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Introduction: During resuscitation from cardiac arrest with Pulseless Electrical Activity (PEA), studies show that adrenaline facilitates return of spontaneous circulation (ROSC) and possibly leads to an isolated increase in the heart rate (HR). In this study, we investigated the immediate effects of adrenaline on ECG characteristics; HR and QRS duration (duration of ventricle depolarization). Method: We studied 19 ECG segments of 300 s duration from emergency defibrillators in 10 adult patients during resuscitation from in-hospital cardiac arrest. Information on the exact timing of adrenaline administration (between 0.5 and 1 mg i.v.) was obtained from the defibrillators or the emergency personnel involved. HR (1/min) and QRS duration (ms) were annotated and registered using an ad-hoc Matlab (Mathworks, Natic, MA) graphical Data Annotator, and interpolated linearly between individual observations. Trends were identified with LOWESS. Results: The plots show the individual observations (red points) along with the trends (blue lines) of HR and QRS Duration during resuscitation, relative to the time of adrenaline administration. We observed a gradual increase in heart rate (peaking at 150 s after adrenaline administration) and a more pronounced narrowing of the QRS (levelling off also at about 150 s). Discussion: In this pilot study, administration of adrenaline was associated with narrowing of the QRS complex, while the relation to heart rate was less apparent. A limitation is that no adjustment for the individual patient’s trajectory was made. However, the results are fairly consistent with earlier studies on out-of-hospital resuscitation, when adrenaline was typically given much later.

Introduction: PEA is commonly observed in in-hospital cardiac arrest. ROSC is currently the only indication of treatment response. Studies suggest that QRS duration (QRSd) and heart rate (HR) develop differently in patients who obtain ROSC or not. The aim of this study was to assess prospectively how QRSd and HR affect the immediate outcome of patients with PEA. Method: We investigated 327 episodes of IHCA in 298 patients, collected at two US and one Norwegian hospital. We assessed the ECG in 559 segments of PEA, measuring QRSd and HR in pauses of compressions, and noted the clinical state that followed PEA. We investigated the development of HR, QRSd, and transitions to ROSC or noROSC in a joint linear mixed/ time-to-event model, using software R version 4.0.3 with the package ‘JMbayes2’. Results: A HR increase by 50bpm increased the intensity (“hazard”) of gaining ROSC by 42% (p<0.01), and a 50ms decrease in QRSd increased the intensity of gaining ROSC by 29% (p<0.01). A decreasing HR had no significant impact; however, if QRSd increased by 50ms this increased the probability of transitioning to other lethal states (ventricular tachycardia or fibrillation, asystole, or death) by 24% (p<0.01). Still, several patients experienced increasing QRSd before obtaining ROSC. The figure shows an example of how QRSd (lower left) and HR (upper left) developed in one PEA segment overlaid the linear model (blue line). The estimated probability of obtaining ROSC (green line with 95% CI) or transitioning to other arrest states (red line) over the next 4 minutes are displayed to the right. This patient obtained ROSC at approx. 7min. Conclusion: HR and QRSd conveys information of the immediate outcome (ROSC/noROSC) in PEA. This may guide the team in their efforts, and possibly allow for individual tailoring of treatment, e.g., by delaying a (potentially harmful) epinephrine administration. Due to low specificity, the model cannot support termination of resuscitation.