Resuscitative Hysterotomy

Written by: Aldo Gonzalez, MD (NUEM ‘23) Edited by: Justine Ko, MD (NUEM ‘21)
Expert Commentary by: Paul Trinquero, MD (NUEM '19) & Pietro Bortoletto, MD

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Introduction

Resuscitative hysterotomy (RH) is the new term for what was previously called perimortem cesarean delivery (PMCD). The new nomenclature is being adopted to highlight the importance of the procedure to a successful resuscitation during maternal cardiopulmonary arrest (MCPA). It is defined as the procedure of delivering a fetus from a gravid mother through an incision in the abdomen during or after MCPA. The goal of the procedure is to improve the survival of the mother and the neonate.

Physiology

There are physiologic changes that occur during pregnancy which reduce the probability of return of spontaneous circulation (ROSC) during cardiac arrest. Physiologic anemia of pregnancy reduces the oxygen carrying capacity of blood and results in decreased delivery of oxygen during resuscitation. The large gravid uterus elevates the diaphragm and reduces the lung’s functional reserve capacity (FRC),  which when combined with increased oxygen demand from the fetus results in decreased oxygen reserves and resultant risk for rapid oxygen desaturations. The size of a gravid uterus at 20 weeks results in aortocaval compression which reduces the amount of venous return from the inferior vena cava and reduces cardiac output during resuscitation. The theory behind resuscitative hysterotomy is to increase the probability of ROSC by reducing the impact of aortocaval compression.

Supporting Evidence 

A 2012 systematic review primarily investigated the neonatal and maternal survival rates after perimortem cesarean delivery and secondarily attempted to evaluate maternal and fetal neurological outcome and the ability to perform the procedure within the recommended time frame.

Inclusion Criteria

• original articles, case series, case reports and letters to the editor, and reports from databases

• had minimum of least five clinical details of the case (e.g. patient age, gravidity, parity, obstetric history, medical history, presenting rhythm, or location of arrest) 

  AND

• the care administered (chest compression, ventilation, monitoring, drug administration)

  AND

• maternal return of spontaneous circulation or survival to hospital discharge or fetal neonatal outcome

Exclusion Criteria

• Post-delivery arrests

• Studies without enough data to understand the details of the arrests

• Studies with unclear maternal and fetal outcomes

Population

• Pregnant woman that

  • (1) had a cardiac arrest or a non-perfusing rhythm 

  • (2) received chest compression and/or advanced life support medications and/or defibrillation

• Average maternal age: 30.5±6.5 years (median 32, range 17–44, IQR, 26.5–35.5, n = 80)

• Gravidity: 2.5±1.5 (median 2, range 1–7, IQR 1–4, n = 59)

• Parity: 1.1±1.3 (median 1, range 0–6, IQR 0–2, n = 57)

• Singleton Pregnancies: 90.4% (n = 85)

• Average gestational age at arrest: 33±7 weeks (median 35, range 10–42, IQR 31–39, n = 85)

Results

• for cases undergoing PMCD, earlier time from arrest to delivery was associated with increased survival (p < 0.001, 95%CI 6.9–18.2)

  • surviving mothers: 27/57; 10.0±7.2 min (median 9, range 1–37)

  • non-surviving mother: 30/57; 22.6±13.3 min (median 20, range 4–60)]

• for neonates delivered by PMCD/RH earlier time from arrest to delivery was associated with increased survival (p = 0.016)

  • surviving neonates: 14±11 min (median = 10, range = 1–47)

  • non-survivor neonates: 22±13 min (median = 20, range = 4–60) 

• Only 4 cases met the timeframe of less than minutes

Take-Aways: Performing a PMCD/RH in the 4-5 minutes time frame is difficult. However, PMCD/RH beyond the proposed time is still beneficial and earlier time to delivery from arrest is associated with better outcomes

Guideline Recommendations

Perform basic life support (BLS) in the same way as non-pregnant patients

• Place patient in supine position

  • Left lateral decubitus (left lateral tilt) positioning is no longer recommended during compressions because of reduced efficacy of chest compressions

• No modification of Chest compressions 

  • Rate: 100-120 per minute

  • Depth: at least 2 inches (5 cm)

  • Allow for full chest recoil between compressions

  • Avoid interruptions as much as possible

• No modification of Ventilation

  • Use bag-ventilation 

  • Compression to breath ratio: 30:2 before advanced airway

Perform advanced cardiac life support (ACLS) as in non-pregnant women

• No modification of Ventilation

  • Once breath every 6 seconds (10 BPM) with advanced airway

• No modification of medications

  • Use 1 mg Epinephrine of epinephrine every 3-5 minutes

• No modification to defibrillation

  • Use adhesive pads on patient

  • Place in anterolateral position 

    • Lateral pad should be placed under breast tissue

  • Defibrillate for Ventricular fibrillation or Ventricular tachycardia

  • Use usual Voltages

    • Biphasic: 120-200 Joules

  • Resume compressions after shock is delivered

Special considerations during resuscitation

• Obtain access above the diaphragm to minimize the effect of aortocaval compression on the administration of drugs

• Perform left uterine deviation during resuscitation to reduce aortocaval compression

• If a gravid patient suffers a cardiac arrest mobilize resources to prepare for the need for resuscitative hysterotomy and the resuscitation of the fetus early

• Palpate the size of the gravid uterus

  • If above the height of the umbilicus then patient is most likely greater than 20 weeks gravid and a candidate for RH

• Strongly consider performing RH (PMCD) if the patient does not achieve ROSC by the 4-minute mark and qualified staff to perform the procedure are present

• Aim to have the procedure done by the 5-minute mark

• Consider performing RH (PMCD) sooner if maternal prognosis is poor or prolonged period of pulselessness

• RH should be performed at the site of the resuscitation

• Do not delay procedure to prepare abdomen

  • May pour iodine solution over abdomen prior to incision

• Do not delay procedure for surgical equipment if scalpel is available

• Continue performing LUD while performing RH

Figure 1: One-handed left uterine deviation technique

Figure 2: Two-handed left uterine deviation technique

Steps for Resuscitative Hysterectomy

Pre-procedure

• Gather supplies to perform RH

  • Personal Protective Equipment

    • Gloves

    • Face mask

    • Apron/gown

  • Resuscitative Hysterotomy Equipment

    • Scalpel(the minimum equipment to perform procedure)

    • Blunted Scissors

    • Clamps/Hemostats

    • Gauze

    • Suction

    • Large absorbable sutures

    • Needle Holder

    • Antiseptic Solution

  • Neonatal resuscitation equipment

    • Dry Linens

    • Neonatal Bag Valve Mask

    • Neonatal Airway supplies

    • Suction

    • Umbilical venous access equipment

    • Neonatal resuscitation drugs

    • Baby Warmer

    • Plastic Bag

• Form teams to perform Resuscitative Hysterotomy

  • Resuscitative Team

  • Resuscitative Hysterotomy Team

  • Neonatal Resuscitation Team

Procedure

• Maintain patient in supine position and continue compressions

• Continue Left Uterine Deviation until the start of incision 

• Quickly prepare the skin with antiseptic solution (do not delay for skin prep)

• Perform midline vertical Incision with scalpel on the abdomen from pubic symphysis to umbilicus and cut through skin and subcutaneous tissue until fascia is reached

• Use fingers to bluntly dissect the rectus muscle fascia access the peritoneum (can use scalpel or blunt scissors)

• Locate the uterus and differentiate it from the bladder (bladder yellow and enveloped in fatty tissue)

• Make a vertical incision from the lower uterus to the fundus with scalpel (can use blunt scissors)

• If the placenta is encountered while entering the uterus, cut through it

• Use a cupped hand to locate the fetal part closest to pelvis

• Elevate the located fetal part and pass through uterine incision while applying transabdominal pressure with other hand

• Use traction and transabdominal pressure to deliver the rest of the baby

• Clamp the cord at two spots and cut in between both clamps

• Hand the baby to the neonatal team

• Deliver placenta with gentle traction

Post-procedure

• Continue performing compressions

• Consider stopping if ROSC not achieved after several rounds and  depending on the cause of PMCA

• Give medications to promote uterine contraction

• Analgesia and sedation may be required if patient achieves ROSC

• Bleeding will be worse if ROSC achieved and may require pharmacologic and nonpharmacologic interventions

• Closure will depend on whether the patient achieves ROSC and may necessitate careful closure to prevent further bleeding. Best performed by an obstetrician. If an obstetrician is unavailable, pack the uterus with gauze and clamps actively bleeding vessels to reduce bleeding. 

• Administer prophylactic antibiotics

References

1. Einav, S., et al. (2012). "Maternal cardiac arrest and perimortem caesarean delivery: evidence or expert-based?" Resuscitation 83(10): 1191-1200.

2. Jeejeebhoy, F. M., et al. (2015). "Cardiac Arrest in Pregnancy: A Scientific Statement From the American Heart Association." Circulation 132(18): 1747-1773.

3. Kikuchi, J. and S. Deering (2018). "Cardiac arrest in pregnancy." Semin Perinatol 42(1): 33-38.

4. Parry, R., et al. (2016). "Perimortem caesarean section." Emerg Med J 33(3): 224-229.

5. Rose, C. H., et al. (2015). "Challenging the 4- to 5-minute rule: from perimortem cesarean to resuscitative hysterotomy." Am J Obstet Gynecol 213(5): 653-656, 653 e651.

6. Soskin, P. N. and J. Yu (2019). "Resuscitation of the Pregnant Patient." Emerg Med Clin North Am 37(2): 351-363.

7. Walls, R. M., et al. (2018). Rosen's emergency medicine: concepts and clinical practice. Philadelphia, PA, Elsevier.

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Expert Commentary

This is an excellent review of an extremely rare, but potentially life-saving procedure. It may seem daunting to perform (and it should), but the evidence would say that a resuscitative hysterotomy (RH), especially if performed promptly, drastically improves survival during the catastrophic scenario of maternal cardiac arrest. This is even more important because these patients are young (and often relatively healthy) and could potentially have decades of meaningful quality of life if they can survive the arrest. That being said, this procedure is so rare that most of us not only have never performed it, but often have never even seen it. Not only that, but unlike other rare lifesaving procedures (such as cricothyroidotomy or resuscitative thoracotomy), RH is extremely difficult to practice in cadaver labs due to the unavailability of pregnant cadavers. So, we are left with the next best thing: familiarizing ourselves with the anatomy, physiology, and simplified technique of the procedure and mentally rehearsing it so that when the time comes, we can be ready.

For these rare procedures, in addition to the excellent and thorough review above, it is also helpful to simplify and rehearse the fundamental steps. I’m not an obstetrician and certainly not an expert on this procedure, but I’ve mentally prepared myself for what I would do in the event that I am faced with this grave situation and categorized it into the following simplified five step plan. Also, prior to writing this commentary I got a curbside consult from a friend from med school and actual obstetrician and gynecologic surgeon, Dr. Pietro Bortoletto. 

First off, the indications-- basically, a pregnant woman estimated to be >20 weeks EGA who has suffered a cardiac arrest. Don’t worry about the 4 minutes, make the decision to perform a RH right away and start prepping. Delegate someone to call the appropriate resuscitation teams if available. Then start the procedure. 

Step 1: Setup. You probably don’t have a c section kit in your trauma bay, so instead open the thoracotomy tray and you’ll have most of what you need. Go ahead and set aside the finochietto rib spreaders so that you don’t have a panic attack trying to remember how to put those together with other people watching. But everything else you’ll need will be in that tray (basically a scalpel, blunt scissors, and hemostats). 

Step 2: Cut into the Abdomen. Splash prep the abdomen with betadine. Then make your long vertical incision from the uterine fundus to the pubic symphysis. Cut through the skin and subcutaneous tissue then bluntly separate the rectus and enter the peritoneum with scalpel or blunt scissors. Extend the peritoneal incision with blunt scissors. 

Step 3: (carefully) Cut into the Uterus. First, locate the uterus. Then, take a deep breath and remember that there is a fetus inside the uterus. With that terrifying thought in mind, cut vertically into the uterus, insert your fingers, and extend the incision upwards with blunt scissors and a steady hand. If you encounter an anterior placenta, cut right through it.

Step 4: Delivery. Deliver the fetus either by cupping the head and elevating it through the incision or by grabbing a leg, wiggling out the shoulders, and then flexing the head. Hand over the neonate to whoever is taking the lead on the neonatal resuscitation (will need to be warmed, stimulated, and potentially aggressively resuscitated). Clamp and cut the cord, leaving a long enough umbilical stump for an easy umbilical line if needed. Then using gentle traction, attempt delivery of the placenta. If it isn’t coming easily, leave it alone so as not to stir up more bleeding. 

Step 5: Extra credit. If you’ve made it this far as an emergency physician and there is still no obstetrician in sight, you can continue resuscitation, focusing on stopping the uterine bleeding. While you don’t need to close the fascia or skin, it can be helpful to close the uterine incision to prevent additional blood loss. You can do this with a whip stitch using 0-0 vicryl (or if that seems like showing off, you can just pack it with sterile gauze. If you’ve got it handy, give 10 IU oxytocin to stimulate uterine contraction and further slow bleeding. Feel free to order some antibiotics as well. Otherwise, continue maternal resuscitation following typical ACLS.

The big picture here is that this is a heroic, potentially life-saving procedure that most of us will never do. But we can all take a few minutes to read an excellent review like the blog post above, watch a video, and mentally walk ourselves through the simplified steps. That preparation will afford us some much-needed confidence if we are ever faced with this terrifying scenario.

Paul Trinquero, MD

Medical Director

Department of Emergency Medicine

US Air Force Hospital - Langley

Pietro Bortoletto, MD

Clinical Fellow

Reproductive Endocrinology & Infertility

Weill Cornell Medical College

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How To Cite This Post:

[Peer-Reviewed, Web Publication] Gonzalez, A. Ko, J. (2021, Dec 13). Resuscitative Hysterotomy. [NUEM Blog. Expert Commentary by Trinquero, P and Bortoletto, P]. Retrieved from http://www.nuemblog.com/blog/resuscitative-hysterotomy.

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Bicarb in Cardiac Arrest

Written by: Kishan Ughreja, MD (NUEM ‘23) Edited by: Sean Watts, MD (NUEM ‘22)
Expert Commentary by: Dana Loke, MD (NUEM ‘21)

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Utility of Sodium Bicarbonate in Cardiac Arrest

Use of sodium bicarbonate as empiric therapy in cardiac arrest has been an area of controversy.  During cardiac arrest hypoxia and hypoperfusion results in severe metabolic acidosis and subsequent impaired myocardial contractility, decreased efficacy of vasopressors, and increased risk of dysrhythmias. Previous ACLS guidelines recommended use of sodium bicarbonate to mitigate these effects; however,  harms are also associated with its routine use  including compensatory respiratory acidosis, hyperosmolarity, increased vascular resistance, and reduction in ionized calcium. 1 Current guidelines no longer recommend routine use of sodium bicarbonate, except in cases of arrest secondary to hyperkalemia, TCA overdose or preexisting metabolic acidosis.2 Regardless of these recommendations, sodium bicarbonate continues to be utilized during routine management of cardiac arrest, and studies are limited in investigating its appropriate use.

The study below investigates the effect of sodium bicarbonate in patients suffering out-of-hospital cardiac arrest with severe metabolic acidosis during prolonged CPR.

Article

Clinical Question

In patients with prolonged, atraumatic out-of-hospital cardiac arrest (OHCA) and severe metabolic acidosis, does sodium bicarbonate (SB) administration with transient hyperventilation improve acidosis without increased CO2 burden, enhance rates of return of spontaneous circulation (ROSC), survival to admission, and favorable neurologic outcomes?

Study Design

Double-blind, prospective, randomized, placebo-controlled, single-center pilot clinical trial 

Population

Inclusion criteria: Atraumatic arrest in patients ≥18yo without ROSC after 10 minutes of CPR in ED and with pH <7.1 or bicarbonate <10 mEq/L on ABG

Exclusion criteria: DNR, ECPR, ROSC w/i 10 minutes of ACLS, absence of severe metabolic acidosis on ABG after 10 minutes of CPR

Data collection over 1 year at Asan Medical Center, a tertiary referral center in Seoul, Korea

Figure 1: Patient Selection

Intervention

Sodium bicarbonate administration of 50 mEq/L over 2 minutes with concurrent increase in ventilation rate from 10 to 20 breaths per minute for 2 minutes

Control

Normal saline administration of 50 mL over 2 minutes (with same transient hyperventilation)

Outcomes

Primary

• Change in acidosis (per methods section)

Secondary

• Sustained ROSC — defined as restoration of a palpable pulse ≥20 min (per methods section, but listed as primary outcome in abstract)

• Survival to hospital admission

• Good neurological survival at 1 and 6 months (defined as cerebral performance category 1 or 2)

Results

• 157 patients presented with cardiac arrest, 50 enrolled per inclusion criteria

• No significant differences between study and control groups regarding demographics, PMH, witnessed arrest, bystander CPR, pre-hospital and initial cardiac rhythm

• 10% (n=5) of enrolled patients with sustained ROSC and admitted

• No patients survived at 6 months follow up

Pre-Intervention

• ABG results at 10 minutes were not significantly different between groups

Post-intervention

• ABG results at 20 minutes demonstrate that pH and HCO3- were higher in the study group than in the control group

  • pH 6.99 vs 6.90, p=0.038

  • HCO3- 21.0 vs 8.00, p=0.007

• Within the study group, the increase in pH was not statistically significant after sodium bicarbonate administration; the increase in HCO3- was statistically significant (using Wilcoxon signed rank test)

• No statistically significant findings in the control group after normal saline administration

• No significant differences in any secondary outcomes (sustained ROSC, survival to admission, good neurologic outcome)

Strengths

• Randomized, double-blinded, placebo-controlled study design

• This study adds additional information to a clinical question that has limited previous research

• This study added a practical clinical intervention (hyperventilation) to counteract excessive CO2 accumulation secondary to sodium bicarbonate administration, a known deleterious effect of this compound.

• Strong control over sodium bicarbonate administration (no pre-hospital administration allowed in South Korea), so authors could control when it was given and analyze ABG results at desired intervals)

Weaknesses 

• Small, single-center study with only 50 enrolled patients

• Primary endpoint unclear from abstract vs methods, whether it was change acidosis or sustained ROSC; however, neither is truly patient-centered clinical outcome (good neurological outcome would be the ideal primary outcome)

• Dosing was universal — 50 mEq/L instead of weight based (1-2 mEq/L/kg), which could result in improper dosing

• Hyperventilation strategy may have benefited sodium bicarbonate administration group by countering respiratory alkalosis, however, it could have harmed the placebo group

• Possible venous sampling rather than arterial for blood gas analysis at 10-minute point, though this would be a concern in any arrest setting if an arterial line could not be established in this time frame

Author’s Conclusion

“The use of sodium bicarbonate during CPR with transient hyperventilation improves acid-base status without CO2 elevation which is one of the most concerned adverse effects of sodium bicarbonate administration, but it had no effect on the improvement of the rate of ROSC and good neurologic survival.  At this point, we could not advise for or against its administration, our pilot data could be used to help design a larger trial to verify the efficacy of sodium bicarbonate.”

Bottom Line

Based on this study, the use of sodium bicarbonate does not appear to improve clinically significant outcomes, though it improved acid-base status.  Sodium bicarbonate should not be indiscriminately used in all cardiac arrests, and larger trials should be performed to further evaluate its impact on patient-centered outcomes.

Citation

Ahn, S., Kim, Y. J., Sohn, C. H., Seo, D. W., Lim, K. S., Donnino, M. W., & Kim, W. Y. (2018). Sodium bicarbonate on severe metabolic acidosis during prolonged cardiopulmonary resuscitation: a double-blind, randomized, placebo-controlled pilot study. Journal of thoracic disease, 10(4), 2295.

References

1. White, S. J., Himes, D., Rouhani, M., & Slovis, C. M. (2001). Selected controversies in cardiopulmonary resuscitation. Seminars in respiratory and critical care medicine, 22(1), 35–50. https://doi.org/10.1055/s-2001-13839

2. Merchant, R. M., Topjian, A. A., Panchal, A. R., Cheng, A., Aziz, K., Berg, K. M., Lavonas, E. J., Magid, D. J., & Adult Basic and Advanced Life Support, Pediatric Basic and Advanced Life Support, Neonatal Life Support, Resuscitation Education Science, and Systems of Care Writing Groups (2020). Part 1: Executive Summary: 2020 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation, 142(16_suppl_2), S337–S357. https://doi.org/10.1161/CIR.0000000000000918

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Expert Commentary

Thank you Dr. Ughreja and Dr. Watts for this excellent blog post on an important topic. In medicine, we often ask “what else can we do?” but less often do we ask “is what we’re already doing effective?” This is especially important for resuscitation and cardiac arrest. Not everything that is standard-of-care is ultimately effective care, and overtreating patients can lead to other untoward effects. 

In addition to the points made in the above blog, I would add a few important notes into the equation. First, the study excluded in-hospital cardiac arrest and therefore should not be considered in those patients. Second, the study also excluded those patients with early ROSC and absence of severe metabolic acidosis, effectively biasing towards inclusion of sicker patients. It is unclear how administration of sodium bicarbonate may have influenced those patients. Third, the study population was quite small and a striking majority of that population were found to have an initial rhythm of asystole. Fourth, ventilation rates were purposefully increased during bicarb administration. Though this may be practical and can potentially counteract excessive CO2 accumulation secondary to sodium bicarbonate administration, this is not common practice which leads to questions of this study’s external validity at other institutions.  

So, despite this study, at this point in time we still must grapple with the “should-we-or-should-we-not” of sodium bicarbonate administration in prolonged cardiac arrest. Some scenarios certainly do require sodium bicarbonate, most notably TCA overdose and hyperkalemia. In these cases, it’s obvious what to do. But so often what we do in emergency medicine is riddled with uncertainty. An unclear cause of cardiac arrest is certainly one of those situations. Perhaps instead of mindlessly giving sodium bicarbonate to cardiac arrest patients, we should give it once or twice and look for evidence that it has had an effect. Is the rhythm narrowing? Did you obtain ROSC shortly after administration? If not, giving dose after dose of sodium bicarbonate in hopes of meaningful recovery may not be the best path forward.

Dana Loke, MD

Department of Emergency Medicine

Northwestern University Feinberg School of Medicine

Northwestern Memorial Hospital

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How To Cite This Post:

[Peer-Reviewed, Web Publication] Ughreja, K. Watts, S. (2021, Dec 6). Bicarb in Cardiac Arrest. [NUEM Blog. Expert Commentary by Loke, D]. Retrieved from http://www.nuemblog.com/blog/bicarb-arrest

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ECMO Initiation in the ED

Written by: Kaitlin Ray, MD (NUEM PGY-3) Edited by: Evan Davis, MD (NUEM Alum ‘18) Expert commentary by: Colin McCloskey, MD (NUEM Alum ‘16)

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ECMO Initiation in the Emergency Department

Introduction:

Extracorporeal membrane oxygenation (ECMO) provides prolonged cardiopulmonary support in severe acute respiratory or cardiac failure. As the science behind ECMO continues to grow and with promising data regarding its use in acute hypoxemic respiratory failure, cardiac arrest, and cardiogenic shock, ECMO use in the United States has increased over 400% in the last ten years. This has stimulated an interest in earlier applications of ECMO both in the emergency department (ED) and even in the prehospital setting [1]. Initiation of ECMO in the ED is a relatively new development, with 65% of programs <5 years old and the majority of programs with <3 cases per year. However, this number continues to grow [2].

There two main types of ECMO: venoarterial (VA) and venovenous (VV). While VV ECMO provides respiratory support, only VA ECMO provides both respiratory and hemodynamic support. ECMO drains blood from the native vascular system, then circulates it outside of the body via a mechanical pump where it passes through an oxygenator and heat exchanger. Hemoglobin then becomes saturated with oxygen, CO2 is removed, and blood then reinfuses into the circulation [4]. Venoarterial ECMO is more commonly utilized in the emergency department as eligible ED patients often have concurrent hemodynamic and respiratory collapse.

Emergency medicine physicians have an increasing responsibility to initiate ECMO and/or make the decision to transfer to an ECMO capable facility. Knowing this, it is critical that we are familiar with the types of ECMO available, understand the indications, contraindications, risks, benefits, and logistics of initiating this form of extracorporeal life support.

Indications/Contraindications:

The specific criteria and contraindications to ECMO vary from institution to institution, often making the decision and ability to initiate ECMO challenging. The Extracorporeal Life Support Organization (ELSO) provides specific guidelines for ECMO initiation. These indications include cardiogenic shock as defined as (1) hypotension and low cardiac output with inadequate tissue perfusion despite adequate intravascular volume and (2) persistent shock despite volume, inotropes, pressors, and possibly an intraaortic balloon pump. The ELSO also provides guidelines for ECMO in acute respiratory collapse, as well as contraindications for ECMO including: unrecoverable heart failure and not a candidate for transplant or LVAD, advanced age, chronic multi-system failure, compliance issues, terminal malignancy and prolonged CPR without adequate tissue perfusion. 

As emergency physicians, which patients should we consider as candidates for ECMO? Generally speaking, consider younger and healthier patients who experience an acute but reversible insult leading to rapid cardiopulmonary collapse.  Recall that ECMO should only be considered as a bridge to more definitive therapy. Examples of scenarios that fit this criterion include:

• Massive pulmonary embolism

• Myocardial infarction causing V-Tach/V-Fib or cardiogenic shock

• Acute myocarditis or cardiomyopathy causing cardiogenic shock

• Drowning

• Hypothermia

• Drug overdose causing cardiovascular collapse (such as beta-blocker or Ca-channel blocker)

• Massive smoke inhalation, pulmonary contusion, or pulmonary hemorrhage causing refractory hypoxemia

As mentioned above, generally those with more chronic conditions such as end-stage heart failure, end-stage COPD, or those with chronic multi-organ failure, do not make good ECMO candidates. Other patient populations to consider in an ICU rather than ED setting include those with septic shock and/or ARDS. Note that patients with traumatic injury leading to hemorrhagic decompensation, although acute in nature, typically are not good candidates for ECMO as ECMO does not prevent further blood loss.

Additionally, we must consider what an ECMO-eligible patient clinically looks like. The majority of the patients who present with one of the above conditions will either be responsive to conventional therapies (intubation, fluids, inotropes), or they will be dead on arrival. However it is the rare, in-between patient that should be considered for ECMO. The condition of a good candidate would include things like: 

• Persistent hypotension despite maximum conventional therapy

• Persistent hypoxemia despite maximum ventilator therapy

• Patients brought in in cardiac arrest but achieve periods of unsustained ROSC

• Patients brought in with vitals but arrest in the ED

Unfortunately patients who arrest in the field, are brought to the ED already in cardiac arrest, or who do not achieve ROSC despite 30-45 minutes of well executed ACLS are unlikely to be appropriate ECMO candidates. The critical ECMO population is truly those who are flirting with life vs. death, especially the patients with intermittent periods of ROSC. Key exceptions to this include drowning and/or hypothermic patients. Generally these patients are better candidates for ECMO even if there has not been a recorded pulse, with the caveat that they should have been pulled out of the water or other environment quickly.

Risks/benefits:

ECMO is unique in that it provides full cardiopulmonary support without the physical trauma of chest compressions, thereby decreasing trauma, stress, and number of interruptions. Additionally, it provides a higher flow state than would otherwise be provided by manual compressions [2]. VV ECMO also minimizes barotrauma, volutrauma, and oxidative stress. However ECMO is not without risks and complications. The risk of bleeding is significant in the context of continuous anticoagulation and platelet dysfunction. Thromboembolism may lead to stroke or limb ischemia [4]. Infection may also occur secondary to indwelling lines/tubes [1].

Logistics:

ECMO is a costly intervention that requires a multi-disciplinary approach and an organizational commitment in order to proceed. Consideration must be given to the required equipment, blood bank capabilities, cannulation, and personnel availability. In order for ECMO to be successfully initiated from the ED, coordination between EMS, emergency medicine physicians, the cath lab, nursing staff, neurocritical care, cardiothoracic surgery, and the ICU is required [3]. When cannulating for VV ECMO, one may use a two cannula approach (femoral vein and internal jugular/SVC), or a single dual-lumen cannula (right atrium/IVC via the IJ). VA ECMO typically involves cannulation through the femoral artery and femoral vein [1]. If CPR is ongoing during cannulation attempts, programs may use a modified ACLS algorithm with a continuous epinephrine infusion at 0.7 mg/kg/min and minimization of pulse checks by utilizing continuous TEE monitoring [3]. Aggressive anticoagulation is required with continuous infusion of either unfractionated heparin or direct thrombin inhibitor, and efforts should be made to maintain platelet counts >50K and hemoglobin >12 mg/dL6,7.

Recap:

While initiation of ECMO from the emergency department is still a relatively new endeavor for many certified ECMO centers, the ED is in a unique position to bridge select patients in acute respiratory or cardiac failure to recovery using ECMO.  While institutional criteria for ECMO varies, the ELSO guidelines may be used as a reference to guide decision making in the absence of formal criteria. Generally speaking, pursue ECMO for younger, healthier patients with acute hemodynamic and/or respiratory collapse that is potentially reversible and unresponsive to conventional therapies. Typically patients with massive PE, MI, hypothermia, drowning, acute cardiomyopathy are the best candidates for ED ECMO. Contraindications generally include severe neurologic injury, end stage malignancy, advanced age, and irreversible multi-organ failure. Knowing that the emergency physicians are often the first to receive patients in acute cardiac and respiratory failure, it is critical that we are familiar with the types of ECMO available, understand the indications, contraindications, risks and benefits, and logistics of initiating this form of extracorporeal life support.

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Expert Commentary 

This is a thoughtful and thorough overview of ECMO within the emergency department. I will limit my commentary to VA ECMO for cardiopulmonary failure (ECPR), given the enthusiasm for the topic in the FOAM world and my experience within a ED based ECMO program. Some broad themes I would like to highlight: Evidence, Patient selection and Systems of Care.

Evidence: There is a signal that ECPR is better than conventional CPR. A systematic review and metanalysis found that those with cardiac arrest who received VA ECMO had an association with increased neurologically intact survival, with a number needed to treat of 7 [1]. However, most of the data is retrospective and from single centers, making it subject to a number of confounders, as well as selection bias. Further, those who received ECPR were more likely to receive therapeutic hypothermia and percutaneous catheterization, both interventions known to improve outcome following cardiac arrest.  Another single center experience has been promising, with 9/18 patients surviving to hospital discharge with good neurological outcome [2]. This protocol involved EMS bypassing the ED and taking the patient to the cardiac catheterization lab where they were placed on ECMO and underwent catheterization. Those who had good outcome all had concomitant intervenable coronary artery disease. There are several centers that have similar experiences with published case series [3,4], but it depends thus far on quality patient selection and a viable system of care.

Patient Selection:  All the above trials had strict inclusion and exclusion criteria. Most established protocols include an age cutoff (65-75 depending on center), initial shockable rhythm, and a time from arrest to cannulation between 30-60 minutes. Pertinent exclusions include advanced comorbidities, initial asystole or prolonged downtime. This is done with the intent of cannulating patients with the best chance of surviving their ECMO run; namely young patients with likely coronary artery disease who need ECMO as a bridge to cardiac catheterization. VA ECMO’s other successful ED applications, namely pulmonary embolism [5], drug overdose [6], and acute myocarditis [7] all share the commonality that ECMO provides time for recovery or as a bridge to a viable intervention. A bridge to recovery must exist prior to any cannulation scenario; this cannot be understated.

Systems of care: Cannulation is just one step in a VA ECMO patients hospital course. When conceptualizing a successful ED ECMO program, the institutional commitment should be visualized: A patient requiring 5-7 days in the ICU, formal neuroprognostication and continuous goals of care discussions with family. You rightly include a logistics session in your review, but this system of care is paramount to a successful ECMO program. Prehospital EMS systems must be designed for quick recognition and transport of ECMO candidates.  Emergency physicians need to be trained, and maintain competency in ECMO cannulation; interventional cardiology must be willing to catheterize appropriate patients; ICU consultants must have a standardized protocol for post-arrest care and neurology/ICU must have an institutionally accepted neuroprognostication scheme. In parallel to this, the family discussions regarding prognosis and any transition of care should include social work, case management and palliative care professionals. Cannulation is as exciting a procedure an emergency physician can perform, but without a thoughtful, multidisciplinary system of care, these patients will do poorly.

In closing, VA ECMO in the emergency department is an exciting development to tertiary ED practice. More experience, and more data, will help define the niche of patients and the necessities of post-arrest care that provide these patients with the best outcome.

1. Ouweneel DM, Schotborgh JV, Limpens J, et al. Extracorporeal life support during cardiac arrest and cardiogenic shock: A systematic review and meta-analysis. Intensive Care Med. 2016;42(12):1922-1934.

2. Yannopoulos D, Bartos JA, Martin C, et al. Minnesota resuscitation consortium's advanced perfusion and reperfusion cardiac life support strategy for out-of-hospital refractory ventricular fibrillation. J Am Heart Assoc. 2016;5(6):10.1161/JAHA.116.003732.

3. Stub D, Bernard S, Pellegrino V, et al. Refractory cardiac arrest treated with mechanical CPR, hypothermia, ECMO and early reperfusion (the CHEER trial). Resuscitation. 2015;86:88-94.

4. Bellezzo JM, Shinar Z, Davis DP, et al. Emergency physician-initiated extracorporeal cardiopulmonary resuscitation. Resuscitation. 2012;83(8):966-970.

5. Yusuff H, Zochios V, Vuylsteke A. Extracorporeal membrane oxygenation in acute massive pulmonary embolism: A systematic review. Perfusion. 2015;30(8):611-616.

6. Wang G, Levitan R, Wiegand T, et al. Extracorporeal membrane oxygenation (ecmo) for severe toxicological exposures: Review of the toxicology investigators consortium (toxic). Journal of Medical Toxicology. 2016;12(1):95-99.

7. Nakamura T, Ishida K, Taniguchi Y, et al. Prognosis of patients with fulminant myocarditis managed by peripheral venoarterial extracorporeal membranous oxygenation support: A retrospective single-center study. Journal of intensive care. 2015;3(1):5.

Colin McCloskey, MD
NUEM Alum ‘16, Critical Care Anesthesiology fellow - University of Michigan Medical Center/University of Michigan Health System

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How To Cite This Post

[Peer-Reviewed, Web Publication]  Ray K, Davis E (2018, November 12). ECMO Initiation in the ED  [NUEM Blog. Expert Commentary by McCloskey C]. Retrieved from http://www.nuemblog.com/blog/ECMO

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Other Posts You May Enjoy

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Resources

1. Mosier, Jarrod M., et al. “Extracorporeal Membrane Oxygenation (ECMO) for Critically Ill Adults in the Emergency Department: History, Current Applications, and Future Directions.” Critical Care, BioMed Central, 17 Dec. 2015, ccforum.biomedcentral.com/articles/10.1186/s13054-015-1155-7.

2. Tonna, Joseph E., et al. “Practice Characteristics of Emergency Department Extracorporeal Cardiopulmonary Resuscitation (ECPR) Programs in the United States: The Current State of the Art of Emergency Department Extracorporeal Membrane Oxygenation (ED ECMO).” Resuscitation, Elsevier Ireland Ltd, 10 Sept. 2016, experts.umich.edu/en/publications/practice-characteristics-of-emergency-department-extracorporeal-c.

3. Tonna, Joseph E., et al. “Development and Implementation of a Comprehensive, Multidisciplinary Emergency Department Extracorporeal Membrane Oxygenation Program.” Annals of Emergency Medicine, Mosby Inc., 1 July 2017, cwru.pure.elsevier.com/en/publications/development-and-implementation-of-a-comprehensive-multidisciplina.

4. Bartlett, Robert. Extracorporeal Membrane Oxygenation (ECMO) in Adults, 16 June 2017, www.uptodate.com/contents/extracorporeal-membrane-oxygenation-ecmo-in-adults.

5. Extracorporeal Life Support Organization - ECMO and ECLS. “Guidelines for Adult Respiratory and Cardiac Failure.” Extracorporeal Life Support Organization - ECMO and ECLS > Resources > Guidelines, ELSO (Extracorporeal Life Support Organization), Dec. 2013, www.elso.org/Resources/Guidelines.aspx.

6. Sklar MC, Sy E, Lequier L, et al. Anticoagulation Practices during Venovenous Extracorporeal Membrane Oxygenation for Respiratory Failure. A Systematic Review. Ann Am Thorac Soc 2016; 13:2242.

7. Spinelli E, Bartlett RH. Anemia and Transfusion in Critical Care: Physiology and Management. J Intensive Care Med 2016; 31:295.

End Tidal CO2 in Cardiac Arrest

Written by: Alex Herndon, MD (NUEM PGY-2) Edited by: Andrew Moore, MD (NUEM Alum '18) Expert commentary by: Seth Trueger, MD, MPH

Introduction:

ER, Grey’s Anatomy, House, Chicago Med, The Good Doctor - across the nation millions tune in to their favorite medical dramas hoping to get a glimpse at what it’s like to be in the business of saving lives. As a newly minted emergency medicine intern, my eye caught on to the most recent addition, The Resident, intrigued by how the show would portray the medical profession. While watching and cringing at dramatized incidences of medical nonsense, one scene particularly stood out.

It was day one of residency and the new intern was leading the resuscitation of a patient who suddenly arrested. Fast-forward, the intern achieves return of spontaneous circulation, however he is immediately chastised by his senior resident who states, “her end-tidal CO2 was less than 15 for the entire code…”

As the credits rolled I was left agreeing with critic Dr. Esther Choo in that “this show feels like a most unfortunate and untimely addition to the medical drama genre”, given it is the least accurate medical show I’ve watched to date, except for this fleeting reference to End Tidal CO2 (ETCO2).

A Review of ETCO2 and its Applications:

Traditionally, ETCO2 has been used in order to assess proper endotracheal tube placement. Approximately 25 years ago anesthesiologists began using ETCO2 capnography because it was revealed that approximately 93% of anesthesia errors could have been prevented with additional capnography monitoring. In particular, the sensitivity of color change of colorimetric devices can be faulty at low concentrations of CO2, a particular concern when there is presumed decreased CO2 released from the lungs due to decreased cardiac output during an arrest, or if the ET tube is placed within the esophagus. The addition of capnography not only reinforces that the ET tube is properly placed, but its use has been extrapolated to indirectly assess cardiac output. (1)

The additional data ETCO2 supplies can be used in two key ways:

1. To assess quality of chest compressions

In cardiac arrest, ETCO2 waveform, while performing CPR, can serve as an indirect measurement of blood flow generated by chest compressions. The height of the ETCO2 waveform during CPR has been used as an indirect measure of adequate chest compressions, helping those involved in resuscitation monitor the effectiveness of their compressions in real time. In the awake adult, normal cardiac index lies between 2.5-4 L/min/m2, with an ETCO2 of 35-45 mmHg. On average during CPR, if adequate chest compressions are being delivered a cardiac index of 1.6-1.9 L/min/m2 can be generated, which correlates with ETCO2 pressures of 20mmHg.(1) ACLS guidelines define high quality chest compressions as achieving ETCO2 pressures of at least 10-20 mmHg. As rotating medical professionals deliver chest compressions, ETCO2 can be used to determine if they need to be deeper, if there is performer fatigue, or if there are other factors that might be inhibiting the ability to maintain ideal cardiac output outside of ineffective chest compressions. All in all, it provides a more accurate assessment of chest compression adequacy than visual estimation of compression depth.

2. To help predict return of spontaneous circulation (ROSC)

Numerous studies have shown that abrupt increases in ETCO2 pressures exceeding 10 mmHg that remain higher than preceding values suggest an increase in cardiac output and is indicative of ROSC, hence the incorporation of such measures in ACLS guidelines.(1) Patients with values less than 10 mmHg are more likely to die during CPR, and those with values greater than 10 during CPR were more likely to get ROSC. (1) However when comparing a mere 10 mmHg ETCO2 pressure to the minimal normal ETCO2 pressure of 35 mmHg, it can be difficult to argue 10 mmHg is enough. Multiple studies have aimed to drive this number up, in particular showing ETCO2 pressures higher than 16mHg were significantly associated with survival from CPR in the emergency department. However, the use of an absolute ETCO2 value was limited by the cause of cardiac arrest. Average ETCO2 pressures that achieved ROSC widely varied depending on whether cardiac arrest was purely cardiac versus pulmonary in etiology. (1) A 2015 meta-analysis of ETCO2 values associated with ROSC showed, on average, patients with ROSC after CPR had an average ETCO2 level of 25 mmHg, significantly higher than the current recommended 10 mmHg threshold.(2) Other than the aforementioned minimal ETCO2 threshold, it is important to follow ETCO2 trends, looking for the sudden increase in ETCO2 and maintenance of elevated levels associated with ROSC.

Furthermore, other studies have attempted to show how ETCO2 can be a tool in deciding to terminate CPR when ROSC isn’t achieved. One study from 1997 reported that ETCO2 less than 10 mmHg at the 20 minute mark is predictive of non-survivability in outside-hospital cardiac arrest patients thus should lead to terminating resuscitation efforts.(3) Current studies of use of ETCO2 in outside hospital arrest trends have shown 3-5 minutes of ETCO2 <10 mmHg are associated with a bad prognosis and has been used to terminate in-field resuscitation efforts.(4)

Next Steps:

While more data is needed in order to potentially reset the ETCO2 threshold used to assess adequate CPR and ultimately long-term survival post-arrest, others are looking at alternate applications of ETCO2. In 2016 Wang et al studied whether or not ETCO2 values could be used as a predictor of survival when looking at in-hospital versus outside-hospital cardiac arrests. They found that an initial ETCO2 level was predictive of not only sustained ROSC, but also survival to discharge.(2) Others have looked at the use of ETCO2 to determine potential effectiveness of defibrillation. It was found that ETCO2 less than 7 mmHg never resulted in effective shocks, whereas shocks delivered with ETCO2 greater than 45 mmHg were always successful. Ultimately the authors attributed the success to performing high quality chest compressions prior to defibrillation.(5)

 

Limitations of ETCO2 Capnography and Conclusions:

Similar to how ETCO2 can vary given the cause of cardiac arrest, ETCO2 can be influenced by other factors, thus altering how physicians interpret capnography. In particular, no studies have assessed the effect or epinephrine or sodium bicarbonate on ETCO2. Further complicating matters, the majority of cardiac arrest patients end up intubated, thus ventilator settings or over bagging can influence expired CO2 levels creating yet another confounding factor. These subtleties regarding ETCO2 need further exploration.   

Next time you are waiting for that outside-hospital cardiac arrest to roll through the Emergency Department entrance, arm yourself with ETCO2 capnography not only to aid your resuscitative efforts, but also help with your decision-making along the way. Its usefulness extends beyond simply achieving ROSC and has the potential to prognosticate whether patients will not only survive but thrive.

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Expert Commentary:

Thanks for this nice overview of the data behind quantitative waveform ETCO2 in arrest. While it’s not the only tool in our armamentarium, it certainly can be helpful in assessing whether compressions are being effectively done, which can help the compressor modify their technique or location, add an element of motivation for the compressor, and help identify when the compressor is tiring out so we can switch someone else in before the official 2 minutes is up. Similarly, if there’s a big jump upward in the ETCO2 (eg, from 12 to 35), it’s reasonable to deviate from the usual 2 minutes and jump to a pulse check.

Using low ETCO2s is helpful in identifying futile codes; the general rule is that if the ETCO2 is consistently <10 after 20 minutes of well-done ACLS, the patient is very unlikely to come back. I find it important to point out that this is not a sensitive test, however, and many arrested patients will continue to have ETCO2 over 10 during long codes. I try to not get too focused on the ETCO2 as the only marker of when to terminate resuscitative efforts. Rather, it can help make a hard decision easier in some cases, but like most things, it’s not a magic bullet.

One other caution: don’t be mislead by a flat ETCO2 waveform during an arrest. If you don’t see any waves, then the airway is not in and either replace it or confirm intubation by other means (eg VL or gentle bougie insertion to holdup).

Here is a short screencast I put together back in 2013 on the 3 major uses of ETCOS: ETT confirmation, arrest, and monitoring in procedural sedation:

https://player.vimeo.com/video/57510987

Seth Trueger, MD, MPH

Assistant Professor of Emergency Medicine, Northwestern University

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How To Cite This Post

[Peer-Reviewed, Web Publication]   Herndon A, Moore A (2018, October 1). End Tidal CO2 in Cardiac Arrest.  [NUEM Blog. Expert Commentary by Trueger NS]. Retrieved from http://www.nuemblog.com/blog/ETCO2

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Other Posts You May Enjoy

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Resources

1. Kodali, B. Urman, R. Capnography during cardiopulmonary resuscitation: Current evidence and future directions. J Emerg Trauma Shock. 2014 Oct-Dec: 7(4): 332-340. Doi: 10.4103/0974-2700.142778

2. Wang, AY. Initial end-tidal CO2 partial pressure predicts outcomes of in-hospital cardiac arrest. Am J Emerg Med. 2016 Dec;34(12):2367-2371. doi: 10.1016/j.ajem.2016.08.052.

3. Morshedi, B. The role of ETCO2 in termination of resuscitation. J Emerg Med Services. 2017 Dec. <http://www.jems.com/articles/print/volume-42/issue-12/features/the-role-of-etco2-in-termination-of-resuscitation.html>

4. Venkatesh, H. Keating, E. Can the value of end tidal CO2 prognosticate ROSC in patients coding into emergency department with an out-of-hospital cardiac arrest. Emerg Med J. 2017 Mar; 34(3): 187-189. doi: 10.1136/emermed-2017-206590.1

5. Savastano, S et al. End-tidal carbon dioxide and defibrillation success in out-of-hospital cardiac arrest. Resuscitation. 2017 Dec;121:71-75. doi: 10.1016/j.resuscitation.2017.09.010.

Approach to Hypothermic Resuscitation

Written by:  Luke Neil, MD (NUEM PGY-2) Edited by: Quentin Rueter, MD, (NUEM PGY-4) Expert commentary by: Kory Gebhardt, MD

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Expert Commentary

This is a good overview of the algorithmic approach to the hypothermic patient. Generally speaking, hypothermia can be divided into various categories of severity, but as you mention, it is really those patients with a core temperature of <32°C (90°F) with cardiac instability or cardiac arrest that will require especially aggressive care.

For any hypothermic patient, the most important initial intervention is to stop any further heat loss. This is especially important for those with damp or wet clothing. Any wet garments should be completely removed, the patient should be dried, and then covered with warm, dry blankets and possibly a forced air rewarming device (i.e. Bair Hugger). Recall that one of the most efficient ways to cool a HYPERthermic patient is with evaporative cooling (spraying with or submerging them in water and then using fans to circulate air over the wet surfaces). Similarly, this heat loss will strongly work against you in rewarming a hypothermic patient if they are not fully dry. After this simple intervention, the majority of mildly hypothermic and stable patients just need time to bring their core temperature back to normal and often can be discharged once this has occurred.

For those patients with a core temp >32°C with severe cardiac instability or in cardiac arrest, you should also consider alternative etiologies for their presentation rather than expect it solely caused by the hypothermia alone. Like you mention, if you are able to rewarm a cardiac arrest patient above this temperature and they remain in asystole, it is likely that irreversible damage has occurred and they are less likely to be able to be successfully resuscitated.

As you detail in the algorithm, those with a temperature less than 32°C (90°F) AND instability or arrest need aggressive and invasive rewarming. The best available means of doing this is ECMO. Much of the research surrounding accidental hypothermia and resuscitation comes from the Nordic countries where freezing temperatures are often combined with outdoor extracurriculars and results in a high “n” for the studies. Outcomes data from many of the expert centers in this area show major benefits of ECMO, including one showing survival post-arrest in nearly 60% of patients and, even more importantly, good neurologic outcomes in 38% compared to only 3% in those without extracorporeal rewarming!

Unfortunately, not all EM physicians will have quick or 24/7 availability of ECMO. While this should be the preferred means of rewarming if available, there are alternatives if it is not. Hemodialysis circuits can also be used to actively rewarm a patient. Generally these can achieve 2-4 degrees/hr of rewarming compared to the 4-6 degrees/hr of ECMO. Thoracic (bilateral chest tubes), gastric (NG tube), and bladder lavage (foley) with warm fluids can also provide several degrees per hour of rewarming if used appropriately. Use a ventilator that can warm and humidify air. Don’t forget about minimizing heat loss by fully drying the patient and keeping as much of them covered as possible.

Lastly, I want to say a word about prognostication. While the mantra is, “you’re not dead until you’re warm and dead”, you can imagine that these patients require a considerable amount of time, effort, and mobilization of resources when they present to the ED. There is information that can help guide which patients are likely to benefit from such aggressive care from those who are, unfortunately, unlikely to be resuscitated. While multiple markers have been studied, the one with the most evidence supporting it, is a potassium value. This value can serve as a sort of surrogate for “warm ischemia time”, or in other words, how long were they warm and dead. This should be obtained and sent early in the resuscitation of the patient. If the value is >12, there is nearly no chance of any meaningful recovery (still very unlikely at >10, and even a cutoff of >8). Conversely, if the potassium level is less than the 8-12 range, the patient still has a good chance at a meaningful recovery if resuscitated to ROSC and these are the patients that should receive everything we have to rapidly and efficiently rewarm them (they are also the patients that can have meaningful recoveries despite impressive downtimes of even hours).

Additionally, historical factors surrounding the hypothermia, if known, can provide valuable prognostic information. Immersion vs. Submersion, which you define in your algorithm, is one example that might influence your decision about whether a patient might have benefit from mobilizing ECMO or other aggressive/invasive rewarming.

Kory Gebhardt, MD

Kaiser Permanente Emergency Medicine

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How to cite this post

[Peer-Reviewed, Web Publication]   Neil L, Rueter Q (2018, June 4 ). Approach to Hypothermic Resuscitation.  [NUEM Blog. Expert Commentary by Gebhardt K]. Retrieved from http://www.nuemblog.com/blog/hypothermia

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