Take Home Pearls from 2017 UM EM Cardiac Arrest Symposium

Below is a review of the key points of each lecture from the 2017 University of Maryland Emergency Cardiology Symposium which was hosted by Amal Mattu, MD in Baltimore, MD. This year’s topic was Cardiac Arrest.

To view video and presentations of all of the lectures, visit: www.livestream.com/UMEmergencyMed.


How Far We’ve Come!

John M. Field, MD; Penn State University

  • JAMA 2016: trial showed LOWER likelihood of survival to discharge and worse neurological outcome for patients with in-hospital cardiac arrest treated with therapeutic hypothermia.
  • JAMA 2017: no mortality benefit for tracheal intubation during cardiac arrest – consider using LMA (quick placement and less compression interruption).

Running the Perfect Code

Michael Winters, MD; University of Maryland

  • Team leadership is key! (Take charge of your resuscitation. Assign roles prior to patient arrival.)
  • Early defibrillation
  • High-Quality CPR:
    • Highest rate of survival at 121-140 compressions/min.
      • Journal of Resuscitation: 120-140 compressions per minute (compared to ACLS taught 100-120) showed improved ROSC at this rate in the year 2017. Single center. Roughly 200 something patients.
    • 5-6 cm depth of compressions with appropriate recoil of chest wall.
    • Avoid leaning on the chest.
    • Chest compression fraction (percentage of time in which chest compressions are done by rescuers during cardiac arrest) should be greater than 60%; goal of 80%.
  • Hemodynamic-Directed CPR
    • Using femoral arterial line, aim for DBP >25-35 mmHg. This is also helpful for determining PEA vs pseudo-PEA.
    • Using end tidal CO2, aim for >20 mmHg.
    • Hold epinephrine if these parameters are met.
    • Aim for a coronary perfusion pressure (CPP = aortic diastolic pressure minus the left ventricular end-diastolic pressure) of >20 mmHg to attain ROSC. Need arterial and central line to obtain the CPP which may be difficult during a resuscitation. Instead, we can guide our resuscitations with the use of early arterial line placement and/or end tidal CO2.
  • Consider video laryngoscopy as first attempt in CPR because DL increases “no flow” time seen bc of holding compressions to optimize view.  Success rate is similar.
  • Code Medications: Epinephrine: ? evidence of efficacy.  There exists no definitive evidence of epi’s benefit to long term survival to date.
  • NEJM 2016:  Amiodarone vs Lidocaine vs Placebo in out of hospital cardiac arrest shockable rhythms:  NO DIFFERENCE.  However, there was a non-statistically significant trend towards benefit to hospital discharge in those getting amio or lido vs placebo.

ECHO Evaluation in Cardiac Arrest

Sarah A. Stahmer, MD; UNC

  • US can interrupt cardiac compressions. Need to use a focused approach to limit delay during CPR
  • Use ultrasound to evaluate pump, tank, pipes during the resuscitation
  • SHoC Study 
    • Look for the Four F’s:  Fluid (pericardial), Form (RV dilatation), Function (wall movement), Filling (IVC diameter
    • RUSH Exam – Rapid Ultrasound for Shock and Hypotension
    • FEEL Study
    • Asystole or PEA with any degree of wall movement had higher rate of survival
    • Use cardiac ultrasound to determine appropriate pacemaker capture; appropriate myocardial squeeze with capture.
    • A twitch in the heart muscle is not cardiac stand still.  Must be no cardiac muscle movement for standstill. However, valvular motion with cardiac stand still is considered cardiac death.
    • Sonographic asystole has a poor prognosis, but not no prognosis.  Small chance of survival exists.  If patient young, continue resuscitative efforts.  Older/Nursing home patients it may be reasonable to call the code.
    • Must consider all patient variables with continuation of resuscitative efforts.

A Rational Approach to PEA 

Laszio Littmann, MD; UNC

  • Almost impossible to remember all H’s and T’s during a code
  • New algorithm for PEA: Based on whether the QRS is Narrow or Wide
    • QRS Narrow:
      • Mechanical (RV) problem (tamponade, tension PTX, PE, mechanical hyperinflation) (US: hyperdynamic LV—PSEUDO PEA).  These patients may benefit from an intervention – fluids/phenylephrine/needle decompression etc. and not CPR.
    • QRS Wide:
      • Metabolic (LV) problem (HyperK, Na channel blocker tox) (US: Hypokinetic—TRUE PEA). These patients likely will benefit from CPR
      • Consider Phenylephrine (NOT Epinephrine) in pseudo-PEA (narrow QRS): 2-10 mcg/kg bolus. 200-500 mcg IVP over 10-30 seconds. May repeat in 10-15 minutes. Approximately 20-minute half-life. No scientific evidence behind using phenylephrine; Littmann’s personal experience.

Optimizing Post-Arrest Care

Joshua C. Reynolds, MD, MSU

  • Hard to share pearls considering detail of lecture
  • Best take home from this lecture is not to settle after initial resuscitation. Must consider domains of injury and phenotypes of injury. Direct care down to the cellular level.

Making ECMO a Reality in the ED

Zack Shinar, MD; San Diego

  • 8% survival to hospital discharge in cardiac arrests – number hasn’t moved in many years
  • JAHA 2016: 50% survival achieved by one hospital in Minnesota with wide use of ECMO
  • Arterial line for all cardiac arrest patients to monitor response
  • Getting ECMO in your ED: 1. Assess your capabilities; 2. Develop relationships (CT surg, Cardio, Intensive care); 3. Become a “professional proceduralist”

Where are we going?

Robert O’Connor, MD, MPH; University of Virginia

  • AHA 2012:  Dispatch pre-arrival instructions (on how to perform CPR until EMS arrives) improve survival in out of hospital cardiac arrest
  • Japan has a cardiac arrest registry. USA does not. Why??
  • Arterial line in codes – helpful in distinguishing PEA from pseudo-PEA.  Compressions may be harmful in the latter
  • What is a pulse?  Finger is not very accurate
  • Chain of Survival is key to appropriate care of out-of-hospital cardiac arrests
  • PulsePoint App for phone: allows those trained in BLS to know when they are close to an active cardiac arrest.
  • EMS Dispatcher guided CPR for bystanders
  • Prolonged prehospital care has increased patient mortality
  • Appropriate Cath lab activation for ROSC patients: refer to Mattu’s ECG weekly lecture.

Panel Discussion: 

  • Cool to 36 if mild sx moving around etc. Cool to 33 if in deep coma /sicker subset (Personal preference)
  • ECMO is reimbursed very well as long as your pt is insured
  • Fingers to palpate a pulse are not very good.  Ultrasound, arterial line, and end tidal may be better resources. One study done in prehospital setting with ultrasound in the field shows those with no pulse but ultrasound showing cardiac motion did better with Meds (pressors) verses starting compressions. These patients have “pseudo pea” bc they actually have a pulse you just can’t feel it.

Case of the Week #1

CC Chest pain and palpitations

HPI Pt is a 23 y/o male with no PMHx presenting with c/o palpitations, chest pain since last night. Pt states the pain is localized to the mid sternal chest wall with radiation to b/l upper extremities at times. Pt states the pain came on suddenly last night and he didn’t think anything of it so he went to bed. He woke up this morning with same pain and now with associated nausea and dizziness prompting the visit to the ED. Pt has never had pain like this in the past. Denies vomiting, F/C, recent illness, sudden cardiac death in the family other than a 70 y/o uncle who was obese. Pt denies drug use and states he was drinking over the weekend 2 days ago.

PMHx: none

Meds: none

Allergies: none

PSHx: none

Social: occasional ETOH, (-) drugs

Pertinent PE and Vitals: BP 90/62 P 186 RR 22 O2 sat 100% RA

General: Awake, alert, mild distress Cardiac: (+) tachycardic; no murmurs Lungs: CTAB, no rales, no rhonchi, no wheezing Abd: soft, nontender, nondistended Skin: diaphoretic; mild pallor

Pertinent Labs (if any) Troponin: 0.439

DDX: SVT with aberrancy vs VTach

ED Course: Pt placed on cardiac monitor immediately and IVF bolus initiated. Adenosine 12 mg IVP given while rhythm strip running with no change. A second dose of Adenosine 12 mg IVP given again with no change. 150 mg Amiodarone given with improvement of HR from 190’s to 170’s still wide complex. Second dose of 150 mg Amiodarone given with improvement of HR from 170‘s to 150’s and eventually converted to a NSR rate 85. Pt remained in stable condition and BP responsive to IVF. Pt admitted to telemetry and Cardiology consulted. While still in the ED, pt reverted back to wide complex tachycardia. 3rd dose of 150 mg Amiodarone given and recommendation from Cardiology was to try a 20 mg IVP of Cardizem. Cardizem given and pt immediately converted to NSR. Pt started on Cardizem drip and upgraded to the CCU. Pt underwent EPS and AV dissociation was noted. Determination was Verapamil Sensitive Ventricular Tachycardia. Pt remained stable throughout hospital course and started on Verapamil. Discharged on hospital day #3 with follow up with cardiology clinic.

Final Dx:  Idiopathic Fascicular Left Ventricular Tachycardia AKA • Fascicular Tachycardia • Verapamil-sensitive VT • Belhassen-type VT

Discussion:  MC type of idiopathic tachycardia of LEFT ventricle ! It is a reentrant tachycardia typically seen in young patients without structural heart disease ! Verapamil is first line treatment • Dose: 10 mg IVP over 1 minute ! EKG features: • Monomorphic V tach • QRS 100-140 ms (narrower than other forms of Tach) • Short RS interval 60-80 ms • RBBB pattern • Axis deviation depends on anatomical site of re-entry circuit ! Often misdiagnosed as SVT with RBBB ! Keys to dx: • Observe features of VT such as caption/fusion beats, AV dissociation • Usually unresponsive to adenosine, vagal maneuvers, or beta blockers

Post by: Kristen Pena, DO

Blunt chest trauma

Being in even the most benign car accident imaginable, can be stressful for patients.  Inherently, if they have any chest pain they’re going to be convinced that they’ve sheared their aorta right off its hinges.  While that may be of concern to them, we are pretty certain that their aorta is still intact if they still are alive, but did they sustain a cardiac contusion? How do we figure out if they had one?  And what the heck do we do with them if they did in fact have a cardiac contusion?

1) What are we concerned about in blunt chest trauma?
There are many clinically significant injuries possible in the setting of blunt chest trauma. One that comes to mind is the nebulus diagnosis of “cardiac contusion.”  A lot of the controversy and uncertainty comes from the unclear definition of cardiac contusion which seems to encompass things like myocardial rupture, valvular injury, arrhythmias, cardiac dysfunction, etc. In my mind these types of patients would be more clinically apparent so we’ll focus on the patients who may appear well or relatively so.

2) Do we need to get a troponin in blunt chest trauma?
The answer is yes and no. There is a “guideline” answer and a practical one.
The guideline answer is yes. The 2012 EAST practice guideline for blunt trauma recommends BOTH an EKG and troponin. They state based on their references that a normal EKG in blunt chest trauma has a NPV of 95%. This increases to 100% with a normal troponin. There are several studies that support the use of troponin in this setting and there are instances when EKGs may be normal with a positive troponin. One recent study showed a troponin at 24 hours had 100% NPV for severe cardiac injury.
But the practical answer may be no. There are other studies that are less optimistic regarding the sensitivity and specificity and discourage the use of troponin as a gold standard for diagnosing cardiac contusion from blunt trauma. Another study showed that positive troponins were not a strong predictor of abnormalities on echocardiogram. So getting a troponin may not even matter. However other studies suggested that a positive troponin may be indicative of cardiac contusion or underlying cardiac issue, which brings us to our next question.

3) What do we do with a positive troponin in blunt chest trauma?
One of the arguments against getting a troponin is not knowing what to do with it. If it is negative can they go home? If it’s positive do they need to stay? A 2013 prospective study out of Iran does not recommend troponin as a gold standard in cardiac injury but does encourage intensive cardiac monitoring if an elevated troponin is found. Another study showed that elevated troponin was linked to arrythmias during the patients stay.  So this would suggest admission and tele monitoring for a patient that may have otherwise gone home.

4) Does this change the patients outcome?
Probably not. Three older studies looked at outcomes of patients with cardiac contusions and they really have no long term sequelae and do well.

What’s the bottom line?
Being in a trauma center I would follow the trauma guidelines of getting both an EKG and troponin in the setting of blunt chest trauma. If this is negative with a negative EKG and the patient appears well clinically then likely discharge. However if they have an isolated positive troponin then I would consider admission for 24 hour monitoring for arrythmias with a consideration for inpatient echocardiogram with a reassuring knowledge that they will almost absolutely do well long term.

Post by: Dr. Jordan Jeong, DO (@jeongjom)

Abdominal CPR?

There was a case report published in the Western Journal of Emergency Medicine last year about interposed abdominal compression CPR (IAC-CPR).  Personally, I’ve never heard anything of the sort and had to take a deeper look into it.  Essentially, you need two people to do compressions, one for the chest and one for the abdomen.  The abdominal compressor performs CPR with their hands about 5cm above the umbilicus and compressing about as deep as you would need to palpate the abdominal aorta pulse.  Both compress at the same rate and alternate their compressions; chest-abdomen-chest-abdomen and so on.  Theoretically, the abdominal compressor is acting as an external intra-aortic balloon pump.  By compressing the aorta during diastole, there is retrograde blood flow back into the coronaries.  Additionally, this abdominal compression increases venous return and promotes forward flow of the intrathoracic blood pool.  There have been no intra-abdominal injuries noted in survivors besides one pediatric traumatic pancreatitis reported in 1984.  The most recent review of IAC-CPR in Resuscitation showed significant improvements in the probability of achieving ROSC in the pre-hospital and in-hospital cardiac arrests when compared to standard CPR.  The question for me is why are we not doing this more? Is there harm in trying it if the person is already in cardiac arrest?

Post by: Terrance McGovern DO, MPH (@drtmcg13)

The Clinical Utility of BNP in Acute CHF

ER physicians diagnose CHF often and actually very well on clinical grounds at the bedside.  So why are we ordering BNP’s when we already know the diagnosis?  The evidence clearly states in which situations the BNP will not help you.  Check out the proposed algorithm recently published in EM Resident and let’s put the evidence into real practice.

Post by: Joe Bove, DO ( @jjbove08 )