Goetting M G, Paradis N A, Appleton T J, Rivers E P, Martin G B, Nowak R M
Department of Pediatrics, Henry Ford Hospital, Detroit, MI 48202.
Crit Care Med. 1991 Aug;19(8):1012-7. doi: 10.1097/00003246-199108000-00007.
Animal studies have shown an aortic-carotid artery pressure difference during cardiopulmonary resuscitation (CPR), which compromises cerebral perfusion. This pressure difference is most marked with prolonged CPR and can be abolished with administration of high doses of epinephrine. To better understand the mechanism of cerebral blood flow during CPR in humans, we determined the aortic-carotid artery pressure difference, the cephalic perfusion pressure (the carotid artery-jugular vein pressure difference), and thoracic inlet venous "valving" (the central venous-jugular vein pressure difference), while administering standard doses of epinephrine.
Prospective study with randomization as to which side the carotid artery was catheterized.
The resuscitation room of a large urban hospital's emergency department.
Fifteen adults in normothermic, nontraumatic prehospital cardiac arrest treated according to Advanced Cardiac Life Support guidelines, including administration of 1 mg epinephrine iv every 5 mins.
The descending aorta, cervical common carotid artery, internal jugular vein, and central venous system were catheterized. Pressures were recorded during standard CPR for 5 mins after administration of 1 mg epinephrine iv.
Most patients received CPR for greater than 20 mins before the first epinephrine dose and for greater than 45 mins before pressure recording as described above. There was no significant difference between aortic and carotid artery compression and relaxation phase pressures. The mean +/- SD compression central venous-jugular vein pressure difference was 22.1 +/- 15.0 mm Hg, and the mean cephalic perfusion pressure was 20.8 +/- 19.5 mm Hg.
There is no clinically important aortic-carotid artery pressure difference during human CPR using the standard dose of epinephrine, even with prolonged CPR. Despite carotid artery patency and thoracic inlet venous valving, the cephalic perfusion pressure is low during CPR in humans.
动物研究表明，心肺复苏（CPR）期间存在主动脉 - 颈动脉压力差，这会损害脑灌注。这种压力差在长时间CPR时最为明显，大剂量肾上腺素给药可消除该压力差。为了更好地了解人类CPR期间脑血流的机制，我们在给予标准剂量肾上腺素时，测定了主动脉 - 颈动脉压力差、头部灌注压（颈动脉 - 颈静脉压力差）和胸廓入口静脉“瓣膜作用”（中心静脉 - 颈静脉压力差）。
前瞻性研究，随机选择一侧颈动脉进行插管。
一家大型城市医院急诊科的复苏室。
15名体温正常、非创伤性院外心脏骤停的成年人，按照高级心脏生命支持指南进行治疗，包括每5分钟静脉注射1毫克肾上腺素。
对降主动脉、颈总动脉、颈内静脉和中心静脉系统进行插管。在静脉注射1毫克肾上腺素后，进行标准CPR 5分钟期间记录压力。
大多数患者在首次给予肾上腺素剂量前接受CPR超过20分钟，在进行上述压力记录前接受CPR超过45分钟。主动脉和颈动脉压缩及舒张期压力之间无显著差异。平均±标准差的压缩期中心静脉 - 颈静脉压力差为22.1±15.0毫米汞柱，平均头部灌注压为20.8±19.毫米汞柱。
即使长时间进行CPR，使用标准剂量肾上腺素进行人类CPR期间，主动脉 - 颈动脉压力差在临床上也无重要意义。尽管颈动脉通畅且胸廓入口静脉有瓣膜作用，但人类CPR期间头部灌注压仍较低。
