Post cardiac arrest syndrome care pathway

Post cardiac arrest syndrome care pathway

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Associate Editor: Cafer Zorkun, M.D., Ph.D. [2]

Please Take Over This Page and Apply to be Editor-In-Chief for this topic: There can be one or more than one Editor-In-Chief. You may also apply to be an Associate Editor-In-Chief of one of the subtopics below. Please mail us [3] to indicate your interest in serving either as an Editor-In-Chief of the entire topic or as an Associate Editor-In-Chief for a subtopic. Please be sure to attach your CV and or biographical sketch.

Post-cardiac arrest is defined as absence of pulses requiring chest compressions, regardless of location or presenting rhythm. The post cardiac arrest syndrome is characterized by resumption of spontaneous systemic circulation after prolonged ischemia of whole body.

Prevalance

Annually 166.200 out of hospital cardiac arrests occur in United States, and only 6.4% of them survive at hospital discharge. Despite of all improvements in pre and in hospital treatment possibilities, there is no significant change in hospital mortality rate.

Pathophysiology

The underlying mechanism of post cardiac arrest syndrome is a combination of:

• Systemic response to ischemia and reperfusion

• Circulatory collapse
• Hyperglycemia
• Hypotension
• Infections
• Multiorgan failure
• Ongoing tissue hypoxia / ischemia
• Fever

• Myocardial dysfunction

• Circulatory collapse
• Dysrhythmias
• Hypotension
• Reduced cardiac output

• Brain injury

• Brain death
• Cognitive dysfunction
• Coma
• Cortical stroke
• Myoclonus
• Persistent vegetative state
• Secondary parkinsonism
• Seizures
• Spinal stroke

• Effects of persistent precipitating pathologies

• Cardiovascular disease (Acute coronary syndromes, cardiomyopathy)
• Chronic obstructive pulmonary disease
• Central nervous system diseases (e.g. cerebrovascular accident)
• Thromboembolic disorders (e.g. pulmonary emboli)
• Drug / substance overdose, poisoning
• Infections (sepsis, pneumonia)
• Volume loss (Hypovolemia: e.g. hemorrhage, dehydration)

Management

(In alphabetical order)

• Arterial blood gases
• Blood glucose
• Cardiac output monitoring with noninvasive methods or pulmonary artery catheter
• Chest x-ray
• Complete blood count
• Computed tomography or MRI
• Continuous ECG monitoring
• Echocardiography
• EEG for early seizure detection and treatment
• Electrolytes
• General blood sampling (blood chemistry and cardiac enzymes)
• Monitoring of central venous pressure
• Oxygen saturation by pulse oximetry
• Placement of an arterial catheter
• ScvO2
• Serum lactate
• Temperature follow up (bladder, esophagus)
• Urine output

Treatment

• Mild therapeutic hypotermia
• PCI if ACS diagnosed (Fibrinolytic therapy if PCI is not available)
• Extracorporeal membrane oxygenation
• Management of adrenal insufficiency

A Complete List of What to Do:

A. Initial Data Gathering (after ABC’s are stabilized)

1. History:

• Review

• eligibility
• contraindications
• advance directives
• overall prognosis

• Discuss issues with health care proxy, if available

2. Physical: Baseline Neurological Evaluation

• Exclude other causes of coma

• mass lesions
• Metabolic coma
• Seizures

• Document Glasgow Motor Score

3. Initial laboratories:

• Arterial blood gas
• CBC
• Platelets
• PT
• PTT
• P7 and Calcium
• Mg
• Phosphate
• Lactate
• CPK-MB
• Troponin
• Cortisol level
• Pan-culture
• Toxicology screen if appropriate

4. Serial laboratories:

• ScvO2 q 6 if PreSEP catheter not used
• Glucose (q 6 hrs x 2 days)
• Potassium q (6 hrs x 2 days)
• Lactate (q 6 hrs x 2 days)
• Repeat CPK-MB and Troponin at 6 hrs
• CBC (q 12 hr x 4)
• Platelets (q 12 hr x 4)
• PT (q 12 hr x 4)
• PTT (q 12 hr x 4)
• P7 (q 12 hr x 4)
• BUN (q 12 hr x 4)
• Creatinine (q 12 hr x 4)
• Calcium (q 12 hr x 4)
• Magnesium (q 12 hr x 4)
• Phosphate (q 12 hr x 4)

5. Chest X-Ray

• Chest x-rays are essential to rule out aspiration pneumonias and other underlying (possible) pulmonary pathologies.

6. Cranial CT:

• Rule out intracranial hemorrhage

7. Consultations:

Cardiology in all cases. Note: If cardiac catheterization is indicated, hypothermia should not be delayed.

8. Echocardiogram:

To r/o regional wall motion abnormality and severe contractile dysfunction.

B. Establish Appropriate Monitoring Immediately:

1. Cardiovascular:

• EKG after initial stabilization and repeat q 8 hours x 2 and prn to r/o acute coronary syndrome
• Arterial-line for continuous arterial blood pressure monitoring (essential prior to initiating hypothermia). Attempt radial artery x 1 and then proceed to femoral artery if necessary.
• Temperature monitoring Foley for continuous urine output and temperature monitoring. If there is no urine output, use an alternative site for temperature measurement – (e.g. esophageal)
• Presep catheter or other central venous catheters for central venous pressure & ScvO2 (subclavian site preferred) though don't delay hypothermia to perform this.

2. Pulmonary:

Continuous SaO2 probe, frequent ABG’s (use temperature correction)

3. Temperature:

Foley with temperature probe (use alternative site if no urine output)

4. Neurologic:

• Continuous EEG monitoring beginning within 6-12 hrs while paralyzed.
• Once in ICU, use BIS monitor to titrate sedation (40-60)
• Neuro checks q 2 hour (while paralyzed follow pupils and titrate paralysis per NMB Nursing Policy)

5. Additional monitoring and follow-up studies

• If net fluid balance is > 5 liters in 24 hrs, monitor intrabdominal pressure (IAP) via Foley catheter after cooling device has been discontinued (call medical resident if IAP is ≥ 20 mmHg).
• Consider to repeat echocardiogram 24-48 hours after return of spontaneous circulation
• Repeat Chest X-ray in AM and after 72 hours to rule out aspiration pneumonia

C. Initiate Appropriate Interventions

NOTE: Interventions should be carried out simultaneously when appropriate and feasible

• Post-Cardiac Arrest Early Goal-Directed Therapy
• Therapeutic hypothermia (if indicated)
• Treat acute coronary syndrome
• Treat hyperglycemia
• Antibiotic prophylaxis
• Fever prophylaxis
• Other ICU protocols if necessary

Therapeutic Hypothermia

• Hypothermia activates the sympathetic nervous system causing vasoconstriction and shivering. Shivering increases O₂ consumption by 40-100%. Sedatives, opiates, and neuromuscular blockers can counteract these responses and enhance the effectiveness of active cooling. However, initiating paralysis in a patient that is already hypothermic should be avoided because it can result in a precipitous drop in core body temperature. Elderly patients will cool more quickly than younger or obese patients.
• Hypothermia shifts the oxyhemoglobin curve to the left may result in decreased O₂ delivery. However, the metabolic rate is also lowered, decreasing O₂ consumption / CO₂ production, cardiac output and cerebral blood flow. Ventilator settings may need to be adjusted due to decreased CO₂ production, using temperature corrected blood gases.
• Hypothermia initially causes sinus tachycardia, then bradycardia. With temp <30º C there is an increased risk for arrhythmias. With temp <28º C there is an increased risk for ventricular fibrillation. The severely hypothermic myocardium (<30°C) is less responsive to defibrillation and medications. Therefore it is extremely important to keep temp >30ºC.
• Hypothermia can induce coagulopathy which is treatable with platelets and FFP.
• Hypothermia-induced diuresis is to be expected and should be treated aggressively with fluid and electrolyte repletion. Magnesium, phosphorus and potassium should be monitored closely and maintained in the normal (because it will rebound to very high) range.
• Decreased insulin secretion and sensitivity leads to hyperglycemia, which should be treated aggressively.
• Re-warming too rapidly can cause vasodilation, hypotension, and rapid electrolyte shifts.

Eligibility Criteria for Post-Cardiac Arrest Therapeutic Hypothermia

• Meets eligibility criteria for Post-Cardiac Arrest Care Pathway
• Comatose at enrollment with a Glasgow Coma Motor Score <6 pre-sedation (i.e., patient doesn’t follow commands)
• No other obvious reasons for coma
• No uncontrolled bleeding
• Hemodynamically stable with no evidence of:

• Uncontrollable dysrhythmias
• Severe cardiogenic shock
• Refractory hypotension (MAP <60 mm Hg) despite preload optimization and use of vasoactive medications

• No existing, multi-organ dysfunction syndrome, severe sepsis, or comorbidities with minimal chance of meaningful survival independent of neurological status

Relative Contraindications for Therapeutic Hypothermia:

• Prolonged arrest time (> 60 minutes)
• Thrombocytopenia or other coagulopathies
• Pregnancy (Therapeutic hypothermia can potentially be performed on pregnant female in consultation with OB/Gyn)

Prognosis

The neurologic prognosis of the majority of comatose cardiac arrest survivors cannot be reliably predicted until at least 72 hours after resuscitation. Furthermore, the reliability of these parameters has not been evaluated in the face of effective interventions such as therapeutic hypothermia. Therefore DNR status should not be established and care should not be withdrawn based on neurologic prognosis before 72 hours after return of spontaneous circulation.

External Links

• Therapeutic hypotermia trial at Clinical Trials.gov

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