Mathias Zuercher

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.

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.

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−2 · min−1 with no leaning to 1.6 ± 0.1 L · M−2 · min−1 with 10% leaning, and 1.4 ± 0.2 L · M−2 · min−1 with 20% leaning (p < .05). The myocardial blood flow decreased from 39 ± 7 mL · min−1 · 100 g−1 with no lean to 30 ± 6 mL · min−1 · 100 g−1 with 10% leaning and 26 ± 6 mL · min−1 · 100 g−1 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.

The use of Glasgow Coma Scale in injury assessment: a critical review.

Primary objective: Patients with brain injuries are assessed using the Glasgow Coma Scale (GCS). This review evaluates the use of GCS scoring in medical literature and identifies the reasons for inaccuracy. Literature selection and critical appraisal: Pubmed and ISI Web of Knowledge SM were searched using specific keywords. The authors critically appraised the current state of GCS scoring, GCS definitions, the time and frequency of assessment, confounders, GCS reporting and GCS assessment schemes. Main outcome and results: More than 90% of the publications using GCS scoring cite the 14-item GCS rather than the 15-item GCS. The timing of the initial GCS assessment is inconstant. GCS components are seldom utilized, contributing to the loss of information. Confounders are often not reported and, if they are, not in a standardized manner. The order of the GCS components is not consistent. Conclusions: The current inconsistent and inappropriate use of GCS diminishes its reliability in both a clinical and a scientific context. A consensus statement is needed to correct this situation. Citing the correct references, early and repeated GCS assessments at defined intervals, standardized reporting of confounders and GCS component plus sum scores, and the utilization of a uniform assessment scheme are recommended.

In-Hospital Pediatric Cardiac Arrest

The understanding of the incidence, epidemiology, etiology, and pathophysiology of pediatric cardiac arrest has evolved greatly in the past two decades. This includes recognition that cardiopulmonary resuscitation delays in cardiac arrest are especially injurious, ventricular arrhythmias are not as uncommon in children as previously believed, and four distinct phases of cardiac arrest can be delineated. Performance of, and technologic advances in, the treatment of cardiac arrest make this an exciting time in the field.

Cardiac arrest during anesthesia.

Purpose of reviewCardiac arrest of patients during anesthesia has been the driving force behind the development of this specialty. Safer procedures, new anesthetics, and technical improvements such as monitoring devices and ventilators have successfully reduced intraoperative mortality. Nevertheless, modern technology itself creates specific risks; and causes, diagnosis, and management of anesthesia-related cardiac arrest differ considerably from situations encountered elsewhere. Recent findingsCardiac arrest attributable to anesthesia occurs from 0.5 to 1 case per 10 000 interventions. Pediatric cases show a higher incidence (1.4–4.6 per 10 000). However, with the increasing age of patients, preexisting disease or trauma, and new surgical interventions cardiac arrests remain a serious concern. Environmental considerations are gradually becoming more important than mere technological improvements, and educational inputs try to create safer surroundings by recognizing human factors such as efficient communication, awareness, error culture, crew resources utilization, and preparedness for more effective crisis management. SummaryThe anesthetic environment has become much safer than it was 50 years ago. For a successful management of cardiac arrest during operative procedures, not only individual knowledge and skills but also institutional safety culture have to be implemented into education, training, and everyday practice of this specialty.

Endotracheal tube intracuff pressure during helicopter transport.

STUDY OBJECTIVE We evaluate changes in endotracheal tube intracuff pressures among intubated patients during aeromedical transport. We determine whether intracuff pressures exceed 30 cm H(2)O during aeromedical transport. METHODS During a 12-month period, a helicopter-based rescue team prospectively recorded intracuff pressures of mechanically ventilated patients before takeoff and as soon as the maximum flight level was reached. With a commercially available pressure manometer, intracuff pressure was adjusted to < or =25 cm H(2)O before loading of the patient. The endpoint of our investigation was the increase of endotracheal tube cuff pressure during helicopter transport. RESULTS Among 114 intubated patients, mean altitude increase was 2,260 feet (95% confidence interval [CI] 2,040 to 2,481 feet; median 2,085 feet; interquartile range [IQR] 1,477.5 to 2,900 feet). Mean flight time was 14.8 minutes (95% CI 13.1 to 16.4 minutes; median 13.5 minutes; IQR 10 to 16.1 minutes). Intracuff pressure increased from 28.7 cm H(2)O (95% CI 27.0 to 30.4 cm H(2)O [median 25 cm H(2)O; IQR 25 to 30 cm H(2)O]) to 62.6 cm H(2)O (95% CI 58.8 to 66.5 cm H(2)O; median 58; IQR 48 to 72 cm H(2)O). At cruising altitude, 98% of patients had intracuff pressures > or =30 cm H(2)O, 72% had intracuff pressures > or =50 cm H(2)O, and 20% even had intracuff pressures > or =80 cm H(2)O. CONCLUSION Endotracheal cuff pressure during transport frequently exceeded 30 cm H(2)O during aeromedical transport. Hospital and out-of-hospital practitioners should measure and adjust endotracheal cuff pressures before and during flight.

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.

Prevalence and hemodynamic effects of leaning during CPR

BACKGROUND Cardiopulmonary resuscitation (CPR) guidelines recommend complete release between chest compressions (CC). OBJECTIVE Evaluate the hemodynamic effects of leaning (incomplete chest wall release) during CPR and the prevalence of leaning during CPR. RESULTS In piglet ventricular fibrillation cardiac arrests, 10% and 20% (1.8 kg and 3.6 kg, respectively), leaning during CPR increased right atrial pressures, decreased coronary perfusion pressures, and decreased cardiac index and left ventricular myocardial blood flow by nearly 50%. In contrast, residual leaning of a 260 g accelerometer/force feedback device did not adversely affect cardiac index or myocardial blood flow. Among 108 adult in-hospital CPR events, leaning ≥ 2.5 kg was demonstrable in 91% of the events and 12% of the evaluated CC. For 12 children with in-hospital CPR, 28% of CC had residual leaning ≥ 2.5 kg and 89% had residual leaning ≥ 0.5 kg. CONCLUSIONS Leaning during CPR increases intrathoracic pressure, decreases coronary perfusion pressure, and decreases cardiac output and myocardial blood flow. Leaning is common during 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.