Authors: Lou Mitchell, Lewis O Jones / Editor: Steve Fordham / Reviewer: Pragya Mallick / Codes: ACCS LO 2, RP3, SLO3, SLO5, SLO6, SLO7 / Publication Date: 26/12/2020


Emergency Physicians must be confident managing the post-cardiac arrest patient with return of spontaneous circulation (ROSC) to continue high quality care once initial resuscitation succeeds. All clinicians must speak the same language to allow effective stabilising, planning and prognostication for these patients.

This session focuses on the Emergency Department (ED) care of patients post cardiac arrest (i.e. after the return of spontaneous circulation), and specifically how to:

  1. Stabilise a post arrest patient
  2. Formulate a plan for their ongoing care and definitive care
  3. Make an evidence based assessment of short term prognosis for the post-arrest patient
  4. Evaluate medicolegal/ethical issues around withdrawing/withholding care

Basic Science and Pathophysiology

The short term mortality of patients who survive cardiac arrest is high. The National Cardiac Arrest Audit 2018-19 UK data found only 23.6% patients with in-hospital cardiac arrest (IHCA) survived to hospital discharge [1]. The ROSC rates for out-of-hospital cardiac arrests (OHCA) were nearly 26.7% but the survival to hospital discharge rates were less than half of that at 12% in another study published by the NHS Ambulance services [2].

This mortality hasnt improved since 1953 despite improvements in resuscitative practice and critical care medicine.

The aim in stabilising the patient with ROSC post cardiac arrest is to manage what has recently been termed post cardiac arrest syndrome [3].

This comprises four areas:

  • Brain injury
  • Myocardial dysfunction
  • The ischaemic/reperfusion response
  • The precipitating pathology

By establishing invasive physiological control of the patient the impact of post cardiac arrest syndrome on long term mortality and morbidity can be ameliorated, and the underlying cause for cardiac arrest can be found and treated.

In any critically ill patient, clinical assessment and treatment must occur simultaneously. Reassessment of response to interventions must be undertaken frequently and rapidly.


Assess airway patency. If an airway cannot be maintained by simple measures or is immediately threatened (e.g. by vomiting or pulmonary oedema) immediate intubation is indicated. If a patent airway can be maintained then the urgency of intubation depends on the patients ventilatory status.

If the post arrest patient is not waking 5-10 minutes after ROSC, intubation should be planned [3].


Controlled ventilation gives indirect control of other homeostatic mechanisms undertaken by a conscious and physiologically normal body.

For example:

  • Changes in PaCO2 affect cerebral blood flow
  • Positive End-Expiratory Pressure (PEEP) can dramatically improve ventilatory status

Hypoxia must be avoided but there is some evidence that hyperoxia may cause harm, so give sufficient oxygen to maintain saturations of 94-98% [3,4].

A nasogastric / orogastric tube will relieve gastric distension. This can improve ventilatory status [5]. Beware of the risk of precipitating vomiting if the airway is not protected.

Monitoring Airway and Breathing:

Standard resuscitation room monitoring should be in place early: Sp02, 3-lead ECG monitoring, Non invasive Blood Pressure every 3-5 minutes, and End Tidal Carbon dioxide (ETCO2) monitoring in the ventilated patient.

The ETCO2 is a guide to the trend of arterial partial pressure of CO2 (PaCO2), while not being the same numerically due to V/Q mismatches. The aim is normocarbia [6].


Post ROSC patients are usually haemodynamically unstable, and their fluid status and fluid-responsiveness are difficult to judge. Post-arrest patients are a heterogeneous group, and the target mean arterial pressure (MAP) should take into account their normal blood pressure, the estimated cardiac (dys)function, and the cause of cardiac arrest. The International Liason Committee on Resuscitation (ILCoR) make a broad recommendation of aiming for a MAP between 65 and 100.

Judicious fluid challenges of 125-500 mls should be given to optimise the patients perfusion and preload. There is a conflicting need to perfuse the post-ischaemic brain (which may have lost autoregulation) without too much strain on the post-ischaemic heart [3].

Invasive Circulatory Monitoring:

An arterial line provides a continuous blood pressure, and facilitates regular blood gas analysis to track response to therapy. A swing in the waveform with respiration can suggest under-filling.

Central venous access is often obtained early, as it gives central and reliable access for the continuous infusion of drugs. CVP readings can be taken pre and post fluid challenges to add to clinical interpretation of fluid status in the patient.

Echocardiography can give a visual guide to the filling status and the cardiac index of the patient.

Non-invasive cardiac output monitoring may be useful and can be rapidly established (e.g. oesophageal or supra-sternal Doppler).

Inotropes and vasopressors are often needed to maintain blood pressure and cardiac output. Choice of inotropic support is beyond the remit of this module, but depends upon the underlying pathology.


Record the GCS prior to administering any sedation it has implications for prognostication.

Be cautious with sedation. If the patient is making inadequate respiratory effort or fighting the ventilator, neuromuscular blockade is necessary to gain control of their ventilation. It then becomes essential to ensure the patient is adequately sedated. Short acting sedating agents are preferred (e.g. propofol) as neurological assessment can be made sooner after a sedation hold [5].

Control seizures as they cause a three-fold increase in brain metabolism [3].


See later for guidance on temperature control post ROSC.

Glucose Control

Tight glycaemic control is not recommended, not least because the comatose patient is at great risk of undiagnosed hypoglycaemia [7].

However, hyperglycaemia must be controlled as it has been correlated with increasing risk of poor neurological outcome [8]. The optimal blood glucse target level in the post arrest group has not been determined [5], but current evidence suggests the BM should not be controlled unless it is more than 8 mmol/l [8].

A chest x-ray confirms line and tube position, rules out iatrogenic complications and may aid diagnosis.

Frequent 12-lead ECGs should be undertaken if ischaemia/infarction or arrhythmia is suspected.

Potassium should be checked on venous or arterial blood gases, and should be maintained at 4-4.5 mmmol/l to try and limit arrhythmias [5].

An improving lactate post arrest demonstrates reducing tissue ischaemia [3]. It is a valuable way to assess physiological response to therapy and is an independent predictor of mortality [9].

Ultrasonography can be useful in diagnosing cause of cardiac arrest the skilled practitioner can rule in / out massive pulmonary embolus, look for pericardial effusion, and assess overall cardiac contractility and filling status. Pleural spaces can be assessed, free fluid can be sought in the abdomen, and abdominal aortic aneurysm can be ruled out [10].

CTPA or echocardiography will reliably diagnose massive PE [11].

Identifying and treating the underlying pathology

Consider the type of arrest, and any pre-hospital clinical context or history that can be obtained. VF / VT can occur post ischaemia. PEA often occurs post PE or secondary to hypovolaemia or hypoxia.

PCI should be considered in all post arrest patients in whom an acute coronary syndrome is suspected. Thrombolysis should be considered if PCI is not available.

If PE is suspected thrombolysis may be indicated without confirmatory investigations, if there is no other obvious pathology 50 mg alteplase as a bolus is recommended by the British Thoracic Society [11].

However: without specific indications there is no role for routine thrombolysis following out of hospital (OOH) arrest. One large study was terminated early due to futility [12].

Post-arrest hypothermia

Mild induced hypothermia is neuroprotective and improves outcome after a period of global cerebral hypoxia-ischaemia. It may suppress the inflammatory cascade associated with reperfusion injury post arrest and there is some evidence that all survivors of cardiac arrest benefit in terms of mortality and neurological outcome from mild hypothermia [3,13].


However, a recent large (939 patients included in analysis) multicentre study has led to controversy showing no survival or neurological outcome benefit from mild hypothermia versus controlled normothermia. The authors argue that the prevention of pyrexia, rather than cooling per se, has led to the outcome differences observed in earlier studies [15].

Based on this TTM trial [15], Resus Council UK has advised targeted temperature management along with the The Advanced Life Support Task Force of the International Liaison Committee on Resuscitation (ILCOR) [5,14]:

  • Maintain a constant, target temperature between 32°C and 36°C for those patients in whom temperature control is used.
  • TTM is recommended for adults after OHCA with an initial shockable rhythm who remain unresponsive after ROSC.
  • TTM is suggested for adults after OHCA with an initial nonshockable rhythm who remain unresponsive after ROSC.
  • TTM is suggested for adults after IHCA with any initial rhythm who remain unresponsive after ROSC.
  • If targeted temperature management is used, it is suggested that the duration is at least 24 h.

The physiological effects and complications of hypothermia such as increased systemic vascular resistance, arrhythmias, diuresis, electrolyte abnormalities, coagulopathy etc need to be managed carefully.

Consensus is that pyrexia must be prohibited post cardiac arrest. It is common in the first 48 hours and the risk of a poor neurological outcome increases with each degree rise over 37 degrees centigrade [3].

Making realistic treatment decisions and predicting prognosis

1. Clinical neurological findings

Retention of any neurological function (e.g. respiratory effort, pupillary light reflex, coughing/swallowing) immediately after CPR is a predictor of good functional outcome [8].

Absent pupillary light reflexes and an absent motor response to pain are of no value in prognosticating in the first few hours post ROSC. But by 72 hours, both are independently predictive of poor outcome [5].

Myoclonic jerks is a very poor prognostic indicator and is used by many physicians in the emergency department as an indicator to support withdrawal of life support [16,17]. However some case reports have contradicted this study [8].

Pathophysiological factors (e.g. hypoglycaemia) and interventions (hypothermia, sedation, atropine administration) will affect the neurological exam and must be considered [3].

2. Comorbidities and age

Advanced age probably increases the short-term mortality post cardiac arrest but importantly does not predict neurological outcome in cardiac arrest survivors [3].

Advanced age and a PEA rhythm combined are significant predictors of poor outcome [8].

Poor outcome is also associated with diabetes, sepsis prior to cardiac arrest, cancer, stroke, or being housebound before cardiac arrest. These, again, have not been found to be reliable predictors of neurological outcome in survivors [3].

3. Type of arrest

A non-cardiac cause of arrest, or asystole as the initial rhythm on commencement of CPR, are unreliable as predictors of poor outcome [3].

4. Downtime, delay to start of CPR, and quality of CPR

Several studies have shown an association with poor outcome with increasing time interval between collapse and start of CPR and/or from the start of CPR to return of spontaneous circulation.

Increasing number of shocks or adrenaline doses correlate with poorer neurological outcome [8].

A low ETCO2 of less than 10 mmHg during resuscitation (i.e. CO2 as a marker of cardiac output during CPR) is associated with poor outcome [3], as is a low PaO2 after ROSC [8].

5. Early blood gas interpretation

The pH on the initial ABG has not been correlated with survival. High lactate levels have been associated with severe neurological impairment in one study but a lactate has to be >16 to give 100% specificity for poor neurological outcome after ROSC [18].

6. CT Brain

The performance of a CT brain has not been shown to affect outcome and should only be done immediately post ROSC if a specific pathology is being sought.


As a rule, post ROSC comatose patients without significant pre-arrest co-morbidities should be taken to the ICU for supportive care and their individual prognosis decided later by the intensive care team.

The best predictor of outcome we have is neurological outcome at 72 hours. Perhaps delaying prognostication in individual patients until 72 hours post ROSC may limit the problem that perception of a likely adverse outcome may well create a self-fulfilling prophecy [3].

Safety pearl

Liaising with hospital colleagues to optimise multi-disciplinary input

A careful but succinct verbal and written hand over of potential causative diagnoses, treatments given / planned, and what has been discussed with relatives, is crucial when handing over care of any critically ill patient. Though the importance of verbal and written handover is obvious, both are often neglected where time-critical care of the post arrest patient is being undertaken.


  • All critically ill patients demand physician presence at the bedside so rapid reassessment of clinical response to interventions can be made. They cannot be managed from afar
  • Post arrest patients have a conflicting need to perfuse the post-ischaemic brain without too much strain on the postischaemic heart
  • The need for adequate sedation must be balanced against the risk of worsening cardiovascular instability
  • An unconscious patient is at great risk of unrecognised hypoglycaemia, so glycaemic control must be done carefully
  • Pyrexia is common post arrest and must be avoided as it correlates with a worse neurological outcome
  • Absent pupillary reflexes and absent motor response to pain are of no prognostic value soon after ROSC (but are of value at 72 hours)
  • Advancing age does NOT predict poorer neurological outcome in patients with ROSC post cardiac arrest
  • pH on initial ABG is not correlated with cardiac arrest survival
  • The perception of a poor outcome being likely may well affect the resuscitative teams efforts and become a self-fulfilling prophecy

Withdrawal of life sustaining treatment (WLST) and withholding care are generally regarded as ethically equivalent.

Withdrawal of life sustaining treatment (WLST) or withholding treatment are regarded as omissions, not acts, and life prolonging treatment may lawfully be withdrawn or withheld if deemed not in the patient’s best interests.

Likewise there is no legal obligation to give treatment if it is futile or deemed burdensome to the individual patient.

Who makes the withdraw / withhold decision?

An adult with capacity can refuse treatment even when this may result in harm or death. Few patients post cardiac arrest have capacity.

The terms of a valid advance decision or the views of an individual with lasting power of attorney for the patient must be followed. In both cases the documentation must specify that issues relating to life sustaining treatment are included within its remit.

When there is no capacity, attorney, or advance decision, the final decision rests with the most senior clinician caring for the patient. This should be a best interests decision but the views of those closest to the patient should be sought to make this.

If the patient does not have capacity, and there is doubt about the appropriateness of providing a treatment which has potential to be of benefit to the patient, it should be started until a clearer assessment can be made [19].

I am text block. Click edit button to change this text. Lorem ipsum dolor sit amet, consectetur adipiscing elit. Ut elit tellus, luctus nec ullamcorper mattis, pulvinar dapibus leo.

Key Learning Points
  • O2 sats of 94-98% and normocapnia should be aimed for. (Sackett strength D)
  • A MAP of 65-100 should be aimed for. (Sackett strength D)
  • Tight glycaemic control is not recommended, as the patient is then at higher risk of missed hypoglycaemia. (Sackett B) Hyperglycaemia must also be avoided. (Sackett B2a)
  • Clearance of lactate demonstrates physiological response to therapy and is an independent predictor of mortality. (Sackett B)
  • CTPA or echo will reliably diagnose massive PE. (Sackett B)
  • There is no role for routine thrombolysis following out of hospital cardiac arrest. (Sackett A1b)
  • Selecting and maintaining a constant, target temperature between 32°C and 36°C for at least 24 hours, in patients with out-of-hospital or in-hospital cardiac arrests who are unresponsive after ROSC, is recommended. Hyperthermia (>= 37.6 degree centigrade) should be avoided.
  • Absent pupillary or corneal reflexes, absent or extensor motor responses to pain are the best predictors of poor prognosis, but only at 72 hours after cardiac arrest
  • Myoclonus status epilepticus in the first day after cardiac arrest predicts poor prognosis. (Sackett B2a)
  • Retention of any neurological function (e.g. respiratory effort, coughing/swallowing, pupillary light reflex) after cardiac arrest is predictive of a good functional outcome. (Sackett B2b)
  • An arterial lactate must be more than 16 to be 100% specific for poor neurological outcome (Sackett B2b)
  • Generally, post ROSC comatose patients without significant pre-arrest co-morbidities should be taken to the ICU for supportive care and their individual prognosis decided later by the intensive care team.
  • Where there is no capacity, attorney, or advance decision, the final decision as to withdraw / withhold treatment lies with the most senior clinician caring for the patient, and should be a best interests decision made with the input of those closest to the patient.
  1. Key statistics from the National Cardiac Arrest Audit 2018/19
  2. Perkins GD, Brace-McDonnell SJ On behalf of the OHCAO Project Group. The UK Out of Hospital Cardiac Arrest Outcome (OHCAO) project.
  3. Neumar RW, Nolan JP et al. Post-Cardiac Arrest Syndrome: Epidemiology, Pathophysiology, Treatment and Prognostication. A Consensus Statement From the International Liaison Committee on Resuscitation (American Heart Association, Australian and New Zealand Council on Resuscitation, European Resuscitation Council, Heart and Stroke Foundation of Canada, Inter American Heart Foundation, Resuscitation Council of Asia, and the Resuscitation Council of Southern Africa); the Council on Cardiovascular Surgery and Anesthesia; the Council on Cardiopulmonary, Perioperative, and Critical Care; the Council on Clinical Cardiology; and the Stroke Council. Circulation 2008;118:2452-2483; originally published online Oct 23, 2008
  4. BTS Guideline for oxygen use in healthcare and emergency settings, 2019
  5. Resus Council UK guidelines: Post-resuscitation care, 2015
  6. Walls RM, Murphy MF. Manual of Emergency Airway Management, 3rd Ed. Philadelphia: Lippincott, Williams & Wilkins, 2008.
  7. Kennedy A, Soar J. Management of glucose post-cardiac arrest. Best BETS 29/8/2005.
  8. Kaye P. Early prediction of individual outcome following cardiopulmonary resuscitation: systematic review. Emerg Med J 2005;22:700-705.
  9. Gnanesegaram D, Hughes N. Lactate Clearance a better predictor of mortality than Initial Lactate Level. BestBETS: 19/9/2008.
  10. Wright J, Jarman R, Connolly J et al. Echocardiography in the Emergency Department. Emerg Med J 2009;26:82-96.
  11. British Thoracic Society Standards of Care Committee Pulmonary Embolism Guideline Development Group. Guidelines for the management of suspected acute pulmonary embolism. Thorax 2003;58:470-484.
  12. Bottiger BW, Arntz HR, Chamberlain DA et al. Thrombolysis during Resuscitation for Out-of-Hospital Cardiac Arrest. N Eng J Med 2008;359:2651-2662.
  13. Donnino, M.W., et al., Temperature Management After Cardiac Arrest: An Advisory Statement by the Advanced Life Support Task Force of the International Liaison Committee on Resuscitation and the American Heart Association Emergency Cardiovascular Care Committee and the Council on Cardiopulmonary, Critical Care, Perioperative and Resuscitation.
  14. Targeted Temperature Management After Cardiac Arrest , 2019. Statement by the Advanced Life Support Task Force of the International Liaison Committee on Resuscitation following publication of the HYPERION trial.
  15. Nielsen, N., et al., Targeted temperature management at 33 degrees C versus 36 degrees C after cardiac arrest. N Engl J Med, 2013. 369(23): p. 2197-206.
  16. Wijdicks, EF, Hijdra A, Young GB et al. Practice Parameter: Prediction of outcome in comatose survivors after cardiopulmonary resuscitation (an evidence-based review). Neurology 2006;67:203-210.
  17. Wijdics EF, Parisi JE, Jarbrough FW. Prognostic value of myoclonus status in comatose survivors of cardiac arrest. Annals of Neurology 2006;35(2):239-243.
  18. Mullner M, Sterz F, Domanovits H et al. The association between blood lactate concentration on admission, duration of cardiac arrest, and functional neurological recovery in patients resuscitated from ventricular fibrillation cardiac arrest. Intensive Care Medicine 1997;23(11):1138-1143.
  19. General Medical Council UK. Treatment and care towards the end of life: good practice in decision making. London, GMC.