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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 are low blood pressure, decreased urine output, and confusion, these may not always be present.[6] While a fast heart rate is common, in 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.[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. 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.[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 the great 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 from sepsis 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 in vasodilation leading to hypotension. Septic shock can be caused by Gram negative bacteria such as (among others) Escherichia coli, Proteus species, Klebsiella pneumoniae (which have an endotoxin on their surface that produces adverse biochemical, immunological and occasionally neurological effects which are harmful to the body), other Gram-positive cocci, such as pneumococci and streptococci, and certain fungi as well as Gram-positive bacterial toxins. Septic shock also includes some elements of cardiogenic shock. In 1992, the ACCP/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 receiving inotropic 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) Systemic leukocyte adhesion to endothelial cells[19] 2) Reduced contractility of the heart[19] 3) Activation of the coagulation pathways, resulting in disseminated intravascular coagulation[19] 4). Increased levels of neutrophils[19]
The main manifestations of septic shock are due to the massive release of histamine which causes intense dilation of the blood vessels. People with septic shock will also likely be positive for SIRS 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 cause neurogenic shock, which is commonly classified as a subset of distributive shock.[21] 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.[21] (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.)
Although not officially classified as a subcategory of shock, many endocrinological disturbances in their severe form can result in shock.[citation needed]
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.
Shock is a common end point of many medical conditions.[9] 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.[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 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.[citation needed]
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.[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 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.[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 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.[19] 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.[19] If the bowel becomes sufficiently ischemic, bacteria may enter the blood stream, resulting in the increased complication of endotoxic shock.[26][19]
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.[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 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.[28]
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]
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.[9] 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.[6] 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.[29] It is important to keep the person warm to avoid hypothermia[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 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.[31]Colloids and crystalloids 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 the hemoglobin 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 for hemorrhagic shock from trauma[39] but may be of use in neurogenic shock.[21]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.[40] Activated protein C was withdrawn from the market in 2011, and clinical trials were discontinued.[40] The use of sodium 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, 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.
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 the intensive 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 that Hippocrates used the word exemia to signify a state of being "drained of blood".[47] 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.)[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 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.[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]
^ abcdefghijklmInternational Trauma Life Support for Emergency Care Providers (8 ed.). Pearson Education Limited. 2018. pp. 172–73. ISBN978-1292-17084-8.
^ abcdefghijklATLS – Advanced Trauma Life Support – Student Course Manual (10 ed.). American College of Surgeons. 2018. pp. 43–52, 135. ISBN978-78-0-9968267.
^"Shock". Red Cross. Archived from the original on 2024-11-04. Retrieved 2024-10-21.
^ abcdefghijTintinalli, Judith E. (2010). Emergency Medicine: A Comprehensive Study Guide. New York: McGraw-Hill Companies. pp. 165–72. ISBN978-0-07-148480-0.
^Tintinalli, Judith E. (2010). Emergency Medicine: A Comprehensive Study Guide. New York: McGraw-Hill Companies. pp. 174–75. ISBN978-0-07-148480-0.
^Assessing dehydration and shock. NCBI Bookshelf. National Collaborating Centre for Women's and Children's Health (UK). April 2009. Archived from the original on 2021-08-29. Retrieved 2019-05-09.
^Olaussen A, Blackburn T, Mitra B, Fitzgerald M (June 2014). "Review article: shock index for prediction of critical bleeding post-trauma: a systematic review". Emergency Medicine Australasia. 26 (3): 223–28. doi:10.1111/1742-6723.12232. PMID24712642. S2CID19881753.
^ abcGuyton, Arthur; Hall, John (2006). "Chapter 24: Circulatory Shock and Physiology of Its Treatment". In Gruliow, Rebecca (ed.). Textbook of Medical Physiology (11th ed.). Philadelphia, Pennsylvania: Elsevier Inc. pp. 278–88. ISBN978-0-7216-0240-0.
^Wu MC, Liao TY, Lee EM, Chen YS, Hsu WT, Lee MG, Tsou PY, Chen SC, Lee CC (November 2017). "Administration of Hypertonic Solutions for Hemorrhagic Shock: A Systematic Review and Meta-analysis of Clinical Trials". Anesthesia and Analgesia. 125 (5): 1549–57. doi:10.1213/ANE.0000000000002451. PMID28930937. S2CID39310937.
^ abBoyd JH, Walley KR (August 2008). "Is there a role for sodium bicarbonate in treating lactic acidosis from shock?". Current Opinion in Critical Care. 14 (4): 379–83. doi:10.1097/MCC.0b013e3283069d5c. PMID18614899. S2CID22613993.
Circulatory shock is a life-threatening syndrome of acute circulatory failure characterized by inadequate tissue perfusion and oxygenation, leading to cellular hypoxia, metabolic acidosis, and progressive organ dysfunction if untreated.[1] It represents a state in which the cardiovascular system fails to deliver sufficient oxygen and nutrients to meet cellular demands, often progressing through compensated, decompensated, and irreversible stages.[2]The condition is classified into four primary types based on underlying pathophysiology: hypovolemic shock, resulting from significant volume loss such as hemorrhage or dehydration; cardiogenic shock, due to primary cardiac pump failure from events like myocardial infarction; distributive shock, involving widespread vasodilation and capillary leakage, as seen in septic, anaphylactic, or neurogenic forms; and obstructive shock, caused by mechanical impediments to blood flow, including pulmonary embolism or cardiac tamponade.[1] Each type shares common clinical features but differs in etiology and management priorities, with distributive shock being the most common in intensive care settings due to its association with sepsis.[3]Pathophysiologically, shock initiates a cascade of reduced cardiac output, hypotension, and tissue hypoperfusion, triggering compensatory mechanisms like tachycardia and vasoconstriction in early stages, followed by multi-organ failure in advanced cases.[1]Diagnosis relies on clinical signs such as hypotension (systolic blood pressure <90 mmHg), tachycardia, altered mental status, oliguria, and lactic acidosis, often confirmed by laboratory tests including elevated lactate levels (>2 mmol/L) and hemodynamic monitoring.[2]Initial management focuses on rapid resuscitation to restore perfusion, including airway stabilization, intravenous fluid administration (e.g., 30 mL/kg crystalloids for distributive shock), vasopressors like norepinephrine for refractory hypotension, and targeted therapies such as antibiotics for sepsis or inotropes for cardiogenic shock.[1] Early intervention is critical, as mortality rates can exceed 40% in severe cases, underscoring the need for prompt recognition and multidisciplinary care in emergency and critical care settings.[3]
Definition and Classification
Definition
Circulatory shock is a life-threatening medical emergency characterized by acute circulatory failure, resulting in inadequate tissue perfusion and cellular hypoxia despite the body's potential for sufficient oxygen delivery.[1] This state leads to impaired cellular metabolism and, if untreated, progressive multi-organ dysfunction and death.[2] The term "shock" entered medical lexicon in the 18th century, originating from descriptions of battlefield trauma, particularly gunshot wounds, where it initially denoted a sudden neurologic collapse but later evolved to emphasize circulatory derangements observed in military contexts.[4]At its core, circulatory shock involves disruptions in key physiological components of the cardiovascular system, including reduced cardiac output due to pump failure, maldistribution of blood flow from vasodilation or shunting, or diminished oxygen-carrying capacity from anemia or hypoxemia.[5] These mechanisms collectively fail to meet the metabolic demands of tissues, triggering a cascade of anaerobic metabolism, lactic acidosis, and inflammatory responses that exacerbate the hypoperfusion.[6]Circulatory shock must be differentiated from non-circulatory forms, such as spinal shock—a temporary areflexia following spinal cord injury—or psychogenic shock, a brief vasovagal episode triggered by emotional stress that resolves without sustained tissue hypoxia.[7][8] Clinical identification relies on hemodynamic indicators, including a mean arterial pressure below 65 mmHg, elevated serum lactate exceeding 2 mmol/L, or the necessity of vasopressor support to sustain perfusion.[2] Circulatory shock encompasses several main types, including hypovolemic, cardiogenic, obstructive, and distributive.[2]
Classification
Circulatory shock is classically classified into four main types based on the underlying pathophysiological mechanism: hypovolemic, cardiogenic, obstructive, and distributive shock.[9]Hypovolemic shock results from absolute intravascular volume loss, leading to reduced cardiac preload and output.[9]Cardiogenic shock arises from primary cardiac pump failure, impairing forward flow.[9]Obstructive shock involves mechanical impedance to blood flow, such as obstruction of great vessels or cardiac filling.[9]Distributive shock is characterized by maldistribution of blood flow due to peripheral vasodilation and relative hypovolemia.[9]Subtypes within these categories provide further granularity. Hypovolemic shock includes hemorrhagic (e.g., due to acute blood loss) and non-hemorrhagic (e.g., from dehydration or third-spacing) forms.[10]Cardiogenic shock encompasses acute myocardial infarction-related and non-ischemic variants, such as those from myocarditis or arrhythmias.[11]Obstructive shock subtypes feature pulmonary embolism and cardiac tamponade as prominent examples.[9]Distributive shock subtypes comprise septic (from infection-induced vasodilation), anaphylactic (allergic reaction-mediated), neurogenic (spinal cord injury-related sympathetic disruption), and endocrine forms like adrenal crisis (cortisol deficiency causing vasoplegia).[12]Classification relies on hemodynamic profiles to differentiate types. For instance, distributive shock typically shows high cardiac output (>8 L/min) with low systemic vascular resistance (SVR <800 dynes·s·cm⁻⁵), contrasting with low cardiac output (<4 L/min) and high SVR (>1200 dynes·s·cm⁻⁵) in cardiogenic shock.[13] Hypovolemic and obstructive shocks often present with low cardiac output and variable SVR, distinguished by preload measures like central venous pressure.[9] These profiles, assessed via invasive monitoring (e.g., pulmonary artery catheter), guide initial diagnosis.[11]This classification system facilitates etiology-specific management, such as volume resuscitation for hypovolemic shock or inotropes for cardiogenic, thereby improving outcomes.[9]Emerging classifications address complexities like mixed shocks, where multiple mechanisms coexist, such as cardiogenic-vasodilatory (low cardiac index with low SVR).[14] Recent frameworks propose dichotomizing mixed cardiogenic shock into primary cardiogenic with secondary contributors (e.g., sepsis) or vice versa, using thresholds like cardiac index <2.5 L/min/m² and SVR <1000 dynes·s·cm⁻⁵.[14] For cardiogenic shock specifically, the Society for Cardiovascular Angiography and Interventions (SCAI) staging (A-E) stratifies severity: A (at-risk, normal hemodynamics), B (beginning, hypotension without hypoperfusion), C (classic, hypoperfusion requiring intervention), D (deteriorating, worsening despite therapy), and E (extremis, near collapse).[15] In hemorrhagic shock, a revised physiological classification emphasizes hemodynamic response to fluid challenge over percentage blood loss, with stages from compensated (responsive to bolus) to decompensated (non-responsive, requiring source control).[16] Updates from 2023-2024 literature highlight phenotypes and mixed states to refine risk stratification and therapy.[17]
Causes
Hypovolemic Causes
Hypovolemic shock arises from a significant reduction in intravascular volume, impairing cardiac output and tissue perfusion. This can occur through absolute hypovolemia, involving direct loss of blood or fluids, or relative hypovolemia, where effective circulating volume decreases due to internal redistribution despite normal total body fluid.[18]Absolute hypovolemia is the most common form and includes hemorrhagic causes such as trauma, gastrointestinal bleeding, and surgical or postoperative hemorrhage. Nonhemorrhagic causes encompass external fluid losses from severe vomiting, diarrhea, burns, and third-spacing of fluids into interstitial spaces, as seen in conditions like pancreatitis or bowel obstruction.[18][19]Relative hypovolemia results from factors that shift fluids away from the intravascular space, such as dehydration due to inadequate intake or excessive output in heatstroke or diabetes insipidus, leading to a disproportionate reduction in circulating volume.[18]The primary mechanism involves diminished venous return, reducing preload and subsequently stroke volume via the Frank-Starling mechanism, which compromises cardiac output. Hypovolemic shock accounts for approximately 20-30% of all shock cases in emergency department settings, with higher rates in trauma contexts.[18][20]Key risk factors include high trauma volumes, where hemorrhage is staged by blood loss percentage: Class I (<15% loss, minimal symptoms), Class II (15-30% loss, tachycardia), Class III (30-40% loss, hypotension), and Class IV (>40% loss, profound shock). Recent studies highlight non-hemorrhagic causes, such as severe gastroenteritis, as prominent in pediatric populations, often leading to rapid dehydration and shock in resource-limited settings.[10][21]
Cardiogenic Causes
Cardiogenic shock arises primarily from cardiac etiologies that impair the heart's pump function, leading to inadequate tissue perfusion. The most common cause is ischemic, accounting for approximately 80% of cases, with acute myocardial infarction (AMI) being the predominant trigger. In AMI, extensive myocardial damage, often involving the left ventricle, results in reduced contractility and diminished cardiac output. Right ventricular infarction, which occurs in about 30-50% of inferior AMIs, further complicates hemodynamics by impairing right heart filling and preload to the left ventricle, exacerbating the shock state.[22][23]Non-ischemic causes constitute the remaining cases and include a variety of conditions that directly compromise myocardial function or electrical stability. Myocarditis, often viral or autoimmune, leads to inflammation and weakened contractility. Cardiomyopathies, such as dilated or hypertrophic forms, cause chronic or acute dilation and systolic dysfunction, respectively. Acute valvular disruptions, like papillary muscle rupture or severe regurgitation from endocarditis, impede forward flow. Sustained arrhythmias, including ventricular tachycardia or bradycardias, disrupt coordinated pumping and reduce effective output. These etiologies collectively impair ventricular contractility, resulting in low cardiac output despite adequate preload, distinguishing cardiogenic shock from other forms.[24][25][26]Cardiogenic shock complicates 5-10% of AMI cases, with higher rates in older patients or those with extensive infarction. Risk is amplified by comorbidities such as diabetes mellitus, which promotes microvascular damage and worsens ischemic tolerance, and prior heart failure, which indicates preexisting systolic dysfunction. Recent data indicate an increasing incidence, driven by aging populations where hospitalizations for cardiogenic shock with AMI rose steadily from 2003 to 2021, alongside emerging contributions from post-COVID-19 myocarditis, which has elevated cardiogenic shock rates in affected myocarditis cases from 7% to 12%.[27][23][28][29][30][31]
Obstructive Causes
Obstructive shock arises from mechanical impediments to blood flow, distinct from cardiogenic shock by involving extrinsic obstructions rather than intrinsic myocardial dysfunction.[32] These obstructions reduce cardiac output by either impairing venous return to the heart or obstructing outflow tracts, leading to systemic hypoperfusion despite preserved myocardial contractility.[1]Cardiac obstructions primarily include cardiac tamponade and tension pneumothorax. Cardiac tamponade occurs when pericardial effusion accumulates rapidly, compressing the cardiac chambers and equalizing intracardiac pressures, which severely limits diastolic filling and venous return.[32] Tension pneumothorax develops from air accumulation in the pleural space under pressure, collapsing the affected lung and shifting the mediastinum, thereby compressing the vena cava and impeding venous return to the right atrium.[1]Vascular obstructions encompass massive pulmonary embolism and aortic dissection. Massive pulmonary embolism involves a large thrombus occluding the pulmonary arterial bed, acutely increasing right ventricular afterload and obstructing right ventricular outflow, which in turn reduces left ventricular preload through ventricular interdependence.[32] This condition leads to shock in approximately 5% of acute pulmonary embolism cases, classified as high-risk due to hemodynamic instability.[33]Aortic dissection, particularly type A involving the ascending aorta, creates a false lumen that disrupts left ventricular outflow, elevating afterload and impairing systemic perfusion.[1]The core mechanisms in obstructive shock involve either preload reduction via impaired venous return (as in tamponade and tension pneumothorax) or afterload elevation via outflow tract obstruction (as in pulmonary embolism and aortic dissection).[32] These processes mimic cardiogenic shock clinically with hypotension and organ hypoperfusion but differ by maintaining normal or hyperdynamic myocardial contractility, without primary pump failure.[1] Key diagnostic clues include elevated central venous pressure reflecting right-sided obstruction, in the absence of left heart failure signs such as pulmonary congestion.[32]
Distributive Causes
Distributive shock arises from conditions that cause profound vasodilation and increased vascular permeability, leading to maldistribution of blood flow and relative hypovolemia despite normal or increased total blood volume.[12] This results in inadequate tissue perfusion, as systemic vascular resistance drops dramatically, often compounded by capillary leak that shifts fluid into the interstitial space.[34]Septic shock, the most prevalent subtype of distributive shock, accounts for about 62% of undifferentiated shock cases in clinical studies and is primarily triggered by bacterial infections such as pneumonia or urinary tract infections.[35] It stems from a dysregulated host immune response to infection, involving widespread release of pro-inflammatory cytokines that induce endothelial dysfunction and vasodilation.[12]Anaphylactic shock develops from severe type I hypersensitivity reactions to allergens, including drugs, foods, or insect stings, which trigger massive mast celldegranulation and histamine release.[36] This mediator release causes rapid onset of systemic vasodilation, bronchospasm, and increased vascular permeability, often progressing to life-threatening hypotension within minutes.[37]Neurogenic shock occurs due to disruption of autonomic nervous system function, commonly from acute spinal cord injury or severe brainstem trauma, leading to loss of sympathetic vasomotor tone.[34] The resultant unopposed parasympathetic activity causes profound bradycardia and vasodilation, particularly in the lower body, exacerbating hypoperfusion.[35]Endocrine etiologies include adrenal insufficiency, as seen in Addisonian crisis, where cortisol deficiency impairs vascular responsiveness to catecholamines and promotes hypotension through reduced cardiac output and vasodilation.[38]Thyroid storm, a hypermetabolic state from excess thyroidhormone, induces distributive shock via direct vasodilatory effects on peripheral vessels and increased metabolic demand.[39]The underlying mechanisms across these causes involve inflammatory cytokine storms (e.g., TNF-α, IL-1) that upregulate inducible nitric oxide synthase, producing excess nitric oxide to mediate smooth muscle relaxation and vasodilation.[12] Concurrently, endothelial barrier dysfunction promotes capillary leak, creating a relative hypovolemic state that further impairs organ perfusion.[34] Recent 2024 investigations have highlighted post-viral distributive components in long COVID, linked to persistent low-grade inflammation mimicking sepsis-like vasodilation.[40]
Signs and Symptoms
General Features
Circulatory shock manifests through a constellation of universal clinical signs reflecting systemic hypoperfusion and inadequate tissue oxygenation, observable across all types of shock. Key vital sign abnormalities include hypotension, typically defined as systolic blood pressure (SBP) less than 90 mmHg, which indicates inadequate cardiac output to maintain perfusion pressure.[1]Tachycardia, often with heart rates exceeding 100 beats per minute, represents a compensatory response to sustain cardiac output despite reduced stroke volume.[5]Tachypnea, with respiratory rates greater than 20 breaths per minute, arises from metabolic acidosis and hypoxemia stimulating respiratory centers.[41]Oliguria, characterized by urine output less than 0.5 mL/kg/hour (or approximately 30 mL/hour in adults), signals renal hypoperfusion and early acute kidney injury.[1]Indicators of impaired tissue perfusion are prominent and include cool, clammy skin due to peripheral vasoconstriction aimed at preserving central blood flow, often accompanied by pallor or cyanosis in extremities.[5] Altered mental status, ranging from mild confusion to obtundation, results from cerebral hypoperfusion and hypoxia.[1] Elevated serum lactate levels, particularly above 4 mmol/L, serve as a biochemical marker of anaerobic metabolism and tissue hypoxia, correlating with shock severity and poor prognosis.[42]Organ dysfunction emerges as hypoperfusion persists, with acute kidney injury evident through rising serum creatinine and oliguria, hepatic dysfunction indicated by elevated transaminases and bilirubin, and coagulopathy manifested as prolonged prothrombin time or thrombocytopenia.[43] These features overlap with systemic inflammatory response syndrome (SIRS) criteria, including fever (temperature >38°C) or hypothermia (<36°C), and leukocytosis (white blood cell count >12,000/μL) or leukopenia (<4,000/μL), reflecting an inflammatory cascade triggered by cellular injury.[44]Early signs of shock often include anxiety and restlessness as sympathetic activation predominates, while late-stage manifestations progress to lethargy, stupor, and ultimately coma due to worsening cerebral ischemia.[45] If untreated, these general features culminate in multi-organ failure, underscoring the need for prompt intervention.[41]
Type-Specific Presentations
In hypovolemic shock, patients often exhibit dry mucous membranes due to significant fluid depletion, alongside flat neck veins reflecting reduced central venous pressure, and a clear history of fluid loss such as from hemorrhage or dehydration.[46][47] These signs distinguish hypovolemic shock from other types by emphasizing volume deficit without primary cardiac or vascular tone abnormalities.Cardiogenic shock presents with pulmonary edema manifesting as severe shortness of breath and crackles on lung auscultation, an S3 gallop indicating ventricular dysfunction, jugular venous distension from elevated filling pressures, and frequently associated chest pain from underlying myocardial ischemia.[25][29] These features highlight the pump failure central to this shock type, contrasting with the peripheral hypoperfusion seen in other forms.Obstructive shock displays type-specific signs depending on the underlying obstruction; in cardiac tamponade, pulsus paradoxus—an exaggerated drop in systolic blood pressure greater than 10 mmHg during inspiration—arises from impaired cardiac filling, while tension pneumothorax is marked by absent breath sounds on the affected side due to lung collapse.[48][49] In massive pulmonary embolism, right heart strain appears as elevated jugular venous pressure and signs of acute cor pulmonale, such as a parasternal heave, reflecting acute right ventricular overload.[50]Distributive shock varies by subtype: early septic shock features warm extremities from peripheral vasodilation, often with bounding pulses before progression to colder skin; anaphylactic shock includes a characteristic rash, such as urticaria or flushing, due to mast cell degranulation; and neurogenic shock shows hypotension without tachycardia (or even bradycardia) from sympathetic disruption, with preserved or warm skin below the injury level.[34][51][52] Additionally, in adrenal crisis—a form of distributive shock from acute adrenal insufficiency—patients may display hyperpigmentation of the skin, particularly in sun-exposed areas or creases, resulting from elevated adrenocorticotropic hormone levels stimulating melanocytes.[53][54]Mixed shocks combine elements from multiple categories, such as cardiogenic-vasodilatory shock, which exhibits low cardiac output typical of pump failure alongside vasodilation leading to relatively low systemic vascular resistance and warmer extremities despite overall hypoperfusion.[55] These hybrid presentations require careful differentiation to guide targeted interventions, as they may mimic pure forms but respond differently to standard therapies.[56]
Pathophysiology
Initial Stage
The initial stage of circulatory shock is triggered by an acute insult that disrupts effective tissue perfusion, such as hemorrhage, myocardial infarction, or systemic vasodilation, leading to inadequate oxygen delivery to cells. This reduction in oxygen delivery (DO2) is fundamentally determined by the equation DO2=CO×CaO2, where CO represents cardiac output and CaO2 denotes arterial oxygen content, which encompasses hemoglobin concentration, oxygen saturation, and dissolved oxygen.[57] In all forms of shock, this early imbalance creates a mismatch between oxygen supply and demand, initiating cellular stress across hypovolemic, cardiogenic, obstructive, and distributive types, though the specific precipitant varies—for instance, volume loss in hypovolemic shock or loss of vascular tone in distributive shock.[58]At the cellular level, the diminished DO2 forces tissues to rely on anaerobic glycolysis for energy production, yielding only 2 moles of ATP per glucose molecule compared to 36 under aerobic conditions, and generating lactic acid as a byproduct. This shift results in elevated lactate levels, often exceeding 1.5 mmol/L, and contributes to local acidosis, impairing cellular function without immediate widespread organ failure.[57] Hemodynamically, the onset manifests as mild hypotension—typically a systolic blood pressure below 90 mm Hg or mean arterial pressure under 65-70 mm Hg—while peripheral perfusion remains relatively preserved, allowing vital organs to function temporarily despite the insult.[1]This initial phase endures for minutes to hours, depending on the insult's severity and the patient's baseline reserves, before advancing to more pronounced decompensation if untreated.[59] The core pathophysiological features, including early hypoxia and metabolic derangements, are consistent across shock classifications, underscoring the universal reliance on adequate DO2 for cellular viability.[58]
Compensatory Stage
In the compensatory stage of circulatory shock, the body initiates adaptive neurohormonal responses to counteract the initial reduction in tissue perfusion and maintain vital organ function. The sympathetic nervous system is activated, leading to a surge in catecholamines that results in tachycardia and peripheral vasoconstriction, thereby redirecting blood flow to essential organs such as the heart and brain.[18] Concurrently, the renin-angiotensin-aldosterone system (RAAS) is stimulated, promoting renal sodium and water retention to expand intravascular volume and support cardiac preload.[60] These mechanisms collectively aim to stabilize hemodynamic parameters following the precipitating insult.A key physiological adjustment during this stage is the increase in systemic vascular resistance (SVR) to preserve mean arterial pressure (MAP), governed by the relationship MAP=CO×SVR, where CO represents cardiac output.[60] This elevation in SVR helps offset any decline in CO due to reduced preload or contractility, ensuring adequate perfusion pressure initially. Clinically, patients often exhibit normal or slightly elevated blood pressure, reflecting successful compensation, along with signs of sympathetic overdrive such as anxiety, pallor, and cool, clammy extremities from cutaneous vasoconstriction.[1]The effectiveness of these compensatory responses depends on the severity of the underlying insult; they are typically sufficient in mild cases, such as modest hypovolemia, where perfusion can be restored without progression.[18] However, in severe shock, these mechanisms may fail as endogenous catecholamine reserves are depleted, leading to inadequate maintenance of vascular tone and perfusion. Variations exist across shock types: in hypovolemic shock, vasoconstriction is robust to compensate for volume loss, whereas in distributive shock, such as sepsis, it is often blunted by concurrent vasodilation, resulting in a hyperdynamic state with relatively preserved cardiac output but lower SVR.[1]
Progressive Stage
In the progressive stage of circulatory shock, the body's compensatory mechanisms begin to fail, leading to decompensation and worsening tissue hypoperfusion despite initial adaptive responses such as tachycardia and vasoconstriction. This phase is characterized by vasoplegia, where systemic vascular resistance falls dramatically due to endothelial dysfunction and excessive nitric oxide production, impairing the ability to maintain blood pressure. Concurrently, myocardial depression occurs, with reduced contractility and cardiac output resulting from inflammatory cytokines and metabolic derangements, further exacerbating hypoperfusion. Microcirculatory dysfunction compounds these issues, as heterogeneous blood flow, capillary leakage, and impaired oxygen extraction at the tissue level lead to localized ischemia even in the presence of normalized macrohemodynamics.[61]Organ dysfunction emerges prominently during this stage, with early manifestations including acute respiratory distress syndrome (ARDS) driven by alveolar-capillary membrane injury and neutrophil activation, leading to impaired gas exchange. Renal involvement progresses to acute tubular necrosis from prolonged ischemia and tubular cell apoptosis, often heralding broader multiorgan failure if unchecked. These changes reflect a shift from reversible hypoperfusion to established cellular injury, with histological evidence of mitochondrial swelling and energy failure in affected tissues.[1][61]Biomarkers provide critical indicators of progression, with serum lactate levels rising above 2 mmol/L due to anaerobic metabolism and impaired clearance, signaling ongoing tissue hypoxia. Base deficit, typically exceeding -6 mEq/L, reflects worsening metabolic acidosis from lactate accumulation and bicarbonate consumption, correlating with the severity of hypoperfusion. Hemodynamically, cardiac output declines persistently despite aggressive fluid resuscitation and vasopressor support, often accompanied by rising pulmonary artery pressures and falling mixed venous oxygen saturation.[1][62]This stage represents a critical transition from compensated shock to an irreversible trajectory, where the balance tips toward refractory hypoperfusion and is a pivotal point in intensive care unit progression models like the Sequential Organ Failure Assessment (SOFA) score. Early recognition of these decompensatory signs is essential, as they underscore the breakdown of prior adaptations and the onset of self-perpetuating inflammatory cascades.[61]
Refractory Stage
The refractory stage of circulatory shock represents the terminal phase, characterized by irreversible multi-organ failure that persists despite aggressive interventions, including high-dose vasopressors and mechanical circulatory support (MCS). In this end-stage, cellular and tissue damage becomes profound and non-reversible, marking a point of futility in reversal efforts. Building briefly on the progressive stage's escalating organ dysfunction, the refractory phase involves a cascade of maladaptive responses that overwhelm compensatory mechanisms.[63]Central to the pathophysiology is mitochondrial dysfunction, where oxidative stress and disrupted oxidative phosphorylation impair ATP synthesis, leading to energetic failure in vital tissues. This is compounded by widespread apoptosis, particularly in ischemic conditions rather than pure hypoxia, resulting in extensive cell death across organs like the kidneys, liver, and brain. Additionally, coagulopathy, often manifesting as disseminated intravascular coagulation (DIC), arises from microthrombi formation in the microcirculation, exacerbating tissue ischemia and contributing to multi-organ failure. These processes are driven by a cytokine storm, which induces excessive nitric oxide production via inducible nitric oxide synthase (iNOS), promoting refractory vasodilation, and endothelial injury, which disrupts microvascular integrity and blood flow distribution.[63]Clinically, patients exhibit profound hypotension unresponsive to catecholamines (e.g., norepinephrine doses ≥0.25-1 μg/kg/min), anuria reflecting renal shutdown from hypoperfusion, and progression to coma or altered mental status due to cerebral hypoperfusion, even under maximal supportive measures. Recent 2024 insights into refractory mixed shocks, such as cardiogenic-vasodilatory types, highlight resistance to MCS like venoarterial extracorporeal membrane oxygenation (VA-ECMO), where persistent vasoplegia limits mean arterial pressure recovery and worsens outcomes due to unresolved systemic inflammation.[55]The prognosis is dismal, with mortality rates ranging from 80% to 90% in refractory cases, though rare recoveries occur with advanced interventions in select patients; however, in mixed shock phenotypes, survival benefits from MCS remain limited, underscoring the need for targeted subphenotype research.[63]
Diagnosis
Clinical Evaluation
The clinical evaluation of circulatory shock begins with a rapid history to identify potential etiologies and guide further assessment. Clinicians should inquire about the onset of symptoms, which is often acute in hypovolemic or obstructive shock but may be more insidious in cardiogenic or distributive types. Key historical elements include recent trauma or hemorrhage suggesting hypovolemia, signs of infection such as fever, chills, or recent illness indicating distributive shock, and cardiac symptoms like chest pain, dyspnea, or palpitations pointing to cardiogenic causes.[64] A focused history helps differentiate shock from mimics and prioritizes urgent interventions.[2]The physical examination starts with assessment of the ABCs—airway, breathing, and circulation—to ensure immediate stabilization and identify life-threatening issues like airway obstruction or tension pneumothorax. Perfusion is evaluated through signs of tissue hypoperfusion, including prolonged capillary refill time greater than 2 seconds, skin mottling, cool and clammy extremities, oliguria, and altered mental status. These findings, when combined, improve diagnostic accuracy over single signs, achieving up to 81-100% sensitivity in predefined profiles for inadequate cardiac output.[65][66][2] Tachycardia, hypotension, and weak pulses further support the diagnosis, though their correlation with cardiac output varies.Classification aids like the quick Sequential Organ Failure Assessment (qSOFA) score assist in identifying high-risk patients, particularly in distributive shock contexts. A qSOFA score of ≥2 points—based on systolic blood pressure ≤100 mmHg, respiratory rate ≥22 breaths per minute, and altered mentation—predicts increased mortality and prompts escalation of care outside intensive settings. Differential diagnosis requires ruling out non-circulatory causes, such as hypoglycemia, which can mimic shock symptoms like altered mentation and tachycardia; early bedside glucose measurement is essential to exclude this.[67][68]Recent updates emphasize structured protocols for initial evaluation, including the 2024 MINUTES bundle and the 2025 European Society of Intensive Care Medicine (ESICM) guidelines on circulatory shock, which recommend serial assessment of tissue perfusion (e.g., capillary refill time, skin mottling, and temperature gradient) and point-of-care echocardiography as the first-line imaging for shock classification within the first 30 minutes of recognition.[69][70] This approach ensures timely identification of shock type and hypoperfusion while avoiding delays in non-circulatory differentials. General features like hypotension and type-specific presentations such as fever in septic shock inform the bedside evaluation.
Laboratory and Imaging Tests
Laboratory tests play a crucial role in confirming the presence of circulatory shock, assessing its severity, and differentiating between types such as hypovolemic, distributive, cardiogenic, and obstructive. Arterial blood gas analysis is essential to detect metabolic acidosis and hypoxemia, while serum lactate levels greater than 2 mmol/L indicate tissue hypoperfusion and guide resuscitation efforts across all shock types; the 2025 ESICM guidelines recommend serial lactate measurements alongside venous-to-arterial carbon dioxide difference (v-a CO₂ >6 mmHg) for evaluating adequacy of tissue perfusion.[65][18][70]A complete blood count (CBC) helps identify anemia from hemorrhage in hypovolemic shock or leukocytosis suggestive of infection in distributive (septic) shock. In cardiogenic shock, elevated high-sensitivity troponin and N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels support myocardial injury or heart failure as the underlying cause. Blood and urine cultures are recommended in suspected septic shock to identify pathogens, alongside coagulation studies to evaluate for disseminated intravascular coagulation.[18][71][65]Imaging modalities provide rapid, non-invasive insights into shock etiology and severity. Point-of-care ultrasound (POCUS), including the Rapid Ultrasound for Shock and Hypotension (RUSH) protocol, is increasingly emphasized for bedside classification, assessing inferior vena cava (IVC) collapsibility to evaluate hypovolemia (>50% collapse suggests volume depletion) and cardiac function for tamponade or right ventricular strain in obstructive shock.[72][18][32]Echocardiography evaluates ejection fraction, valvular abnormalities, and pericardial effusion in cardiogenic or obstructive shock, with guidelines recommending its urgent use as the first-line modality in suspected cases.[65][32][70]Computed tomography (CT) angiography is the gold standard for diagnosing pulmonary embolism or aortic dissection in obstructive shock, particularly when patients are stable enough for transport. Chest radiography aids in identifying pneumothorax or cardiomegaly, while abdominal ultrasound or CT can detect intra-abdominal sources of hypovolemia or infection in distributive shock.[32][71][18]Hemodynamic monitoring refines shock classification through direct measurements. Pulmonary artery catheterization (Swan-Ganz) measures pulmonary capillary wedge pressure (PCWP ≥15 mmHg with low cardiac output indicates cardiogenic shock), cardiac output, and systemic vascular resistance (SVR), with guidelines supporting its use in complex or refractory cases to guide therapy.[73][65] Advanced systems like PiCCO (pulse contour analysis with transpulmonary thermodilution) and FloTrac (arterial waveform analysis) offer less invasive continuous cardiac output monitoring, particularly useful in septic or mixed shock for tracking volume responsiveness without calibration; the 2025 ESICM guidelines advocate monitoring cardiac output/stroke volume in non-responders using such methods and dynamic predictors (e.g., end-expiratory occlusion test) over static preload markers like central venous pressure for assessing fluid responsiveness.[74][75][70]
Management
Initial Resuscitation
Initial resuscitation in circulatory shock prioritizes the airway, breathing, and circulation (ABCs) to stabilize the patient and prevent immediate deterioration. Airway patency must be ensured immediately, with supplemental oxygen administered to maintain adequate oxygenation, typically targeting an SpO2 of 94-98%.[5] Endotracheal intubation and mechanical ventilation are indicated if there is respiratory failure, altered mental status, or severe shock impairing ventilation.[69] These steps address hypoxia, which exacerbates tissue hypoperfusion in all shock types.[5]Circulatory support follows, beginning with rapid establishment of intravenous (IV) access using two large-bore (14- to 16-gauge) peripheral catheters, or intraosseous access if peripheral veins are inaccessible.[5]Fluid resuscitation is the cornerstone for hypovolemic and distributive shock, with an initial bolus of crystalloids such as 0.9% saline or lactated Ringer's solution at 20-30 mL/kg administered over 15-30 minutes, repeated as needed based on response.[5] In septic shock, guidelines recommend at least 30 mL/kg within the first 3 hours to restore intravascular volume. For hemorrhagic shock, blood products may be used early in a balanced 1:1:1 ratio of red blood cells, plasma, and platelets if massive transfusion is anticipated.[5]Fluid administration should be cautious or limited in cardiogenic shock to avoid pulmonary edema.[69]The primary goals of initial resuscitation are to restore tissue perfusion and hemodynamic stability, targeting a mean arterial pressure (MAP) of at least 65 mmHg to ensure coronary and cerebral perfusion.[69] In traumatic hemorrhagic shock, permissive hypotension is employed prior to hemostasis, aiming for a systolic blood pressure of 80-90 mmHg (or MAP 50-65 mmHg) in patients without traumatic brain injury, to minimize bleeding while preserving vital organ function; this approach remains supported in 2024 guidelines.[76] Other perfusion markers include normalization of mental status, skin perfusion, and lactate clearance.Continuous monitoring is essential during resuscitation, including vital signs (heart rate, blood pressure via noninvasive or arterial catheter, respiratory rate), pulse oximetry, and electrocardiography.[5] An indwelling urinary catheter should be placed to track urine output, targeting greater than 0.5 mL/kg/hour as an indicator of renal perfusion.[69] Point-of-care ultrasound and initial labs (e.g., lactate, hemoglobin) guide ongoing adjustments within the first 30 minutes.[69]
Pharmacologic Interventions
Pharmacologic interventions in circulatory shock focus on restoring hemodynamic stability after initial fluid resuscitation, with agents selected based on the shock etiology to support blood pressure, cardiac output, and tissue perfusion. Vasopressors and inotropes are titrated to achieve target mean arterial pressure (MAP) goals, typically ≥65 mmHg in septic shock or higher in other forms, while monitoring for adverse effects like arrhythmias or ischemia.[77] These therapies address vasodilation in distributive shock or myocardial dysfunction in cardiogenic shock, often guided by invasive monitoring of systemic vascular resistance (SVR) and cardiac output (CO).[78]In septic shock, norepinephrine serves as the first-line vasopressor, initiated at doses of 0.01 to 0.5 mcg/kg/min via continuous intravenous infusion to counteract vasodilation and maintain MAP ≥65 mmHg.[77]Vasopressin is recommended as an adjunct when norepinephrine doses exceed 0.25 to 0.5 mcg/kg/min without achieving hemodynamic goals, typically at a fixed dose of 0.03 units/min, to reduce catecholamine requirements and lower the risk of atrial fibrillation.[77]Titration of these agents is based on SVR (target 800-1200 dynes·s·cm⁻⁵) and CO, with escalation or weaning guided by serial lactate levels and urine output to avoid excessive vasoconstriction.[78]For cardiogenic shock characterized by low cardiac output, dobutamine is commonly employed as an inotrope at doses of 2 to 20 mcg/kg/min to enhance myocardial contractility and increase CO without significantly raising heart rate in most cases.[79] In right ventricular (RV) failure complicating shock, such as in pulmonary embolism or acute respiratory distress syndrome, milrinone is preferred due to its pulmonary vasodilatory effects, administered at 0.375 to 0.75 mcg/kg/min after a loading dose, providing comparable outcomes to dobutamine in terms of composite endpoints like mortality and sustained hypotension.[79]Inotrope selection and dosing are titrated against CO (target >2.2 L/min/m²) and SVR, with caution in patients with tachycardia to prevent worsening ischemia.[78]Specific etiologies require targeted agents beyond vasopressors and inotropes. In adrenal crisis presenting as shock, hydrocortisone is administered as an initial intravenous bolus of 100 mg, followed by 200 mg over 24 hours via continuous infusion or intermittent dosing (50 mg every 6 hours), to replace deficient glucocorticoids and support vascular tone.[80] For anaphylactic shock, after epinephrine stabilization, adjunctive antihistamines (e.g., diphenhydramine 25-50 mg IV) and corticosteroids (e.g., methylprednisolone 125 mg IV) are used to mitigate histamine-mediated vasodilation and prevent biphasic reactions, though they do not reverse acute hypotension.[81]In refractory septic shock unresponsive to fluids and vasopressors, hydrocortisone at 200 mg/day (via continuous infusion or divided doses) is suggested to address relative adrenal insufficiency, potentially accelerating shock reversal without increasing mortality risk.[77] Overall dosing and titration across agents prioritize invasive hemodynamic parameters, with norepinephrine and dobutamine often combined in mixed shock to balance SVR elevation and CO augmentation.[78]Recent updates, including 2024 consensus reviews, endorse angiotensin II as a salvage therapy for vasodilatory shock (e.g., septic or post-cardiotomy) refractory to high-dose catecholamines, infused at 20 ng/kg/min and titrated up to 80 ng/kg/min to raise MAP by activating the renin-angiotensin system, as demonstrated in the ATHOS-3 trial where it reduced vasopressor needs compared to placebo.[82] This approach is particularly relevant when norepinephrine equivalents exceed 0.2 mcg/kg/min, though its use remains adjunctive pending further outcome data.[83]
Mechanical Circulatory Support
Mechanical circulatory support (MCS) devices are employed in patients with refractory cardiogenic shock who do not respond adequately to initial resuscitation and pharmacologic interventions, providing temporary augmentation of cardiac output to maintain organ perfusion.[84] These devices are particularly indicated in severe cases of cardiogenic shock due to acute myocardial infarction (AMI) or other etiologies, as well as obstructive shock such as massive pulmonary embolism, where hemodynamic instability persists despite maximal medical therapy.[85][86]Key MCS devices include the intra-aortic balloon pump (IABP), which uses counterpulsation to reduce afterload and augment diastolic coronary perfusion by inflating in diastole and deflating in systole via a balloon in the descending aorta.[87] The Impella system, a microaxial flow pump, provides left ventricular (LV) unloading by aspirating blood from the LV and expelling it into the ascending aorta, thereby decreasing LV workload and improving cardiac output.[88] Venoarterial extracorporeal membrane oxygenation (VA-ECMO) offers full circulatory and respiratory support by draining deoxygenated blood from the venous system, oxygenating it externally, and returning it to the arterial circulation, often used when biventricular failure or profound hypoxemia is present.[89]Indications for these devices are primarily in cardiogenic shock complicating AMI (AMI-CS), where Impella is frequently utilized for LV support in high-risk percutaneous coronary interventions or post-infarction pump failure, and in obstructive shock requiring rapid decompression alongside support.[90] VA-ECMO is reserved for profound refractory cases needing complete hemodynamic rescue, while IABP may serve as a less invasive initial option despite limited efficacy in some trials.[91]Complications associated with MCS devices include vascular issues such as limb ischemia from arterial cannulation, particularly with Impella and VA-ECMO due to larger sheath sizes, and bleeding risks from anticoagulation requirements or access site hematomas across all devices.[92]Hemolysis is a notable concern with Impella, resulting from high shear stress on red blood cells, while VA-ECMO carries additional risks of systemic inflammation and oxygenator thrombosis.[93] IABP-related issues often involve balloon rupture or aortic dissection, though rates are lower with modern systems.[94]The DanGer Shock trial, a 2024 randomized controlled study, demonstrated that routine use of a microaxial flow pump (Impella CP) in patients with ST-elevation myocardial infarction-related cardiogenic shock reduced 180-day mortality by 12.7% compared to standard care (45.8% vs. 58.5%; hazard ratio 0.74, 95% CI 0.55-0.99). Long-term follow-up as of August 2025 showed an absolute mortality reduction of 16.3% at up to 10 years.[95][96] This evidence supports selective application in AMI-CS, though broader outcomes vary by device and patient selection.[97]MCS devices are typically used as a bridge to myocardial recovery, durable ventricular assist device implantation, or heart transplantation, with durations varying by device; for instance, the Impella 5.5 is FDA-approved for up to 14 days but 2025 registry data indicate safe prolonged support beyond 30 days in select cases without increased complications.[91][98][99]
Emerging Therapies
Emerging therapies for circulatory shock aim to address unmet needs in specific etiologies and phenotypes by targeting underlying pathophysiological mechanisms beyond conventional resuscitation and support. These approaches include immunomodulation, lipid-targeted interventions, phenotype-guided stratification, regenerative strategies, and predictive technologies, with ongoing clinical trials evaluating their efficacy in improving outcomes for septic, cardiogenic, and mixed shock states.[100]In septic shock, cytokine modulators represent a promising targeted therapy to mitigate the cytokine storm driving systemic inflammation and organ dysfunction. Extracorporeal cytokine adsorption devices, such as polymyxin B-immobilized fibers, have shown potential in reducing circulating inflammatory mediators like IL-6 and TNF-α, with preclinical and early clinical data indicating improved hemodynamics and reduced vasopressor requirements in severe cases.[101] Biomarker-guided use of cytokine blockers, including anti-IL-6 agents, allows for precision immunomodulation tailored to hyperinflammatory profiles, potentially decreasing mortality in subsets of patients unresponsive to standard antibiotics and fluids.[102] For cardiogenic shock complicated by hyperlipidemia, particularly post-acute myocardial infarction, in-hospital initiation of PCSK9 inhibitors like evolocumab has demonstrated rapid LDL-C reduction and attenuation of myocardial inflammation, which may stabilize plaque and prevent further deterioration in high-risk patients.[103] Early administration in acute coronary syndrome settings, where shock risk is elevated, has also been associated with plaque regression and favorable safety profiles, suggesting a role in preventing progression to refractory states.[104]The 3-axis model for cardiogenic shock, introduced in 2022 by the Society for Cardiovascular Angiography and Interventions (SCAI), integrates shock severity staging with etiology, phenotype, and comorbidity risk to enable tailored therapeutic escalation. This framework stratifies patients across axes of hemodynamic compromise, clinical phenotypes (e.g., hypovolemic vs. distributive overlays), and modifiers like age or renal function, facilitating personalized decisions on interventions from vasopressors to advanced support.[100] By incorporating non-cardiac factors, the model addresses limitations in prior classifications, with preliminary data showing improved prognostic accuracy and guidance for timely de-escalation in recovering patients.[105]Gene and cell therapies, particularly stem cell approaches, are under investigation for myocardial recovery in refractory cardiogenic shock, where irreversible damage limits conventional recovery. Intramyocardial or intracoronary delivery of mesenchymal stem cells has promoted angiogenesis and reduced fibrosis in animal models of ischemia-induced shock, with phase I/II trials reporting modest improvements in left ventricular ejection fraction and survival in end-stage heart failure patients bridged to transplant.[106] These therapies target cardiomyocyte regeneration and paracrine effects to halt progressive remodeling, though challenges like cell retention and immune rejection persist in clinical translation.[107]AI-assisted predictive algorithms are emerging to anticipate shock escalation in intensive care settings, enabling proactive interventions. Machine learning models using vital signs and electronic health record data have achieved high accuracy (AUC >0.85) in forecasting new-onset shock within 4 hours of ICU admission, outperforming traditional scoring systems like SOFA.[108] In 2025 pilot programs within cardiac ICUs, AI tools integrated with mechanical circulatory support monitoring predict decompensation in high-risk patients, optimizing timing for escalation and reducing unnecessary device use.[109]For mixed shock states, such as cardiogenic-distributive phenotypes, combined mechanical circulatory support (MCS) with vasopressors addresses overlapping hypoperfusion and vasodilation, as highlighted in 2024 reviews. This multimodal strategy, involving devices like Impella alongside norepinephrine, stabilizes hemodynamics in up to 60% of cases refractory to monotherapy, though optimal sequencing remains under study to minimize complications like right ventricular failure.[17] While current MCS options have limitations in vasodilatory components, these hybrid regimens fill critical gaps in management.[55]
Epidemiology
Incidence and Prevalence
Hospitals in the United States report more than 1 million cases of shock annually.[110]Septic shock, the most common type of distributive shock, affects approximately 1.7 million individuals annually and accounts for about 20% of intensive care unit (ICU) admissions.[111][112] This substantial burden underscores its role as a leading cause of critical illness, with over 5 million ICU admissions occurring each year in the country.[111]Among cases of undifferentiated shock in ICU settings, septic shock is the most prevalent type, accounting for about 62% of instances, followed by cardiogenic shock at 16%, hypovolemic shock at 16%, and obstructive shock at 2%.[35] These proportions highlight the dominance of distributive mechanisms, particularly sepsis-related, in driving shock epidemiology within critical care environments.Trends indicate a rising incidence of cardiogenic shock, driven by an aging population and increasing cardiovascular disease (CVD) prevalence; in the United States, the number of adults with clinical CVD is projected to grow from 28 million in 2020 to 45 million by 2050, a 61% increase.[113] Globally, the burden is disproportionately higher in low- and middle-income countries (LMICs), where infections and trauma contribute to elevated rates; according to 2020 data, an estimated 48.9 million sepsis cases occur worldwide each year, with the majority of related morbidity and mortality concentrated in these regions.[114] Recent analyses (as of 2021) estimate 166 million sepsis cases globally, resulting in 21.4 million deaths, representing nearly one-third of all global deaths.[115] In Japan, 2024 data reveal a post-pandemic surge in distributive shocks, including a 433% increase in septic phenotypes such as septic shock associated with invasive infections.[116]
Mortality and Trends
Mortality rates for circulatory shock vary by type but remain substantial overall, typically ranging from 20% to 50% across hypovolemic, distributive, cardiogenic, and obstructive categories.[117]Hypovolemic shock often carries lower rates, around 20% to 40% at 90 days, while distributive forms like septic shock exhibit 30% to 40% in-hospital mortality, and cardiogenic shock shows the highest burden at 40% to 50%.[1][118][119]Despite advances in critical care, mortality trends in circulatory shock have remained stubbornly high, with little overall improvement over the past decade.[120] In 2025 analyses, acute myocardial infarction-related cardiogenic shock (AMI-CS) continues to exceed 40% in-hospital mortality in real-world U.S. settings.[121] Recent reports highlight persistent lethality, particularly in septic and cardiogenic subtypes.[1]Delayed recognition and treatment significantly elevate mortality risk, with each hour of postponement in interventions like antibiotics for septic shock increasing death odds by up to 7%.[122] Conversely, advancements in mechanical circulatory support (MCS) devices, such as Impella and intra-aortic balloon pumps, have contributed to modest reductions in some cohorts, lowering in-hospital mortality for cardiogenic shock from historical peaks, though overall rates stay elevated.[123][124]Global disparities exacerbate outcomes, with mortality approaching 70% in resource-poor settings due to limited access to timely diagnostics and advanced care, compared to 20% to 40% in high-income regions.[118] Low- and middle-income countries bear a disproportionate sepsis-related burden, where septic shock fatality can reach 50% to 80%, underscoring the need for equitable interventions.[125]
Prognosis
Overall Outcomes
Short-term survival in circulatory shock varies widely by type, with 30-day survival rates generally ranging from 50% to 80% following initial resuscitation. Hypovolemic shock demonstrates the highest survival, often exceeding 70% at 30 days due to its responsiveness to fluid replacement and source control, while cardiogenic shock has lower rates around 57-60%, and distributive (septic) shock falls in the 50-62% range owing to multi-organ involvement.[117][20][1]Long-term outcomes for survivors include substantial challenges in quality of life and high readmission risks, with 20-30% experiencing rehospitalization within six months, often due to recurrent cardiovascular events or complications like heart failure. Post-discharge quality of life is frequently impaired by cognitive deficits, physical limitations, and post-intensive care syndrome, affecting up to 70% of cardiogenic shock survivors despite overall hospital discharge survival of 60-70%. One-year mortality among discharged patients remains elevated at approximately 25-40%, underscoring persistent morbidity.[126][127]Recovery patterns depend on etiology, with full restoration possible in reversible causes such as anaphylactic shock through prompt allergen removal and supportive care, achieving near-complete resolution in most cases. In contrast, cardiogenic shock often results in partial recovery, with survivors facing ongoing cardiac dysfunction and reduced functional capacity due to myocardial damage.[1][128]The Sequential Organ Failure Assessment (SOFA) score serves as a key metric for evaluating ICU outcomes in circulatory shock, quantifying multi-organ dysfunction to predict mortality, where higher scores (e.g., ≥10) correlate with ICU death rates exceeding 50% in septic and cardiogenic cases.[129][130]As of 2025, early mechanical circulatory support (MCS) in select cardiogenic shock patients has shown improved 30-day survival rates up to 68-76% compared to delayed initiation, particularly when deployed prior to percutaneous coronary intervention in acute myocardial infarction-related cases.[131][132]
Prognostic Factors
Patient factors significantly influence outcomes in circulatory shock, with advanced age greater than 65 years associated with increased mortality risk due to reduced physiological reserve and higher comorbidity prevalence.[133] Comorbidities such as chronic kidney disease and diabetes further worsen prognosis by exacerbating organ dysfunction and complicating resuscitation efforts.[134] Frailty, often measured by clinical scales, independently predicts poor survival by impairing recovery from hemodynamic instability.[135]Disease-related variables also play a critical role, including elevated lactate levels above 4 mmol/L, which indicate tissue hypoperfusion and are linked to higher short-term mortality across shock types.[67] Multi-organ failure, as evidenced by sequential organ failure assessment, amplifies risk by reflecting systemic decompensation.[136] Delayed initiation of therapy beyond 1 hour from shock recognition correlates with adverse outcomes, as timely intervention mitigates irreversible damage.[137]Type-specific prognostic indicators provide nuanced predictions; in cardiogenic shock, left ventricular ejection fraction below 30% signals severe myocardial impairment and elevated in-hospital mortality.[138] In septic shock, the presence of bacteremia has been associated with higher in-hospital mortality in some studies.[139] In hypovolemic shock, the volume and rate of fluid loss serve as key determinants, while obstructive shock outcomes hinge on rapid relief of mechanical obstruction, such as in pulmonary embolism.[1][140]Prognostic scoring systems enhance risk stratification; the APACHE II score, incorporating physiological and chronic health variables, demonstrates acceptable accuracy in predicting in-hospital mortality, with higher scores indicating poorer outcomes.[141] In cardiogenic shock, Society for Cardiovascular Angiography and Interventions (SCAI) stages C through E denote deteriorating hemodynamics and are tied to substantially higher mortality rates compared to earlier stages.[142]Recent analyses from the Cardiogenic Shock Working Group registry underscore the 2024 emphasis on comorbidity burden as a pivotal prognostic element in cardiogenic shock, revealing its independent association with mortality and highlighting the need for integrated risk assessment beyond acute presentation.[134]
History
Early Concepts
The earliest recorded descriptions of circulatory shock trace back to ancient Greek medicine, particularly in the Hippocratic Corpus around the 5th century BCE, where the condition was termed exemia to denote a state of profound collapse or depletion associated with trauma, hemorrhage, or severe illness, characterized by pallor, cold extremities, and weak pulse. These observations captured the clinical syndrome of patients "drained of blood" following injuries, emphasizing collapse as a response to bodily insult without a mechanistic explanation.In the 18th and 19th centuries, battlefield medicine brought greater attention to "wound shock" amid large-scale conflicts like the Napoleonic Wars (1799–1815). French surgeon Henri-François Le Dran first applied the term "shock" in 1743 to describe the acute neurologic-like prostration and insensibility following gunshot wounds, viewing it as a direct nervous system reaction to trauma rather than mere blood loss. British military surgeon George James Guthrie, drawing from his experiences treating casualties during the Peninsular Campaign, expanded on this in 1827, associating shock with the physics of injury—such as contusion and tissue disruption—and its neurophysiologic aftermath, noting symptoms like rapid pulse, anxiety, and eventual coma in wounded soldiers.Key figures advanced these ideas through foundational works on pathology and physiology. Scottish surgeon John Hunter, in his 1794 treatise A Treatise on the Blood, Inflammation, and Gun-Shot Wounds, detailed the inflammatory response to injuries, describing systemic debility, fever, and collapse as constitutional effects of local wound inflammation, which foreshadowed shock as a whole-body disturbance beyond the injury site. Mid-century, French physiologist Claude Bernard's experiments (1851–1852) revealed vasomotor nerves' role in controlling blood vessel dilation and constriction via the sympathetic system, providing a physiological basis for how nervous impulses could precipitate vascular instability in shock.[143][144]Debates over shock's etiology pitted the dominant nervous theory against nascent toxic explanations. The nervous theory, prevalent through much of the 19th century, attributed shock to central nervous system overload or inhibition—exemplified by "spinal shock," a transient paralysis and sensory loss after spinal trauma—leading to vasomotor paralysis and circulatory failure. Opposing views, influenced by observations of wound sepsis, proposed a toxic theory where absorbed substances from injured tissues altered blood composition, causing vasodilation and toxemia. By the late 1800s, experimental physiology began shifting focus to circulatory dynamics; American surgeon George Crile's 1897–1899 studies on surgical shock used animal models to demonstrate blood pressure drops and oligemia as core features, marking a transition toward recognizing hypovolemia and vascular tone as pivotal mechanisms.[145]
Modern Developments
During World War I, physiologist Walter B. Cannon conducted pivotal studies on traumatic shock among wounded soldiers, attributing the condition primarily to hypovolemia from blood loss rather than nervous system failure, as previously thought; his 1917 report emphasized fluid replacement to restore circulating volume.[146] Concurrently, the introduction of blood transfusions revolutionized shock management, with British pathologist Oswald Robertson establishing the first blood bank in 1917 and performing over 500 transfusions on battlefield casualties, significantly reducing mortality from hemorrhagic shock.In the mid-20th century, shock classification evolved to distinguish major etiologies, with hypovolemic shock formalized in the 1940s based on volume depletion models, followed by recognition of cardiogenic shock in the 1950s as a distinct entity complicating acute myocardial infarction, driven by clinical observations and early hemodynamic studies.[146] Vasopressor therapy emerged as a cornerstone during this period, with norepinephrine adopted in the late 1940s for refractory hypotension in shock states, marking a shift toward pharmacologic support of vascular tone.[147]The late 20th century saw refinement of shock subtypes, culminating in the 1992 consensus definitions from the Society of Critical Care Medicine (SCCM) and American College of Chest Physicians, which delineated sepsis, severe sepsis, and septic shock as part of distributive shock, emphasizing systemic inflammatory response and organ dysfunction. By the 1980s and 1990s, the four principal types of circulatory shock—hypovolemic, cardiogenic, distributive, and obstructive—were solidified in clinical guidelines and textbooks, providing a standardized framework for diagnosis and research.[146]Entering the 21st century, the Surviving Sepsis Campaign, launched in 2002 by the SCCM and European Society of Intensive Care Medicine, established evidence-based bundles for early recognition and management of septic shock, reducing global mortality through iterative guideline updates.[148] In cardiogenic shock, the Society for Cardiovascular Angiography and Interventions (SCAI) introduced staged classifications in 2019, with updates through 2022 and 2025 incorporating validation studies to enhance prognostic accuracy across stages A-E, while recent work has emphasized mixed shock phenotypes combining cardiogenic and distributive elements for tailored interventions. Mechanical circulatory support (MCS) trials advanced understanding, as the 2012 IABP-SHOCK II study demonstrated no 30-day mortality benefit from routine intra-aortic balloon pump use in myocardial infarction-related cardiogenic shock, leading to guideline de-escalation.[149] Conversely, the 2024 DanGer Shock trial reported improved 180-day survival (45.8% vs. 58.4% mortality) with early Impella CP microaxial flow pump versus standard care in refractory cardiogenic shock post-percutaneous intervention, highlighting selective MCS efficacy.Addressing gaps in heterogeneity, 2024-2025 research has advanced shock phenotyping through unsupervised machine learning on clinical and echocardiographic data, identifying sub-phenotypes in cardiogenic and septic shock to predict outcomes and guide therapy.[150] AI-driven monitoring tools, including predictive algorithms for early sepsis detection and real-time hemodynamic analysis, have shown promise in intensive care settings, with models achieving high sensitivity for shock progression using electronic health record data.[151]
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