Pulmonary

Complications in the pulmonary system are numerous following cardiac arrest. Such causes may be related to pulmonary edema, atelectasis, and aspiration events. Consequently, patients are at risk of perfusion- ventilation mismatch that can negatively affect oxygen content in the arteries. A low PaO₂/FiO₂ ratio (under 300 mm Hg) usually indicates lung injury. Other signs may include diffuse infiltrates on chest x-ray, reduce pulmonary artery pressures under 18 mm Hg, or lack of left atrial hypertension. This situation may be confused with acute respiratory distress, which is differentiated by an even lower PaO₂/FiO₂ of under 200 mm Hg. For either condition, however, providing positive end expiration pressure and managing FiO₂ levels will help manage the pulmonary damage. 

Chest x-ray and arterial blood gasses can be useful in this setting. Titration of the settings of mechanical ventilation depended on oxygen saturation, blood gases, and minute ventilations is useful for treating this condition. Currently, the best FiO₂ is unclear, and the benefits of oxygen must be evaluated alongside its toxicities from free oxygen radicals. High oxygen also increases PaO₂ (up to 350 mm Hg in the first 15-60 minutes following ROSC), which can lead to acute brain injury via metabolic derangement and lipid peroxidation when compared with maintenance of oxygen saturation at 94% or more. 

Following ROSC, monitor arterial oxyhemoglobin saturation and wean FiO₂ to keep and SpO₂ of 94% or higher. If arterial oxyhemoglobin saturation is not available, use the highest oxygen concentration available so hypoxia is avoided until measuring is available.  Avoid hyperventilation and low CO₂ as this can worse brain perfusion via vasoconstriction of the cerebral vasculature. Additionally, the associated rise in thoracic pressure decreases cardiac function. In patients on temperature management, PaO₂ can be corrected for temperature. 

Pulmonary Embolism

The management of cardiac arrest secondary to pulmonary emboli is thrombolysis, mechanical, or surgical embolectomy. (Class IIa, Evidence level C-LD). Traditionally, patients with significant PE would only receive fibrinolytic therapy if they have not received CPR. However, patients who have received CPR can still benefit from fibrinolytics as the risk of bleeding may not outweigh the benefits of treatment in this disease. (Class IIa, Evidence level C-LD). Alternatively, if it is available, surgery with embolectomy is another treatment modality.  

Sedative Use

Many patients after a cardiac arrest will need pain management as well as therapies to reduce anxiety, minimizing “fighting” the ventilator, and minimize catecholamine excess. Patients will experience pain and discomfort from interventions, including advanced airways and temperature management. They will likely have some anxiety associated with therapies. Sedative, narcotics, anxiolytics, and other treatments are commonly used. Always titrate medications to the patient’s response; scales to evaluate motor response, as well as the level of sedation, can be helpful. 

Occasionally, the patient’s agitation may interfere with care, and the use of neuromuscular blockade is required. This therapy is also used for patients who are prone to seizures and are monitored using EEG. These agents should be minimized, however.  

Cardiovascular

Assess for ACS as the cause for cardiac arrest with 12 lead EKG. (Class I, Evidence level B). If STEMI is identified, the team should begin management as for patients without a cardiac arrest, regardless of comatose status or need for temperature management. Provide PCI, if the patient is eligible, as quickly as possible. 

Do not routinely use lidocaine or beta-blockade following arrest. However, in patients with VF or V-Tach, research indicates that lidocaine may minimize arrhythmia recurrence, although this may not improve long-term outcomes.  Research shows that beta-blockade in VF/V-Tach associated cardiac arrest is correlated with increased survival. This medication should be used cautiously as they are also associated with hypotension, bradycardias, and worsened heart failure following cardiac arrest. The risk and benefits must be weighed for the individual patient.