Haynes W G, Hamer D W, Robertson C E, Webb D J
Department of Medicine, University of Edinburgh, Western General Hospital, UK.
Resuscitation. 1994 Mar;27(2):117-22. doi: 10.1016/0300-9572(94)90003-5.
Cardiac 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.
