The severity of PCAS is highly dependent on many variables including: the underlying cause of the<unk> , 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 predicable 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. As a result, any amount of cerebral ischemia, especially when it is prolonged in cases of<unk><unk> , typically results in brain injury.. Increasingly severe injury can lead to long term consequences such as cognitive dysfunction, persistent vegetative state and finally brain death. The brain starts suffering irreversible injury after about 20 minutes of ischemia. Even after blood flow is restored to the brain, patients can experience hours-days of hypotension, hypoxemia, impaired cerebrovascular autoregulation, brain edema, fever, hyperglycemia and/or seizures which further insult cerebral tissue. Diagnosis of brain injury involves neurological examination, EEG, brain imaging and/or biomarker evaluation (such as S100B and NSE). For out-of-hospital<unk><unk> , brain injury is the cause of death in most patients who undergo ROSC but ultimately die. Heart After the brain, the heart is the second most sensitive organ to ischemia. If the cause of the<unk><unk>  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<unk> . In this case, PCAS very frequently presents with myocardial dysfunction in the first minute-hours post-ROSC. This myocardial dysfunction may present as prolonged cardiogenic shock, highly variable blood pressures, reduced<unk>  output and/or dysrhythmias. PCAS myocardial dysfunction seems to start almost immediately after ROSC. Unlike brain tissue, evidence suggests that the myocardial injury is generally transient and can mostly recover within 72 hours; though full recovery may take months. Lungs While the lungs are generally oxygenated during the ischemic period of<unk> , they are still susceptible to ischemic damage. While ischemia is not the mechanism of injury, evidence suggests that the lack of perfusion through the pulmonary vasculature during an<unk>  reduces the Alveolar–arterial gradient which creates dead space. The oxygen accumulation in the alveoli encourages ROS production which then leads to pulmonary damage. This pulmonary-specific damage, together with the systemic inflammation, causes ARDS in about 50% of ROSC patients who survive for at least 48 hours. Lung complications, such as pulmonary contusion and pulmonary edema, may result from other aspects of PCAS such as CPR and left-ventricular dysfunction, respectively. Finally, pneumonia is a common pulmonary complication due to multifactoral mechanisms including: loss of airway protection, aspiration, emergency intubation, and mechanical ventilation. Kidneys The kidneys are the third most sensitive organ to ischemia. Prolonged renal ischemia from<unk><unk>  leads to Acute Kidney Injury (AKI) in about 40% of patients. While PCAS may independently present with AKI, the development of AKI can be exacerbated by the administration of intravenous contrast if the patient undergoes angiography. It is unclear if the development of AKI worsens PCAS overall prognosis, but it does not seem to be a major contributor to death or poor neurological outcome at this time. PCAS patients, both as a cause and a consequence of the<unk> , present with acid-base and electrolyte abnormalities. Accumulation of lactate and CO2 during the ischemic period largely accounts for the metabolic acidosis seen in PCAS patients, though strong ion gaps and phosphate also plays a role. Worse acidosis is generally predictive of worse outcomes. Finally, though electrolytes can present variably, PCAS patients most often demonstrate hypokalemia, hypocalcemia and hypomagnesaemia Liver PCAS patients, especially those with longer ischemic times, can present with hepatic complications. About 50% of PCAS patients present with Acute Liver Failure (ALF), while about 10% may present with the more severe hypoxic hepatitis. Development of hypoxic hepatitis predicts poor PCAS outcomes, however ALF-similar to AKI- is not necessarily associated with poor outcomes Coagulation PCAS is associated with pro-thrombotic coagulopathy. The coagulopathy is, itself, pathophysiological, but thrombi can additionally contribute to co-morbidiities in the aforementioned organ systems. The ischemia-reperfusion injury promotes Damage Associated Molecular Patterns (DAMPs) which encourage pro-inflammatory cytokine circulation, which then induces a pro-coagulopathic state. Major mechanisms of pro-coagulation in PCAS include: multiimodal activation of factors 5, 7,8 and 9 leading to a thrombin burst, decreased activity of Proteins C & S, and decreased anti-thrombin and tissue factor pathway inhibitor levels. Early PCAS (first 24 hours) is generally defined by hyperfibrinolysis, due to increased tPA activity, resulting in a risk of disseminated intravascular coagulation. However late PCAS generally presents with hypofibrinolysis, due to increased PAI-1 levels, resulting in a risk of multiorgan dysfunction. PCAS patients also generally show some degree of thrombocytopenia within the first 48 hours. Endocrine The endocrine functions most clinically relevant to PCAS are glycemic control and the 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. 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. Regarding the HPA axis, PCAS can present with elevated cortisol levels from the stress of the<unk> , but relative adrenal insufficiency is not uncommon in PCAS. Lower cortisol levels have been associated with poor PCAS outcomes. Newer research suggests that<unk><unk>  may damage the pituitary gland, thus explaing some of the HPA dysregulation.
Post-Cardiac Arrest Syndrome
Post-intensive care syndrome
Postpericardiotomy syndrome
Acute coronary syndrome
Acute aortic syndrome
Acute chest syndrome
Fat embolism syndrome
Edwards syndrome