Post-cardiac arrest syndrome

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Post-cardiac arrest syndrome
Other namesPost-resuscitation disease
Symptoms Brain injury, myocardial injury, systemic ischemia/reperfusion response
Usual onsetAfter resuscitation from a cardiac arrest
DurationWeeks
CausesGlobal ischemia-reperfusion injury
Risk factors Prolonged cardiac arrest
Differential diagnosis Systemic inflammatory response syndrome
ManagementHemodynamic stabilization and supportive care

Post-cardiac arrest syndrome (PCAS) is an inflammatory state of pathophysiology that can occur after a patient is resuscitated from a cardiac arrest. [1] While in a state of cardiac arrest, the body experiences a unique state of global ischemia. This ischemia results in the accumulation of metabolic waste which instigate the production of inflammatory mediators. If return of spontaneous circulation (ROSC) is achieved after CPR, then circulation resumes, resulting in global reperfusion and the subsequent distribution of the ischemia products throughout the body. While PCAS has a unique cause and consequences, it can ultimately be thought of as type of global ischemia-reperfusion injury. [2] The damage, and therefore prognosis, of PCAS generally depends on the length of the patient's ischemic period; therefore the severity of PCAS is not uniform across different patients.

Contents

Causes and mechanisms

Before cardiac arrest, the body is in a state of homeostasis. Arterial blood circulates appropriately through the body, supplying oxygen to tissues while the venous blood collects metabolic waste products to be utilized elsewhere and/or eliminated from the body. However, during cardiac arrest, the body is in circulatory and pulmonary arrest. Oxygen is no longer being ventilated by the lungs, and blood ceases to circulate throughout the body. As a result, all tissues in the body start to enter a state of ischemia. In this state, metabolic waste products, such as lactic acid and carbon dioxide, begin to accumulate as there is no circulation to move these products to the appropriate organs. This state of ischemia will continue until ROSC is achieved through CPR, at which time, blood starts to be reperfused throughout the body. This reperfusion results in inflammatory injury through three overlapping mechanisms. Some complimentary combination of, first, mitochondrial damage and, second, endothelial activation, causes a release of reactive oxygen species (ROS), which initiates and/or exacerbates a pathophysiological inflammatory response. Third, reperfusion initiates an immune, inflammatory response resulting in the circulation of pro-inflammatory cytokines such as TNFα, IL-6 and IL-8 as well as complement activation (such as TCC and C3bc). [3] Unlike other causes of ischemia-reperfusion injury, such as organ transplants, PCAS results from global ischemia-reperfusion and subsequently has global organ damage.

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. [4] As a result, any amount of brain ischemia, especially when it is prolonged in cases of cardiac arrest, 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 sustains irreversible injury after about 20 minutes of ischemia. [4] 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 brain tissue. [5] Diagnosis of brain injury involves neurological examination, EEG, brain imaging and/or biomarker evaluation (such as S100B and NSE). [6] For out-of-hospital cardiac arrest, brain injury is the cause of death in most patients who undergo ROSC but ultimately die. [7]

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[ clarification needed ] that the lack of perfusion through the pulmonary vasculature during an arrest 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 acute respiratory distress syndrome in about 50% of ROSC patients who survive for at least 48 hours. [12] 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. [13]

Kidneys

The kidneys are the third most sensitive organ to ischemia. [4] Prolonged renal ischemia from cardiac arrest leads to acute kidney injury (AKI) in about 40% of patients. [14] 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. [15] PCAS patients, both as a cause and a consequence of the arrest, present with acid-base and electrolyte imbalances. Accumulation of lactate and carbon dioxide during the ischemic period largely accounts for the metabolic acidosis seen in PCAS patients, though strong ion gaps and phosphate also plays a role. [16] Worse acidosis is generally predictive of worse outcomes. [17] Finally, though electrolytes can present variably, PCAS patients most often demonstrate hypokalemia, hypocalcemia and hypomagnesaemia [8] Acute kidney injury is not the leading cause of death after cardiac arrest. However, evidence suggests that the kidney damage after a cardiac arrest should be highly considered in the prognosis of the patients' health outcome. [18]

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 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 V, VII, VIII and IX leading to a thrombin burst, decreased activity of proteins C and S, and decreased anti-thrombin and tissue factor pathway inhibitor levels. Early PCAS (first 24 hours) is generally defined by hyperfibrinolysis, due to increased tissue plasminogen activator 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. [20] PCAS patients also generally show some degree of thrombocytopenia within the first 48 hours. [21]

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.

SystemCommon complicationsCommon supportive treatments
BrainHypoxic brain injury, seizures Hemodynamic monitoring and optimization, Ventilator management, glucose control, antiepileptics
CardiovascularHemodynamic instability, cardiogenic shock, myocardial infarction, dysrhythmia Hemododynamic monitoring, vasopressors, antiarrhythmics, diuretics, blood transfusion, crystalloid therapy, ACLS, PCI, ECMO
PulmonaryARDS, pneumonia, pulmonary contusion, pulmonary edema Intubation, ventilator management, oxygen therapy, antibiotics
RenalAcute Kidney Injury, electrolyte imbalances, metabolic acidosis Dialysis, electrolyte replacement, diuretics
HepaticAcute Liver Injury, hypoxic hepatitis Transplantation
CoagulatoryThrombosis (Pulmonary embolism, DVTs), DIC Anti-Coagulation, fibrinolytics, platelet transfusion, IVCF
EndocrineDysglycemia, 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, 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

Related Research Articles

<span class="mw-page-title-main">Cardiac arrest</span> Sudden stop in effective blood flow due to the failure of the heart to beat

Cardiac arrest, also known as sudden cardiac arrest, is when the heart suddenly and unexpectedly stops beating. As a result blood will not be pumped around the body in normal circulation, consciousness will be rapidly lost, and breathing will be abnormal or absent. Without immediate intervention such as cardiopulmonary resuscitation (CPR), and possibly defibrillation, death will occur within minutes.

<span class="mw-page-title-main">Cardiopulmonary resuscitation</span> Emergency procedure for cardiac arrest

Cardiopulmonary resuscitation (CPR) is an emergency procedure consisting of chest compressions often combined with artificial ventilation, or mouth to mouth in an effort to manually preserve intact brain function until further measures are taken to restore spontaneous blood circulation and breathing in a person who is in cardiac arrest. It is recommended for those who are unresponsive with no breathing or abnormal breathing, for example, agonal respirations.

Clinical death is the medical term for cessation of blood circulation and breathing, the two criteria necessary to sustain the lives of human beings and of many other organisms. It occurs when the heart stops beating in a regular rhythm, a condition called cardiac arrest. The term is also sometimes used in resuscitation research.

<span class="mw-page-title-main">Ischemia</span> Restriction in blood supply to tissues

Ischemia or ischaemia is a restriction in blood supply to any tissue, muscle group, or organ of the body, causing a shortage of oxygen that is needed for cellular metabolism. Ischemia is generally caused by problems with blood vessels, with resultant damage to or dysfunction of tissue i.e. hypoxia and microvascular dysfunction. It also implies local hypoxia in a part of a body resulting from constriction. Ischemia causes not only insufficiency of oxygen, but also reduced availability of nutrients and inadequate removal of metabolic wastes. Ischemia can be partial or total blockage. The inadequate delivery of oxygenated blood to the organs must be resolved either by treating the cause of the inadequate delivery or reducing the oxygen demand of the system that needs it. For example, patients with myocardial ischemia have a decreased blood flow to the heart and are prescribed with medications that reduce chronotrophy and ionotrophy to meet the new level of blood delivery supplied by the stenosed vasculature so that it is adequate.

<span class="mw-page-title-main">Reperfusion injury</span> Tissue damage after return of blood supply following ischemia or hypoxia

Reperfusion injury, sometimes called ischemia-reperfusion injury (IRI) or reoxygenation injury, is the tissue damage caused when blood supply returns to tissue after a period of ischemia or lack of oxygen. The absence of oxygen and nutrients from blood during the ischemic period creates a condition in which the restoration of circulation results in inflammation and oxidative damage through the induction of oxidative stress rather than restoration of normal function.

<span class="mw-page-title-main">Brain ischemia</span> Medical condition

Brain ischemia is a condition in which there is insufficient bloodflow to the brain to meet metabolic demand. This leads to poor oxygen supply or cerebral hypoxia and thus leads to the death of brain tissue or cerebral infarction/ischemic stroke. It is a sub-type of stroke along with subarachnoid hemorrhage and intracerebral hemorrhage.

Myocardial stunning or transient post-ischemic myocardial dysfunction is a state of mechanical cardiac dysfunction that can occur in a portion of myocardium without necrosis after a brief interruption in perfusion, despite the timely restoration of normal coronary blood flow. In this situation, even after ischemia has been relieved and myocardial blood flow (MBF) returns to normal, myocardial function is still depressed for a variable period of time, usually days to weeks. This reversible reduction of function of heart contraction after reperfusion is not accounted for by tissue damage or reduced blood flow, but rather, its thought to represent a perfusion-contraction "mismatch". Myocardial stunning was first described in laboratory canine experiments in the 1970s where LV wall abnormalities were observed following coronary artery occlusion and subsequent reperfusion.

Ischemic preconditioning (IPC) is an experimental technique for producing resistance to the loss of blood supply, and thus oxygen, to tissues of many types. In the heart, IPC is an intrinsic process whereby repeated short episodes of ischaemia protect the myocardium against a subsequent ischaemic insult. It was first identified in 1986 by Murry et al. This group exposed anesthetised open-chest dogs to four periods of 5 minute coronary artery occlusions followed by a 5-minute period of reperfusion before the onset of a 40-minute sustained occlusion of the coronary artery. The control animals had no such period of “ischaemic preconditioning” and had much larger infarct sizes compared with the dogs that did. The exact molecular pathways behind this phenomenon have yet to be fully understood.

Deep hypothermic circulatory arrest (DHCA) is a surgical technique in which the temperature of the body falls significantly and blood circulation is stopped for up to one hour. It is used when blood circulation to the brain must be stopped because of delicate surgery within the brain, or because of surgery on large blood vessels that lead to or from the brain. DHCA is used to provide a better visual field during surgery due to the cessation of blood flow. DHCA is a form of carefully managed clinical death in which heartbeat and all brain activity cease.

Targeted temperature management (TTM) previously known as therapeutic hypothermia or protective hypothermia is an active treatment that tries to achieve and maintain a specific body temperature in a person for a specific duration of time in an effort to improve health outcomes during recovery after a period of stopped blood flow to the brain. This is done in an attempt to reduce the risk of tissue injury following lack of blood flow. Periods of poor blood flow may be due to cardiac arrest or the blockage of an artery by a clot as in the case of a stroke.

The Arctic Sun Temperature Management System is a non-invasive targeted temperature management system. It modulates patient temperature by circulating chilled water in pads directly adhered to the patient's skin. Using varying water temperatures and a computer algorithm, a patient's body temperature can be better controlled. It is produced by Medivance, Inc. of Louisville, Colorado.

<span class="mw-page-title-main">Coronary perfusion pressure</span>

Coronary perfusion pressure (CPP) refers to the pressure gradient that drives coronary blood pressure. The heart's function is to perfuse blood to the body; however, the heart's own myocardium must, itself, be supplied for its own muscle function. The heart is supplied by coronary vessels, and therefore CPP is the blood pressure within those vessels. If pressures are too low in the coronary vasculature, then the myocardium risks ischemia with subsequent myocardial infarction or cardiogenic shock.

A diagnosis of myocardial infarction is created by integrating the history of the presenting illness and physical examination with electrocardiogram findings and cardiac markers. A coronary angiogram allows visualization of narrowings or obstructions on the heart vessels, and therapeutic measures can follow immediately. At autopsy, a pathologist can diagnose a myocardial infarction based on anatomopathological findings.

Return of spontaneous circulation (ROSC) is the resumption of a sustained heart rhythm that perfuses the body after cardiac arrest. It is commonly associated with significant respiratory effort. Signs of return of spontaneous circulation include breathing, coughing, or movement and a palpable pulse or a measurable blood pressure. Someone is considered to have sustained return of spontaneous circulation when circulation persists and cardiopulmonary resuscitation has ceased for at least 20 consecutive minutes.

<span class="mw-page-title-main">Rearrest</span>

Rearrest is a phenomenon that involves the resumption of a lethal cardiac dysrhythmia after successful return of spontaneous circulation (ROSC) has been achieved during the course of resuscitation. Survival to hospital discharge rates are as low as 7% for cardiac arrest in general and although treatable, rearrest may worsen these survival chances. Rearrest commonly occurs in the out-of-hospital setting under the treatment of health care providers.

Remote ischemic conditioning (RIC) is an experimental medical procedure that aims to reduce the severity of ischaemic injury to an organ such as the heart or the brain, most commonly in the situation of a heart attack or a stroke, or during procedures such as heart surgery when the heart may temporary suffer ischaemia during the operation, by triggering the body's natural protection against tissue injury. Although noted to have some benefits in experimental models in animals, this is still an experimental procedure in humans and initial evidence from small studies have not been replicated in larger clinical trials. Successive clinical trials have failed to identify evidence supporting a protective role in humans.

Ischemia-reperfusion (IR) tissue injury is the resultant pathology from a combination of factors, including tissue hypoxia, followed by tissue damage associated with re-oxygenation. IR injury contributes to disease and mortality in a variety of pathologies, including myocardial infarction, ischemic stroke, acute kidney injury, trauma, circulatory arrest, sickle cell disease and sleep apnea. Whether resulting from traumatic vessel disruption, tourniquet application, or shock, the extremity is exposed to an enormous flux in vascular perfusion during a critical period of tissue repair and regeneration. The contribution of this ischemia and subsequent reperfusion on post-traumatic musculoskeletal tissues is unknown; however, it is likely that similar to cardiac and kidney tissue, IR significantly contributes to tissue fibrosis.

<span class="mw-page-title-main">Resuscitative endovascular balloon occlusion of the aorta</span> Temporary procedure to support blood pressure and stem blood loss

Resuscitative endovascular balloon occlusion of the aorta (REBOA) is a minimally invasive procedure performed during resuscitation of critically injured trauma patients. Originally developed as a less invasive alternative to emergency thoracotomy with aortic cross clamping, REBOA is performed to gain rapid control of non-compressible truncal or junctional hemorrhage. REBOA is performed first by achieving access to the common femoral artery (CFA) and advancing a catheter within the aorta. Upon successful catheter placement, an occluding balloon may be inflated either within the descending thoracic aorta (Zone 1) or infrarenal abdominal aorta (Zone 3). REBOA stanches downstream hemorrhage and improves cardiac index, cerebral perfusion, and coronary perfusion. Although REBOA does not eliminate the need for definitive hemorrhage control, it may serve as a temporizing measure during initial resuscitation. Despite the benefits of REBOA, there are significant local and systemic ischemic risks. Establishing standardized REBOA procedural indications and mitigating the risk of ischemic injury are topics of ongoing investigation. Although this technique has been successfully deployed in adult patients, it has not yet been studied in children.

Kidney ischemia is a disease with a high morbidity and mortality rate. Blood vessels shrink and undergo apoptosis which results in poor blood flow in the kidneys. More complications happen when failure of the kidney functions result in toxicity in various parts of the body which may cause septic shock, hypovolemia, and a need for surgery. What causes kidney ischemia is not entirely known, but several pathophysiology relating to this disease have been elucidated. Possible causes of kidney ischemia include the activation of IL-17C and hypoxia due to surgery or transplant. Several signs and symptoms include injury to the microvascular endothelium, apoptosis of kidney cells due to overstress in the endoplasmic reticulum, dysfunctions of the mitochondria, autophagy, inflammation of the kidneys, and maladaptive repair.

<span class="mw-page-title-main">LUCAS device</span> Device to provide mechanical CPR

The Lund University Cardiopulmonary Assist System (LUCAS) device provides mechanical chest compressions to patients in cardiac arrest. It is mostly used in emergency medicine as an alternative to manual CPR because it provides consistent compressions at a fixed rate through difficult transport conditions and eliminates the physical strain on the person performing CPR. The first generation of the LUCAS device was pneumatic, while the second and third generations are battery-operated.

References

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