Critical Care

Topic 1 - Summary
1. Citation: Warren, Sam A., Ella Huszti, Steven M. Bradley, Paul S. Chan, Chris L. Bryson, Annette L. Fitzpatrick, and Graham Nichol. "Adrenaline (epinephrine) Dosing Period and Survival after In-hospital Cardiac Arrest: A Retrospective Review of Prospectively Collected Data." Resuscitation 85 (2013): 350-58
2. Summary/Bottom Lines:
  • The paper suggests less frequent epinephrine dosing (as defined by time from first dose to resuscitation endpoint divided by total doses) during in-hospital cardiac arrest (IHCA) results in increase survival to discharge. The benefits of epinephrine and its dosing period remain unclear. This article is yet another paper questioning epinephrine during cardiac arrest, asking physicians to keep in mind the benefits versus risks of its use
3. Methods:
  • This was a retrospective review of prospectively collected data of 20,909 IHCA, using only patients located in a hospital ward or ICU bed. The adjusted odds ratio in their logistic regression models found that there is improved survival to discharge with longer epinephrine dosing period when compared to their reference category, epinephrine average doing period of 4 to <5min/dose
4. Limits:
  • Does not include patients in the ED or pre-hospital.

  • Includes data from differing CPR guideline time periods, where part of the patient population received CPR when there was less emphasis on quality.

  • No defined epinephrine dose.

  • Data was all self-reported

5. Additional Info:
  • Patients who received less epinephrine could have been doing better clinically, requiring less doses
6. Author: Dr. Michael Tran

 

Topic 2 - Summary
1. Citation: Eisuke K, Keigo D, Masaya K, et al. Should We Emergently Revascularize Occluded Coronaries for Cardiac Arrest? Rapid-Response Extracorporeal Membrane Oxygenation and Intra-Arrest Percutaneous Coronary Intervention. Circulation. 2012;126:1605-1613
2. Summary/Bottom Lines:

CPR, ECMO, and PCI have all been used in the treatment of patients suffering cardiac arrest. This is the first study exploring the associations among extracorporeal CPR, intra-arrest PCI, and patient outcomes. In this study, rapid-response ECMO was performed in 86 patients with acute coronary syndrome who were unresponsive to conventional CPR, 61 of which underwent intra-arrest PCI. This study showed a definitively higher rate of return of spontaneous heartbeat (100%) and improved outcomes in cardiac arrest patients with acute coronary syndrome treated with ECMO and intra-arrest PCI. PCI is feasible in this setting and can increase return of spontaneous heartbeat and improve outcomes. Randomized studies of intra-arrest PCI based on these findings are needed

3. Methods:

This was a retrospective chart review from two hospitals in Hiroshima City, Japan between 2004-2011. Data pertaining to ROSB, weaning from ECMO, 30-day survival, and favorable neurological outcome were collected from medical records. When CPR was performed, a quick evaluation was conducted to verify eligibility for ECPR, which was: age 18 to 74 years, ventricular fibrillation on ECG during CPR, estimated interval of <15 minutes from the time of collapse to CPR, arrest presumed to be of cardiac origin or due to pulmonary embolism, and failure to achieve ROSC within 20 minutes of conventional CPR. Both out- and in-patients were included in this study. If ROSC was not achieved after the second epinephrine dose, the patient was taken to the catheter laboratory where ECMO was initiated and patients underwent coronary angiography to determine whether or not they had vessel lesions potentially treatable by PCI. The endpoints of those patients who underwent PCI while on ECMO were then compared to those who had ECMO only and showed benefit in every category favoring ECMO with PCI

4. Limits:

The major limitations of this study were that it was a retrospective review and not a randomized controlled trial and it’s applicability. The percentage of hospitals with access to both ECMO and PCI is low. However, anything that shows improved outcomes in both survivability and favorable neurologic outcomes in a disease that already has a very poor prognosis should be considered for further investigation

5. Additional Info:

 

6. Author: Dr. Mark Crosby

 

Topic 1 - Summary
1. Citation:

Effect of Heart Rate Control With Esmolol on Hemodynamic and Clinical Outcomes in Patients With Septic Shock; A Randomized Clinical Trial; JAMA. 2013;310(16):1683-1691

2. Summary/Bottom Lines:
  • In patients with septic shock, can beta-blocker therapy be of benefit?

  • There were many improvements in the hemodynamic status of patients on beta-blocker therapy:

  • a greater decrease in heart rate

  • less requirement of Norepinephrine

  • better Stroke Volume, SVR, and LV stroke work

  • greater reduction in oxygen consumption

  • less need for Levosimendan (Ca-sensitizer that enhances myocardial contractility without increasing oxygen demand)

  • less fluid requirement

  • a higher (better) arterial pH

  • a lower lactate

  • better renal function

  • best of all, a lower 28-day mortality

3. Methods:
  • open label, randomized, phase 2 study

  • ICU patients from Nov 2010 to July 2012

  • patients became eligible if: they still required Norepinephrine & HR still > 95 after 24hr & hemodynamic optimization (PA occlusion pressure  > 12, CVP > 8, mixed venous saturation >65%, MAP >65)

  • randomized to get either “standard Tx” or standard Tx + Esmolol

  • start at 25mg/hr; incr at 20min intervals by increments of 50mg/hr (or by discretion of provider) to reach predefined threshold rate within 12hr

  • continued gtt until either ICU discharge, or death

  • max dose 2g/hr

  • all patients received:

         I) RBCs if Hgb dropped below 7 g/dL OR if pt “exhibited clinical signs of inadequate O2 supply”

         II) Norepi to keep MAP > 65

         III) hydrocortisone 300mg/day continuous infusion

         IV) Levosimendan if needed

    2.  Results

       A.  77 patients in each arm

       B. median Esmolol dose 100 mg/hr

         I) this was the required amount for the target HR range of 80-94bpm

       C. results above, see paper for specifics

4. Limits:
  • arbitrary HR range was chosen

  • nonblinded

  • why did the “standard Tx group” have such a high mortality rate?

5. Additional Info:
  • Dr Nelson raised the question of how do we know that its not the Norepinephrine that is causing the harm?

  • He also asked could we possibly do a study to see how patients do if no Norepinephrine was given

  • the question was asked of whether this would be ethical?  The counterargument was there’s no evidence supporting Norepinephrine/vasopressors  does not decrease mortality

6. Author: Dr. Jessica Herrera

 

Topic 2 - Summary
1. Citation:

Study:  Shehabi Y, Bellomo R, Reade M, et al. Early Intensive Care Sedation Predicts Long-Term Mortality in Ventilated Critically Ill Patients . J Am Resp Crit Care 2012; 186: 724-731.

2. Summary/Bottom Lines:

Bottom Line: This study focused on how early deep sedation, measured based on the Richmond Agitation Sedation Score (RASS), would affect long term outcome. Specifically, the study found that early deep sedation increased length of time to extubation, hospital death, and 180 day mortality. Early deep sedation did not have statistically significant effects on measurable delirium after 48 hours.  While this study does provide interesting conclusions about early sedation and the deleterious effects therein, it may not be practical given that many patients are given early sedation after intubation for immediate benefit.

3. Methods:

Methods and Results: Two hundred fifty one patients were included from 25 ICUs in New Zealand. Inclusion criteria included patients over 18 who were intubated within 24 hours and expected to be intubated for at least another 24 hours. Early sedation was defined as within four hours of starting ventilation. Deep sedation was defined as RASS of -3 to -5. The study found that early deep sedation led to statistically significant increases in extubation time, hospital death and 180 day mortality. However, early deep sedation did not lead to statistically significant increased delirium after 48 hours.

4. Limits:

Limitations and applicability: Delirium assessment was only done during light sedation to avoid over diagnosis. Patients who were not receiving intravenous sedatives were not included in the assessment. Adjustments for illness confounders, such as shock, sepsis, etc, could not be performed. This last point is problematic for EM practice. Many of the patients intubated in the ER are very unstable with many of these confounders changing their clinical condition many times per hour. These confounders would necessarily affect mortality and extubation time independently of early deep sedation. 

5. Additional Info:

 

6. Author: Dr. Joshua Larson