Post Cardiac Arrest Care

The management of the patient after return of spontaneous circulation. Achieving a pulse is the beginning rather than the end of the resuscitation, and the majority of deaths after successful resuscitation occur in the following days from brain injury and from myocardial dysfunction rather than from re arrest.

Post cardiac arrest syndrome, comprising four components

• Post cardiac arrest brain injury, which is the leading cause of death in out of hospital arrest survivors. It results from the initial ischaemia and from reperfusion injury with excitotoxicity, calcium influx, free radical generation and disrupted cerebral autoregulation. Cerebral blood flow becomes pressure passive, so hypotension directly causes further brain injury and normal blood pressure becomes a neuroprotective intervention.
• Post cardiac arrest myocardial dysfunction, with global hypokinesia and a reduced ejection fraction appearing within minutes and typically recovering over 48 to 72 hours. It is reversible and is supported through rather than treated definitively.
• Systemic ischaemia and reperfusion response, which is a sepsis like state with cytokine release, vasoplegia, capillary leak, coagulopathy and adrenal insufficiency.
• The persisting precipitating pathology, which is most often coronary occlusion and which must be identified and treated.

Why the first hours matter disproportionately

Hypotension, hypoxia, hyperoxia, hypocapnia, hyperthermia and hypoglycaemia after return of circulation each independently worsen neurological outcome, and all are iatrogenic and preventable. The essential message is that overshooting is as harmful as undershooting.

• Return of spontaneous circulation with a palpable pulse and a measurable blood pressure.
• A spectrum of consciousness from fully alert to deep coma. Most patients are initially comatose.
• Haemodynamic instability with hypotension, which is present in the majority.
• Arrhythmia and a risk of re arrest.
• Evidence of the precipitating cause: chest pain, electrocardiographic changes, respiratory failure, sepsis, haemorrhage.
• Seizures and myoclonus, which occur in up to a third and which are associated with severe brain injury, although status myoclonus is no longer considered independently sufficient to predict a poor outcome.
• Pulmonary oedema, aspiration pneumonitis and rib and sternal fractures from compressions.

• Continuous monitoring of rhythm, blood pressure, oxygen saturation, temperature and where possible end tidal carbon dioxide.
• Twelve lead electrocardiogram immediately, and repeated. This is the single most important early investigation, since a substantial proportion of arrests are coronary in origin.
• Capillary blood glucose.
• Arterial blood gas, with an arterial line inserted where possible for continuous pressure monitoring and repeated sampling.
• Full blood count, urea, electrolytes, creatinine, magnesium, calcium, liver function, coagulation screen, lactate and troponin.
• Chest radiography to confirm the depth of the endotracheal tube, to identify pulmonary oedema, aspiration, pneumothorax and rib fractures, and to confirm central line position.
• Echocardiography to assess ventricular function, to identify regional wall motion abnormality, tamponade and right ventricular strain.
• Computed tomography of the head where the cause is unclear, where there was a preceding headache or neurological event, or where trauma occurred, since intracranial haemorrhage is an under recognised cause of arrest.
• Computed tomography pulmonary angiography where pulmonary embolism is suspected.
• Toxicology where poisoning is possible.
• Coronary angiography, which is performed urgently in ST elevation and in unstable patients with a suspected coronary cause. In stable patients without ST elevation, immediate angiography has not shown a survival benefit over a delayed strategy and can be deferred.
• Electroencephalography where seizures are suspected or where the patient remains comatose, since non convulsive status epilepticus occurs and is treatable.

Immediate priorities

• Activate or retain the resuscitation team, since re arrest is common in the first minutes.
• Monitor and support airway, breathing and circulation, and remain prepared to resume compressions and defibrillation.
• Full vital signs including blood pressure, pulse, respiratory rate, oxygen saturation, temperature and blood glucose.

Optimise ventilation and oxygenation

• Consider an advanced airway with waveform capnography in the patient who is not following commands or who cannot protect the airway.
• Titrate the inspired oxygen fraction to the minimum required to maintain a saturation of 94 to 98 percent. Do not leave the patient on 100 percent oxygen. Hyperoxia generates free radicals, worsens reperfusion injury and is associated with increased mortality, and the reflex to leave the oxygen at maximum after a successful resuscitation is a genuine and common harm.
• Ventilate at 10 to 12 breaths per minute, that is one breath every 5 to 6 seconds, targeting an end tidal carbon dioxide of 35 to 45 mmHg and a normal arterial carbon dioxide.
• Avoid hyperventilation. Hypocapnia causes cerebral vasoconstriction, reduces cerebral blood flow in an already injured brain, and raises intrathoracic pressure with reduced venous return. Deliberate hyperventilation has no place unless there is documented raised intracranial pressure with herniation, and even then only as a brief bridge.
• Use lung protective ventilation with a tidal volume of 6 to 8 mL/kg predicted body weight.

Treat hypotension

Defined as a systolic pressure below 100 mmHg or a mean arterial pressure below 65 mmHg. Hypotension after arrest is common and directly worsens neurological outcome, so it is corrected promptly.

• Give an intravenous or intraosseous fluid bolus of 1 to 2 litres of Ringer lactate or Hartmann solution, unless contraindicated by pulmonary oedema or renal failure. Give it in aliquots with reassessment rather than as a single unmonitored infusion.
• If there is no response to fluid, or if fluid is contraindicated, start a vasopressor infusion:
• Noradrenaline 0.1 to 0.5 micrograms/kg/min, which is approximately 7 to 35 micrograms/min in a 70 kg adult, titrated to effect.
• Adrenaline 0.1 to 0.5 micrograms/kg/min as an alternative, particularly where myocardial dysfunction with a low cardiac output coexists, since it provides inotropy as well.
• Dobutamine 2.5 to 20 micrograms/kg/min where there is demonstrated myocardial dysfunction with a low cardiac output despite adequate filling and pressure.
• Target a mean arterial pressure of at least 65 mmHg, and higher, at 80 mmHg or above, in patients with chronic hypertension or where perfusion markers remain poor.
• Judge adequacy by urine output above 0.5 mL/kg/hour, a normal or falling lactate, and improving mental status, rather than by the number on the monitor alone.
• Insert an arterial line for continuous monitoring, and central venous access for vasopressors, without delaying peripheral vasopressor initiation.
• Insert a urinary catheter for hourly output measurement.

Identify and treat the cause

• Obtain a twelve lead electrocardiogram immediately if a cardiac cause is likely.
• Consult an interventional cardiologist immediately for ST elevation, for unstable cardiogenic shock, and where mechanical circulatory support may be required.
• Work systematically through the reversible causes again: hypoglycaemia, hypovolaemia, hypoxia, acidosis, hypokalaemia and hyperkalaemia, hypothermia, tension pneumothorax, tamponade, toxins, pulmonary thrombosis and coronary thrombosis. A cause that was missed during the arrest is frequently identifiable once there is a circulation and time to look.

Temperature management

• Prevent fever actively. Target a temperature of 37.5 degrees Celsius or below for at least 36 hours in every patient who remains unresponsive to verbal commands after return of circulation. Fever after arrest is common and is independently associated with worse neurological outcome.
• Use antipyretics, surface cooling, cooled intravenous fluids and where available a feedback controlled cooling device.
• Avoid and treat shivering, which raises metabolic demand and defeats cooling: use adequate sedation, magnesium, and neuromuscular blockade if necessary.
• Deliberate deep hypothermia to 33 degrees Celsius has not been shown superior to strict normothermia in recent trials, and current practice emphasises avoidance of fever rather than induced hypothermia. Whichever is chosen, avoid rebound hyperthermia during and after rewarming, and rewarm slowly at no more than 0.25 to 0.5 degrees per hour.

Other supportive measures

• Sedation and analgesia to facilitate ventilation and temperature control, using short acting agents that permit neurological assessment, such as propofol and fentanyl infusions.
• Seizure treatment: benzodiazepine followed by levetiracetam or sodium valproate. Do not use prophylactic anticonvulsants.
• Glycaemic control targeting 7.8 to 10 mmol/L, avoiding both hyperglycaemia and hypoglycaemia, which is particularly damaging to the injured brain.
• Correct electrolytes, particularly potassium and magnesium, since arrhythmia risk is high.
• Head elevation to 30 degrees.
• Venous thromboembolism prophylaxis once bleeding risk allows.
• Stress ulcer prophylaxis and early enteral nutrition.
• Treat aspiration pneumonitis and consider antibiotics where there is evidence of aspiration or infection.

Transfer

Once stable, transfer to a critical care or coronary care unit connected to a defibrillator, with continuous monitoring and an escort capable of managing re arrest. The transfer is a high risk period and requires the same monitoring and preparation as the resuscitation itself.

Neurological prognostication

• Do not prognosticate early. Sedation, hypothermia, organ dysfunction and neuromuscular blockade all confound assessment, and premature withdrawal of treatment is a self fulfilling prophecy that is a genuine cause of avoidable death.
• Delay formal prognostication until at least 72 hours after return of circulation, and longer where sedation or temperature management has been used.
• Use a multimodal approach: bilaterally absent pupillary and corneal reflexes, bilaterally absent N20 somatosensory evoked potentials, a highly malignant electroencephalogram pattern, neuron specific enolase levels, and imaging showing diffuse anoxic injury. No single finding is sufficient.
• Involve the family throughout with honest and repeated communication.

Follow up

Survivors require cardiological assessment including consideration of an implantable defibrillator, rehabilitation, cognitive and psychological assessment given the high rate of memory impairment, anxiety and post traumatic stress, and screening of family members where an inherited arrhythmia syndrome or cardiomyopathy is identified.