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Chest compression moves blood during cardiac arrest by generating changes in intrathoracic pressure
AMERICAN
JOURNAL
OF EMERGENCY
MEDICINE
H Volume
2, Number
both inspiratory and expiratory muscles are stimulated and there is no air flow into or out of the trachea. Ideally, electrodes will be positioned to produce maximum inspiratory effort with minimum applied current. The optimum site for thoracic electrodes to produce a strong inspiration in the dog is just below the axilla. This site corresponds to the motor point for the long and lateral thoracic nerves which innervate the muscles of inspiration. The optimum stimulus is a short burst (0.5 seconds) of short duration (50 microseconds) pulses having a frequency of 60 per second. This type of stimulus produces a smooth tetanic contraction of the inspiratory muscles. ‘&pically, one tidal volume (160 ml) is produced with 40 mA of current. The choice of short-duration pulses enables the current required for electroventilation to be many times lower than that which produces cardiac stimulation. Preliminary studies in dogs have shown that it is possible to provide a tidal volume five times that of the animal’s normal tidal volume. The studies have also shown that electroventilation can maintain oxygen saturation. Furthermore, electroventilation is effective even after 5 minutes of circulatory arrest. Moreover, in these studies, no cardiac arrhythmias have been encountered.
ulated,
Chest Compression Moves Blood during Cardiac Arrest by Generating Changes in Intrathoracic Pressure. Henry R. Halperin, Joshua E. Tsitlik, Alan Guerci, Nisha Chandra, Myron L. Weisfeldt. Johns Hopkins Medical Institutions, Baltimore, MD 21205. Chest compression during cardiac arrest can move blood because of changes in intrathoracic pressure (ITP) or because of direct cardiac compression. In this study the authors examined myocardial (aortic to right atria1 mean diastolic pressure) and cerebral (carotid to intracranial mean pressure) perfusion pressures produced by manual cardiopulmonary resuscitation (CPR) at rates of 60 and 150/min in eight 21-32 kg dogs, and compared them with perfusion pressures produced by pure ITP fluctuations in the same animals at the same rate and similar peak right atria1 pressures as manual CPR. Perfusion pressures are estimates of blood flow because both myocardial and cerebral flow correlate with their perfusion pressures (r = 0.87, P < 0.001; r = .89, P < 0.001, respectively) in these eight dogs. If blood moves because of cardiac compression, then (1) increasing the rate should move more blood and generate higher perfusion pressures, and (2) perfusion pressures produced by manual CPR should be higher than those produced by ITP fluctuations at any level of vascular pressure. In these eight dogs, with no surgical manipulation of the chest, increasing perfusion pressures were obtained by manual CPR at increasing sternal forces from 100-400 N, and by ITP fluctuations from a pneumatically cycled vest (vest CPR) around the thorax. Sternal displacement with the vest was less than 0.6 cm, precluding direct compression of the heart. Perfusion pressures were normalized across dogs by dividing the perfusion pressures of the four CPR techniques for each dog by the perfusion pressure produced at a peak right atrial pressure of 80 mm Hg by manual CPR at 6O/min in that dog. Perfusion pressures correlated with right atrial pressure for all techniques (P < 0.001 for each). The relation between 350
4 n July 1984
cerebral perfusion pressure and peak right atrial pressure for manual CPR did not vary with rate (slope 0.018 c 0.003, intercept -0.46 rt 0.11 at 60/min versus slope 0.016 + 0.001, intercept -0.24 + 0.07 at 150/min, P = NS) and was not steeper than that of vest CPR (slope 0.018 * 0.002, intercept -0.34 f 0.19 at 60/min versus slope 0.022 ? 0.002, intercept -0.72 ? 0.17 at 1501min). Similarly, there was no relationship between rate and myocardial perfusion gradients. Thus, because of rate insensitivity and the similarity of manual and vest CPR, even if chest compression produces changes in shape of the heart, there is no significant contribution of cardiac compression to blood flow. The Contribution of Left Ventricular Stroke Volume to CPR Blood Flow Depends upon the Duty Cycle. M. J. Hausknecht, R. Brower, R. Wise, S. Permutt. Johns Hopkins Medical Institutions. Baltimore, MD 21205. Controversy exists whether volume changes of the left ventricle (LV) contribute to blood flow in CPR. Some investigators have found that the LV acts as a passive conduit, while others have shown that the LV volume decreases during compression. The authors have analyzed a mathematical model of CPR in which the intrathoracic vasculature is modeled as two compliances, an upstream pulmonary compartment and a downstream LV compartment with a common surrounding pleural pressure. Analysis of this model could account for these apparently conflicting observations. This model makes the following predictions: (1) There is an optimum duty cycle at which CPR blood flow is maximal. (2) The contribution of LV stroke volume to CPR blood flow increases as the duty cycle decreases. (3) The change in pleural pressure that generates the maximum CPR blood flow (Pplmax) increases as the duty cycle decreases. In order to test this model, five fibrillated canine heartlung preparations were placed in an artificial thorax where pleural pressure could be controlled and accurately measured. The heart and lungs were connected to an analogue of the peripheral circulation with a Starling resistor, a peripheral venous reservoir, and a one-way valve attached to the venous conduit. Pleural pressure was cycled at Pplmax at a frequency of 6 cycles per minute. The duty cycle (fraction of cycle spent in compression) was varied from 0.1 to 0.9 in increments of 0.1. Constant conditions included static vascular pressure of 15 mm Hg, Starling resistor pressure of 30 mm Hg, and peripheral compliance of 20 ml/mm Hg, Starling resistor pressure of 30 mm Hg, and peripheral compliance of 20 ml/mm Hg. The CPR blood flow (Qcpr) was measured by integration of the instantaneous aortic blood flow, as well as the change in transmural pressure of the left ventricle (Plvtm), which was used as an index of LV stroke volume. The results are listed below:
outv cyc/e Pplmax mm Hg Qcpr ml/min
0.9
0.6
0.7
0.6
0.5
0.4
0.3
0.2
34
40
40
40
46
50
58
68
89
217
287
355
392
427
406
332
214
1.95
3.10
4.25
5.45
6.25
7.40
7.35
6.75
96 Plvtm mm Hg 0.85
0.1
JOURNAL
OF EMERGENCY
MEDICINE
H Volume
2, Number
both inspiratory and expiratory muscles are stimulated and there is no air flow into or out of the trachea. Ideally, electrodes will be positioned to produce maximum inspiratory effort with minimum applied current. The optimum site for thoracic electrodes to produce a strong inspiration in the dog is just below the axilla. This site corresponds to the motor point for the long and lateral thoracic nerves which innervate the muscles of inspiration. The optimum stimulus is a short burst (0.5 seconds) of short duration (50 microseconds) pulses having a frequency of 60 per second. This type of stimulus produces a smooth tetanic contraction of the inspiratory muscles. ‘&pically, one tidal volume (160 ml) is produced with 40 mA of current. The choice of short-duration pulses enables the current required for electroventilation to be many times lower than that which produces cardiac stimulation. Preliminary studies in dogs have shown that it is possible to provide a tidal volume five times that of the animal’s normal tidal volume. The studies have also shown that electroventilation can maintain oxygen saturation. Furthermore, electroventilation is effective even after 5 minutes of circulatory arrest. Moreover, in these studies, no cardiac arrhythmias have been encountered.
ulated,
Chest Compression Moves Blood during Cardiac Arrest by Generating Changes in Intrathoracic Pressure. Henry R. Halperin, Joshua E. Tsitlik, Alan Guerci, Nisha Chandra, Myron L. Weisfeldt. Johns Hopkins Medical Institutions, Baltimore, MD 21205. Chest compression during cardiac arrest can move blood because of changes in intrathoracic pressure (ITP) or because of direct cardiac compression. In this study the authors examined myocardial (aortic to right atria1 mean diastolic pressure) and cerebral (carotid to intracranial mean pressure) perfusion pressures produced by manual cardiopulmonary resuscitation (CPR) at rates of 60 and 150/min in eight 21-32 kg dogs, and compared them with perfusion pressures produced by pure ITP fluctuations in the same animals at the same rate and similar peak right atria1 pressures as manual CPR. Perfusion pressures are estimates of blood flow because both myocardial and cerebral flow correlate with their perfusion pressures (r = 0.87, P < 0.001; r = .89, P < 0.001, respectively) in these eight dogs. If blood moves because of cardiac compression, then (1) increasing the rate should move more blood and generate higher perfusion pressures, and (2) perfusion pressures produced by manual CPR should be higher than those produced by ITP fluctuations at any level of vascular pressure. In these eight dogs, with no surgical manipulation of the chest, increasing perfusion pressures were obtained by manual CPR at increasing sternal forces from 100-400 N, and by ITP fluctuations from a pneumatically cycled vest (vest CPR) around the thorax. Sternal displacement with the vest was less than 0.6 cm, precluding direct compression of the heart. Perfusion pressures were normalized across dogs by dividing the perfusion pressures of the four CPR techniques for each dog by the perfusion pressure produced at a peak right atrial pressure of 80 mm Hg by manual CPR at 6O/min in that dog. Perfusion pressures correlated with right atrial pressure for all techniques (P < 0.001 for each). The relation between 350
4 n July 1984
cerebral perfusion pressure and peak right atrial pressure for manual CPR did not vary with rate (slope 0.018 c 0.003, intercept -0.46 rt 0.11 at 60/min versus slope 0.016 + 0.001, intercept -0.24 + 0.07 at 150/min, P = NS) and was not steeper than that of vest CPR (slope 0.018 * 0.002, intercept -0.34 f 0.19 at 60/min versus slope 0.022 ? 0.002, intercept -0.72 ? 0.17 at 1501min). Similarly, there was no relationship between rate and myocardial perfusion gradients. Thus, because of rate insensitivity and the similarity of manual and vest CPR, even if chest compression produces changes in shape of the heart, there is no significant contribution of cardiac compression to blood flow. The Contribution of Left Ventricular Stroke Volume to CPR Blood Flow Depends upon the Duty Cycle. M. J. Hausknecht, R. Brower, R. Wise, S. Permutt. Johns Hopkins Medical Institutions. Baltimore, MD 21205. Controversy exists whether volume changes of the left ventricle (LV) contribute to blood flow in CPR. Some investigators have found that the LV acts as a passive conduit, while others have shown that the LV volume decreases during compression. The authors have analyzed a mathematical model of CPR in which the intrathoracic vasculature is modeled as two compliances, an upstream pulmonary compartment and a downstream LV compartment with a common surrounding pleural pressure. Analysis of this model could account for these apparently conflicting observations. This model makes the following predictions: (1) There is an optimum duty cycle at which CPR blood flow is maximal. (2) The contribution of LV stroke volume to CPR blood flow increases as the duty cycle decreases. (3) The change in pleural pressure that generates the maximum CPR blood flow (Pplmax) increases as the duty cycle decreases. In order to test this model, five fibrillated canine heartlung preparations were placed in an artificial thorax where pleural pressure could be controlled and accurately measured. The heart and lungs were connected to an analogue of the peripheral circulation with a Starling resistor, a peripheral venous reservoir, and a one-way valve attached to the venous conduit. Pleural pressure was cycled at Pplmax at a frequency of 6 cycles per minute. The duty cycle (fraction of cycle spent in compression) was varied from 0.1 to 0.9 in increments of 0.1. Constant conditions included static vascular pressure of 15 mm Hg, Starling resistor pressure of 30 mm Hg, and peripheral compliance of 20 ml/mm Hg, Starling resistor pressure of 30 mm Hg, and peripheral compliance of 20 ml/mm Hg. The CPR blood flow (Qcpr) was measured by integration of the instantaneous aortic blood flow, as well as the change in transmural pressure of the left ventricle (Plvtm), which was used as an index of LV stroke volume. The results are listed below:
outv cyc/e Pplmax mm Hg Qcpr ml/min
0.9
0.6
0.7
0.6
0.5
0.4
0.3
0.2
34
40
40
40
46
50
58
68
89
217
287
355
392
427
406
332
214
1.95
3.10
4.25
5.45
6.25
7.40
7.35
6.75
96 Plvtm mm Hg 0.85
0.1