Shock is an event of Organhypoperfusion with resultant cellular dysfunction and cell death. Among the pathological mechanisms decreased circulating volume, reduced cardiac ejection and vasodilation and occasionally peripheral shunts may belong to bypass the capillary region. Symptoms include a change of consciousness, tachycardia, hypotension and oliguria. The diagnosis is made clinically, it includes a blood pressure measurement and occasionally the use of markers for Gewebehypoperfusion (z. B. lactate, base deficit). The treatment is effected by fluid administration, including blood products, if necessary, correction of the underlying disorder and in need for vasopressor.

Shock is an event of Organhypoperfusion with resultant cellular dysfunction and cell death. Among the pathological mechanisms decreased circulating volume, reduced cardiac ejection and vasodilation and occasionally peripheral shunts may belong to bypass the capillary region. Symptoms include a change of consciousness, tachycardia, hypotension and oliguria. The diagnosis is made clinically, it includes a blood pressure measurement and occasionally the use of markers for Gewebehypoperfusion (z. B. lactate, base deficit). The treatment is effected by fluid administration, including blood products, if necessary, correction of the underlying disorder and in need for vasopressor. Pathophysiology The fundamental error when shock is reduced perfusion of vital organs. If the perfusion reduced as much once that the O2 supply to the cells for the aerobic metabolism is no longer sufficient, it comes to an increased anaerobic metabolism in the cells, thus increasing CO2 production and accumulation of lactate. The cellular functions decrease. Holds the shock of it can cause irreversible cell damage or cellular death. In shock both the cascade of inflammatory mediators as well as the coagulation of blood in the hypoperfundierten regions may be triggered. Hypoxic vascular endothelial cells to activate leukocytes that bind to endothelium and there directly damaging agents (eg. B. O2 reactive compounds, proteolytic enzymes) and inflammatory mediators (cytokines, leukotrienes, tumor necrosis factor [TNF]) release. Some of these mediators bind to cell surface receptors and activate the “nuclear factor kappa B” (NFkB), which leads to the formation of other cytokines and nitric oxide (NO), a potent vasodilator. Septic shock (sepsis and septic shock) can take a more inflammatory progressive form than other types of shock, because there the action of bacterial toxins, mainly the endotoxins dominated. In septic shock, vasodilation of the capacitance vessels to blood “pooling” and thus leads to hypotension due to the relative hypovolemia (so that a large vessel volume is a relatively seen low blood volume opposite). Due to localized vasodilation blood is on capillary bypasses (shunting). Thus, a circumscribed focal hypoperfusion is possible, although the cardiac pumping capacity and blood pressure are normal. Significantly increased formation of NO results in the conversion in peroxynitrite (PN). These free radicals cause mitochondrial damage and decrease in ATP production. The circulation of the microvessels including capillaries is reduced, although the circulation of large vessels is maintained in the case of septic shock. The mechanical transfer of the microvessels can, at least partially, leading to a reduced substrate supply to the cells. Leukocytes and platelets adhere to the endothelium. At the same time, the coagulation cascade is activated, and it comes to the deposition of fibrin. Numerous mediators enhance capillary permeability together with the dysfunction of the endothelial cells. Thus, liquids and partly plasma proteins get into the interstitial space. In the gastrointestinal tract, this increased permeability leads to the translocation of Enterobacteriaceae from the lumen, possibly with the consequence of sepsis and metastatic infection. Neutrophil apoptosis may be inhibited, so that lead to an enhanced release of inflammatory mediators. In other cells, apoptosis can be increased. Increased cell death and thus worsening organ function are the consequences. In the early stages of shock, blood pressure does not always reduced (although it probably comes to hypotension, when the shock is not canceled). all patients nor have low blood pressure in shock. The extent and consequences of hypotension vary with the extent of physiological compensation mechanisms and the underlying disease. Thus, a mild hypotension, which can be well tolerated by a healthy young patients lead in older people with significant atherosclerosis in severe cerebral damage or cardiac and renal dysfunction. Compensation When beginning the O2 delivery (DO2) decreases, the fabric compensate for this by an increased O2 extraction. The low arterial pressure triggers adrenergic receptors that lead to sympathikusvermittelter vasoconstriction and often also cause an increase in heart rate. Input vasoconstriction is selectively and pumps the blood to the central nervous system and heart and away from the circulation in the Splanchnikusgefäßen. Circulating ?-adrenergic amines (epinephrine, norepinephrine) increase cardiac pump power and provide increased release of corticosteroids from the adrenal cortex, as well as of renin from the kidney and glucose from the liver. The increased accumulation of glucose can thereby cause further damage to already damaged mitochondria and thus lactate intensivieren.Reperfusion reperfusion already ischemic cells can cause further damage. Where substrates are washed in again, the activity of neutrophils may increase, continue to increase the production of damaging superoxide and hydroxyl radicals. After blood flow is restored, inflammatory acting mediators can then in the various organs zirkulieren.Multiorganversagen (multiple organ dysfunction syndrome, MODS): The combination of direct and caused by reperfusion injury may for MODS with functional failure of ? 2 organs as a result of a life-threatening disease lead or injury. A MODS can develop from any form of shock, but is usually found associated with infections. Organ failure is one of the typical signs of septic shock (sepsis and septic shock). A MODS results in> 10% of patients with severe trauma and is the most common reason for a fatal outcome in the patients who survive the first 24 hours. Each organ system can be affected. However, the most common target organ is the lung. Here the increased membrane permeability leads to accumulation of fluid in the alveoli and additional inflammation. The progressive hypoxia is often refractory to an increased O2 supply are. This is called acute lung injury or in accordance with severe forms as acute lung injury ( “acute respiratory distress syndrome”, ARDS) denotes (acute hypoxic respiratory failure (AHRF ARDS)). The kidneys are affected if the renal perfusion drops below a critical value. It comes to acute tubular necrosis and renal insufficiency, which are expressed in serum by oliguria and continued rise in creatinine. In the heart of the coronary perfusion is reduced and increase in the mediators reduced the contractility (including TNF and IL-1), myocardial compliance deteriorated and the ? receptors are in their responsiveness reduced ( “down-regulation”). These factors reduce the cardiac output and worsen both myocardial and systemic perfusion. There is therefore an often lethal ending vicious circle. Arrhythmias can occur. In the gastrointestinal tract to ileus and submucosal hemorrhage can develop. The perfusion of the liver can cause focal or extensive hepatocellular necrosis. This leads to increases in transaminases and bilirubin and decreased production of clotting factors. Etiology and Classification There are various pathological mechanisms of Organhypoperfusion and shock. A shock may be of a volume shortage out develop (hypovolemic shock), by vasodilation caused (distributive shock), by a primary drop of the cardiac pumping performance (both in cardiogenic and during obstructive shock) or a combination of these pathological mechanisms are triggered. Hypovolemic shock A hypovolemic shock caused by a critical waste of intravascular volume. Reduced venous return (preload) results in decreasing ventricular filling and reduced stroke volume. Can not in this situation, the heart rate increased, there is a decrease in cardiac output. A common cause of shock is the bleeding (hemorrhagic shock). Typical triggers include trauma, surgical interventions, peptic ulcers, esophageal varices or a ruptured aortic aneurysm. The bleeding can thereby obviously (as hematemesis, melena) or hard to see his (bleeding in ectopic pregnancy). Hypovolemic shock can set up as a result of the increased loss of other body fluids other than blood (hypovolemic shock due to fluid loss). Hypovolemic shock due to fluid loss localization of the fluid loss type of loss skin thermally or chemically induced burns, sweating from exposure to extreme heat gastrointestinal vomiting, diarrhea kidney diabetes mellitus or insipidus, adrenal insufficiency, “salt-wasting” nephritis, polyurische phase after acute tubular lesion, use of potent diureticsCrossing intravascular fluid into the extravascular space Increased capillary permeability as a result of inflammation or traumatic injury (eg. B. contusion), anoxia, cardiac arrest, sepsis, intestinal ischemia, acute pancreatitis So may be (with increased losses) a reason, inadequate fluid intake. Can not be met, the amount consumed, perhaps a thirst impaired perception leads due to neurological damage or other physical weakness to further reduce the water supply. In hospitalized patients hypovolemia may result in that the first signs of circulatory insufficiency be misinterpreted as cardiogenic and therefore, the liquid supply by concomitant administration of diuretics reduced wird.Distributiver shock The total circulating blood volume is normal. A distributive shock arising from a relative imbalance of intravascular volume due to arterial or venous vasodilation. In some cases, cardiac output (and the DO2) normal, but the increased blood flow through arteriovenous shunts bypasses the capillary bed. This bypass and decoupled O2 transport lead to hypoperfusion of cells (shown on decreasing O2 consumption). In other situations, the blood in the venous capacity vessels collected ( “venous pooling”), and the cardiac ejection decreases. A distributive shock can be caused by anaphylaxis (anaphylactic shock, anaphylaxis), by bacterial infections with release of endotoxins (septic shock, sepsis and septic shock), by severe spinal cord injuries, generally above T4 (neurogenic shock) or by ingestion of certain drugs or toxins (eg., nitrates, opioids, Sympathikusantagonisten). Both anaphylactic and septic shock often did you also a Hypovolämiekomponente.Kardiogener and obstructive shock A cardiogenic shock caused by relative or absolute reduction in cardiac output due to a primary cardiac disorder. The obstructive shock resulting from mechanical factors that interfere with the filling and emptying of the heart or great vessels. A list of causes can be found in pathological mechanisms of cardiogenic and obstructive shock. Pathological mechanisms of cardiogenic shock and obstructive type mechanism basic Obstructive Mechanical interference with the vetrikulären filling Tension, compression of the vena cava, cardiac tamponade, atrial tumor or -thrombus interference with ventricular emptying cardiogenic pulmonary embolism deterioration of myocardial contractility Myokardisch ämie or myocardial infarction, myocarditis, drug heart rhythm abnormalities tachycardia, bradycardia Structural cardiac disorders Acute mitral or aortic regurgitation, rupture of the ventricular septum, malfunction of a replacement valve symptoms and complaints of inertia, confusion and sleepiness are common signs. The hands and feet are pale, cold and damp, often livid, as are the earlobes, nose and the nail bed. The capillary refill time is extended. With the exception of distributive shock, the skin color appears grayish or dark and damp. A significant Schwitzneigung can draw near. Often, only the femoral pulses or the carotid pulse can be palpated. The peripheral pulses are weak and usually fast. Tachypnea and hyperventilation are possible. Blood pressure is rather low (<90 mmHg systolic) or undetectable. Is a direct measurement with an intra-arterial catheter (vascular access: Procedure) performed often resulting higher and more accurate values. Urine production is also reduced. A distributive shock causes similar symptoms. However, the skin appears here rather hot or flushed, especially during sepsis. The pulses are usually well palpable. In septic shock chills usually precedes the ever-present fever. Some patients with anaphylactic shock show urticaria or wheezing. Numerous other symptoms (chest pain, dyspnea, abdominal pain) can depending on the underlying disease or even draw near secondarily as a result of organ failure. Diagnosis Clinical evaluation trends in test results Diagnosis is usually clinical and based on the detection of the insufficient tissue perfusion (clouding, oliguria, peripheral cyanosis), and the presence of appropriate compensation mechanisms (tachycardia, tachypnea, sweating). Specific criteria are the clouding of consciousness, tachycardia> 100 / min, respiratory rate> 22 / min, hypotension (systolic blood pressure <90 mmHg), or a drop in blood pressure by 30 mmHg compared to the pre-value, and a urine production of <0.5 ml / kg / h. The laboratory findings support the diagnosis by a lactate> 3 mmol / l, a base deficit <- 4 mEq / l and a PaCO2 <32 mmHg. However, none of these individual values ??is proving itself, and each must be considered in the clinical context, given its tendency (d. E. Deterioration or improvement) and to which in each case include the appropriate physical findings. Recently, the measurement of sublingual PCO2 and the near-infrared spectroscopy were introduced as a non-invasive and fast techniques with which one can determine the shock level. However, these methods have not yet been validated in a larger scale until now. to recognize diagnosis of the causes The cause is important to determine as the form of shock accurate. Mostly these causality is easy to clear up by history or physical examination and simple tests. Chest pain (with or without accompanying dyspnea) suggests a myocardial infarction, aortic dissection or pulmonary embolism. A systolic murmur may indicate a Ventrikelseptumruptur or mitral regurgitation as a result of acute myocardial infarction. A diastolic murmur is considered evidence of aortic regurgitation of aortic dissection with inclusion of the aortic root. Pericardial tamponade should be suspected in Jugularvenendistension, muffled heart sounds, and a paradoxical pulse. A pulmonary embolism, which is pronounced enough to pull a shock after themselves, leading to a decrease in O2 saturation and occurs more frequently under special circumstances, including prolonged bed rest and after surgery. Necessary investigation procedures include ECG, troponin I, chest x-ray image, lung scan, spiral CT and echocardiography. Abdominal or back pain and strained abdominal let pancreatitis, suggests the rupture of an abdominal aortic aneurysm, peritonitis, or in women of childbearing age, even a rupture in ectopic pregnancy. A pulsating mass in the midline must make one think of a ruptured aortic aneurysm. A painful tumor in the adnexal region can be considered as an indication of an ectopic pregnancy. Typical investigation process includes a abdominal CT (if the patient is unstable, it is also an ultrasound at the bedside to make). Furthermore, a complete blood count should be created. The determination of amylase and in women of childbearing age to carry out a pregnancy test in the urine is additionally required. Fever, chills and infectious focal signs suggest septic shock. This is especially true for immunocompromised patients. Isolated fever, connected to the corresponding medical history and clinical situation can indicate a heat stroke. Among the studies of the chest x-ray, urine examination, a complete blood count, Wunden-, blood and urine cultures and bacterial testing of other body fluids include. In a few patients, the cause remains unclear. In patients without evidence of focal symptoms or stove characters that help to determine the cause, an ECG, a measurement of the cardiac enzymes, a chest X-ray and an arterial blood gas analysis should be made. When such investigations turn out normal, are among the most probable causes have not yet done a drug overdose, an infection not previously recognized (with the possible consequence of toxic shock), anaphylactic or obstructive Schock.Zusatzuntersuchungen If, ECG and chest X-ray are performed. Among the laboratory tests include complete blood counts, electrolytes, serum urea, creatinine, prothrombin time according to Quick, liver function tests, fibrinogen and fibrin. With these provisions, the present output status of the patient can be raised. Provided that the volume status is difficult to determine, the monitoring of central venous pressure can (CVP) or the Pulmonalarterienverschlussdrucks (PCWP or PAOP) provide important orientation. A CVP <5 mm Hg (<7 cm H2O) or PCWP <8 mmHg can indicate hypovolemia. However, the CVP may also have higher values ??with pre-existing pulmonary hypertension despite hypovolemia. A quick echocardiography at bedside (by the attending physician) to determine the adequacy of cardiac filling is increasingly used to evaluate the shock. Prognosis and Treatment The untreated shock usually ends deleterious. Even with treatment, the mortality in cardiogenic shock after myocardial infarction (60-65%) or in septic shock (30-40%) is high. The prognosis depends on the trigger mechanism of the underlying or adventitious disease, the period between the beginning and diagnosis of shock events and the adequacy of early stage onset of therapeutic measures. General Stroke Treatment One of the first measures is to keep the patient sufficiently warm. External bleeding have stopped, kept the airway and ensure the ventilation and respiratory support to start if needed. Any oral delivery is prevented. The patient's head must be stored to one side to prevent aspiration in case of vomiting. The treatment begins concurrently with the clinical findings. Via mask increases the O2 offer. (Restoring and Backing up the airways: Endotracheal intubation) in severe shock or inadequate spontaneous breathing, a Luftwegintubation machine with arterial ventilation is required. Two large (14-16 gauge) intravenous catheters are inserted into separate peripheral veins. If a peripheral venipuncture first is not feasible, alternatively, a central venous catheter, or, especially in children, an intraosseous access can be used (Vascular Access: Intraosseous infusion). Most 1000 ml (or 20 ml / kg in children) are infused a 0.9% NaCl solution for 15 min. With greater blood flow Ringer's lactate solution is usually selected. The infusion is continued until normal clinical parameters. Smaller volumes (eg. B. 250-500 ml) are added in such patients, signs of right heart failure show high (jammed neck veins) or have suffered an acute myocardial infarction. Such volume administration ( "fluid challenge") should not be done in patients with pulmonary edema. All other fluid therapy is based on the underlying clinical conditions. To this end, a more extensive monitoring with CVP and PAOP measurement is often required. cava cardiac ultrasound at the bedside to assess contractility and respiratory variability of V. can help to balance the need for additional fluid against the need for inotropic support. Patients in shock are seriously ill and thus be laid on an intensive care unit. To the monitoring measures the ECG monitoring, measurement of systolic, diastolic and arterial medium pressure and preferably an arterial blood pressure measurement by an intra-arterial catheter and the pulse oximetry, further monitoring of respiratory rate and tidal depth, urine excretion (with horizontal urinary catheter), body temperature, pulse quality , skin temperature and color as well as the other clinical status, including the sensory situation (for example, using the Glasgow coma scale, see table. Glasgow coma scale *). CVP and PAOP measurement and the determination of cardiac output by thermodilution via pulmonary artery catheter (Monitoring and analysis of intensive care patients: Procedure) can be useful in diagnosis and therapy management of shock patients. This is especially true for the shock of undetermined etiology or complex and severe cases in which draw near oliguria or pulmonary edema. With echocardiography (transthoracic at the bedside or transesophageal made) is only a less invasive alternative monitoring method. Regular determination of arterial blood gases and hematocrit, electrolytes, serum creatinine and blood lactate are standard. The sublingual CO2 determination (Other forms of monitoring) is, where available, an option for non-invasive monitoring of visceral perfusion. A clearly structured schedule facilitates the therapeutic approach considerably. Clinical Calculator: Mean vessel pressure (systemic or pulmonary) Due to the Gewebeminderperfusion intramuscular absorption of drugs is unreliable. All parenteral agents to be administered intravenously. Opioids should generally be avoided, as they lead to vasodilation. Severe pain treated with morphine (1-4 mg i.v. over 2 min, if necessary every 10-15 min re-dose). Although the cerebral hypoperfusion can cause anxiety, sedatives or tranquilizers are not used routinely. After the start of the first measures the specific treatment to the particular clinical conditions is aligned. Complementary therapy is based on the type of shock Schocks.Hämorrhagischer In hemorrhagic shock, surgical restoration of the bleeding site has first priority. Forced fluid replacement (intravenous fluid replacement) and surgical treatment must be made at the same time as possible. Blood products and crystalloid solutions are used for resuscitation. Packed red blood cells and plasma are, however, earlier and at a ratio of 1: 1 considered in patients likely to need a massive transfusion (blood products). Such lack of response to volume administration should be seen as an indication of a still inadequate infusion or not previously recognized persistent bleeding. Vasopressors are not displayed in this situation. These substances are only used if, in addition, a cardiac, obstructive or distributive shock component vorliegt.Distributiver shock When distributive shock with extended hypotension after the initial volume replacement with 0.9% NaCl solution, the administration of positive inotropic agents or vasopressors be considered ( z. B. dopamine, Norarenalin, inotropes and vasoactive catecholamines). Patients with septic shock are with broad-spectrum antibiotic treatment (antibiotics). In anaphylactic shock regardless of the extent of the volume administration (especially while bronchoconstriction) should epinephrine (0.05-0.1 mg iv and subsequent Epinephrininfusion of 5 mg in 500 ml of 5% glucose solution at a dose of 10 ml / h or 0, are given 02 ug / kg / min) (anaphylaxis). Inotropic agents and vasoactive catecholamines active agent dosage Hemodynamic effect of noradrenaline 4 mg / 250 ml or 500 ml of 5% glucose solution as a continuous intravenous infusion of 8-12 g / min initially, then 2-4 g / min until stabilization; often large dose variability ?-adrenergic: ?-adrenergic vasoconstriction: inotropic and chronotropic action * dopamine 400 mg / 500 ml 5% glucose solution as a continuous intravenous infusion of 0.3 to 1.25 ml (250-1000 .mu.g) / min 2- in the low dose range at high dose requirements ?-adrenergic 10 ug / kg / min 20 ug / kg / min: vasoconstriction ?-adrenergic: inotropic and chronotropic action, vasodilating Nonadrenerg: vasodilation renal and splanchnic dobutamine 250 mg / 250 ml 5% glucose solution ‡ inotropic effect: as a continuous intravenous infusion of 2.5-10 ug / kg / min ?-adrenergic * No noticeable effect due to excessive increase in arterial pressure. † effect depending on dose and underlying pathophysiology. ‡ Chronotropic, arrhythmogenic and direct vascular effect in the lower dose range minimal. In cardiogenic shock cardiogenic shock have structural damage (flap malfunction, Ventrikelseptumruptur) be restored by surgery immediately. Koronararterienverschlüsse be addressed either by percutaneous intervention (angioplasty, stent insertion), operating system of a coronary artery bypass or thrombolysis (Overview for coronary heart disease). A Tachydysrhythmie (z. B. rapid atrial fibrillation, ventricular tachycardia) is adjusted by electrical cardioversion or drug. In the presence of a bradycardia pacemaker or transcutaneous administration of atropine (0.5 mg i.v., up to 4 individual doses per 5 min) displayed until contact of the Pacers. Isoproterenol (2 mg / 500 ml in 5% glucose solution at a dose of 1-4 g / min [0.25-1 ml / min]) is useful in some cases, when the administration of atropine had no effect. However, it is not recommended in patients with myocardial ischemia due to coronary artery disease. A shock after acute myocardial infarction is treated with fluid resuscitation, when the pulmonary capillary wedge pressure is decreased or normalwertig. 15-18 mmHg are considered as optimal values. PAC is not present, the careful administration of liquid (250-500 ml bolus of a 0.9% NaCl solution) can be tried. Through careful and repeated auscultation signs of fluid overload must be detected early. A shock after right ventricular myocardial infarction is usually little responsive to fluid resuscitation. Hier sind in der Regel Vasopressoren erforderlich. Eine kardiale Sonographie am Krankenbett zur Beurteilung von Kontraktilität und Atemvariabilität der V. cava kann helfen, den Bedarf an zusätzlicher Flüssigkeit gegen Vasopressoren abzuwägen. Inotrope Unterstützung ist ein besserer Ansatz bei Patienten mit normaler oder übernormaler Füllung. Ist die Hypotonie nur mäßig (z. B. mit einem arteriellen Mitteldruck [MAP] von 70–90 mmHg), kann mit einer Dobutamininfusion das Herzzeitvolumen gesteigert und der linksventrikuläre Füllungsdruck reduziert werden. Tachykardie und Arrhythmien treten gelegentlich im Zuge der Dobutamingabe auf, besonders im höheren Dosisbereich. In diesen Fällen ist eine Dosisreduktion erforderlich. Vasod

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