Manual vs device-assisted CPR: reconciling apparently contradictory results.
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Cardiopulmonary Resuscitation↗
Biomedical subjects
James T Niemann
Publications and source records attributed to James T Niemann.
A new device producing manual sternal compression with thoracic constraint for cardiopulmonary resuscitation.
OBJECTIVE: Blood flow during conventional cardiopulmonary resuscitation (CPR) is usually less than adequate to sustain vital organ perfusion. A new chest compression device (LifeBelt) which compresses both the sternum and the lateral thoraces (compression and thoracic constraint) has been developed. The device is light weight, portable, manually powered and mechanically advantaged to minimize user fatigue. The purpose of this study was to evaluate the mechanism of blood flow with the device, determine the optimal compression force and compare the device to standard manual CPR in a swine arrest model. METHODS: Following anesthesia and instrumentation, intravascular contrast injections were performed in four animals and the performance characteristics of the device were evaluated in eight animals. In a comparative outcome study, 42 anesthetized and instrumented swine were randomized to receive LifeBelt or manual CPR. Ventricular fibrillation (VF) was induced electrically and was untreated for 7.5 min. After 7.5 min, countershocks were administered and chest compressions initiated. Pulseless electrical activity (PEA) was observed after one to three shocks in all animals. CPR was continued until restoration of spontaneous circulation (ROSC) or for 10 min after the first shock. If ROSC had not occurred within 5 min of beginning CPR, 0.01 mg/kg of epinephrine (adrenaline) was administered. During CPR, peak systolic aortic pressure (Ao), diastolic coronary perfusion pressure (CPP-diastolic aortic minus diastolic right pressure) and end-tidal CO(2) were measured. RESULTS: Angiographic studies demonstrated cardiac compression as the mechanism of blood flow. Optimal performance, determined by coronary perfusion pressure, was observed at a sternal force of 100-130 lb (45-59 kg). In the comparative trial, significant differences in the measured CPP were observed between LifeBelt and manual CPR both at 1 min (15+/-8 mmHg versus 10+/-6 mmHg, p<0.05) and 5 min (17+/-4 mmHg versus 13+/-7 mmHg, p<0.02) of chest compression. A greater (p<0.05) ETCO(2), a marker of cardiac output and systemic perfusion, was observed with LifeBelt CPR (20+/-7 mmHg) than with manual CPR (15+/-5 mmHg) at 1 min. Peak Ao pressures were not different between methods. With the device, 86% of animals were resuscitated compared to 76% in the manual group. CONCLUSIONS: Blood flow with the LifeBelt device is primarily the result of cardiac compression. At a sternal force of 100-130 lb (45-59 kg), the device produces greater CPP than well-performed manual CPR during resuscitation from prolonged VF.
Animals↗
Post-resuscitation plasma catecholamines after prolonged arrest in a swine model.
OBJECTIVE: A dramatic increase in plasma catecholamines has been demonstrated consistently following cardiac arrest and during CPR. The time course of this initial catecholamine surge after successful resuscitation has not been well studied. The purpose of this study was to measure plasma catecholamines after successful resuscitation and to determine their relationship to post-resuscitation hemodynamics. METHODS: VF cardiac arrest was induced in eight anesthetized and instrumented swine. After 5 min of VF, conventional CPR was initiated followed 2 min later by transthoracic defibrillation. Restoration of spontaneous circulation (ROSC) was achieved in six animals. Following resuscitation, hemodynamic variables and plasma catecholamines were measured at intervals. RESULTS: Myocardial contractility (peak systolic dP/dt), stoke volume, left ventricular stroke work (LVSW), and mean arterial pressure (MAP) were significantly decreased from pre-arrest values within 15 min of ROSC and remained depressed during 60 min of observation. Systemic vascular resistance (SVR) was significantly increased within 15 min and remained elevated. Significant negative correlations were observed between SVR and plasma epinephrine (adrenaline) (r=-0.72, p<0.001) and norepinephrine (noradrenaline) (r=-0.76, p<0.001). Significant negative correlations were also observed between MAP and these catecholamines. A negative correlation was also observed between norepinephrine and LVSW (r=-0.50, p=0.039). Catecholamine levels were not related to other indices of cardiac function. CONCLUSIONS: A post-resuscitation adrenergic state is driven by a decline in MAP and PVR. Although seemingly compensatory, it may also contribute to the observed decline in cardiac function.
Animals↗
Intracardiac voltage gradients during transthoracic defibrillation: implications for postshock myocardial injury.
UNLABELLED: In-vitro studies indicate that the electric-field intensity, or voltage gradient (VG), generated by a defibrillation shock is a determinant of defibrillation success as well as potential shock-induced cardiac injury. It is not clear how common descriptors of shock dose, e.g., joules (J), relate to VGs. OBJECTIVES: To assess the relationships between shock energy descriptors and VG. METHODS: One monophasic and three biphasic waveforms were compared using transthoracic shocks and standard electrodes in five swine. VG measurements via intracavitary multielectrode-tipped catheters were compared with delivered energy and peak current. Shock variables were recorded at native transthoracic impedance and an adjusted impedance approximating that of typical humans. RESULTS: For shocks at the same energy setting, peak current and VGs varied widely among the four defibrillators. At simulated human impedance (75 Omega), shocks at each device's maximum energy setting produced similar VGs among the three biphasic defibrillators, despite different delivered energies. For both native impedance (35 Omega) and at 75 Omega, VG correlated with peak current (r = 0.81 and 0.77, respectively) but not energy setting (r = 0.61, 0.52) or delivered energy (r = 0.58, 0.56). At the maximum energy setting of each device, maximum recorded VGs for both monophasic (33 V/cm) and biphasic (24 V/cm) defibrillators were less than those reported to cause myocardial injury (>60 to 80 V/cm). CONCLUSIONS: Energy descriptors correlate poorly to actual shock intensities. When compared with reported VG thresholds of myocardial injury, this study suggests that risk of injury from critically strong VGs is low for all of these defibrillators and equivalent among tested biphasic waveforms.
Animals↗
Prediction rules for estimating neurologic outcome following out-of-hospital cardiac arrest.
BACKGROUND: No valid model has been developed to predict survival following out-of-hospital cardiac arrest. The purpose of this study was to develop a prediction model for meaningful survival following out-of-hospital cardiac arrest using variables available during resuscitation. METHODS: This was a retrospective cohort study. Consecutive adult cardiac arrest patients were studied between 1994 and 2001. Variables included age, sex, race/ethnicity, arrest location, whether the arrest was witnessed, initial rhythm, whether CPR was performed, patient downtime, paramedic response time, survival to hospital discharge, and Glasgow Coma Score (GCS) at hospital discharge. Classification and Regression Tree analysis was used to develop decision rules to predict meaningful survival, as defined by the patient's discharge GCS. RESULTS: Of the 754 patients, 16 (2%) survived with a GCS > or =13, 15 (2%) survived with a GCS = 14, and 5 (0.7%) survived with a GCS = 15. The decision rule for survival with a GCS > or = 13 incorporated whether the arrest was witnessed and the patient's age, resulting in a negative predictive value (NPV) of 99.8%. The rule for survival with a GCS > or = 14 incorporated the initial arrest rhythm, whether the arrest was witnessed, and the patient's age, resulting in a NPV of 99.6%. The rule for survival with a GCS = 15 incorporated only the interval between collapse and the initiation of life support, resulting in a NPV of 99.8%. CONCLUSIONS: This study reports decision rules for potential meaningful survival following out-of-hospital cardiac arrest with high NPVs for each. Future studies need to be performed to prospectively validate these models.
Aged↗
Tumor necrosis factor-alpha is associated with early postresuscitation myocardial dysfunction.
OBJECTIVE: Left ventricular dysfunction after successful cardiopulmonary resuscitation contributes to early death following resuscitation. The stress-induced proinflammatory cytokines, particularly tumor necrosis factor-alpha and interleukin-1beta, are known to depress myocardial function. We hypothesized that tumor necrosis factor-alpha and interleukin-1beta, synthesized and released in response to the stress of global ischemia accompanying cardiac arrest, play a role in development of postresuscitation left ventricular dysfunction. METHODS: Hemodynamic variables, tumor necrosis factor-alpha , interleukin-1beta, interleukin-6 (enzyme-linked immunosorbent assay method), and ionized calcium were measured in ten anesthetized swine before and after 7 mins of cardiac arrest and during the early postresuscitation period (60-90 mins). RESULTS: Tumor necrosis factor-alpha increased three-fold within 15 mins of restoration of circulation and remained elevated throughout the observation period. A significant negative correlation was observed between tumor necrosis factor-alpha and left ventricular systolic change in pressure over time (r = -.54, p <.001). Interleukin-1beta was undetectable before and after resuscitation, and interleukin-6 was detectable in only two animals after resuscitation. Although a significant decline in ionized calcium was observed and correlated with left ventricular systolic change in pressure over time, an independent role for ionized calcium in postresuscitation left ventricular dysfunction was not demonstrated. CONCLUSION: Tumor necrosis factor-alpha increases during the early postresuscitation period and may play a role in postresuscitation myocardial dysfunction.
Animals↗
A model of ischemically induced ventricular fibrillation for comparison of fixed-dose and escalating-dose defibrillation strategies.
OBJECTIVES: Fixed- and escalating-dose defibrillation protocols are both in clinical use. Clinical observations suggest that the probability of successful defibrillation is not constant across a population of patients with ventricular fibrillation (VF). Common animal models of electrically induced VF do not represent a clinical VF etiology or reproduce clinical heterogeneity in defibrillation probability. The authors hypothesized that a model of ischemically induced VF would exhibit heterogeneous defibrillation shock strength requirements and that an escalating-dose strategy would more effectively achieve prompt defibrillation. METHODS: Forty-six swine were randomized to fixed, lower-energy (150 J) transthoracic shocks (group 1) or escalating, higher-energy (200 J-300 J-360 J) shocks (group 2). VF was induced by balloon occlusion of a coronary artery. After 1 or 5 minutes of VF, countershocks with a biphasic waveform were administered. The primary endpoint was successful defibrillation (termination of VF for 5 seconds) with < or =3 shocks. RESULTS: VF was induced with occlusion or after reperfusion in 35 animals. Only five of 17 group 1 animals (29%, 95% CI = 10 to 56) could be defibrillated with < or =3 shocks; 15 of 18 group 2 animals (83%, 95% CI = 59 to 96) were defibrillated with < or =3 shocks (p < 0.002 vs. group 1). Nine of the group 1 animals (75%) that could not be defibrillated with 150-J shocks were rescued with < or =3 shocks ranging from 200 to 360 J. CONCLUSIONS: In this ischemic VF animal model, defibrillation shock strength requirements varied among individuals, and when defibrillation was difficult, an escalating-dose strategy was more effective for prompt defibrillation than fixed, lower-energy shocks.
Animals↗
Milrinone facilitates resuscitation from cardiac arrest and attenuates postresuscitation myocardial dysfunction.
BACKGROUND: Left ventricular (LV) dysfunction with a low cardiac index after successful CPR contributes to early death attributable to multiorgan failure, and an effective treatment has not been identified. The purpose of this study was to investigate the use of milrinone, a selective phosphodiesterase III inhibitor, as treatment for LV dysfunction after resuscitation. METHODS AND RESULTS: Ventricular fibrillation (VF) was induced electrically in 32 swine. After 5 minutes of VF, CPR was initiated and animals were randomized to receive either saline (control group, n=16) as a bolus and infusion or milrinone 50 microg/kg as a bolus and then 0.5 microg/kg per min for 60 minutes (treatment group, n=16). After 2 minutes of CPR (total VF time, 7 minutes), countershocks were given. Coronary perfusion pressures during CPR were similar for the groups (24+/-2 versus 21+/-4 mm Hg). All animals were defibrillated; 6 of 16 control animals developed refractory postcountershock pulseless electrical activity compared with 0 of 16 treated animals (P=0.018). At 30 minutes after restoration of spontaneous circulation, stroke volume (16+/-3 versus 26+/-7 mL, P<0.01) and LV dp/dt (793+/-197 versus 1108+/-316 mm Hg/s, P<0.02) were higher in the treatment group. Similar differences were observed 60 minutes after restoration of spontaneous circulation. Significant differences in heart rates between groups were not observed, and peripheral vascular resistance was significantly greater in the control group 30 and 60 minutes after resuscitation. CONCLUSIONS: Milrinone facilitates resuscitation from prolonged VF and attenuates LV dysfunction after resuscitation without worsening major determinants of myocardial oxygen demand.
3',5'-Cyclic-AMP Phosphodiesterases↗
Transthoracic impedance does not decrease with rapidly repeated countershocks in a swine cardiac arrest model.
STUDY PURPOSE: Successful defibrillation is dependent upon the delivery of adequate electrical current to the myocardium. One of the major determinant of current flow is transthoracic impedance. Prior work has suggested that impedance falls with repeated shocks during sinus rhythm. The purpose of this study was to evaluate changes in transthoracic impedance with repeated defibrillation shocks in an animal model of cardiac arrest due to ventricular fibrillation (VF). METHODS: VF was electrically induced in anesthetized swine. After 5 min of untreated VF, monophasic or biphasic waveform defibrillation was attempted using a standard sequence of 'stacked shocks' (200, 300, then 360 J, if necessary) administered via adhesive electrodes. If one of the first three shocks failed to convert VF, conventional CPR was initiated and defibrillation (360 J) attempted 1 min later. Strength-duration curves for delivered voltage and current were measured during each shock and transthoracic impedance calculated. Animals requiring a minimum of four shocks were selected for study inclusion. Impedance data from sequential shocks were analyzed using mixed linear models to account for the repeated-measures design and the variability of the initial impedance of individual animals. RESULTS: Thirteen animals (monophasic waveform, n=7, biphasic waveform, n=6) required at least four shocks to terminate VF (range 4-6). Transthoracic impedance did not change from the first shock in the 13 animals (46+/-8 Omega) to the fourth shock (46+/-9 Omega). In animals receiving more than four shocks, transthoracic impedance likewise did not change significantly from the first to the last shock, which terminated VF. The lack of a significant change in impedance was also observed when animals were analyzed according to defibrillation waveform. CONCLUSION: Transthoracic impedance does not change significantly with repeated shocks in a VF cardiac arrest model. This is likely due to the lack of reactive skin and soft tissue hyperemia and edema observed in non-arrest models.
Animals↗
Is the ACLS score a valid prediction rule for survival after cardiac arrest?
UNLABELLED: The ACLS (advanced cardiac life support) Score was previously developed to predict survival from out-of-hospital cardiac arrest. Whether the arrest was witnessed, initial cardiac rhythm, performance of bystander cardiopulmonary resuscitation (CPR), and the response time of the paramedic unit were determined to be predictive of survival. However, the ACLS Score has not been validated in other emergency medical services systems. OBJECTIVES: The purpose of this study was to externally validate the ACLS Score in one patient population. METHODS: This was a retrospective cohort study performed at an urban county teaching hospital. The study population consisted of consecutive adult patients treated for out-of-hospital, nontraumatic cardiac arrest, and transported to the authors' institution between November 1, 1994, and September 30, 2001. Patient records for all cardiac arrests during the study period were reviewed. Study variables included witnessed arrest, initial arrest rhythm, bystander CPR, paramedic response time, and survival to hospital discharge. Predicted probability of survival to hospital discharge was calculated for each patient using the ACLS Score. The overall predicted and observed survival rates were compared using Flora's Z score. The Hosmer-Lemeshow test was used to evaluate the model's goodness-of-fit over a range of survival probabilities. RESULTS: Of 754 cardiac arrest patients enrolled in the study period, 575 (76%) patients had documentation that allowed scoring using the ACLS Score. Twenty-five (4%) patients survived to hospital discharge. The predicted number of survivors based on the ACLS Score was 104 (18%), yielding a Flora's Z statistic of -4.46 (p < 0.0001). After categorizing predicted survival probabilities into four categories, the resulting Hosmer-Lemeshow statistic was 210 (p << 10(-6)). Both goodness-of-fit statistics demonstrated extremely poor fit of the model. A receiver operating characteristic (ROC) curve was created, yielding an area under the ROC curve of 0.33 (95% CI = 0.19 to 0.47), signifying extremely poor discrimination. CONCLUSIONS: The previously published ACLS Score was not valid when applied to an external cohort of out-of-hospital cardiac arrest patients. An externally valid model is needed to predict survival to hospital discharge following out-of-hospital cardiac arrest.
Advanced Cardiac Life Support↗
Left ventricular function after monophasic and biphasic waveform defibrillation: the impact of cardiopulmonary resuscitation time on contractile indices.
UNLABELLED: Previous work has suggested that low-energy biphasic waveform defibrillation (BWD) is followed by less post-resuscitation left ventricular (LV) dysfunction when compared with higher-energy monophasic waveform defibrillation (MWD). To the best of the authors' knowledge, the effect of cardiopulmonary resuscitation (CPR) duration and total ischemia time on LV function after countershock, controlling for waveform type, has not been evaluated. OBJECTIVE: To determine the effect of CPR duration on LV function after MWD and BWD. METHODS: VF was electrically induced in anesthetized and instrumented swine. After 5 minutes of VF, the animals were randomized to MWD (n = 22) or one of two BWDs (n = 46). If countershock terminated VF but was followed by a nonperfusing rhythm, conventional manual CPR without drug therapy was performed until restoration of spontaneous circulation (ROSC), defined as a systolic arterial pressure >60 mm Hg for 10 minutes without vasopressor support. Systolic LV pressure (LVP), LV dP/dt (first derivative of pressure measured over time), and cardiac output (CO) were measured at intervals for 60 minutes postresuscitation. CPR times (times to ROSC) and hemodynamic variables for the three groups were compared. Multivariable linear regression was performed to assess the contribution of defibrillation waveform, total joules, and CPR time on LVP, LV dP/dt, and CO at 15, 30, and 60 minutes postresuscitation. RESULTS: When analyzed as groups, significant differences in median number of shocks to terminate VF, total joules, or CPR time were not observed between waveform groups. Regression analysis demonstrated that increasing CPR time was associated with a significant effect on indices of LV function at 15 and 30 minutes postresuscitation. Global LV function was not influenced by waveform type or total joules. CONCLUSIONS: Adjustment for CPR time, a determinant of total myocardial ischemia time, is necessary when defibrillation waveforms are compared for their effect on postresuscitation cardiac function and short-term outcome.
Animals↗
Endotracheal drug administration during out-of-hospital resuscitation: where are the survivors?
BACKGROUND: Drugs administered endotracheally are effectively absorbed during normal spontaneous cardiac activity. However, animal cardiac arrest studies and limited clinical investigations do not support either the use of endotracheal (ET) drugs in doses currently recommended for adults or the method of direct endotracheal instillation. The purpose of this study was to compare the effect of intravenous (IV) and ET drug therapy on outcome from out-of-hospital cardiac arrest secondary to all cardiac arrest rhythms. DESIGN: Five and one-half year retrospective cohort study. SETTING: Municipal, university affiliated hospital. PATIENTS: Consecutive patients >18 years of age in nontraumatic out-of-hospital cardiac arrest who received advanced cardiac life support (ACLS) medications by only the ET or IV route were included. INTERVENTIONS: None. RESULTS: Five hundred and ninety-six patients met inclusion criteria (IV drugs=495, ET drugs=101). There was no difference between groups in the rate of witnessed arrest and the frequency of bystander cardiopulmonary resuscitation (CPR). In the ET drug group, a significantly greater number of patients had an initial documented arrest rhythm of asystole compared to the IV drug group (56 vs 37%, P=0.01). The rate of return of spontaneous circulation (27 vs 15%, P=0.01) and survival to hospital admission rate (20 vs 9%, P=0.01) were significantly greater in the IV drug group. No patient who received ET drugs survived to hospital discharge compared to 5% of those receiving IV drugs (P=0.01). CONCLUSION: For our out-of-hospital advanced rescuer system, ET drugs at recommended doses (twice the IV dose) injected into an ET tube during cardiac arrest and CPR were of no benefit.
Adrenergic Agonists↗
Reconsideration of proximate Utstein-style end points.
The Utstein-style template defines core and supplementary data for reporting out-of-hospital cardiac arrest information. The primary outcome statistic of the Utstein template is survival to hospital discharge (SHD). The SHD statistic is dependent on Utstein-defined out-of-hospital variables and multiple in-hospital variables that are undefined and uncontrolled. An example of one of these undefined in-hospital variables is the decision to place a patient on do-not-resuscitate status. At our municipal teaching hospital, 418 patients who had out-of-hospital cardiac arrest presented over a 4-yr period; 79 (19%; 95% confidence interval [CI], 15% to 23%) survived to hospital admission, with 54 (68%; 95% CI, 57% to 78%) subsequently being placed on do-not-resuscitate status. When patients on do-not-resuscitate status were included in the SHD calculation, the SHD rate was 5.3% (95% CI, 3.3% to 7.8%), and when patients on do-not-resuscitate status were excluded from the SHD calculation, the SHD rate was 6.1% (95% CI, 3.8% to 9.0%). These data show a relative 15% change in SHD resulting from a single in-hospital variable. Cardiac arrest survivors represent a small proportion of a total population; therefore, large numbers of study subjects are required for a statistically significant interpretation of the SHD statistic. This requirement for large study populations has resulted in recent studies that report results by using end points proximate to SHD when assessing the effect of individual interventions. It is logical that success of a specific intervention should be determined by the ability of the intervention to accomplish its purpose rather than the ability to improve SHD that is dependent on multiple variables. Furthermore, because in-hospital care is not standardized and uncontrolled variables exist, the primary Utstein end point of SHD should be reconsidered when evaluating cardiac arrest interventions.
Data Collection↗
Vasopressin in piglet "pediatric models" of cardiac arrest.
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Animals↗