Determinants of elevated creatine kinase activity and creatine kinase MB-fraction following cardiopulmonary resuscitation

We undertook this study to determine the occurrence and the determinants of elevation of serum creatine kinase (CK) levels and CK MB-fraction following cardiopulmonary resuscitation (CPR). Four hundred twenty consecutive adult admissions to the Long Island Jewish Medical Center from January 1989 thr...

Full description

Saved in:
Bibliographic Details
Published inChest Vol. 101; no. 5; p. 1386
Main Authors Mattana, J, Singhal, P C
Format Journal Article
LanguageEnglish
Published United States 01.05.1992
Subjects
Online AccessGet more information

Cover

Loading…
More Information
Summary:We undertook this study to determine the occurrence and the determinants of elevation of serum creatine kinase (CK) levels and CK MB-fraction following cardiopulmonary resuscitation (CPR). Four hundred twenty consecutive adult admissions to the Long Island Jewish Medical Center from January 1989 through December 1990 with a diagnosis of cardiac arrest were reviewed. The Long Island Jewish Medical Center, New Hyde Park, NY, the Long Island Campus for the Albert Einstein College of Medicine, Bronx, NY. Sixty-three patients survived for at least 12 h following cardiac arrest for evaluation of post-CPR CK levels and were included into the study. Clinical features, biochemical profiles, and administered drug profiles were studied in these patients. The clinical and biochemical features of the patients with (CK greater than 224 IU/L [3.7 mu kat/L]) and without rhabdomyolysis were also compared. Two major determinants responsible for elevated CK levels emerged, including physical injury (number of chest compressions during CPR) and electrical injury (cumulative number of joules administered during defibrillation). Post-CPR CK levels showed positive correlations with both the number of chest compressions given (p less than 0.001) and the number of joules administered during defibrillation (p less than 0.001). Post-CPR CK-MB levels also showed a positive correlation with the number of joules administered (p less than 0.005) and the number of chest compressions (p less than 0.02). Forty-three (68.3 percent) of the 63 patients developed rhabdomyolysis. Serum CK levels were higher (p less than 0.005) in the patients who received electrical countershock therapy as well as chest compressions when compared with patients who received chest compressions alone. There were no significant differences in electrolyte levels between patients with and without rhabdomyolysis. Thirty patients had a history of coronary artery disease (CAD) and 18 (60.0 percent) of these had a positive MB-fraction post-CPR while only ten of the 33 patients without known CAD had a positive MB-fraction post-CPR (30.3 percent, p less than 0.05). Patients with no known CAD but positive CK-MB fraction had significantly higher total CK levels, physical injury, and electrical injury compared with patients with negative CK-MB fraction. Twenty patients survived CPR and were discharged from the hospital without significant neurologic sequelae. The remaining 43 either died or suffered severe neurologic injury. The patients who survived CPR had a significantly shorter duration of CPR (p less than 0.01) compared with those who did not. Patients who did not have long-term survival following CPR were more likely to have elevated serum potassium, phosphate, and creatinine values. CK elevation is a common finding following successful CPR after cardiac arrest and this elevation of post-CPR CK levels is related to both physical as well as electrical injury sustained during CPR. Elevation of post-CPR CK-MB fraction seems to be only a crude indicator of preexisting CAD; however, a positive CK-MB fraction in patients without CAD is related to severity of physical injury and electrical injury during CPR. Patients who survive CPR without neurologic impairment appear to be those with a shorter duration of CPR. Elevated serum potassium, phosphate, and creatinine values may be related to an adverse effect on long-term survival.
ISSN:0012-3692
DOI:10.1378/chest.101.5.1386