Surviving OHCA by Prof. Richard Lyon

This is the talk by Prof. Richard Lyon at The Bick Sick in Zermatt, 2018

Dr. Lyon is a consultant in Emergency Medicine and clinical lead for Medic1 at the Royal Infirmary of Edinburgh. He is the associate medical director of Kent, Surrey & Sussex Air Ambulance and chair or Pre-hospital Emergency Care at the University of Surrey. He completed a unique doctorate thesis on out-of-hospital cardiac arrest (OHCA) – the TOPCAT study, which has formed the basis of a successful programme of work to improve outcome from OHCA across Scotland. He has won numerous national and international awards for his work. 

Posted by:

              

     Lakshay Chanana

     

     ST4 Trainee

     Royal Infirmary of Edinburgh

     Department of Emergency Medicine

     Edinburgh

     Scotland

     @EMDidactic

Pulseless Electrical Activity Demystified

Pulseless Electrical Activity by Amal Mattu (From Resuscitation 2015) 

This video is also available on youtube. 

More thoughts on PEA:

http://rebelem.com/a-new-pulseless-electrical-activity-algorithm/

http://adelaideemergencyphysicians.com/2014/08/a-new-pea-diagnostic-algorithm-ecg-and-ultrasound/

The Intracerebral Bleeder

Intracerebral haemorrhage (ICH) is a subtype of stroke AKA Haemorrhagic stroke. Often the outcome turns out to be dismal and unfortunately we cannot do much about it. But luckily ICH makes up only about 10-15% of the total strokes and it is a neurosurgical emergency where we need to act fast and do the best to at least prevent the secondary brain injury. There are two schools of thought about this depending on the circumstances in which you are working. Some physicians go all out and do everything possible for these patients while others have a pretty nihilistic attitude about this. 

Regardless of these, there are some things that we must do in the initial few hours of intracranial haemorrhage that can possibly change the outcome of these patients. Let us go through each one of them.

Rapid and accurate diagnosis using neuroimaging

First and foremost, we should always suspect ICH in anyone presenting with acute CNS symptoms. Some patients might walk into the ED if they have a small bleed but usually they have other worrisome symptoms like acute onset weakness, headache, vomiting, seizures, altered mental status. It is not reliable to distinguish between an Acute Ischemic Stroke (AIS) and Intracerebral Haemorrhage (ICH) based on the history and clinical examination alone and this is the sole reason why a Non-Contrast head CT is ordered for these symptoms. 

If CT shows blood --> ICH

CT Normal --> Probable AIS 

Other information that a CT can give us:

• Based on the location of blood

Classical hypertensive ICH - seen at basal ganglia, thalamus, pons, cerebellum 

Amyloid Antipathy bleeds/ AVM bleeds - Lobar bleed

Common causes that lead to ICH are chronic hypertension leading to charcot bouchard aneurysms, cerebral amyloid angiopathy, AV malformations, Berry Aneurysms (SAH).

• Calculate the ICH Volume

Concise clinical assessment regarding ICH characteristics and patient condition

We will one again start with the mantra of emergency medicine and start off with ABCs. These patients are often comatose and require RSI. 

Avoid ketamine here if they already have a high blood pressure. I prefer using rocorunium with a sedative. This eases the process of intubation and also brings down the blood pressure a bit. Remember with succinyl choline (sux), there is a concern for transient rise in ICP. Though some physicians are of the opinion that this transient bump in ICP with sux in insignificant, I don't recommend using sux here. 

A full neuro exam is hard to perform in these patients but we can do a ICH score to assess the mortality. Each point increase in the ICH score is associated with an increased risk of mortality and a decreased likelihood of good functional outcome. 

Targeted assessment for potential early interventions including:

1. Control of elevated blood pressure
   The exact number to which the blood pressure should be reduced remains unclear. But a reduction SBP of 140mmHg appress safe. There has been a concern that acutely lowering blood pressure could lead to ischemic brain injury in the peri-hematoma region, but this risk has not been supported by recent studies. 
   
   
   American Heart Association/American Stroke Association Guidelines for the Management of Intracerebral Hemorrhage suggest reducing the blood pressure to <160/90 mmHg or a mean arterial pressure (MAP) <110 mmHg. In patients with potential for elevated ICP, a cerebral perfusion pressure (CPP) of >60 mmHg should be maintained.
   
   
   Go for quick acting and titratable agents like IV calcium channel blocker infusions (nicardipine or clevidipine) or Labetalol. The worst thing that you can do for these patients is to start them on a nitroprusside or nitroglycerine drip. These dugs cause cerebral vasodilation and can further increase the ICP. 
   
   
2. Correction of coagulopathy
   For some reason, we tend to forget this. But reversing blood thinners and anticoagulants is one of the most crucial steps while managing these patients. A quick guide on reversing these medication is mentioned in the table below:
   
   
   
   
   
   
   
   
   
3. Need for early surgical intervention and hematoma evacuation

Current AHA ICH guidelines recommend surgical intervention if:

• Patients with cerebellar hemorrhage who are deteriorating neurologically 
• Brainstem compression  
• Lobar ICH with hematoma volume >30 cc and within 1 cm of the cortical surface 
• Significant life-threatening mass effect

Always correct coagulopathy in patients undergoing surgical hematoma evacuation.  

Other issues:

Prophylactic AEDs

Current guidelines do not recommend routine use of prophylactic anticonvulsants though some practitioners still use a short course in patients with lobar ICH and those undergoing hematoma evacuation. Clinical seizures should be treated.  

Need for intracranial pressure (ICP) or other neuromonitoring

ICP monitoring is recommended in patients with GCS < 9, large hematomas with mass effect suggestive of elevated ICP, or hydrocephalus. As a goal, an ICP <20 mmHg and a CPP> 60 should be maintained.

  

Patient disposition from emergency department (ED):

‘‘I have a 62 year man with known DM/HTN/A fib who was on warfarin. He was found at home this morning at 7 AM by his wife who last saw him normal at 5 AM. He had left-sided weakness, pre hospital GCS was 12, and BP was 190/100.’’

‘‘On arrival to the ED, he was the same, so we took labs and sent him for a head CT.’’

‘‘CT completed at 10 AM showed a 20-mL right thalamic ICH with mild IVH, but no hydrocephalus. There is about 4 mm of right-to-left midline shift. CTA/CTP showed no AVM or aneurysm."

‘‘When he returned to the ED, he was comatose with a GCS of 10, and his left-sided weakness was worse. So he has an ICH Score of 2. His labs came back with an INR of 2.8.’’

‘‘We intubated him using rocuronium and etomidate and transfused PCC. He also had 10 mg of IV vitamin K.’’

‘‘Neurosurgery has been called, and they are on their way to see him. He is in ED, intubated and sedated now on propofol drip. His BP is 150/85 with no other treatment.’’

‘‘They are ready to take him in Bed 2 in the ICU in 5 min.

The first 24 h are critical for blood pressure management, identification of seizures, ICP management, and maintaining a secure airway. Avoidance of fever, hyperglycemia/hypoglycemia, and hypoxia are also important, as these may affect outcomes. In addition, patients with ICH are at increased risk for the development of deep venous thrombosis (DVT); current guidelines recommend use of compression stockings and pneumatic compression devices at hospital admission, as well as initiation of prophylaxis-dose UFH/LMWH within 1–4 days following onset (assuming cessation of bleeding).

Take Home

• DNR is a self fulfilling prophecy. Give them the best chance.
• Do the ABCs, reverse blood thinners/anticoags and control BP (140 SBP is acceptable)
• Get neurosurgery involved ASAP
• When you handover, make sure to convey the volume, location, medication reversal.

References:

1. www.neurocriticalcare.org
2. Morgenstern LB, Hemphill JC 3rd, Anderson C, et al. Guidelines for the management of spontaneous intracerebral hemorrhage: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2010;41: 2108–29. 
3. Kothari RU, Brott T, Broderick JP, et al. The ABCs of measuring intracerebral hemorrhage volumes. Stroke. 1996;27:1304–5.
4. Hemphill JC 3rd, Newman J, Zhao S, Johnston SC. Hospital usage of early do-not-resuscitate orders and outcome after intracerebral hemorrhage. Stroke. 2004;35:1130–4.
5. Hemphill JC 3rd, White DB. Clinical nihilism in neuroemer- gencies. Emerg Med Clin North Am. 2009;27:27–37. vii-viii. Qureshi AI, Wilson DA, Hanley DF, Traystman RJ. No evidence for an ischemic penumbra in massive experimental intracerebral hemorrhage. Neurology. 1999;52:266–72.
6. Zazulia AR, Diringer MN, Videen TO, et al. Hypoperfusion without ischemia surrounding acute intracerebral hemorrhage. J Cereb Blood Flow Metab. 2001;21:804–10.
7. Antihypertensive Treatment of Acute Cerebral Hemorrhage Investigators. Antihypertensive treatment of acute cerebral hemorrhage. Crit Care Med. 2010;38:637–48.
8. Anderson CS, Huang Y, Wang JG, et al. Intensive blood pressure reduction in acute cerebral haemorrhage trial (INTERACT): a randomised pilot trial. Lancet Neurol. 2008;7:391–9.
9. Kirollos RW, Tyagi AK, Ross SA, van Hille PT, Marks PV.Management of spontaneous cerebellar hematomas: a prospective treatment protocol. Neurosurgery. 2001;49:1378–86. Discussion: 86–7. 
10. Frontera, Jennifer A., et al. "Guideline for Reversal of Antithrombotics in Intracranial Hemorrhage." Neurocritical care (2015): 1-41.

Capnography beyond ROSC

What is Capnography?

It is a non-invasive technique where CO2 is analysed continuously, in the gases entering and leaving the lungs. Look at it like a non-invasive way of estimating the PaCO2. Normal ETCO2 ranges between 35-45mmHg.

Different ways of estimating ETCO2:

1. Waveform capnography (Quantitative): When ETCO2 is graphically displayed and analysed quantitatively (real time quantitative waveform as depicted below). Capnograph is the device that measures and displays the waveform. It gives us a number i.e very close to the PaCO2 (typically underestimates PaCO2 by 5mmHg in healthy adults). Therefore, a high ETCO2 is almost always associated with hypercapnia. 

Normal Capnograph (Adults)

2. Capnometry (Quantitative): When only the numerical value is displayed without the waveform.

                         

3. Qualitative: Does not tell us one fixed number instead gives a range of ETCO2 using the calorimetric device. Ex. 21-30mmHg. Hence, utility is limited to ET tube placement verification.

Calorimeter device

How is it different from SpO2?

SpO2 measures O2 saturation in the blood whereas ETCO2 measures CO2 in the airway. ETCO2 reflects the elimination of CO2 by the lungs and thus paints an immediate picture of patient's condition on the monitor, in contrast to SpO2 that remains normal for several minutes (even when you hold your breath).

SpO2 and ETCO2                             

When interpreting ETCO2, look at both, the numeric value as well as the waveform. If you look only at the numeric value, this is like only looking at the heart rate without the ECG wave pattern!

Normal ETCO2 waveform:

Phase I aka Dead space ventilation/ Inspiratory baseline: Beginning of exhalation, no gas exchange here. There is almost no CO2 in airway during inspiration, so baseline is normally zero.

Phase II aka Ascending/Expiratory upstroke/ Early exhalation phase: CO2 from alveoli reaches the upper airway and causes a rapid rise in the amount of CO2 that is detected on the monitor.

Phase III aka Expiratory plateau phase: CO2 rich air is exhaled out

ETCO2 i.e. end of exhalation contains the highest concentration of CO2 (normal value is about 35-45 mmHg).

Phase IV aka Descending/ Expiratory downstroke: Inspiration begins and CO2 in the airways drops down to zero.

Normal capnograph wave

Note: The baseline represents the inspiratory phase (not expiratory)

Normal capnograph

Increase in ETCO2 (See the waveform below)

Hypoventilation

Increased muscular activity

Malignant hyperthermia

Increased Cardiac Output or Bicarbonate infusion

Relief from bronchospasm

Increasing ETCO2 (Ex. Hypoventilation during procedural sedation)

Decrease in ETCO2 (See the waveform below)

Hyperventilation

Muscle relaxants and hypothermia

Decrease cardiac output

Pulmonary embolism 

Bronchospasm

Decreasing ETCO2

Clinical Applications:

1. Airway management: To confirm the ET tube placement, also for continuous confirmation of the airway
2. Monitoring CPR efficacy: Target ETCO2 >20 during CPR
3. Estimates prognosis during CPR: An end-tidal CO2 value < 10 mm Hg after 20 min of resuscitation has been shown to be very accurate in predicting death
4. Confirming ROSC without stopping chest compressions: With ROSC ETCO2 shows as a sudden increase
5. Monitoring PaCo2 in a Traumatic Brain Injury/ Post Cardiac Arrest care
6. Guide to ventilation during procedural sedation: Shows hypoventilation i.e increasing ETCO2 at least 60 seconds prior to hypoxia 
7. Fluid responsiveness (5% or greater increase in ETCO2 following a passive leg raise is a non invasive way of predicting fluid responsiveness)
8. Diagnosing other pathologies (PE, DKA)

ETCO2 waveform in other pathologies:

Airway obstruction pattern (Bronchospasm)

Rebreathing

Esophageal intubation

On Muscle relaxants

Take Home

• ETCO2 is a surrogate marker for arterial CO2. If increased, it confirms hypercapnia.
• ETCO2 changes immediately with changes in the amount of CO2 in the airway (unlike SpO2 that shows a lag)
• When using waveform capnography, look at the ETCO2 numeric value as well as the waveform.
• Eliminate pulse checks during CPR, use ETCO2 instead.

References:

1. Heradstveit BE, Heltne JK. PQRST - A unique aide-memoire for capnography interpretation during cardiac arrest. Resuscitation 2014; 85:1619-20.
2. Monnet, X. et al. ETCO2 is better than arterial pressure for predicting volume responsiveness by PLRT. Intensive Care Med. 2013 Jan;39 (1): 93-100
3. http://www.medscape.com/viewarticle/812011
4. http://edtech2.boisestate.edu/meganjacobson/502/capno.html
5. http://www.carefusion.com/pdf/Center_for_Safety/Documents/RC1706-L3017-Capnography-Handbook.final.pdf

Running the code

This week, lets go through some key points on cardiac arrest. Some of these form the fundamentals of CPR in addition to other important points which are not talked about when we do the routine life support courses.

1. High quality CPR
Well, we all know this, Right?

• Rate:100-120/min
• Depth: 5cm approximately
• Allowing full chest recoil
• Not to hyperventilate
• Minimising interruptions

This is something that is really stressed on during the life support courses. Well, this is because survival is linked to the quality of CPR and there should not be any excuses here. This is very basic simple stuff that can make a difference. So how are doing it so far?

Current literature says we are slow/ shallow with chest compressions and do not allow adequate recoil. So next time when you run a code, make sure that you stick to these points and especially stay away from interruptions.

Reasons for interruptions: 

a) Airway: Securing the airway should be individualised for every patient. There is no magic number here. For a witnessed arrest with presumed cardiac cause, airway can be delayed for 8-10 minutes whereas early airway control should be done for a hypoxic arrest (drowning, pulmonary edema). In India, pre-hospital intubations are rare and by the time patients are brought to a hospital, airway should be secured ASAP on arrival with minimal interruptions to chest compressions. This is not the time for a novice to try intubation, it should be done by the most experienced provider around. 

b) Pulse Checks: Checking pulse during CPR is unreliable and should not be done, instead use ETCO2 to look for the ROSC. DO NOT STOP COMPRESSIONS TO CHECK FOR PULSE. 

c) Peri shock pauses: Shock can be delivered with transcutaneous pads or paddles and in India, the use of paddles is far more common than pads. 
With every 5 seconds of peri shock pause, there is an 18% decrease in survival. It is recommended to continue to deliver compressions while charging the defibrillator and once it is charged, only then hold the chest compressions for probably < 5 seconds, deliver the shock and resume compressions. It is painful to see those providers, who stop compressions as soon as they touch the paddles, then charge the defibrillator and then deliver the shock. This way it roughly takes about 20-30 seconds.

If there is expertise available, use intra arrest ECHO to pick up a tamponade or dilated RV, but again minimise compressions (Transesophageal ECHO is coming to the ED's soon..)


2. Hemodynamics Guided Resuscitation
Choose one of these three to judge your performance and hemodynamic status:

a) Coronary Perfusion Pressure (needs an arterial line and central line to monitor CPP)

• Our goal is to achieve an adequate Coronary Perfusion Pressure (CPP) i.e. CPP > 20mm Hg
• CPP = Aortic DBP - Right Atrial Pressure (RAP) 

OR

b) Diastolic Blood Pressure (needs just an arterial line)

• Insert a intra arrest femoral arterial line and target DBP > 40mm Hg 
• If < 40, improve CPR or give epinephrine
• If > 40, no need to give epinephrine, continue high quality CPR

OR

c) ETCO2 

• When you can't get an arterial line, use waveform capnography
• It is the continuous non invasive measurement end tidal CO2 using a sensor, the value is displayed on the monitor as a number.
• ETCO2 acts as a surrogate marker of cardiac output in addition to confirming the ET tube placement and ROSC.
• Target ETCO2 > 20mmHg 

3. Medications
Theoretical benefit: Improve CPP, CPP
Detrimental effects: Increase myocardial O2 demand, post ROSC myocardial dysfunction

Epinephrine (Adrenaline)

• No difference in outcomes, but we are finding it hard to stop using it!!
• Literature says more epi = no change or worse outcomes.
• With epi you are more likely to achieve ROSC, but worsen the neurological outcomes.
• Read more on epinephrine here by Dr. Anand Swaminathan (@EMSwami)

Give q5min epi now if you have been doing q3min so far and watch out for the next ACLS update OR use Hemodynamics Guided Resuscitation. 


3. Team Leadership

• This is by far the most important take home point from this post. Your leadership skills, ability to mobilise resources and getting things done can affect the outcome of a code. With experience we need to learn how to take control of the situation and communicate effectively under stress. Just knowing the algorithms is not enough.
• Good Leadership: Appropriate role assignment, better communication, reduces errors and establishes ROSC faster
• Errors are made due to indecisive and weak leadership which can cost a life.
• If there is time available, brief your team prior to the code and always debrief after you are done with the code regardless of the outcome. This will improve the team dynamics for future resuscitations. 
• 

So take the charge, assign tasks, be decisive, communicate early, clearly and effectively.

Take Home:

• Don't forget the basics, focus on high quality CPR
• Don't flood them with epinephrine instead use Hemodynamics guided resuscitation (CPP, DBP or ETCO2)
• Communicate early, clearly and effectively. Good leadership saves lives..

Thank You

References:

1. Michael Winters, MD: Running the Perfect Code in 2015 (AAEM Scientific Assembly) 
2. Castelao, Ezequiel Fernandez, et al. "Effects of team coordination during cardiopulmonary resuscitation: A systematic review of the literature." Journal of critical care 28.4 (2013): 504-521.CPR quality- Consensus 
3. Panesar, Sukhmeet S., Agnieszka M. Ignatowicz, and Liam J. Donaldson. "Errors in the management of cardiac arrests: An observational study of patient safety incidents in England." Resuscitation 85.12 (2014): 1759-1763.
4. Cheskes, Sheldon, et al. "Perishock Pause An Independent Predictor of Survival From Out-of-Hospital Shockable Cardiac Arrest." Circulation 124.1 (2011): 58-66.
5. Sunde, Kjetil, and Theresa M. Olasveengen. "Towards cardiopulmonary resuscitation without vasoactive drugs." Current opinion in critical care 20.3 (2014): 234-241.
6. Stiell, Ian G., et al. "Advanced cardiac life support in out-of-hospital cardiac arrest." New England Journal of Medicine 351.7 (2004): 647-656.Johnson NJ et al Resuscitation 2014
7. Sutton, Robert M., et al. "Hemodynamic-directed cardiopulmonary resuscitation during in-hospital cardiac arrest." Resuscitation 85.8 (2014): 983-986.

Auto-resuscitation: Lazarus Syndrome!

What is Lazarus Syndrome?

Lazarus syndrome/ phenomenon is a rare and probably under reported condition where delayed return of spontaneous circulation (ROSC) after cessation of cardiopulmonary resuscitation (CPR) is seen. This was first reported in 1982, so far 38 cases of delayed ROSC have been published and majority of them come from anaesthesia and critical care literature. 

In the cases reported so far, ROSC very often occurred within 10 minutes of stopping CPR. Less than half of them achieved good neurological recovery following ROSC and the rest died soon after.

What are the possible mechanisms that explain Lazarus Syndrome?

The exact mechanism of delayed ROSC is unclear and not well understood. This is possibly multifactorial:

1. Positive end expiratory pressure

Dynamic hyperinflation of the lung causing increased positive end expiratory pressure (PEEP) is one of the proposed mechanisms.

2. Delayed action of drugs

Some authors suggest delayed action of drugs administered during CPR as a mechanism for delayed ROSC. It is possible that drugs injected through a peripheral vein are inadequately delivered centrally due to impaired venous return, and when venous return improves after stopping the dynamic hyperinflation, delivery of drugs could contribute to return of circulation.

3. Myocardial stunning

Prolonged myocardial dysfunction can occur following myocardial ischaemia, taking up to several hours before normal function returns. Myocardial Infarction was present in about 1/3 of the cases reported so far which could have contributed to transient myocardial ischaemia and stunning.

What can be the implications for emergency health care providers with delayed ROSC?

Delayed ROSC can lead to serious professional and legal consequences. Questions can be raised about the quality of resus and whether it was stopped too soon. The  physicians might also be accused of negligence or incompetence and even be sued for the damages.

In such a scenario, the conduct of resuscitation can only be assessed from the documentation, so it is vital to record the events during cardiac arrest as accurately as possible. It is absolutely essential to get a consensus from the arrest team and to document the reason for termination of CPR. 

So, What makes Lazarus Syndrome important for us?

We need to realize that death is not an event, but a process. It is a process during which various organs supporting the continuation of life fail. Cessation of circulation and respiration is such an example. The physical findings to support this—absence of heartbeat and respiration—are the traditional and the most widely used criteria to certify death. Since these findings alone are not a sign of definitive death, it is quite possible to declare death in the interval between cessation of CPR and delayed ROSC.

Some recommend that the patients should be passively monitored for few minutes following unsuccessful CPR. It should also be mentioned that the patient is being closely monitored to establish death. Death should not be certified in any patient immediately after stopping CPR, and one should wait at least 5-10 minutes, if not longer, to verify and confirm death beyond doubt.  

The time honoured criteria of the stoppage of the heart beat and circulation are indicative of death only when they persist long enough for the brain to die.

KEY POINTS

• Lazarus phenomenon is delayed ROSC after cessation of CPR.
• Understand death: It is a process, Stop looking at it like a single event.
• Observe the patients for 5-10 minutes the cessation of CPR before confirming death. (Get an EKG or bedside ECHO before you declare death)
• Re-read and scrutinise the chart before signing it off. 

References: 

1. Adhiyaman V, Adhiyaman S, Sundaram R. The Lazarus phenomenon. Journal of the Royal Society of Medicine. 2007;100(12):552-557.Bray JG. The Lazarus phenomenon revisited. Anesthesiology 1993;78: 991
2. Linko K, Honkavaara P, Salmenpera M. Recovery after discontinued cardiopulmonary resuscitation. Lancet 1982;1: 106-7  
3. Martens P, Vandekerckhove Y, Mullie A. Restoration of spontaneous circulation after cessation of cardiopulmonary resuscitation. Lancet 1993;341: 841 
4. Braunwald E, Kloner RA. The stunned myocardium: prolonged, postischemic ventricular dysfunction. Circulation 1982;66: 1146-9 
5. De Salvia A, Guardo A, Orrico M, De Leo D. A new case of Lazarus phenomenon? Forensic Sci Int2004;146: S13-5  
6. Monticelli F, Bauer N, Meyer HJ. Lazarus phenomenon. Current resuscitation standards and questions for the expert witness (German). Rechtmedizin 2006;16: 57-63
7. Lantos JD. The Lazarus Case: Life and Death Issues in Neonatal Intensive Care. Baltimore: Johns Hopkins University Press, 2001
8. Conference of Medical Royal Colleges and their Faculties in the United Kingdom 1979. Diagnosis of death. BMJ 1979;1: 332. 
9. Sweet WH. Brain death. NEJM 1978;299: 410-2  

Resuscitation: When do we call it off?

I have a case this week, that made me question some of the dogmas that I was always taught:

DOGMAS:

1. CPR > 20 min is of no use
2. No pupillary reaction means they are dead - do not resuscitate
3. pH < 7.0, too bad - they are not gonna come back

0900AM: I was signing off after the night shift, when they wheeled in this man,

50/M, unresponsive, H/O preceding chest pain

Downtime: 10 minutes

No comorbid conditions 

and this is was his initial rhythm

Our team braced up and we started running the code. Eventually he ended up getting these meds/procedures over the course of next 45 minutes in addition to high quality compressions via a mechanical device.

• Intubation
• IV access
• 200J X 8 Shocks
• 13 amps Epinephrine
• Amiodarone 300mg then 150mg
• Lidocaine 100mg
• 2gm Magnesium
• + Dopamine was started during the compressions
• Intra arrest ECHO

Just when all of us were loosing the hopes, we got his pulses back and this was the ECG.

Cardiology was already paged during the compressions on the basis of the ECHO that demonstrated RWMA. Cardio registrar was with us during the later half of the resus, witnessing everything with a fair amount of skepticism.

On getting the pulses back, his first remark was "Ahh. Why are you guys even doing this for the last 45 minutes". He is in Hypoxic encephalopathy, there is no pupillary reaction. He is never going to make it. Did you look at his blood gas!!  And then he insisted on a Neurology Consult to comment about his CNS function. But this chap was lucky enough because he coded during the morning hours, so we could get things moving fast in terms of getting the consult and convincing cardiology to push him to the cathlab. No surprise here, he had a >95% LAD lesion that was taken care off.

Post Resus ABG 

Next morning the ED docs were upstairs in the ICU to review this guy, and guess what he was propped up, ready for extubation, looking around, GCS: E4M6VT!! And the same cardiology registrar was right next to him. And then, much to my surprise he said "You guys saved him".

So, This guy who was almost "brought dead", walked out of the hospital after about 14 days, neurologically intact.

This leaves us with a few questions:

1. When should we stop resuscitation? 20 minutes?

The general consensus about CPR, at least among the other specialists (non-EM) is to "STOP AFTER 20 MINUTES" or else you are going to leave them in a persistent vegetative state. Some specialities those are far away from resuscitation consider cardiac arrest - an irreversible event and have a really pessimistic attitude towards it. Well this is not always true and this was a perfect example. And as Emergency Physicians, we all have seen such scenarios. In this particular case, we got the pulses back after about 45 minutes, in addition to the downtime of 10 minutes.

Key Message: Traditionally prolonged CPR is recommended for LA toxicity, Intra arrest lysed PE, Hypothermia aka special situations. But individualise this timeline with every patient. 20 minutes is not a deadline for everyone. Use age and co morbidities before you make the decision to stop.

2. What is the role of pupillary reaction and blood gas in terms of gauging the prognosis in the immediate post resus period?

Pupils - NOT RELIABLE

This guy had non reactive pupils post resus, but he had a favourable outcome. Therefore, we cannot rely on pupils in the immediate post resus period.  

Blood Gas (ABG) - NEVER!

His initial blood gas was thought to be "incompatible with life". Well to compare and contrast, this was his ABG the next morning in the ICU (about 21 hours after the first ABG).

ABG next morning

Key Message: Pupillary reaction suggests a favourable prognosis but non reactive pupils in post resus period do not convey anything. Though after a period of 72 hours, if they still have non reactive pupils, then that suggests a bad outcome.
And numbers on the blood gas cannot dictate the prognosis and your decision to stop/continue the resuscitation should never be based on them.

3. What can be done to avoid the delays when dealing with specialists in such situations?

We lost 10-15 crucial minutes, while getting neurology to see him and also convincing the cardiologists to take him for cath. Fortunately, it was a clean and smooth conversation without any clash of egos. Still we ROSC to balloon time 45 minutes!

Well, these potential delays can be avoided if you have pre-existing protocols about these issues. For this particular case, it could have been anything from "taking them to Cath with mechanical CPR" or "treating with thrombolytics" based on the ECHO findings. You can't be discussing these logistics in the heat of resus when you should be providing the post arrest care!

There is a ton of stuff that we can do depending on the resources we have:

Mechanichal CPR

Double Shocks/Mg/Beta blockers for incessant VF

Intra arrest ECHO/Thrombolytics

Empirical thrombolytics

Intraarrest PCI

PCI for all cardiac arrests with a worrisome history

ED initiated intra peritoneal dialysis

ECMO

Resuscitative Thoracotomy

REBOA

This is only possible when all the team members are completely aware of the resus plan. For instance, If you are planning a resuscitative thoracotomy, better make sure that your Cardiothoracic team of surgeons is okay with that and they must be on the same page with ED in terms of indications of doing this procedure because surgeons often refuse to take up a patient if they were never in favour of doing this procedure at the first place, and things get ugly from there.

Key message: Have set written protocols to avoid the delays and keep everyone on the same page.

Learning Points:

• 20 minutes -  does not fit all.
• Don't be fooled by those numbers on the blood and non reacting pupils are not good enough.
• Have pre existing protocols, don't not fight with the logistics when you are stressed.