Definition, classification, etiology, and pathophysiology of shock in adults - UpToDate 19/02/17 3:07 p.m.

Official reprint from UpToDate

www.uptodate.com 2017 UpToDate

Definition, classification, etiology, and pathophysiology of shock in adults

Authors: David F Gaieski, MD, Mark E Mikkelsen, MD, MSCE

Section Editor: Polly E Parsons, MD
Deputy Editor: Geraldine Finlay, MD

All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Jan 2017. | This topic last updated: May 25, 2016.

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 and
management of shock in adult trauma" and "Clinical presentation, evaluation, and diagnosis of the 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 irreversible organ dysfunction. "Undifferentiated
shock" refers to the situation where shock is recognized but the cause is unclear.

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.)

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].

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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].

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 [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) 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, Enterococcus), 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) and
noninfectious (list below). (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 "Complications and long-term outcomes of a severe burn")

Hypoperfusion caused by trauma (see "Initial evaluation and management of shock in adult trauma")

Significant blunt trauma and crush injury (see "Initial evaluation and management of shock in adult trauma")

Amniotic fluid embolism (see "Amniotic fluid embolism syndrome")

Air embolism (see "Air embolism")

Fat embolism (see "Fat embolism syndrome")

Idiopathic systemic capillary leak syndrome (see "Idiopathic systemic capillary leak syndrome")

Post-successful return of spontaneous circulation after a cardiac arrest [7], myocardial infarction, or cardio-

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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 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. In addition to
hemodynamic collapse, bronchospasm and increased airway resistance are cardinal features of anaphylaxis.
However, it can also be seen in patients with allergies to natural rubber 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 "Epidemiology, clinical manifestations, and
diagnosis of streptococcal toxic shock syndrome".)

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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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
"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 "Approach to the
diagnosis of wide QRS complex tachycardias" and "Clinical features and treatment of ventricular arrhythmias
during acute myocardial infarction" 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 "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 mitral stenosis".)

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

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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 and management of shock in adult
trauma", section on 'Pathophysiology and classification' 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, aorticenteric 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'):

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 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).

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 adult with suspected acute pulmonary embolism", section on
'Hemodynamically unstable patients' and "Overview of pulmonary hypertension in adults", section on
'Classification'.)

Acute right heart syndrome can, given ventricular interdependence, mimic left ventricular dysfunction resulting in

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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 "Primary spontaneous pneumothorax in adults", section on 'Clinical

presentation')
Pericardial tamponade (see "Cardiac tamponade", section on 'Physiology' and "Cardiac tamponade", section
on 'Etiology')
Constrictive pericarditis (see "Constrictive pericarditis", section on 'Physiology' and "Constrictive
pericarditis", section on 'Etiology')
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

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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 syndrome", section on 'Pathophysiology')
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 'pathogenesis')
Myxedema coma (see "Myxedema coma", section on 'Pathogenesis' 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 [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

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CO is the product of heart rate (HR) and stroke volume (SV):

CO = HR X SV

The stroke volume is determined by:

Preload
Myocardial contractility
Afterload

SVR is governed by:

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.

Pre-shock Pre-shock is also known as compensated shock, or cryptic shock. It is characterized by

compensatory responses to diminished tissue perfusion [15]. 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 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 [16].

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Potentially, with timely and appropriate management, deterioration can be prevented and signs of impending
deterioration can be reversed (eg, normalization of 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 [19].

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, 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

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, 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).

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Hypovolemic shock may be due to hemorrhagic (eg, trauma) or nonhemorrhagic fluid losses (eg,
vomiting).

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.)

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GRAPHICS
Classification of shock

Septic Gram positive (Pneumococcus, Staphylococcus, Streptococcus,

Enterococcus, Legionella, Listeria)
Gram negative (Klebsiella, Pseudomonas, Escherichia,
Haemophilus, Neisseria, Moraxella, Rickettsia, Francisella
[tularemia])
Fungal (Candida, Aspergillus)
Viral (influenza, cytomegalovirus, Ebola, varicella)
Parasitic (Plasmodium, Ascaris, Babesia)
Mycobacterium (Mycobacterium tuberculosis, Mycobacterium
abscessus)

Non-septic Inflammatory shock (systemic inflammatory response syndrome)

Distributive Burns, trauma, pancreatitis, postmyocardial infarction, post
coronary bypass, post cardiac arrest, viscus perforation, amniotic
fluid embolism, fat embolism, idiopathic systemic capillary leak
syndrome
Neurogenic shock Traumatic brain injury, spinal cord injury
(quadriparesis with bradycardia or paraplegia with tachycardia),
neuro-axial anesthesia
Anaphylactic shock - IgE-mediated (eg, foods, medications, insect
bites or stings), IgE-independent (eg, iron dextran),
nonimmumnologic (eg, exercise or heat-induced), idiopathic
Other Liver failure, transfusion reactions, vasoplegia (eg,
vasodilatory agents, cardiopulmonary bypass), toxic shock
syndrome, toxicologic (eg, heavy metals), beriberi

Cardiomyopathic Myocardial infarction (involving >40% of the left ventricle or with

extensive ischemia)
Severe right ventricle infarction
Acute exacerbation of severe heart failure from dilated
cardiomyopathy
Stunned myocardium from prolonged ischemia (eg, cardiac
arrest, hypotension, cardiopulmonary bypass)
Advanced septic shock
Myocarditis
Myocardial contusion
Cardiogenic
Drug-induced (eg, beta blockers)

Arrhythmogenic Tachyarrhythmia Atrial tachycardias (fibrillation, flutter,

reentrant tachycardia), ventricular tachycardia and fibrillation
Bradyarrhythmia Complete heart block, Mobitz type II second
degree heart block

Mechanical Severe valvular insufficiency, acute valvular rupture (papillary or

chordae tendineae rupture, valvular abscess), critical valvular
stenosis, acute or severe ventricular septal wall defect, ruptured
ventricular wall aneurysm, atrial myxoma

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Hemorrhagic Trauma, gastrointestinal bleeding (eg, varices, peptic ulcer),

intraoperative and postoperative bleeding, retroperitoneal
bleeding (eg, ruptured aortic aneurysm), aortic-enteric fistula,
hemorrhagic pancreatitis, iatrogenic (eg, inadvertent biopsy of
arteriovenous malformation, or left ventricle), tumor or abscess
erosion into major vessels, ruptured ectopic pregnancy,
postpartum hemorrhage, uterine or vaginal hemorrhage (eg,
infection, tumors, lacerations), spontaneous peritoneal
Hypovolemic hemorrhage from bleeding diathesis

Non- Gastrointestinal losses (eg, diarrhea, vomiting, external

hemorrhagic drainage); 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)

Pulmonary Hemodynamically significant pulmonary embolus, severe

vascular pulmonary hypertension, severe or acute obstruction of the
pulmonic or tricuspid valve, venous air embolus

Mechanical Tension pneumothorax or hemothorax (eg, trauma, iatrogenic),

Obstructive pericardial tamponade, constrictive pericarditis, restrictive
cardiomyopathy, severe dynamic hyperinflation (eg, elevated
intrinsic PEEP), left or right ventricular outflow tract obstruction,
abdominal compartment syndrome, aorto-caval compression (eg,
positioning, surgical retraction)

Endocrine (eg, adrenal insufficiency, thyrotoxicosis, myxedema

coma)
Metabolic (eg, acidosis, hypothermia)
Mixed/unknown
Other - Polytrauma with more than one shock category, acute
shock etiology with pre-existing cardiac disease, late under-
resuscitated shock, miscellaneous poisonings

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.

PEEP: positive end-expiratory pressure.

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Causes of anaphylaxis

Allergens (IgE-dependent immunologic mechanism)

Foods, especially peanut, tree nut, crustacean shellfish, finned fish, milk, egg

Insect stings (eg, Hymenoptera venom) and insect bites (eg, kissing bugs)

Medications (eg, antibiotics, NSAIDs)

Biological materials, including allergen immunotherapy, monoclonal antibodies, chemotherapy agents, and
vaccines*

Natural rubber latex

Food additives, including spices, insect-derived colorants (eg, carmine), and vegetable gums

Inhalants (rare) (eg, horse dander, cat dander, grass pollen)

Human seminal fluid (rare trigger of anaphylaxis in women)

Occupational allergens (eg, stinging insects, natural rubber latex)

Immunologic triggers (IgE-independent mechanism)

IgG-dependent (rare) (eg, to high-molecular weight dextran, infliximab)

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

Nonimmunologic triggers (direct activation of mast cells and basophils)

Physical factors (eg, exercise , cold, heat)

Medications (eg, opioids, NSAIDs)

Radiocontrast agents

Alcohol (ethanol) (may augment, rarely induces)

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.

IgE: immunoglobulin E; NSAIDs: nonsteroidal anti-inflammatory drugs; IgG: immunoglobulin G.

* Reactions to vaccines are rare and typically involve an excipient, such as gelatin, rather than microbial content.
Usually involves a cofactor, such as a food, medication (eg, an NSAID), or exposure to cold air or water.

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Hemodynamic values of normal recumbent adults

Mean Range

Cardiac index, liters/min/m 2 3.4 2.8-4.2

Stroke volume index, mL/m 2/beat 47 30-65

Arteriovenous oxygen difference, mL per liter of blood 38 30-48

Arterial saturation, percent 98 94-100

Pressure*, mmHg

Left ventricle
Systolic 130 90-140

End-diastolic 7 4-12

Left atrium
Maximum 13 6-20

Minimum 3 -2-+9

Mean 7 4-12

Pulmonary artery wedge ("PC")

Maximum 16 9-23

Minimum 6 1-12

Mean 9 6-15

Pulmonary artery

Systolic 24 15-28

Diastolic 10 5-16

Mean 16 10-22

Right ventricle

Systolic 24 15-28

End-diastolic 4 0-8

Right atrium

Maximum 7 2-14

Minimum 2 -2-+6

Mean 4 -1-+8

Venae cavae

Maximum 7 2-14

Minimum 5 0-8

Mean 6 1-10

End-diastolic volume index

Left ventricular, mL/m 2 70 50-90

Resistance, dyns/cm 5

Total systemic 1150 900-1400

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Systemic arteriolar 850 600-900

Total pulmonary 200 150-250

Pulmonary arteriolar 70 45-120

* 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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Hemodynamic profiles of shock on pulmonary artery catheter in adults

Physiologic Tissue
Preload Pump function Afterload
variable perfusion

Pulmonary Mixed venous

Clinical Systemic vascular
capillary wedge Cardiac output* oxyhemoglobin
measurement resistance
pressure saturation

Hypovolemic (early) or (late) (early) or (late) >65% (early) or

<65% (late)

Cardiogenic <65%

Distributive (early) or (late) or (occasionally) >65%

Obstructive

PE, PH, (early) or (late) (early) or (late) >65%

tension
pneumothorax

Pericardial <65%
tamponade

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%.
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.

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