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The Initial Assessment and Management of the Post-Cardiac Arrest Patient

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Amad Hania

Submitted: May 8th, 2021Reviewed: August 25th, 2021Published: March 9th, 2022

DOI: 10.5772/intechopen.100132

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Cardiac arrest is the most common cause of death in North America and in the developed world. Advances in care have resulted in improved survival and favorable neurological outcomes in recent times. The initial management and interventions of the post-cardiac arrest patient are reviewed here. Following the return of spontaneous circulation (ROSC) the priorities are to (A) determine and treat the cause of the cardiac arrest, and (B) optimize the cardiorespiratory function of the to prevent further cardiac arrests. The European Resuscitation Council (ERC) and the European Society of Intensive Care Medicine (ESICM) have collaborated to produce post-resuscitation care guidelines for adults following cardiac arrest.


  • resuscitation
  • return of spontaneous circulation
  • cardiac arrest
  • management
  • targeted temperature management

1. Introduction

Cardiac arrest is the most common cause of death in North America and in the developed world [1]. Advances in care have resulted in improved survival and favorable neurological outcome in recent times [2]. The initial management and interventions of the post-cardiac arrest patient are reviewed here. Following the return of spontaneous circulation (ROSC) the priorities are to (A) determine and treat the cause of the cardiac arrest, and (B) optimize the cardiorespiratory function of the to prevent further cardiac arrests. The European Resuscitation Council (ERC) and the European Society of Intensive Care Medicine (ESICM) have collaborated to produce post-resuscitation care guidelines for adults following cardiac arrest.


2. Determining the cause of the cardiac arrest

In cases of cardiac arrest, the cause determines further interventions that are required. A thorough history and examination can help identify the underlying causes and subsequent interventions required to avoid an imminent threat to life. While cardiovascular disease is a common cause of cardiac arrest, there is a broad range of differential diagnosis for potential causes (Table 1).

Cardiac arrest—causes
  • Thrombosis—MI

  • Thromboembolism—PE

  • Tension pneumothorax

  • Tamponade—cardiac

  • Trauma

  • Tablets—drugs/toxins

  • Hypovolemia

  • Hypoxia

  • Hydrogen ions—acidosis

  • Hyper/hypokalemia

  • Hypothermia

  • Hypo/hyperglycemia

Table 1.

Common causes of cardiac arrest; H’s and T’s.


3. History

Most patients will not be able to give a history of the events leading up to their cardiac arrest, so it is important to obtain relevant details about the preceding events from any individuals who can give an insight into the patients pre-existing medical condition and the event leading up to the cardiac arrest. These can include family members, friends, witnesses, emergency service personnel, etc. This can help identify the potential cause and help guide management.


4. Physical examination

An initial assessment of the patient is made of the patient using a systematic approach (Table 2).

  1. Airway—If the patient is able to speak coherently and is responsive then the airway is patent. Perform either a chin lift or jaw thrust if airway obstruction is identified. A jaw thrust only is preferred if cervical spine injury is suspected, and the cervical spine should be immobilized and maintained in-line.

    Foreign bodies, secretions, and facial fractures should be identified if present.

  2. Breathing—Initial inspection should identify tracheal deviation, an open pneumothorax or significant chest wounds, flail chest, paradoxical chest movement, or asymmetric chest wall excursion. Auscultation of both lungs should be conducted to identify decreased or asymmetric lung sounds.

  3. Circulation—This is evaluated by assessing the level of responsiveness, obvious hemorrhage, skin color, pulse (presence, quality, and rate), and blood pressure. Capillary refill time can be used to assess the adequacy of tissue perfusion. A capillary refill time of more than 2 s may indicate poor perfusion. Auscultate the heart to identify any abnormalities as described.

  4. Disability—Assessment of neurological status is made by patient’s Glasgow coma scale (GCS), pupil size and reaction, and any abnormal neurological signs. A reduced GCS of ≤8 may suggest diminished airway reflexes and may require a definitive airway to help protect the airway.

  5. Environment—The patient should be exposed to ensure that no injuries are missed.

Table 2.

Initial assessment.

4.1 Airway and breathing

Following the return of spontaneous circulation (ROSC), an initial examination of airway, breathing, circulation, and disability (ABCs) is performed. Airway and ventilation support should continue after the return of spontaneous circulation (ROSC) is achieved [3]. Airway potency is assessed, and endotracheal intubation is required for the patient patients if unable to maintain the airway. If the patient is already intubated, then the position of the endotracheal tube should be checked, as a misplaced endotracheal tube can lead to hypoxia and re-arrest.

Once the patient’s airway is secured, an assessment of breathing is to be done. Abnormal examination such as asymmetrical sounds, wheeze, crackles, etc. can help identify potential cause or precipitant. This may reveal potential causes such as pneumothorax, mal-positioned endotracheal, cardiac, and respiratory issues.

4.2 Circulation

Circulation and end-organ perfusion are next assessed. The pulse (weak, thread), blood pressure, skin color (pale, mottled, cold), and prolonged capillary refill time (>2 s) can be indicative of poor peripheral perfusion and the need for IV fluids and vasopressor support. Abnormal cardiac sounds such as the presence of harsh cardiac murmurs, rubs can suggest a cardiac mechanical cause. Diminished heart sounds, jugular venous distension, and hypotension can suggest cardiac tamponade as a potential cause.

4.3 Disability

A detailed neurological exam is required following the return of circulation to help determine the likely cause and indication for immediate investigations such as a computerized tomography (CT) brain scan. A comprehensive exam may be delayed depending on the use of long-acting sedation and muscle relaxant; however, the presence of asymmetrical neurological findings may suggest intracranial pathology and the need for urgent imaging. Brainstem responses, including the pupillary, corneal, oculocephalic, gag, and cough response to stimulation, correlate with prognostication and survival and should be assessed.

4.4 Environment

An abnormal abdominal examination such as a rigid abdomen, presence of blood in the rectum and stomach can indicative of a surgical emergency and a potential cause. The rest of the patient’s body should be examined for the possible source of sepsis, bleeding, and presence of deep vein thrombosis (unilateral leg swelling).


5. Diagnostic tests

Diagnostic tests, including an electrocardiogram (ECG), imaging studies, and laboratory tests, are usually required to help determine the cause of the cardiac arrest, confirm endotracheal tube position, and assess for chest trauma from cardiopulmonary resuscitation (CPR), and to assess the involvement of specific organ systems.

ECG: This can help to identify common causes of cardiac arrest such as acute myocardial infarction (MI), cardiomyopathy, and primary arrhythmia. Following ROSC, a 12-lead electrocardiogram (ECG) should be rapidly obtained and evaluated for signs of ST-elevation myocardial infarction (STEMI) (including a new left bundle branch block) that requires emergency reperfusion therapy. Abnormalities of conduction intervals, the electrical axis may indicate possible etiology, e.g., a prolonged QTc interval may reflect a primary arrhythmia, accidental hypothermia, or an electrolyte abnormality. Evidence of right heart strain (e.g., right axis deviation) may be present in the setting of pulmonary embolus.

In the setting of cardiac arrest, significant coronary artery lesions may be present in the absence of signs of acute STEMI [4]. The incidence of coronary artery lesions is highest in those presenting with arrhythmia such as ventricular fibrillation (VF) or pulseless ventricular tachycardia (VT). Thus, emergency coronary revascularisation may be required for patients without presenting with initial signs of STEMI.

When the diagnosis of the acute coronary syndrome (ACS) is uncertain based on ECG findings, bedside echocardiography may demonstrate focal wall motion abnormalities, suggesting acute or previous myocardial infarction.

Imaging studies: A chest x-ray can identify possible pulmonary pathology and confirm correct positioning of the endotracheal tube and central venous catheter if applicable. Pulmonary edema and evidence of aspiration are common findings after CPR but may be unrelated to the possible cause of the arrest. Pneumothorax may be present as a possible cause of the arrest or may be secondary to the chest compressions, this should be further evaluated and require immediate treatment if indicated. Enlarged aorta or concerning mediastinal findings on chest radiograph may indicate an aortic dissection and should urge prompt CT scan imaging and likely immediate intervention.

FAST examination is the “Focused Assessment with Sonographyin Trauma” is performed, to identify free fluid in the abdomen and can help to identify possible causes of the arrest that represent ongoing threats to life, including pericardial tamponade, pneumothorax, pulmonary embolism (PE), and intraperitoneal bleeding. Cardiac ultrasound can be used to assess right ventricular size and function (which may be abnormal with PE), determine the diameter of the inferior vena cava (which may be abnormal with a reduced diameter or inadequate dilation following fluid resuscitation can indicate hypovolemia) [5], and assess global cardiac function.

Computerized tomography (CT) of the brain can detect early cerebral edema or intracranial hemorrhage in the comatose post-cardiac arrest patient. This will guide appropriate referral to the neurosurgical unit and may preclude possible anticoagulation administration. A CT of the chest is useful in cases of suspected pulmonary embolism (PE). In cases of traumatic injury, presence of peritonitis, and markedly raised lactate a CT of the abdomen and pelvis can be useful to identify the potential abdominal cause of the arrest.

Laboratory testing: Laboratory can give an insight into the cause of the arrest but also give an indication on the extent of organ damage from the hypoperfusion event resulting from the cardiac arrest. Particularly, electrolyte and acid-base disturbances require close monitoring during the resuscitation and ongoing management following the return of circulation.

Arterial vascular access is frequently obtained in comatose post-cardiac arrest patients given the need for frequent arterial blood gasmeasurements. The frequent use of vasopressor and inotropic drugs for hemodynamic support requires continuous invasive blood pressure monitoring. Arterial blood gasses will give important and immediate data such as acid-base balance, electrolytes disturbance, glucose, and lactate levels.

Serum electrolyte concentrations, including sodium, potassium, chloride, and bicarbonate are monitored as rapid fluctuations in serum electrolytes particularly potassium may occur because of ischemia, acidosis, and catecholamine administration such as adrenaline and noradrenaline through activation of alpha and beta adrenoreceptors [6].

Full blood countsare measured to detect anemia and other hematologic disorders. Profound anemia can suggest blood loss as a factor contributing to cardiac arrest.

Serum troponinis measured to detect myocardial injury. Cardiac arrest, CPR, and defibrillation often cause mild increases in the serum troponin. Rising levels of serum troponin may suggest an acute coronary artery occlusion.

Serum lactateis measured and is usually elevated following cardiac arrest, the rate of clearance of lactate correlates with the likelihood of survival [7]. Lactate should clear over time once reperfusion is restored. Markedly raised serum lactate and rising levels may suggest ongoing intra-abdominal or muscle compartment ischemia.

Specific toxicologystudies can be of use in patients with a history of drug ingestion, signs of a toxicologic syndrome (e.g., sympathomimetic poisoning), or clinical suspicion of poisoning. For example, myocardial infarction or arrhythmia may be caused by acute cocaine or methamphetamine intoxication. The cardiopulmonary arrest may be precipitated by antidepressant overdose. Sedative overdose e.g., benzodiazepine and opioids may contribute to a prolonged coma independent of any brain injury sustained during the cardiac arrest. The presence of long-acting opioids or benzodiazepine may prompt treatment with the necessary reversal agent for e.g., naloxone for opioids and flumazenil for benzodiazepines.

Hypoperfusion from cardiac arrest can impair kidney and liver function. Frequent monitoring of liver function tests, and renal function testsare required to assess organ function which can alter drug prescribing and dosing. Coagulation testsare also recommended as blood clotting can become impaired following ischaemic injury to the liver during a cardiac arrest.


6. Respiratory management

Airway and ventilation support should continue after the return of spontaneous circulation (ROSC) is achieved. Patients who are the comatose following return of circulation require endotracheal intubation by experienced operators in airway management. Correct placement of the endotracheal tube should be confirmed by waveform capnography. In the absence of a skilled incubator, it may be reasonable to insert a supraglottic airway device e.g., laryngeal mask, laryngeal tube until endotracheal intubation is achieved [3]. Gastric decompression with a nasogastric tube is indicated to help prevent aspiration.

Patients who have returned normal cerebral function following brief cardiac arrest may not require endotracheal intubation if airway and breathing are normal. Patients should receive oxygen to maintain arterial oxygen saturation above 94% [3].

Patients should receive FiO2 of 1.0 until arterial oxygen saturations can be measured reliably. Titrate FiO2 to the lowest level to achieve arterial oxygen saturations above 94% or arterial partial pressure of oxygen (PaO2) of 10–13 kPa [3].

In patients requiring mechanical ventilation after ROSC, ventilation should be adjusted to target a normal arterial partial pressure of carbon dioxide (PaCO2), i.e., 4.5–6.0 kPa or 35–45 mmHg. This should be achieved using lung-protective strategies e.g. tidal volume of 6–8 mL kg−1 ideal body weight, in a unit experienced managing intubated patients on mechanical ventilation (Figure 1).

Figure 1.

Haemodynamic, oxygenation, and ventilation targets in patients following ROSC (MAP—mean arterial pressure, PaO2—partial pressure of oxygen, SaO2—saturation of oxygen, PaCO2—partial pressure of carbon dioxide, TV—tidal volume).


7. Circulation management

Patients should be monitored with an arterial line for continuous invasive blood pressure measurements, and it may be reasonable to monitor cardiac output in hemodynamically unstable patients. Aim for mean arterial pressure greater than 65 mmHg using intravenous fluids, vasopressor, and/or ionotropic support to achieve urine output (> 0.5 mL kg−1 h−1) and also target normal or decreasing serum lactate [3]. This may require central venous access.

Emergency cardiac catheterization laboratory evaluation (and immediate percutaneous coronary intervention (PCI) if required) should be performed in adult patients with ROSC after cardiac arrest of suspected cardiac origin with ST-elevation on the ECG or patient’s high probability of acute coronary occlusion [3].

Perform early echocardiography in all patients to detect any underlying cardiac pathology and quantify the degree of myocardial dysfunction. Persistent cardiogenic shock not responsive to vasopressors and inotropes may require mechanical circulatory support such as intra-aortic balloon pump, veno-arterial extracorporal membrane oxygenation and for the longer duration a left- or bi-ventricular assist device.


8. Disability management

Patients should be monitored for seizure-like activity using electroencephalography (EEG) to diagnose electrographic seizures in patients with clinical convulsions and to monitor the effects of treatment of seizures. The EEG can also be used in the diagnosis of subclinical seizures in patients under neuromuscular blockade. Treatment of seizures following cardiac arrest should be with levetiracetam or sodium valproate as first-line antiepileptic drugs in addition to sedative drugs [3]. Seizure prophylaxis is not recommended for routine use [3]. Short-acting sedatives and opioids should be used to assess neurological recovery in a timely fashion to allow for prognostication.


9. Temperature management

Targeted temperature management (TTM) reduces neurologic injury and promotes patient survival. Adult patients who remain unresponsive following ROSC from an out-of-hospital cardiac arrest (OHCA) or an in-hospital cardiac arrest (IHCA) with any initial rhythm should have a constant temperature between 32 and 36°C for at least 24 h. Avoid fever (>37.7°C) for at least 72 h after ROSC in patients who remain in a coma [3]. A recent randomized trial (n = 351) investigated TTM at 33°C during 48 h or 24 h in unconscious patients after OHCA [8]. There was no significant difference in neurological outcome between the groups—relative risk (RR) for a cerebral performance category 1–2 at 6 months 1.08, 95% CI 0.93–1.25). Adverse events were more common in the prolonged cooling group (RR 1.06, 95% CI 1.01–1.12). Rewarming should be slow, with a target rate of 0.25°C (0.5°F) every hour (0.25°C/h) until the patient returns to normothermia (37°C [98.6°F]). It will take ≈12–16 h to rewarm. The greatest risks during rewarming are hypotension, hyperkalemia, and hypoglycemia [9]. The complications of TTM include cardiovascular effects such as bradycardia, decreased cardiac output, and vasoconstriction which can lead to a rise in blood pressure [10]. TTM can also cause shivering, increased risk of infection, increased insulin resistance, impaired drug metabolism, decreased gastrointestinal motility, and impaired hemostasis [10]. The routine use of neuromuscular blockade in patients undergoing targeted temperature management (TTM) is not recommended, but may be used in cases of severe shivering during TTM [3]. It is important to be aware of these potential complications of TTM and the known complications need to be recognized for immediate treatment.


10. General critical care management

Provide stress ulcer prophylaxis routinely in cardiac arrest patients may decrease the risk of gastrointestinal bleeding [11]. Provide deep venous thrombosis prophylaxis. Target blood glucose of 7.8–10 mmol L−1 (140–180 mg dL−1) using an infusion of insulin if required; avoid hypoglycemia [12]. Start enteral feeding at low rates (trophic feeding) during TTM and increase after rewarming if indicated. Patients should be nursed 30° head-up. This may decrease intracranial pressure (ICP) and decrease the risk of aspiration pneumonia [3].

11. Prognostication

In patients who are comatose after resuscitation from cardiac arrest, neurological prognostication should be performed using a multimodal approach by clinical examination, electrophysiology, and imaging to help inform clinicians and relatives of the likelihood of meaningful neurological recovery.

The clinical neurological examination is central to prognostication. To avoid falsely pessimistic predictions, clinicians should ensure the examination is not carried out with confounding factors such as residual sedation and hypothermia which might give an inaccurate assessment.

The start of the prognostication process begins with accurate clinical assessment ≥72 h from ROSC. In a comatose patient with a motor score of ≤3 at ≥72 h from ROSC, in the absence of confounders, a poor outcome is likely when two or more of the following predictors are present (Figure 2) [3]:

  • The absence of the pupillary light reflex.

  • The absence of corneal reflex.

  • The presence of status myoclonus within 72 h.

  • Highly malignant EEG at >24 h.

  • Diffuse and extensive anoxic injury on brain CT/MRI.

  • Bilaterally absent negative potential at 20 ms post sensory stimulation-somatosensory evoked potentials (N20 SSEP) wave.

  • Neuron-specific enolase (NSE) > 60 μg L−1 at 48 h and/or 72 h.

Figure 2.

Summary of prognostication factors resulting in likely poor outcome (EEG—electroencephalogram, SSEP—somatosensory evoked potentials, CT—computerized tomography, MRI—magnetic resonance imaging, N20 wave—negative potential at 20 ms post sensory stimulation, NSE—neuron-specific enolase).

12. Clinical examination

Clinical examination can be prone to misinterpretation from interference from confounding factors such as sedatives, muscle relaxants, and opioids. The presence of any confounding factors should be excluded to achieve a reliable interpretation from clinical examination of the patient. A motor score of ≤3 in the Glasgow coma score (abnormal flexion or worse in response to pain) at 72 h or later after ROSC, may indicate poor neurological outcome and the need for neurological prognostication. The poor neurological outcome can be predicted by the following test results from clinical examination [3].

13. Neurophysiology

An EEG should be performed on all comatose patients following cardiac arrest. The presence of subclinical seizure activity on EEG in the first 72 h following ROSC is an indicator of poor prognosis. Highly malignant EEG patterns include suppressed background with or without periodic discharges and burst suppression. After cardiac arrest, the EEG is suppressed in many patients but returns to normal voltage activity within the first 24 h in patients who achieve a good outcome [13].

Somatosensory evoked potentials can be performed by electrically stimulating a nerve e.g., the median nerve, and the ascending signals can be recorded from the peripheral plexus brachialis, cervical level, subcortical level, and the sensory cortex (N20-potential). A bilateral absence of the short-latency N20-potentials over the sensory cortex is a reliable sign of a poor prognosis after cardiac arrest with high specificity [3].

14. Biomarkers

Neuron-specific enolase (NSE) is an acidic protease unique to neurons and is sensitive to damage to nerve cells. NSE decreases after 24 h in patients with good outcomes and typically increases in patients with a poor outcome to peak at 48–96 h [14].

15. Imaging

The use of brain imaging studies can help predict patients with poor neurological outcomes. The presence of generalized brain edema, manifested by a marked reduction of the gray matter/white matter ratio on CT brain scan, or extensive diffusion restriction on brain MRI can predict poor neurological outcomes after cardiac arrest. Further signs of diffuse and extensive hypoxic-ischemic brain injury on brain CT include an effacement of cortical sulci and reduced ventricle size [3].

16. Long term outcome in cardiac arrest survivors

Cognitive impairments, emotional problems, and fatigue are common following cardiac arrest [15]. The morbidities can be missed by healthcare professionals. These can have a significant impact on the quality of life of patients and should be addressed for cardiac arrest survivors and monitored on follow-up to allow early detection and intervention with appropriate care [3].

Functional assessments of physical and emotional impairments should be performed before discharge from the hospital to help identify patients requiring early intervention and rehabilitation. Cardiac arrest survivors should be followed up within 3 months post-discharge and be screened for cognitive, emotional problems, and be provided information and support [3].


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Written By

Amad Hania

Submitted: May 8th, 2021Reviewed: August 25th, 2021Published: March 9th, 2022