Components of the post-cardiac arrest syndrome are shown in Box 8.1.

The severity of the post-cardiac arrest syndrome varies with the duration and cause of cardiac arrest; it may be absent if the cardiac arrest is brief. Post-cardiac arrest brain injury manifests as coma, seizures, myoclonus, varying degrees of neurological dysfunction and brain death. Post-cardiac arrest brain injury may be exacerbated by microcirculatory failure, impaired autoregulation, hypercarbia, hypoxaemia and hyperoxaemia, pyrexia, hyperglycaemia and seizures. Significant myocardial dysfunction is common after cardiac arrest but typically recovers by 2–3 days. The whole body ischaemia/reperfusion that occurs with resuscitation from cardiac arrest activates immunological and coagulation pathways contributing to multiple organ failure and increasing the risk of infection. Thus, the post-cardiac arrest syndrome has many features in common with sepsis, including intravascular volume depletion and vasodilation. About 60% of patients initially comatose after out-of-hospital cardiac arrest (OHCA) will develop pneumonia.

Airway and breathing

Patients who have had brief period of cardiac arrest may recover consciousness, maintain their airway safely and breathe adequately without the need for tracheal intubation. Patients remaining comatose and those with inadequate breathing will need support with mechanical ventilation via a tracheal tube.

Several animal studies indicate that hyperoxaemia causes oxidative stress and harms post-ischaemic neurones. Although the clinical data supporting this phenomenon are inconsistent, current recommendations are to titrate the inspired oxygen concentration to maintain the arterial blood oxygen saturation in the range of 94–98% as soon as arterial blood oxygen saturation can be monitored reliably (by blood gas analysis and/or pulse oximetry (SpO₂)). Adjust ventilation to achieve normocarbia and monitor this using the end-tidal CO₂ with waveform capnography and arterial blood gas values.

Circulation

Coronary artery disease is the most common cause of OHCA and many of these arrests will be associated with ST-segment elevation myocardial infarction (STEMI) for which early reperfusion therapy is required. Reperfusion can be achieved with primary percutaneous coronary intervention (PCI), fibrinolysis or both. Primary PCI is the preferred treatment if a first medical contact-to-balloon time of <90 min can be achieved because it is much more likely to establish full reperfusion than using fibrinolytic therapy. The early post-resuscitation 12-lead electrocardiogram (ECG) is less reliable for predicting acute coronary occlusion than it is in those who have not had a cardiac arrest. Recent evidence suggests that about 25% of patients with no obvious extra cardiac cause for their cardiac arrest but who do not have evidence of STEMI on their initial 12-lead ECG, will have a coronary lesion on angiography that is amenable to stenting. The trend is to consider immediate coronary artery angiography in all OHCA patients with no obvious non-cardiac cause of arrest.

Post-cardiac arrest myocardial dysfunction causes haemodynamic instability, which manifests as hypotension, a low cardiac output and arrhythmias. Early echocardiography will enable the extent of myocardial dysfunction to be quantified. In the ICU, an arterial line for continuous blood pressure monitoring is essential. Treatment with fluid, inotropes and vasopressors may be guided by blood pressure, heart rate, urine output, and rate of plasma lactate clearance and central venous oxygen saturations. Non-invasive cardiac output monitors may help to guide treatment. If treatment with fluid resuscitation and vasoactive drugs is insufficient to support the circulation, consider insertion of an intra-aortic balloon pump. In the absence of definitive data supporting a specific goal for blood pressure, target the mean arterial blood pressure to achieve an adequate urine output (1 ml kg⁻¹ h⁻¹) and normal or decreasing plasma lactate values, taking into consideration the patient’s normal blood pressure, the cause of the arrest and the severity of any myocardial dysfunction.

Brain

In patients surviving to ICU admission but subsequently dying in hospital, brain injury is the cause of death in 68% after OHCA and in 23% after in-hospital cardiac arrest.

Cerebral perfusion

Immediately after ROSC, there is a period of cerebral hyperaemia. After asphyxial cardiac arrest, brain oedema may occur transiently after ROSC but it is associated only rarely with clinically relevant increases in intracranial pressure. Autoregulation of cerebral blood flow is impaired after cardiac arrest; thus, cerebral perfusion varies with cerebral perfusion pressure instead of being linked to neuronal activity. Maintain mean arterial pressure near the patient’s normal level.

Sedation

There are no data to support a defined period of ventilation, sedation and neuromuscular blockade after cardiac arrest; however, patients need to be well sedated during treatment with therapeutic hypothermia, and the duration of sedation and ventilation is influenced by this treatment. Sedation is achieved typically with a combination of opioids and hypnotics. Short-acting drugs (e.g. propofol, alfentanil, remifentanil) will enable earlier neurological assessment. Adequate sedation will reduce oxygen consumption. During hypothermia, optimal sedation can reduce or prevent shivering, which enables the target temperature to be achieved more rapidly. Mild hypothermia reduces clearance of many drugs by at least a third and may make later prognostication unreliable.

Control of seizures

Seizures or myoclonus or both occur in 10–40% of those who remain comatose after cardiac arrest. Although patients with seizures have four times the mortality rate of comatose patients without seizures, good neurological recovery has been documented in 17% of those with seizures. Seizures increase cerebral metabolism by up to threefold and may cause cerebral injury: treat with benzodiazepines, phenytoin, sodium valproate, propofol, or a barbiturate. Myoclonus can be particularly difficult to treat; phenytoin is often ineffective and may be best avoided. Clonazepam is the most effective antimyoclonic drug, but sodium valproate, levetiracetam and propofol can also be effective.

Glucose control

There is a strong association between high blood glucose after resuscitation from cardiac arrest and poor neurological outcome. However, severe hypoglycaemia is associated with increased mortality in critically ill patients and comatose patients are at particular risk from unrecognised hypoglycaemia. Based on the available data and expert consensus, following ROSC, blood glucose should be maintained at ≤10 mmol l⁻¹. Avoid hypoglycaemia (<4.0 mmol l⁻¹).

Targeted temperature management

Pyrexia is common in the first 48 h after cardiac arrest and is associated with poor outcome; therefore, treat any hyperthermia occurring after cardiac arrest with antipyretics or active cooling.

Mild hypothermia is neuroprotective and improves outcome after a period of global cerebral hypoxia-ischaemia. Cooling suppresses many of the pathways leading to delayed cell death, including apoptosis (programmed cell death). Hypothermia decreases the cerebral metabolic rate for oxygen by about 6% for each 1 °C reduction in temperature and this may reduce the release of excitatory amino acids and free radicals.

Which post-cardiac arrest patients should be cooled?

All studies of post-cardiac-arrest therapeutic hypothermia have included only patients in coma. There is good evidence supporting the use of induced hypothermia in comatose survivors of OHCA caused by VF. Two randomised trials demonstrated improved neurological outcome at hospital discharge or at 6 months in comatose patients after out-of-hospital VF cardiac arrest. Cooling was initiated within minutes to hours after ROSC and a temperature range of 32–34 °C was maintained for 12–24 h. The evidence supporting the use of hypothermia after cardiac arrest from non-shockable rhythms and after in-hospital cardiac arrest is much weaker and based only on non-randomised observational studies.

How to cool

The practical application of therapeutic hypothermia comprises induction, maintenance and rewarming. Earlier cooling after ROSC probably produces better outcome. External and/or internal cooling techniques can be used to initiate cooling. An infusion of 30 ml kg⁻¹ of 4 °C 0.9% sodium chloride or Hartmann’s solution decreases core temperature by approximately 1.5 °C and this technique can be used to initiate cooling pre-hospital. Other methods of inducing and/or maintaining hypothermia are listed in Box 8.2.