Introduction

Patients suffering from cardiac arrest in the community and surviving it are frequently transferred to a cardiothoracic centre where further investigations and treatment are possible. The majority of these patients have already been intubated and ventilated, and are transferred directly to an angiography laboratory where percutaneous interventions are performed. Once the investigations and treatment in the angiography laboratory are completed the patients are then transferred to the cardiothoracic intensive care unit for further management.

With the advent and increasing availability of mechanical circulatory support (MCS) devices (including mechanical chest compression devices (MCCD) and extracorporeal membrane oxygenation (ECMO)/extracorporeal CPR (ECPR)) there are likely to be increasing numbers of out-of-hospital cardiac arrest patients transported to hospitals whilst still in cardiac arrest. Critical care clinicians must be comfortable with continuing high quality CPR and ACLS and with the operation of MCS devices.

Survival

Survival after out-of-hospital cardiac arrest (OHCA) is increasing but remains low, and varies across geographic regions and institutions. Where outcomes have improved it appears to be in younger patients and in those who have an initial shockable rhythm. This has been attributed to a focused improvement in each of basic life support (BLS), advanced cardiac life support (ACLS) and post-resuscitation care (PRC) – the elements that form a continuum of links in the ‘chain of survival’ (Figure 25B.1) outlined by the International Liaison Committee on Resuscitation (ILCOR):

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  early recognition and call for help to prevent cardiac arrest;

  
  
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  early cardiopulmonary resuscitation (CPR) to buy time;

  
  
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  early defibrillation to restart the heart;

  
  
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  post-resuscitation care to restore quality of life.

Figure 25B.1 Chain of survival, courtesy of the Adult Basic Life Support Guidelines of the Resuscitation Council.

ILCOR publishes a five yearly update to the International Consensus on cardiopulmonary resuscitation (CPR) and emergency cardiovascular care (ECC) Science with Treatment Recommendations (CoSTR). This document forms the basis for guidelines that are subsequently produced and endorsed by member organisations. An in-depth discussion of basic and advanced life support is beyond the scope of this chapter.

Strategies that have led to increased survival in a variety of settings have included systematic community based projects to enhance first responder CPR training, increased numbers of public access automated external defibrillators (AEDs) and protocolised in-hospital care pathways.

The Post-cardiac Arrest Syndrome

Overall survival and long-term outcomes after OHCA are related to the underlying cause of the arrest, the hypoxaemic/ischaemic insult to the brain and other organs during the period of circulatory arrest, and to the severity of the post-cardiac arrest syndrome (PCAS) that occurs with reperfusion – in the setting of a return of spontaneous circulation (ROSC) or with institution of MCS.

Post-cardiac arrest care begins immediately on reinstitution of circulation. Some patients with a readily reversible cause and short duration of cardiac arrest will suffer very little, if any, systemic insult. Immediate goals of treatment having achieved restoration of circulation (ROSC or MCS) include the diagnosis and management of the underlying cause of the cardiac arrest in order to prevent recurrence, minimising ongoing injury from both the cardiac arrest itself and the insults from reperfusion injury, and multiple organ support.

Four key components of PCAS have been described:

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  Post-cardiac arrest brain injury;

  
  
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  Post-cardiac arrest myocardial dysfunction;

  
  
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  Systemic ischaemia/reperfusion response;

  
  
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  Persistent precipitating pathology.

Post-cardiac Arrest Brain Injury

The brain is particularly vulnerable to hypoxic ischaemic injury in the setting of circulatory arrest. Reperfusion is associated with an ongoing cascade of cerebral injury. Mechanisms are incompletely understood but are thought to include: disruptions to calcium homeostasis, excitotoxicity, alterations in membrane permeability with resultant cellular oedema, free radical generation, mitochondrial dysfunction and activation of apoptotic pathways. Cerebrovascular autoregulation may be impaired for an extended period of time following cardiac arrest.

Clinical findings in post-cardiac arrest brain injury include coma, seizures, myoclonus, neurocognitive dysfunction and in the most severe cases, brain death. Post-cardiac arrest brain injury is the leading cause of morbidity and mortality after cardiac arrest. The protracted pattern of neuronal cell death suggests a wide therapeutic window with multiple potential pharmacological and physiological interventions to optimise outcome. To date, only therapeutic temperature management has shown any likelihood of improved outcomes. Post-cardiac arrest brain injury may be compounded by the other features of PCAS (persistent cardiovascular instability, complications from systemic ischaemia-reperfusion (hypo/hypergycaemia, hyperthermia), and persistent precipitating pathology (hypoxaemia)) as well as potentially by therapeutic interventions (hypo/hypercarbia, hyperoxia).

Post-cardiac Arrest Myocardial Dysfunction

Haemodynamics in the immediate post-ROSC setting can be extremely labile, reflecting circulating endogenous and exogenous catecholamines, and an ischaemia-reperfusion injury to the myocardium (regardless of the initial cause of arrest). Following cardiac arrest there is a period of myocardial ‘stunning’ that occurs despite evidence of preserved coronary blood flow (where coronary ischaemia was not the primary cause of cardiac arrest) characterised by global hypokinesis and elevated filling pressures. Observational data and animal studies suggest that this reversible period of myocardial stunning lasts for up to 72 hours.

Clinically this can manifest as dysrhythmia, hypotension and evidence of a low cardiac output state with systemic hypoperfusion. Treatment is supportive and can include judicious fluid administration, inotropes, vasopressors, temporary pacing and MCS (intra-aortic balloon counterpulsation pump (IABP), venoarterial ECMO or left ventricular assist device (LVAD)). Cardiovascular instability and complications remain a leading cause of death in patients who survive an initial cardiac arrest.

Systemic Ischaemia-Reperfusion Response

Circulatory arrest prevents tissue oxygen and nutrient delivery and metabolic waste removal. Even with continuous CPR there is an accumulated systemic oxygen debt that causes endothelial activation and cellular (and subsequently organ) dysfunction and results in generalised activation of the inflammatory and coagulation cascades. The endothelial glycocalyx appears to play a central role in these processes. Systemic hypoperfusion may self-propagate and progress even with reinstitution of circulation due to post-cardiac arrest myocardial dysfunction, vasodilatation and microcirculatory failure. This ‘systemic inflammatory response syndrome’ (SIRS) shares many features with sepsis and can result in the clinical appearance of relative hypovolaemia (with interstitial oedema and capillary leak), abnormal circulatory autoregulation, impaired oxygen delivery and uptake, and an increased susceptibility to infection. The severity of the syndrome and markers of inflammation are associated with a poorer prognosis.

Persistent Precipitating Pathology

Primary myocardial disease is the most common cause of OHCA. However, circulatory arrest can be the presenting feature or final common pathway in any number (if not all) pathologies. More common etiologies can include the following:

Respiratory

pulmonary embolus; pneumothorax; hypoxaemia – drowning, aspiration, asphyxiation; end-stage chronic obstructive airways disease (COAD), asthma

Neurological

subarachnoid haemorrhage (SAH), cerebrovascular accident, prolonged seizures

Sepsis

Metabolic

including electrolyte abnormalities and temperature derangement

Trauma

hypovolaemia (haemorrhage), tension pneumothorax, tamponade

Toxicology

envenomation and overdoses

Where cardiac arrest has occurred as a result of a systemic illness, the likelihood of sustained ROSC when the underlying pathology has not been treated is remote. Addressing potentially reversible causes remains a key component of ACLS resuscitation algorithms with the 4 Hs and 4 Ts mnemonic:

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  Hypoxia

  
  
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  Hypovolaemia

  
  
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  Hypokalaemia/hyperkalaemia/other metabolic

  
  
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  Hypothermia/hyperthermia

  
  
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  Thrombosis – coronary or pulmonary

  
  
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  Tension pneumothorax

  
  
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  Tamponade – cardiac

  
  
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  Toxins

Assessment of likely antecedent cause(s) for the cardiac arrest must occur contemporaneously with ACLS and post-resuscitation care. This involves collateral history from first responders, paramedics, family members and medical staff as well as a focused clinical examination and investigations where appropriate.

Persistent precipitating pathology can both confound and complicate management of the post-cardiac arrest patient. Asphyxiation is associated with more severe cerebral oedema and post-cardiac arrest brain injury than other causes of circulatory arrest. A SIRS response in the setting of sepsis may potentiate the haemodynamic instability and multiple organ dysfunction associated with systemic ischaemia-reperfusion. Acute coronary syndrome (ACS) as a cause for cardiac arrest will exacerbate post-arrest myocardial dysfunction, and early percutaneous coronary intervention has been associated with improved neurologically intact survival.

Intensive Care Management

The intensive care management of OHCA patients involves the diagnosis and treatment of the underlying cause for the arrest, managing subsequent cardiovascular dysfunction, minimising and managing any further organ damage, and prognostication. Critical care physicians are increasingly involved in the very early management of cardiac arrest patients – as part of rapid response teams (RRTs) attending in-hospital cardiac arrest (IHCA) and as an integral part of protocolised in-hospital care pathways for OHCA patients.

Due to a relative paucity of high quality research in post-resuscitative care, there are only limited data to support specific interventions. However, several hospital level critical care interventions have consistently been associated with improved outcomes after OHCA (see Figure 25B.2):

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  Early percutaneous coronary intervention (PCI);

  
  
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  Targeted temperature management (TTM);

  
  
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  Delayed prognostication before withdrawal of cardiorespiratory supports.

Figure 25B.2 Post-resuscitation care algorithm. SBP systolic blood pressure; PCI percutaneous coronary intervention; CTPA computerised tomography pulmonary angiogram; ICU intensive care unit; MAP mean arterial pressure; ScvO₂ central venous oxygenation; CO/CI cardiac output/cardiac index; EEG electroencephalography; ICD implanted cardioverter defibrillator.

Image courtesy of Elsevier Limited.

A Practical Approach

Assessment and management of the post-ROSC OHCA patient should occur simultaneously, using a team-based approach with an initial focus on the airway, breathing and circulation. History, examination, investigations and treatment should occur contemporaneously.

In the unconscious patient collateral history must be obtained from first responders, paramedic and emergency staff, medical records, and family members.

Physical examination should focus on excluding persistent precipitating pathologies and an assessment of the adequacy of circulation and end-organ perfusion.

Important investigations to aid diagnosis and subsequent management include the following:

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  12-lead electrocardiogram (ECG): to identify evidence of coronary ischaemia, abnormal conduction such as a prolonged QT interval, or right heart strain (suggestive of a pulmonary embolus).

  
  
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  Transthoracic echocardiography (TTE): ultrasound is playing an increasing role in emergency and critical care medicine and is now incorporated into ALS algorithms. Early focused and/or formal TTE may help to differentiate the aetiology of OHCA and guide treatment decisions.

  
  
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  Blood tests: these include a full blood count, a blood group and screen, electrolytes, urea and creatinine, troponin, and early arterial blood gas to help establish the cause of the arrest, assess the severity of insults and provide baseline information. Toxicology analysis may be considered.

  
  
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  Chest X-ray: evaluation of primary pulmonary pathology, potential injuries sustained during resuscitation and the correct position of an endotracheal tube and central vascular access.

  
  
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  Computerised tomography (CT) brain/chest: may reveal intracranial haemorrhage as the cause of the arrest, or cerebral oedema as a result of ischaemic-hypoxic injury. In selected patients a CT chest scan may reveal a pulmonary embolus or aortic pathology.

Treatment algorithms should include general management of the OHCA patient and specific interventions depending on the cause of the arrest.

Early Percutaneous Coronary Intervention (PCI)

In patients where there is not an obvious non-cardiac cause of arrest, early PCI is associated with improved overall survival, and improved neurological outcomes. This includes patients without obvious ST segment elevation myocardial infarction (STEMI).

However, routine PCI in OHCA involves significant resource utilisation and further randomised controlled trials are required to clearly define the optimum timing and role for PCI in this cohort (Table 25B.1).

Table 25B.1 Percutaneous coronary intervention

Emergency coronary angiography is reasonable for select (e.g. electrically or haemodynamically unstable) adult patients who are comatose after OHCA of suspected cardiac origin with ST elevation on ECGb

Emergency coronary angiography is reasonable for select (e.g. electrically or haemodynamically unstable) adult patients who are comatose after OHCA of suspected cardiac origin but without ST elevation on ECGd

^a Class I, Level of Evidence B – randomised studies.

^b Class I, Level of Evidence B – non-randomised studies.

^c Class I, Level of Evidence C – expert opinion.

^d Class IIa, Level of Evidence B – non-randomised studies.

^e Class IIa, Level of Evidence C – limited data.

^f Class IIa, Level of Evidence C – expert opinion.

^g Class IIb, Level of Evidence B – non-randomised studies.

^h Class IIb, Level of Evidence C – expert opinion.

ⁱ Class III, Level of Evidence B – non-randomised studies.

^j Class III, Level of Evidence C – limited data.

Haemodynamics

Invasive arterial monitoring is recommended for continuous assessment of blood pressure, titration of fluids/vasoactive agents and to facilitate blood sampling. Large bore peripheral access may be used for fluid administration to correct any hypovolaemia. Where vasoactive agents (inotropes/vasopressors) are being considered, a central venous line should be inserted.

There is no evidence that defines an optimal target for mean arterial pressure (MAP). The aim should be to deliver adequate coronary, cerebral and systemic organ perfusion that is balanced against increasing the metabolic demands of an already stressed heart through the use of fluids and vasoactive agents. A recent meta-analysis associated higher MAP with improved neurological outcome but it is not clear that improving MAP was responsible for the improved outcomes.

MCS theoretically offers improved systemic and coronary perfusion without necessarily increasing myocardial oxygen consumption. The role of the intra-aortic counterpulsation balloon pump (IABP) remains controversial; and newer devices including ECMO and left ventricular assist devices (LVADs) are being used in selected patients in some specialist centres.

Routine antiarrhythmic prophylaxis is not recommended in the absence of persistent dysrhythmia.