(Circulation. 1995;91:215-221.)
© 1995 American Heart Association, Inc.
Articles |
Vasopressin Improves Vital Organ Blood Flow During Closed-Chest Cardiopulmonary Resuscitation in Pigs
From the Department of Anesthesiology and Critical Care Medicine, University of Ulm, Germany (K.H.L., A.W.P., E.G.P., I.M.L., H.U.S., M.G.), and the Cardiovascular Division, Department of Medicine, University of Minnesota, Minneapolis (K.G.L.).
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Abstract |
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Background This study was designed to compare the effects of epinephrine with those of vasopressin on vital organ blood flow during closed-chest cardiopulmonary resuscitation (CPR) in a pig model of ventricular fibrillation.
Methods and Results Vasopressin was compared with epinephrine by randomly allocating 28 pigs to receive either 0.2 mg/kg epinephrine (n=7), 0.2 U/kg vasopressin (low dose) (n=7), 0.4 U/kg vasopressin (medium dose) (n=7), or 0.8 U/kg vasopressin (high dose) (n=7) after 4 minutes of ventricular fibrillation and 3 minutes of closed-chest CPR. Left ventricular myocardial blood flow, determined by use of radiolabeled microspheres during CPR, before and then 90 seconds and 5 minutes after drug administration was 17±2, 43±5, and 22±3 mL · min-1 · l00 g-1 (mean±SEM) in the epinephrine group; 18±2, 50±6, and 29±3 mL · min-1 · 100 g-1 in the low-dose vasopressin group; 17±3, 52±8, and 52±6 mL · min-1 · 100 g-1 in the medium-dose vasopressin group; and 18±2, 95±9, and 57±6 mL · min-1 · 100 g-1 in the high-dose vasopressin group (P<.001 at 90 seconds and 5 minutes between epinephrine and high-dose vasopressin, and P<.01 at 5 minutes between epinephrine and medium-dose vasopressin). At the same times, calculated coronary systolic perfusion pressures were 12±2, 36±5, and 18±2 mm Hg in the epinephrine group; 10±1, 39±6, and 26±5 mm Hg in the low-dose vasopressin group; 11±2, 49±6, and 38±5 mm Hg in the medium-dose vasopressin group; and 10±2, 70±5, and 47±6 mm Hg in the high-dose vasopressin group (P<.01 at 90 seconds and 5 minutes between epinephrine and high-dose vasopressin); and calculated coronary diastolic perfusion pressures were 15±2, 24±2, and 19±2 mm Hg in the epinephrine group; 13±1, 25±2, and 20±1 mm Hg in the low-dose vasopressin group; 13±2, 25±2, and 21±2 mm Hg in the medium-dose vasopressin group; and 13±2, 35±3, and 24±2 mm Hg in the high-dose vasopressin group (P<.05 at 90 seconds between epinephrine and high-dose vasopressin). Total cerebral blood flow was significantly higher after high-dose vasopressin than after epinephrine (P<.05 at 90 seconds and P<.01 at 5 minutes between groups). Five animals in the epinephrine, 5 in the low-dose vasopressin, 7 in the medium-dose vasopressin, and 6 in the high-dose vasopressin groups were successfully resuscitated and survived the 1-hour observation period.
Conclusions We conclude that administration of vasopressin leads to a significantly higher coronary perfusion pressure and myocardial blood flow than epinephrine during closed-chest CPR in a pig model of ventricular fibrillation.
Key Words: fibrillation • microspheres • regional blood flow • acid-base imbalance
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Introduction |
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In an effort to improve the currently dismal outcome for most victims of cardiac arrest, a number of fundamental endocrinologic responses of the body to cardiac arrest and CPR have been investigated.1 2 3 4 We recently reported that circulating endogenous vasopressin concentrations are very high in patients in cardiac arrest undergoing cardiopulmonary resuscitation (CPR) and that levels were significantly higher in resuscitated than in nonresuscitated patients.5 These results suggested that endogenously released vasopressin might be a crucial factor in enhancing the pressor response to endogenously released epinephrine, norepinephrine, angiotensin II, and endothelin.
More recently, we demonstrated in a pig model of ventricular fibrillation that administration of exogenous vasopressin during open-chest CPR significantly improves blood flow to vital organs.6 Although this study was promising, it was limited in that we were able to assess only the effects of single doses of vasopressin and epinephrine. Moreover, we did not know whether the effects of vasopressin would be similar during closed-chest CPR. In a pig model, Brown et al7 demonstrated that 0.2 mg/kg of epinephrine administered during ventricular fibrillation was the dose at which maximum vital organ blood flow takes place. Thus, the aim of our investigation was to compare the effects of different doses of vasopressin with those of epinephrine (0.2 mg/kg) on vital organ perfusion during closed-chest CPR.
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Methods |
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Surgical Preparation
This study was performed on 28 healthy, 12- to 14-week-old domestic pigs weighing 26 to 31 kg. It was approved by our institutional animal investigation committee. The animals were managed in accordance with the guidelines of the American Physiological Society. Before surgery, they were all fasted overnight but had free access to water. The pigs were premedicated with azaperon (4 mg/kg IM) and atropine (0.1 mg/kg IM) 1 hour before surgery. Anesthesia was induced with 15 mg/kg pentobarbital given via an ear vein. The pigs were then fixed in the dorsal recumbent position, and their tracheas were intubated during spontaneous respiration. They were ventilated with a Servo ventilator 900 (Servo, Siemens) with 65% nitrous oxide in oxygen at 20 breaths per minute and with a tidal volume adjusted to maintain the mean arterial PCO2 at 35 mm Hg. Anesthesia was maintained with a continuous intravenous infusion of pentobarbital (0.4 mg · kg-1 · h-1) and a single dose of buprenorphine (0.015 mg/kg). Ringer's solution (6 mL · kg-1 · h-1) was administered continuously throughout the preparation and study period with an infusion pump (Infusomat, Braun). A standard lead II ECG was used to monitor cardiac rhythm.
Multiple catheters were used for hemodynamic monitoring and measurement of organ blood flow. Two 7F catheters were advanced by femoral cutdown into the descending aorta for monitoring of blood pressure and withdrawal of blood samples. Reference blood samples for measurement of organ blood flow were withdrawn from a 5F catheter placed in the descending aorta by femoral cutdown. A separate 5F catheter was placed into the right atrium for drug administration. A 7F pigtail catheter with multiple distal side ports used to inject radionuclide microspheres was placed under pressure control via femoral cutdown into the left ventricle. This catheter was also used to inject iced saline solution (5 mL) to measure cardiac output. A 5F pulmonary artery catheter (Swan-Ganz, Baxter Edwards Laboratories) was placed under pressure control via a branch of the external jugular vein into the pulmonary artery. For the measurement of body temperature, a thermistor probe was placed via femoral artery cutdown into the abdominal aorta. Body temperature was recorded from this catheter (blood temperature) and maintained between 37.5°C and 38.5°C with a heating pad. All catheters were pressure flushed with saline containing 5 U heparin/mL at a rate of 3 mL/h (Intraflo II, Abbott Laboratories) to prevent obstruction during the preparation phase. After completion of surgery and before induction of cardiac arrest, 300 U/kg sodium heparin was administered intravenously to prevent intracardiac clot formation. All animals were autopsied to check correct positioning of the catheters and to look for damage to the rib cage and internal organs.
Measurements
Aortic and right atrial pressures were measured
via the
saline-filled catheters with calibrated pressure transducers (model
1290A, Hewlett Packard) that were calibrated to atmospheric pressure at
the level of the right atrium. Pressure tracings were continuously
recorded (Hewlett Packard 7 758 multichannel recorder), and mean
pressures were obtained by electronic integration. Heart rate was
determined from a simultaneously recorded ECG signal. Coronary
perfusion pressure calculated during systole (compression) and diastole
(relaxation) was defined as the arteriovenous pressure difference
(time-coincident difference between aortic and right atrial diastolic
pressure) and was measured with an electronic subtraction unit.
Measurements were recorded before arrest and during the period of
closed-chest CPR with two monitors (model 78342A, Hewlett Packard) and
a data acquisition/control unit (model 9133, Hewlett Packard). On-line
measurements were performed at intervals of 30 seconds before induction
of cardiac arrest and after restoration of spontaneous circulation
(ROSC) and at intervals of 1 second during CPR. Arterial blood gases
were measured with a blood gas analyzer (IL 1302, Allied
Instrumentation Laboratories) and corrected for body temperature.
Hemoglobin content and oxygen saturation were measured with a
co-oximeter (model 282, Allied Instrumentation Laboratories). Arterial
lactate concentrations were determined by a lactate analyzer (2300 STAT
lactate analyzer, Yellow Springs Instruments). The CO2
concentration of expired gas was measured continuously by an infrared
absorption analyzer (Capnomac Ultima, Datex Instrumentarium). A Fleisch
pneumotachometer (7319, Dynasciences) was used to measure tidal volume.
Accuracy of measurement was <0.2% in the range between 0% and 5%.
The sample manifold of the analyzer was attached to the proximal end of
the endotracheal tube with a side-port connector. Gas was withdrawn at
a rate of 200 mL/min.
Vital organ blood flow was measured by use of radiolabeled microspheres as previously described.8 9 Organ blood flow was measured in the present study before and at 90 seconds and 5 minutes after drug administration during CPR. Microspheres radioactively labeled with 141Ce, 95Nb, or 103Ru (New England Nuclear) had a mean diameter of 15±1.5 µm and a specific activity of 10 mCi/g. Each microsphere vial was placed in a water bath and subjected to ultrasonic vibration for 1 minute before injection. Approximately 5x105 microspheres, diluted in 10 mL saline, were then immediately injected into the left ventricle. With an automatic pump (Perfusor, Braun), arterial blood was continuously withdrawn from the descending aorta at a rate of 9.9 mL/min from 10 seconds before to 80 seconds after microsphere injection. At the end of the experiment, the entire heart, cerebrum, both kidneys, and samples of head muscle, head fat, and small intestine were removed. The left ventricular free wall was sectioned into three layers. Aliquots of each tissue were weighed, homogenized, and then placed into vials. Radioactivities from tissues and blood were measured with a gamma scintillation spectrometer (LB 5300, Berthold).
Experimental Protocol
Before induction of cardiocirculatory
arrest, hemodynamic
parameters, arterial and blood gases, and lactate concentrations were
measured simultaneously. A 50-Hz, 60-V AC was applied via two
subcutaneous needle electrodes to induce ventricular fibrillation.
Cardiocirculatory arrest was defined as that point at which the aortic
pulse pressure decreased to zero and ECG showed ventricular
fibrillation. Ventilation was stopped at this point. After 4 minutes of
arrest, closed-chest CPR was performed with a pneumatically driven
automatic piston device (Thumper, model 1003, Michigan Instruments),
and mechanical ventilation (900, Servo ventilator, Siemens) was
simultaneously initiated. The compression pad of the device was placed
on the midsternum, the chest compression rate was 80 per minute, and
the duration of compression was 50% of the total cycle time. The
velocity of compression (5 in/s) was held constant during the course of
CPR. During closed-chest CPR, the compression force applied to the
sternum and the resulting sternal displacement are crucial determinants
for the blood flow achieved. Based on experiments using the same animal
model,10 the chest compression force was adjusted to
produce 25% sternal displacement of the pig's anteroposterior chest
diameter. Relaxation (decompression) was allowed to occur passively.
Mechanical ventilation with an FIO2 of 1.0 at
20 breaths per minute was performed independently of chest compression
at a tidal volume shown to result in an arterial
PCO2 of 35 mm Hg before induction of cardiac
arrest.
After 3 minutes of CPR, animals were randomly assigned to receive either 0.2 mg/kg epinephrine (n=7), 0.2 U/kg vasopressin (low dose) (n=7), 0.4 U/kg vasopressin (medium dose) (n=7), or 0.8 U/kg vasopressin (high dose) (n=7) given via right atrial catheter over a period of 5 seconds. All drugs were diluted to 10 mL in physiological saline, and during the arrest the animals were allocated to drug treatment by random numbers. The investigators were blinded to use of drugs. Hemodynamic measurements, measurement of variables, and acquisition of aortic blood samples were performed before induction of ventricular fibrillation, before drug administration (ie, after a total of 7 minutes of arrest, including 3 minutes of CPR), and 90 seconds and 5 minutes after drug administration, as well as at 5, 15, 30, and 60 minutes when resuscitation was successful. Immediately after acquiring the last blood sample during CPR (ie, after a total of 12 minutes of arrest, including 8 minutes of CPR), we attempted to restore spontaneous circulation with DC shocks. The time needed for ROSC was measured from that point in time. Three DC countershocks were initially administered in rapid succession at an energy setting of 3 J/kg. If ventricular fibrillation or ventricular tachycardia persisted, the same drug was administered at the same dose as previously given, and closed-chest CPR was reinitiated for an additional 90 seconds. Three DC shocks (5 J/kg) were then again delivered in rapid sequence. The same protocol (without defibrillation) was used if asystole or pulseless electrical activity developed. Successful resuscitation was defined as the presence of coordinated electrical activity, a systolic blood pressure >90 mm Hg, and a diastolic blood pressure >40 mm Hg for at least 5 minutes, during which no further resuscitative measures were applied.
Statistical Analysis
Values are expressed as mean±SEM.
All data were stored on a
computer system (Hewlett Packard 9000, type 300). One-way ANOVA was
used to determine statistical significance of the differences between
the four groups, followed by the Student-Newman-Keuls post hoc test.
Where necessary, a square root transformation was performed on the data
before calculation to satisfy the assumption of approximate equality of
variance of the sample distribution. Paired Student's t
test (two-tailed) was used to determine differences during CPR before
and 90 seconds after drug administration. Because time intervals
between the first defibrillation and ROSC were distributed unevenly,
they are expressed as medians and as minimum and maximum. For these
variables, the Mann-Whitney U test (two-tailed) was used to
determine differences between the groups. For multiple comparisons
within one group, the Bonferroni method was applied. Statistical
significance was considered at P<.05.
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Results |
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TopAbstractIntroductionMethods Results Discussion References |
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After induction of ventricular fibrillation and performance of CPR, 5 animals in the epinephrine group, 5 in the low-dose vasopressin group, 7 in the medium-dose vasopressin group, and 6 in the high-dose vasopressin group were successfully resuscitated and survived the 1-hour observation period. Two animals in the epinephrine group stayed in ventricular fibrillation, and 2 of the low-dose vasopressin and 1 of the high-dose vasopressin group were defibrillated into pulseless electrical activity. After removal of the last blood sample during CPR, which was immediately followed by defibrillation (ie, after a total of 12 minutes of arrest, including 8 minutes of CPR), spontaneous circulation was restored within 247 (85 to 296) seconds in the epinephrine group, 88 (20 to 256) seconds in the low-dose vasopressin group, 39 (4 to 152) seconds in the medium-dose vasopressin group, and 14 (8 to 152) seconds in the high-dose vasopressin group (P<.05 epinephrine versus medium-dose vasopressin and versus high-dose vasopressin). Five epinephrine, 4 low-dose vasopressin, 2 medium-dose vasopressin, and 1 high-dose vasopressin animals required one further injection of the same drug and dose as initially given. In the first minutes after ROSC, 2 of 5 epinephrine-treated and 5 of 6 vasopressin-treated animals (2 in the medium-dose and 3 in the high-dose group) required lidocaine infusions (1.5 mg/kg bolus followed by 0.14 mg · kg-1 · min-1) to treat sustained ventricular dysrhythmias. Autopsy revealed no damage to the thoracic cage or the internal organs in any of the groups. In each vasopressin animal of all three groups, a striking skin pallor occurred within approximately 30 seconds after drug administration, which was not present after epinephrine. Especially in the high-dose vasopressin group, this phenomenon was still present during the first 30 minutes after ROSC.
End-tidal CO2, which correlates closely with
cardiac output, decreased from a prearrest value of 4.4±0.1%,
4.3±0.1%, 4.4±0.2%, and 4.3±0.1% in the epinephrine,
low-dose
vasopressin, medium-dose vasopressin, and high-dose vasopressin groups,
respectively, to approximately 0.1% in all animals immediately after
induction after ventricular fibrillation but before initiation of
mechanical measures (Fig 1
). During CPR but before
drug administration, the end-tidal CO2 was 2.2±0.3%,
2.0±0.2%, 2.0±0.3%, and 2.3±0.2% in the four groups,
respectively. Ninety seconds after drug administration, end-tidal
CO2 decreased significantly (P<.05) in all
groups compared with values before drug during CPR. Intergroup
comparison showed a significant difference between the epinephrine
group and the high-dose vasopressin group at 90 seconds after drug
administration.
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There were no differences in hemodynamic variables before induction of
arrest between groups (Table 1). Systolic and
diastolic coronary perfusion pressures during CPR and before and after
drug administration are shown in Fig 2. Ninety seconds
after drug administration, systolic and diastolic coronary perfusion
pressures were significantly higher in the high-dose vasopressin group
than in the epinephrine group. Heart rate was significantly lower in
the high-dose vasopressin group than in the epinephrine group at 5
minutes after ROSC (Table 1). At both points during CPR after
drug
administration, mean arterial pressure was significantly higher in the
high-dose vasopressin group than in the epinephrine group. However,
cardiac index was significantly lower at 90 seconds after drug
administration in the medium-dose vasopressin and in the high-dose
vasopressin compared with the epinephrine group. Right atrial pressures
and pulmonary artery wedge pressures were not significantly different
between the groups either during or after resuscitation. A
significantly higher systemic vascular resistance was found in the
high-dose vasopressin group at 90 seconds and 5 minutes after drug
administration during CPR compared with the epinephrine group (Fig
3).
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Differences in regional organ blood flow between treatment groups are
shown in Fig 4 and Tables 2 and
3. Before drug administration during CPR, left
ventricular myocardial blood flow was 17±2
mL · min-1 · 100 g-1 in the
epinephrine, 18±2 mL · min-1 · 100
g-1 in the low-dose vasopressin, 17±1
mL · min-1 · 100 g-1 in the
medium-dose vasopressin, and 18±2
mL · min-1 · 100 g-1 in the
high-dose
vasopressin groups (Fig 4). In these four groups, left
ventricular
myocardial blood flow was 43±5, 50±6, 52±8, and
95±9
mL · min-1 · 100 g-1 at 90
seconds
and 22±3, 29±3, 52±6, and 57±6
mL · min-1 · 100 g-1 at 5
minutes
after drug administration (P<.001 at 90 seconds and 5
minutes between epinephrine and high-dose vasopressin, and
P<.01 at 5 minutes between epinephrine and low-dose
vasopressin). At 90 seconds and 5 minutes after high-dose vasopressin,
epicardial and endocardial blood flow remained significantly higher
than after epinephrine (Table 2). Since high-dose vasopressin
increased
epicardial blood flow more than endocardial blood flow, the ratio of
endocardial to epicardial blood flow was significantly lower in this
group compared with the epinephrine group. Total cerebral blood flow
after drug administration was significantly higher in the high-dose
vasopressin group at 90 seconds, and at 5 minutes after drug
administration it was significantly higher in all three vasopressin
groups than in the epinephrine group (Fig 5). In
contrast, nonvital organ blood flow, including head muscle, fat, and
small intestine blood flow, was significantly lower or even zero in all
three vasopressin groups compared with the epinephrine group.
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Arterial blood gas analyses and lactate concentrations before arrest, during CPR, and in the postresuscitation phase were not significantly different between the four groups.
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Discussion |
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TopAbstractIntroductionMethods Results Discussion References |
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The sustained release of extraordinary levels of the potent vasoconstrictor vasopressin in victims of cardiac arrest receiving CPR suggested the possibility that exogenous vasopressin administration during CPR may be beneficial. Results from this study comparing different doses of vasopressin with the dose of epinephrine known to maximize vital organ blood flow in pigs during cardiac arrest demonstrate that vasopressin causes higher arterial pressures and greater coronary perfusion and vital organ blood flow compared with optimal epinephrine administration during ventricular fibrillation and CPR. In addition to higher perfusion pressures and improved vital organ blood flow, these effects of vasopressin lasted significantly longer than those of epinephrine. Five minutes after epinephrine administration, left ventricular and total cerebral blood flow were only 29% and 22% greater than baseline, respectively. In contrast, 5 minutes after high-dose vasopressin, left ventricular and total cerebral perfusion were 217% and 111% greater than baseline flow, respectively.
End-tidal CO2 measurement during CPR has been postulated to correlate with cardiac index, coronary perfusion pressure, and the possibility of restoring spontaneous circulation.11 In a recent study in pigs, high-dose epinephrine resulted in a decrease in cardiac index and end-tidal CO2 while improving myocardial blood flow.14 The effects of vasopressin on cardiac index and end-tidal CO2 were previously unknown. The lower end-tidal CO2 and cardiac index and the higher systemic vascular resistance after high-dose vasopressin compared with epinephrine clarify the mechanism of vasopressin action during CPR. Analogous to profound hypovolemia secondary to hemorrhage, vasopressin therapy during CPR appears to work by acutely increasing systemic vascular resistance.15 Vasopressin may increase peripheral vasoconstriction directly via the "V1" receptor and/or by potentiating the vasoconstrictor effects of endogenous catecholamines.16 17 In so doing, it appears to shunt blood away from noncritical organs (skeletal muscle, small intestine, and fatty tissues) more than epinephrine does. Renal blood flow was not significantly different between the groups. This is in agreement with a report by Liard18 demonstrating that during vasopressin infusion, blood flow to skin, skeletal muscle, and fat is reduced more than cardiac output but that other organs, in particular the kidney and the liver, do not show any fall in blood flow at all. Our results are similar to others, finding a similar pattern of preferential shunting of blood to more vital organs, especially the brain, by an endothelium-mediated cerebral artery relaxation.19 20 21 Our study clearly demonstrates that the dissociation between cardiac index and end-tidal CO2 on the one hand and myocardial and cerebral perfusion on the other hand is stronger after high-dose vasopressin than after epinephrine.
When a high compression force was used, coronary perfusion pressures during the compression and decompression phases were approximately the same before drug administration in all groups. Like epinephrine, vasopressin improves coronary perfusion pressure during both compression and decompression.22 In humans, it has been demonstrated that vasopressin releases nitric oxide to cause vasodilation in forearm resistance arteries.23 It is hypothesized that the effects of this substance are biphasic, causing an initial strong peripheral vasoconstriction, followed by an increased production of nitric oxide and a consecutive vasodilation, leveling off the vasoconstriction in the immediate postresuscitation phase.24 Postdefibrillation dysrhythmias were observed in both the epinephrine and the vasopressin medium-dose and high-dose groups in the immediate postresuscitation phase, but they were successfully treated with lidocaine and did not lead to renewed cardiac arrest. The lower heart rate immediately after ROSC in the high-dose vasopressin group may have been caused by stimulation of the arterial baroreceptor reflex or lack of ß1-adrenergic receptor stimulation.
This study is limited in that we were able to assess only regional organ blood flow and not the metabolic status of the myocardium during CPR. A myocardial blood flow of at least 20 to 25 mL · min-1 · 100 g-1 seems to be necessary for successful defibrillation and ROSC in experimental animals.25 Because in all instances myocardial blood flow was above that threshold after drug administration, it is not surprising that the majority of animals could be resuscitated. It may well be that a different treatment regime with a third repetition of drug administration and the use of sodium bicarbonate could have restored spontaneous circulation in all animals. Although no differences in cardiac index or right atrial or pulmonary artery wedge pressure were measured in the postresuscitation phase, an impairment of myocardial function following high-dose vasopressin administration cannot be excluded. Long-term survival and neurological outcome in the postresuscitation phase were not evaluated in this study; in addition, this study included only healthy animals. Long-term animal studies should assess whether renal and gut function after ROSC are worse after vasopressin because of greater ischemia during CPR and after ROSC. In dogs in which an area of myocardium had been rendered collateral dependent without producing myocardial infarction, vasopressin impaired perfusion of the collateral-dependent region during physiological conditions and during exercise.24 One important aspect that remains to be elucidated is whether after myocardial infarction and cardiac arrest, vasopressin administration might enlarge the ischemic area. Because of the marked skin pallor after vasopressin administration, blinding the investigators to the drug administered was not possible.
In conclusion, these experiments support the hypothesis that administration of 0.8 U/kg vasopressin during closed-chest CPR significantly improves blood flow to vital organs compared with 0.2 mg/kg epinephrine. No deleterious side effects of vasopressin on cardiac index and gas exchange were observed during the 1-hour postresuscitation phase. It is possible that in the future, we may be able to develop a "CPR cocktail" that contains a number of vasoactive substances, including vasopressin, to improve the chances for survival after a cardiac arrest.
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Acknowledgments |
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This study was supported in part by a grant donated from the Laerdal Foundation, Stavanger, Norway.
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Footnotes |
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Reprint requests to Dr Karl H. Lindner, Universitätsklinik für Anästhesiologie, Klinikum der Universität Ulm, Steinhövelstr 9, 89075 Ulm, FRG.
Received May 13, 1994; accepted July 31, 1994.
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