**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,

#### *Cardiac Arrhythmias - Translational Approach from Pathophysiology to Advanced Care*

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 *Sonography* in 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 gas* measurements. 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 counts* are measured to detect anemia and other hematologic disorders. Profound anemia can suggest blood loss as a factor contributing to cardiac arrest.

#### *The Initial Assessment and Management of the Post-Cardiac Arrest Patient DOI: http://dx.doi.org/10.5772/intechopen.100132*

*Serum troponin* is 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 lactate* is 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 *toxicology* studies 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 tests* are required to assess organ function which can alter drug prescribing and dosing. *Coagulation tests* are 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].

#### **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).*

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**).

#### **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

*The Initial Assessment and Management of the Post-Cardiac Arrest Patient DOI: http://dx.doi.org/10.5772/intechopen.100132*

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]:


*Cardiac Arrhythmias - Translational Approach from Pathophysiology to Advanced Care*

#### **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).*

