Electrical induction of ventricular fibrillation for resuscitation from postcountershock pulseless and asystolic cardiac arrests.

BACKGROUND: There is increasing evidence that defibrillation from prolonged ventricular fibrillation (VF) before CPR decreases survival. It remains unclear, however, whether harmful effects are due primarily to initial countershock of ischemic myocardium or to resultant postdefibrillation rhythms (ie, pulseless electrical activity [PEA] or asystole). METHODS AND RESULTS: We induced 15 dogs into 12 minutes of VF and randomized them to 3 groups. Group 1 was defibrillated at 12 minutes and then administered advanced cardiac life support (ACLS); group 2 was allowed to remain in VF and was subsequently defibrillated after 4 minutes of ACLS; group 3 was defibrillated at 12 minutes, electrically refibrillated, and then defibrillated after 4 minutes of ACLS. All group 1 and 3 animals were defibrillated into PEA/asystole at 12 minutes. After 4 minutes of ACLS, group 2 and 3 animals were effectively defibrillated into sinus rhythm. The extension of VF in group 2 and 3 subjects paradoxically resulted in shorter mean resuscitation times (251+/-15 and 245+/-7 seconds, respectively, versus 459+/-66 seconds for group 1; P<0.05) and improved 1-hour survival (10 of 10 group 2 and 3 dogs versus 1 of 5 group 1 dogs; Fisher's exact, P<0.005) compared with more conservatively managed group 1 subjects. CONCLUSIONS: Precountershock CPR during VF appears more conducive to resuscitation than CPR during postcountershock PEA or asystole. The intentional induction of VF may prove useful in the management of PEA and asystolic arrests.

Resuscitation after prolonged ventricular fibrillation with use of monophasic and biphasic waveform pulses for external defibrillation.

BACKGROUND: Survival after prolonged ventricular fibrillation (VF) appears severely limited by 2 major factors: (1) low defibrillation success rates and (2) persistent post-countershock myocardial dysfunction. Biphasic (BP) waveforms may prove capable of favorably modifying these limitations. However, they have not been rigorously tested against monophasic (MP) waveforms in clinical models of external defibrillation, particularly where rescue from prolonged VF is the general rule. METHODS AND RESULTS: We randomized 26 dogs to external countershocks with either MP or BP waveforms. Hemodynamics were assessed after shocks applied during sinus rhythm, after brief VF (>10 seconds), and after resuscitation from prolonged VF (>10 minutes). Short-term differences in percent change in left ventricular +dP/dt(max) (MP -16+/-28%, BP +9.1+/-24%; P=0.03) and left ventricular -dP/dt(max) (MP -37+/-26%, BP -18+/-20%; P=0.05) were present after rescue from brief VF, with BP animals exhibiting less countershock-induced dysfunction. After prolonged VF, the BP group had lower mean defibrillation thresholds (107+/-57 versus 172+/-88 J for MP, P=0.04) and significantly shorter resuscitation times (397+/-73.7 versus 488+/-74.3 seconds for MP, P=0.03). CONCLUSIONS: External defibrillation is more efficacious with BP countershocks than with MP countershocks. The lower defibrillation thresholds and shorter resuscitation times associated with BP waveform defibrillation may improve survival after prolonged VF arrest.

Is a pressor necessary during aortic perfusion and oxygenation therapy of cardiac arrest?

STUDY OBJECTIVE: Occlusion of the descending aorta and infusion of oxygenated ultrapurified polymerized bovine hemoglobin may improve the efficacy of advanced cardiac life support (ACLS). Because selective aortic perfusion and oxygenation (SAPO) directly increases coronary perfusion pressure, exogenous epinephrine may not be required. The purpose of this study was to determine whether exogenous epinephrine is necessary during SAPO by comparing the rate of return of spontaneous circulation and aortic and coronary perfusion pressures during ACLS-SAPO in animals treated with either intra-aortic epinephrine or saline solution. METHODS: A prospective, randomized, interventional before-after trial with a canine model of ventricular fibrillation cardiac arrest and ACLS based on external chest compression was performed. The ECG, right atrial, aortic arch, and esophageal pulse pressures were measured continuously. A descending aortic occlusion balloon catheter was placed through the femoral artery. Ventricular fibrillation was induced, and no therapy was given during the 10-minute arrest time. Basic life support was then initiated and normalized by standardization of esophageal pulse pressure and central aortic blood gases. After 3 minutes of basic life support, the aortic occlusion balloon was inflated, and 0.01 mg/kg epinephrine or saline solution was administered through the aortic catheter followed by 450 mL of ultrapurified polymerized bovine hemoglobin over 2 minutes. Defibrillation was then attempted. The outcomes and changes in intravascular pressures were compared. RESULTS: Aortic pressures were higher during infusions in animals treated with epinephrine. During infusion, the mean aortic relaxation pressure increased by 58+/-5 mm Hg in animals that had received epinephrine versus 20+/-11 mm Hg in those that had received saline placebo. The coronary perfusion pressure during infusion increased by 52+/-8 mm Hg in animals that had received epinephrine versus 26+/-10 mm Hg in those that had received saline. Only 2 of 7 animals in the placebo group had return of spontaneous circulation versus 7 of 8 in the epinephrine group. CONCLUSION: The addition of epinephrine to ACLS-SAPO increases vital organ perfusion pressures and improves outcome from cardiac arrest. There appears to be a profound loss of arterial vasomotor tone after prolonged arrest. This loss of vasomotor tone may make exogenous pressors necessary for resuscitation after prolonged cardiac arrest.

Emergency department cardiopulmonary bypass in the treatment of human cardiac arrest.

OBJECTIVE: To study the use of emergency department (ED) femoro-femoral cardiopulmonary bypass (CPB) in the resuscitation of medical cardiac arrest patients. DESIGN: Prospective, uncontrolled trial. SETTING: Urban academic ED staffed with board-certified emergency physicians (EPs). PARTICIPANTS: Ten patients with medical cardiac arrest unresponsive to standard therapy. INTERVENTIONS: Femoro-femoral CPB instituted by EPs. RESULTS: The time of cardiac arrest prior to CPB (mean+/-SD) was 32.0+/-13.6 min. The cardiac output while on CPB was 4.09+/-1.03 L/min with an average of 229+/-111 min on bypass. All 10 patients had resumption of spontaneous cardiac activity while on CPB. Seven of these were weaned from CPB with intrinsic spontaneous circulation. Of these, six patients were transferred from the ED to the operating room for cannula removal and vessel repair while the other patient died in the ED soon after discontinuing CPB. Mean survival was 47.8+/-44.7 h in the six patients leaving the ED. Although these patients had successful hemodynamic resuscitation, there were no long-term survivors. CONCLUSION: CPB instituted by EPs is feasible and effective for the hemodynamic resuscitation of cardiac arrest patients unresponsive to advanced cardiac life support therapy. Future efforts need to focus on improving long-term outcome.

Objective measurements for guiding initiation, sequencing, and discontinuation of life-support intervention.

At present, there are only a limited number of objective measures available to clinicians resuscitating patients from cardiac arrest. The electrocardiogram and end-tidal CO2 are easily applied, but the data they produce are of only limited utility in evaluating the efficacy of chest compression and in choosing the sequence of therapies. In particular, we are in need of an objective test that can tell us when the myocardium will defibrillate into a perfusing rhythm. The ventricular fibrillation waveform holds information that we have not yet begun to utilize. Parameters derived from power spectrum analysis, such as ventricular fibrillation median frequency, appear promising. Combination of both old and new parameters may allow us to more accurately evaluate the efficacy of therapy.

Hematocrit as a predictor of significant injury after penetrating trauma.

A study was undertaken to determine if there are differences in hematocrit (HCT) during the initial evaluation of patients with and without significant visceral intrathoracic or intraabdominal injury after penetrating trauma and, if so, the predictive value of this parameter. Sixty consecutive adults with potentially significant penetrating trauma who presented to an urban municipal trauma center during a 10-week period were studied. Diagnostic variables were recorded for all patients at risk for significant injury, defined as intrathoracic or intraabdominal injury requiring surgical intervention. Patients were ultimately grouped on the basis of operative findings or observation to discharge. Acquired variables included vital signs, initial HCT (HCT-0), HCT at 15 minutes (HCT-15), HCT at 30 minutes (HCT-30), and fluid administered. Twenty-one patients had significant injuries (INJ), and 39 did not (NO-INJ). INJ patients had lower HCT values than NO-INJ on presentation (35% +/- 6% and 41% +/- 5%, respectively). At presentation, a low HCT was predictive of significant injury, but a normal HCT did not preclude injury. The changes in HCT from arrival to 15 minutes, between INJ and NO-INJ patients, were similar (-1.5% +/- 3% and -0.6% +/- 3% respectively). Only when the decrease in HCT was > or =6.5% from presentation measurements was it predictive of injury. During the first 15 minutes a decrease in HCT of > or =6.5% had a positive predictive value and specificity of 1.0. The change in HCT between 15 and 30 minutes was less useful. There was a large difference between the amounts of fluid given to injured and uninjured patients, which may have been responsible for some of the differences in HCT between the two groups. These results show that HCT may have some diagnostic utility during the early management of penetrating trauma. Presentation with an HCT below normal, or an early decrease in HCT, is an indicator of potential injury. Although many patients with serious internal injuries do not manifest large decreases early after presentation, those who do have a high probability of internal injury. The lower the HCT, or the greater the decrease, the greater the probability that a significant injury exists.

Dose-response relationship between aortic infusions of polymerized bovine hemoglobin and return of circulation in a canine model of ventricular fibrillation and advanced cardiac life support.

OBJECTIVES: Return of spontaneous circulation after cardiac arrest may be a function of vital organ perfusion. Selective aortic perfusion and oxygenation with oxygenated ultrapurified polymerized bovine hemoglobin improves vital organ perfusion and is an effective adjunct in the treatment of cardiac arrest. This study determined the dose-response relationship between intra-aortic oxygenated ultrapurified polymerized bovine hemoglobin and return of spontaneous circulation. DESIGN: Randomized, interventional study, using a clinically relevant model of ventricular fibrillation with a prolonged arrest time and cardiopulmonary resuscitation based on external chest compression and aortic occlusion with oxygenated ultrapurified polymerized bovine hemoglobin infusion. SETTING: University, resuscitation research laboratory. SUBJECTS: Fasted, mongrel dogs (> 20 kg). INTERVENTIONS: After alpha-chloralose anesthesia, blood gases and vital signs were normalized. Electrocardiogram, aortic arch, and intraesophageal pressures were measured continuously. A descending aortic occlusion-infusion balloon catheter was placed through the femoral artery. Ventricular fibrillation was induced and basic life support was begun after 10 mins. Interanimal differences in basic life support were minimized by standardization of the esophageal pulse pressure and aortic blood gases. At 13 mins, the aortic occlusion balloon was inflated and a dose of 10, 20, or 30 mL/kg of ultrapurified polymerized bovine hemoglobin was infused at 300 mL/min. Defibrillation was attempted at the end of the infusion. MEASUREMENTS AND MAIN RESULTS: Only two of five animals given 10 mL/kg of ultrapurified polymerized bovine hemoglobin had return of spontaneous circulation, vs. four of five animals given 20 mL/kg, and all seven animals given 30 mL/kg. All resuscitated animals were alive at 1 hr after return of spontaneous circulation. CONCLUSIONS: There is a dose-response relationship between the volume of oxygenated ultrapurified polymerized bovine hemoglobin administered by selective aortic perfusion and oxygenation and return of spontaneous circulation after prolonged cardiac arrest. This result supports the hypothesis that vital organ flow is causally related to improved outcome.

Aortic-based therapy for cardiac arrest.

After the failure of electrical countershock, the successful treatment of cardiac arrest is a function of raising aortic pressure so as to improve vital organ perfusion. Pharmacologic pressor agents have until recently been the most direct means of increasing aortic pressure. We have now begun to reevaluate direct aortic techniques including occlusion, infusion, counter-pulsation, and combinations of these. Clinical studies have demonstrated that the aorta can be accessed quickly and reliably even under emergency conditions. Initial laboratory studies indicate that some nonpharmacologic aortic therapies hold promise as adjuncts to external chest compression, or even as stand-alone therapies. Considerable research will be needed to identify the most effective approach before clinical trials can be considered.

Cardiac arrest research in humans--insights into failure.

Cardiac arrest research in humans has failed to fulfil expectations generated by laboratory studies. This reflects a number of factors. It is difficult to perform clinical research in the setting of emergency cardiac resuscitation. Both the epidemiology and pathophysiology of sudden death present special problems to the clinical researcher. Laboratory studies and clinical trials have failed to faithfully mimic each other. Estimation of sample size and application of inclusion/exclusion criteria present special problems in methodology. Our focus on improving long term survival by changing one component of therapy may have been premature and obscured the utility of extant data. Many of these problems can be addressed through refinements in: laboratory models, our understanding of the underlying pathophysiology, estimation of sample size, the application of inclusion/exclusion criteria, the identification of the primary dependent variables and subgroups of interest, the overall quality of therapy. Clinical studies will not generate useful data until these issues, among others, have been addressed.

High atrial natriuretic peptide concentrations blunt the pressor response during cardiopulmonary resuscitation in humans.

OBJECTIVE: To determine the relationship of circulating atrial natriuretic peptide concentrations to the pressor response to high-dose epinephrine in patients undergoing cardiopulmonary resuscitation (CPR) for cardiac arrest. DESIGN: Prospective study. PATIENTS: Fourteen normothermic, adult, prehospital and emergency department patients suffering unexpected cardiac arrest. INTERVENTION: Patients received high-dose epinephrine (0.2 mg/kg) i.v. when standard advanced cardiac life support (including multiple 1-mg dosages of epinephrine) failed to result in return of spontaneous circulation. MEASUREMENTS AND MAIN RESULTS: Cardiac arrest patients were separated into those patients with and without detectable serum atrial natriuretic peptide concentrations, and were termed the "low atrial natriuretic peptide" and "high atrial natriuretic peptide" groups, respectively. Their aortic pressure response to high-dose (0.02 mg/kg) epinephrine was compared. The proportion with positive assays was compared with a group of healthy control subjects. Fourteen patients were studied. Eight patients had low serum atrial natriuretic peptide concentrations and six patients had high circulating atrial natriuretic peptide concentrations. The mean concentration in the high atrial natriuretic peptide group was 151 +/- 82 pg/mL. The proportion with positive assays (six of 14 patients) was greater than in the group in spontaneous circulation (three of 29 patients) (p = .002). The maximal increase in the aortic relaxation-phase pressures after high-dose epinephrine was 9 +/- 7 torr (1.2 +/- 0.9 kPa) in the low atrial natriuretic peptide group and 0 +/- 5 torr (0 +/- 0.7 kPa) in the high atrial natriuretic peptide group (p = .03). The maximal increase in the aortic compression pressures after high-dose epinephrine was 17 +/- 13 torr (2.3 +/- 1.7 kPa) in the low atrial natriuretic peptide group and 2 +/- 10 torr (0.3 +/- 1.3 kPa) in the high atrial natriuretic peptide group (p = .03). Thus, pressor responses after high-dose epinephrine administration were observed in patients in the low atrial natriuretic peptide group, but this response was absent in patients in the high atrial natriuretic peptide group. CONCLUSIONS: Cardiac arrest patients receiving CPR have higher circulating atrial natriuretic peptide concentrations than healthy subjects. High serum atrial natriuretic peptide concentrations may antagonize the vasopressor response to epinephrine. Blocking this effect of atrial natriuretic peptide may improve outcomes in patients suffering cardiac arrest.

Selective aortic perfusion and oxygenation: an effective adjunct to external chest compression-based cardiopulmonary resuscitation.

OBJECTIVES: The purpose of this study was to compare the perfusion pressure and rate of return of spontaneous circulation produced by standard advanced cardiac life support with that resulting from advanced cardiac life support with simultaneous aortic occlusion and proximal infusion with oxygenated fluid. BACKGROUND: Cardiopulmonary resuscitation based solely on external chest compression is unable to achieve return of spontaneous circulation in most patients with cardiac arrest. Adjunctive therapies that enhance myocardial oxygen supply may improve outcomes. METHODS: We conducted a prospective, randomized study in mongrel dogs using a fibrillatory model of cardiac arrest with a 20-min arrest time. Dogs were randomized to two groups. Aortic arch and right atrial micromanometers were placed to measure intravascular pressure. Manual external chest compression was used and standardized to an esophageal pulse pressure of 50 mm Hg. Two minutes after initiation of advanced cardiac life support, selective aortic perfusion and oxygenation were initiated in dogs assigned to one group by inflation of an occluding balloon in the descending aorta and infusion of 450 ml of ultrapurified polymerized bovine hemoglobin through a large bore central infusion port. RESULTS: Maximal aortic pressure during standard advanced cardiac life support was 42 +/- 23 (mean +/- SD) versus 69 +/- 28 mm Hg during advanced cardiac life support with selective aortic perfusion and oxygenation. Maximal coronary perfusion pressure during standard therapy was 33 +/- 21 versus 62 +/- 26 mm Hg during combined therapy. Only 2 of 10 dogs receiving standard therapy had return of spontaneous circulation versus 6 of 7 dogs receiving combined therapy. Balloon occlusion alone did not increase perfusion pressure significantly. CONCLUSIONS: The use of selective aortic perfusion and oxygenation increases aortic and coronary perfusion pressures during cardiopulmonary resuscitation, resulting in a large increase in the rate of return of spontaneous circulation. This technique may be an effective adjunct to advanced cardiac life support based on any method of external chest compression and may improve the poor prognosis of patients with cardiac arrest.

The effect of global ischemia and reperfusion on the plasma levels of vasoactive peptides. The neuroendocrine response to cardiac arrest and resuscitation.

OBJECTIVE: Return of spontaneous circulation with CPR is a function of coronary perfusion pressure, which is determined by vasomotor tone and the force of compression. Vasomotor tone is affected by the relative stimulation of arterial vasoconstricting and vasorelaxing receptors by vasoactive substances. We measured the plasma levels of the endogenous vasoactive peptides arginine vasopressin (AVP) angiotensin II (ANG-II) and atrial natriuretic peptide (ANP) during cardiac arrest and resuscitation. DESIGN: A fibrillatory canine model of canine arrest was used. 'Down time' was greater than 10 min, during which no therapy, including BLS, was given. Standard ACLS was initiated at the end of the down time with manual external chest compression standardized to an esophageal pulse pressure of 50 mmHg. Blood samples were collected through an aortic catheter during spontaneous circulation and 3 min after initiation of ACLS. Peptide levels were measured using standard RIA techniques. Results are reported as the mean +/- S.D. in pg/ml. RESULTS: AVP levels increased from a baseline of 1.7 +/- 1.0 pg/ml during spontaneous circulation to 29.9 +/- 33.3 during cardiac arrest and CPR (P = 0.01). There was a moderate positive correlation between aortic pressure and circulating AVP levels after the first dose of epinephrine (R = 0.5). There was a trend towards higher AVP levels in animals with return of spontaneous circulation (P = 0.12). ANG-II levels increased from a baseline of 14.7 +/- 12.9 pg/ml during spontaneous circulation to 151 +/- 105 during cardiac arrest and CPR (P < 0.05). ANP levels increased from a baseline of 55 +/- 46 pg/ml during spontaneous circulation to 293 +/- 73 during cardiac arrest and CPR (P < 0.01). CONCLUSION: There were significant increases in the levels of these endogenous vasoactive peptides. This reflects the neuroendocrine response to global ischemia and CPR reperfusion. Plasma levels of these peptides may effect the vital organ perfusion pressures, response to exogenous vasopressors, and outcome of resuscitative efforts. Future therapies may be directed at enhancing or blocking the effect of these peptides so as to optimize perfusion pressure which is one of the principle determinants of outcome during CPR.

Simultaneous radial, femoral, and aortic arterial pressures during human cardiopulmonary resuscitation.

OBJECTIVE: To examine the validity of interchanging arterial sites and their responses to graded doses of epinephrine during human cardiopulmonary resuscitation (CPR). DESIGN: Consecutive case series. SETTING: Large, urban Emergency Department. PATIENTS: Adult, normothermic, nonhemorrhagic cardiac arrest patients. INTERVENTIONS: While receiving advanced cardiac life support, patients received right atrial (n = 40), aortic (n = 40), radial (n = 40), and femoral (n = 17) artery catheters. Pressures were measured simultaneously at baseline, after 0.01 mg/kg and 0.2 mg/kg of epinephrine. MEASUREMENTS AND MAIN RESULTS: The mean aortic compression-phase pressure was 9.3 +/- 10 (SD), 8.1 +/- 11, and 4.4 +/- 9.5 mm Hg higher than radial artery pressure at baseline, after 0.01 mg/kg, and 0.2 mg/kg of epinephrine, respectively (all statistically significant). When compared with the femoral artery at the same time points, the mean aortic compression-phase pressure was also 3.0 +/- 6.8, 1.9 +/- 8, and 0.6 +/- 7.7 mm Hg higher, respectively (none statistically significant). The aortic relaxation-phase pressure was 1.3 +/- 3.6, 1.1 +/- 3.8, and 1.6 +/- 2.5 mm Hg lower than the radial artery at baseline, after 0.01 mg/kg and 0.2 mg/kg of epinephrine, respectively (all statistically significant). When compared with the femoral artery at the same time points, the aortic relaxation-phase pressure was 0.6 +/- 2.0, 0.3 +/- 3.3, and 0.3 +/- 2.4 mm Hg lower, respectively (none statistically significant). CONCLUSIONS: Radial artery relaxation-phase pressure, although statistically higher, correlated with aortic relaxation-phase pressure. Femoral artery relaxation-phase pressure was not statistically different from aortic relaxation-phase pressure. Aortic pressure was statistically higher and had a lower correlation with radial artery pressures during compression phase. The aortic to radial artery and aortic to femoral artery compression-phase gradients abated with increasing doses of epinephrine therapy. Caution must be used when substituting compression-phase pressure obtained at radial or femoral artery sites for aortic pressure during human CPR. Coronary artery perfusion pressures obtained with radial and femoral arteries correlate with aortic pressure when measuring the response to vasopressor therapy during CPR when an interpretable waveform exists.

Functional responses to extremely high plasma epinephrine concentrations in cardiac arrest.

OBJECTIVE: To evaluate the action of high-dose epinephrine by measuring simultaneously its vasopressor and norepinephrine releasing effects in humans during cardiac arrest. DESIGN: A prospective study on consecutive patients admitted with cardiac arrest. SETTING: Emergency Department in a large, urban hospital. PATIENTS: Eighteen patients with out-of-hospital cardiac arrest undergoing cardiopulmonary resuscitation (CPR). INTERVENTIONS: Catheterization of both the aorta and right atrium for the recording of pressure and collection of blood samples. Throughout the study period (12.5 mins), 18 patients received epinephrine at both the standard dose (1 mg, approximately 0.015 mg/kg) and high dose (0.2 mg/kg). Blood samples were drawn five times, every 2.5 mins. MEASUREMENTS AND MAIN RESULTS: Plasma epinephrine and norepinephrine concentrations; aorta, right atrial, and coronary perfusion pressures. Epinephrine concentrations (normal at rest = 160 +/- 10 [SEM] pmol/L) were increased at the time of the first sample (2.5 mins) by approximately 3,000-fold (to approximately 0.5 mumol/L), and, increased further to 12,000-fold (approximately 2.0 mumol/L) during the study. Aortic pressure increased from 20 +/- 3 to 28 +/- 3 mm Hg (p < .001), and coronary perfusion pressure increased from 4 +/- 3 to 10 +/- 3 mm Hg (p < .001). Simultaneous plasma norepinephrine concentrations were 30-fold higher than the normal resting value of 1.30 +/- 0.04 nmol/L, and increased by 90-fold during the study (p < .001). The spectral distributions of the individual correlations between plasma epinephrine and norepinephrine concentrations were segregated into high correlations (r > .83) in 12 of 18 patients and low r values (r = .29 to .79) in the remaining six patients. The distribution of the correlations was nonuniform by the Kolmogorov-Smirnov goodness-of-fit test with p < .001; this profile suggests that norepinephrine responsiveness to epinephrine can separate two populations, one of which (r > .83) would have preserved viability of the corresponding epinephrine receptors. The correlations between plasma epinephrine concentrations and coronary perfusion pressures were distributed more evenly, also in a nonuniform pattern (p < .02 by Kolmogorov-Smirnov goodness-of-fit test) and the relationship between the two sets of correlations was not significant. CONCLUSIONS: Despite the very high prevailing plasma epinephrine concentrations during cardiac arrest, further epinephrine increases still elicit biological responses. The present work provides physiologic support for the use of large doses of epinephrine during the course of CPR.

Use of open chest cardiopulmonary resuscitation after failure of standard closed chest CPR: illustrative cases.

Compared to standard closed chest CPR, open chest cardiac massage improves vital organ perfusion and survival in animal models of medical cardiac arrest. Yet its use is essentially limited to the treatment of traumatic arrest. Three cases of medical cardiac arrest are presented in which open chest compression was used after failure of external chest compression. These cases illustrate the range of potential outcomes and how this therapy can be optimally applied. Approaches we have used to prevent application of futile intensive therapy in patients unlikely to be neurologically intact survivors are described. Replacement of open chest CPR by closed chest CPR as the standard of care for the in-hospital cardiac arrest was not justified by experimental data. The circumstances of refractory cardiac arrest make it unlikely that well controlled human studies will be able to demonstrate the superiority of open chest CPR in selected patients. The decision to use this therapy will likely remain within the art of medicine.

Aortic pressure during human cardiac arrest. Identification of pseudo-electromechanical dissociation.

We measured aortic pressure during clinically apparent cardiac electromechanical dissociation (EMD). Patients with pulse pressures were designated as having pseudo-EMD; those without, as having true EMD. Of the 200 patients studied, 54 presented with EMD, and 40 others developed it during resuscitation. Of the 94 with EMD, 39 were found to have pseudo-EMD. We compared the two types of EMD for electrocardiographic duration, return of palpable pulses, and response to standard- and high-dose epinephrine. The mean resting aortic pressure was 18 +/- 11 mm Hg in patients with true EMD and 28 +/- 11 mm Hg in those with pseudo-EMD. The mean pulse pressure in patients with pseudo-EMD was 6.3 +/- 3.5 mm Hg. Patients with pseudo-EMD had a higher proportion of witnessed arrests, higher PaO2, and lower PaCO2 than patients with true EMD. Patients with pseudo-EMD had shorter QR and QRS durations than patients with true EMD. They had a better response to standard- and high-dose epinephrine than patients with true EMD. Many patients diagnosed clinically to be in EMD have mechanical cardiac activity; this should be considered when interpreting the results of cardiac arrest research.