Management of Post-Arrest Patients Including Prognostication

The short-term mortality of patients who survive cardiac arrest is high. A recent meta-analysis by Yan et al found that, of all-cause cardiac arrests with return of spontaneous circulation (ROSC) globally, the rate to survival to hospital admission was 22%, and the rate to survival to hospital discharge was 8.8%. [1]

Emergency physicians must be confident managing patients who gain ROSC post arrest to maximise the chance of meaningful recovery.

This session focusses on six key areas for the emergency physician to consider in their initial management of the post-arrest patient.

Introduction

Despite improvements in resuscitative practice and critical care medicine, the short term mortality of patients with ROSC has not improved since the first large study was published in 1953.

This describes the complex pathophysiological processes that occur following whole body ischaemia during cardiac arrest and the subsequent reperfusion response during CPR and following successful resuscitation.

Management must follow an ABCDE approach with assessment and treatment occurring simultaneously.

The response to any intervention must be rapidly and frequently measured, preferably with invasive monitoring.

Airway Patency

Fig.1 Intubation with a pillow under the patient’s head to give a better view of the cords

In the absence of concerns regarding an unstable c-spine injury, a pillow placed under the head and the patient positioned with neck flexed and head extended provides optimal conditions for intubation.

If an airway cannot be maintained by simple measures or is immediately threatened, for example by vomiting or pulmonary oedema, prompt intubation is indicated. If a patent airway can be maintained, the urgency of intubation depends on the patient’s ventilatory status.

Awake patients with appropriate respiratory effort and able to maintain their airway can be monitored without intubation. Those with suboptimal or no respiratory effort should be intubated (if not done already during the arrest). [2]

Breathing

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 gas exchange

While hypoxia is well known to cause increased mortality, there is increasing evidence that prolonged periods of hyperoxia is also harmful, and independently associated with decreased survival to hospital discharge. Target oxygen saturations post-ROSC are 94-98%. [4]

BEWARE of the risk of precipitating vomiting if ventilating without a definitive airway.

Circulation

• Post-arrest patients are a heterogeneous group
• Post-ROSC patients are usually haemodynamically unstable
• Their fluid status and fluid-responsiveness is difficult to judge

The target mean arterial pressure (MAP) should take into account the following:

• Their normal blood pressure
• The estimated cardiac (dys)function
• The cause of cardiac arrest

Current evidence recommends aiming for a MAP of around 65mmHg. [2,5]

Judicious fluid challenges of 125-500ml should be given to optimise pre-load and perfusion with early consideration of inotropic support.

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]

Circulatory Assessment

Arterial line/invasive blood pressure monitoring

An arterial line provides continuous blood pressure monitoring, and facilitates blood gas sampling to track response to therapy.

A swing in the waveform with respiration can suggest under-filling. Invasive cardiac output monitoring can be established via an arterial line (e.g. LiDCO), usually once on the intensive care unit.

Central venous access

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

Most patients post-ROSC should have a central line and arterial line sited if they are felt to be suitable for ongoing resuscitation/intensive supportive care.

Echocardiography

This gives a visual guide to the filling status and the cardiac index of the patient, allowing as ejection fraction estimation to be made. It may also be used to assist in establishing the aetiology of the cardiac arrest: the existence of regional wall abnormalities (in combination with ECG changes) may point towards a primarily cardiac cause, whereas a dilated right ventricle may suggest PE as the underlying cause.

It can be useful early in the management of a patient with ROSC, both diagnostically and by guiding fluid and inotrope/pressor therapy.

However, a suitably skilled clinician must be available to perform and interpret sonographic images.

Non-invasive cardiac output monitoring

Although there is no patient-orientated evidence supporting its use in the emergency department, non-invasive cardiac output monitoring can be rapidly and easily instigated (e.g. via oesophageal or suprasternal doppler) and adds further data aiding circulatory assessment and management.

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

Disability and Glucose Control

Disability

Record the Glasgow coma scale (GCS) prior to administering any sedation – it has implications for prognostication.

If the patient is making inadequate respiratory effort or ‘fighting’ the ventilator then deepening of sedation and/or administration of neuromuscular blockade (e.g. Rocuronium) is required to optimise ventilation.

Seizures occur in 20-30% of post cardiac arrest patients and can cause a three-fold increase in brain metabolism. Routine seizure prophylaxis is not recommended in post-cardiac arrest patients, but any seizures that do occur should be treated aggressively. First line treatments are Levetiracetam or Sodium Valproate. [4]

Short-acting sedating agents are preferred (e.g. propofol) as neurological assessment can be made sooner after a sedation hold [5].

Caution with sedation; most agents can worsen cardiovascular instability.

Glucose control [6]

Tight glycaemic control is not recommended, not least because the comatose patient is at risk of undiagnosed hypoglycaemia. However, hyperglycaemia has been correlated with increasing risk of poor neurological outcome.

Based on the available data, following ROSC, blood glucose should be maintained at <= 10 mmol/ L-1.

Introduction

As the immediate ABCDE priorities are being attended to, consider the five further issues highlighted in the introduction to this session.

What key questions should be considered following a cardiac arrest?

• What caused the arrest?
• What immediate further investigation and treatment is needed?
• What can be done to optimise outcome?
• Do I cool them?
• Is this patient salvageable?
• Is the proposed course of action in the patient’s best interests?
• Who is going to continue caring for this patient and what information do they need?

After initial basic care, five broader areas merit consideration.

Underlying Pathology

It will be necessary to consider the type of arrest, and any pre-hospital clinical context or history that can be obtained.

Ventricular fibrillation (VF)/ventricular tachycardia (VT) can occur as part of acute coronary syndrome, as a primary arrhythmia, due to electrolyte disturbance, poisoning, or electrocution. Pulseless electrical activity (PEA) often occurs post-pulmonary embolus or secondary to hypovolaemia or hypoxia.

The CT pulmonary angiogram shows a large pulmonary embolus. Click on the CT to enlarge.

Percutaneous coronary intervention (PCI) should be considered in all post-arrest patients in whom an acute myocardial infarction (AMI) is strongly suspected regardless of the presence or absence of ST segment elevation of ROSC ECG. A study by Elfwen, et al. found that short and long-term survival rates were improved in those receiving early coronary angiography where OHCA was witnessed and the patient had a shockable rhythm, but where no ST-elevation was demonstrated on the ECG. [4,8,9]

Therapeutic Hypothermia

Mild hypothermia may suppress chemical reactions associated with reperfusion injury post- arrest. Therapeutic hypothermia was in vogue up until recent years where more recent evidence has shown prevention of hyperpyrexia to be associated with better outcomes.

Guidelines have shifted towards supporting targeted temperature management rather than therapeutic hypothermia. TTM aims to maintain temperature between 32-36 degrees Celsius. TTM should be initiated immediately post-ROSC in all patients who remain comatose, regardless of initial rhythm. These measures should be maintained for at least 24 hours.

It is likely that it is the prevention of pyrexia, rather than cooling per se, which leads to outcome differences in the post-arrest patient.

Local preference and guidelines should be followed for exact temperature target but in all cases, pyrexia should be avoided.

Pyrexia must be avoided 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 37oC. [4]

The Advanced Life Support Task Force of the International Liaison Committee on Resuscitation (ILCOR) have recommended that the term Targeted Temperature Management (TTM) replace the historic term Therapeutic Hypothermia.

ILCOR recommend:

1. Maintain a constant, target temperature between 32-36 degrees centrigrade for those patients in whom temperature control is used
2. TTM is recommended for adults after OHCA with an initial shockable rhythm who remain unresponsive after ROSC
3. TTM is suggested for adults after OHCA with an initial non shockable rhythm who remain unresponsive after ROSC
4. TTM is suggested for adults after IHCA with any initial rhythm who remain unresponsive after ROSC
5. If TTM is used, it is suggested that the duration is at least 24 hours

Most ITU clinicians in the UK now use 36 degrees centigrade as the TTM post cardiac arrest.

Treatment Decisions

The following areas will be important in the on going management of a patient post-ROSC:

Clinical neurological findings

Neurological prognostication should be performed using a multimodal strategy, to include clinical examination, electrophysiology, biomarkers and imaging.

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

Fig.1 From: European Resuscitation Council and European Society of Intensive Care Medicine guidelines 2021: post-resuscitation care

Prognostication strategy algorithm. EEG electroencephalography, NSE neuron specific enolase, SSEP somatosensory evoked potential, ROSC return of spontaneous circulation. 1. Major confounders may include sedation, neuromuscular blockade, hypothermia, severe hypotension, hypoglycaemia, sepsis, and metabolic and respiratory derangements. 2. Use an automated pupillometer, when available, to assess pupillary light reflex. 3. Suppressed background ± periodic discharges or burst-suppression, according to ACNS. 4. Increasing NSE values between 24 h-48 h or 24/48 h and 72 h further confirm a likely poor outcome. 5. Defined as a continuous and generalised myoclonus persisting for 30 min or more. *Caution in case of discordant signs indicating a potentially good outcome (see text for details)

Pupillary light reflex and corneal reflex, when both absent together bilaterally, at 72 hours or more post-ROSC, are very specific for poor outcome.

Comorbidities and age

Advanced age has been shown to be associated with worse survival rates in older patients. Neurological outcome also deteriorates with increasing age, but this deterioration isn’t always marked, and older patients have been shown to survive with favourable neurological outcomes.

The general consensus is that biological age should not form part of the decision to withdraw care post-ROSC, as age has no significant predictive value on mortality. [10]

Increasing comorbidity has also been shown to impact the 30-day survival rate after OHCA. This is particularly true of:

• Diabetes
• Renal disease
• Congestive heart failure
• Metastatic carcinoma

Older patients are more like to have comorbidities and so age may indirectly impact survival rates in this way instead. [11] However, there is no significant association between comorbidities and favourable neurological outcome. [12]

Type of arrest

The initial rhythm at first discovery of an out-of-hospital cardiac arrest also affects the prognosis. [13]

• • People experiencing ventricular tachycardia (VT) or ventricular fibrillation (VF) have the greatest chance of survival.
  • People who are found in pulseless electrical activity or asystole have the lowest chance of survival.

Downtime, delay to start of CPR and quality of CPR

Several studies have shown an association between poor outcome and increasing time interval between collapse and start of CPR and/or from the start of CPR to return of spontaneous circulation. [8]

This is also true of poor quality CPR. A low ETCO2of <10mmHg during resuscitation (i.e. CO2 as a marker of cardiac output – and therefore the quality of chest compressions – during CPR) is associated with poor outcome as is a low PaO2 after ROSC. [14]

Learning bite

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

Early blood gas interpretation

Following an OHCA, patients with a favourable outcome have been shown to have lower lactate and high pH values compared with those with an unfavourable outcome, according to retrospective analyses. [15]

In one study, the optimal cut-off point for lactate was found to be 80mg/dL and the pH found to be 7.05. pH is thought to be a better predictor for neurological outcome than lactate levels. [15]

CT/MRI Brain

This set of images shows a selection of CT scans obtained post ROSC. Click on the CTs to enlarge.

Fig 2: CT image of a normal brain	Fig 3: CT image of a posterior fossa bleed	Fig 4: CT image of extradural haematoma with overlying skull fracture

Conclusion

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 function we have is neurological outcome at 72 hours.

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’. [4]

Medico-legal Decisions

Withdrawing and withholding care are generally regarded as ethically equivalent.

Withdrawing 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. [16,17]

Further information can be found from the joint Guidance from the BMA, RCUK and RCN.

Handover Strategies

A careful but succinct verbal and written handover 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.

Whilst this seems obvious, both are often neglected between busy departments, and where rapid time – critical management decisions are being made.

• All critically-ill patients demand physician presence at the bedside so that 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 post-ischaemic 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 cautious glycaemic control is preferred.
• Pyrexia is common post-arrest and must be avoided – 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).
• Advanced age does NOT predict poorer neurological outcome in patients with ROSC post-cardiac arrest.
• a pH lower than 7.05 is associated with a worse outcome post-ROSC.
• The perception of a poor outcome being likely may well affect the resuscitative teams’ efforts and become a ‘self-fulfilling prophecy’.

1. Yan S, Gan Y, Jiang N, Wang R, Chen Y, Luo Z, et al. The global survival rate among adult out-of-hospital cardiac arrest patients who received cardiopulmonary resuscitation: a systematic review and meta-analysis. Crit Care [Internet]. 2020 Dec 22 [cited 2024 May 30];24(1):61.
2. Mangla A, Daya MR, Gupta S. Post-resuscitation care for survivors of cardiac arrest. Indian Heart J. 2014 Jan-Feb;66 Suppl 1(Suppl 1):S105-12. doi: 10.1016/j.ihj.2013.12.028. [cited 2024 May 30].
3. del Castillo J, López-Herce J, Matamoros M, Cañadas S, Rodriguez-Calvo A, Cechetti C, et al. Hyperoxia, hypocapnia and hypercapnia as outcome factors after cardiac arrest in children. Resuscitation. 2012 Dec 1;83(12):1456–61.
4. Nolan JP, Sandroni C, Böttiger BW, Cariou A, Cronberg T, Friberg H, et al. European Resuscitation Council and European Society of Intensive Care Medicine guidelines 2021: post-resuscitation care. Intensive Care Medicine 2021 47:4 [Internet]. 2021 Mar 25 [cited 2024 May 30];47(4):369–421.
5. Skrifvars MB, Ameloot K, Aneman A. Blood pressure targets and management during post-cardiac arrest care. 2023 [cited 2024 May 30];
6. Padkin A. Glucose control after cardiac arrest. Resuscitation. 2009 Jun;80(6):611-2.
7. Towards evidence based emergency medicine: Best BETs from the Manchester Royal Infirmary SEARCH STRATEGY SEARCH OUTCOME. 1950;
8. Elfwén L, Lagedal R, James S, Jonsson M, Jensen U, Ringh M, et al. Coronary angiography in out-of-hospital cardiac arrest without ST elevation on ECG—Short- and long-term survival. Am Heart J. 2018 Jun 1;200:90–5.
9. Dumas F, Cariou A, Manzo-Silberman S, Grimaldi D, Vivien B, Rosencher J, et al. Immediate Percutaneous Coronary Intervention Is Associated With Better Survival After Out-of-Hospital Cardiac Arrest. Circ Cardiovasc Interv [Internet]. 2010 Jun [cited 2024 Jun 4];3(3):200–7.
10. Kovacs E, Pilecky D, Szakal-Toth Z, Fekete-Gyor A, Gyarmathy VA, Geller L, et al. The role of age in post-cardiac arrest therapy in an elderly patient population. Physiol Int [Internet]. 2020 Jul 20 [cited 2024 Jun 4];107(2):319–36.
11. Hirlekar G, Jonsson M, et al. Comorbidity and survival in out-of-hospital cardiac arrest. Resuscitation. 2018 Dec;133:118-123.
12. Terman SW, Shields TA, Hume B, Silbergleit R. The influence of age and chronic medical conditions on neurological outcomes in out of hospital cardiac arrest. Resuscitation. 2015 Apr 1;89(C):169–76.
13. National Institute for Health and Care Excellence (NICE). Cardiac arrest – out of hospital care: | What is the Prognosis? | CKS | [Internet]. [cited 2024 May 31].
14. Kaye P. Early prediction of individual outcome following cardiopulmonary resuscitation: systematic review. Emerg Med J. 2005 Oct;22(10):700-5. [cited 2024 Jun 4];
15. Momiyama Y, Yamada W, Miyata K, Miura K, et al. Prognostic values of blood pH and lactate levels in patients resuscitated from out-of-hospital cardiac arrest. Acute Medicine & Surgery [Internet]. 2017 Jan 1 [cited 2024 Jun 4];4(1):25–30.
16. Decisions relating to cardiopulmonary resuscitation. Guidance from the British Medical Association, the Resuscitation Council (UK) and the Royal College of Nursing.
17. Treatment and care towards the end of life – professional standards – GMC [Internet]. [cited 2024 Jun 4].