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Anesth Analg 2000;90:1067-1075
© 2000 International Anesthesia Research Society

CARDIOVASCULAR ANESTHESIA

The Effects of Repeated Doses of Vasopressin or Epinephrine on Ventricular Fibrillation in a Porcine Model of Prolonged Cardiopulmonary Resuscitation

Ulrich Achleitner, MSc*, Volker Wenzel, MD*, Hans-Ulrich Strohmenger, MD*, Anette C. Krismer, MD*, Keith G. Lurie, MD{dagger}, Karl H. Lindner, MD*, and Anton Amann, PhD*

*Department of Anesthesiology and Critical Care Medicine, Leopold-Franzens-University of Innsbruck, Innsbruck, Austria; and the {dagger}Cardiac Arrhythmia Center, Cardiovascular Division, Department of Medicine, University of Minnesota, Minneapolis, Minnesota

Address correspondence and reprint requests to Anton Amann, PhD, The Leopold-Franzens University of Innsbruck, Department of Anesthesiology and Critical Care Medicine, Anichstrasse 35, 6020 Innsbruck, Austria. Address e-mail to anton.amann{at}uibk.ac.at


   Abstract
Top
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 References
 
This study evaluated ventricular fibrillation mean frequency and amplitude to predict defibrillation success in a porcine cardiopulmonary resuscitation (CPR) model using repeated administration of vasopressin or epinephrine. After 4 min of cardiac arrest and 3 min of CPR, 10 pigs were randomly assigned to receive either vasopressin (early vasopressin: 0.4, 0.4, and 0.8 units/kg, respectively, n = 5) or epinephrine (early epinephrine: 45, 45, and 200 µg/kg, respectively, n = 5). Another 11 animals were randomly allocated after 4 min of cardiac arrest and 8 min of CPR to receive every 5 min either vasopressin (late vasopressin: 0.4 and 0.8 units/kg, respectively, n = 5) or epinephrine (late epinephrine: 45 and 200 µg/kg, n = 6). Ventricular fibrillation mean frequency and amplitude on defibrillation were significantly higher in the vasopressin groups than in the epinephrine groups, respectively. In vasopressin versus epinephrine animals, mean frequency immediately before defibrillation was 9.6 ± 1.5 Hz vs 7.0 ± 0.7 Hz (P < 0.001), mean amplitude was 0.65 ± 0.26 mV vs 0.21 ± 0.14 mV (P < 0.001, and coronary perfusion pressure was 27 ± 9 mm Hg vs 8 ± 4 mm Hg (P < 0.00001), respectively. In contrast to no epinephrine animals, all vasopressin animals were successfully defibrillated and survived 1 h (P < 0.05). Mean fibrillation frequency and amplitude predicted successful defibrillation and may serve as noninvasive markers to monitor continuing CPR efforts. Furthermore, vasopressin was superior to epinephrine in maintaining these variables above a threshold necessary for successful defibrillation.

Implications: Mean frequency and amplitude of ventricular fibrillation predicted successful defibrillation in pigs. Vasopressin was superior to epinephrine in maintaining these variables above a success defibrillation threshold.


   Introduction
Top
 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 References
 
The lack of a reliable and simple monitoring tool for the efficacy of continuing cardiopulmonary resuscitation (CPR) partly constraints resuscitation strategy. For example, although coronary perfusion pressure is the best single predictor of successful defibrillation resulting in return of spontaneous circulation in both animals (1–4) and humans (5,6), measurement of that variable is not possible in out-of-hospital and in-hospital CPR outside intensive care units. The best monitoring technique to estimate cardiac output during CPR may be end-tidal carbon dioxide (7,8); unfortunately, cardiac output does not correlate with coronary perfusion, especially after vasopressor administration. Accordingly, a technique similar to monitoring coronary perfusion pressure that predicts the best time for successful defibrillation may increase CPR outcome by avoiding unnecessary defibrillation attempts, and interruption of chest compressions (9).

Previous laboratory and clinical CPR studies showed that both ventricular fibrillation amplitude (10–13) and mean frequency (5,14) were able to predict success of defibrillation. Although amplitude and mean frequency are established variables for the prediction of successful defibrillation in models with basic life support only (15), or with vasopressin and epinephrine administration (16,17), several problems have not been addressed. It is unknown whether ventricular fibrillation amplitude and/or mean frequency are of equal importance for successful defibrillation during prolonged CPR efforts, with repeated drug administration, when rescuers are repetitively recycling through an algorithm of vasopressor administration and defibrillation (18,19). Accordingly, the purpose of our study was to determine whether ventricular fibrillation mean frequency and/or amplitude may be able to predict defibrillation success in a porcine CPR model of prolonged cardiac arrest with repeated administration of vasopressin or epinephrine (20). The effects of different drugs on defibrillation success and coronary perfusion pressure in this model have been previously reported (20), and the data reported in the current study were obtained from a subset of the animals used to evaluate the latter effects (20).


   Materials and Methods
Top
 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 References
 
Surgical Preparation and Measurements
This project was approved by the Austrian Federal Animal Investigational Committee, and the animals were managed in accordance with the American Physiological Society and institutional guidelines. This study was performed according to Utstein-style guidelines (21) on 21 healthy, 12- to 16-week-old swine of either gender weighing 30 to 40 kg. The animals were fasted overnight, but had free access to water. The pigs were premedicated with azaperone (neuroleptic drug; 4 mg/kg IM) and atropine (0.1 mg/kg IM) 1 h before surgery, and anesthesia was induced with thiopental (7–15 mg/kg IV). After intubation during spontaneous ventilation, the pigs were ventilated with a volume-controlled ventilator (Draeger EV-A, Lübeck, Germany) with 100% oxygen at 20 breaths/min, and with a tidal volume adjusted to maintain normocapnia. Anesthesia was maintained with propofol (6–8 mg · kg-1 · h-1) and a single dose of piritramid (30 mg). We achieved muscle paralysis with 8 mg pancuronium after intubation and subsequently with repeated doses of 8 mg pancuronium as needed. Ringer’s solution (6 mL · kg-1 · h-1) and a 3% gelatin solution (4 mL · kg-1 · h-1) were administered for plasma volume expansion in the preparation phase before induction of cardiac arrest and in the postresuscitation phase. A standard lead III electrocardiogram (ECG) was used to monitor cardiac rhythm; depth of anesthesia was judged according to blood pressure and heart rate. If necessary, we increased the propofol dose, and additional piritramid was given to provide maximum comfort for the animal, and to keep blood pressure variables within a specified range (diastolic <90 mm Hg, systolic <140 mm Hg) before induction of cardiac arrest. Body temperature was maintained with a heating blanket between 38.0° and 39.0°C.

A 7F catheter was advanced into the descending aorta for measurement of arterial blood pressure, another 7F catheter was placed into the right atrium to measure right atrial pressure and for drug administration. Blood pressures were measured with saline-filled catheters attached to pressure transducers (model 1290A, Hewlett Packard, Böblingen, Germany) that were calibrated to atmospheric pressure at the level of the right atrium. Coronary perfusion pressure was defined as the difference between aortic and right atrial diastolic pressure.

Experimental Protocol
Fifteen minutes before cardiac arrest, 5000 units of heparin were administered IV to prevent intracardiac clot formation, a single dose of 15 mg piritramid and 8 mg pancuronium was given, and hemodynamic variables were measured. A 50-Hz, 60-V alternating current was then applied via two subcutaneous needle electrodes to induce ventricular fibrillation. Onset of cardiopulmonary arrest was defined as the time when the ECG showed ventricular fibrillation and aortic pressure decreased profoundly and was nonpulsatile. Ventilation was stopped at that point. After 4 min of untreated ventricular fibrillation, closed-chest CPR was performed manually, and mechanical ventilation was resumed with the same setting as before induction of cardiac arrest. Chest compression rate was always performed by the same investigator at a rate of 80/min guided by acoustical audiotones. This investigator was blinded to hemodynamic and end-tidal carbon dioxide monitor tracings.

After 4 min of ventricular fibrillation, followed by 3 min of CPR, 10 animals were randomly assigned to receive either vasopressin (early vasopressin group: 0.4, 0.4, and 0.8 units/kg; n = 5) or epinephrine (early epinephrine group: 45, 45, and 200 µg/kg; n = 5) after 3, 8, and 13 min of CPR, respectively. Another 11 animals were randomly allocated after 4 min of ventricular fibrillation, and 8 min of CPR, to receive either vasopressin (late vasopressin group: 0.4 and 0.8 units/kg; n = 5) or epinephrine (late epinephrine group: 45 and 200 µg/kg; n = 6) after 8 and 13 min of CPR, respectively.

All drugs were diluted to 10 mL with normal saline and subsequently injected into the right atrium, which was followed by 20 mL saline flush (investigators were blinded to the drugs). Hemodynamic variables were measured before induction of cardiac arrest, after 3 min of CPR, as well as 90 s and 5 min after each drug administration, respectively. After 22 min of cardiac arrest, including 18 min of CPR, up to five countershocks were administered with an energy of 3, 4, and 6 Joules/kg, respectively. If asystole or pulseless electrical activity was present after defibrillation, the experiment was terminated. Return of spontaneous circulation was defined as an unassisted pulse with a systolic arterial pressure of >=80 mm Hg, lasting for at least 5 min. After finishing the experimental protocol, the animals were killed and necropsied to document correct positioning of the catheters and injuries to the rib cage.

ECG Signal Recording
The ventricular fibrillation ECG signal (standard lead III) was monitored continuously and electronically stored using a PC-based data acquisition system (Dewetron, Graz, Austria; Datalog GmbH, Mönchengladbach, Germany). Digitization was performed at a sampling rate of 1000 Hz, with an amplitude resolution of 12 bits (4096 equal steps between minimum and maximum amplitude). Because of technical difficulties, we were only able to analyze data of 5 animals in the early and late vasopressin groups and in the early epinephrine group.

ECG Analysis
The recorded ECG signals were analyzed using the mathematical software package MatLab (The MathWorks, Inc., Natick, MA). The signals were divided into consecutive 10-s epochs, and each epoch was transformed into the frequency domain by Fourier transformation. For signal analysis, the frequency domain was restricted to the range from 4.33 to 30 Hz, as previously described (22). Using the transformed ECG signal, the maximum of mean fibrillation frequency within 90 s after each drug administration, as well as the maximum within 20 s before the second and third drug administrations, and before defibrillation was calculated. Also, the maximum of mean fibrillation frequency within 20 s before and within 90 s after the start of CPR was calculated. Mean ventricular fibrillation peak-trough-amplitude (difference between a peak and the next following trough of the ECG signal) was calculated for the same time instants. For amplitude analysis, the signal was constrained to the frequency range of 4.33–30 Hz by digital filtering (finite impulse response filter of order 500, passband 4.66–33.5 Hz). For each 10-s epoch of the signal, the amplitude was the average of all peak-trough-amplitudes within this epoch.

Statistical Analysis
Values are expressed as the means ± SD. The comparability of weight, baseline data, and mean frequency during ventricular fibrillation was verified using the unpaired Student’s t test for continuous variables. Analysis of variance was used to identify statistically significant differences of mean frequency, mean amplitude, coronary perfusion pressure, and number of countershocks between groups. Fisher’s exact test was used to test the null hypothesis that the number of surviving animals is independent of treatment. Sensitivity, specificity, positive and negative predictive value of the variables, mean frequency, mean amplitude and coronary perfusion pressure regarding countershock success were determined. The sensitivity of a variable is calculated as the number of successful countershocks that have a variable value within a specific range divided by the total number of successful countershocks. The specificity of a variable is calculated as the number of unsuccessful countershocks that have a variable value outside a specific range divided by the total number of unsuccessful countershocks. The positive predictive value is calculated as the number of successful countershocks that have a variable value within a specific range divided by the total number of countershocks that have a variable value within a specific range. The negative predictive value is calculated as the number of unsuccessful countershocks that have a variable value outside a specific range divided by the total number of countershocks that have a variable value outside a specific range. Thresholds were determined using binary logistic regression (Fig. 1), these thresholds also maximize the sum of sensitivity and specificity of mean amplitude, coronary perfusion pressure, and mean frequency. Statistical significance was considered with a two-tailed P < 0.05.



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  		Figure 1. Using binary logistic regression, the thresholds (vertical lines) distinguishing survivors from nonsurvivors were determined. Rounded threshold values are a ventricular fibrillation mean frequency of 8.4 Hz, a ventricular fibrillation mean amplitude of 0.4 mV, and a coronary perfusion pressure of 15 mm Hg.

 

   Results
Top
 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 References
 
Mean ventricular fibrillation frequency was comparable in all groups during cardiac arrest and basic life support CPR. Mean fibrillation frequency after early vasopressin was significantly higher than after early epinephrine during the entire experiment (Fig. 2). In Fig. 3, the raw ECG signal and the corresponding power spectrum in a 5-s interval before (Fig. 3a,b) and after Fig. 3c,d) early vasopressin administration are shown. Similarly, mean fibrillation frequency after late vasopressin was significantly higher than after late epinephrine 5 min after the first drug administration until defibrillation (Fig. 4). Ventricular fibrillation mean amplitude was comparable during cardiac arrest and basic life support CPR. Ventricular fibrillation mean amplitude after early vasopressin was significantly higher than after early epinephrine, only after the third drug administration (Fig. 5). Ventricular fibrillation mean amplitude after late vasopressin was significantly higher than after late epinephrine for the entire experiment (Fig. 6).



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  		Figure 2. Mean fibrillation frequency in the early vasopressin ({nabla}; mean ± SD of five observations) and early epinephrine groups ({nabla}; mean ± SD of five observations) during untreated cardiac arrest, and basic and advanced life support CPR. *P < 0.05, **P < 0.01, ***P < 0.001 for vasopressin versus epinephrine. BLS, basic life support; CPR, cardiopulmonary resuscitation; VF, ventricular fibrillation.

 


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  		Figure 3. Representative spectrum and 5 s electrocardiogram signal during basic life support (a,b) and 90 s after drug administration (c,d) in a pig of the early vasopressin group. Vasopressin resulted in an increase of ventricular fibrillation mean frequency, as indicated by the rightward shift of the frequency spectrum (a,c). Also, vasopressin resulted in an increase of electrocardiogram mean amplitude (b,d).

 


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  		Figure 4. Mean fibrillation frequency in the late vasopressin ({circ}; mean ± SD of five observations) and late epinephrine groups ({square}; mean ± SD of six observations) during untreated cardiac arrest, and basic and advanced life support CPR. *P < 0.05, **P < 0.01, ***P < 0.001 for vasopressin versus epinephrine. BLS, basic life support; CPR, cardiopulmonary resuscitation; VF, ventricular fibrillation.

 


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  		Figure 5. Ventricular fibrillation mean amplitude in the early vasopressin ({Delta}; mean ± SD of five observations) and early epinephrine groups ({nabla}; mean ± SD of five observations) during untreated cardiac arrest, and basic and advanced life support CPR. *P < 0.05 for vasopressin versus epinephrine. BLS, basic life support; CPR, cardiopulmonary resuscitation; VF, ventricular fibrillation.

 


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  		Figure 6. Ventricular fibrillation mean amplitude in the late vasopressin ({circ}; mean ± SD of five observations) and late epinephrine groups ({square}; mean ± SD of six observations) during untreated cardiac arrest, and basic and advanced life support CPR. *P < 0.05, **P < 0.01 for vasopressin versus epinephrine. BLS, basic life support; CPR, cardiopulmonary resuscitation; VF, ventricular fibrillation.

 
Before drug administration, coronary perfusion pressure was comparable in all groups. Immediately before defibrillation, coronary perfusion pressure was 30 ± 12 mm Hg after early vasopressin vs. 7 ± 4 mm Hg after early epinephrine (P < 0.0001); and 23 ± 4 mm Hg after late vasopressin vs. 9 ± 5 mm Hg after late epinephrine (P < 0.01). All animals in the early and late vasopressin group had return of spontaneous circulation (1.4 ± 0.5 vs. 4.4 ± 2.3 countershocks, respectively, P < 0.03), and survived the 60-min postresuscitation phase, whereas all epinephrine pigs died (P < 0.05). Mean frequency, mean amplitude, and coronary perfusion pressure before defibrillation in resuscitated vs. nonresuscitated animals were 9.6 ± 1.5 vs. 7.0 ± 0.7 Hz (P < 0.001); 0.65 ± 0.26 vs. 0.21 ± 0.14 mV (P < 0.001); and 27 ± 9 vs. 8 ± 4 mm Hg (P < 0.00001). Sensitivity, specificity, positive and negative predictive value of thresholds of mean frequency >=8.4 Hz, mean amplitude >=0.4 mV, and a coronary perfusion pressure >=15 mm Hg regarding defibrillation success are given in Table 1, as well as the numbers of true positives, false positives, true negatives, and false negatives for each of these variables.


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  		Table 1. True Positives, True Negatives, False Positives, False Negatives, and Predictive Power for Mean Fibrillation Frequency, Mean Fibrillation Amplitude, and Coronary Perfusion Pressure
 

   Discussion
Top
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
References
 
During CPR, adequate coronary perfusion pressure and myocardial blood flow are crucial for restarting the arrested heart (23–25). Since it is technically impossible to measure these variables in out-of-hospital and most in-hospital cardiac arrest patients, ventricular fibrillation mean frequency and mean amplitude may be an alternative to monitor continuing CPR efforts. Accordingly, in our study simulating prolonged CPR and repeated drug administration, ventricular fibrillation mean frequency, mean amplitude, and coronary perfusion pressure were significantly higher in resuscitated than in nonresuscitated pigs. Moreover, sensitivity, specificity, positive and negative predictive value of ventricular fibrillation mean frequency, mean amplitude, and coronary perfusion pressure for predicting successful defibrillation were comparable.

The present model closely simulates a short and prolonged duration of basic life support, followed by advanced cardiac life support. The first dosages of both vasopressin (0.4 units/kg) and epinephrine (45 µg/kg) reflect an established optimal dose in this pig model (26). Furthermore, the escalating doses of 0.8 units/kg vasopressin and 200 µg/kg epinephrine are the maximum effective dosages in swine (23,24,26). A vasopressor-induced increased systemic vascular resistance (27) due to a marked peripheral vasoconstriction (28) may shift blood toward the myocardium. Thus, our animal model reflects simulated repetitive cycling of an algorithm of vasopressor administration during CPR, as recommended by the European Resuscitation Council (18) and the American Heart Association (19).

Variables derived from an ECG signal may serve as a tool to monitor efficacy of continuing CPR efforts. As such, this strategy may enable the rescuers to predict the optimal point in time for successful defibrillation. As observed in other studies, the increase in mean frequency and amplitude of our pigs most likely reflects an increase of myocardial blood flow during CPR. Accordingly, mean frequency in 8 of 10 and amplitude levels in 9 of 10 vasopressin pigs were above thresholds of 8.4 Hz (16) and 0.4 mV that were only surpassed in a single nonsurvivor. These observations may be explained by effects of the drugs administered in our experiment. Epinephrine during CPR increases myocardial oxygen consumption fundamentally (29–31); therefore, myocardial blood flow is insufficient to meet the metabolic demands of the fibrillating myocardium. Interestingly, in one clinical study, epinephrine was no better than saline placebo for restoration of spontaneous circulation (32). As such, after initiating CPR in our epinephrine pigs, mean fibrillation frequency decreased from ~12 Hz that may have been sufficient to restore spontaneous circulation to ~7 Hz shortly before defibrillation, which may reflect the imbalance of cardiac oxygen delivery versus metabolic needs during CPR with epinephrine. Thus, our results may demonstrate that repeated administration of epinephrine was not able to maintain a critical level of myocardial blood flow that usually correlates with successful defibrillation.

Mean frequency and amplitude have been shown to be predictors of countershock success after cardiac arrest with or without basic or advanced cardiac life support using a single drug administration (15–17,22). Our data confirm that the findings derived from single drug administration during a short duration of CPR may be safely extrapolated to models with repeated drug administration and significantly prolonged CPR.

When sensitivity, specificity, and positive and negative predictive values were calculated for mean frequency, amplitude, and coronary perfusion pressure, this reveals that the predictive power for defibrillation success of these three variables is comparable. The thresholds for this calculation were chosen to maximize the sum of sensitivity and specificity. Moreover, the 8.4 Hz threshold for mean frequency fulfilling this condition could be assigned the identical value as reported in an earlier study (16). Accordingly, we suggest that monitoring ventricular fibrillation mean frequency and mean amplitude during prolonged CPR attempts may be useful to predict and/or manage successful defibrillation. This may have significant clinical implications, since after the first cycles of advanced cardiac life support, a large variety of interventions (such as different vasopressors, buffers, antiarrhythmics, and CPR adjuncts) may be administered. Furthermore, different patients most likely respond to these CPR strategies in a different way; as such, it may be even more important to monitor efficacy of continuing CPR efforts in real time. Thus, ventricular fibrillation mean frequency and mean amplitude may serve as a guide to determine the optimal time for increasing success of defibrillation (33).

Some limitations of this study should be noted and include the impossibility to exactly control effectiveness of manually performed CPR. Due to design limitations, defibrillation attempts had to be omitted until the end of the protocol. Furthermore, the absolute values of ventricular fibrillation mean frequency differ significantly between animals and humans (14,17,34). Due to the small sample size of the study, our results may be preliminary, especially regarding ventricular fibrillation mean amplitude due to a large standard deviation. Also, myocardial blood flow was not measured in this study, since a correlation of mean fibrillation frequency and myocardial blood flow, and a high degree of correlation of myocardial blood flow and coronary perfusion pressure have been shown explicitly in pigs (17,22,35). The use of two different drugs for anesthesia induction and maintenance (thiopental and propofol) may have introduced a confounding variable. However, our baseline values almost matched reference values for pigs (36), indicating that appropriate and balanced anesthesia was provided.

In conclusion, mean frequency and amplitude predicted successful defibrillation in this porcine model, and may serve as noninvasive surrogates for coronary perfusion pressure as a predictor of successful defibrillation. Vasopressin was superior over epinephrine in keeping ventricular fibrillation mean frequency and amplitude above a threshold necessary for successful defibrillation.


   Acknowledgments
 
This study was supported, in part, by Science Project 7276 and 7280 of the Austrian National Bank, Vienna, Austria; Science Project 98/05 of the Austrian Heart Fund, Vienna, Austria; the Laerdal Foundation for Acute Medicine, Stavanger, Norway; a Dean’s grant of the Leopold-Franzens University, Innsbruck, Austria; and the Department of Anaesthesiology and Critical Care Medicine, The Leopold-Franzens University of Innsbruck, Innsbruck, Austria.

We thank Martin Stoffaneller, BS, for assistance with data acquisition.


   References
Top
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 References
 

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Accepted for publication December 28, 1999.




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J. H. Indik, R. W. Hilwig, M. Zuercher, K. B. Kern, M. D. Berg, and R. A. Berg
Preshock Cardiopulmonary Resuscitation Worsens Outcome From Circulatory Phase Ventricular Fibrillation With Acute Coronary Artery Obstruction in Swine
Circ Arrhythmia Electrophysiol, April 1, 2009; 2(2): 179 - 184.
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 Arch Intern MedHome page
S. D. Mentzelopoulos, S. G. Zakynthinos, M. Tzoufi, N. Katsios, A. Papastylianou, S. Gkisioti, A. Stathopoulos, A. Kollintza, E. Stamataki, and C. Roussos
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Arch Intern Med, January 12, 2009; 169(1): 15 - 24.
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J. Heath, D. Hanson, R. Long, and N. A. Crowell
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 Anesth. Analg.Home page
M. Holzer, W. Behringer, F. Sterz, J. Kofler, E. Oschatz, E. Schuster, and A. N. Laggner
Ventricular Fibrillation Median Frequency May Not Be Useful for Monitoring During Cardiac Arrest Treated with Endothelin-1 or Epinephrine
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K. H. Stadlbauer, K. Rheinberger, V. Wenzel, C. Raedler, A. C. Krismer, H.-U. Strohmenger, S. Augenstein, H. G. Wagner-Berger, W. G. Voelckel, K. H. Lindner, et al.
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A. Amann, K. Rheinberger, U. Achleitner, A. C. Krismer, W. Lingnau, K. H. Lindner, and V. Wenzel
The Prediction of Defibrillation Outcome Using a New Combination of Mean Frequency and Amplitude in Porcine Models of Cardiac Arrest
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H.-U. Strohmenger, T. Eftestol, K. Sunde, V. Wenzel, M. Mair, H. Ulmer, K. H. Lindner, and P. A. Steen
The Predictive Value of Ventricular Fibrillation Electrocardiogram Signal Frequency and Amplitude Variables in Patients with Out-Of-Hospital Cardiac Arrest
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R. V. DiGregorio
Pharmacotherapeutic Advances in Cardiac Resuscitation: A Review of the Advanced Cardiac Life Support (ACLS) 2000 Guidelines and Their Impact on Pharmacy Practice
Journal of Pharmacy Practice, February 1, 2001; 14(1): 41 - 53.
[Abstract] [PDF]

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Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press