INTRODUCTION — Shock is a life-threatening condition of circulatory failure, causing inadequate oxygen delivery to meet cellular metabolic needs and oxygen consumption requirements, producing cellular and tissue hypoxia. The effects of shock are initially reversible, but rapidly become irreversible, resulting in multiorgan failure (MOF) and death. When a patient presents with undifferentiated shock, it is important that the clinician immediately initiate therapy while rapidly identifying the etiology so that definitive therapy can be administered to reverse shock and prevent MOF and death.
The definition, classification, etiology, and pathophysiology of shock are discussed in this review. The clinical presentation and diagnostic evaluation of undifferentiated shock and the evaluation of patients with specific forms of shock are discussed separately. (See "Evaluation of and initial approach to the adult patient with undifferentiated hypotension and shock" and "Evaluation and management of suspected sepsis and septic shock in adults" and "Clinical manifestations and diagnosis of cardiogenic shock in acute myocardial infarction" and "Etiology, clinical manifestations, and diagnosis of volume depletion in adults" and "Approach to shock in the adult trauma patient" and "Clinical presentation, evaluation, and diagnosis of the nonpregnant adult with suspected acute pulmonary embolism".)
DEFINITION — Shock is defined as a state of cellular and tissue hypoxia due to either reduced oxygen delivery, increased oxygen consumption, inadequate oxygen utilization, or a combination of these processes. This most commonly occurs when there is circulatory failure manifested as hypotension (ie, reduced tissue perfusion); however, it is crucial to recognize that a patient in shock can present hypertensive, normotensive, or hypotensive. Shock is initially reversible, but must be recognized and treated immediately to prevent progression to irreversible organ dysfunction. "Undifferentiated shock" refers to the situation where shock is recognized but the cause is unclear.
EPIDEMIOLOGY — Septic shock, a form of distributive shock, is the most common form of shock among patients admitted to the intensive care unit, followed by cardiogenic and hypovolemic shock; obstructive shock is rare [1,2]. As an example, in a trial of 1600 patients with undifferentiated shock, septic shock occurred in 62 percent, cardiogenic shock in 16 percent, hypovolemic shock in 16 percent, other types of distributive shock in 4 percent (eg, neurogenic shock, anaphylaxis), and obstructive shock in 2 percent .
In the emergency department (ED), the percentage of each type of shock seen depends upon the population served by the ED [3,4]. As an example, busy, urban, level-I trauma centers will see a higher percentage of hemorrhagic shock. In one study of 103 patients with undifferentiated shock presenting to a busy, urban ED, 36 percent of patients had hypovolemic shock, 33 percent had septic shock, 29 percent had cardiogenic shock, and 2 percent had other forms of shock .
CLASSIFICATION AND ETIOLOGY — Four types of shock are recognized: distributive, cardiogenic, hypovolemic, and obstructive. However, these are not exclusive, and many patients with circulatory failure have a combination of more than one form of shock (multifactorial shock) (table 1). There are many etiologies within each class, all of which are discussed in detail in the sections below. (See 'Distributive' below and 'Cardiogenic' below and 'Hypovolemic' below and 'Obstructive' below and 'Combined' below.)
Distributive — Distributive shock is characterized by severe peripheral vasodilatation (vasodilatory shock). Molecules that mediate vasodilatation vary among the etiologies discussed in the sections below.
Septic shock — Sepsis, defined as a dysregulated host response to infection resulting in life-threatening organ dysfunction , is the most common cause of distributive shock. Septic shock is a subset of sepsis associated with mortality in the 40 to 50 percent range that can be identified  by the use of vasopressor therapy and the presence of elevated lactate levels (>2 mmol/L) despite adequate fluid resuscitation. The type of pathogen causing sepsis varies with the population studied. In the United States, gram-positive bacteria (eg, Pneumococcus, Enterococcus) are the most common pathogens responsible for severe sepsis and septic shock. However, antibiotic-resistant organisms (eg, methicillin-resistant staphylococcus), gram-negative organisms (eg, Pseudomonas, Klebsiella, Enterobacter), and fungi (eg, Candida) are more commonly encountered in those with shock from sepsis, when compared with patients who have sepsis without the features of shock. The definition, epidemiology, prognosis, and evaluation of patients with suspected sepsis and septic shock are discussed separately. (See "Sepsis syndromes in adults: Epidemiology, definitions, clinical presentation, diagnosis, and prognosis" and "Evaluation and management of suspected sepsis and septic shock in adults".)
Systemic inflammatory response syndrome (SIRS) — SIRS is a clinical syndrome that is characterized by a robust inflammatory response, usually induced by a major body insult that can be infectious (see above) or noninfectious (list below). The majority of patients presenting to the ED or admitted to the hospital who have SIRS are not in shock and will not develop shock during their admission; the presence of SIRS, however, should increase a clinician’s vigilance for progression of disease severity. (See "Sepsis syndromes in adults: Epidemiology, definitions, clinical presentation, diagnosis, and prognosis", section on 'Definitions'.)
Examples of noninfectious conditions that can be complicated by SIRS include the following:
●Pancreatitis (see "Clinical manifestations and diagnosis of acute pancreatitis", section on 'Natural history and complications')
●Burns (see "Overview of complications of severe burn injury")
●Hypoperfusion caused by trauma (see "Approach to shock in the adult trauma patient")
●Significant blunt trauma and crush injury (see "Approach to shock in the adult trauma patient")
●Amniotic fluid embolism (see "Amniotic fluid embolism")
●Air embolism (see "Air embolism")
●Fat embolism (see "Fat embolism syndrome")
●Idiopathic systemic capillary leak syndrome (see "Idiopathic systemic capillary leak syndrome")
●Post-cardiac arrest syndrome following return of spontaneous circulation after a cardiac arrest , myocardial infarction, or cardio-pulmonary bypass (see "Sepsis syndromes in adults: Epidemiology, definitions, clinical presentation, diagnosis, and prognosis")
Neurogenic shock — Hypotension and, in some cases, overt shock are common in patients with severe traumatic brain injury and spinal cord injury. Interruption of autonomic pathways, causing decreased vascular resistance and altered vagal tone, is thought to be responsible for distributive shock in patients with spinal cord injury. However, hypovolemia from blood loss and myocardial depression may also contribute to shock in this population. (See "Acute traumatic spinal cord injury", section on 'Cardiovascular complications' and "Management of acute moderate and severe traumatic brain injury", section on 'Initial evaluation and treatment'.)
Anaphylactic shock — Shock from anaphylaxis is most commonly encountered in patients with severe, immunoglobulin-E (Ig-E) mediated, allergic reactions to insect stings, food, and drugs (table 2). The term anaphylaxis also applies to acute systemic reactions caused by direct release of mediators from mast cells and basophils produced by various triggers (eg, exercise, contrast media, natural rubber latex, idiopathic). (See "Anaphylaxis: Acute diagnosis", section on 'Causes and mechanisms'.)
Drug and toxin-induced shock — Drug or toxin reactions that can be associated with shock or SIRS-like syndromes include those associated with drug overdoses (eg, long-acting narcotics); snake bites; insect bites including scorpion envenomation and various spider bites; transfusion reactions; heavy-metal poisoning including arsenic, iron, and thallium; and infections associated with toxic shock syndrome (eg, Streptococcus and Escherichia spp). (See "Use of blood products in the critically ill" and "Invasive group A streptococcal infection and toxic shock syndrome: Epidemiology, clinical manifestations, and diagnosis".)
Cyanide and carbon monoxide cause shock from mitochondrial dysfunction. (See "Cyanide poisoning" and "Carbon monoxide poisoning" and "Inhalation injury from heat, smoke, or chemical irritants".)
Endocrine shock — Addisonian crisis (adrenal failure due to mineralocorticoid deficiency) and myxedema can be associated with hypotension and states of shock. In states of mineralocorticoid deficiency, vasodilatation can occur due to altered vascular tone and aldosterone-deficiency-mediated hypovolemia. Although thyroid hormone plays a role in blood pressure homeostasis, the exact mechanism of vasodilation in patients with myxedema is unclear; concurrent myocardial depression or pericardial effusions likely contribute to hypotension and shock in this population. (See "Myxedema coma", section on 'Cardiovascular abnormalities' and "Cardiovascular effects of hypothyroidism" and "Clinical manifestations of adrenal insufficiency in adults", section on 'Postural hypotension'.)
Patients with thyrotoxicosis can develop high-output cardiac failure and do not develop shock per se. However, with progression, these patients can develop left ventricular systolic dysfunction and/or tachyarrhythmia, leading to hypotension. (See "Cardiovascular effects of hyperthyroidism", section on 'Heart failure' and "Overview of the clinical manifestations of hyperthyroidism in adults", section on 'Cardiovascular'.)
Cardiogenic — Cardiogenic shock is due to intracardiac causes of cardiac pump failure that result in reduced cardiac output (CO). Causes of cardiac pump failure are diverse, but can be divided into the following three categories listed in the sections below (table 1).
Cardiomyopathic — Cardiomyopathic causes of shock include myocardial infarction involving greater than 40 percent of the left ventricular myocardium, myocardial infarction of any size if accompanied by severe extensive ischemia due to multivessel coronary artery disease, severe right ventricular infarction, acute exacerbation of heart failure in patients with severe underlying dilated cardiomyopathy, stunned myocardium following cardiac arrest, prolonged ischemia or cardiopulmonary bypass, myocardial depression due to advanced septic or neurogenic shock, and myocarditis. (See "Clinical manifestations and diagnosis of cardiogenic shock in acute myocardial infarction", section on 'Pathophysiology' and "Clinical manifestations and diagnosis of cardiogenic shock in acute myocardial infarction", section on 'Etiology' and "Right ventricular myocardial infarction" and "Coronary artery bypass graft surgery in patients with acute ST-elevation myocardial infarction", section on 'Cardiogenic shock' and "Clinical manifestations and diagnosis of myocarditis in adults".)
Patients with hypertrophic cardiomyopathy or severe diastolic heart failure rarely present with cardiogenic shock, but these underlying conditions may contribute to hypotension and shock from other causes (eg, sepsis, hypovolemia). (See "Hypertrophic cardiomyopathy: Clinical manifestations, diagnosis, and evaluation" and "Heart failure with preserved ejection fraction: Clinical manifestations and diagnosis".)
Arrhythmic — Both atrial and ventricular tachyarrhythmias and bradyarrhythmias may induce hypotension, often contributing to states of shock. However, when CO is severely compromised by significant rhythm disturbances (eg, sustained ventricular tachycardia, complete heart block), patients can present with cardiogenic shock. If CO is absent because of the underlying rhythm (eg, pulseless ventricular tachycardia, ventricular fibrillation), patients present in cardiac arrest. (See "Atrial fibrillation: Overview and management of new-onset atrial fibrillation" and "Wide QRS complex tachycardias: Approach to the diagnosis" and "Ventricular arrhythmias during acute myocardial infarction: Incidence, mechanisms, and clinical features" and "Third-degree (complete) atrioventricular block".)
Mechanical — Mechanical causes of cardiogenic shock include severe aortic or mitral valve insufficiency, and acute valvular defects due to rupture of a papillary muscle or chordae tendineae (mitral valve defect) or retrograde dissection of the ascending aorta into the aortic valve ring or an abscess of the aortic ring (aortic insufficiency). Additional causes include severe ventricular septal defects or acute rupture of the intraventricular septum, atrial myxomas, and a ruptured ventricular free wall aneurysm. While a ruptured ventricular aneurysm can cause cardiogenic shock due to reduced output from the left ventricle, it can also present with the features of obstructive shock, when bleeding is contained by the pericardial sac, or catastrophic hemorrhagic shock, when the pericardial sac is breached and hemorrhage is ongoing. (See "Acute mitral regurgitation in adults" and "Acute aortic regurgitation in adults" and "Clinical manifestations and diagnosis of ventricular septal defect in adults" and "Acute myocardial infarction: Mechanical complications" and "Cardiac tumors".)
Critical aortic stenosis or mitral stenosis rarely present with cardiogenic shock, but often contribute to hypotension and shock from other causes (eg, sepsis, hypovolemia). (See "Clinical manifestations and diagnosis of aortic stenosis in adults" and "Rheumatic mitral stenosis: Clinical manifestations and diagnosis".)
Hypovolemic — Hypovolemic shock is due to reduced intravascular volume (ie, reduced preload), which, in turn, reduces CO. Hypovolemic shock can be divided into two categories: hemorrhagic and nonhemorrhagic (table 1).
Hemorrhagic — Reduced intravascular volume from blood loss can result in shock. There are multiple causes of hemorrhagic shock, of which blunt or penetrating trauma (includes multiple fractures without vessel injury) is the most common, followed by upper (eg, variceal hemorrhage, peptic ulcer) or lower (eg, diverticular, arteriovenous malformation) gastrointestinal bleeding. (See "Approach to shock in the adult trauma patient" and "Initial management of moderate to severe hemorrhage in the adult trauma patient", section on 'Classification of hemorrhage' and "Causes of upper gastrointestinal bleeding in adults" and "Etiology of lower gastrointestinal bleeding in adults".)
Less common causes include intraoperative and postoperative bleeding, ruptured abdominal aortic or left ventricle aneurysm, aortic–enteric fistula, hemorrhagic pancreatitis, iatrogenic (eg, inadvertent biopsy of arteriovenous malformation, severed artery), tumors or abscess erosion into major vessels, postpartum hemorrhage, uterine or vaginal hemorrhage from other causes (eg, infection, tumors, lacerations), spontaneous peritoneal hemorrhage from bleeding diathesis, and ruptured hematoma. (See "Management of symptomatic (non-ruptured) and ruptured abdominal aortic aneurysm", section on 'Ruptured AAA' and "Left ventricular aneurysm and pseudoaneurysm following acute myocardial infarction" and "Clinical manifestations and diagnosis of acute pancreatitis" and "Overview of postpartum hemorrhage" and "Managing an episode of acute uterine bleeding", section on 'Etiology' and "Overview of complications of peptic ulcer disease", section on 'Penetration'.)
Nonhemorrhagic — Reduced intravascular volume from fluid loss other than blood can cause shock. Volume depletion from loss of sodium and water can occur from a number of anatomic sites (see "Etiology, clinical manifestations, and diagnosis of volume depletion in adults", section on 'Etiology'):
●Gastrointestinal losses (eg, diarrhea, vomiting, external drainage)
●Skin losses (eg, heat stroke, burns, severe dermatologic conditions including Stevens-Johnson syndrome)
●Renal losses (eg, excessive drug-induced or osmotic diuresis, salt-wasting nephropathies, hypoaldosteronism)
●Third space losses into the extravascular space or body cavities (eg, postoperative and trauma, intestinal obstruction, crush injury, pancreatitis, cirrhosis)
Obstructive — Obstructive shock is mostly due to extracardiac causes of cardiac pump failure and often associated with poor right ventricular output. The causes of obstructive shock can be divided into the following two categories, listed in the sections below (pulmonary vascular and mechanical) (table 1).
Pulmonary vascular — Most cases of obstructive shock are due to right ventricular failure from hemodynamically significant pulmonary embolism (PE) or severe pulmonary hypertension (PH). In these cases, the right ventricle fails because it is unable to generate enough pressure to overcome the high pulmonary vascular resistance associated with PE or PH. While hemodynamic collapse in the setting of PE is traditionally attributed to mechanical obstruction, pulmonary vasoconstriction mediated by vasoactive mediators such as serotonin and thromboxane also contribute to the observed pathophysiology . Patients with severe stenosis or with acute obstruction of the pulmonary or tricuspid valve may also fall into this category. (See "Clinical presentation, evaluation, and diagnosis of the nonpregnant adult with suspected acute pulmonary embolism", section on 'Hemodynamically unstable patients' and "Clinical features and diagnosis of pulmonary hypertension of unclear etiology in adults", section on 'Postdiagnostic testing and classification'.)
Acute right heart syndrome can, given ventricular interdependence, mimic left ventricular dysfunction resulting in cardiogenic shock. Acute right heart syndrome is associated with myocardial infarction localizing to the right ventricle, massive volume overload, hypoxemic vasoconstriction resulting in acute pulmonary hypertension, and pulmonary embolism. In patients with pre-existing pulmonary hypertension and right ventricular dysfunction, ischemia, volume overload, or hypoxemia should be avoided as these insults can result in acute-on-chronic right ventricular dysfunction resulting in cardiovascular collapse. (See 'Cardiogenic' above.)
Mechanical — Patients in this category present clinically as hypovolemic shock because their primary physiologic disturbance is decreased preload, rather than pump failure (eg, reduced venous return to the right atrium or inadequate right ventricle filling). Mechanical causes of obstructive shock include the following:
●Tension pneumothorax (see "Pneumothorax in adults: Epidemiology and etiology")
●Pericardial tamponade (see "Cardiac tamponade", section on 'Physiology' and "Cardiac tamponade", section on 'Etiology')
●Constrictive pericarditis (see "Constrictive pericarditis: Clinical features and causes", section on 'Pathophysiology' and "Constrictive pericarditis: Clinical features and causes", section on 'Incidence and causes' and "Constrictive pericarditis: Diagnostic evaluation and management")
●Restrictive cardiomyopathy (see "Definition and classification of the cardiomyopathies", section on 'Restrictive cardiomyopathy')
Abdominal compartment syndrome (ACS), defined as sustained intra-abdominal hypertension associated with organ dysfunction can exacerbate shock. Primary ACS develops in patients with an intra-abdominal injury, whereas secondary ACS is frequently the result of massive volume resuscitation. ACS impairs cardiovascular function by both reducing venous return and by impairing myocardial contractility. (See "Abdominal compartment syndrome in adults".)
Combined — Patients often present with combined forms of shock. Examples include:
●Patients with shock from sepsis or pancreatitis primarily have distributive shock (due to the effects of inflammatory and anti-inflammatory cascades on vascular permeability and peripheral vasodilation); however, they also often have a hypovolemic component (due to decreased oral intake, insensible losses, vomiting, diarrhea) and a cardiogenic component (due to inflammation-related myocardial depression).
●Patients with underlying cardiomyopathy may present with hypovolemic shock (from over-diuresis) and cardiogenic shock (from inadequate compensatory tachycardia and/or stroke volume).
●Patients with severe traumatic injury may have hemorrhagic shock from blood loss as well as distributive shock from SIRS or, less commonly, fat embolism.
●Patients with trauma to the spinal cord can have distributive shock from injury-related autonomic dysfunction and cardiogenic shock from myocardial depression.
●Patients with a ruptured left ventricular free wall aneurysm can have cardiogenic shock from primary pump failure, obstructive shock from cardiac tamponade when blood loss is contained by the pericardial sac, and hemorrhagic shock when blood loss is not contained by the pericardial sac.
●Patients with septic shock may transition from a distributive (low systemic vascular resistance [SVR]) shock state to multifactorial shock state after massive volume resuscitation that results in abdominal compartment syndrome and/or acute right heart syndrome.
PATHOGENESIS AND PATHOPHYSIOLOGY — The general mechanisms, physiology, and stages of shock are discussed in the sections below (see 'Mechanisms of shock' below and 'Physiology' below and 'Stages of shock' below). The pathogenesis and physiology of specific forms of shock are discussed separately:
●Septic shock (see "Pathophysiology of sepsis")
●Burns (see "Burn wound infection and sepsis", section on 'Pathogenesis')
●Amniotic fluid embolism (see "Amniotic fluid embolism", section on 'Pathogenesis')
●Air embolism syndrome (see "Air embolism", section on 'Terminology and pathophysiology')
●Fat embolism syndrome (see "Fat embolism syndrome", section on 'Pathogenesis')
●Idiopathic systemic capillary leak syndrome (see "Idiopathic systemic capillary leak syndrome", section on 'Pathogenesis')
●Spinal cord injury (see "Acute traumatic spinal cord injury", section on 'Pathophysiology')
●Anaphylactic shock (see "Pathophysiology of anaphylaxis")
●Toxic shock syndrome (see "Staphylococcal toxic shock syndrome", section on 'Microbiology and pathogenesis')
●Myxedema coma (see "Myxedema coma", section on 'Epidemiology and risk factors' and "Myxedema coma", section on 'Cardiovascular abnormalities')
●Cardiogenic shock (see "Pathophysiology of cardiogenic pulmonary edema")
●Pulmonary embolism (PE) (see "Overview of acute pulmonary embolism in adults", section on 'Pathogenesis and pathophysiology')
●Pericardial tamponade (see "Cardiac tamponade", section on 'Physiology')
●Constrictive pericarditis and restrictive cardiomyopathy (see "Differentiating constrictive pericarditis and restrictive cardiomyopathy")
Mechanisms of shock — Cellular hypoxia occurs as a result of reduced tissue perfusion/oxygen delivery and/or increased oxygen consumption or from inadequate oxygen utilization [9-11]. Cellular hypoxia, in turn, causes cell membrane ion pump dysfunction, intracellular edema, leakage of intracellular contents into the extracellular space, and inadequate regulation of intracellular pH. These biochemical processes, when unchecked, progress to the systemic level, resulting in acidosis, and endothelial dysfunction, as well as further stimulation of inflammatory and anti-inflammatory cascades. Compounding this process is a further reduction in tissue perfusion from complex humoral and microcirculatory processes that impair regional blood flow [11,12].
Serum lactate levels, when elevated, have traditionally been used as surrogates for hypoperfusion and tissue hypoxia. Admittedly, lactate flux is more complex than the tissue hypoxia hypothesis suggests, as epinephrine-mediated aerobic glycolysis in skeletal muscle contributes to hyperlactatemia  as well. However, elevations in serum lactate level are useful risk-stratification tools in undifferentiated shock.
Physiology — The major physiologic determinants of tissue perfusion (and systemic blood pressure [BP]) are cardiac output (CO) and systemic vascular resistance (SVR):
BP = CO X SVR
CO is the product of heart rate (HR) and stroke volume (SV):
CO = HR X SV
The stroke volume is determined by:
SVR is governed by:
●Vessel diameter (ie, vessel tone)
Thus, biologic processes that change any one of these physiologic parameters can result in hypotension and shock.
The hemodynamic profiles, which can be measured on pulmonary artery catheterization or noninvasive CO devices, which distinguish each class of shock are shown in the tables (table 3 and table 4). Common to most forms of shock is diminished CO and/or SVR. Occasionally, the SVR is low relative to a high CO (eg, thyrotoxicosis), which can result in poor tissue perfusion. In general, severe hypovolemia, cardiogenic shock, and late-stage obstructive shock are characterized by a low CO and compensatory increase in the SVR in an attempt to maintain perfusion to vital organs, whereas distributive shock is classically associated with reduced SVR and compensatory (but insufficient) increase in the CO to maintain adequate oxygen delivery. However, the CO may be normal in the early phases of hypovolemic and obstructive shock. Similarly, in some cases of severe distributive shock (eg, sepsis and neurogenic shock) or combined shock, both CO and SVR may be reduced.
Some forms of shock have normal CO and SVR. As an example, patients with profound mitochondrial dysfunction (eg, inheritable mitochondrial disease, carbon monoxide, and cyanide poisoning) have a shock state that occurs despite normal CO, SVR, and tissue perfusion because of inadequate oxygen utilization. (See "Mitochondrial myopathies: Clinical features and diagnosis" and "Carbon monoxide poisoning" and "Cyanide poisoning" and "Inhalation injury from heat, smoke, or chemical irritants".)
Stages of shock — Shock is a physiologic continuum [10,14]. It begins with an inciting event, such as a focus of infection (eg, abscess) or an injury (eg, gunshot wound), triggering pathophysiological changes, which can progress through several stages. The early stages of shock (pre-shock, shock) are more amenable to therapy and are more likely to be reversible, compared with end-stage shock, which is associated with irreversible end-organ damage and death.
●Pre-shock – Pre-shock is also known as compensated shock, or cryptic shock. It is characterized by compensatory responses to diminished tissue perfusion . As an example, in early hypovolemic pre-shock, a compensatory tachycardia and peripheral vasoconstriction may allow an otherwise healthy adult to be asymptomatic and preserve a normal or mildly elevated blood pressure despite a 10 percent reduction in total effective arterial blood volume. Thus, tachycardia, a modest change in systemic blood pressure (increase or decrease), or mild to moderate hyperlactatemia, may be the only clinical signs of early shock . Potentially, with timely and appropriate management, deterioration can be prevented and signs of impending deterioration can be reversed (eg, normalization of heart rate and serum lactate levels).
●Shock – During shock, the compensatory mechanisms become overwhelmed, and signs and symptoms of organ dysfunction appear including symptomatic tachycardia, dyspnea, restlessness, diaphoresis, metabolic acidosis, hypotension, oliguria, and cool, clammy skin.
The signs and symptoms of organ dysfunction typically correspond to a significant pathophysiologic perturbation [17-19]. As examples, in hypovolemic shock, clinical signs and symptoms are associated with a 20 to 25 percent reduction in arterial blood volume, and, in cardiogenic shock, a fall in the cardiac index to less than 2.5 L/min/m2 is required before signs and symptoms appear .
●End-organ dysfunction – Progressive shock leads to irreversible organ damage, multiorgan failure (MOF), and death. During this stage, anuria and acute renal failure develop, acidemia further depresses CO, hypotension becomes severe and recalcitrant to therapy, often related to vasoplegia, hyperlactatemia often worsens, and restlessness evolves into obtundation and coma. Death is common in this phase of shock.
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
●Basics topic (see "Patient education: Shock (The Basics)")
SUMMARY AND RECOMMENDATIONS
●Definition – Shock is defined as a state of cellular and tissue hypoxia due to reduced oxygen delivery, increased oxygen consumption, inadequate oxygen utilization, or a combination of the three. "Undifferentiated shock" refers to the situation where shock is recognized but the cause is unclear. (See 'Definition' above.)
●Classification – Four types of shock are recognized. However, many patients have a combination of more than one of the forms of shock listed below (table 1):
•Distributive shock has many causes, including septic shock, systemic inflammatory response syndrome (SIRS; eg, pancreatitis), neurogenic shock, anaphylactic shock, toxin-related shock, and endocrine shock (eg, addisonian crisis).
•Cardiogenic shock may be cardiomyopathic (eg, myocardial infarction), or due to an arrhythmia (eg, sustained ventricular tachycardia) or a mechanical abnormality (eg, acute valvular rupture).
•Hypovolemic shock may be due to hemorrhagic (eg, trauma) or nonhemorrhagic fluid losses (eg, diarrhea).
•Obstructive shock may be pulmonary vascular related (eg, pulmonary embolism [PE]) or due to a mechanical cause of reduced preload (eg, tension pneumothorax, pericardial tamponade).
•Mechanisms – Cellular hypoxia results in cell membrane ion pump dysfunction, intracellular edema, leakage of intracellular contents into the extracellular space, and inadequate regulation of intracellular pH. These biochemical processes, in turn, progress to acidosis, endothelial dysfunction, and further stimulation of inflammatory and anti-inflammatory cascades. (See 'Mechanisms of shock' above.)
•Pathophysiology – Common to most forms of shock is diminished cardiac output (CO) and/or systemic vascular resistance (SVR (table 3 and table 4)). In general, severe hypovolemia, cardiogenic shock, and late-stage obstructive shock are characterized by a low CO and compensatory increase in the SVR that attempts to maintain perfusion to vital organs, whereas distributive shock is classically associated with reduced SVR and a compensatory increase in the CO. Shock due to disorders of mitochondrial function (eg, carbon monoxide poisoning) have normal CO and SVR but inadequate oxygen utilization. (See 'Physiology' above.)
•Stages of shock – Shock begins with an inciting event and may progress through several stages: pre-shock, shock, and end-organ dysfunction. The progression can culminate in irreversible end-organ damage and death. (See 'Stages of shock' above.)
3 : The use of end-tidal carbon dioxide monitoring in patients with hypotension in the emergency department.
4 : Diagnostic accuracy of left ventricular function for identifying sepsis among emergency department patients with nontraumatic symptomatic undifferentiated hypotension.
6 : Developing a New Definition and Assessing New Clinical Criteria for Septic Shock: For the Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3).
8 : Pathophysiology and treatment of haemodynamic instability in acute pulmonary embolism: the pivotal role of pulmonary vasoconstriction.
15 : Temporal physiologic patterns of shock and circulatory dysfunction based on early descriptions by invasive and noninvasive monitoring.
18 : Plasma cytokine and endotoxin levels correlate with survival in patients with the sepsis syndrome.
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