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Delivery of oxygenated blood during cardiac arrest and CPR is critically dependent on the effectiveness of chest compressions. The major thrust of current CPR research has been directed toward optimizing blood flow by means of variations in compression techniques. The recommended chest compression rate is 100/min with a depth (1.5 to 2.0 inches) sufficient to generate a palpable carotid or femoral pulse. A compression-to-relaxation ratio of 50:50 is advocated. During one-person CPR, the recommended compression-ventilation ratio is 15:2. In two-person CPR when the patient's airway is not secured with a tracheal tube, the recommended compression-ventilation ratio is also 15:2. Once the trachea is intubated, a compression-ventilation ratio of 5:1 is recommended with continuous chest compressions and asynchronous ventilation. In both one- and two-person CPR, the chest compression rate is 100/minute.
Figure 78-1
A, Schematic representation
of a cardiac compression pump. B, An intrathoracic
pressure pump. C, collapse of airways and venous structures; LV, left ventricle;
RV, right ventricle. (Redrawn with modification from Halperin HR: Mechanisms
of forward flow during external chest compression. In
Paradis NA, Halperin HR, Nowak RM [eds]: Cardiac Arrest: The Science and Practice
of Resuscitation Medicine. Baltimore, Williams & Wilkins, 1995, p 252.)
Since the early 1960s, when CPR became a widespread clinical technique, it has been assumed that blood is ejected as a direct result of actual compression of the heart between the sternum and the vertebral column. This is commonly referred to as the cardiac pump mechanism. Echocardiographic and hemodynamic measurements obtained during experimental porcine CPR have demonstrated that both the mitral and tricuspid valves open during the upstroke phase of external compression and close during downstroke. A reduction in left ventricular area occurred during downstroke.[41] These observations support direct cardiac compression as the mechanism producing forward blood flow during CPR. Transesophageal echocardiography in arrested humans provides an opportunity to assess changes in cardiac dimensions and valve positions during chest compressions, as well as the direction of blood flow. With this method of assessment it has been confirmed that at least in some patients, direct cardiac compression is the predominant mechanism of blood flow during external chest compression.[42] [43] [44] Right and left ventricular compression, mitral valve closure during downstroke of the compression phase, and opening of the mitral valve during the upstroke or relaxation phase are all consistent with direct cardiac compression, or the cardiac pump mechanism ( Fig. 78-1A ).[42] [43]
The finding that repeated, forceful coughing (cough CPR) can sustain consciousness during ventricular fibrillation (VF) for as long as 100 seconds suggests that
Interposed abdominal counterpulsation (IAC) is a form of CPR in which the abdomen is compressed midway between the xiphoid process and the umbilicus during the upstroke of the chest compression phase in an attempt to sustain aortic diastolic pressure and thus improve coronary perfusion pressure, a critical determinant of successful restoration of spontaneous circulation. Experimental evidence has shown that carotid blood flow[49] and end-diastolic arteriovenous pressure differences,[50] indexes of coronary perfusion pressure, are increased with IAC-CPR. A randomized controlled trial comparing IAC-CPR with standard CPR in humans in asystolic and electromechanical dissociation arrest indicated that IAC-CPR conferred a significantly more frequent return of spontaneous circulation, but no patient in either the IAC-CPR group or the standard CPR group survived to hospital discharge.[51] When sufficient personnel trained in the technique are available, IAC-CPR can be considered a reasonable alternative to standard CPR.
Active compression-decompression (ACD) CPR accomplishes compression and active decompression of the thorax by means of a device containing a suction header, bellows, and a compression area within the bellows. Preliminary data in arrested humans comparing ACD-CPR with standard CPR have provided evidence of hemodynamic benefit, with higher systolic arterial pressure and PETCO2 and echocardiographic demonstration of an increased velocity time integral, an analog of cardiac output. In a study of 16 patients with out-of-hospital cardiac arrest, peak PETCO2 was significantly higher during ACD-CPR than during standard manual CPR (27.6 ± 3 versus 15.6 ± 2.2 mm Hg).[52] This finding was interpreted to reflect higher cardiac output with ACD-CPR.
In humans studied during implantation of cardioverter-defibrillators (also see Chapter 35 ), ACD-CPR increased systemic arterial pressure, coronary perfusion pressure, and minute ventilation when compared with standard CPR.[53] Although these observations provided clinical support for experimental studies indicating improved hemodynamic (and perhaps ventilatory) function with ACD-CPR versus standard CPR, still lacking was evidence of benefit on patient outcome. Several studies have been undertaken to address this critical question. In one such study of patients experiencing in-hospital cardiac arrest, initial return of spontaneous circulation was higher with ACD-CPR than with standard manual CPR, but there was no statistically significant improvement in survival to hospital discharge.[54]
Several studies of ACD-CPR have been carried out in patients with out-of-hospital cardiac arrest,[55] [56] [57] but none has demonstrated an improvement in patient outcome in terms of hospital discharge when ACD-CPR was compared with standard CPR. The largest study comparing ACD-CPR with standard CPR included 1784 adults with in-hospital and prehospital cardiac arrest. This study, like its predecessors, concluded that ACD-CPR does not improve survival or neurologic outcomes.[58] Thus, despite the earlier experimental and clinical evidence that ACD-CPR may confer benefit to victims of cardiac arrest by virtue of enhanced hemodynamic variables, no evidence to date supports the hypothesis that ACD-CPR improves outcome from cardiac arrest in humans when compared with standard manual CPR.
Circumferential compression of the chest with a pneumatic vest (vest CPR) has been described as a mechanism for generating intrathoracic pressure fluctuations and thereby improving blood flow by exploiting the thoracic pump mechanism ( Fig. 78-2 ).[59] [60] The increased intrathoracic pressure fluctuations are apparently mediated through increased chest compression force and increased airway collapse during chest compression by trapping of air in the lungs. The latter may also increase the effectiveness of transmission of vest pressure to the intrathoracic space. The increased intrathoracic pressure with vest CPR is the presumed major mechanism of hemodynamic benefit. As with ACD-CPR, vest CPR has been shown in a preliminary study to increase both aortic and coronary perfusion pressure,[61] but no data are yet available relative to its impact on survival, the ultimate determinant of benefit.
Much more information is needed before any of these observations can be extended to modification of currently recommended CPR practice as described earlier. It is likely that both direct cardiac compression and intrathoracic pressure changes contribute to forward blood flow and that they are not mutually exclusive. In some patients, the cardiac pump may be primarily operative, whereas in others, the thoracic pump may predominate.[62] [63] Continued transesophageal echocardiographic observations in human victims of cardiac arrest may provide insight into which mechanism of blood flow is functional in which patients. Most important, until the clinical relevance of any of these observations is established, standard CPR techniques as described are recommended. What is certain is that CPR, regardless of the mechanism of blood flow and technique, is only a temporizing procedure in need of rapid supplementation with ACLS, most critically, rapid defibrillation of the fibrillating heart.
Figure 78-2
Comparison of the thoracic vest system (A)
for cardiopulmonary resuscitation (vest CPR) and standard manual CPR (B).
The vest contains a bladder that is inflated and deflated by a pneumatic system.
The lower panels show schematic representations
of transverse sections of the midthorax during vest CPR and manual CPR. Thoracic
size during chest relaxation is shown by the solid lines.
The arrows indicate force applied to the thorax
during chest compression. Vest inflation produces a relatively uniform decrease
in dimensions of the thorax. With manual CPR, the sternum is displaced during compression
(arrow) and the lateral aspect of the thorax can
bulge, thereby increasing thoracic volume and reducing the intrathoracic pressure
generated during compression. (Redrawn with modification from Halperin HR,
Tsitlik JE, Gelfand M, et al: A preliminary study of cardiopulmonary resuscitation
by circumferential compression of the chest with use of a pneumatic vest. N Engl
J Med 329:762, 1993.)
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