Paradis N A, Wortsman J, Malarkey W B, Martin G B, Goetting M G, Feingold M, Nowak R M
Department of Critical Care Medicine, New York University Medical Center, NY.
Crit Care Med. 1994 Feb;22(2):213-8. doi: 10.1097/00003246-199402000-00010.
To determine the relationship of circulating atrial natriuretic peptide concentrations to the pressor response to high-dose epinephrine in patients undergoing cardiopulmonary resuscitation (CPR) for cardiac arrest.
Prospective study.
Fourteen normothermic, adult, prehospital and emergency department patients suffering unexpected cardiac arrest.
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.
Cardiac arrest patients were separated into those patients with and without detectable serum atrial natriuretic peptide concentrations, and were termed the "low atrial natriuretic peptide" and "high 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 peptide concentrations and six patients had high circulating atrial natriuretic peptide concentrations. The mean concentration in the high atrial natriuretic peptide 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 peptide group and 0 +/- 5 torr (0 +/- 0.7 kPa) in the high atrial natriuretic peptide 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 peptide group and 2 +/- 10 torr (0.3 +/- 1.3 kPa) in the high atrial natriuretic peptide group (p = .03). Thus, pressor responses after high-dose epinephrine administration were observed in patients in the low atrial natriuretic peptide group, but this response was absent in patients in the high atrial natriuretic peptide group.
Cardiac arrest patients receiving CPR have higher circulating atrial natriuretic peptide concentrations than healthy subjects. High serum atrial natriuretic peptide concentrations may antagonize the vasopressor response to epinephrine. Blocking this effect of atrial natriuretic peptide may improve outcomes in patients suffering cardiac arrest.
确定心脏骤停接受心肺复苏（CPR）患者循环心房利钠肽浓度与高剂量肾上腺素升压反应之间的关系。
前瞻性研究。
14名体温正常、成年、院前及急诊科意外心脏骤停患者。
当标准的高级心脏生命支持（包括多次1mg剂量的肾上腺素）未能使自主循环恢复时，患者静脉注射高剂量肾上腺素（0.2mg/kg）。
心脏骤停患者被分为血清心房利钠肽浓度可检测和不可检测的两组，分别称为“低心房利钠肽组”和“高心房利钠肽组”。比较两组患者对高剂量（0.02mg/kg）肾上腺素的主动脉压力反应。将检测呈阳性的患者比例与一组健康对照者进行比较。共研究了14名患者。8名患者血清心房利钠肽浓度低，6名患者循环心房利钠肽浓度高。高心房利钠肽组的平均浓度为151±82pg/mL。检测呈阳性的比例（14名患者中的6名）高于自主循环组（29名患者中的3名）（p = 0.002）。高剂量肾上腺素后，低心房利钠肽组主动脉舒张期压力的最大增加值为9±7托（1.2±0.9kPa），高心房利钠肽组为0±5托（0±0.7kPa）（p = 0.03）。高剂量肾上腺素后，低心房利钠肽组主动脉收缩期压力的最大增加值为17±13托（2.3±1.7kPa），高心房利钠肽组为2±10托（0.3±1.3kPa）（p = 0.03）。因此，低心房利钠肽组患者在给予高剂量肾上腺素后出现升压反应，而高心房利钠肽组患者无此反应。
接受CPR的心脏骤停患者循环心房利钠肽浓度高于健康受试者。高血清心房利钠肽浓度可能拮抗肾上腺素的升压反应。阻断心房利钠肽的这种作用可能改善心脏骤停患者的预后。
