Glucagon-like peptide-1 preserves coronary microvascular endothelial function after cardiac arrest and resuscitation: potential antioxidant effects.

Glucagon-like peptide-1 (GLP-1) has protective effects in the heart. We hypothesized that GLP-1 would mitigate coronary microvascular and left ventricular (LV) dysfunction if administered after cardiac arrest and resuscitation (CAR). Eighteen swine were subjected to ventricular fibrillation followed by resuscitation. Swine surviving to return of spontaneous circulation (ROSC) were randomized to receive an intravenous infusion of either human rGLP-1 (10 pmol·kg(-1)·min(-1); n = 8) or 0.9% saline (n = 8) for 4 h, beginning 1 min after ROSC. CAR caused a decline in coronary flow reserve (CFR) in control animals (pre-arrest, 1.86 ± 0.20; 1 h post-ROSC, 1.3 ± 0.05; 4 h post-ROSC, 1.25 ± 0.06; P < 0.05). GLP-1 preserved CFR for up to 4 h after ROSC (pre-arrest, 1.31 ± 0.17; 1 h post-ROSC, 1.5 ± 0.01; 4 h post-ROSC, 1.55 ± 0.22). Although there was a trend toward improvement in LV relaxation in the GLP-1-treated animals, overall LV function was not consistently different between groups. 8-iso-PGF(2α), a measure of reactive oxygen species load, was decreased in post-ROSC GLP-1-treated animals [placebo, control (NS): 38.1 ± 1.54 pg/ml; GLP-1: 26.59 ± 1.56 pg/ml; P < 0.05]. Infusion of GLP-1 after CAR preserved coronary microvascular and LV diastolic function. These effects may be mediated through a reduction in oxidative stress.

Mild hypothermia delays the development of stone heart from untreated sustained ventricular fibrillation--a cardiovascular magnetic resonance study.

BACKGROUND: 'Stone heart' resulting from ischemic contracture of the myocardium, precludes successful resuscitation from ventricular fibrillation (VF). We hypothesized that mild hypothermia might slow the progression to stone heart. METHODS: Fourteen swine (27 ± 1 kg) were randomized to normothermia (group I; n=6) or hypothermia groups (group II; n=8). Mild hypothermia (34 ± 2 °C) was induced with ice packs prior to VF induction. The LV and right ventricular (RV) cross-sectional areas were followed by cardiovascular magnetic resonance until the development of stone heart. A commercial 1.5T GE Signa NV-CV/i scanner was used. Complete anatomic coverage of the heart was acquired using a steady-state free precession (SSFP) pulse sequence gated at baseline prior to VF onset. Un-gated SSFP images were obtained serially after VF induction. The ventricular endocardium was manually traced and LV and RV volumes were calculated at each time point. RESULTS: In group I, the LV was dilated compared to baseline at 5 minutes after VF and this remained for 20 minutes. Stone heart, arbitrarily defined as LV volume <1/3 of baseline at the onset of VF, occurred at 29 ± 3 minutes. In group II, there was less early dilation of the LV (p<0.05) and the development of stone heart was delayed to 52 ± 4 minutes after onset of VF (P<0.001). CONCLUSIONS: In this closed-chest swine model of prolonged untreated VF, hypothermia reduced the early LV dilatation and importantly, delayed the onset of stone heart thereby extending a known, morphologic limit of resuscitability.

Epinephrine improves 24-hour survival in a swine model of prolonged ventricular fibrillation demonstrating that early intraosseous is superior to delayed intravenous administration.

BACKGROUND: Vasopressors administered IV late during resuscitation efforts fail to improve survival. Intraosseous (IO) access can provide a route for earlier administration. We hypothesized that IO epinephrine after 1 minute of cardiopulmonary resuscitation (CPR) (an "optimal" IO scenario) after 10 minutes of untreated ventricular fibrillation (VF) cardiac arrest would improve outcome in comparison with either IV epinephrine after 8 minutes of CPR (a "realistic" IV scenario) or placebo controls with no epinephrine. METHODS: Thirty swine were randomized to IO epinephrine, IV epinephrine, or placebo. Important outcomes included return of spontaneous circulation (ROSC), 24-hour survival, and 24-hour survival with good neurological outcome (cerebral performance category 1). RESULTS: ROSC after 10 minutes of untreated VF was uncommon without administration of epinephrine (1 of 10), whereas ROSC was nearly universal with IO epinephrine or delayed IV epinephrine (10 of 10 and 9 of 10, respectively; P = 0.001 for either versus placebo). Twenty-four hour survival was substantially more likely after IO epinephrine than after delayed IV epinephrine (10 of 10 vs. 4 of 10, P = 0.001). None of the placebo group survived at 24 hours. Survival with good neurological outcome was more likely after IO epinephrine than after placebo (6 of 10 vs. 0 of 10, P = 0.011), and only 3 of 10 survived with good neurological outcome in the delayed IV epinephrine group (not significant versus either IO or placebo). CONCLUSION: In this swine model of prolonged VF cardiac arrest, epinephrine administration during CPR improved outcomes. In addition, early IO epinephrine improved outcomes in comparison with delayed IV epinephrine.

Predictors of resuscitation in a swine model of ischemic and nonischemic ventricular fibrillation cardiac arrest: superiority of amplitude spectral area and slope to predict a return of spontaneous circulation when resuscitation efforts are prolonged.

OBJECTIVE: We have demonstrated that a return of spontaneous circulation in the first 3 mins of resuscitation in swine is predicted by ventricular fibrillation waveform (amplitude spectral area or slope) when untreated ventricular fibrillation duration or presence of acute myocardial infarction is unknown. We hypothesized that in prolonged resuscitation efforts that return of spontaneous circulation immediately after a second or later shock with postshock chest compression is independently predicted by end-tidal CO2, coronary perfusion pressure, and ventricular fibrillation waveform measured before that shock in a swine model of ischemic and nonischemic ventricular fibrillation arrest. DESIGN: Animal intervention study with comparison to a control group. SETTING: University animal laboratory. SUBJECTS: Twenty swine. INTERVENTIONS: Myocardial infarction was induced by steel plug occlusion of the left anterior descending coronary artery. Ventricular fibrillation was untreated for 8 mins in normal swine (n=10) and acute myocardial infarction swine (n=10). MEASUREMENTS AND MAIN RESULTS: End-tidal CO2, coronary perfusion pressure, and ventricular fibrillation waveform characteristics of amplitude spectral area and slope were analyzed before second or later shocks. For an amplitude spectral area>35 mV-Hz, the odds ratio for achieving return of spontaneous circulation after that shock was 72 (95% confidence interval, 3.8-1300; p=.004) compared with an amplitude spectral area<28 mV-Hz and with an area under the receiver operator characteristic curve of 0.86. For slope>3.6 mV/s, the odds ratio for achieving return of spontaneous circulation was 36 (95% confidence interval, 2.7-480; p=.007) compared with slope<2.72 mV/s with an area under the curve of 0.86. End-tidal CO2 and coronary perfusion pressure were not predictive of return of spontaneous circulation after a shock, although coronary perfusion pressure was significantly related to both amplitude spectral area (p<.001) and slope (p<.001). CONCLUSIONS: : In prolonged untreated ventricular fibrillation arrest, the waveform characteristics of amplitude spectral area and slope predict the attainment of return of spontaneous circulation with a second or later shock. This has implications for the ideal means to customize the timing of shocks and chest compressions when return of spontaneous circulation is not promptly obtained.

Leaning during chest compressions impairs cardiac output and left ventricular myocardial blood flow in piglet cardiac arrest.

OBJECTIVE: Complete recoil of the chest wall between chest compressions during cardiopulmonary resuscitation is recommended, because incomplete chest wall recoil from leaning may decrease venous return and thereby decrease blood flow. We evaluated the hemodynamic effect of 10% or 20% lean during piglet cardiopulmonary resuscitation. DESIGN: Prospective, sequential, controlled experimental animal investigation. SETTING: University research laboratory. SUBJECTS: Domestic piglets. INTERVENTIONS: After induction of ventricular fibrillation, cardiopulmonary resuscitation was provided to ten piglets (10.7 +/- 1.2 kg) for 18 mins as six 3-min epochs with no lean, 10% lean, or 20% lean to maintain aortic systolic pressure of 80-90 mm Hg. Because the mean force to attain 80-90 mm Hg was 18 kg in preliminary studies, the equivalent of 10% and 20% lean was provided by use of 1.8- and 3.6-kg weights on the chest. MEASUREMENTS AND MAIN RESULTS: Using a linear mixed-effect regression model to control for changes in cardiopulmonary resuscitation hemodynamics over time, mean right atrial diastolic pressure was 9 +/- 0.6 mm Hg with no lean, 10 +/- 0.3 mm Hg with 10% lean (p < .01), and 13 +/- 0.3 mm Hg with 20% lean (p < .01), resulting in decreased coronary perfusion pressure with leaning. Microsphere-determined cardiac index and left ventricular myocardial blood flow were lower with 10% and 20% leaning throughout the 18 mins of cardiopulmonary resuscitation. Mean cardiac index decreased from 1.9 +/- 0.2 L . M . min with no leaning to 1.6 +/- 0.1 L . M . min with 10% leaning, and 1.4 +/- 0.2 L . M . min with 20% leaning (p < .05). The myocardial blood flow decreased from 39 +/- 7 mL . min . 100 g with no lean to 30 +/- 6 mL . min . 100 g with 10% leaning and 26 +/- 6 mL . min . 100 g with 20% leaning (p < .05). CONCLUSIONS: Leaning of 10% to 20% (i.e., 1.8-3.6 kg) during cardiopulmonary resuscitation substantially decreased coronary perfusion pressure, cardiac index, and myocardial blood flow.

Continued breathing followed by gasping or apnea in a swine model of ventricular fibrillation cardiac arrest.

BACKGROUND: Continued breathing following ventricular fibrillation has here-to-fore not been described. METHODS: We analyzed the spontaneous ventilatory activity during the first several minutes of ventricular fibrillation (VF) in our isoflurane anesthesized swine model of out-of-hospital cardiac arrest. The frequency and type of ventilatory activity was monitored by pneumotachometer and main stream infrared capnometer and analyzed in 61 swine during the first 3 to 6 minutes of untreated VF. RESULTS: During the first minute of VF, the air flow pattern in all 61 swine was similar to those recorded during regular spontaneous breathing during anesthesia and was clearly different from the patterns of gasping. The average rate of continued breathing during the first minute of untreated VF was 10 breaths per minute. During the second minute of untreated VF, spontaneous breathing activity either stopped or became typical of gasping. During minutes 2 to 5 of untreated VF, most animals exhibited very slow spontaneous ventilatory activity with a pattern typical of gasping; and the pattern of gasping was crescendo-decrescendo, as has been previously reported. In the absence of therapy, all ventilatory activity stopped 6 minutes after VF cardiac arrest. CONCLUSION: In our swine model of VF cardiac arrest, we documented that normal breathing continued for the first minute following cardiac arrest.

Gasping during cardiac arrest in humans is frequent and associated with improved survival.

BACKGROUND: The incidence and significance of gasping after cardiac arrest in humans are controversial. METHODS AND RESULTS: Two approaches were used. The first was a retrospective analysis of consecutive confirmed out-of-hospital cardiac arrests from the Phoenix Fire Department Regional Dispatch Center text files to determine the presence of gasping soon after collapse. The second was a retrospective analysis of 1218 patients with out-of-hospital cardiac arrests in Arizona documented by emergency medical system (EMS) first-care reports to determine the incidence of gasping after arrest in relation to the various EMS arrival times. The primary outcome measure was survival to hospital discharge. An analysis of the Phoenix Fire Department Regional Dispatch Center records of witnessed and unwitnessed out-of-hospital cardiac arrests with attempted resuscitation found that 44 of 113 (39%) of all arrested patients had gasping. An analysis of 1218 EMS-attended, witnessed, out-of-hospital cardiac arrests demonstrated that the presence or absence of gasping correlated with EMS arrival time. Gasping was present in 39 of 119 patients (33%) who arrested after EMS arrival, in 73 of 363 (20%) when EMS arrival was <7 minutes, in 50 of 360 (14%) when EMS arrival time was 7 to 9 minutes, and in 25 of 338 (7%) when EMS arrival time was >9 minutes. Survival to hospital discharge occurred in 54 of 191 patients (28%) who gasped and in 80 of 1027 (8%) who did not (adjusted odds ratio, 3.4; 95% confidence interval, 2.2 to 5.2). Among the 481 patients who received bystander cardiopulmonary resuscitation, survival to hospital discharge occurred among 30 of 77 patients who gasped (39%) versus only 38 of 404 among those who did not gasp (9%) (adjusted odds ratio, 5.1; 95% confidence interval, 2.7 to 9.4). CONCLUSIONS: Gasping or abnormal breathing is common after cardiac arrest but decreases rapidly with time. Gasping is associated with increased survival. These results suggest that the recognition and importance of gasping should be taught to bystanders and emergency medical dispatchers so as not to dissuade them from initiating prompt resuscitation efforts when appropriate.

Passive oxygen insufflation is superior to bag-valve-mask ventilation for witnessed ventricular fibrillation out-of-hospital cardiac arrest.

STUDY OBJECTIVE: Assisted ventilation may adversely affect out-of-hospital cardiac arrest outcomes. Passive ventilation offers an alternate method of oxygen delivery for these patients. We compare the adjusted neurologically intact survival of out-of-hospital cardiac arrest patients receiving initial passive ventilation with those receiving initial bag-valve-mask ventilation. METHODS: The authors performed a retrospective analysis of statewide out-of-hospital cardiac arrests between January 1, 2005, and September 28, 2008. The analysis included consecutive adult out-of-hospital cardiac arrest patients receiving resuscitation with minimally interrupted cardiopulmonary resuscitation (CPR) consisting of uninterrupted preshock and postshock chest compressions, initial noninvasive airway maneuvers, and early epinephrine. Paramedics selected the method of initial noninvasive ventilation, consisting of either passive ventilation (oropharyngeal airway insertion and high-flow oxygen by nonrebreather facemask, without assisted ventilation) or bag-valve-mask ventilation (by paramedics at 8 breaths/min). The authors determined adjusted neurologically intact survival from hospital and public records and by telephone interview and mail questionnaire. The authors compared adjusted neurologically intact survival between ventilation techniques by using generalized estimating equations. RESULTS: Among the 1,019 adult out-of-hospital cardiac arrest patients in the analysis, 459 received passive ventilation and 560 received bag-valve-mask ventilation. Adjusted neurologically intact survival after witnessed ventricular fibrillation/ventricular tachycardia out-of-hospital cardiac arrest was higher for passive ventilation (39/102; 38.2%) than bag-valve-mask ventilation (31/120; 25.8%) (adjusted odds ratio [OR] 2.5; 95% confidence interval [CI] 1.3 to 4.6). Survival between passive ventilation and bag-valve-mask ventilation was similar after unwitnessed ventricular fibrillation/ventricular tachycardia (7.3% versus 13.8%; adjusted OR 0.5; 95% CI 0.2 to 1.6) and nonshockable rhythms (1.3% versus 3.7%; adjusted OR 0.3; 95% CI 0.1 to 1.0). CONCLUSION: Among adult, witnessed, ventricular fibrillation/ventricular tachycardia, out-of-hospital cardiac arrest resuscitated with minimally interrupted cardiac resuscitation, adjusted neurologically intact survival to hospital discharge was higher for individuals receiving initial passive ventilation than those receiving initial bag-valve-mask ventilation.

Improved neurological outcome with continuous chest compressions compared with 30:2 compressions-to-ventilations cardiopulmonary resuscitation in a realistic swine model of out-of-hospital cardiac arrest.

BACKGROUND: The 2005 Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care changed the previous ventilations-to-chest-compression algorithm for bystander cardiopulmonary resuscitation (CPR) from 2 ventilations before each 15 chest compressions (2:15 CPR) to 30 chest compressions before 2 ventilations (30:2 CPR). It was acknowledged in the guidelines that the change was based on a consensus rather than clear evidence. This study was designed to compare 24-hour neurologically normal survival between the initial applications of continuous chest compressions without assisted ventilations with 30:2 CPR in a swine model of witnessed out-of-hospital ventricular fibrillation cardiac arrest. METHODS AND RESULTS: Sixty-four animals underwent 12 minutes of ventricular fibrillation before defibrillation attempts. They were divided into 4 groups, each with increasing durations (3, 4, 5, and 6 minutes, respectively) of untreated ventricular fibrillation before the initiation of bystander resuscitation consisting of either continuous chest compression or 30:2 CPR. After the various untreated ventricular durations plus bystander resuscitation durations, all animals were given the first defibrillation attempt 12 minutes after the induction of ventricular fibrillation, followed by the 2005 guideline-recommended advanced cardiac life support. Neurologically normal survival at 24 hours after resuscitation was observed in 23 of 33 (70%) of the animals in the continuous chest compression groups but in only 13 of 31 (42%) of the 30:2 CPR groups (P=0.025). CONCLUSIONS: In a realistic model of out-of-hospital ventricular fibrillation cardiac arrest, initial bystander administration of continuous chest compressions without assisted ventilations resulted in significantly better 24-hour postresuscitation neurologically normal survival than did the initial bystander administration of 2005 guideline-recommended 30:2 CPR.

The influence of myocardial substrate on ventricular fibrillation waveform: a swine model of acute and postmyocardial infarction.

OBJECTIVE: In cardiac arrest resulting from ventricular fibrillation, the ventricular fibrillation waveform may be a clue to its duration and predict the likelihood of shock success. However, ventricular fibrillation occurs in different myocardial substrates such as ischemia, heart failure, and structurally normal hearts. We hypothesized that ventricular fibrillation is altered by myocardial infarction and varies from the acute to postmyocardial infarction periods. DESIGN: An animal intervention study was conducted with comparison to a control group. SETTING: This study took place in a university animal laboratory. SUBJECTS: Study subjects included 37 swine. INTERVENTIONS: Myocardial infarction was induced by occlusion of the midleft anterior descending artery. Ventricular fibrillation was induced in control swine, acute myocardial infarction swine, and in postmyocardial infarction swine after a 2-wk recovery period. MEASUREMENTS AND MAIN RESULTS: Ventricular fibrillation was recorded in 11 swine with acute myocardial infarction, ten postmyocardial infarction, and 16 controls. Frequency (mean, median, dominant, and bandwidth) and amplitude-related content (slope, slope-amp [slope divided by amplitude], and amplitude-spectrum area) were analyzed. Frequencies at 5 mins of ventricular fibrillation were altered in both acute myocardial infarction (p < .001 for all frequency characteristics) and postmyocardial infarction swine (p = .015 for mean, .002 for median, .002 for dominant frequency, and <.001 for bandwidth). At 5 mins, median frequency was highest in controls, 10.9 +/- .4 Hz; lowest in acute myocardial infarction, 8.4 +/- .5 Hz; and intermediate in postmyocardial infarction, 9.7 +/- .5 Hz (p < .001 for acute myocardial infarction and p = .002 for postmyocardial infarction compared with control). Slope and amplitude-spectrum area were similar among the three groups with a shallow decline after minute 2, whereas slope-amp remained significantly altered for acute myocardial infarction swine at 5 mins (p = .003). CONCLUSIONS: Ventricular fibrillation frequencies depend on myocardial substrate and evolve from the acute through healing phases of myocardial infarction. Amplitude related measures, however, are similar among these groups. It is unknown how defibrillation may be affected by relying on the ventricular fibrillation waveform without considering myocardial substrate.

Myocardial microcirculatory dysfunction after prolonged ventricular fibrillation and resuscitation.

OBJECTIVE: The etiology of postresuscitation myocardial stunning is unknown but is thought to be related to either ischemia occurring during cardiac arrest and resuscitation efforts and/or reperfusion injury after restoration of circulation. A potential common pathway for postischemia/reperfusion end-organ dysfunction is microvascular injury. We hypothesized that myocardial microcirculatory function is markedly abnormal in the postresuscitation period. DESIGN: In vivo study of myocardial microvascular function. SETTING: University animal laboratory. SUBJECTS: Five swine (25 +/- 2 kg). INTERVENTIONS: Measurements before and after cardiac arrest and resuscitation. MEASUREMENTS AND MAIN RESULTS: Baseline data were not different among the five subjects. Left ventricular ejection fraction was significantly lower at all postresuscitation time periods (p < .05), reaching a nadir of 19% at 1 hr postresuscitation. Cardiac output declined following fibrillation and resuscitation and was significantly lower than baseline at 1 and 4 hrs postresuscitation (p < .05). Prearrest coronary flow reserve, a ratio of normal to maximal intracoronary flow velocity, was 3.4 ("normal" ratio is 2:4), but was below normal (<2) throughout the 4-hr post resuscitation period (p < .05). CONCLUSION: This in vivo study showed that normal myocardial microcirculatory function is quickly lost after prolonged ventricular fibrillation and resuscitation. As early as 30 min postresuscitation the myocardial microcirculatory function is less than 50% of its prearrest baseline level. This dysfunction persists for at least 4 hrs. During the postresuscitation period, both left ventricular ejection fraction and cardiac output decline from their prearrest levels. No cause and effect relationship was proven, but a parallel decline in left ventricular function and coronary flow reserve is evident.

Immediate post-shock chest compressions improve outcome from prolonged ventricular fibrillation.

AIM: This study was designed to test the hypothesis that immediate post-shock chest compressions improve outcome from prolonged ventricular fibrillation (VF) compared with typical "hands off" period (i.e., delayed post-shock compressions) associated with AED use. MATERIALS AND METHODS: After 7.5 min of untreated VF, 36 domestic swine (26+/-1 kg) were treated with 200 J biphasic shocks and randomly assigned to: (1) 1 min of immediate post-shock chest compressions or (2) simulated pre-hospital automated external defibrillator (AED) care with delays in post-shock chest compressions. Return of spontaneous circulation (ROSC) occurred in 7/18 immediate chest compressions animals within 2 min of the first shock versus 0/18 AED animals (P<0.01). Ten of 18 immediate chest compressions animals attained ROSC compared with 3/18 AED animals (P<0.05). Nine of 18 immediate chest compressions swine were alive at 24 and 48 h compared with 3/18 AED swine (P<0.05). All 48-h survivors had good neurologic outcomes. Among the 21 animals that defibrillated with the first shock, ROSC was attained in 7/10 immediate chest compressions animals within 2 min of the first shock compared with 0/11 AED animals (P=0.001), and 48-h survival was attained in 8/10 versus 3/11, respectively (P<0.05). CONCLUSIONS: Immediate post-shock chest compressions can substantially improve outcome from prolonged VF compared with simulated pre-hospital AED care.

Attenuating the defibrillation dosage decreases postresuscitation myocardial dysfunction in a swine model of pediatric ventricular fibrillation.

OBJECTIVE: The optimal biphasic defibrillation dose for children is unknown. Postresuscitation myocardial dysfunction is common and may be worsened by higher defibrillation doses. Adult-dose automated external defibrillators are commonly available; pediatric doses can be delivered by attenuating the adult defibrillation dose through a pediatric pads/cable system. The objective was to investigate whether unattenuated (adult) dose biphasic defibrillation results in greater postresuscitation myocardial dysfunction and damage than attenuated (pediatric) defibrillation. DESIGN: Laboratory animal experiment. SETTING: University animal laboratory. SUBJECTS: Domestic swine weighing 19 +/- 3.6 kg. INTERVENTIONS: Fifty-two piglets were randomized to receive biphasic defibrillation using either adult-dose shocks of 200, 300, and 360 J or pediatric-dose shocks of approximately 50, 75, and 85 J after 7 mins of untreated ventricular fibrillation. Contrast left ventriculograms were obtained at baseline and then at 1, 2, 3, and 4 hrs postresuscitation. Postresuscitation left ventricular ejection fraction and cardiac troponins were evaluated. MEASUREMENTS AND MAIN RESULTS: By design, piglets in the adult-dose group received shocks with more energy (261 +/- 65 J vs. 72 +/- 12 J, p < .001) and higher peak current (37 +/- 8 A vs. 13 +/- 2 A, p < .001) at the largest defibrillation dose needed. In both groups, left ventricular ejection fraction was reduced significantly at 1, 2, and 4 hrs from baseline and improved during the 4 hrs postresuscitation. The decrease in left ventricular ejection fraction from baseline was greater after adult-dose defibrillation. Plasma cardiac troponin levels were elevated 4 hrs postresuscitation in 11 of 19 adult-dose piglets vs. four of 20 pediatric-dose piglets (p = .02). CONCLUSIONS: Unattenuated adult-dose defibrillation results in a greater frequency of myocardial damage and worse postresuscitation myocardial function than pediatric doses in a swine model of prolonged out-of-hospital pediatric ventricular fibrillation cardiac arrest. These data support the use of pediatric attenuating electrodes with adult biphasic automated external defibrillators to defibrillate children.

Continuous passive oxygen insufflation results in a similar outcome to positive pressure ventilation in a swine model of out-of-hospital ventricular fibrillation.

BACKGROUND: The deleterious effects of positive pressure ventilation may be prevented by substituting passive oxygen insufflation during advanced cardiac life support (ACLS) cardiopulmonary resuscitation (CPR). METHODS: We compared 24-h neurologically normal survival among three different ventilation scenarios for ACLS in a realistic swine model of out-of-hospital prolonged ventricular fibrillation (VF) cardiac arrest. No bystander CPR was provided during the first 8 min of untreated VF before the simulated arrival of an emergency medical system (EMS). Thirty-six swine were randomly assigned to one of three experimental groups. Group I (standard ventilation) was mechanically ventilated at 10 respirations per minute (RPM) at a tidal volume (TV) of 10 ml/kg with 100% oxygen. Group II (hyperventilation) was ventilated at 35 RPM at a TV of 20 ml/kg with 100% oxygen. In Group III (insufflation) animals, a nasal cannula was placed in the oropharynx to administer oxygen continuously at 10 l/min. RESULTS: There was no significant difference in the 24h neurologically normal survival among groups (standard: 2/12, hyperventilation: 2/12, insufflation: 4/12; p=.53). CONCLUSIONS: Passive insufflation may be an acceptable alternative to the currently recommended positive pressure ventilation during resuscitation efforts for out-of-hospital VF cardiac arrest. Potential advantages of this technique include: (1) easier to teach, (2) easier to administer, (3) prevention of the adverse effects of positive pressure ventilation and (4) allows EMS personnel to concentrate upon other critically important duties.

Cardiac magnetic resonance imaging investigation of sustained ventricular fibrillation in a swine model--with a focus on the electrical phase.

OBJECTIVES: We sought to develop a method to evaluate the rapidly changing cardiac dimensions during sustained ventricular fibrillation (VF). We also present details of our CPR research imaging program to facilitate this avenue of clinically important research. BACKGROUND: The changes in cardiac dimensions occurring during the initial critical electrical phase of sustained VF are not entirely known. Conventional cardiac magnetic resonance imaging (CMR) functional imaging lacks the temporal resolution necessary to capture the dynamic changes within this early time period of sustained VF. We hypothesized that changes in the middle short axis slice of the ventricles will reflect changes in ventricular volumes accurately. METHODS: Ventricular dimensions were determined from CMR for 30 min of untreated VF in a closed chest, closed pericardium model in seven swine. Ungated steady-state free precession images (SSFP) from the cardiac base to the apex were acquired, taking care to align the anatomical short axis (SAX) imaging planes maximally. The middle slice of the ventricles was determined as the mathematical center of the stack of SAX slices. We then compared the relative changes of right ventricle (RV) and left ventricle (LV) volumes to relative changes in mid-ventricular single slice area. RESULTS: During 30 min of sustained VF, there was an excellent correlation between the changes in exact mid-slice area and the quantitative changes in ventricular volumes (r(2)>0.95). CONCLUSIONS: Mid-slice area data can be used as a surrogate marker of prompt ventricular volume changes during VF. By imaging the heart 10 times faster, the rapid anatomical changes occurring during the initial few minutes of sustained VF can be understood better.

Magnetic resonance imaging during untreated ventricular fibrillation reveals prompt right ventricular overdistention without left ventricular volume loss.

BACKGROUND: Most out-of-hospital ventricular fibrillation (VF) is prolonged (>5 minutes), and defibrillation from prolonged VF typically results in asystole or pulseless electrical activity. Recent visual epicardial observations in an open-chest, open-pericardium model of swine VF indicate that blood flows from the high-pressure arterial system to the lower-pressure venous system during untreated VF, thereby overdistending the right ventricle and apparently decreasing left ventricular size. Therefore, inadequate left ventricular stroke volume after defibrillation from prolonged VF has been postulated as a major contributor to the development of pulseless rhythms. METHODS AND RESULTS: Ventricular dimensions were determined by MRI for 30 minutes of untreated VF in a closed-chest, closed-pericardium model in 6 swine. Within 1 minute of untreated VF, mean right ventricular volume increased by 29% but did not increase thereafter. During the first 5 minutes of untreated VF, mean left ventricular volume increased by 34%. Between 20 and 30 minutes of VF, stone heart occurred as manifested by dramatic thickening of the myocardium and concomitant substantial decreases in left ventricular volume. CONCLUSIONS: In this closed-chest swine model of VF, substantial right ventricular volume changes occurred early and did not result in smaller left ventricular volumes. The changes in ventricular volumes before the late development of stone heart do not explain why defibrillation from brief duration VF (<5 minutes) typically results in a pulsatile rhythm with return of spontaneous circulation, whereas defibrillation from prolonged VF (5 to 15 minutes) does not.

Interruptions of chest compressions during emergency medical systems resuscitation.

BACKGROUND: Survival after nontraumatic out-of-hospital (OOH) cardiac arrest in Tucson, Arizona, has been flat at 6% (121/2177) for the decade 1992 to 2001. We hypothesized that interruptions of chest compressions occur commonly and for substantial periods during treatment of OOH cardiac arrest and could be contributing to the lack of improvement in resuscitation outcome. METHODS AND RESULTS: Sixty-one adult OOH cardiac arrest patients treated by automated external defibrillator (AED)-equipped Tucson Fire Department first responders from November 2001 through November 2002 were retrospectively reviewed. Reviews were performed according to the code arrest record and verified with the AED printout. Validation of the methodology for determining the performance of chest compressions was done post hoc. The median time from "9-1-1" call receipt to arrival at the patient's side was 6 minutes, 27 seconds (interquartile range [IQR, 25% to 75%], 5 minutes, 24 seconds, to 7 minutes, 34 seconds). An additional 54 seconds (IQR, 38 to 74 seconds) was noted between arrival and the first defibrillation attempt. Initial defibrillation shocks never restored a perfusing rhythm (0/21). Chest compressions were performed only 43% of the time during the resuscitation effort. Although attempting to follow the 2000 guidelines for cardiopulmonary resuscitation, chest compressions were delayed or interrupted repeatedly throughout the resuscitation effort. Survival to hospital discharge was 7%, not different from that of our historical control (4/61 versus 121/2177; P=0.74). CONCLUSIONS: Frequent interruption of chest compressions results in no circulatory support during more than half of resuscitation efforts. Such interruptions could be a major contributing factor to the continued poor outcome seen with OOH cardiac arrest.

Better outcome after pediatric defibrillation dosage than adult dosage in a swine model of pediatric ventricular fibrillation.

OBJECTIVES: This study was designed to compare outcome after adult defibrillation dosing versus pediatric dosing in a piglet model of prolonged prehospital ventricular fibrillation (VF). BACKGROUND: Weight-based 2 to 4 J/kg monophasic defibrillation dosing is recommended for children in VF, but impractical for automated external defibrillator (AED) use. Present AEDs can only provide adult shock doses or newly developed attenuated adult doses intended for children. A single escalating energy sequence (50/75/86 J) of attenuated adult-dose biphasic shocks (pediatric dosing) is at least as effective as escalating monophasic weight-based dosing for prolonged VF in piglets, but this approach has not been compared to standard adult biphasic dosing. METHODS: Following 7 min of untreated VF, piglets weighing 13 to 26 kg (19 +/- 1 kg) received either biphasic 50/75/86 J (pediatric dose) or biphasic 200/300/360 J (adult dose) therapies during simulated prehospital life support. RESULTS: Return of spontaneous circulation was attained in 15 of 16 pediatric-dose piglets and 14 of 16 adult-dose piglets. Four hours postresuscitation, pediatric dosing resulted in fewer elevations of cardiac troponin T (0 of 12 piglets vs. 6 of 11 piglets, p = 0.005) and less depression of left ventricular ejection fraction (p < 0.05). Most importantly, more piglets survived to 24 h with good neurologic scores after pediatric shocks than adult shocks (13 of 16 piglets vs. 4 of 16 piglets, p = 0.004). CONCLUSIONS: In this model, pediatric shocks resulted in superior outcome compared with adult shocks. These data suggest that adult defibrillation dosing may be harmful to pediatric patients with VF and support the use of attenuating electrodes with adult biphasic AEDs to defibrillate children.

Importance of continuous chest compressions during cardiopulmonary resuscitation: improved outcome during a simulated single lay-rescuer scenario.

BACKGROUND: Interruptions to chest compression-generated blood flow during cardiopulmonary resuscitation (CPR) are detrimental. Data show that such interruptions for mouth-to-mouth ventilation require a period of "rebuilding" of coronary perfusion pressure to obtain the level achieved before the interruption. Whether such hemodynamic compromise from pausing to ventilate is enough to affect outcome is unknown. METHODS AND RESULTS: Thirty swine (weight 35 +/- 2 kg) underwent 3 minutes of untreated ventricular fibrillation before 12 minutes of basic life support CPR. Animals were randomized to receive either standard airway (A), breathing (B), and compression (C) CPR with expired-gas ventilation in a 15:2 compression-to-ventilation ratio or continuous chest compression CPR. Those randomized to the standard 15:2 group had no chest compressions for a period of 16 seconds each time the 2 ventilations were delivered. Defibrillation was attempted at 15 minutes of cardiac arrest. All resuscitated animals were supported in an intensive care environment for 1 hour, then in a maintenance facility for 24 hours. The primary end point of neurologically normal 24-hour survival was significantly better in the experimental group receiving continuous chest compression CPR (12 of 15 versus 2 of 15; P<0.0001). CONCLUSIONS: Mouth-to-mouth ventilation performed by single layperson rescuers produces substantial interruptions in chest compression-supported circulation. Continuous chest compression CPR produces greater neurologically normal 24-hour survival than standard ABC CPR when performed in a clinically realistic fashion. Any technique that minimizes lengthy interruptions of chest compressions during the first 10 to 15 minutes of basic life support should be given serious consideration in future efforts to improve outcome results from cardiac arrest.

Effects of intravenous arginine vasopressin on epicardial coronary artery cross sectional area in a swine resuscitation model.

Although arginine vasopressin (AVP) has been shown to be a promising drug during cardiopulmonary resuscitation (CPR), concern has been raised about the potential for AVP-mediated vasoconstriction of the coronary arteries. In a prospective, randomized laboratory investigation employing an established porcine model, the effects of AVP on haemodynamic variables, left anterior descending (LAD) coronary artery cross sectional area employing intravascular ultrasound (IVUS), and return of spontaneous circulation were studied. During sinus rhythm, the LAD coronary artery cross sectional area was measured by IVUS at baseline, and 90 s and 5 min after AVP (0.4 U/kg IV). Following a 60 min recovery, ventricular fibrillation was induced. At 4 min, chest compressions were initiated; AVP (0.4 U/kg IV) was injected at 5.5 min, and defibrillation performed at 8 min. LAD coronary artery cross sectional area was measured by IVUS at the pre-arrest baseline, 90 s after drug injection during CPR, and 5 min after return of spontaneous circulation. Compared with baseline, the mid-LAD coronary artery cross sectional area increased significantly (P<.05) 90 s and 5 min after AVP administration (9.2+/-.5mm2 versus 10.7+/-.6mm2 versus 11.7+/-.6mm2, respectively) during normal sinus rhythm. Similarly during ventricular fibrillation and CPR plus AVP, the mid-LAD coronary artery cross sectional area increased at 90 s after AVP compared with baseline (9.5+/-.6mm2 versus 11.0+/-.7mm2; P<.05). Moreover, the cross sectional area increased further 5 min after return of spontaneous circulation (9.5+/-.6mm2 versus 14.0+/-.8mm2, P<.05). In conclusion, in this experimental model with normal coronary arteries, AVP resulted in significantly increased LAD coronary artery cross sectional area during normal sinus rhythm, during ventricular fibrillation with CPR, and after return of spontaneous circulation.