Background

The American Heart Association (AHA) released guidelines to improve survival rates from out-of-hospital cardiac arrest in 2005. We sought to identify what barriers delayed the implementation of these guidelines in EMS agencies.

Methods

We surveyed 178 EMS agencies as part of a larger quantitative survey regarding guideline implementation and conducted a single-question semi-structured interview using the Grounded Theory method. We asked “What barriersm if any, delayed implementation of the (2005 AHA) guidelines in your EMS agency?” Data were coded and member validation was employed to verify our findings.

Results

176/178 agencies completed the quantitative survey. Qualitative data collection ceased after reaching theoretical saturation with 34 interviews. Ten unique barriers were identified. We categorized these ten barriers into three themes. The theme Instruction Delays (reported by 41% of respondents) included three barriers: booking/training instructors (9%), receiving training materials (15%), and scheduling staff for training (18%). The second theme, Defibrillator Delays (38%), included two barriers; reprogramming defibrillators (24%) and receiving new defibrillators to replace non-upgradeable units (15%). The third theme was Decision-Making (38%) and included five barriers; coordinating with allied agencies (9%), government regulators such as state and provincial health authorities (9%), medical direction and base hospitals (9%), ROC participation (9%), and internal crises (3%).

Conclusion

Many barriers contributed to delays in the implementation of the 2005 AHA guidelines in EMS agencies. These identified barriers should be proactively addressed prior to the 2010 Guidelines to facilitate rapid translation of science into clinical practice.

Introduction

In 2005, the American Heart Association (AHA) released guidelines to improve survival rates from out-of-hospital cardiac arrest (OHCA).

Objective

To determine if, and when, emergency medical services (EMS) agencies participating in the Resuscitation Outcomes Consortium (ROC) implemented these guidelines.

Methods

We contacted 178 EMS agencies and completed structured telephone interviews with 176 agencies. The survey collected data on specific treatment protocols before and after implementation of the 2005 guidelines as well as the date of implementation crossover (the “crossover date”). The crossover date was then linked to a database describing the size, type, and structure of each agency. Descriptive statistics and regression were used to examine patterns in time to crossover.

Results

The 2005 guidelines were implemented by 174 agencies (99%). The number of days from guideline release to implementation was as follows: mean 416 (standard deviation 172), median 415 (range 49–750). There was no difference in time to implementation in fire-based agencies (mean 432), nonfire municipal agencies (mean 365), and private agencies (mean 389, p = 0.31). Agencies not providing transport took longer to implement than agencies that transported patients (463 vs. 384 days, p = 0.004). Agencies providing only basic life support (BLS) care took longer to implement than agencies who provided advanced life support (ALS) care (mean 462 vs. 397 days, p = 0.03). Larger agencies (>10 vehicles) were able to implement the guidelines more quickly than smaller agencies (mean 386 vs. 442 days, p = 0.03). On average, it took 8.9 fewer days to implement the guidelines for every 50% increase in EMS-treated runs/year to which an agency responded.

Conclusion

ROC EMS agencies required an average of 416 days to implement the 2005 AHA guidelines for OHCA. Small EMS agencies, BLS-only agencies, and nontransport agencies took longer than large agencies, agencies providing ALS care, and transport agencies, respectively, to implement the guidelines. Causes of delays to guideline implementation and effective methods for rapid EMS knowledge translation deserve investigation.

Background

Fatigue is common among medical professionals and has been linked to poor performance and medical error.

Objective

To characterize sleep quality and its association with severe fatigue in emergency medical services (EMS) providers.

Methods

We studied a convenience sample of EMS providers who completed three surveys: the Pittsburgh Sleep Quality Index (PSQI), the Chalder Fatigue Questionnaire (CFQ), and a demographic survey. We used established measures to examine survey psychometrics and performed t-tests, analysis of variance (ANOVA), and chi- square tests to identify differences in PSQI and CFQ scores.

Results

One hundred nineteen surveys were completed. The eight-hour shift was most commonly reported (35.4%). A majority of subjects were overweight (41.9%) or obese (42.7%), and 59.6% had been diagnosed with one or more health conditions (e.g., diabetes). Results from psychometric tests were positive. The mean (± standard deviation) PSQI score was 9.2 (± 3.7). A CFQ score >4, indicating severe mental and physical fatigue, was present in 44.5% of the subjects. The mean PSQI score was higher among those reporting severe fatigue (11.3 ± 3.2) than among those not reporting fatigue (7.5 ± 3.0, p < 0.0001).

Conclusions

The results from this study suggest that the sleep quality and fatigue status of EMS workers are at unhealthy levels. The health and safety of the EMS worker and patient population should be considered in light of these results.

Background

Hypothermia has been shown to improve survival and neurological outcomes for ventricular fibrillation (VF) cardiac arrest. The electrophysiological mechanisms of hypothermia are not well-understood, nor are the effects of beginning cooling during the resuscitation.

Methods and Results

We hypothesized that inducing hypothermia prior to the onset of VF would slow the deleterious changes seen in the ECG during VF and that inducing hypothermia at the start of resuscitation would increase the rates of ROSC and short-term survival in a porcine model of prolonged VF. We randomly assigned 42 domestic swine (27.2 ±2.3 kgs) to either pretreatment with hypothermia before induction of VF (PRE), normothermic resuscitation (NORM) or intra-resuscitation hypothermia (IRH). During anesthesia, animals were instrumented via femoral cutdown. Lead II ECG was recorded continuously. PRE animals were cooled before the induction of VF, with a rapid infusion of 4° normal saline (30 mL/kg). VF was induced electrically, left untreated for 8 minutes, then mechanical CPR began. During CPR the NORM animals got 30 mL/kg body-temperature saline and the IRH animals got 30 mL/kg 4° saline. In all groups first rescue shocks were delivered after 13 minutes of VF. We calculated the VF scaling exponent (ScE) for the entire 8 minute period (compared using GEE). ROSC and survival were compared with Fisher's exact test. Mean temperature in °C at the onset of VF was PRE=34.7° (±0.8), NORM=37.8 (±0.9), and IRH=37.9 (±0.9). The ScE values over time were significantly lower after 8 minutes in the PRE group (p=0.02). ROSC: PRE=10/14 (71%), NORM=6/14 (43%) and IRH=12/14 (86%); p for IRH vs. NORM=0.02. Survival: PRE=9/14 (64%), NORM=5/14 (36%), IRH 8/14 (57%).

Conclusion

Hypothermia slowed the decay of the ECG waveform during prolonged VF. IRH improved ROSC but not short-term survival compared to NORM. It is possible to rapidly induce mild hypothermia during CPR using an IV infusion of ice-cold saline.

Introduction

The optimum duration of cardiopulmonary resuscitation (CPR) prior to first rescue shock is unknown. Clinical trials have used 90s and 180s. Neither of these durations may be optimal. We sought to determine the optimum duration of CPR prior to first defibrillation attempt and whether this varied depending on the duration of ventricular fibrillation (VF). In this porcine model of basic life support, our outcomes were rates of return of spontaneous circulation (ROSC), survival, and coronary perfusion pressure (CPP).

Methods

We anesthetized and instrumented 45 swine and then induced VF. After 5 or 8 minutes of untreated VF, we randomized the swine to mechanical CPR for 90, 180, or 300s. A single rescue shock (150J biphasic) was then administered. If this shock failed, 2 minutes of mechanical CPR were completed prior to the next rescue shock. CPP was calculated for each 30 second epoch. ROSC was defined as a blood pressure >80mmHg sustained for 60s. Survival was defined as sustained ROSC for 20 minutes. Data were analyzed with descriptive statistics, Fisher’s exact test, and ANOVA.

Results

In the 5 minute VF cohort, the rate of ROSC did not differ between the three groups (90s: 25%; 180s: 38%; 300s: 38%, p>.05). Survival rates did not differ (90s: 25%; 180s: 25%; 300s: 25%, p>0.05). In the 8 minute VF cohort, no animals experienced ROSC or survival. CPP were calculated by 30 second epoch and did not differ between the three groups (p>0.05). CPPs decline after 180s of CPR.

Conclusions

ROSC and survival were equivalent regardless of VF duration and CPR duration. When CPR begins late, CPPs are low, stressing the importance of early CPR. We do not recommend 300s of CPR unless a defibrillator is unavailable.

P0 glycoprotein is the major structural protein of peripheral nerve myelin where it is thought to modulate inter-membrane adhesion at both the extracellular apposition, which is labile upon changes in pH and ionic strength, and the cytoplasmic apposition, which is resistant to such changes. Most studies on P0 have focused on structure-function correlates in higher vertebrates. Here, we focused on its role in the structure and interactions of frog (Xenopus laevis) myelin, where it exists primarily in a dimeric form. As part of our study, we deduced the full sequence of Xenopus laevis P0 (xP0) from its cDNA. The xP0 sequence was found to be similar to P0 sequences of higher vertebrates, suggesting that a common mechanism of PNS myelin compaction via P0 interaction might have emerged through evolution. As previously reported for mouse PNS myelin, a similar change of extracellular apposition in frog PNS myelin as a function of pH and ionic strength was observed, which can be explained by a conformational change of P0 due to protonation-deprotonation of His52 at P0’s putative adhesive interface. On the other hand, the cytoplasmic apposition in frog PNS myelin, like that in the mouse, remained unchanged at different pH and ionic strength. The contribution of hydrophobic interactions to stabilizing the cytoplasmic apposition was tested by incubating sciatic nerves with detergents. Dramatic expansion at the cytoplasmic apposition was observed for both frog and mouse, indicating a common hydrophobic nature at this apposition. Urea also expanded the cytoplasmic apposition of frog myelin likely owing to denaturation of P0. Removal of the fatty acids that attached to the single Cys residue in the cytoplasmic domain of P0 did not change PNS myelin structure of either frog or mouse, suggesting that the P0-attached fatty acyl chain does not play a significant role in PNS myelin compaction and stability. These results help clarify the present understanding of P0’s adhesion role and the role of its acylation in compact PNS myelin.