Babbs C F
Resuscitation. 1987 Mar;15(1):37-50. doi: 10.1016/0300-9572(87)90096-7.
Experimental work over the past decade has revealed three distinct mechanisms for generating artificial circulation during cardiac arrest and resuscitation. To isolate these mechanisms and study them in pure form, and in particular to characterize circulation during open vs. closed chest cardiopulmonary resuscitation (CPR), we developed an electrical model of the human circulatory system. Heart and blood vessels were modeled as resistive-capacitive networks, pressures in the chest, abdomen, and vascular compartments as voltages, blood flow as electric current, blood inertia as inductance, and the cardiac and venous valves as diodes. External pressurization of thoracic and abdominal vessels, as would occur in CPR, was simulated by application of half-sinusoidal voltage pulses. Simulations included two modes of creating artificial circulation: the cardiac pump mechanism, in which the atria and ventricles of the model were pressurized simultaneously, as occurs during open chest cardiac massage, and the thoracic pump mechanism, in which all intrathoracic elements of the model were pressurized simultaneously, as is likely to occur in closed chest CPR. The two mechanisms were compared for the same peak applied pressure (80 mmHg). Pure cardiac pump CPR generated near normal systemic perfusion pressures throughout the compression cycle. Pure thoracic pump CPR generated much lower systemic perfusion pressure only during the diastolic phase of the compression cycle. Simulation of cardiac compression at rates from 40 to 100/min produced total flows of 2500-3300, myocardial flows of 150-250 and cranial flows of 600-800 ml/min, depending on the compression rate. In contrast, thoracic pump CPR produced a total flow of approx. 1200, myocardial flow of 70, and cranial flow of 450 ml/min, independently of the compression rate. Direct cardiac compression is an inherently superior hemodynamic mechanism, because it can generate greater perfusion pressure throughout the compression cycle. If one presumes that improved blood flow during CPR is the key to more successful resuscitation, then it is reasonable to conclude that direct heart massage is the most effective available way to achieve this end.
过去十年的实验工作揭示了在心脏骤停和复苏过程中产生人工循环的三种不同机制。为了分离这些机制并以纯粹的形式对其进行研究，特别是为了表征开胸与闭胸心肺复苏（CPR）期间的循环情况，我们开发了一种人体循环系统的电学模型。心脏和血管被建模为电阻 - 电容网络，胸部、腹部和血管腔室中的压力被视为电压，血流被视为电流，血液惯性被视为电感，心脏瓣膜和静脉瓣膜被视为二极管。通过施加半正弦电压脉冲来模拟CPR中会出现的胸腹部血管的外部加压。模拟包括两种创建人工循环的模式：心脏泵机制，即模型的心房和心室同时受压，如同开胸心脏按摩时的情况；以及胸泵机制，即模型的所有胸腔内元件同时受压，这可能发生在闭胸CPR过程中。对这两种机制在相同的峰值施加压力（80 mmHg）下进行了比较。纯粹的心脏泵CPR在整个按压周期中产生接近正常的全身灌注压力。纯粹的胸泵CPR仅在按压周期的舒张期产生低得多的全身灌注压力。以40至100次/分钟的速率模拟心脏按压，根据按压速率的不同，产生的总血流量为2500 - 3300 ml/分钟，心肌血流量为150 - 250 ml/分钟，颅脑血流量为600 - 800 ml/分钟。相比之下，胸泵CPR产生的总血流量约为1200 ml/分钟，心肌血流量为70 ml/分钟，颅脑血流量为450 ml/分钟，与按压速率无关。直接心脏按压是一种本质上更优越的血流动力学机制，因为它可以在整个按压周期中产生更大的灌注压力。如果假定CPR期间改善的血流是更成功复苏的关键，那么合理的结论是直接心脏按摩是实现这一目标的最有效方法。
