HIGH ATRIAL-NATRIURETIC-PEPTIDE CONCENTRATIONS BLUNT THE PRESSOR-RESPONSE DURING CARDIOPULMONARY-RESUSCITATION IN HUMANS

Objective: To determine the relationship of circulating atrial natriur etic peptide concentrations to the presser response to high-dose epine phrine in patients undergoing cardiopulmonary resuscitation (CPR) for cardiac arrest. Design: Prospective study. Patients: Fourteen normothe rmic, adult, prehospital and emergency department patients suffering u nexpected cardiac arrest. Intervention: Patients received high-dose ep inephrine (0.2 mg/kg) iv when standard advanced cardiac life support ( including multiple 1-mg dosages of epinephrine) failed to result in re turn of spontaneous circulation. Measurements and Main Results: Cardia c arrest patients were separated into those patients with and without detectable serum atrial natriuretic peptide concentrations, and were t ermed the ''low atrial natriuretic peptide'' and ''high atrial natriur etic 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 n atriuretic peptide concentrations and six patients had high circulatin g atrial natriuretic peptide concentrations. The mean concentration in the high atrial natriuretic peptide group was 151 +/- 82 pg/mL. The p roportion with positive assays (six of 14 patients) was greater than i n the group in spontaneous circulation (three of 29 patients) (p = .00 2). The maximal increase in the aortic relaxation-phase pressures afte r high-dose epinephrine was 9 +/- 7 torr (1.2 +/- 0.9 kPa) in the low atrial natriuretic peptide group and 0 +/- 5 torr (0 +/- 0.7 kPa) in t he high atrial natriuretic peptide group (p = .03). The maximal increa se in the aortic compression pressures after high-dose epinephrine was 17 +/- 13 torr (2.3 +/- 1.7 kPa) in the low atrial natriuretic peptid e group and 2 +/- 10 torr (0.3 +/- 1.3 kPa) in the high atrial natriur etic peptide group (p = .03). Thus, presser responses after high-dose epinephrine administration were observed in patients in the low atrial natriuretic peptide group, but this response was absent in patients i n the high atrial natriuretic peptide group. Conclusions: Cardiac arre st patients receiving CPR have higher circulating atrial natriuretic p eptide concentrations than healthy subjects High serum atrial natriure tic peptide concentrations may antagonize the vasopressor response to epinephrine. Blocking this effect of atrial natriuretic peptide may im prove outcomes in patients suffering cardiac arrest.