Return of a spontaneous circulation (ROSC) is an important step in the continuum of resuscitation. However the next goal is to return the patient to a state of normal cerebral function, and to establish and maintain a stable cardiac rhythm and normal haemodynamic function.
Post-cardiac arrest syndrome
The post-cardiac arrest syndrome comprises:
- Post-cardiac arrest brain injury
- manifests as coma, seizures, myoclonus, varying degrees of neurocognitive dysfunction and brain death
- exacerbated by microcirculatory failure, impaired autoregulation, hypotension, hypercarbia, hypoxaemia, hyperoxaemia, pyrexia, hypoglycaemia, hyperglycaemia, seizures
- Post-cardiac arrest myocardial dysfunction
- common after cardiac arrest but typically starts to recover by 2-3 days although full recovery make take significantly longer
- Systemic ischaemia/reperfusion response
- activation of immunological and coagulation pathways contributes to multiple organ failure and increased risk of infection
- Persistent precipitating pathology
The severity of this syndrome will vary with the duration and cause of cardiac arrest. It may not occur at all if the cardiac arrest is brief.
Immediate post-resuscitation management
- Use ABCDE approach
- Airway and Breathing
- Maintain SpO2 94 - 98%
- Establish advanced airway
- Monitor waveform capnography
- Ventilate lungs to normocapnia
- Examine chest
- Ensure correct placement of tracheal tube
- Assess for rib fracture, pneumothorax, flail chest from CPR
- Assess for pulmonary oedema or pulmonary aspiration
- Insert gastric tube to decompress the stomach, prevent splinting of the diaphragm and enable drainage of gastric contents
- Circulation
- Perform 12-lead ECG
- Obtain reliable intravenous access (ideally central venous access)
- Aim for systolic blood pressure (SBP) > 100 mmHg
- Administer fluid (crystalloid) to restore normovolaemia
- Establish intra-arterial blood pressure monitoring
- Consider vasopressor/inotrope to maintain SBP
- Disability and Exposure
- Identify any precipitating cause
- Assess Glasgow Coma Scale score
- Control temperature
- Maintain constant temperature 32 - 36°C
- Sedation to control shivering
Investigations
- Full blood count
- To exclude anaemia as contributor to myocardial ischaemia
- To provide baseline values
- Biochemistry
- To assess renal function
- To assess electrolyte concentrations (K+, Mg2+, Ca2+)
- To ensure normoglycaemia
- To commence serial cardiac troponin measurements
- To provide baseline values
- 12-lead ECG
- To record cardiac rhythm
- To look for evidence of acute coronary syndrome (ACS)
- To look for evidence of old myocardial infarction
- To provide a baseline record
- Chest radiograph
- To establish the position of a tracheal tube, a gastric tube or a central venous catheter
- To check for evidence of pulmonary oedema
- To check for evidence of pulmonary aspiration
- To exclude pneumothorax
- To assess cardiac contour
- Arterial blood gas
- To ensure adequacy of ventilation and oxygenation
- To ensure correction of acid/base balance
- Echocardiography
- To identify contributing causes to cardiac arrest
- To assess LV and RV structure and function
- CT scan
- CT brain to rule out intracranial bleed or stroke as primary cause of cardiac arrest
- CTPA to rule out pulmonary embolism or other respiratory cause of cardiac arrest
- Coronary angiography +/- PCI
- To investigate/treat acute coronary occlusion as cause of cardiac arrest
ICU management
- Maintain normoxaemia and normocapnia with protective ventilation
- Optimise haemodynamics
- mean arterial pressure (MAP)
- lactate
- central venous oxygenation (ScvO2)
- cardiac output/cardiac index (CO/CI)
- urine output (≥ 1 mL/kg/hr)
- Maintain normoglycaemia (4 – 10 mmol/L)
- Maintain normokalaemia (4.0 - 4.5 mmol/L)
- Temperature control
- control temperature 32 - 36°C for ≥ 24 h
- prevent fever for at least 72 h
- Diagnose/treat seizures
- EEG, sedation, anticonvulsants
- Delay prognostication for at least 72 h
Targeted temperature management (TTM)
Rationale for TTM:
- Mild induced hypothermia is neuroprotective and improves outcomes after a period of global cerebral hypoxia-ischaemia.
- Hypothermia suppresses many of the pathways leading to delayed cell death, including apoptosis
- Hypothermia decreases the cerebral metabolic rate for oxygen (CMRO2) by about 6% for each 1°C reduction in core temperature and this may reduce the release of excitatory amino acids and free radicals
- Hypothermia blocks the intracellular consequences of excitotoxin exposure (high calcium and glutamate concentrations) and reduces the inflammatory response associated with the post-cardiac arrest syndrome
Recommendations for TTM:
- Maintain a constant, target temperature between 32 - 36°C for those patients in whom temperature control is used
- TTM is recommended for adults after out-of-hospital cardiac arrest with an initial shockable rhythm who remain unresponsive after ROSC
- TTM is suggested for adults after out-of-hospital cardiac arrest with an initial non-shockable rhythm who remain unresponsive after ROSC
- TTM is suggested for adults after in-hospital cardiac arrest with any initial rhythm who remain unresponsive after ROSC
- If TTM is used, it is suggested that the duration is at least 24 h
Methods of inducing/maintaining TTM:
- IV fluid infusion
- Simple ice packs and/or wet towels
- Cooling blankets or pads
- Water or air-circulating blankets
- Water circulating gel-coated pads
- Transnasal evaporative cooling
- Intravascular heat exchanger placed in femoral or subclavian vein
- Extracorporeal circulation
Complications of hypothermia:
- Shivering will increase metabolic and heat production thus reducing cooling rates
- Hypothermia increases systemic vascular resistance and can cause arrhythmias (usually bradycardia)
- Hypothermia causes a diuresis and electrolyte abnormalities such as hypophosphataemia, hypokalaemia, hypomagnesaemia and hypocalcaemia
- Hypothermia causes insulin sensitivity and insulin secretion causing hypoglycaemia
- Hypothermia impairs coagulation and increases bleeding
- Hypothermia impairs the immune system and increases rates of infection
- Hypothermia decreases clearance of sedative drugs and neuromuscular blockers