Complications
Data from 2022 shows that survival to hospital discharge is 9.3% for patients with out-of-hospital cardiac arrest, and 21.2% for patients with in-hospital cardiac arrest.[2]
Considerations include termination of resuscitative efforts and consultation with family members. The American Heart Association recommends that organ donation is considered in all resuscitated patients who meet the neurologic criteria for death or before planned withdrawal of life-sustaining therapies.[54]
Traumatic injury due to CPR manifests as rib and/or sternal fractures. It occurs in approximately one third of patients, but the rate of serious complications as a result is quite low.[127] Care should be taken to evaluate for further sequelae, such as penetrating trauma to internal organs.
Therapy is directed at analgesia and maintaining adequate secretion clearance.
Impaired circulation deprives the brain of nutrients and oxygen. The degree of injury spans the spectrum from brain death to persistent vegetative state to coma to recovery.
Prognosis is affected by the duration of arrest and CPR.[128] It is estimated that almost 50% of survivors of sudden cardiac arrest face some degree of diminished neurologic dysfunction.[129] This may be due to increased cerebral oxygen consumption, the generation and accumulation of oxygen free radicals, activation of the inflammatory cascade, or a rise in intracranial pressure seen after cardiac arrest.[130]
Maintaining hemodynamic stability is of paramount importance. Targeted temperature management decreases mortality and improves neurologic outcome.[91]
Due to the loss of splanchnic circulation during cardiac arrest, the liver faces hypoxic-ischemic injury, propagated by the inflammatory response of hepatocytes, Kupffer cells, and the endothelium.[131] Furthermore, restoration of oxygen to the liver through resuscitation results in reperfusion injury via the generation of reactive oxygen species.[132] The degree of damage is proportional to the duration of impaired circulation.
The management of shock liver is supportive. Maintaining hemodynamic stability and avoiding further damage to the liver are the mainstays of treatment.
Loss of circulation initiates the process of ischemic renal injury.[133] This causes endothelial damage, which further propagates injury through mechanisms of impaired vascular regulation, infiltration of inflammatory mediators, and a procoagulant state; this is called the "extension" phase of ischemic ATN.[134]
Management of ischemic ATN is supportive. Maintaining hemodynamic stability, optimizing volume status, avoiding nephrotoxins, and potential hemodialysis are the mainstays of therapy.
The median time to recurrence is 20 weeks after the sentinel event.[135] In a study of 234 patients having out-of-hospital sudden cardiac arrest due to ventricular fibrillation (VF), almost 40% of patients developed recurrent VF or death.[135] The risk of death in survivors varies depending on whether sudden cardiac arrest was due to a major cardiovascular event.[136]
Treating underlying coronary artery disease, electrolyte disturbances, or other causes is instrumental in decreasing the risk of repeat cardiac arrest. Judicious use of implantable cardioverter defibrillators in select patients is of paramount importance.[7]
Use of this content is subject to our disclaimer