Shock (circulatory)

The presentation of shock is variable, with some people having only minimal symptoms such as confusion and weakness. While the general signs for all types of shock are low blood pressure, decreased urine output, and confusion, these may not always be present. Specific subtypes of shock may have additional symptoms. Dry mucous membrane, reduced skin turgor, prolonged capillary refill time, weak peripheral pulses, and cold extremities can be early signs of shock. Low volume Hypovolemic shock is the most common type of shock and is caused by insufficient circulating volume. The severity of hemorrhagic shock can be graded on a 1–4 scale on the physical signs. The shock 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. This relationship has not been well established in pregnancy-related bleeding. Cardiogenic Cardiogenic shock is caused by the failure of the heart to pump effectively. Several conditions can result in this form of shock. • Cardiac tamponade, in which fluid in the pericardium prevents inflow of blood into the heart (venous return). Increased intra-abdominal pressure can result from sepsis and severe abdominal trauma. This increased pressure reduces venous return, thereby reducing lung-heart function, resulting in signs and symptoms of shock. Many of the signs of obstructive shock are similar to cardiogenic shock, although treatments differ. Symptoms of obstructive shock include: • Abnormal heart rhythms, often a fast heart rate. • Reduced blood pressure. • Cool, clammy, mottled skin, often due to low blood pressure and vasoconstriction. • Decreased urine output. Distributive Distributive shock is low blood pressure due to a dilation of blood vessels within the body. This can be caused by systemic infection (septic shock), a severe allergic reaction (anaphylaxis), or spinal cord injury (neurogenic shock). • Septic shock is the most common cause of distributive shock. • Signs of septic shock include: • Abnormal heart rhythms, often a fast heart rate • Reduced blood pressure • Decreased urine output • Altered mental status • Anaphylactic shock is caused by a severe anaphylactic reaction to an allergen, antigen, drug, or foreign protein causing the release of histamine which causes widespread vasodilation, leading to hypotension and increased capillary permeability. Signs typically occur after exposure to an allergen and may include: • Skin changes, such as hives, itching, flushing, and swelling. • Wheezing and shortness of breath. • Abdominal pain, diarrhea, and vomiting. • Lightheadedness, confusion, headaches, loss of consciousness. • High spinal injuries may cause neurogenic shock, which is commonly classified as a subset of distributive shock. The classic symptoms include a slow heart rate due to loss of cardiac sympathetic tone and warm skin due to dilation of the peripheral blood vessels. (This term can be confused with spinal shock which is a recoverable loss of function of the spinal cord after injury and does not refer to the hemodynamic instability.) Endocrine Although not officially classified as a subcategory of shock, many endocrinological disturbances in their severe form can result in shock. • Hypothyroidism (can be considered a form of cardiogenic shock) in people who are critically ill patients reduces cardiac output and can lead to hypotension and respiratory insufficiency. • Thyrotoxicosis (cardiogenic shock) may induce a reversible cardiomyopathy. • Acute adrenal insufficiency (distributive shock) is frequently the result of discontinuing corticosteroid 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. • Relative adrenal insufficiency (distributive shock) in critically ill patients where present hormone levels are insufficient to meet the higher demands. ==Cause==

Shock is a common end point of many medical conditions. Shock triggered by a serious allergic reaction is known as anaphylactic shock, shock triggered by severe dehydration or blood loss is known as hypovolemic shock, shock caused by sepsis is known as septic shock, etc. Shock itself is a life-threatening condition as a result of compromised body circulation. It can be divided into four main types based on the underlying cause: hypovolemic, distributive, cardiogenic, and obstructive. A few additional classifications are occasionally used, such as endocrinologic shock. ==Pathophysiology==

Shock is a complex and continuous condition, and there is no sudden transition from one stage to the next. At a cellular level, shock is the process of oxygen demand becoming greater than oxygen supply. Initial During the Initial stage (Stage 1), the state of hypoperfusion causes hypoxia. Due to the lack of oxygen, the cells perform lactic acid fermentation. Since oxygen, the terminal electron acceptor in the electron transport chain, is not abundant, this slows down entry of pyruvate into the Krebs cycle, resulting in its accumulation. The accumulating pyruvate is converted to lactate (lactic acid) by lactate dehydrogenase. The accumulating lactate causes lactic acidosis. Compensatory 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 the acidosis, the person will begin to hyperventilate in order to rid the body of carbon dioxide (CO2) since it indirectly acts to acidify the blood; the body attempts to return to acid–base homeostasis by removing that acidifying agent. The baroreceptors in the arteries detect the hypotension resulting from large amounts of blood being redirected to distant tissues, and cause the release of epinephrine and norepinephrine. Norepinephrine causes predominately vasoconstriction with a mild increase in heart rate, whereas epinephrine predominately causes an increase in heart rate with a small effect on the vascular tone; the combined effect results in an increase in blood pressure. The renin–angiotensin axis is activated, and arginine vasopressin (anti-diuretic hormone) is released to conserve fluid by reducing its excretion via the renal system. These hormones cause the vasoconstriction of the kidneys, gastrointestinal tract, and other organs to divert blood to the heart, lungs and brain. The lack of blood to the renal system causes the characteristic low urine production. However, the effects of the renin–angiotensin axis take time and are of little importance to the immediate homeostatic mediation of shock. Progressive/decompensated 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 while potassium ions leak out. Due to lack of oxygen, cellular respiration diminishes and anaerobic metabolism predominates. As anaerobic metabolism continues, the arteriolar smooth muscle and precapillary sphincters relax such that blood remains in the capillaries. Due to this, the hydrostatic pressure will increase and, combined with histamine release, will lead to leakage of fluid and protein into the surrounding tissues. As this fluid is lost, the blood concentration and viscosity increase, causing sludging of the micro-circulation. The prolonged vasoconstriction will also cause the vital organs to be compromised due to reduced perfusion. If the bowel becomes sufficiently ischemic, bacteria may enter the blood stream, resulting in the increased complication of endotoxic shock. Refractory At Refractory stage (stage 4), the vital organs 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 cellular ATP (the basic energy source for cells) has been degraded into adenosine in the absence of oxygen as an electron receptor in the mitochondrial matrix. Adenosine easily perfuses out of cellular membranes into extracellular fluid, furthering capillary vasodilation, and then is transformed into uric 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 to phosphorylate into ATP. ==Diagnosis==

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. Shock is, hemodynamically speaking, inadequate blood flow or cardiac 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. Tissue oxygenation is critically dependent on blood flow. When the oxygenation of tissues is compromised anaerobic metabolism will begin and lactic acid will be produced. ==Management==

Treatment of shock is based on the likely underlying cause. 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%. It is important to keep the person warm to avoid hypothermia as well as adequately manage pain and anxiety as these can increase oxygen consumption. Colloids and crystalloids appear to be equally effective with respect to outcomes., Balanced crystalloids and normal saline also appear to be equally effective in critically ill patients. If the person remains in shock after initial resuscitation, packed red blood cells should be administered to keep the hemoglobin greater than 100 g/L. Targets include a mean arterial pressure of 60 mmHg, a systolic blood pressure of 70–90 mmHg, Hypertonic fluid may also be an option in this group. Medications Vasopressors may be used if blood pressure does not improve with fluids. Common vasopressors used in shock include: norepinephrine, phenylephrine, dopamine, and dobutamine. There is no evidence of substantial benefit of one vasopressor over another; however, using dopamine leads to an increased risk of arrhythmia when compared with norepinephrine. Vasopressors have not been found to improve outcomes when used for hemorrhagic shock from trauma but may be of use in neurogenic shock. Activated protein C (Xigris), while once aggressively promoted for the management of septic shock, has been found not to improve survival and is associated with a number of complications. Activated protein C was withdrawn from the market in 2011, and clinical trials were discontinued. If used at all it should only be considered if the blood pH is less than 7.0. • 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. • Artificial heart (TAH) • Extracorporeal membrane oxygenation (ECMO) – an external device that completely replaces the work of the heart. Treatment goals The goal of treatment is to achieve a urine output of greater than 0.5 mL/kg/h, a central venous pressure of 8–12 mmHg and a mean 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. == Epidemiology ==

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. Of these, cardiogenic shock accounts for approximately 20%, hypovolemic about 20%, and septic shock about 60% of cases. ==Prognosis==

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. ==History==

There is no evidence of the word shock being used in its modern-day form prior to 1743. However, there is evidence that Hippocrates used the word exemia to signify a state of being "drained of blood". Shock or "choc" was first described in a trauma victim in the English translation of Henri-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 on gun-shot wounds.) 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. Prior to World War I, there were several competing hypotheses behind the pathophysiology of shock. Of the various theories, the most well regarded was a theory penned by George 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. 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. 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. In 1972 Hinshaw and Cox suggested the classification system for shock which is still used today. == References ==