Post-cardiac Arrest Syndrome
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Post-cardiac Arrest Syndrome
Post-cardiac arrest syndrome (PCAS) is an inflammatory state of pathophysiology that can occur after a patient is Cardiopulmonary resuscitation, resuscitated from a cardiac arrest. 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. 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. Causes and mechanisms Before cardiac arrest, the body is in a state of homeostasis. Arte ...
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Cardiac Arrest
Cardiac arrest is when the heart suddenly and unexpectedly stops beating. It is a medical emergency that, without immediate medical intervention, will result in sudden cardiac death within minutes. Cardiopulmonary resuscitation (CPR) and possibly defibrillation are needed until further treatment can be provided. Cardiac arrest results in a rapid loss of consciousness, and breathing may be abnormal or absent. While cardiac arrest may be caused by heart attack or heart failure, these are not the same, and in 15 to 25% of cases, there is a non-cardiac cause. Some individuals may experience chest pain, shortness of breath, nausea, an elevated heart rate, and a light-headed feeling immediately before entering cardiac arrest. The most common cause of cardiac arrest is an underlying heart problem like coronary artery disease that decreases the amount of oxygenated blood supplying the heart muscle. This, in turn, damages the structure of the muscle, which can alter its function. ...
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Brain Ischemia
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. Ischemia leads to alterations in brain metabolism, reduction in metabolic rates, and energy crisis. There are two types of ischemia: focal ischemia, which is confined to a specific region of the brain; and global ischemia, which encompasses wide areas of brain tissue. The main symptoms of brain ischemia involve impairments in vision, body movement, and speaking. The causes of brain ischemia vary from sickle cell anemia to congenital heart defects. Symptoms of brain ischemia can include unconsciousness, blindness, problems with coordination, and weakness in the body. Other effects that may result from brain ischemia are stroke, cardiorespiratory ...
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Left Ventricular Dysfunction
Heart failure (HF), also known as congestive heart failure (CHF), is a syndrome, a group of signs and symptoms caused by an impairment of the heart's blood pumping function. Symptoms typically include shortness of breath, excessive fatigue, and leg swelling. The shortness of breath may occur with exertion or while lying down, and may wake people up during the night. Chest pain, including angina, is not usually caused by heart failure, but may occur if the heart failure was caused by a heart attack. The severity of the heart failure is measured by the severity of symptoms during exercise. Other conditions that may have symptoms similar to heart failure include obesity, kidney failure, liver disease, anemia, and thyroid disease. Common causes of heart failure include coronary artery disease, heart attack, high blood pressure, atrial fibrillation, valvular heart disease, excessive alcohol consumption, infection, and cardiomyopathy. These cause heart failure by altering the st ...
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Pulmonary Edema
Pulmonary edema, also known as pulmonary congestion, is excessive edema, liquid accumulation in the parenchyma, tissue and pulmonary alveolus, air spaces (usually alveoli) of the lungs. It leads to impaired gas exchange and may cause hypoxemia and respiratory failure. It is due to either failure of the left ventricle of the heart to remove oxygenated blood adequately from the pulmonary circulation (cardiogenic pulmonary edema), or an injury to the lung parenchyma, lung tissue directly or blood vessels of the lung (non-cardiogenic pulmonary edema). Treatment is focused on three aspects: firstly improving respiratory function, secondly, treating the underlying cause, and thirdly preventing further damage and assuring full recovery to the lung. Pulmonary edema, especially when sudden (acute), can lead to respiratory failure or cardiac arrest due to Hypoxia (medical), hypoxia. It is a cardinal feature of congestive heart failure. The term edema is from the Greek language, Greek (''oi ...
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Pulmonary Contusion
A pulmonary contusion, also known as lung contusion, is a bruise of the lung, caused by chest trauma. As a result of damage to capillaries, blood and other fluids accumulate in the lung tissue. The excess fluid interferes with gas exchange, potentially leading to inadequate oxygen levels ( hypoxia). Unlike pulmonary laceration, another type of lung injury, pulmonary contusion does not involve a cut or tear of the lung tissue. A pulmonary contusion is usually caused directly by blunt trauma but can also result from explosion injuries or a shock wave associated with penetrating trauma. With the use of explosives during World Wars I and II, pulmonary contusion resulting from blasts gained recognition. In the 1960s its occurrence in civilians began to receive wider recognition, in which cases it is usually caused by traffic accidents. The use of seat belts and airbags reduces the risk to vehicle occupants. Diagnosis is made by studying the cause of the injury, physical examinati ...
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Acute Respiratory Distress Syndrome
Acute respiratory distress syndrome (ARDS) is a type of respiratory failure characterized by rapid onset of widespread inflammation in the lungs. Symptoms include shortness of breath (dyspnea), rapid breathing (tachypnea), and bluish skin coloration (cyanosis). For those who survive, a decreased quality of life is common. Causes may include sepsis, pancreatitis, trauma, pneumonia, and aspiration. The underlying mechanism involves diffuse injury to cells which form the barrier of the microscopic air sacs of the lungs, surfactant dysfunction, activation of the immune system, and dysfunction of the body's regulation of blood clotting. In effect, ARDS impairs the lungs' ability to exchange oxygen and carbon dioxide. Adult diagnosis is based on a PaO2/FiO2 ratio (ratio of partial pressure arterial oxygen and fraction of inspired oxygen) of less than 300 mm Hg despite a positive end-expiratory pressure (PEEP) of more than 5 cm H2O. Cardiogenic pulmonary edema, a ...
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Dead Space (physiology)
Dead space is the volume of air that is inhaled that does not take part in the gas exchange, because it either remains in the conducting airways or reaches alveoli that are not perfused or poorly perfused. It means that not all the air in each breath is available for the exchange of oxygen and carbon dioxide. Mammals breathe in and out of their lungs, wasting that part of the inhalation which remains in the conducting airways where no gas exchange can occur. Components ''Total dead space'' (also known as physiological dead space) is the sum of the anatomical dead space and the alveolar dead space. Benefits do accrue to a seemingly wasteful design for ventilation that includes dead space. #Carbon dioxide is retained, making a bicarbonate-buffered blood and interstitium possible. #Inspired air is brought to body temperature, increasing the affinity of hemoglobin for oxygen, improving O2 uptake. #Particulate matter is trapped on the mucus that lines the conducting airways, allow ...
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Alveolar–arterial Gradient
The Alveolar–arterial gradient (A-, or A–a gradient), is a measure of the difference between the alveolar concentration (A) of oxygen and the arterial (a) concentration of oxygen. It is a useful parameter for narrowing the differential diagnosis of hypoxemia. The A–a gradient helps to assess the integrity of the alveolar capillary unit. For example, in high altitude, the arterial oxygen is low but only because the alveolar oxygen () is also low. However, in states of ventilation perfusion mismatch, such as pulmonary embolism or right-to-left shunt, oxygen is not effectively transferred from the alveoli to the blood which results in an elevated A-a gradient. In a perfect system, no A-a gradient would exist: oxygen would diffuse and equalize across the capillary membrane, and the pressures in the arterial system and alveoli would be effectively equal (resulting in an A-a gradient of zero). However even though the partial pressure of oxygen is about equilibrated between the p ...
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Cardiogenic Shock
Cardiogenic shock (CS) is a medical emergency resulting from inadequate blood flow due to the dysfunction of the ventricles of the heart.Textbooks of Internal MedicinHarrison's Principles of Internal Medicine 16th Edition, The McGraw-Hill CompaniesCecil Textbook of Medicine by Lee Goldman, Dennis Ausiello, 22nd Edition (2003), W. B. Saunders CompanyThe Oxford Textbook of Medicine Edited by David A. Warrell, Timothy M. Cox and John D. Firth with Edward J. Benz, Fourth Edition (2003), Oxford University Press, Shock: An Overview
PDF by Michael L. Cheatham, MD, Ernest F.J. Block, MD, Howard G. Smith, MD, John T. Promes, MD, Surgical Critical Care Service, Department of Surgical Education,

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Myocardial Infarction Complications
Myocardial infarction complications may occur immediately following a heart attack (in the acute phase), or may need time to develop (a chronic problem). After an infarction, an obvious complication is a second infarction, which may occur in the domain of another atherosclerotic coronary artery, or in the same zone if there are any live cells left in the infarct. Post-myocardial complications occur after a period of ischemia, these changes can be seen in gross tissue changes and microscopic changes. Necrosis begins after 20 minutes of an infarction. Under 4 hours of ischemia, there are no gross or microscopic changes noted.Kumar, V., Abbas, A. K., & Aster, J. C. (2015). Robbins and Cotran pathologic basis of disease (Ninth edition.). Philadelphia, PA: Elsevier/Saunders. From 4-24 hours coagulative necrosis begins to be seen, which is characterized by the removal of dead cardiomyocytes through heterolysis and the nucleus through karyorrhexis, karyolysis, and pyknosis. On gross exa ...
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Neuron Specific Enolase
Gamma-enolase, also known as enolase 2 (ENO2) or neuron specific enolase (NSE), is an enzyme that in humans is encoded by the ''ENO2'' gene. Gamma-enolase is a phosphopyruvate hydratase. Gamma-enolase is one of the three enolase isoenzymes found in mammals. This isoenzyme, a homodimer, is found in mature neurons and cells of neuronal origin. A switch from alpha enolase to gamma enolase occurs in neural tissue during development in rats and primates. Interactive pathway map Utility Detection of NSE with antibodies can be used to identify neuronal cells and cells with neuroendocrine differentiation. NSE is produced by small-cell carcinomas, which are neuroendocrine Neuroendocrine cells are cells that receive neuronal input (through neurotransmitters released by nerve cells or neurosecretory cells) and, as a consequence of this input, release messenger molecules ( hormones) into the blood. In this way they b ... in origin. NSE is therefore a useful tumor marker for distinguish ...
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S100B
S100 calcium-binding protein B (S100B) is a protein of the S-100 protein family. S100 proteins are localized in the cytoplasm and nucleus of a wide range of cells, and involved in the regulation of a number of cellular processes such as cell cycle progression and differentiation. S100 genes include at least 13 members which are located as a cluster on chromosome 1q21; however, this gene is located at 21q22.3. Function S100B is glial-specific and is expressed primarily by astrocytes, but not all astrocytes express S100B. It has been shown that S100B is only expressed by a subtype of mature astrocytes that ensheath blood vessels and by NG2-expressing cells. This protein may function in neurite extension, proliferation of melanoma cells, stimulation of Ca2+ fluxes, inhibition of PKC-mediated phosphorylation, astrocytosis and axonal proliferation, and inhibition of microtubule assembly. In the developing CNS it acts as a neurotrophic factor and neuronal survival protein. In the ...
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