High atrial natriuretic peptide concentrations blunt the pressor response during cardiopulmonary resuscitation in humans

Abstract

OBJECTIVE To determine the relationship of circulating atrial natriuretic concentrations to the pressor response to high-dose epinephrine in patients undergoing cardiopulmonary resuscitation (CPR) for cardiac arrest. DESIGN Prospective study. PATIENTS Fourteen normothermic, adult, prehospital and emergency department patients suffering unexpected cardiac arrest. INTERVENTION Patients received high-dose epinephrine (0.2 mg/kg) i.v. when standard advanced cardiac life support (including multiple 1-mg dosages of epinephrine) failed to result in return of spontaneous circulation. MEASUREMENTS AND MAIN RESULTS Cardiac arrest patients were separated into those patients with and without detectable serum atrial natriuretic concentrations, and were termed the atrial natriuretic peptide and atrial natriuretic peptide groups, respectively. Their aortic pressure response to high-dose (0.02 mg/kg) epinephrine was compared. The proportion with positive assays was compared with a group of healthy control subjects. Fourteen patients were studied. Eight patients had low serum atrial natriuretic concentrations and six patients had high circulating atrial natriuretic concentrations. The mean concentration in the high atrial natriuretic group was 151 +/- 82 pg/mL. The proportion with positive assays (six of 14 patients) was greater than in the group in spontaneous circulation (three of 29 patients) (p = .002). The maximal increase in the aortic relaxation-phase pressures after high-dose epinephrine was 9 +/- 7 torr (1.2 +/- 0.9 kPa) in the low atrial natriuretic group and 0 +/- 5 torr (0 +/- 0.7 kPa) in the high atrial natriuretic group (p = .03). The maximal increase in the aortic compression pressures after high-dose epinephrine was 17 +/- 13 torr (2.3 +/- 1.7 kPa) in the low atrial natriuretic group and 2 +/- 10 torr (0.3 +/- 1.3 kPa) in the high atrial natriuretic group (p = .03). Thus, pressor responses after high-dose epinephrine administration were observed in patients in the low atrial natriuretic group, but this response was absent in patients in the high atrial natriuretic group. CONCLUSIONS Cardiac arrest patients receiving CPR have higher circulating atrial natriuretic concentrations than healthy subjects. High serum atrial natriuretic concentrations may antagonize the vasopressor response to epinephrine. Blocking this effect of atrial natriuretic may improve outcomes in patients suffering cardiac arrest.