• W G Haynes, D W Hamer, C E Robertson, and D J Webb.
• Department of Medicine, University of Edinburgh, Western General Hospital, UK.
• Resuscitation. 1994 Mar 1; 27 (2): 117-22.

AbstractCardiac arrest is associated with major metabolic disturbances, including severe hypoxia and large increases in circulating catecholamines, both of which are known to stimulate generation of the potent endothelium-derived vasoconstrictor peptide endothelin-1. We have, therefore, examined plasma immunoreactive endothelin concentrations following cardiac arrest. Blood was sampled at 10-min intervals from a central venous catheter inserted at onset of resuscitation in 38 patients (13 female; mean age, 67 years) presenting with cardiac arrest to the Accident and Emergency Department at the Royal Infirmary of Edinburgh. Plasma immunoreactive endothelin concentrations (mean +/- S.D.) in patients following cardiac arrest (5.4 +/- 2.3 pg/ml) were no different from those in healthy subjects (5.1 +/- 1.2 pg/ml). There was no significant difference between endothelin concentrations at presentation in survivors and non-survivors of cardiac arrest. However, non-survivors had a significant fall in endothelin concentrations with time from onset of resuscitation from 5.4 +/- 2.2 pg/ml to 3.5 +/- 1.8 pg/ml (P = 0.002), while survivors had a non-significant increase in concentrations. On multiple regression analysis there was a significant association between higher plasma endothelin concentration and survival (r = 0.37; P = 0.009). The failure of plasma endothelin to increase after cardiac arrest is unexpected. Although the fall in plasma endothelin with time in non-survivors may reflect the adverse physiological milieu that occurs during cardiac arrest, it is also possible that low endothelin concentrations contribute to the poor prognosis in this condition.

18 keywords...

hide…