Sunday, April 17, 2016

A Perfect Resuscitation Saves a Patient with Refractory Ventricular Fibrillation

This was contributed by Dr. Johanna Moore, one of my Hennepin Colleagues who researches CPR, along with Keith Lurie and Demetris Yannopoulos.  She translated her research knowledge into a spectacular resuscitation.

Case 

A 54 year old male presented via ambulance to the Emergency Department (ED) in cardiac arrest. He was found down outside a clinic, where bystander CPR was initiated by clinic staff. The amount of down time was unclear but thought to be minimal as this was a high traffic pedestrian area.
He received an estimated 5 minutes of manual CPR, then, after medic arrival, 20 minutes of LUCAS CPR, including use of the inspiratory threshold device (ITD, ResQPod) pre-hospital. He was noted to be in refractory ventricular fibrillation by paramedics. As part of his pre-hospital care, a King airway was placed, he was defibrillated 7 times, and received 300 mg IV amiodarone, followed by 150 mg IV amiodarone. He also received 2 mg epinephrine. He was noted to be “chewing” on the King airway and was also given 2 mg IV versed for this.

On arrival to the ED (after 25 minutes of pre-hospital CPR), the patient had agonal respirations and had brief movements of his upper and lower extremities while on LUCAS. [The presence of gasping, or agonal, respirations during cardiac arrest is associated with improved survival1,2.]  His continuous end tidal CO2 readings throughout the case averaged in the 30s mmHg (a sign of effective CPR and good outcome).

LUCAS CPR, with ITD use, was continued. The King airway was exchanged for an endotracheal tube without interruption of CPR, and blood was noted to be pooling in the posterior oropharynx at that time. Blood in scant amounts was also noted to be coming out of the endotracheal tube intermittently. The source of the blood was unclear. 

He was noted to be hypoxic at that time, with initial recorded oxygen saturation of 70%, and a nadir of 49%.  Post intubation, the oxygen saturation remained low, in the 70-80% range.  Several rounds of ACLS medications including epinephrine, sodium bicarbonate, and calcium gluconate were given along with further defibrillation attempts. The rhythm would intermittently convert to ventricular tachycardia after defibrillation but would rapidly degenerate into fibrillation.

Here is an ultrasound of the heart during ventricular fibrillation:

This is fascinating: The septum is fibrillating, but the lateral wall (lower right) is not.  As you will see later, this is because the lateral wall is where the STEMI is.  It is too ischemic to even fibrillate!



At around 15-20 minutes into the case, the head of the bed was elevated as much as the LUCAS would allow (10-20 degrees) in an attempt to improve oxygenation and preserve neurologic function (“Head Up” CPR3,4). The patient remained in refractory VF. Lidocaine 100 mg IV was given, as well as 2 g of magnesium empirically. 20 mEq KCL was given after the initial potassium returned at 2.6 mEq/L. The patient remained in refractory VF and an esmolol bolus, then drip, was started for treatment of ventricular storm.5 Further defibrillation shocks were administered without ROSC. Movement of the patient during CPR had stopped, but the end tidal CO2 remained over 20 mmHg. His oxygenation saturation had improved after intubation and placement in the Head Up position.
Double defibrillation6,7 was then performed by placing two separate sets of pads on the patient at once, then performing a simultaneous shock. After 38 minutes of ED CPR and 25 minutes of out of hospital CPR (total, 63 minutes), ROSC was obtained, with a corresponding increase in end tidal CO2 from the 30 mmHg range to 50 mmHg range. The patient was kept in the Head Up position. His Chest X-Ray showed diffuse right lung airspace opacities.


Here is a post-ROSC ultrasound:



There is very poor LV function.  There is no movement of the lateral wall (lower right).  There is also apparent thrombus in the right atrium.  With prolonged stasis in cardiac arrest, such thrombi can form.  Of course, one must also entertain the possibility of pulmonary embolism as the etiology of the arrest.  Ventricular fibrillation is the initial rhythm in less than 5% of arrest from pulmonary embolism.

Here is a parasternal short axis view:






An ECG was obtained:
Sinus rhythm with huge infero-postero-lateral STEMI




The cardiac catheterization lab was activated. Aspirin, ticagrelor, and heparin were given. Unfortunately, the catheterization lab team had just started an emergent and complex case, so the cath lab was occupied indefinitely.  

Consideration was given to tPA administration for treatment of STEMI, due to the delayed catheterization time. However, after discussion between the Emergency Physicians and Cardiology physicians, tPA was not given for the following reasons 1) The patient still had scant blood coming from the endotracheal tube 2) The consequences of giving tPA after over 60 min of CPR were unclear and the risk here was thought to be greater than the benefit 3) The patient would get to cath, albeit not as fast as the team would like. The ED physicians arranged for the patient to be transferred to a nearby hospital that had a cardiac catheterization team available.

The esmolol drip was continued and a low dose epinephrine drip was started due to hypotension to maintain a MAP greater than 60 mmHg. An intravascular cooling catheter was placed and therapeutic hypothermia was begun. Transport arrived for the patient, and he went for catheterization at the outside hospital, which showed a culprit lesion in the proximal left circumflex artery. A drug eluting stent was placed.

The patient remains hospitalized at this time, nearly 1 month after his arrest. His hospital course was complicated by an episode of ventricular tachycardia less than 48 hours post cooling. His post arrest echocardiogram showed an EF of around 30%, and he had an AICD placed as an inpatient. At this time, he is being evaluated for vocal cord/speech/swallow dysfunction, but is otherwise doing well neurologically.

Take Home Points
1.       We all already know this, but it is well worth it to mention again: High quality CPR, with minimal interruption, as well as bystander CPR, saves lives.

2.       There is no absolute way to tell how the brain is doing during CPR. This is an active area of research among resuscitation researchers. In this case, good prognostic indicators included the patient “chewing” on the King airway, agonal respirations noted during CPR, intermittent movement at the beginning of the ED case during CPR, and end tidal CO2 readings > 20 mmHg throughout the case. 

      In spite of these good prognostic signs, many of the treating ED physicians thought this patient had a very poor chance of neurologic survival.

3.       Head Up position was initiated in the middle of the case and the patient tolerated it well, with no immediate complications noted. His oxygen saturation level and bloody secretions from the endotracheal tube also improved in this position. 

      The animal work performed in this area uses an angle of 30 degrees for Head Up CPR, which we were not able to achieve.  It is also important to remember the theory behind Head Up CPR is not that it will improve rates of ROSC, but will possibly improve subsequent neurologic function.

4.       Remember esmolol is an option in refractory ventricular fibrillation, and to use both the bolus and drip dosing.

5.       Double defibrillation can also be used in refractory ventricular fibrillation.

   -   Use of lidocaine or amiodarone is now proven to increase survival (NNT = 20 for witnessed arrest).  Just published in NEJM Apr 13 online.

       Targeted Temperature Management for coma after cardiac arrest is critical.  We believe that hypothermia is better than normathermia (the study equating the two had a 12 hour interval to target temperature and thus does not prove equivalence of the two).

 

      Key aspects of the resuscitation:
      1) Uninterrupted CPR
      2) Use of the ITD
      3) Use of Esmolol
      4) Head Up CPR
      5) Amiodarone and/or lidocaine
      6) Magnesium and Potassium supplementation
      7) Double defibrillation
      8) Cooling

References:

1.       Clark JJ, Larsen MP, Culley LL, Graves JR, Eisenberg MS. Incidence of agonal respirations in sudden cardiac arrest. Ann Emerg Med. 1992 Dec;21(12):1464-7.

2.       Bobrow BJ, Zuercher M, Ewy GA, Clark L, Chikani V, Donahue D, Sanders AB, Hilwig RW, Berg RA, Kern KB. Gasping during cardiac arrest in humans is frequent and associated with improved survival. Circulation. 2008 Dec 9;118(24):2550-4.

3.       Ryu HH, Moore JC, Lick M, McKnite S, Shin SD, Kim TY, Metzger A, Rees J, Tsangaris A, Yannopoulos D, Debaty G, Lurie KG. The Effect of Head Up Cardiopulmonary Resuscitation on Cerebral and Systemic Hemodynamics Resuscitation. 2016 Feb;102:29-34. doi:10.1016/j.resuscitation.2016.01.033 [Epub ahead of print]

4.       Debaty G, Shin SD, Metzger A, Kim T, Ryu HH, Rees J, McKnite S, Matsuura T, Lick M, Yannopoulos D, Lurie K. Tilting for perfusion: head-up position during cardiopulmonary resuscitation improves brain flow in a porcine model of cardiac arrest. Resuscitation. 2015 Feb;87:38-43.

5.      Driver BE, Debaty G, Plummer DW, Smith SW. Use of esmolol after failure of standard cardiopulmonary resuscitation to treatpatients with refractory ventricular fibrillation. Resuscitation. 2014 Oct;85(10):1337-41.

6.       Merlin MA, Tagore A, Bauter R, Arshad FH. A Case Series of Double Sequence Defibrillation. Prehosp Emerg Care. 2016 Feb 5:1-4.

7.       CabaƱas JG, Myers JB, Williams JG, De Maio VJ, Bachman MW. Double Sequential External Defibrillation in Out-of-Hospital Refractory Ventricular Fibrillation: A Report of Ten Cases. Prehosp Emerg Care. 2015 January-March;19(1):126-130.

       Kudenchuk PJ et al.  Amiodarone, Lidocaine, or Placebo in Out-of-Hospital Cardiac Arrest.  http://www.nejm.org/doi/full/10.1056/NEJMoa1514204

      Aufderheide, T. P. et al.  Standard cardiopulmnary resuscitation versus active compression-decompression cardiopulmonary resuscitation with augmentation of negative intrathoracic pressure for out-of-hospital cardiac arrest: a randomised trial.  Lancet 2011;377(9762):301-11.  (Use of ITD)




7 comments:

  1. Rewarding case with detailed description of a series of interventions leading to ultimate survival for the patient with surprisingly good neurologic function. While difficult to determine which interventions had greatest impact — there are MANY Take-Home points that Dr. Smith emphasizes. It is fascinating for us to see a quality Echo during VFIb, showing fibrillation of the ventricles but with lateral wall akinesis (the area of the infarct being too ischemic to even fibrillate!) — prognostic value of serial ET CO2 readings that suggested all along NOT to give up on resuscitation despite markedly prolonged CPR times (persistent ET CO2 values > 20 mmHg should convey ongoing hope of potential ultimate success) — value of LUCAS CPR — and, the pearl that Beta-Blockers may relieve VFib “Storm” when nothing else does. Truly a team effort wth positive end result!

    I’ll add comment about the 12-lead ECG, which is a “pearl” in itself regarding prediction of the culprit lesion. There is sinus rhythm with obvious acute infero-postero-lateral STEMI. But unlike the case with the much more common RCA-occlusion, in which ST elevation tends to be greater in lead III > II with lesser ST elevation (if any) in lateral chest leads and usually marked reciprocal ST depression in lead aVL — we have a VERY different picture here! ST elevation is clearly much greater in lead II compared to lead III. There is obvious posterior infarction — but unlike typical RCA occlusion in which associated RV involvement generally attenuates the amount of ST depression in lead V1 (which is almost always less than in V2,V3) — we have the opposite here, with maximal ST depression in lead V1. That’s because there is no RV involvement. We also have maximal ST elevation in lateral leads typical supplied by the LCx (Left Circumflex) = leads V5, V6 and lead I — with already significant loss of R wave in virtually all lateral leads. This looks like a huge acutely evolving STEMI with a dominant LCx as the “culprit artery” (supported at the bedside by the Echo findings).

    THANKS to Dr. Smith for posting this highly insightful case of successful cardiopulmonary resuscitation!

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  2. Thanks for publishing this case. Any thoughts of esmolol vs propranolol which I've read possibly has a better mechanism for treating refractory ventricular fibrillation?

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  3. Dillon,
    I would not want beta 2 blockade and I would not want a long acting agent. You can turn off esmolol if the patient's contractility is affected and they are in cardiogenic shock.
    Steve

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  4. I once took a previously healthy patient in his 60s with refractory v fib out of hospital cardiac arrest after a short period of chest pain to cath lab with ongoing LUCAS where a LAD occlusion was opened and stented. The v fib could then be defibrillated in to stable sinus. The patient was admitted to the ICU but had an unsucessful outcome due to recurrent episodes of ventricular arrythmias. Thoughts?

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    1. We have taken many patients to the cath lab on LUCAS, but have not yet had ROSC AND neurologic recovery. Demetris Yannopoulos (researches arrest with Lurie) has reported great success with this.

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  5. Excellent case with great videos of the heart. I would like to share one case series where 32 patients underwent interventions in the cath lab with ongoing chest compression. They had 25% survival rate with good neurological outcome. It is important to note that all of these cases had cardiac arrest in the cath lab so the time to intervention is definitely an advantage compared to the ED . The overall survival for in hospital arrests is 23%. But what is more attractive about these cases is the good neurological outcome.

    http://sjtrem.biomedcentral.com/articles/10.1186/s13049-016-0198-3

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    Replies
    1. Thanks for pointing us to this interesting paper!

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