Shock (circulatory)

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Shock
US Navy 120203-N-CD652-004 U.S. Naval Hospital Guantanamo Bay emergency technician (EMT) trainees work with Naval Station Guantanamo Bay firemen to.jpg
US Navy EMT trainees and firemen using IV fluid replacement in treating a trauma training mannequin to prevent hypovolemic shock.
Specialty Critical care medicine
Symptoms Initial: Weakness, fast heart rate, fast breathing, sweating, anxiety, increased thirst [1]
Later: Confusion, unconsciousness, cardiac arrest [1]
Types Low volume, cardiogenic, obstructive, distributive [2]
CausesLow volume: Severe bleeding, vomiting, diarrhea, dehydration, or pancreatitis [1]
Cardiogenic: severe heart attack (especially of the left or right ventricles), severe heart failure, cardiac contusion [1]
Obstructive: Cardiac tamponade, tension pneumothorax [1]
Distributive: Sepsis, spinal cord injury, certain overdoses [1]
Diagnostic method Based on symptoms, physical exam, laboratory tests [2]
TreatmentBased on the underlying cause [2]
Medication Intravenous fluid, vasopressors [2]
Prognosis Risk of death 20 to 50% [3]
Frequency1.2 million per year (US) [3]

Shock is the state of insufficient blood flow to the tissues of the body as a result of problems with the circulatory system. [1] [2] Initial symptoms of shock may include weakness, fast heart rate, fast breathing, sweating, anxiety, and increased thirst. [1] This may be followed by confusion, unconsciousness, or cardiac arrest, as complications worsen. [1]

Contents

Shock is divided into four main types based on the underlying cause: low volume, cardiogenic, obstructive, and distributive shock. [2] Low volume shock, also known as hypovolemic shock, may be from bleeding, diarrhea, or vomiting. [1] Cardiogenic shock may be due to a heart attack or cardiac contusion. [1] Obstructive shock may be due to cardiac tamponade or a tension pneumothorax. [1] Distributive shock may be due to sepsis, anaphylaxis, injury to the upper spinal cord, or certain overdoses. [1] [4]

The diagnosis is generally based on a combination of symptoms, physical examination, and laboratory tests. [2] A decreased pulse pressure (systolic blood pressure minus diastolic blood pressure) or a fast heart rate raises concerns. [1] The heart rate divided by systolic blood pressure, known as the shock index (SI), of greater than 0.8 supports the diagnosis more than low blood pressure or a fast heart rate in isolation. [5] [6]

Treatment of shock is based on the likely underlying cause. [2] An open airway and sufficient breathing should be established. [2] Any ongoing bleeding should be stopped, which may require surgery or embolization. [2] Intravenous fluid, such as Ringer's lactate or packed red blood cells, is often given. [2] Efforts to maintain a normal body 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]

Signs and symptoms

The presentation of shock is variable, with some people having only minimal symptoms such as confusion and weakness. [7] While the general signs for all types of shock are low blood pressure, decreased urine output, and confusion, these may not always be present. [7] While a fast heart rate is common, those on β-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. [8] 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. [9]

Low volume

Hypovolemic shock is the most common type of shock and is caused by insufficient circulating volume. [7] The most common cause of hypovolemic shock is hemorrhage (internal or external); however, vomiting and diarrhea are more common causes in children. [10] Other causes include burns, as well as excess urine loss due to diabetic ketoacidosis and diabetes insipidus. [10]

Hemorrhage classes [11]
ClassBlood loss (liters)ResponseTreatment
I<15% (0.75 L)min. fast heart rate, normal blood pressureminimal
II15–30% (0.75–1.5 L)fast heart rate, min. low blood pressureintravenous fluids
III30–40% (1.5–2 L)very fast heart rate, low blood pressure, confusionfluids and packed RBCs
IV>40% (>2 L)critical blood pressure and heart rateaggressive interventions

Signs and symptoms of hypovolemic shock include:

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. [5] This relationship has not been well established in pregnancy-related bleeding. [12]

Cardiogenic

Cardiogenic shock is caused by the failure of the heart to pump effectively. [7] This can be due to damage to the heart muscle, most often from a large myocardial infarction. Other causes of cardiogenic shock include dysrhythmias, cardiomyopathy/myocarditis, congestive heart failure (CHF), myocardial contusion, or valvular heart disease problems. [10]

Symptoms of cardiogenic shock include:

Obstructive

Obstructive shock is a form of shock associated with physical obstruction of the great vessels of the systemic or pulmonary circulation. [13] Several conditions can result in this form of shock.

Many of the signs of obstructive shock are similar to cardiogenic shock, however treatments differ. Symptoms of obstructive shock include:

Distributive

Systemic inflammatory response syndrome [16]
FindingValue
Temperature <36 °C (96.8 °F) or >38 °C (100.4 °F)
Heart rate >90/min
Respiratory rate >20/min or PaCO2<32 mmHg (4.3 kPa)
WBC <4x109/L (<4000/mm3), >12x109/L (>12,000/mm3), or ≥10% bands

Distributive shock is low blood pressure due to a dilation of blood vessels within the body. [7] [17] This can be caused by systemic infection (septic shock), a severe allergic reaction (anaphylaxis), or spinal cord injury (neurogenic shock).

Endocrine

Although not officially classified as a subcategory of shock, many endocrinology disturbances in their severe form can result in shock.[ citation needed ]

Cause

TypeCause
Low volumeFluid loss such as bleeding or diarrhea
CardiogenicIneffective pumping due to heart damage
ObstructiveBlood flow to or from the heart is blocked
DistributiveAbnormal flow within the small blood vessels [21]

Shock is a common end point of many medical conditions. [10] 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. [22] It can be divided into four main types based on the underlying cause: hypovolemic, distributive, cardiogenic, and obstructive. [23] A few additional classifications are occasionally used, such as endocrinologic shock. [10]

Pathophysiology

Effects of inadequate perfusion on cell function. Shock-cell2.svg
Effects of inadequate perfusion on cell function.

There are four stages of shock. Shock is a complex and continuous condition, and there is no sudden transition from one stage to the next. [24] At a cellular level, shock is the process of oxygen demand becoming greater than oxygen supply. [7]

One of the key dangers of shock is that it progresses by a positive 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.

As such, shock is a runaway condition of homeostatic 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. [6]

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). CO2 indirectly acts to acidify the blood, so 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.[ citation needed ]

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. [18] 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. [18] If the bowel becomes sufficiently ischemic, bacteria may enter the blood stream, resulting in the increased complication of endotoxic shock. [6] [18]

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. [6]

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. [25] A high degree of suspicion is necessary for the proper diagnosis of shock.

The first change seen in shock is increased cardiac output followed by a decrease in mixed venous oxygen saturation (SmvO2) as measured in the pulmonary artery via a pulmonary artery catheter. [26] Central venous oxygen saturation (ScvO2) as measured via a central line correlates well with SmvO2 and are easier to acquire. If shock progresses anaerobic metabolism will begin to occur with an increased blood lactic acid as the result. While many laboratory tests are typically performed, there is no test that either conclusively makes or excludes the diagnosis. A chest X-ray or emergency department ultrasound may be useful to determine volume status. [7] [8]

Management

The best evidence exists for the treatment of septic shock in adults. However, the pathophysiology of shock in children appears to be similar so treatment methodologies have been extrapolated to children. [10] Management may include securing the airway via intubation if necessary to decrease the work of breathing and for guarding against respiratory arrest. Oxygen supplementation, intravenous fluids, passive leg raising (not Trendelenburg position) should be started and blood transfusions added if blood loss is severe. [7] In select cases, compression devices like non-pneumatic anti-shock garments (or the deprecated military anti-shock trousers) can be used to prevent further blood loss and concentrate fluid in the body's head and core. [27] It is important to keep the person warm to avoid hypothermia [28] as well as adequately manage pain and anxiety as these can increase oxygen consumption. [7] Negative impact by shock is reversible if it's recognized and treated early in time. [22]

Fluids

Aggressive intravenous fluids are recommended in most types of shock (e.g. 1–2 liter normal saline bolus over 10 minutes or 20 mL/kg in a child) which is usually instituted as the person is being further evaluated. [29] Colloids and crystalloids appear to be equally effective with respect to outcomes., [30] Balanced crystalloids and normal saline also appear to be equally effective in critically ill patients. [31] 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. [7]

For those with hemorrhagic shock, the current evidence supports limiting the use of fluids for penetrating thorax and abdominal injuries allowing mild hypotension to persist (known as permissive hypotension). [32] Targets include a mean arterial pressure of 60 mmHg, a systolic blood pressure of 70–90 mmHg, [7] [33] or until the patient has adequate mentation and peripheral pulses. [33] Hypertonic fluid may also be an option in this group. [34]

Medications

Epinephrine auto-injector Epipen.jpg
Epinephrine auto-injector

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; [35] however, using dopamine leads to an increased risk of arrhythmia when compared with norepinephrine. [36] Vasopressors have not been found to improve outcomes when used for hemorrhagic shock from trauma [37] but may be of use in neurogenic shock. [20] 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. [38] Activated protein C was withdrawn from the market in 2011, and clinical trials were discontinued. [38] The use of sodium bicarbonate is controversial as it has not been shown to improve outcomes. [39] If used at all it should only be considered if the blood pH is less than 7.0. [39]

People with anaphylactic shock are commonly treated with epinephrine. Antihistamines, such as Benadryl (diphenhydramine) or ranitidine are also commonly administered. Albuterol, normal saline, and steroids are also commonly given.

Mechanical support

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. [33] Overall, up to one-third of people admitted to the intensive care unit (ICU) are in circulatory shock. [41] Of these, cardiogenic shock accounts for approximately 20%, hypovolemic about 20%, and septic shock about 60% of cases. [42]

Prognosis

Sepsis mortality Sepsis mortality.png
Sepsis mortality

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. [43]

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". [44] 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.) [45] 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. [46] 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. [47] 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. [48] [49] In 1972 Hinshaw and Cox suggested the classification system for shock which is still used today. [50] [43]

Related Research Articles

<span class="mw-page-title-main">Sepsis</span> Life-threatening organ dysfunction triggered by infection

Sepsis is a potentially life-threatening condition that arises when the body's response to infection causes injury to its own tissues and organs.

<span class="mw-page-title-main">Respiratory failure</span> Inadequate gas exchange by the respiratory system

Respiratory failure results from inadequate gas exchange by the respiratory system, meaning that the arterial oxygen, carbon dioxide, or both cannot be kept at normal levels. A drop in the oxygen carried in the blood is known as hypoxemia; a rise in arterial carbon dioxide levels is called hypercapnia. Respiratory failure is classified as either Type 1 or Type 2, based on whether there is a high carbon dioxide level, and can be acute or chronic. In clinical trials, the definition of respiratory failure usually includes increased respiratory rate, abnormal blood gases, and evidence of increased work of breathing. Respiratory failure causes an altered mental status due to ischemia in the brain.

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

Fluid replacement or fluid resuscitation is the medical practice of replenishing bodily fluid lost through sweating, bleeding, fluid shifts or other pathologic processes. Fluids can be replaced with oral rehydration therapy (drinking), intravenous therapy, rectally such as with a Murphy drip, or by hypodermoclysis, the direct injection of fluid into the subcutaneous tissue. Fluids administered by the oral and hypodermic routes are absorbed more slowly than those given intravenously.

<span class="mw-page-title-main">Pulmonary edema</span> Fluid accumulation in the tissue and air spaces of the lungs

Pulmonary edema, also known as pulmonary congestion, is excessive liquid accumulation in the tissue and air spaces 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, or an injury to the lung tissue directly or blood vessels of the lung.

<span class="mw-page-title-main">Septic shock</span> Dangerously low blood pressure due to damage from an organ infection

Septic shock is a potentially fatal medical condition that occurs when sepsis, which is organ injury or damage in response to infection, leads to dangerously low blood pressure and abnormalities in cellular metabolism. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3) defines septic shock as a subset of sepsis in which particularly profound circulatory, cellular, and metabolic abnormalities are associated with a greater risk of mortality than with sepsis alone. Patients with septic shock can be clinically identified by requiring a vasopressor to maintain a mean arterial pressure of 65 mm Hg or greater and having serum lactate level greater than 2 mmol/L (>18 mg/dL) in the absence of hypovolemia. This combination is associated with hospital mortality rates greater than 40%.

<span class="mw-page-title-main">Hypotension</span> Abnormally low blood pressure

Hypotension is low blood pressure. Blood pressure is the force of blood pushing against the walls of the arteries as the heart pumps out blood. Blood pressure is indicated by two numbers, the systolic blood pressure and the diastolic blood pressure, which are the maximum and minimum blood pressures, respectively. A systolic blood pressure of less than 90 millimeters of mercury (mmHg) or diastolic of less than 60 mmHg is generally considered to be hypotension. Different numbers apply to children. However, in practice, blood pressure is considered too low only if noticeable symptoms are present.

<span class="mw-page-title-main">Hypovolemia</span> Low blood volume

Hypovolemia, also known as volume depletion or volume contraction, is a state of abnormally low extracellular fluid in the body. This may be due to either a loss of both salt and water or a decrease in blood volume. Hypovolemia refers to the loss of extracellular fluid and should not be confused with dehydration.

<span class="mw-page-title-main">Internal bleeding</span> Medical condition

Internal bleeding is a loss of blood from a blood vessel that collects inside the body, and is not usually visible from the outside. It can be a serious medical emergency but the extent of severity depends on bleeding rate and location of the bleeding. Severe internal bleeding into the chest, abdomen, pelvis, or thighs can cause hemorrhagic shock or death if proper medical treatment is not received quickly. Internal bleeding is a medical emergency and should be treated immediately by medical professionals.

In immunology, systemic inflammatory response syndrome (SIRS) is an inflammatory state affecting the whole body. It is the body's response to an infectious or noninfectious insult. Although the definition of SIRS refers to it as an "inflammatory" response, it actually has pro- and anti-inflammatory components.

<span class="mw-page-title-main">Hypovolemic shock</span> Medical condition

Hypovolemic shock is a form of shock caused by severe hypovolemia. It could be the result of severe dehydration through a variety of mechanisms or blood loss. Hypovolemic shock is a medical emergency; if left untreated, the insufficient blood flow can cause damage to organs, leading to multiple organ failure.

<span class="mw-page-title-main">Cardiogenic shock</span> Medical emergency resulting from inadequate blood flow due to dysfunction of heart ventricles

Cardiogenic shock is a medical emergency resulting from inadequate blood flow to the body's organs due to the dysfunction of the heart. Signs of inadequate blood flow include low urine production, cool arms and legs, and decreased level of consciousness. People may also have a severely low blood pressure and heart rate.

<span class="mw-page-title-main">Neurogenic shock</span> Insufficient blood flow due to autonomic nervous system damage

Neurogenic shock is a distributive type of shock resulting in hypotension, often with bradycardia, caused by disruption of autonomic nervous system pathways. It can occur after damage to the central nervous system, such as spinal cord injury and traumatic brain injury. Low blood pressure occurs due to decreased systemic vascular resistance resulting from loss of sympathetic tone, which in turn causes blood pooling within the extremities rather than being available to circulate throughout the body. The slowed heart rate results from a vagal response unopposed by a sympathetic nervous system (SNS) response. Such cardiovascular instability is exacerbated by hypoxia, or treatment with endotracheal or endobronchial suction used to prevent pulmonary aspiration.

Distributive shock is a medical condition in which abnormal distribution of blood flow in the smallest blood vessels results in inadequate supply of blood to the body's tissues and organs. It is one of four categories of shock, a condition where there is not enough oxygen-carrying blood to meet the metabolic needs of the cells which make up the body's tissues and organs. Distributive shock is different from the other three categories of shock in that it occurs even though the output of the heart is at or above a normal level. The most common cause is sepsis leading to a type of distributive shock called septic shock, a condition that can be fatal.

End organ damage is severe impairment of major body organs due to high blood pressure or states of low blood pressure or low blood volume. This can present as a heart attack or heart failure, pulmonary edema, neurologic deficits including a stroke, or acute kidney failure.

<span class="mw-page-title-main">Amniotic fluid embolism</span> Potentially fatal complication of pregnancy

An amniotic fluid embolism (AFE) is a life-threatening childbirth (obstetric) emergency in which amniotic fluid enters the blood stream of the mother, triggering a serious reaction which results in cardiorespiratory collapse and massive bleeding (coagulopathy). The rate at which it occurs is 1 instance per 20,000 births and it comprises 10% of all maternal deaths.

Pediatric advanced life support (PALS) is a course offered by the American Heart Association (AHA) for health care providers who take care of children and infants in the emergency room, critical care and intensive care units in the hospital, and out of hospital. The course teaches healthcare providers how to assess injured and sick children and recognize and treat respiratory distress/failure, shock, cardiac arrest, and arrhythmias.

Obstructive shock is one of the four types of shock, caused by a physical obstruction in the flow of blood. Obstruction can occur at the level of the great vessels or the heart itself. Causes include pulmonary embolism, cardiac tamponade, and tension pneumothorax. These are all life-threatening. Symptoms may include shortness of breath, weakness, or altered mental status. Low blood pressure and tachycardia are often seen in shock. Other symptoms depend on the underlying cause.

<span class="mw-page-title-main">Norepinephrine (medication)</span> Therapeutic use of norepinephrine

Norepinephrine, also known as noradrenaline, is a medication used to treat people with very low blood pressure. It is the typical medication used in sepsis if low blood pressure does not improve following intravenous fluids. It is the same molecule as the hormone and neurotransmitter norepinephrine. It is given by slow injection into a vein.

<span class="mw-page-title-main">Angiotensin II (medication)</span> Treatment for low blood pressure

Angiotensin II is a medication that is used to treat hypotension resulting from septic shock or other distributive shock. It is a synthetic vasoconstrictor peptide that is identical to human hormone angiotensin II and is marketed under the brand name Giapreza. The Food and Drug Administration approved the use of angiotensin II in December 2017 to treat low blood pressure resulting from septic shock.

Vasodilatory shock, vasogenic shock, or vasoplegic shock is a medical emergency belonging to shock along with cardiogenic shock, septic shock, allergen-induced shock and hypovolemic shock. When the blood vessels suddenly relax, it results in vasodilation. In vasodilatory shock, the blood vessels are too relaxed leading to extreme vasodilation and blood pressure drops and blood flow becomes very low. Without enough blood pressure, blood and oxygen will not be pushed to reach the body's organs. If vasodilatory shock lasts more than a few minutes, the lack of oxygen starts to damage the body's organs. Vasodilatory shock like other types of shock should be treated quickly, otherwise it can cause permanent organ damage or death as a result of multiple organ dysfunction.

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