Authors: Aaron Tiffee, MD and Joel C. Mosley, MD (LSUHSC Baton Rouge Emergency Medicine Residency Program, Our Lady of the Lake Regional Medical Center) // Editors: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) and Manpreet Singh, MD (@MPrizzleER)

“I’ve got a pulse,” you hear the nurse shout. Finally, a sigh of relief comes over the crowded resuscitation room and you take a moment to reflect on what just happened… but, your work is just now about to truly begin. It is up to you to determine why the patient died in the first place and determine which crucial steps need to be initiated to increase your patient’s chance of survival.

A detailed history is paramount to the survival of your patient. Question the paramedics if this was a prehospital arrest.  How long was the down time, how long have they worked the arrest, what was going on at the scene, were there any empty pill bottles at the scene or reported exposure to any toxins? Was there prolonged exposure to extreme temperatures?  Take the time to question the family about the recent symptoms that led up to the arrest, were there any medication changes, or new diagnoses?

A brief differential diagnosis for most all cardiac arrest adult patients should include:

• ACS, arrhythmias
• Electrolyte disorders
• Tamponade
• Airway obstruction, asthma, COPD, pneumonia, PE, tension pneumothorax
• Trauma, GI bleed, AAA rupture, ICH
• Overdose either intentional or accidental

Once your patient has achieved return of spontaneous circulation (ROSC), the next step is to determine extent of injury sustained during, before, or after arrest by performing a brief physical and neurological exam.  As always, start with the basics, the ABCs (i.e. airway, breathing, and circulation). Check the endotracheal tube (ETT) placement, assess the correct depth, cuff pressure and ensure that the tube is adequately secured to the patient.  Listen for equal bilateral breath sounds, does the ETT need to be retracted? Did the CPR cause a pneumothorax that is rapidly worsening with the controlled ventilations?  Abnormal breath sounds may also clue you into a pulmonary origin as the cause of arrest such as CHF or COPD.

A thorough cardiovascular exam should also be performed, listen to heart sounds; assess the quality of the pulse in all extremities. Is there a tamponade or valvular abnormality suggesting a cardiac etiology of their arrest? What is the heart rate and rhythm?  Look at the rhythm strip on the monitor; is there a QRS segment abnormality, suggestive of an electrolyte imbalance?  A brief full body examination should also be performed looking for abnormalities suggesting trauma, neurological, or gastrointestinal origin of the arrest. Are there any injuries or an exsanguinating wound; is the abdomen distended or rigid, suggestive of a surgical abdomen? Do you see any blood on your rectal exam?  These are all questions that you should be asking yourself in the post arrest phase of every patient.

To complete the physical exam, a thorough neurological exam should be performed. This should be done in the absence of neuromuscular blockade. Neurological assessment is becoming more and more important as research becomes evident pertaining to which patients should undergo hypothermic therapy or at least normothermic therapy after the latest Targeted Temperature Management trial by Nielsen et al.¹ In the post-arrest patient we should determine the post arrest GCS, as well as the pupillary, corneal, gag and cough responses.²   Patients who do not have any purposeful movements to follow commands are candidates for therapeutic hypothermia.³

To complete the initial assessment, all cardiac arrest patients with ROSC should have an ECG, blood gas (ABG/VBG), complete blood count (CBC), complete metabolic panel (CMP), troponin, coagulation studies, a chest x-ray, and point of care ultrasound (POCUS) of the cardiac activity. You should also consider a non-contrasted CT of the brain if you have any concern for intracranial hemorrhage.⁴

Of these, perhaps the most important in the acute setting is the 12 lead ECG.  In the United States the most common cause of out of hospital arrest is acute coronary syndrome (ACS). Patients with evidence of coronary artery occlusion or active STEMI on a 12 lead ECG must immediately go to the cardiac catheterization lab  for coronary revascularization.⁵  If your facility is not a 24/7 revascularization center you should be on the phone with the closest appropriate facility quickly arranging a transfer.

Interventional Measures

After the initial assessment has been completed, there are several interventions that you must initiate to maintain a perfusing rhythm. Once you have ascertained that you have an adequate airway as detailed above, the ventilator settings should be set to maintain an end-tidal CO2 from 35-45 mmHg and maintaining SpO2 of at least 94%.⁶ This is important to prevent hypocapnia induced cerebral vasoconstriction, which supports our overall goal of post arrest care of achieving not only coronary perfusion but adequate cerebral perfusion.

Hypoxia must be avoided, but hyperoxia may be harmful as well. Increased oxygen levels are known to also decrease cerebral blood flow and can decrease systemic pCO2 causing further vasoconstriction and more pronounced decrease in cerebral blood flow.⁷ One study conducted by Kilgannon et al in 2010 of 6,326 patients showed an odds ratio for death with patients with PaO2 greater than 300 mmHg of 1.8 (95% CI 1.5-2.2).⁶  However another study in 2011 by Bellomo et al.⁸ with a study population of 12,108 patients found no difference in mortality between hyperoxic and normoxic patients. Although there is still no definitive evidence-based answer about the appropriate level of oxygenation in the post arrest patient the general consensus of the community is to keep the PaO2 under 300 mmHg.

Maintaining an adequate perfusing pressure is necessary to avoid end-organ damage. The mean arterial pressure (MAP) should be greater than 65 mmHg; for optimal cerebral perfusion, the MAP should be increased to 80 to 100 mmHg.⁹ An arterial line should be placed and intravenous inotropes, vasopressors and isotonic fluids should be vigorously administered. There is no evidence that supports the superiority of any one pressor or inotropic drug in post cardiac arrest care, so use what you and your department are comfortable with.  However, in a trial versus dopamine, norepinephrine showed fewer adverse effects and a trend toward decreased mortality in cardiogenic shock patients.¹⁰ A few of the first line medications for consideration include:

• Norepinephrine at 0.01 to 1 mcg/kg/minute
• Epinephrine at 0.01 to 1 mcg/kg/minute
• Dopamine 5-20 mcg/kg/minute

If there is concern for cardiogenic shock in the post arrest patient, you should consider the addition of dobutamine at 2 to 15 mcg/kg/minute in discussion with your cardiology consultant; these patients should be carefully monitored for vasodilatory hypotension or tachydysrhythmias.

As briefly discussed above, an emergent cardiac revascularization should be performed for any patient with findings of ST segment elevation on ECG or with a presenting rhythm of ventricular fibrillation (VF) or ventricular tachycardia (VT). A review of 435 patients with VF/VT revealed that 70% had significant coronary artery disease.⁷ The patients who were treated by interventional cardiologists were twice as likely to be discharged home.⁵ Many facilities send all cardiac arrest patients presenting for cardiac catheterization after ROSC regardless of ECG findings. Again, it is crucial to be quick to be on the phone with your interventional cardiologist or the nearest revascularization center for patients presenting in VF/VT or with ST segment changes.

Treatment with antiarrhythmic drugs should only be considered for recurrent or persistent unstable rhythms.  There is no evidence to support the prophylactic use of antiarrhythmic drugs even if the presenting rhythm was VT or VF and antiarrhythmic drugs were administered during the initial resuscitation.¹² Instead the focus should be on correcting the underlying pathogenic cause of the dysrhythmia such as MI, electrolyte imbalance, or toxin exposure.⁹

Targeted Therapeutic Hypothermia

This topic could easily span the course of several articles as there have been multiple recent and ongoing studies revealing new evidence.  The following will discuss which patients should be cooled and what we as emergency physicians should do to begin the hypothermia therapy.

The greatest prognostic indicator of post-arrest survival and discharge home is preventing neurological injury; this is the goal of therapeutic hypothermia (TH). The core body temperature in post cardiac arrest patients has been shown to have a significant effect on their outcome.  Zeiner et al.³ found that for each degree over 37℃ carried an increased risk of death with an odds ratio of 2.25 (95% CI 1.24-4.12). A large contributor to post arrest complications and neurological injury is due to cerebral edema. This edema has been found in 22%-50% of post arrest patients.¹³ Cerebral edema causes an increase in intracranial pressure (ICP) which decreases cerebral blood flow, leading to neurological injury.¹⁴ TH has been shown to decrease the cerebral edema by decreasing the metabolic demands of the brain. The 2010 guidelines for ACLS recommend therapeutic hypothermia for all adult post cardiac arrest patients,¹⁵ however there are no randomized controlled studies that support the use of TH in any patients other than those in VT or VF.

As described above, patients who are not following commands or showing any purposeful movements should all have their temperature managed.  This includes patients who are pregnant, hemodynamically unstable, or undergoing cardiac catheterization.^3,16  The only absolute contraindications of initiating TH is active non-compressible bleeding or going against an advanced directive.  The most recent data published in the New England Journal of Medicine suggests there is no statistical difference in neurological outcome or survival in cooling patients to either 33℃ or 36℃¹ and International Liaison Committee on Resuscitation support the individual clinician’s decision of which targeted goal they would like to reach.¹⁷

The cooling should be initiated as soon as possible. In the ED, you can initiate TH by infusing a 30cc/kg bolus of IV isotonic saline that has been chilled to 4℃.  The use of a pressure bag can reduce the core temperature by 2℃ per hour.¹⁸ Cold packs placed in the axilla and groin and cooling blankets may also be utilized to help achieve a hypothermic temperature.   Shivering increases body temperature and can cause delays in achieving goal temperatures, therefore suppression of shivering should be initiated in the ED.¹⁸  A propofol infusion of 30 mcg/kg/minute to 50 mcg/kg/minute is generally sufficient to achieve appropriate levels of sedation.  Caution should be used in using neuromuscular blockade, as it can mask seizures which have been found in 3% to 44% of post arrest patients.¹⁹

There are several potential complications that you must be cognizant of while cooling your post arrest patients in the acute setting.  With temperatures below 35℃ platelet function may be altered²⁰ and studies have shown that the clotting cascade can be slowed,¹¹ some bleeding is seen in up to 20% of patients undergoing TH.²¹ Bradycardia and prolongation of the QT interval may be seen as well.¹⁹ If the blood pressure is adequate there is generally no intervention required to reverse the bradycardia. If VT or VF rhythms occur stemming from the prolonged QT, normal defibrillation should be performed and evidence shows good success with single shock therapy in animal studies.²²

For further reading on therapeutic hypothermia, go here: http://www.emdocs.net/therapeutic-hypothermia-after-cardiac-arrest-with-rosc/

Conclusion

The post arrest phase may potentially be as hectic as the arrest phase. You have multiple systems to think about and often must be thinking about them all simultaneously. In summary, keep the following in mind:

• Perform a focused and detailed history and physical examination
• Evaluate the airway and ETT placement, control the ventilator settings to maintain a PaCO2 to 35 to 45 mmHg and an oxygen saturation of above 94%  while keeping the PaO2 below 300 mmHg
• Assess for neurological dysfunction in absence of neuromuscular blockade
• Send labs including CBC, CMP, troponin, coagulation studies
• Obtain a plain film chest X-Ray, Point of Care Ultrasound, and ECG
• Early consultation of interventional cardiology for patients in VF/VT or with ST segment changes on ECG
• Pressor support and isotonic crystalloid boluses to maintain a MAP of 80-100
• Infusion of chilled IV isotonic normal saline to 4℃ to induce therapeutic hypothermia to a goal of 33℃ to 36℃

References

1. Nielsen N, Wetterslev J, Cronberg, T, et al. Targeted Temperature Management at 33°C versus 36°C after Cardiac Arrest. N Engl J Med.2013 Dec 5;369(23):2197-206
2. Rittenberger JC, Tisherman SA, Holm MB, et al. An early, novel illness severity score to predict outcome after cardiac arrest. Resuscitation 2011;82:1399.
3. Zeiner A, Holzer M, Sterz F, et al. Hyperthermia after cardiac arrest is associated with an unfavorable neurologic outcome. Arch Intern Med 2001;161:2007
4. Arnaout M, Mongardon N,Deye N, et al.  Out-of-Hospital Cardiac Arrest From Brain Cause: Epidemiology, Clinical Features, and Outcome in a Multicenter Cohort. Crit Care Med 2015;43(2):453-6
5. Reynolds JC, Callaway CW, El Khoudary SR, et al. Coronary angiography predicts improved outcome following cardiac arrest: propensity-adjusted analysis. J Intensive Care Med 2009;24:179.65
6. Bisschops LL, Hoedemaekers CW, Simons KS, van der Hoeven JG. Preserved metabolic coupling and cerebrovascular reactivity during mild hypothermia after cardiac arrest. Crit Care Med 2010;38:1542
7. Floyd, Thomas F., Clark, James M., Gelfand Robert, et al.  Independent cerebral vasoconstrictive effects of hyperoxia and accompanying arterial hypocapnia at 1 ATA. Journal of applied Physiology 2003;95(6):2453-2461
8. Bellomo R, Bailey M, Eastwood GM, et al. Arterial hyperoxia and in-hospital mortality after resuscitation from cardiac arrest. Crit Care 2011;15:R90
9. Nichol G, Thomas E, Calaway CW, et al. Regional variation in out of hospital cardiac arrest incidence and outcome. JAMA 2008;300:1423
10. De Backer, Daniel, et al. “Comparison of Dopamine and Norepinephrine in the Treatment of Shock”. NEJM 362(9):11.
11. Reed RL 2nd, Bracey AW JR, Hudson JD, Et al. Hypothermia and blood coagulation: dissociation between enzyme activity and clotting factor levels. Circ Shock 1990;32:141
12. Sunde K, Pytte M, Jacobsen D, et al. Implementation of a standardised treatment protocol for post resuscitation care after out of hospital cardiac arrest. Resuscitation 2007;72:29
13. Metter RB, Rittenberger JC, Guyette FX, Callaway CS. Association between a quantitative CT scan measure of brain edema and outcome after cardiac arrest. Resuscitation 2011;82:1180
14. Schwab S, Schwarz S, Spranger M, et al. Moderate hypothermia in the treatment of patients with severe middle cerebral artery infarction. Stroke 1998;29:2461
15. Peberdy MA, Callaway, CW, Neumar RW, et al. Part 9: post cardiac arrest care: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency cardiovascular Care. Circulation 2010;122:S768
16. Nielsen N, Sunde K, Hovdenes J, et al. Adverse events and their relation to mortality in out of hospital cardiac arrest patients treated with therapeutic hypothermia. Crit Care Med.2011 Jan;39(1):57-64.
17. Jacobs I, Nadkarni V. Targeted temperature management following cardiac arrest An update. International Liaison Committee on Resuscitation.  http://www.ilcor.org/data/TTM-ILCOR-update-Dec-2013.pdf, Accessed January 18, 2015
18. Kim F, Olsufka M, Longstreth WT Jr, et al. Pilot randomized clinical trial of prehospital induction of mild hypothermia in out of hospital cardiac arrest patients with a rapid infusion of 4℃ normal saline. Circulation 2007;115:3064
19. Polderman KH, Herold I. Therapeutic hypothermia and controlled normothermia in the intensive care unit: practical considerations, side effects and cooling methods. Crit Care Med 2009;37:1101
20. Michelson AD, MacGregor H, Barnard MR, et al. Reversible inhibition of human platelet activation by hypothermia in vivo and in vitro. Thromb Haemost. 1994 May;71(5):633-40
21. Jarrah S, Dziodzio J, Lord C, et al. Surface cooling after cardiac arrest: effectiveness, skin safety, and adverse events in routine clinical practice. Neurocrit Care 2011;1:382
22. Rhee BJ, Zhang Y, Boddicker KA, et al. Effect of hypothermia on transthoracic defibrillation in a swine model. Resuscitation 2005;65:79. 

Further Reading

1. Kilgannon JH, Jones AE, Shapiro NI, et al. Association between arterial hyperoxia following resuscitation from cardiac arrest and in hospital mortality. JAMA 2010;303:21
2. Rudolf J, Ghaemi M, Ghaemi M, et al. Cerebral glucose metabolism in acute and persistent vegetative state. J Neurosurg Anesthesiol 1999;11:17.
3. Coba V et al. The incidence and significance of bacteremia in out of hospital cardiac arrest. Resuscitation 2014;85(2):196-202
4. Dumas F, Cariou A, Manzo-Silberman S, et al.  Immediate percutaneous coronary intervention is associated with better survival after out of hospital cardiac arrest: insights from the PROCAT registry. Circ Cardiovasc Interv 2010;3:200
5. http://www.ncbi.nlm.nih.gov/pubmed/25654175
6. http://www.ncbi.nlm.nih.gov/pubmed/23916552
7. http://www.ncbi.nlm.nih.gov/pubmed/23103887
8. http://www.ncbi.nlm.nih.gov/pubmed/22824170
9. http://www.ncbi.nlm.nih.gov/pubmed/22281034