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Hemodynamic effects of continuous abdominal binding during cardiac arrest and resuscitation
JANUARY
The American
Journal
15, 1984
of CARDIOLOGY@ VOLUME 53 NUMBER 2
EXPERIMENTAL STUDIES
Hemodynamic Effects of Continuous Abdominal Binding During Cardiac Arrest and Resuscitation JAMES T. NIEMANN, MD, JOHN P. ROSBOROUGH, PhD, STEVEN UNG, MD, and J. MICHAEL CRILEY, MD
Abdominal binding improves arterial pressure and flow during cardiopulmonary resuscitation (CPR). This study was undertaken to assess the mechanisms of improved hemodynamics during cardiac arrest and CPR with continuous abdominal binding in a canine model (n = 8). Carotid and inferior vena caval (IVC) flow probes and cineangiography were used to observe magnitude and direction of blood flow. CPR with binding significantly increased (p < 0.001) systolic aortic (Ao) (49 f 11 vs 34 f 12 mm Hg), right atrial (RA) (49 f 11 vs 31 f 10 mm Hg) and IVC pressure (50 f 7 versus 31 f 11 mm Hg) and common carotid flow (1.1 f 0.4 vs 0.7 f 0.4 ml/min/kg, p <0.05) compared with CPR without binding. Aortic, RA and IVC diastolic pressures increased similarly. Binding decreased the diastolic Ao-IVC pressure difference by 8 f 12 mm Hg and
decreased net IVC flow (0.5 f 1.4 vs 1.4 f 1.2 ml/min/kg, p <0.05). Binding also decreased coronary perfusion pressure (Ao-RA) in 5 of 8 dogs. Cineangiograms showed tricuspid incompetence and reflux from the right atrium to the inferior vena cava during chest compression and IVC-to-right heart inflow during relaxation, which was confirmed by the flowmeter data. Abdominal binding during CPR decreased the size of the perfused vascular bed by inhibiting subdiaphragmatic flow and increased intrathoracic pressure for a given chest compression force, leading to preferential cephalad flow. However, coronary perfusion pressure was often adversely affected. Further studies should be undertaken before the widespread clinical application of continuous abdominal binding during CPR. (Am J Cardiol 1984;53:269-274)
Almost 4 decades ago, Thompson and Rockey showed that anterograde blood flow could be produced during cardiac arrest solely by manipulating intrathoracic pressure.’ Contemporary investigations suggest that
systemic perfusion during circulatory arrest and cardiopulmonary resuscitation (CPR) is largely the result of cyclic variations in intrathoracic pressure.2J Specifically, chest compression during CPR produces an abrupt increase in intrathoracic pressure, which is directly transmitted to the intrathoracic vascular compartments and the extrathoracic arterial bed. The increase in central venous pressure results in closure of competent venous valves at the superior thoracic inlets and a low pressure is maintained in the brachiocephalic venous bed.3*4 A peripheral arteriovenous gradient is thus established to facilitate flow through the intracranial resistance vessels. The absence of subdiaphragmatic venous valves in close proximity to the right heart may mitigate subdi-
From the UCLA School of Medicine, Los Angeles, California, the Departments of Emergency Medicine, Medicine and Radiology, Los Angeles County Harbor-UCLA Medical Center, Torrance, California and the Baylor College of Medicine, Department of Physiology, Houston, Texas. This study was supported in part by Investigative Group Award 421Gll from the American Heart Association Greater Los Angeles Affiliate, Los Angeles, California, and by General Research Support Grant PR-05551 from the National Institutes of Health, Bethesda, Maryland. Manuscript received July 14, 1983, revised manuscript received September 12, 1983, accepted September 19, 1983. Address for reprints: J. Michael Criley, MD, Harbor-UCLA Medical Center, 1000 West Carson Street, Torrance, California 90509. 269
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ABDOMINAL BINDING DURING CARDIOPULMONARY RESUSCITATION
aphragmatic perfusion during CPR due to the lack of a mechanism to assure unidirectional flo~.~ In addition, recent studies have demonstrated a relation between pressure changes within the thoracic and abdominal cavities and the magnitude of anterograde flow during CPR.6s7 The abdominal and thoracic cavities may be simplistically viewed as a single compartment with respect to pressure fluctuations induced by thoracic compression when the diaphragm is flaccid, as during cardiopulmonary arrest. Subdiaphragmatic pressure is almost identical to intrathoracic pressure during chest compression. Manipulation of intraabdominal pressure during CPR theoretically could have salutary effects on circulatory dynamics. This theoretical consideration has been borne out by studies that have used tight circumferential abdominal binding or manual abdominal compression during closed-chest CPR. Abdominal binding increases carotid blood flow and both systolic and diastolic arterial pressure during CPR in animal models2svg and humans.lO External abdominal counterpulsation during CPR produces similar effects.li The present study was undertaken to determine if the absence of anatomic venous valves in the abdominal venous bed alters the timing and direction of subdiaphragmatic flow during cardiac arrest and CPR, and to assess the effect of circumferential abdominal binding on supra- and subdiaphragmatic circulatory dynamics.
Methods Eight mongrel dogs that weighed 16 to 24 kg were anesthetized with a single dose of ketamine hydrochloride, 10 mg/kg i.m., and sodium pentobarbital, 20 mg/kg i.v. Additional pentobarbital (5 mg/kg) was administered as needed during the surgical procedures. The dogs were intubated with a cuffed endotracheal tube and mechanically ventilated with ambient air during instrumentation. Heart rate and rhythm were monitored continuously with a lead II surface ECG. Transducer-tipped catheters (Millar Mikro-Tip@, size 5Fr) were positioned in the right atrium (RA) through a side branch of the external jugular vein, in the subdiaphragmatic inferior vena cava (IVC) via a femoral vein and in the ascending aorta (Ao) through a femoral or axillary artery. Catheter tip position was confirmed fluoroscopically, by characteristic pressure tracings and at necropsy after the study. Airway pressure was measured with a No. 7Fr transducer-tipped catheter through a side hole in the endotracheal tube connector. After systemic heparin administration (1 to 2 mg/kg i.v.), a cannulating electromagnetic flow probe (3 mm i.d.) was inserted into the left common carotid artery at the midcervical level in all dogs. A fiow probe (6 mm i.d.) was positioned in the IVC at the level of the renal vein via a right flank incision and retroperitoneal dissection. The flank incision was tightly closed in layers. Both flow probes had been previously calibrated in vitro and flow was measured with a square-wave flow meter (Narcomatic RT 50@‘, Narco-Biosystems). All pressure and flow data were recorded on a Gould 260 or 280 Brush@ recorder. During instrumentation, 50 to 150 ml of 0.9% saline was administered i.v. to replace estimated blood loss during the surgical procedures. No attempt was made to expand intravascular volume before ventricular fibrillation (VF) and CPR.
After control flows and intravascular pressures had been recorded over a lo-minute period, VF was induced with a transthoracic 120-V, 60-Hz shock; fibrillation was confirmed with surface electrocardiographic monitoring. Thirty to 60 seconds after the induction of VF, CPR was performed using a commercially available pneumatic, cylinder-piston device (Thumper@, Michigan Instruments). The sternum of the supine dog was depressed 2.0 to 2.5 inches with a piston force of 1.8 to 7.5 lb/kg body weight at a rate of 60 compression cycles/min and maintained for 0.5 second. A positive pressure lung inflation to an airway pressure of 40 mm Hg was interposed after every fifth compression. CPR with and CPR without abdominal binding were alternated for 5-minute periods. Abdominal binding was performed with a large blood pressure cuff inflated to 80 mm Hg and the binder remained inflated during both the compression and relaxation phases (continuous abdominal counterpressure). The binder was positioned below the costal margins and extended to the level of the pelvic brim. At the completion of each experiment, the thoracic and abdominal cavities were opened and visceral organs were visually inspected for evidence of trauma. Intravascular pressures during chest compression (systole), the mean intravascular pressure per cycle and arterial and venous flows (ml/min/kg) during systole, during the relation phase (diastole), and net flow (systolic plus diastolic flow) were calculated by an on-line microcomputer. Inferior vena caval resistance during chest compression was calculated by dividing the IVC pulse pressure (peak systolic minus end-diastolic) by systolic IVC flow. Diastolic coronary perfusion pressure was calculated by subtracting the right atrial pressure from the simultaneously recorded aortic pressure, both measured at the end of the relaxation phase. Reported data thus represent end-diastolic values. Differences in intravascular pressures and venous and arterial flows during CPR with and without abdominal binding were assessed using the t test for paired samples or analysis of variance with multiple comparison testing (Bonferroni t
***
T
60 1
CPR CPR w,th Bmdmq *p
**p
***p<0.001
**
T
A0
SYSTOLIC
A0
PRESSURE
DIASTOLIC
RA
IVC
PRESSURE
FIGURE 1. Intravascular pressures during cardiopulmonary resuscitation (CPR) with and without continuous abdominal binding. Systolic and diastolic ascending aortic (AO), right atrial (RA) and inferior vena caval (NC) pressures are shown. Continuous abdominal binding during CPR significantly increased all pressures (2-tailed, paired Student t test).
January 15, 1984
venous circulation through the femoral vessels and positioned in various cardiac chambers or great vessels. Cineangiograms were obtained at 60 frames/s after the manual injection of
Renografine or Dionosil@ droplets in lo-ml boluses. The timing and direction of blood flow through the great veins and right heart were also assessed using a free-floating 2-mm radiopaque bead attached to a short length of 00 silk suture and positioned in the central venous circulation through a conventional No. 8Fr catheter. During conventional CPR, the timing and direction of venous and right heart flow were reflected by movements of the bead within the intravascular compartments and were confirmed with contrast injections. All cinegraphic studies were performed with the dog in the right lateral decubitus position while compression was performed in the anteroposterior plane.
Results Mean aortic and right atria1 pressures after the induction of VF and before the initiation of CPR averaged 16 f 4 mm Hg and 12 f 4 mm Hg, respectively. During CPR without abdominal binding, each chest compression produced positive pressure pulses of comparable magnitude in the Ao and RA, and inferior vena cava and systolic pressures were not significantly different (analysis of variance, F = 0.120) (Fig. 1). However, the rate of increase of right atria1 pressure exceeded that of inferior vena caval pressure, a RA-IVC pressure gradient of 14 f 5 mm Hg was present during early systole and retrograde flow from the right heart to IVC was consistently demonstrated during each chest compression (Table I and Fig. 2). During the relaxation phase (diastole), inferior vena caval pressure exceeded right atria1 pressure by 12 f 4 mm Hg due to a more abrupt decrease in right atria1 pressure with the onset of relaxation, and IVC to right heart inflow occurred. Diastolic ascending aortic pressure (15 f 7 mm Hg) was significantly greater (p <0.05) than diastolic inferior vena caval pressure (9 f 2 mm Hg). During CPR without abdominal binding, net inferior vena caval flow averaged 1.4 f 1.2 ml/min/kg (14% of prearrest flow) and left common carotid arterial flow averaged 0.7 f 0.4 ml/min/kg (12% of prearrest flow). Abdominal binding to a cuff bladder pressure of 80 mm Hg during CPR produced a significant increase in all systolic and end-diastolic intravascular pressures
Discussion The results of this study suggest that subdiaphragmatic hemodynamic events differ considerably from
Carotid Arterial and Inferior Vena Caval Flow Carotid Flow
Systolic IVC Flow
Diastolic WC Flow
Net WC Flow
(ml/min/ka) Control
CPR
CPR with binding
5.7 f 2.3 0.7 f 0.4 1.1 f 0.4’
-5.4 -8.8
t 2.4 f 3.4
7.o.j.1.9 9.3 f 3.6
p <0.05 versus CPR without binding. CPR = cardiopulmonary resuscitation; IVC = inferior vena caval. l
271
(Fig. 1 and 2) as well as common carotid arterial flow (Table I and Fig. 3) compared with values recorded during CPR without binding. Systolic aortic, right atrial, and inferior vena caval pressures were again not significantly different (analysis of variance, F = 0.04). Tight abdominal binding did not prevent retrograde systolic flow from the right heart to the IVC and subdiaphragmatic venous return was again observed only during CPR diastole. Binding significantly decreased net inferior vena caval flow (subdiaphragmatic venous return) (Table I) and decreased the diastolic aorticinferior vena caval pressure difference by 8 f 12 mm Hg. Diastolic aortic (18 f 6 mm Hg) and inferior vena caval pressures (22 f 10 mm Hg) were not significantly different during binding. Abdominal binding did not significantly alter venous resistance (Table I), calculated by subtracting the end-diastolic inferior vena caval pressure from the systolic inferior vena caval pressure and dividing this value by the measured flow (ml/s) during each chest compression. End-diastolic coronary perfusion pressure (aortic minus right atria1 pressure) averaged 10 f 8 mm Hg during CPR without binding. Continuous abdominal binding increased both ascending aortic and right atria1 end-diastolic pressure (Fig. 1) and had a variable effect on the measured coronary perfusion gradient: it decreased in 5 dogs, did not change in 1 dog and increased in 2 dogs. For the group as a whole, end-diastolic coronary perfusion pressure during binding averaged 7 f 6 mm Hg and was not significantly different from the reported value during CPR without binding. Postexperiment necropsies on all dogs revealed no hepatic, splenic or intestinal lacerations and no intraperitoneal hemorrhage. Cinefluoroscopic observations: Cinefluoroscopy of the opaque bead as well as cineangiographic studies confirmed the timing and direction of subdiaphragmatic venous flow during CPR. Each chest compression resulted in marked tricuspid valve regurgitation and reflux into the IVC, and anterograde flow to the right heart occurred during the relaxation phase (Fig. 3). Retrograde flow into the superior vena cava was minimal.
when applicable. A p value of <0.05 was considered statistically significant. Cinefluoroscopic studies: In 6 additional dogs, angiographic catheters (Cordib No. 8Fr) were introduced into the test)
TABLE I
THE AMERICAN JOURNAL OF CARDIOLOGY Volume 53
9.7 f 2.4 1.4 f 1.2 0.5 f 1.4’
IVC Resistance (U) 1.6 f 0.8 12.9 f 9.5 12.7 f 9.3
272
ABDOMINAL BINDING DURING CARDIOPULMONARYRESUSCITATION
A0 (mmHg)
RA (mmHg)
IVC (mmHg)
CBF (ml/min)
IVCF (ml/min)
A0 (mmHg)
RA (mmHg)
IVC (mmHg)
0
3
2501 CBF (ml/min)
IVCF (ml/min)
O
C
C
lsec
FIGURE 2. Intravascular pressures and arterial and venous flows during cardiopulmonary resuscitation. Ascending aortic (Ao), right atrial (RA) and inferior vena caval (IVC) pressures and left common carotid blood flow (CBF) and IVC flow are shown. Top, 3 compression cycles (hatched bars) during CPR without binding are highlighted. In early systole, a large RA-IVC pressure difference occurred and resulted in retrograde flow into the inferior vena cava. With the onset of relaxation, RA pressure decreased abruptly but the decrease in IVC pressure was more gradual, resulting in a favorable gradient for IVC to right heart inflow. The open arrow (top) marks a positive pressure lung inflation. Tight abdominal binding during both the compression and relaxation phases (bottom) significantly increased Ao, RA and IVC pressures and CBF. Binding failed to prevent reflux from the right heart into the inferior vena cava during compression (C), but did result in a decrease in net IVC to right heart inflow. The open arrows (top) indicate lung inflation. These tracings were recorded in the same dog.
those observed in the brachiocephalic circulation during CPR. Inferior vena caval pressure fluctuations recorded during chest compression are the result of right heart to IVC reflux, while the presence of functioning venous valves at the superior thoracic inlets minimizes superior vena caval reflux and facilitates unidirectional flow across the brachiocephalic vessels during CPR.sr4 The absence of subdiaphragmatic venous valves in close proximity to the right heart results in retrograde inferior vena caval flow during chest compression, and venous return appears dependent upon a favorable IVC to right heart pressure gradient, initially due to the rapid early diastolic decline in the right atria1 pressure. These studies confirm that continuous abdominal binding during CPR increases intravascular systolic and diastolic pressures and common carotid arterial flow. Previous investigations demonstrated similar effects but differ from the present study with respect to flow measurement techniques and measured intravascular pressures, method of induction of circulatory arrest, rates at which chest compressions and lung ventilations were delivered, the force of sternal depression and the magnitude and method of abdominal binding. These variations may explain differences in results and their presumed mechanisms. Rudikoff et a1,2 using a canine cardiac arrest and CPR model similar to ours, proposed that the hemodynamic improvement noted during CPR with tight abdominal binding resulted from an increase in effective circulatory blood volume due to redistribution of blood from the splanchnic bed to the central circulation-an “autotransfusion” effect; a reduction in the size of the perfused arterial bed below the diaphragm via an unspecified mechanism; or an increase in intrathoracic pressure. In addition, tight abdominal binding could increase subdiaphragmatic venous resistance and “buffer venous backflow” during CPR, thereby inhibiting reflux from the central venous bed during chest compression and improving cardiac filling between compressions,8 or increasing transpulmonary blood flow during compression. Rudikoff et al2 demonstrated with volume infusions of 1 to 2 liters of normal saline that improved intravascular pressures and carotid arterial flow during CPR with abdominal binding (to an unspecified pressure) could not be ascribed exclusively to salutary changes in effective blood volume, i.e., a transfusion effect. Redding reached a similar conclusion using a manual CPR canine model subjected to cardiopulmonary bypass.9 In the present study, an increase in IVC to right heart electromagnetic flow was not appreciated during inflation of the abdominal binder. In our canine model, diastolic right atria1 pressures were lower than reported values by other investigators using animals of similar weight and using similar mechanical CPR techniques.lsJ3 This discrepancy may result from the fact that our experimental dogs received limited volumes of normal saline, calculated to replace only intraoperative blood loss, before cardiac arrest and CPR. Abdominal external binding to higher levels (>lOO mm Hg) could produce a redistribution of splanchnic blood volume in volume-expanded animals.
January 15. 1984
In this study, abdominal binding during CPR produced a significant increase in diastolic right atria1 and inferior vena caval pressures compared with CPR without abdominal binding. The present study suggests that the decrease in subdiaphragmatic venous return is the result of both an increase in central venous pressure and an unfavorable subdiaphragmatic arteriovenous pressure gradient during CPR diastole. With binding, a high venous pressure during relaxation decreased or reversed the arteriovenous pressure gradient, limiting arterial to venous inflow, and effectively reduced the size of the perfused vascular bed. Abdominal binding did not inhibit central venous reflux into the IVC, as originally suggested by Harris et a1.8 The present study demonstrates that retrograde flow actually increases and confirms an earlier observation by Redding.g Greater central venous to inferior vena caval reflux during abdominal binding appears to result from a higher RA-IVC pressure gradient during early chest compression. Coronary perfusion pressure (aortic minus right atria1 pressure) was low during cardiac arrest and CPR. The reported values are considerably below the estimated values required for minimal myocardial perfusion during VF.14 Other investigators have proposed that abdominal counterpressure improves myocardial blood flow by increasing coronary perfusion pressure,@ but
FIGURE 3. Cinefluoroscopic documentation of venous flow during cardioresuscitation (CPR). Venous flow patterns were studied using a radiopaque bead attached to a catheter with silk thread. Flow toward or away from the heart could be seen by the direction of displacement of the bead. The line drawing at the left illustrates the position of the cardiac chambers and intravascular catheters during CPR diastole (relaxation). Transducer-tipped catheters are positioned in the right atrium (RA) and descending thoracic aorta. Bead flow-indicator catheters were sequentially positioned in the superior vena cava (WC) and inferior vena cava (IVC) (dashed rectangles). The timing and direction of venous flow during CPR diastole are shown in tine frames A (WC) and C (IVC). The small dark arrows indicate the direction of venous flow. Flow toward the heart was seen only during the relaxation phase. During CPR systole (chest compression), the heart was displaced dorsally (large arrows), and the SVC radiopaque bead remained stationary (frame 6). However, retrograde flow (small arrows) was consistently demonstrated in the IVC (frame D).
THE AMERICAN JOURNAL OF CARDIOLOGY
Volume 53
273
right atria1 pressure was not measured and this conclusion is based solely on the increase in aortic diastolic pressure observed during counterpressure. Our data confirmed the significant increase in aortic end-diastolic pressure during abdominal counterpressure but there was also a similar rise in right atria1 pressure. In 5 of the 8 dogs, coronary perfusion pressure decreased; in 1 dog, perfusion pressure did not change. For the group as a whole, differences in coronary perfusion pressure during CPR with (7 f 6 mm Hg) and without binding (10 f mm Hg) failed to attain statistical significance. Abdominal binding should increase intravascular pressures and carotid arterial flow (and, by inference, cerebral perfusion) regardless of the presumed mechanism of blood flow during closed-chest resuscitation. If cardiac or vascular compression occurs during chest compression, the effect of abdominal binding on subdiaphragmatic venous pressure will limit subdiaphragmatic flow and produce a cephalad redistribution of cardiac output. If cyclic changes in intrathoracic pressure are responsible for anterograde flow during external CPR, binding will not only restrict subdiaphragmatic perfusion but will also increase intrathoracic pressuring during CPR systole and diastole. During chest compression, the diaphragm descends passively as intrathoracic pressure increases and thus attenuates the compression-induced increase in intrathoracic pressure. Abdominal binding increases intraabdominal pressure, restricts passive descent of the diaphragm and results in a higher intrathoracic pressure for a given compression force. Intraabdominal pressure remains elevated during the relaxation phase and may be responsible, in part, for the higher intrathoracic diastolic vascular pressures. The findings of this study have a number of potential clinical implications. First, the rise in inferior vena caval pressure during chest compression is the result not of arterial to venous inflow, but of right heart reflux. A palpable femoral “pulse” during CPR is as likely to be of venous origin as arterial and therefore may not be a reliable indicator of the “adequacy” of CPR. Second, drug administration during advanced cardiac life support via a subdiaphragmatic venous access site may not be an effective route, as drug delivery may be substantially delayed due to the “to-and-fro” movement of subdiaphragmatic venous blood. Third, although carotid arterial flow and cerebral blood flow may be improved with abdominal binding, this study suggests that such an intervention does not increase the aortic-right atria1 pressure difference, the gradient responsible for coronary perfusion. In 5 of the study dogs, binding decreased coronary perfusion pressure. Although continuous abdominal binding increases carotid blood flow, it may not improve coronary flow and is thus unlikely to facilitate restoration of spontaneous cardiac activity, i.e., cardiac resuscitation. References 1. ThompsonSA, Rockey EE. The effect of mechanical artificial respiration on maintenance of the circulation. Surg Gynecol Obstet 1947;84:10591062. 2. Rudikoff MT, Maughan WL, EffronM, FreundP, Weldektt ML. Mechanisms
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3. 4. 5. 6. 7. 6.
ABDOMINAL BINDING DURING CARDIOPULMONARY RESUSCITATION
of blood flow during cardiopulmonary resuscitation. Circulation 1980;61: 345-352. Niemann JT, Rosborough JP, Hausknechi M, Garner D, Criley JM. Pressure-synchronized cineangiography during experimental cardiopulmonary resuscitation. Circulation 1981;64:985-991. Fisher J, Vaghaiwalla F, Tsitlik J, Levin H, Brinker J, Weisfeldt M, Yin F. Determinants and clinical significance of jugular venous valve competence. Circulation 1982;65:188-196. Niemann JT, Ung S, Rosborough JP, Suzuki J, Criley JM. Preferential brachiocephalic flow during CPR-a hemodynamic explanation (abstr). Circulation 1981;64:suppl IV:IV-303. Rosborough JP, Niemann JT, Criley JM, D’Bannon W, Rouse D. Lower abdominal compression with synchronized ventilation: a CPR modality (abstr). Circulation 1981;64:suppl IV-IV-303. Ducas J, Roussos C, Karsardis C, Angle M, Magder S. Factors affecting the intrathoracic pressure during CPR (abstr). Circulation 1981;64:suppl IV-IV-302. Harris LC, Klrimll B, Safar P. Augmentation of artificial circulation during
cardiopulmonary resuscitation. Anesthesiology 1967;28:730-734. 6. Redding JS. Abdominal compression in cardiopulmonary resuscitation. Anesth Analg 1971;50:668-675. 10. Chandra N, Snyder LD, Weisfeldt ML. Abdominal binding during cardiopulmonary resuscitation in man. JAMA 1981;246:351-353. 11. Voorhees WD, Niebauer MJ, Babbs CF. Improved oxygen delivery during 12.
13. Ditchey RV, Winkler JV, Rhodes CA. Relative lack of coronary blood flow during closed chest resuscitation in dogs. Circulation 1982;66:297-302. 14. Downey JM, Chagrasulis RW, Hemphill V. Quantitative study of intramyocardial compression in the fibrillating heart. Am J Physiol 1979;237: H191-H196.
The American
Journal
15, 1984
of CARDIOLOGY@ VOLUME 53 NUMBER 2
EXPERIMENTAL STUDIES
Hemodynamic Effects of Continuous Abdominal Binding During Cardiac Arrest and Resuscitation JAMES T. NIEMANN, MD, JOHN P. ROSBOROUGH, PhD, STEVEN UNG, MD, and J. MICHAEL CRILEY, MD
Abdominal binding improves arterial pressure and flow during cardiopulmonary resuscitation (CPR). This study was undertaken to assess the mechanisms of improved hemodynamics during cardiac arrest and CPR with continuous abdominal binding in a canine model (n = 8). Carotid and inferior vena caval (IVC) flow probes and cineangiography were used to observe magnitude and direction of blood flow. CPR with binding significantly increased (p < 0.001) systolic aortic (Ao) (49 f 11 vs 34 f 12 mm Hg), right atrial (RA) (49 f 11 vs 31 f 10 mm Hg) and IVC pressure (50 f 7 versus 31 f 11 mm Hg) and common carotid flow (1.1 f 0.4 vs 0.7 f 0.4 ml/min/kg, p <0.05) compared with CPR without binding. Aortic, RA and IVC diastolic pressures increased similarly. Binding decreased the diastolic Ao-IVC pressure difference by 8 f 12 mm Hg and
decreased net IVC flow (0.5 f 1.4 vs 1.4 f 1.2 ml/min/kg, p <0.05). Binding also decreased coronary perfusion pressure (Ao-RA) in 5 of 8 dogs. Cineangiograms showed tricuspid incompetence and reflux from the right atrium to the inferior vena cava during chest compression and IVC-to-right heart inflow during relaxation, which was confirmed by the flowmeter data. Abdominal binding during CPR decreased the size of the perfused vascular bed by inhibiting subdiaphragmatic flow and increased intrathoracic pressure for a given chest compression force, leading to preferential cephalad flow. However, coronary perfusion pressure was often adversely affected. Further studies should be undertaken before the widespread clinical application of continuous abdominal binding during CPR. (Am J Cardiol 1984;53:269-274)
Almost 4 decades ago, Thompson and Rockey showed that anterograde blood flow could be produced during cardiac arrest solely by manipulating intrathoracic pressure.’ Contemporary investigations suggest that
systemic perfusion during circulatory arrest and cardiopulmonary resuscitation (CPR) is largely the result of cyclic variations in intrathoracic pressure.2J Specifically, chest compression during CPR produces an abrupt increase in intrathoracic pressure, which is directly transmitted to the intrathoracic vascular compartments and the extrathoracic arterial bed. The increase in central venous pressure results in closure of competent venous valves at the superior thoracic inlets and a low pressure is maintained in the brachiocephalic venous bed.3*4 A peripheral arteriovenous gradient is thus established to facilitate flow through the intracranial resistance vessels. The absence of subdiaphragmatic venous valves in close proximity to the right heart may mitigate subdi-
From the UCLA School of Medicine, Los Angeles, California, the Departments of Emergency Medicine, Medicine and Radiology, Los Angeles County Harbor-UCLA Medical Center, Torrance, California and the Baylor College of Medicine, Department of Physiology, Houston, Texas. This study was supported in part by Investigative Group Award 421Gll from the American Heart Association Greater Los Angeles Affiliate, Los Angeles, California, and by General Research Support Grant PR-05551 from the National Institutes of Health, Bethesda, Maryland. Manuscript received July 14, 1983, revised manuscript received September 12, 1983, accepted September 19, 1983. Address for reprints: J. Michael Criley, MD, Harbor-UCLA Medical Center, 1000 West Carson Street, Torrance, California 90509. 269
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ABDOMINAL BINDING DURING CARDIOPULMONARY RESUSCITATION
aphragmatic perfusion during CPR due to the lack of a mechanism to assure unidirectional flo~.~ In addition, recent studies have demonstrated a relation between pressure changes within the thoracic and abdominal cavities and the magnitude of anterograde flow during CPR.6s7 The abdominal and thoracic cavities may be simplistically viewed as a single compartment with respect to pressure fluctuations induced by thoracic compression when the diaphragm is flaccid, as during cardiopulmonary arrest. Subdiaphragmatic pressure is almost identical to intrathoracic pressure during chest compression. Manipulation of intraabdominal pressure during CPR theoretically could have salutary effects on circulatory dynamics. This theoretical consideration has been borne out by studies that have used tight circumferential abdominal binding or manual abdominal compression during closed-chest CPR. Abdominal binding increases carotid blood flow and both systolic and diastolic arterial pressure during CPR in animal models2svg and humans.lO External abdominal counterpulsation during CPR produces similar effects.li The present study was undertaken to determine if the absence of anatomic venous valves in the abdominal venous bed alters the timing and direction of subdiaphragmatic flow during cardiac arrest and CPR, and to assess the effect of circumferential abdominal binding on supra- and subdiaphragmatic circulatory dynamics.
Methods Eight mongrel dogs that weighed 16 to 24 kg were anesthetized with a single dose of ketamine hydrochloride, 10 mg/kg i.m., and sodium pentobarbital, 20 mg/kg i.v. Additional pentobarbital (5 mg/kg) was administered as needed during the surgical procedures. The dogs were intubated with a cuffed endotracheal tube and mechanically ventilated with ambient air during instrumentation. Heart rate and rhythm were monitored continuously with a lead II surface ECG. Transducer-tipped catheters (Millar Mikro-Tip@, size 5Fr) were positioned in the right atrium (RA) through a side branch of the external jugular vein, in the subdiaphragmatic inferior vena cava (IVC) via a femoral vein and in the ascending aorta (Ao) through a femoral or axillary artery. Catheter tip position was confirmed fluoroscopically, by characteristic pressure tracings and at necropsy after the study. Airway pressure was measured with a No. 7Fr transducer-tipped catheter through a side hole in the endotracheal tube connector. After systemic heparin administration (1 to 2 mg/kg i.v.), a cannulating electromagnetic flow probe (3 mm i.d.) was inserted into the left common carotid artery at the midcervical level in all dogs. A fiow probe (6 mm i.d.) was positioned in the IVC at the level of the renal vein via a right flank incision and retroperitoneal dissection. The flank incision was tightly closed in layers. Both flow probes had been previously calibrated in vitro and flow was measured with a square-wave flow meter (Narcomatic RT 50@‘, Narco-Biosystems). All pressure and flow data were recorded on a Gould 260 or 280 Brush@ recorder. During instrumentation, 50 to 150 ml of 0.9% saline was administered i.v. to replace estimated blood loss during the surgical procedures. No attempt was made to expand intravascular volume before ventricular fibrillation (VF) and CPR.
After control flows and intravascular pressures had been recorded over a lo-minute period, VF was induced with a transthoracic 120-V, 60-Hz shock; fibrillation was confirmed with surface electrocardiographic monitoring. Thirty to 60 seconds after the induction of VF, CPR was performed using a commercially available pneumatic, cylinder-piston device (Thumper@, Michigan Instruments). The sternum of the supine dog was depressed 2.0 to 2.5 inches with a piston force of 1.8 to 7.5 lb/kg body weight at a rate of 60 compression cycles/min and maintained for 0.5 second. A positive pressure lung inflation to an airway pressure of 40 mm Hg was interposed after every fifth compression. CPR with and CPR without abdominal binding were alternated for 5-minute periods. Abdominal binding was performed with a large blood pressure cuff inflated to 80 mm Hg and the binder remained inflated during both the compression and relaxation phases (continuous abdominal counterpressure). The binder was positioned below the costal margins and extended to the level of the pelvic brim. At the completion of each experiment, the thoracic and abdominal cavities were opened and visceral organs were visually inspected for evidence of trauma. Intravascular pressures during chest compression (systole), the mean intravascular pressure per cycle and arterial and venous flows (ml/min/kg) during systole, during the relation phase (diastole), and net flow (systolic plus diastolic flow) were calculated by an on-line microcomputer. Inferior vena caval resistance during chest compression was calculated by dividing the IVC pulse pressure (peak systolic minus end-diastolic) by systolic IVC flow. Diastolic coronary perfusion pressure was calculated by subtracting the right atrial pressure from the simultaneously recorded aortic pressure, both measured at the end of the relaxation phase. Reported data thus represent end-diastolic values. Differences in intravascular pressures and venous and arterial flows during CPR with and without abdominal binding were assessed using the t test for paired samples or analysis of variance with multiple comparison testing (Bonferroni t
***
T
60 1
CPR CPR w,th Bmdmq *p
**p
***p<0.001
**
T
A0
SYSTOLIC
A0
PRESSURE
DIASTOLIC
RA
IVC
PRESSURE
FIGURE 1. Intravascular pressures during cardiopulmonary resuscitation (CPR) with and without continuous abdominal binding. Systolic and diastolic ascending aortic (AO), right atrial (RA) and inferior vena caval (NC) pressures are shown. Continuous abdominal binding during CPR significantly increased all pressures (2-tailed, paired Student t test).
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venous circulation through the femoral vessels and positioned in various cardiac chambers or great vessels. Cineangiograms were obtained at 60 frames/s after the manual injection of
Renografine or Dionosil@ droplets in lo-ml boluses. The timing and direction of blood flow through the great veins and right heart were also assessed using a free-floating 2-mm radiopaque bead attached to a short length of 00 silk suture and positioned in the central venous circulation through a conventional No. 8Fr catheter. During conventional CPR, the timing and direction of venous and right heart flow were reflected by movements of the bead within the intravascular compartments and were confirmed with contrast injections. All cinegraphic studies were performed with the dog in the right lateral decubitus position while compression was performed in the anteroposterior plane.
Results Mean aortic and right atria1 pressures after the induction of VF and before the initiation of CPR averaged 16 f 4 mm Hg and 12 f 4 mm Hg, respectively. During CPR without abdominal binding, each chest compression produced positive pressure pulses of comparable magnitude in the Ao and RA, and inferior vena cava and systolic pressures were not significantly different (analysis of variance, F = 0.120) (Fig. 1). However, the rate of increase of right atria1 pressure exceeded that of inferior vena caval pressure, a RA-IVC pressure gradient of 14 f 5 mm Hg was present during early systole and retrograde flow from the right heart to IVC was consistently demonstrated during each chest compression (Table I and Fig. 2). During the relaxation phase (diastole), inferior vena caval pressure exceeded right atria1 pressure by 12 f 4 mm Hg due to a more abrupt decrease in right atria1 pressure with the onset of relaxation, and IVC to right heart inflow occurred. Diastolic ascending aortic pressure (15 f 7 mm Hg) was significantly greater (p <0.05) than diastolic inferior vena caval pressure (9 f 2 mm Hg). During CPR without abdominal binding, net inferior vena caval flow averaged 1.4 f 1.2 ml/min/kg (14% of prearrest flow) and left common carotid arterial flow averaged 0.7 f 0.4 ml/min/kg (12% of prearrest flow). Abdominal binding to a cuff bladder pressure of 80 mm Hg during CPR produced a significant increase in all systolic and end-diastolic intravascular pressures
Discussion The results of this study suggest that subdiaphragmatic hemodynamic events differ considerably from
Carotid Arterial and Inferior Vena Caval Flow Carotid Flow
Systolic IVC Flow
Diastolic WC Flow
Net WC Flow
(ml/min/ka) Control
CPR
CPR with binding
5.7 f 2.3 0.7 f 0.4 1.1 f 0.4’
-5.4 -8.8
t 2.4 f 3.4
7.o.j.1.9 9.3 f 3.6
p <0.05 versus CPR without binding. CPR = cardiopulmonary resuscitation; IVC = inferior vena caval. l
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(Fig. 1 and 2) as well as common carotid arterial flow (Table I and Fig. 3) compared with values recorded during CPR without binding. Systolic aortic, right atrial, and inferior vena caval pressures were again not significantly different (analysis of variance, F = 0.04). Tight abdominal binding did not prevent retrograde systolic flow from the right heart to the IVC and subdiaphragmatic venous return was again observed only during CPR diastole. Binding significantly decreased net inferior vena caval flow (subdiaphragmatic venous return) (Table I) and decreased the diastolic aorticinferior vena caval pressure difference by 8 f 12 mm Hg. Diastolic aortic (18 f 6 mm Hg) and inferior vena caval pressures (22 f 10 mm Hg) were not significantly different during binding. Abdominal binding did not significantly alter venous resistance (Table I), calculated by subtracting the end-diastolic inferior vena caval pressure from the systolic inferior vena caval pressure and dividing this value by the measured flow (ml/s) during each chest compression. End-diastolic coronary perfusion pressure (aortic minus right atria1 pressure) averaged 10 f 8 mm Hg during CPR without binding. Continuous abdominal binding increased both ascending aortic and right atria1 end-diastolic pressure (Fig. 1) and had a variable effect on the measured coronary perfusion gradient: it decreased in 5 dogs, did not change in 1 dog and increased in 2 dogs. For the group as a whole, end-diastolic coronary perfusion pressure during binding averaged 7 f 6 mm Hg and was not significantly different from the reported value during CPR without binding. Postexperiment necropsies on all dogs revealed no hepatic, splenic or intestinal lacerations and no intraperitoneal hemorrhage. Cinefluoroscopic observations: Cinefluoroscopy of the opaque bead as well as cineangiographic studies confirmed the timing and direction of subdiaphragmatic venous flow during CPR. Each chest compression resulted in marked tricuspid valve regurgitation and reflux into the IVC, and anterograde flow to the right heart occurred during the relaxation phase (Fig. 3). Retrograde flow into the superior vena cava was minimal.
when applicable. A p value of <0.05 was considered statistically significant. Cinefluoroscopic studies: In 6 additional dogs, angiographic catheters (Cordib No. 8Fr) were introduced into the test)
TABLE I
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9.7 f 2.4 1.4 f 1.2 0.5 f 1.4’
IVC Resistance (U) 1.6 f 0.8 12.9 f 9.5 12.7 f 9.3
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A0 (mmHg)
RA (mmHg)
IVC (mmHg)
CBF (ml/min)
IVCF (ml/min)
A0 (mmHg)
RA (mmHg)
IVC (mmHg)
0
3
2501 CBF (ml/min)
IVCF (ml/min)
O
C
C
lsec
FIGURE 2. Intravascular pressures and arterial and venous flows during cardiopulmonary resuscitation. Ascending aortic (Ao), right atrial (RA) and inferior vena caval (IVC) pressures and left common carotid blood flow (CBF) and IVC flow are shown. Top, 3 compression cycles (hatched bars) during CPR without binding are highlighted. In early systole, a large RA-IVC pressure difference occurred and resulted in retrograde flow into the inferior vena cava. With the onset of relaxation, RA pressure decreased abruptly but the decrease in IVC pressure was more gradual, resulting in a favorable gradient for IVC to right heart inflow. The open arrow (top) marks a positive pressure lung inflation. Tight abdominal binding during both the compression and relaxation phases (bottom) significantly increased Ao, RA and IVC pressures and CBF. Binding failed to prevent reflux from the right heart into the inferior vena cava during compression (C), but did result in a decrease in net IVC to right heart inflow. The open arrows (top) indicate lung inflation. These tracings were recorded in the same dog.
those observed in the brachiocephalic circulation during CPR. Inferior vena caval pressure fluctuations recorded during chest compression are the result of right heart to IVC reflux, while the presence of functioning venous valves at the superior thoracic inlets minimizes superior vena caval reflux and facilitates unidirectional flow across the brachiocephalic vessels during CPR.sr4 The absence of subdiaphragmatic venous valves in close proximity to the right heart results in retrograde inferior vena caval flow during chest compression, and venous return appears dependent upon a favorable IVC to right heart pressure gradient, initially due to the rapid early diastolic decline in the right atria1 pressure. These studies confirm that continuous abdominal binding during CPR increases intravascular systolic and diastolic pressures and common carotid arterial flow. Previous investigations demonstrated similar effects but differ from the present study with respect to flow measurement techniques and measured intravascular pressures, method of induction of circulatory arrest, rates at which chest compressions and lung ventilations were delivered, the force of sternal depression and the magnitude and method of abdominal binding. These variations may explain differences in results and their presumed mechanisms. Rudikoff et a1,2 using a canine cardiac arrest and CPR model similar to ours, proposed that the hemodynamic improvement noted during CPR with tight abdominal binding resulted from an increase in effective circulatory blood volume due to redistribution of blood from the splanchnic bed to the central circulation-an “autotransfusion” effect; a reduction in the size of the perfused arterial bed below the diaphragm via an unspecified mechanism; or an increase in intrathoracic pressure. In addition, tight abdominal binding could increase subdiaphragmatic venous resistance and “buffer venous backflow” during CPR, thereby inhibiting reflux from the central venous bed during chest compression and improving cardiac filling between compressions,8 or increasing transpulmonary blood flow during compression. Rudikoff et al2 demonstrated with volume infusions of 1 to 2 liters of normal saline that improved intravascular pressures and carotid arterial flow during CPR with abdominal binding (to an unspecified pressure) could not be ascribed exclusively to salutary changes in effective blood volume, i.e., a transfusion effect. Redding reached a similar conclusion using a manual CPR canine model subjected to cardiopulmonary bypass.9 In the present study, an increase in IVC to right heart electromagnetic flow was not appreciated during inflation of the abdominal binder. In our canine model, diastolic right atria1 pressures were lower than reported values by other investigators using animals of similar weight and using similar mechanical CPR techniques.lsJ3 This discrepancy may result from the fact that our experimental dogs received limited volumes of normal saline, calculated to replace only intraoperative blood loss, before cardiac arrest and CPR. Abdominal external binding to higher levels (>lOO mm Hg) could produce a redistribution of splanchnic blood volume in volume-expanded animals.
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In this study, abdominal binding during CPR produced a significant increase in diastolic right atria1 and inferior vena caval pressures compared with CPR without abdominal binding. The present study suggests that the decrease in subdiaphragmatic venous return is the result of both an increase in central venous pressure and an unfavorable subdiaphragmatic arteriovenous pressure gradient during CPR diastole. With binding, a high venous pressure during relaxation decreased or reversed the arteriovenous pressure gradient, limiting arterial to venous inflow, and effectively reduced the size of the perfused vascular bed. Abdominal binding did not inhibit central venous reflux into the IVC, as originally suggested by Harris et a1.8 The present study demonstrates that retrograde flow actually increases and confirms an earlier observation by Redding.g Greater central venous to inferior vena caval reflux during abdominal binding appears to result from a higher RA-IVC pressure gradient during early chest compression. Coronary perfusion pressure (aortic minus right atria1 pressure) was low during cardiac arrest and CPR. The reported values are considerably below the estimated values required for minimal myocardial perfusion during VF.14 Other investigators have proposed that abdominal counterpressure improves myocardial blood flow by increasing coronary perfusion pressure,@ but
FIGURE 3. Cinefluoroscopic documentation of venous flow during cardioresuscitation (CPR). Venous flow patterns were studied using a radiopaque bead attached to a catheter with silk thread. Flow toward or away from the heart could be seen by the direction of displacement of the bead. The line drawing at the left illustrates the position of the cardiac chambers and intravascular catheters during CPR diastole (relaxation). Transducer-tipped catheters are positioned in the right atrium (RA) and descending thoracic aorta. Bead flow-indicator catheters were sequentially positioned in the superior vena cava (WC) and inferior vena cava (IVC) (dashed rectangles). The timing and direction of venous flow during CPR diastole are shown in tine frames A (WC) and C (IVC). The small dark arrows indicate the direction of venous flow. Flow toward the heart was seen only during the relaxation phase. During CPR systole (chest compression), the heart was displaced dorsally (large arrows), and the SVC radiopaque bead remained stationary (frame 6). However, retrograde flow (small arrows) was consistently demonstrated in the IVC (frame D).
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right atria1 pressure was not measured and this conclusion is based solely on the increase in aortic diastolic pressure observed during counterpressure. Our data confirmed the significant increase in aortic end-diastolic pressure during abdominal counterpressure but there was also a similar rise in right atria1 pressure. In 5 of the 8 dogs, coronary perfusion pressure decreased; in 1 dog, perfusion pressure did not change. For the group as a whole, differences in coronary perfusion pressure during CPR with (7 f 6 mm Hg) and without binding (10 f mm Hg) failed to attain statistical significance. Abdominal binding should increase intravascular pressures and carotid arterial flow (and, by inference, cerebral perfusion) regardless of the presumed mechanism of blood flow during closed-chest resuscitation. If cardiac or vascular compression occurs during chest compression, the effect of abdominal binding on subdiaphragmatic venous pressure will limit subdiaphragmatic flow and produce a cephalad redistribution of cardiac output. If cyclic changes in intrathoracic pressure are responsible for anterograde flow during external CPR, binding will not only restrict subdiaphragmatic perfusion but will also increase intrathoracic pressuring during CPR systole and diastole. During chest compression, the diaphragm descends passively as intrathoracic pressure increases and thus attenuates the compression-induced increase in intrathoracic pressure. Abdominal binding increases intraabdominal pressure, restricts passive descent of the diaphragm and results in a higher intrathoracic pressure for a given compression force. Intraabdominal pressure remains elevated during the relaxation phase and may be responsible, in part, for the higher intrathoracic diastolic vascular pressures. The findings of this study have a number of potential clinical implications. First, the rise in inferior vena caval pressure during chest compression is the result not of arterial to venous inflow, but of right heart reflux. A palpable femoral “pulse” during CPR is as likely to be of venous origin as arterial and therefore may not be a reliable indicator of the “adequacy” of CPR. Second, drug administration during advanced cardiac life support via a subdiaphragmatic venous access site may not be an effective route, as drug delivery may be substantially delayed due to the “to-and-fro” movement of subdiaphragmatic venous blood. Third, although carotid arterial flow and cerebral blood flow may be improved with abdominal binding, this study suggests that such an intervention does not increase the aortic-right atria1 pressure difference, the gradient responsible for coronary perfusion. In 5 of the study dogs, binding decreased coronary perfusion pressure. Although continuous abdominal binding increases carotid blood flow, it may not improve coronary flow and is thus unlikely to facilitate restoration of spontaneous cardiac activity, i.e., cardiac resuscitation. References 1. ThompsonSA, Rockey EE. The effect of mechanical artificial respiration on maintenance of the circulation. Surg Gynecol Obstet 1947;84:10591062. 2. Rudikoff MT, Maughan WL, EffronM, FreundP, Weldektt ML. Mechanisms
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3. 4. 5. 6. 7. 6.
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of blood flow during cardiopulmonary resuscitation. Circulation 1980;61: 345-352. Niemann JT, Rosborough JP, Hausknechi M, Garner D, Criley JM. Pressure-synchronized cineangiography during experimental cardiopulmonary resuscitation. Circulation 1981;64:985-991. Fisher J, Vaghaiwalla F, Tsitlik J, Levin H, Brinker J, Weisfeldt M, Yin F. Determinants and clinical significance of jugular venous valve competence. Circulation 1982;65:188-196. Niemann JT, Ung S, Rosborough JP, Suzuki J, Criley JM. Preferential brachiocephalic flow during CPR-a hemodynamic explanation (abstr). Circulation 1981;64:suppl IV:IV-303. Rosborough JP, Niemann JT, Criley JM, D’Bannon W, Rouse D. Lower abdominal compression with synchronized ventilation: a CPR modality (abstr). Circulation 1981;64:suppl IV-IV-303. Ducas J, Roussos C, Karsardis C, Angle M, Magder S. Factors affecting the intrathoracic pressure during CPR (abstr). Circulation 1981;64:suppl IV-IV-302. Harris LC, Klrimll B, Safar P. Augmentation of artificial circulation during
cardiopulmonary resuscitation. Anesthesiology 1967;28:730-734. 6. Redding JS. Abdominal compression in cardiopulmonary resuscitation. Anesth Analg 1971;50:668-675. 10. Chandra N, Snyder LD, Weisfeldt ML. Abdominal binding during cardiopulmonary resuscitation in man. JAMA 1981;246:351-353. 11. Voorhees WD, Niebauer MJ, Babbs CF. Improved oxygen delivery during 12.
13. Ditchey RV, Winkler JV, Rhodes CA. Relative lack of coronary blood flow during closed chest resuscitation in dogs. Circulation 1982;66:297-302. 14. Downey JM, Chagrasulis RW, Hemphill V. Quantitative study of intramyocardial compression in the fibrillating heart. Am J Physiol 1979;237: H191-H196.