Post Cardiac Arrest Care

Summary Algorithm
Background
Post-Cardiac Arrest Syndrome
ED Management of the Post-Cardiac Arrest Patient

Summary Algorithm

Background

• Most deaths following cardiac arrest occur in the first 24 hours
• Systematic post-cardiac arrest care can:
  • Reduce early mortality caused by hemodynamic instability
  • Reduce morbidity and mortality from multi-organ failure and brain injury
  • Improve the likelihood of patient survival with good quality of life
• A comprehensive, structured system of care should be implemented to:
  • Optimise haemodynamics and organ perfusion
  • Optimise oxygenation and ventilation
  • Initiate therapeutic hypothermia
  • Emergent PCI when indicated
  • Identify and treat precipitating causes
  • Provide critical supportive care including targeted temperature management (TTM)

Post-Cardiac Arrest Syndrome

• “A complex array of pathophysiologic processes that occur after ROSC”
• Systemic ischemia-reperfusion response
  • Mediated by:
    • Increased cytokine production: activates neutrophils leading to a potent pro-inflammatory response
    • Alterations in coagulation: an overall pro-coagulant state
    • Oxygen free radical formation
    • Adrenal dysfunction: a relative adrenal insufficiency
    • Disruption of the blood brain barrier
  • Extent of injury dependent upon duration of ischemia, co-morbidities, and cause of arrest
  • Overall characterized by intravascular volume depletion, impaired vaso-regulation, pro-thrombotic state, and increased susceptibility to infection
• Brain injury
  • Most deaths in patients with ROSC from out-of-hospital cardiac arrest are due to neurologic injury
  • Reactive oxygen species
    • Generated by mitochondria in ischemic neuronal tissues
    • Trigger cascade of events including protein oxidation, lipid peroxidation, and DNA damage
    • Hyperoxia can further increase the quantity of reactive species
    • Activation of transcription factors – induces apoptosis, inflammation, and sustained oxidative stress
  • Impaired auto-regulation
  • Cerebral oedema: common in the early post-cardiac arrest period – association with increases in ICP controversial
• Myocardial dysfunction
  • Common – may be seen in up to 70% of patients
  • May contribute to increased morbidity and mortality
  • Typically occurs within 8 hours following ROSC
  • Manifested by increased cardiac filling pressures, decreased cardiac index, decreased systolic and diastolic function
  • Aetiologies may include:
    • Direct injury of myocardium from compressions or defibrillation
    • Surge of catecholamines
    • Depletion of ATP stores
    • Generation of oxygen free radicals
    • Alterations in sarcoplasmic calcium metabolism
    • Up-regulation of heat shock proteins
  • Cardiac index returns to baseline within 24-48 hours in most patients; may persist in a few patients for weeks
• Persistent Precipitating Cause
  • Cardiac causes
  • PE: 5-10% of cases
  • Respiratory failure
  • Drug overdose
  • Electrolyte imbalances
  • Sepsis
  • Intracranial catastrophes

ED Management of the Post-Cardiac Arrest Patient

Oxygenation and Ventilation

• Pulmonary dysfunction common after cardiac arrest
  • Hydrostatic pulmonary oedema – LV dysfunction
  • Non-cardiogenic oedema – inflammatory, infective, physical injury
  • Atelectasis
  • Aspiration
• Patients develop regional V/Q mismatch; decreases arterial oxygen content
• Mechanical ventilation
  • Adjust based on S_pO₂, ABG, minute ventilation, and pt synchrony
  • Setting the mode
    • Assist control
    • No data to recommend a unique ventilator mode
  • Setting the tidal volume
    • Patients at high risk for ALI/ARDS: use a lung protective strategy
    • V_t: 6 – 8 ml/kg
  • Setting the F_iO₂ – “controlled re-oxygenation”
    • Optimal level remains controversial
    • Common practice to place all patients with ROSC on 100% F_iO₂
    • Animal data suggests hyperoxia increases brain lipid peroxidation, metabolic dysfunction, neurological degeneration, and worsens short-term outcome
    • Adjust F_iO₂ to the minimum concentration to achieve S_pO₂ ≥ 94%
    • Maintain P_aO₂ ≈ 100 mm Hg; avoid hyperoxia
  • Setting the respiratory rate
    • Tendency to hyperventilate to correct the metabolic acidosis immediately after ROSC
    • Hyperventilation can be detrimental
      • Can lower P_aCO₂, cause cerebral vasoconstriction, and exacerbate cerebral ischemic injury
      • Can also compromise systemic blood flow due to increases in intrathoracic pressure – decreases venous return and cardiac output
  • Adjust respiratory rate to maintain normocapnia
    • P_aCO₂ of 40-45 mm Hg OR
    • P_etCO₂ of 35-40 mm Hg

Hemodynamic Optimisation

• Hemodynamic instability common after ROSC
• Essential components of hemodynamic optimisation include restoring intravascular volume, maintaining adequate perfusion pressure, monitoring oxygen delivery, and supporting myocardial dysfunction
• Restore intravascular volume
  • Patients generally volume depleted due to increased vascular permeability
  • Administer isotonic crystalloid fluid boluses; use cold IVFs (4^oC) if therapeutic hypothermia is implemented
  • Monitoring volume status
    • CVP unreliable
    • Use respirophasic changes of IVC on ultrasound, pulse pressure variation, systolic pressure variation
• Maintain adequate perfusion pressure
  • Place an arterial line for continuous blood pressure monitoring
  • MAP
    • Better physiologic surrogate for organ perfusion pressure than SBP
    • The optimum post-resuscitation blood pressure has not been defined can vary among individuals.
    • AHA recommendation: MAP > 65 mm Hg
    • Some patients may require a higher MAP (80-100 mm Hg) to maintain adequate CPP and oxygen delivery; small studies of MAP 80-100 mm Hg combined with therapeutic hypothermia show a trend towards improved survival rates
• Vasopressors
  • Paucity of data about which drug to select first
  • All can increase or decrease HR, increase arrhythmias, increase myocardial oxygen demand
  • Administration through central line preferred
  • No standard recommended infusion rates; typical starting doses:
    • Noradrenaline: 0.1-0.5 mcg/kg/min
    • Adrenaline: 0.1-0.5 mcg/kg/min
    • Dopamine: 5-10 mcg/kg/min
    • Phenylephrine: 0.5-2.0 mcg/kg/min
• Monitor oxygen delivery
  • Hemodynamic optimization also dependent on assessing adequacy of oxygen delivery
  • Current guidelines recommend:
    • Serial lactate levels
    • ScvO2 ≥ 70%
• Support myocardial dysfunction
  • Common following ROSC; up to 70% of patients
  • Typically occurs within 8 hours and resolves within 72 hours
  • Perform bedside echo to determine global EF
  • No proven harm to IVFs and vasoactive medications for patients with myocardial stunning
  • Inotropic medications
    • Dobutamine: 5-10 mcg/kg/min
    • Milrinone: load 50 mcg/kg over 10 min then 0.375 mcg/kg min
  • Mechanical assistance
    • IABP
    • LVAD
    • Routine use not recommended since studies have not demonstrated consistent survival benefit

Early Cardiac Catheterisation

• ACS a common cause of cardiac arrest – up to 70%
• Obtain a 12-lead ECG as soon as possible; place on continuous cardiac monitor
• The early post-resuscitation ECG is less reliable for predicting acute coronary occlusion than it is in those who have not had a cardiac arrest.
• Pts with evidence of a STEMI should go for emergent PCI regardless of coma
• Strongly consider emergent PCI even in the absence of STEMI
• PCI should not be delayed because of the use of therapeutic hypothermia – PCI in the setting of hypothermia safe & associated with improved survival and outcome

Supportive Care

• Arrhythmias
  • Prophylactic administration of antiarrhythmics not recommended
  • Treatment of arrhythmias during post-cardiac arrest period does not differ from treatment in the non-cardiac arrest patient
• Hyperglycemia
  • Common in post-cardiac arrest patients and is associated with increased mortality and worse neurologic outcomes
  • Optimal glucose value/treatment strategy however remain controversial
  • Only prospective, randomised trial of glucose control in patients with OOHCA showed no difference in 30-day mortality between those with strict control and those with moderate control; those with strict control had increase in neuron-specific enolase suggesting more severe brain injury.
  • Current guidelines recommend a target glucose of 144-180 mg/dL for post-cardiac arrest patients
• Hyperthermia
  • Increases the risk of poor neurologic outcome
  • Aetiology may be related to activation of inflammatory cytokines
  • Temperatures > 37.6^o C should be treated aggressively with antipyretics or surface cooling techniques
  • Targeted Temperature Management – section attached
• Seizures
  • Seizures are common in post arrest period: 5-20%
  • Prolonged seizure activity can have detrimental neurologic effects and is associated with increased mortality
  • Current guidelines recommend
    • EEG for comatose survivors of cardiac arrest
    • Same anticonvulsant regiment used for status epilepticus for those who have seizure activity on EEG
    • No benefit to the prophylactic administration of anticonvulsants

Targeted Temperature Management (TTM)

• Aims of TTM
  • Cooling to 33˚C or 36˚C has been shown to be beneficial for patients with ROSC from cardiac arrest  according to recent trials  (2013)
  • TTM in the Western Cape setting should be implemented to aggressively prevent hyperthermia / pyrexia in post arrest patients.
  • Therapeutic hypothermia will only be implemented in selected patients in tertiary institutions by critical care specialists.
• Complications of Hypothermia
  • Seizures (myoclonic and generalised tonic-clonic seizures.)
  • Haemorrhage (IV sites, GIT, Oral, Nasal, Genital, Intracranial)
  • Infection / Sepsis
  • Arrhythmias (Atrial fibrillation/flutter, VT,VF, Bradyarrhythmias)
  • Electrolyte & metabolic abnormalities (↓K+, ↓Mg, ↓PO4, ↓Glycaemia)
• Methods of cooling
  • Cold IV fluids (4˚C)
  • Ice packs – axillae & groins
  • Commercial Temperature devices – Intravascular / Airflow mattress devices
• Monitoring
  • Patients require monitoring in intensive care or equivalent area with continuous monitoring of Core Temp, ECG, BP, SaO2, and preferable EtCO2.
• Sedation
  • Intravenous sedation is indicated to prevent patients from hyperthermia –institutional protocols to be followed.
  • Analgesia first sedation with minimal or no benzodiazepines has been proven to decrease delirium in patients admitted to ICU.

Drafted Nov 2014, Review Nov 2016

Courtesy of: Michael Winters, MD, FAAEM FACEP. Associate Professor of Emergency Medicine and Medicine. Director, Critical Care Education. Co-Director, Combined EM/IM/Critical Care Program. University of Maryland School of Medicine, Baltimore, Maryland.

Useful References

Peberdy MA, Callaway CW, Neumar RW, et al. Post cardiac arrest care: 2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation 2010; 122:S768-786.

Kory P, Weiner J, Mathew JP, et al. A rapid, safe, and low-cost technique for the induction of mild therapeutic hypothermia in post-cardiac arrest patients. Resuscitation 2011; 82:15-20.

Nolan JP, Soar J. Post-resuscitation care: entering a new era. Curr Opin Crit Care 2010; 16:216-22.

Sunde K, Soreide E. Therapeutic hypothermia after cardiac arrest: where are we now? Curr Opin Crit Care 2011; 17:247-253.

Walters JH, Morley PT, Nolan JP. The role of hypothermia in post-cardiac arrest patients with return of spontaneous circulation: a systematic review. Resuscitation 2011; 82:508-16.

Zia A, Kern KB. Management of postcardiac arrest myocardial dysfunction. Curr Opin Crit Care 2011; 17:241-6.

Nielsen N, Wetterslev J, Cronberg T, et al. Targeted temperature management at 33˚C  versus 36˚C after cardiac arrest. N Engl J Med 2013;369:2197-2206.