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All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Feb 2019. | This topic last updated: Feb 18, 2018.
INTRODUCTION
Shock is a life-threatening condition of circulatory failure. 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 "Initial evaluation of shock in the
adult trauma patient and management of NON-hemorrhagic shock" 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 reduced oxygen delivery and/or
increased oxygen consumption or inadequate oxygen utilization. This most commonly occurs
when there is circulatory failure manifested as hypotension (ie, reduced tissue perfusion). Shock is
initially reversible, but must be recognized and treated immediately to prevent progression to
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irreversible organ dysfunction. "Undifferentiated shock" refers to the situation where shock is
recognized but the cause is unclear.
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.)
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 [2].
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, and 2 percent had other forms of shock [3].
Septic shock — Sepsis, defined as a dysregulated host response to infection resulting in life-
threatening organ dysfunction [5], 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 [6]
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
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adults: Epidemiology, definitions, clinical presentation, diagnosis, and prognosis" and "Evaluation
and management of suspected sepsis and septic shock in adults".)
Examples of noninfectious conditions that can be complicated by SIRS include the following:
● Hypoperfusion caused by trauma (see "Initial evaluation of shock in the adult trauma patient
and management of NON-hemorrhagic shock")
● Significant blunt trauma and crush injury (see "Initial evaluation of shock in the adult trauma
patient and management of NON-hemorrhagic shock")
● Idiopathic systemic capillary leak syndrome (see "Idiopathic systemic capillary leak
syndrome")
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 severe
traumatic brain injury", section on 'Initial evaluation and treatment'.)
latex, and clinically similar but physiologically different anaphylactoid reactions are seen in patients
with allergies to iodinated contrast (table 2). (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 "Clinical manifestations of adrenal insufficiency in adults", section on 'Hypotension' and
"Myxedema coma", section on 'Cardiovascular abnormalities' and "Cardiovascular effects of
hypothyroidism".)
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).
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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 "Clinical manifestations and diagnosis of heart
failure with preserved ejection fraction".)
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 can present in cardiac
arrest. (See "Overview of 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 "Mechanical complications of acute myocardial infarction" 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 "Clinical manifestations and
diagnosis of rheumatic mitral stenosis".)
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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
"Initial evaluation of shock in the adult trauma patient and management of NON-hemorrhagic
shock", section on 'Pathophysiology' and "Causes of upper gastrointestinal bleeding in adults" and
"Etiology of lower gastrointestinal bleeding in adults" and "Initial management of moderate to
severe hemorrhage in the adult trauma patient", section on 'Classification of hemorrhage'.)
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 the complications of peptic ulcer disease", section on 'Penetration'
and "Overview of postpartum hemorrhage" and "Managing an episode of severe or prolonged
uterine bleeding", section on 'Etiology'.)
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'):
Obstructive — Obstructive shock is mostly due to extracardiac causes of cardiac pump failure
and often associated with poor right ventricle 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).
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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 [8]. 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 "Classification and prognosis of
pulmonary hypertension in adults", section on '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:
Combined — Patients often present with combined forms of shock. Examples include:
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● 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.
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:
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● 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")
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 [13] as well, 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 = HR X SV
● Preload
● Myocardial contractility
● Afterload
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● Vessel length
● Blood viscosity
● 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 measured on pulmonary artery catheterization that 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 to maintain perfusion to vital organs, whereas distributive shock is classically associated with
reduced SVR and compensatory increase in the CO. 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) are shock states that occur despite normal CO, SVR, and tissue perfusion because
they are due to 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), 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.
● Shock – During shock, the compensatory mechanisms become overwhelmed, and signs and
symptoms of organ dysfunction appear including symptomatic tachycardia, dyspnea,
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restlessness, diaphoresis, metabolic acidosis, hypotension, oliguria, and cool, clammy skin.
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.)
● Shock is defined as a state of cellular and tissue hypoxia due to reduced oxygen delivery
and/or increased oxygen consumption or inadequate oxygen utilization. "Undifferentiated
shock" refers to the situation where shock is recognized but the cause is unclear. (See
'Definition' above.)
● Four types of shock are recognized. However, many patients have a combination of more
than one form 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,
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• 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).
● 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.)
● Common to most forms of shock is diminished cardiac output (CO) and/or systemic vascular
resistance (SVR). In general, severe hypovolemia, cardiogenic shock, and late-stage
obstructive shock are characterized by a low CO and compensatory increase in the SVR to
maintain perfusion to vital organs, whereas distributive shock is classically associated with
reduced SVR and compensatory increase in the CO. Shock due to disorders of mitochondrial
function (eg, carbon monoxide poisoning) have normal CO and SVR. (See 'Physiology'
above.)
● Shock begins with an inciting event that 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.)
REFERENCES
3. Kheng CP, Rahman NH. The use of end-tidal carbon dioxide monitoring in patients with
hypotension in the emergency department. Int J Emerg Med 2012; 5:31.
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4. Jones AE, Craddock PA, Tayal VS, Kline JA. Diagnostic accuracy of left ventricular function
for identifying sepsis among emergency department patients with nontraumatic symptomatic
undifferentiated hypotension. Shock 2005; 24:513.
5. Singer M, Deutschman CS, Seymour CW, et al. The Third International Consensus
Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA 2016; 315:801.
6. Shankar-Hari M, Phillips GS, Levy ML, et al. 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). JAMA 2016; 315:775.
7. Adrie C, Laurent I, Monchi M, et al. Postresuscitation disease after cardiac arrest: a sepsis-
like syndrome? Curr Opin Crit Care 2004; 10:208.
9. Barber AE, Shires GT. Cell damage after shock. New Horiz 1996; 4:161.
10. Kristensen SR. Mechanisms of cell damage and enzyme release. Dan Med Bull 1994;
41:423.
11. Angus DC, van der Poll T. Severe sepsis and septic shock. N Engl J Med 2013; 369:840.
13. James JH, Luchette FA, McCarter FD, Fischer JE. Lactate is an unreliable indicator of tissue
hypoxia in injury or sepsis. Lancet 1999; 354:505.
14. Abboud, FM. Pathophysiology of hypotension and shock. In: The Heart, Hurst, JW (Eds), Mc
Graw-Hill, New York 1982. p.452.
15. Shoemaker WC. Temporal physiologic patterns of shock and circulatory dysfunction based
on early descriptions by invasive and noninvasive monitoring. New Horiz 1996; 4:300.
16. Chien S. Role of the sympathetic nervous system in hemorrhage. Physiol Rev 1967; 47:214.
17. Tuchschmidt JA, Mecher CE. Predictors of outcome from critical illness. Shock and
cardiopulmonary resuscitation. Crit Care Clin 1994; 10:179.
18. Casey LC, Balk RA, Bone RC. Plasma cytokine and endotoxin levels correlate with survival
in patients with the sepsis syndrome. Ann Intern Med 1993; 119:771.
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19. Levy MM, Fink MP, Marshall JC, et al. 2001 SCCM/ESICM/ACCP/ATS/SIS International
Sepsis Definitions Conference. Crit Care Med 2003; 31:1250.
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GRAPHICS
Classification of shock
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hemorrhagic skin losses (eg, heat stroke, burns, dermatologic conditions); 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)
Aortic dissection causes shock when retrograde dissection results in cardiac tamponade, acute aortic insufficiency,
and myocardial infarction; please refer to the UpToDate topic text for details.
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Causes of anaphylaxis
Insect stings (eg, Hymenoptera venom) and insect bites (eg, kissing bugs)
Biologic materials, including allergen immunotherapy, monoclonal antibodies, chemotherapy agents, and
vaccines*
Food additives, including spices, insect-derived colorants (eg, carmine), and vegetable gums
Coagulation system activation (eg, heparin contaminated with oversulfated chondroitin sulfate)
Idiopathic anaphylaxis
Consider the possibility of a hidden or previously unrecognized trigger
Consider the possibility of a mast cell activation syndrome, including systemic mastocytosis
Radiocontrast agents
Any food, insect sting or bite, or medication or biologic can potentially trigger anaphylaxis. Novel or unusual
allergen triggers include storage mite-contaminated flour and saliva from kissing bugs. They also
include mosquitoes, pigeon ticks, green ants, and pharaoh ants and venoms from jellyfish, scorpions, and snakes.
Medications include taxanes, platins, and other chemotherapy drugs, biologic agents, including monoclonal
antibodies, such as rituximab, cetuximab, infliximab, and uncommonly, omalizumab. Some triggers, such as
radiocontrast media, insect venoms, and medications (such as NSAIDs) can act through more than one
mechanism.
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Mean Range
Pressure* (mmHg)
Left ventricle
Systolic 130 90 to 140
End-diastolic 7 4 to 12
Left atrium
Maximum 13 6 to 20
Minimum 3 –2 to +9
Mean 7 4 to 12
Pulmonary artery
Systolic 24 15 to 28
Diastolic 10 5 to 16
Mean 16 10 to 22
Right ventricle
Systolic 24 15 to 28
End-diastolic 4 0 to 8
Right atrium
Maximum 7 2 to 14
Minimum 2 –2 to +6
Mean 4 –1 to +8
Venae cavae
Maximum 7 2 to 14
Minimum 5 0 to 8
Mean 6 1 to 10
Resistance (dyn×s/cm 5)
Total systemic 1150 900 to 1400
Systemic arteriolar 850 600 to 900
Total pulmonary 200 150 to 250
Pulmonary arteriolar 70 45 to 120
* Baseline for pressure measurements one-half of anteroposterior chest diameter. 1 mmHg = 133.332 Pascal (PA) =
0.133 kPa.
Reproduced with permission from: Hurst JW, Rackley CE, Sonnenblick EH, Wenger NK. The Heart: Arteries and veins. 7th
ed. McGraw-Hill, Inc, New York 1990. Copyright © 1990 McGraw-Hill Companies, Inc.
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Physiologic Tissue
Preload Pump function Afterload
variable perfusion
Cardiogenic ↑ ↓ ↑ <65%
Obstructive
Pericardial ↑ ↓ ↑ <65%
tamponade Δ
PE: pulmonary embolus; PH: pulmonary hypertension; PAC: pulmonary artery catheter.
* Cardiac output is generally measured using the cardiac index.
¶ Mixed venous oxyhemoglobin saturation cutoff measured on PAC is 65%, but on triple lumen catheter is 70%.
Δ Equalization of right atrial, right ventricular end-diastolic and pulmonary artery wedge pressures is classic in pericardial
tamponade and distinguishes it from primary cardiogenic shock.
https://www.uptodate.com/contents/definition-classification-etiology-and-pathophysiology-of-shock-in-adults/print 19/20
5/3/2019 Definition, classification, etiology, and pathophysiology of shock in adults - UpToDate
Contributor Disclosures
David F Gaieski, MD Nothing to disclose Mark E Mikkelsen, MD, MSCE Nothing to disclose Polly E
Parsons, MD Nothing to disclose Geraldine Finlay, MD Nothing to disclose
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are
addressed by vetting through a multi-level review process, and through requirements for references to be
provided to support the content. Appropriately referenced content is required of all authors and must conform
to UpToDate standards of evidence.
https://www.uptodate.com/contents/definition-classification-etiology-and-pathophysiology-of-shock-in-adults/print 20/20