or hypertonic-hyperoncotic hydroxyethyl starch, on hemodynamics, metabolics, blood loss and short-term survival in hemorrhagic shock.METHOD:Twenty-nine pigs were subjected to severe liver injury and treated 30 min later with either: (1) 2 mg terlipressin in a bolus, (2) placebo-treated controls, (3) 4 mL/kg 7.5% hypertonic NaCl, (4) 4 mL/kg 7.2% hypertonic-hyperoncotic hydroxyethyl starch 200/0.5, or (5) normal saline at three times lost blood volume.RESULTS:The overall mortality rate was 69%. Blood loss was significantly higher in the hypertonic-hyperoncotic hydroxyethyl starch and normal saline groups than in the terlipressin, hypertonic NaCl and placebo-treated controls groups (p<0.005). Hyperkalemia (K>5 mmol/L) before any treatment occurred in 66% of the patients (80% among non-survivors vs. 22% among survivors, p=0.019). Post-resuscitation hyperkalemia occurred in 86.66% of non-survivors vs. 0% of survivors (p<0.001). Hyperkalemia was the first sign of an unsuccessful outcome for the usual resuscitative procedure and was not related to arterial acidemia. Successfully resuscitated animals showed a significant decrease in serum potassium levels relative to the baseline value.CONCLUSION:Hyperkalemia accompanies hemorrhagic shock and, in addition to providing an early sign of the acute ischemic insult severity, may be responsible for cardiac arrest related to hemorrhagic shock.

Survival Rates and Biomarkers in a Large Animal Model of Traumatic Brain Injury Combined With Two Different Levels of Blood Loss

“…Measurements of pulse pressure and shock index were abnormal in both the TBIþ40% and 55% cohorts immediately post-blood loss, with significant evidence of a dose-dependent response for pulse pressure at 85 min post-trauma. Similarly, a parametric response was observed for potassium, sodium, and pH across the 40% and 55% models, all of which are common bloodbased biomarkers of shock, hypoxia, and cardiac functioning (16,32,36). Evidence of a worsening metabolic acidosis (i.e., increased lactate and decreased bicarbonate) was observed in the surviving members of the TBIþ55% cohort at approximately 85 min, confirming the critical role for this process in mortality following severe blood loss (16,19,21).…”

Heart Rate Variability Analysis in an Experimental Model of Hemorrhagic Shock and Resuscitation in Pigs

“…Serum potassium has been shown to increase early during hemorrhagic shock and its increase is related to mortality in animal models of hemorrhagic shock. A high correlation between potassium and lactate, SvO 2 , pH and ΔCO 2 was also observed [ 35 , 36 ].…”

Arterial blood gases, electrolytes, and metabolic indices associated with hemorrhagic shock: inter- and intrainbred rat strain variation

“…Hemorrhage-induced metabolic acidosis is reported to affect K ϩ homeostasis and increase blood K ϩ concentrations (67), which may result in death (68). Each inbred rat strain (except SS) demonstrated the expected increase in K ϩ associated with severe hemorrhage (48,55,(67)(68), and in two inbred rat strains (BN/Mcwi and FHH) the increases in K ϩ during hemorrhage were correlated with reduced survival time. Rapidly occurring hyperkalemia can also have adverse effects on cardiovascular and neuromuscular function (42,58,66).…”