Post-cardiac arrest syndrome
This article may be too technical for most readers to understand.(March 2022) |
Post-cardiac arrest syndrome | |
---|---|
Other names | Post-resuscitation disease |
Symptoms | Brain injury, myocardial injury, systemic ischemia/reperfusion response |
Usual onset | After resuscitation from a cardiac arrest |
Duration | Weeks |
Causes | Global ischemia-reperfusion injury |
Risk factors | Prolonged cardiac arrest |
Differential diagnosis | Systemic inflammatory response syndrome |
Management | Hemodynamic stabilization and supportive care |
Post-cardiac arrest syndrome (PCAS) is an inflammatory state of
Causes and mechanisms
Before cardiac arrest, the body is in a state of
Signs and symptoms
The severity of PCAS is highly dependent on many variables including: the underlying cause of the arrest, the length of the ischemic period, the quality of CPR received, and a patient's physiologic reserve. However, organs generally respond to an ischemic period in predictable ways and therefore PCAS has an average presentation. The symptoms of PCAS are related to the effect of ischemia-reperfusion injury on individual systems, though there is significant co-morbidity between all organs' responses.
Brain
Being highly metabolic with low blood reserves, the brain is the most sensitive organ to ischemia.
Heart
After the brain, the heart is the second most sensitive organ to ischemia.[4] If the cause of the cardiac arrest was fundamentally a coronary pathology, then the consequences to the heart may include myocardial infarction complications. However, if the fundamental cause was non-coronary, then the heart becomes ischemic as a consequence, not a cause, of the arrest. In this case, PCAS very frequently presents with myocardial dysfunction in the first minute-hours post-ROSC.[8] This myocardial dysfunction may present as prolonged cardiogenic shock, highly variable blood pressures, reduced cardiac output and/or dysrhythmias. PCAS myocardial dysfunction seems to start almost immediately after ROSC.[9] Unlike brain tissue, evidence suggests that the myocardial injury is generally transient and can mostly recover within 72 hours,[10] though full recovery may take months.[11]
Lungs
While the lungs are generally oxygenated during the ischemic period of arrest, they are still susceptible to ischemic damage. While ischemia is not the mechanism of injury, evidence suggests[
Kidneys
The kidneys are the third most sensitive organ to ischemia.
Liver
PCAS patients, especially those with longer ischemic times, can present with liver complications. About 50% of PCAS patients present with acute liver failure (ALF), while about 10% may present with the more severe hypoxic hepatitis.[19] Development of hypoxic hepatitis predicts poor PCAS outcomes, however ALF-similar to AKI- is not necessarily associated with poor outcomes.[19]
Coagulation
PCAS is associated with pro-thrombotic
Endocrine
The endocrine functions most clinically relevant to PCAS are glycemic control and the hypothalamic–pituitary–adrenal axis (HPA axis). Regarding blood glucose levels, it is very common for PCAS to present with hyperglycemia; the hyperglycemia is usually higher in diabetic patients than non-diabetic patients.[8] Mechanisms for hyperglycemia in PCAS are mostly similar as those in stress-induced hyperglycemia and therefore include elevated cortisol levels, catchecholamine surges and elevated cytokine levels. Blood glucose levels are associated with poor outcomes in a U-shaped distribution, meaning that both very high and very low levels of glucose are associated with poor outcomes.[22] Regarding the HPA axis, PCAS can present with elevated cortisol levels from the stress of the arrest, but relative adrenal insufficiency is not uncommon in PCAS. Lower cortisol levels have been associated with poor PCAS outcomes.[5] Newer research suggests that cardiac arrest may damage the pituitary gland, thus explaining some of the HPA dysregulation.[23]
Management
PCAS consist of five phases: the immediate phase (20 minutes after ROSC), early phase (from 20 minutes to 6–12 hours after ROSC), intermediate phase (from 6–12 to 72 hours after ROSC), recovery phase (3 days after ROSC), and the rehabilitation phase.[2] Management of PCAS is inherently variable, as it depends on the phase, organ systems affected and overall patient presentation. With the exception of targeted temperature management, there is no treatment that is unique to the pathophysiology of PCAS; therefore PCAS treatment is largely system-dependent, supportive treatment.
Targeted temperature management
Targeted temperature management (TTM) is the use of various cooling methods to reduce a patient's internal temperature. The main methods of cooling include using either cold intravenous solutions or by circulating cool fluids through an external, surface blanket/pad.[24] While most commonly applied as a post-ROSC intervention, there are some studies and EMS systems that start the cooling process in the initial intra-arrest stage.[25][26] Patients are generally cooled to a range of 32-36 °C. As of January 2021, there is active debate about the ideal cooling temperature but there is generally agreement that PCAS patients benefit by not being hyperthermic.[27]
TTM is an important therapy in PCAS because it directly targets the systemic nature of the pathophysiological inflammatory and metabolic processes. TTM works through three major mechanisms. First, it decreases metabolism 6% to 7% per 1 °C decrease in temperature. Second, it decreases cell apoptosis which reduces tissue damage. Third, TTM directly reduces inflammation and ROS production.[26]
System-based treatment
PCAS can present variably depending on intra-arrest dynamics and patient-specific variables. Therefore, there is no universally applicable treatments for PCAS other than TTM. However, because there are generally predictable problems, the table below presents some of the more common treatments; supporting one organ system generally has mutual benefits for the healing of other body systems.[28] These treatments, while common, may not be applicable to every patient.
System | Common complications | Common supportive treatments |
---|---|---|
Brain | Hypoxic brain injury, seizures | Hemodynamic monitoring and optimization, Ventilator management, glucose control, antiepileptics |
Cardiovascular | Hemodynamic instability, cardiogenic shock, myocardial infarction, dysrhythmia | Hemododynamic monitoring, vasopressors, antiarrhythmics, diuretics, blood transfusion, crystalloid therapy, ACLS, PCI, ECMO |
Pulmonary | ARDS, pneumonia, pulmonary contusion, pulmonary edema | Intubation, ventilator management, oxygen therapy, antibiotics |
Renal | Acute Kidney Injury, electrolyte imbalances, metabolic acidosis | Dialysis, electrolyte replacement, diuretics |
Hepatic | Acute Liver Injury, hypoxic hepatitis | Transplantation |
Coagulatory | Thrombosis (Pulmonary embolism, DVTs), DIC | fibrinolytics, platelet transfusion, IVCF
|
Endocrine | Dysglycemia, adrenal disorders | Insulin therapy, glucose therapy, corticosteroids |
Prognosis
Survival from PCAS is convoluted with survival from cardiac arrest generally. There are two common metrics used to define "survival" from cardiac arrest and subsequent PCAS. First is survival-to-hospital-discharge which binarily describes whether one survived long enough to leave the hospital. The second metric is neurological outcome which describes the cognitive function of a patient who survives arrest. Neurological outcome is frequently measured with a CPC score or mRS score.[29] Cardiac arrest and PCAS outcomes are influenced by many complicated patient and treatment variables which allows for a wide array of outcomes ranging from full physical and neurological recovery to death.
PCAS outcomes are generally better under certain conditions including: fewer patient comorbidities, initial shockable rhythms, rapid CPR responses, and treatment at a high-volume cardiac arrest center.[30][31][32] Cardiac arrest survival-to-hospital-discharge, as of 2020[update], is around 10%.[33] Common long term complications of cardiac arrest and subsequent PCAS include: anxiety, depression, PTSD, fatigue, post–intensive care syndrome, muscle weakness, persistent chest pain, myoclonus, seizures, movement disorders and risk of re-arrest.[34][35][36]
Research
Research on PCAS benefits from disease-specific work as well as general improvements in critical care treatments. As of 2022,[37] research on PCAS includes, non-exclusively, work on early resolution of ischemia through pre-hospital extracorporeal membrane oxygenation,[38] and wide distribution of defibrillators and CPR-trained bystanders, continued investigation of TTM,[39] use of immunosuppressive drugs such as steroids[40] and tocilizumab,[41] the use of cytoprotective perfusates,[42] and the use cerebral tissue oxygen extraction fraction.[43]
See also
References
- ^ Abella, Benjamin S.; Bobrow, Bentley J. (2020), Tintinalli, Judith E.; Ma, O. John; Yealy, Donald M.; Meckler, Garth D. (eds.), "Post–Cardiac Arrest Syndrome", Tintinalli's Emergency Medicine: A Comprehensive Study Guide (9 ed.), New York, NY: McGraw-Hill Education, retrieved 2022-01-19
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