68 minutes with chest compressions, full recovery. Plus recommendations from a 5-member panel on cardiac arrest.

The following is told with full permission of the patient, who is a paramedic who also started, owns and runs with his wife a company for teaching CPR.  He has taught CPR to over 100,000 people.  And he's a wonderful guy.   Here is his story:

Near midnight in December, this 56 yo very healthy and vigorous paramedic was out on a run with a critical case when his partner found him unresponsive in the front seat of the ambulance.  The partner began manual chest compressions immediately and called for help.  He was found to be in ventricular fibrillation and was defibrillated 4 times, unsuccessfully.  After a few minutes of manual chest compressions, the LUCAS device was applied.  Due to jaw clenching, he could not be intubated and so was ventilated with bag-valve-mask.  He received 1 mg of epinephrine and 300 mg of amiodarone and still could not be defibrillated. 

On arrival in the ED, he was in full arrest and undergoing LUCAS CPR.  He had been in arrest for 30 minutes at this point.  O2 saturations were 70% with a waveform.  He was given succinylcholine and intubated and the inspiratory threshold device (ResQPod) was attached to the end of the tube.  Slow ventilations were guided by the timing light on the ResQPod.  Continous cardiac ultrasound revealed good cardiac contraction with each compression.  CPR was very briefly held and the rhythm was ventricular fibrillation with no ultrasonic cardiac activity. 

He was given 1 mg of epinephrine, 3g of calcium gluconate, 100 mEq of bicarb, and 100 mg of lidocaine.  At approximately 40 minutes (10 min in the ED), a 2nd mg of epinephrine (6th overall) and 2 g of MgSO4 were given.  The monitor confirmed V fib and he was defibrillated again, with conversion to sinus rhythm.  The LUCAS was paused.  There was good cardiac activity on ultrasound and strong pulses.

With successful return of spontaneous circulation, the cath lab was activated based on the presumption that this would be a coronary event (a greater than 50% probability even without a 12-lead ECG).

A 12-lead ECG was obtained:

Sinus tachycardia.  The QRS is very wide, with a right bundle branch block (RBBB).  The initial r-wave is replaced by a Q-wave in V1 and V2.  There is also left anterior fascicular block.  New RBBB + LAFB is a very bad combination and suggests a huge STEMI, either proximal LAD or left main. 

 

Is there ST elevation in addition to RBBB and LAFB?  To find out, you must find the end of the QRS.  In this case, it is best seen in lead V1, and if you draw a line down to lead II, which is across the bottom of the tracing, you can establish the end of the QRS in II.  Then you can find the end of the QRS is every lead, as below:

This is very similar to a case I posted a couple years ago (one of the most read posts of all time).  You can see that in leads V2, V5, and V6, as well as leads aVR and aVL, there is ST elevation. There is reciprocal ST depression in leads II, III, and aVF.

Case continued:

He had return of ventricular fibrillation immediately after the ECG was recorded (total time in regular rhythm was 2 minutes.)  LUCAS was restarted.  100 mg lidocaine was given.  Defibrillated again, no response.  100 mEq of bicarbonate, 40 U of vasopressin, 1 mg of epinephrine were given.  LUCAS was held briefly and there was wide complex pulseless electrical activity with no cardiac activity seen on ultrasound.  Then the patient reverted to V Fib again.  He was defibrillated again into sinus for only a few moments, then V Fib again.

At this point we realized we were dealing with incessant ventricular dysrhythmias, also known as "electrical storm," a condition seen almost exclusively during severe ischemia/STEMI.  We have had previous success with beta blockade using esmolol (which is short acting and can be turned off if it results in cardiogenic shock), so we gave 40 mg (500mcg/kg) of esmolol in a bolus, and started a 4 mg/min drip (50 mcg/kg/min).  We gave another 3 g of calcium, 1 mg of epinephrine, and 1 mg of atropine.

A venous blood gas returned: pH = 7.05/pCO2 = 101/pO2 = 25 (venous, remember)/HCO3 = 27.  A lactate returned at 12.8 mEq/L.  Another 50 mEq of bicarb was given.  The patient was defibrillated again after 38 minutes in the ED, and 68 minutes since his arrest.  He converted to sinus.  LUCAS was held.  Cardiac ultrasound showed function with poor ejection fraction.  Therapeutic hypothermia was started.

A repeat ECG was recorded while waiting for the cath team to arrive:

It appears to be a junctional rhythm at a rate of 55, with one PVC.  Now the anterolateral STEMI is clearly seen.  Interestingly, the ST elevation in V1-V3 is best seen in the PVC, with proportionally excessively discordant ST elevation (ST/S ratio V2 = 4/7 = 0.57, V3 = 4.5/14.5 = 0.31)

He was given aspirin and heparin and taken to the cath lab where a proximal LAD occlusion was opened.  A balloon pump was placed.

There were difficult critical care issues with  shock, low systemic vascular resistance and poor cardiac output, as well as pneumonia. Next day ejection fraction was 25% and peak troponin I was 250 ng/ml.

48 hours after arrest, he was awake and following commands. Within a few days, his wife could not tell any difference from his baseline functioning.  There was complete neurologic recovery.

His ejection fraction 3 months later is 40% and he is able to go 14 minutes on the Bruce protocol stress test (most normal people cannot even do that).  He will be back to work shortly.



Dr. Brian Driver, 4th year emergency medicine/internal medicine resident at Hennepin County Medical Center, gathered a 5-member panel to discuss: Cardiac Arrest: New Innovations and Best Practices.  

Panel members:

• Dr. Brian Mahoney, HCMC EMS director and HCMC site investigator of the ResQTrial.  HCMC EMS has among the highest resuscitation rates in the country (2010 Utstein number, before use of LUCAS, = 49%, overall resuscitation success = 17%)
• Dr. Demetris Yannopoulos, is an interventionalist at the University of Minnesota and is also a prolific cardiac arrest researcher at Minneapolis Medical Research Foundation (MMRF).  He and Dr. Keith Lurie do some amazing work in that laboratory.
• Dr. Mark Sprenkle, of the Division of Pulmonary and Critical Care Medicine at HCMC
• Dr. Gautam Shroff, staff Cardiologist, HCMC
• Dr. Steve Smith of Dr. Smith's ECG Blog and staff emergency physician at HCMC

Dr. Driver wrote this concise summary of the panel discussion:

High-quality CPR is critical in cardiac arrest, and can increase the rates of successful

defibrillation and survival.(1) CPR should be performed with a compression depth of two inches at a rate of 100 per minute, allowing full chest recoil after each compression.

Ideal CPR can be difficult to maintain with manual chest compressions, and recent technologic advances have made it possible for devices such as the LUCAS to provide high-quality longlasting mechanical chest compressions at the proper rate and depth. Investigations are underway to determine the impact of the LUCAS on cardiac arrest survival.(2,3) Because high-quality CPR is known to improve outcomes, results are likely to be promising.

The impedance threshold device (ITD) is another new adjunct in cardiac arrest. This device

temporarily prevents airflow through the bag-valve mask or endotracheal tube during chest expansion (decompression phase of CPR), thereby augmenting negative intrathoracic pressure and increasing venous return and cardiac output. The ResQTrial, which compared standard CPR to a combination of active compression-decompression CPR coupled with an ITD improved survival in cardiac arrest from 6% to 9%.(4) Another trial using the ITD in pre-hospital cardiac arrest failed to show a benefit, but conclusions drawn from these data are limited because time to ITD placement was delayed.(5)  There is some data from this trial which was discussed and which further supports ITD use, but which cannot be published here, as it will be published in July 2013 and is embargoed at the moment.  The ITD should be used in conjunction with active compression-decompression CPR to fully realize the benefits of increased chest expansion with augmented negative intrathoracic pressure.

Hyperventilation is deadly: during cardiac arrest, it creates excessive positive intrathoracic pressure and decreases venous return and cardiac output. In an animal model, hyperventilation was associated with a decrease in coronary perfusion pressure and survival.(6) Patients in cardiac arrest should be ventilated at a rate of 10 breaths per minute.

Epinephrine, although featured in the ACLS cardiac arrest algorithm and used every day throughout the world, has never been shown to improve survival to hospital discharge. The benefits of epinephrine are currently limited only to increased rates of return of spontaneous circulation. Epinephrine is potentially harmful; in a recent large well-performed Japanese study pre-hospital epinephrine administration in cardiac arrest was associated with decreased survival and functional outcome at 1 month.(7) The best dose and time interval for epinephrine administration has not been defined, but because of these recent data it is prudent to minimize total epinephrine administered in cardiac arrest. Novel investigations into therapies such as nitroprusside that optimize blood flow instead of blood pressure are extremely promising, but have only been demonstrated in animal models.(8) (There are many more novel therapies being actively studied in the MMRF laboratory, especially by Drs. Yannopoulos and Lurie).  Our patient received 8 mg of epinephrine and survived.  How much did epinephrine contribute to his successful resuscitation, if at all?

In cases of refractory ventricular fibrillation or tachycardia, beta-blockade can result in less electrical instability.  One might worry that it would contribute to cardiogenic shock, but, paradoxically, it has the potential to improve inotropy by relaxing the semi-permanent state of left ventricular (LV) contraction and functional mitral stenosis induced by epinephrine.  It can thus improve LV filling and outflow. There are several case reports, as in this case, in which esmolol and other beta-blockers rapidly terminated refractory ventricular fibrillation and were associated with ROSC.(9,10) Certainly, administration of a beta-blocker should be strongly considered before terminating resuscitative efforts for a patient in incessant ventricular dysrhythmia. 

Additionally, there are a number of case reports in which even beta-blockade was ineffective, but in which a bedside left stellate ganglion block was performed and immediately terminated ventricular fibrillation.(11-13) A recent post detailing this procedure can be found here:

To the cath lab with ongoing chest compressions?  Finally, patients who arrest while in the ED and cannot be resuscitated may survive if transported with ongoing mechanical CPR to the cardiac catheterization lab for restoration of flow to an occluded coronary artery. During the panel discussion, the question arose as to whether percutaneous coronary intervention (PCI) is more easily completed without the motion artifact of chest compressions, and the utility of initiating extracorporeal membrane oxygenation (ECMO) to create ideal procedural conditions (14).  Dr. Yannopoulos, an interventional cardiologist and leading resuscitation researcher, stated that taking the time to place ECMO was not beneficial as PCI can readily be performed during chest compressions.  ECMO can be placed in the cardiac catheterization lab or in the ICU after the procedure, if indicated. PCI during mechanical CPR is probably only warranted when the time between arrest and intervention is extremely short.

Finally, all patients who are comatose due to cardiac arrest should undergo therapeutic hypothermia (this is so well established that it needs no elaboration).

Key Points:

• High-quality CPR is critical. Compressions should be 2” deep at a rate of 100 with full

chest recoil after each compression.

• Mechanical CPR can provide high-quality, long-lasting CPR.

• Active compression-decompression CPR with an ITD significantly increased survival in

cardiac arrest. These two adjuncts should always be used together to maximize benefit.

• Hyperventilation is fatal. Bag at a rate of 10 ventilations per minute.

• Epinephrine has no documented benefit of any clinical significance apart from ROSC,

and may be harmful. Total epinephrine dosing in cardiac arrest should be limited.

• Esmolol or other beta-blockers should be administered in refractory ventricular

fibrillation, and can lead to rapid ROSC. Ultrasound-guided left stellate ganglion blocks

are a last-line option for ventricular dysrhythmias that persist after all other therapies.

Use therapeutic hypothermia!

References

1. Wallace, S. K., Abella, B. S. & Becker, L. B. Quantifying the Effect of Cardiopulmonary Resuscitation Quality on Cardiac Arrest Outcome: A Systematic Review and Meta-Analysis. Circulation: Cardiovascular Quality and Outcomes 6, 148–156 (2013).

2. Rubertsson, S. et al. The study protocol for the LINC (LUCAS in cardiac arrest) study: a study comparing conventional adult out-of-hospital cardiopulmonary resuscitation with a concept with mechanical chest compressions and simultaneous defibrillation.

Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine 21, 5 (2013).

3. Perkins, G. D. et al. Prehospital randomised assessment of a mechanical compression device in cardiac arrest (PaRAMeDIC) trial protocol. Scandinavian Journal of Trauma,Resuscitation and Emergency Medicine 18, 58 (2010).

4. MD, P. T. P. A. et al. Standard cardiopulmonary resuscitation versus active compressiondecompression cardiopulmonary resuscitation with augmentation of negative intrathoracic pressure for out-of-hospital cardiac arrest: a randomised trial. Lancet 377, 301–311 (2011).

5a. 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.

5b. Aufderheide, T. P. et al. A trial of an impedance threshold device in out-of-hospital cardiac arrest. N. Engl. J. Med. 365, 798–806 (2011).

6. Aufderheide, T. P. Hyperventilation-Induced Hypotension During Cardiopulmonary

Resuscitation. Circulation 109, 1960–1965 (2004).

7. Hagihara, A. et al. Prehospital epinephrine use and survival among patients with out-ofhospital cardiac arrest. JAMA 307, 1161–1168 (2012).

8. Yannopoulos, D. et al. Sodium nitroprusside enhanced cardiopulmonary resuscitation improves survival with good neurological function in a porcine model of prolonged cardiac arrest.  Critical Care Medicine 39, 1269–1274 (2011).

9. Miwa, Y. et al. Effects of Landiolol, an Ultra-Short-Acting β1-Selective Blocker, on Electrical Storm Refractory to Class III Antiarrhythmic Drugs. Circ J 74, 856–863 (2010).

10. Srivatsa, U. N., Ebrahimi, R., El-Bialy, A. & Wachsner, R. Y. Electrical Storm: Case Series and Review of Management. Journal of Cardiovascular Pharmacology and Therapeutics 8, 237–246 (2003).

11. Loyalka, P. et al. Left stellate ganglion block for continuous ventricular arrhythmias during percutaneous left ventricular assist device support. Tex Heart Inst J 38, 409–411 (2011).

12. Patel, R. A., Priore, D. L., Szeto, W. Y. & Slevin, K. A. Left stellate ganglion blockade for the management of drug-resistant electrical storm. Pain Med 12, 1196–1198 (2011).

13. Nademanee, K., Taylor, R., Bailey, W. E., Rieders, D. E. & Kosar, E. M. Treating Electrical Storm : Sympathetic Blockade Versus Advanced Cardiac Life Support-Guided Therapy.  Circulation 102, 742–747 (2000).

14. Kagawa E et al. Should we emergently revascularize occluded coronaries for cardiac arrest? Rapid-response extracorporeal membrane oxygenation and intra-arrest percutaneous coronary intervention. Circulation 2012 Sep 25; 126:1605.