Shock is a medical emergency and requires urgent medical care. If shock is suspected, emergency help should be called immediately. While waiting for medical care, the individual should be, if safe, laid down (except in cases of suspected head or back injuries). The legs should be raised if possible, and the person should be kept warm. If the person is unresponsive, breathing should be monitored and CPR may need to be performed.[5]
The presentation of shock is variable, with some people having only minimal symptoms such as confusion and weakness.[6] While the general signs for all types of shock arelow blood pressure, decreasedurine output, and confusion, these may not always be present.[6] While a fast heart rate is common, in those onβ-blockers, those who are athletic, and in 30% of cases of those with shock due to intra abdominal bleeding, heart rate may be normal or slow.[7] Specific subtypes of shock may have additional symptoms.[citation needed]
Thirst and dry mouth, due to fluid depletion[citation needed]
Cold and mottled skin (livedo reticularis), especially extremities, due to insufficient perfusion of the skin[11]
The severity of hemorrhagic shock can be graded on a 1–4 scale on the physical signs. Theshock index (heart rate divided by systolic blood pressure) is a stronger predictor of the impact of blood loss than heart rate and blood pressure alone.[12] This relationship has not been well established in pregnancy-related bleeding.[13]
Obstructive shock is a form of shock associated with physical obstruction of thegreat vessels of the systemic or pulmonary circulation.[14] Several conditions can result in this form of shock.
Abdominal compartment syndrome defined as an increase in intra-abdominal pressure to > 20 mmHg with organ dysfunction.[15] Increased intra-abdominal pressure can result fromsepsis and severe abdominal trauma. This increased pressure reduces venous return, thereby reducing lung-heart function, resulting in signs and symptoms of shock.[16]
Many of the signs of obstructive shock are similar to cardiogenic shock, although treatments differ. Symptoms of obstructive shock include:
Septic shock is the most common cause of distributive shock.[9] It is caused by an overwhelming systemic infection resulting invasodilation leading to hypotension. Septic shock can be caused byGram negative bacteria such as (among others)Escherichia coli,Proteus species,Klebsiella pneumoniae (which have anendotoxin on their surface that produces adverse biochemical, immunological and occasionally neurological effects which are harmful to the body), otherGram-positive cocci, such aspneumococci andstreptococci, and certain fungi as well as Gram-positivebacterial toxins. Septic shock also includes some elements of cardiogenic shock. In 1992, theACCP/SCCM Consensus Conference Committee defined septic shock: " ... sepsis-induced hypotension (systolic blood pressure < 90 mmHg or a reduction of 40 mmHg from baseline) despite adequate fluid resuscitation along with the presence of perfusion abnormalities that may include, but are not limited to:lactic acidosis, oliguria, or an acute alteration in mental status. Patients who are receivinginotropic or vasopressor agents may have a normalized blood pressure at the time that perfusion abnormalities are identified. The pathophysiology behind septic shock is as follows: 1) Systemicleukocyte adhesion to endothelial cells[19] 2) Reducedcontractility of the heart[19] 3) Activation of thecoagulation pathways, resulting indisseminated intravascular coagulation[19] 4). Increased levels ofneutrophils[19]
The main manifestations of septic shock are due to the massive release ofhistamine which causes intense dilation of the blood vessels. People with septic shock will also likely be positive forSIRS criteria. The most generally accepted treatment for these patients is early recognition of symptoms, and early administration of broad spectrum and organism specific antibiotics.[20]
High spinal injuries may causeneurogenic shock, which is commonly classified as a subset of distributive shock.[21] The classic symptoms includea slow heart rate due to loss of cardiacsympathetic tone and warm skin due to dilation of the peripheral blood vessels.[21] (This term can be confused withspinal shock which is a recoverable loss of function of thespinal cord after injury and does not refer to the hemodynamic instability.)
Although not officially classified as a subcategory of shock, manyendocrinological disturbances in their severe form can result in shock.[citation needed]
Acuteadrenal insufficiency (distributive shock) is frequently the result of discontinuingcorticosteroid treatment without tapering the dosage. However, surgery and intercurrent disease in patients on corticosteroid therapy without adjusting the dosage to accommodate for increased requirements may also result in this condition.
Shock is a common end point of many medical conditions.[9] Shock triggered by a seriousallergic reaction is known asanaphylactic shock, shock triggered by severedehydration orblood loss is known ashypovolemic shock, shock caused by sepsis is known asseptic shock, etc. Shock itself is a life-threatening condition as a result of compromisedbody circulation.[23] It can be divided into four main types based on the underlying cause: hypovolemic, distributive, cardiogenic, and obstructive.[24] A few additional classifications are occasionally used, such as endocrinologic shock.[9]
Shock is a complex and continuous condition, and there is no sudden transition from one stage to the next.[25] At a cellular level, shock is the process of oxygen demand becoming greater than oxygen supply.[6]
One of the key dangers of shock is that it progresses by apositive feedback loop. Poor blood supply leads to cellular damage, which results in an inflammatory response to increase blood flow to the affected area. Normally, this causes the blood supply level to match with tissue demand for nutrients. However, if there is enough increased demand in some areas, it can deprive other areas of sufficient supply, which then start demanding more. This then leads to an ever escalating cascade.[citation needed]
As such, shock is arunaway condition ofhomeostatic failure, where the usual corrective mechanisms relating to oxygenation of the body no longer function in a stable way. When it occurs, immediate treatment is critical in order to return an individual's metabolism into a stable, self-correcting trajectory. Otherwise the condition can become increasingly difficult to correct, surprisingly quickly, and then progress to a fatal outcome. In the particular case of anaphylactic shock, progression to death might take just a few minutes.[26]
The Compensatory stage (Stage 2) is characterised by the body employing physiological mechanisms, including neural, hormonal, and bio-chemical mechanisms, in an attempt to reverse the condition. As a result of theacidosis, the person will begin tohyperventilate in order to rid the body of carbon dioxide (CO2) since it indirectly acts to acidify the blood; the body attempts to return toacid–base homeostasis by removing that acidifying agent. Thebaroreceptors in thearteries detect thehypotension resulting from large amounts of blood being redirected to distant tissues, and cause the release ofepinephrine andnorepinephrine. Norepinephrine causes predominatelyvasoconstriction with a mild increase inheart rate, whereasepinephrine predominately causes an increase inheart rate with a small effect on thevascular tone; the combined effect results in an increase inblood pressure. Therenin–angiotensin axis is activated, andarginine vasopressin (anti-diuretic hormone) is released to conserve fluid by reducing its excretion via therenal system. These hormones cause the vasoconstriction of thekidneys,gastrointestinal tract, and other organs to divert blood to the heart,lungs andbrain. The lack of blood to the renal system causes the characteristic lowurine production. However, the effects of the renin–angiotensin axis take time and are of little importance to the immediatehomeostatic mediation of shock.[citation needed]
The Progressive stage (stage 3) results if the underlying cause of the shock is not successfully treated. During this stage, compensatory mechanisms begin to fail. Due to the decreased perfusion of the cells in the body,sodium ions build up within the intracellular space whilepotassium ions leak out. Due to lack of oxygen,cellular respiration diminishes andanaerobic metabolism predominates. As anaerobic metabolism continues, the arteriolar smooth muscle and precapillarysphincters relax such that blood remains in thecapillaries.[19] Due to this, thehydrostatic pressure will increase and, combined withhistamine release, will lead toleakage of fluid andprotein into the surrounding tissues. As this fluid is lost, the blood concentration andviscosity increase, causing sludging of the micro-circulation. The prolonged vasoconstriction will also cause the vital organs to be compromised due toreduced perfusion.[19] If the bowel becomes sufficientlyischemic, bacteria may enter the blood stream, resulting in the increased complication ofendotoxic shock.[26][19]
At Refractory stage (stage 4), the vitalorgans have failed and the shock can no longer be reversed.Brain damage and cell death are occurring, and death will occur imminently. One of the primary reasons that shock is irreversible at this point is that much of the cellularATP (the basic energy source for cells) has been degraded intoadenosine in the absence of oxygen as an electron receptor in themitochondrial matrix. Adenosine easily perfuses out of cellular membranes into extracellular fluid, furthering capillaryvasodilation, and then is transformed intouric acid. Because cells can only produce adenosine at a rate of about 2% of the cell's total need per hour, even restoring oxygen is futile at this point because there is no adenosine tophosphorylate into ATP.[26]
The diagnosis of shock is commonly based on a combination of symptoms,physical examination, and laboratory tests. Many signs and symptoms are not sensitive or specific for shock, thus many clinical decision-making tools have been developed to identify shock at an early stage.[27]
Shock is,hemodynamically speaking, inadequate blood flow orcardiac output, Unfortunately, the measurement of cardiac output requires an invasive catheter, such as a pulmonary artery catheter.Mixed venous oxygen saturation (SmvO2) is one of the methods of calculating cardiac output with a pulmonary artery catheter.Central venous oxygen saturation (ScvO2) as measured via a central line correlates well with SmvO2 and is easier to acquire.Tissueoxygenationis critically dependent on blood flow. When the oxygenation of tissues is compromisedanaerobic metabolism will begin and lactic acid will be produced.[28]
Treatment of shock is based on the likely underlying cause.[2] An openairway and sufficientbreathing should be established.[2] Any ongoing bleeding should be stopped, which may require surgery orembolization.[2]Intravenous fluid, such asRinger's lactate orpacked red blood cells, is often given.[2] Efforts to maintain a normalbody temperature are also important.[2]Vasopressors may be useful in certain cases.[2] Shock is both common and has a high risk of death.[3] In the United States about 1.2 million people present to the emergency room each year with shock and their risk of death is between 20 and 50%.[3]
The best evidence exists for the treatment ofseptic shock in adults. However, the pathophysiology of shock in children appears to be similar so treatment methodologies have been extrapolated to children.[9] Management may include securing the airway viaintubation if necessary to decrease the work of breathing and for guarding against respiratory arrest.Oxygen supplementation,intravenous fluids,passive leg raising (notTrendelenburg position) should be started andblood transfusions added if blood loss is severe.[6] In select cases, compression devices likenon-pneumatic anti-shock garments (or the deprecatedmilitary anti-shock trousers) can be used to prevent further blood loss and concentrate fluid in the body's head and core.[29] It is important to keep the person warm to avoidhypothermia[30] as well as adequately manage pain and anxiety as these can increase oxygen consumption.[6] Negative impact by shock is reversible if it's recognized and treated early in time.[23]
Aggressive intravenous fluids are recommended in most types of shock (e.g. 1–2 liternormal saline bolus over 10 minutes or 20 mL/kg in a child) which is usually instituted as the person is being further evaluated.[31]Colloids andcrystalloids appear to be equally effective with respect to outcomes.,[32] Balanced crystalloids and normal saline also appear to be equally effective in critically ill patients.[33] If the person remains in shock after initial resuscitation,packed red blood cells should be administered to keep thehemoglobin greater than 100 g/L.[6]
There is no evidence of substantial benefit of one vasopressor over another;[37] however, using dopamine leads to an increased risk of arrhythmia when compared with norepinephrine.[38] Vasopressors have not been found to improve outcomes when used forhemorrhagic shock fromtrauma[39] but may be of use inneurogenic shock.[21]Activated protein C (Xigris), while once aggressively promoted for the management ofseptic shock, has been found not to improve survival and is associated with a number of complications.[40] Activated protein C was withdrawn from the market in 2011, and clinical trials were discontinued.[40] The use ofsodium bicarbonate is controversial as it has not been shown to improve outcomes.[41] If used at all it should only be considered if the blood pH is less than 7.0.[41]
Intra-aortic balloon pump (IABP) – a device inserted into the aorta that mechanically raises the blood pressure. Use of Intra-aortic balloon pumps is not recommended in cardiogenic shock.[42]
Ventricular assist device (VAD) – A mechanical pump that helps pump blood throughout the body. Commonly used in short term cases of refractory primary cardiogenic shock.[citation needed]
The goal of treatment is to achieve a urine output of greater than 0.5 mL/kg/h, acentral venous pressure of 8–12 mmHg and amean arterial pressure of 65–95 mmHg. In trauma the goal is to stop the bleeding which in many cases requires surgical interventions. A good urine output indicates that the kidneys are getting enough blood flow.
Septic shock (a form of distributive shock) is the most common form of shock. Shock from blood loss occurs in about 1–2% of trauma cases.[35] Overall, up to one-third of people admitted to theintensive care unit (ICU) are in circulatory shock.[44] Of these, cardiogenic shock accounts for approximately 20%, hypovolemic about 20%, and septic shock about 60% of cases.[45]
The prognosis of shock depends on the underlying cause and the nature and extent of concurrent problems. Low volume, anaphylactic, and neurogenic shock are readily treatable and respond well to medical therapy.Septic shock, especially septic shock where treatment is delayed or the antimicrobial drugs are ineffective, however has a mortality rate between 30% and 80%; cardiogenic shock has a mortality rate of up to 70% to 90%, though quick treatment with vasopressors and inotropic drugs, cardiac surgery, and the use of assistive devices can lower the mortality.[46]
There is no evidence of the word shock being used in its modern-day form prior to 1743. However, there is evidence thatHippocrates used the wordexemia to signify a state of being "drained of blood".[47] Shock or "choc" was first described in a trauma victim in the English translation ofHenri-François LeDran's 1740 text, Traité ou Reflexions Tire'es de la Pratique sur les Playes d'armes à feu (A treatise, or reflections, drawn from practice ongun-shot wounds.)[48] In this text he describes "choc" as a reaction to the sudden impact of a missile. However, the first English writer to use the word shock in its modern-day connotation was James Latta, in 1795.[citation needed]
Prior toWorld War I, there were several competing hypotheses behind thepathophysiology of shock. Of the various theories, the most well regarded was a theory penned byGeorge W. Crile who suggested in his 1899 monograph, "An Experimental Research into Surgical Shock", that shock was quintessentially defined as a state of circulatory collapse (vasodilation) due to excessive nervous stimulation.[49] Other competing theories around the turn of the century included one penned by Malcom in 1907, in which the assertion was that prolonged vasoconstriction led to the pathophysiological signs and symptoms of shock.[50] In the following World War I, research concerning shock resulted in experiments by Walter B. Cannon of Harvard and William M. Bayliss of London in 1919 that showed that an increase in permeability of the capillaries in response to trauma or toxins was responsible for many clinical manifestations of shock.[51][52] In 1972 Hinshaw and Cox suggested the classification system for shock which is still used today.[53][46]
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