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Evaluation of and initial approach to the adult patient with undifferentiated hypotension and shock

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


Section Editors: Polly E Parsons, MD, Robert S Hockberger, MD, FACEP
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: Jul 2018. | This topic last updated: Feb 08, 2018.

INTRODUCTION — Shock is a life-threatening condition of circulatory failure that most commonly presents with hypotension. It can also be heralded by other
vital sign changes or the presence of elevated serum lactate levels. The effects of shock are initially reversible but can rapidly become irreversible, resulting
in multi-organ failure (MOF) and death. Thus, when a patient presents with undifferentiated hypotension and/or is suspected of having shock, it is important
that the clinician rapidly identify the etiology so that appropriate therapy can be administered to prevent MOF and death [1,2].

This topic reviews the clinical presentation as well as the initial diagnostic and therapeutic approaches to the adult patient with hypotension and suspected
shock of unknown etiology (ie, undifferentiated shock). The definition, classification, etiology, and pathophysiology of shock are discussed separately. (See
"Definition, classification, etiology, and pathophysiology of shock in adults".)

DEFINITION AND CLASSIFICATION — 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 manifest as hypotension (ie, reduced tissue
perfusion). “Undifferentiated shock” refers to the situation where shock is recognized, but the cause is unclear.

While patients often have a combination of more than one form of shock (multifactorial shock), four classes of shock are recognized (table 1):

● Distributive (eg, septic shock, systemic inflammatory response syndrome, neurogenic shock, anaphylactic shock, toxic shock, end-stage liver disease,
endocrine shock)

● Cardiogenic (eg, myocardial infarction, atrial and ventricular arrhythmias, valve or ventricle septal rupture)

● Hypovolemic (eg, hemorrhagic and nonhemorrhagic fluid losses)

● Obstructive (eg, pulmonary embolism, pulmonary hypertension, tension pneumothorax, constrictive pericarditis, restrictive cardiomyopathy)

Detailed discussion of the classification, etiology, and pathogenesis of shock is provided separately. (See "Definition, classification, etiology, and
pathophysiology of shock in adults".)

WHEN TO SUSPECT SHOCK

Clinical manifestations — The clinical findings associated with undifferentiated shock (ie, cause unknown) vary according to the etiology and stage of
presentation (pre-shock, shock, end-organ dysfunction) (see "Definition, classification, etiology, and pathophysiology of shock in adults", section on 'Stages of
shock'). Features that are highly suspicious of shock include:

● Hypotension

● Tachycardia

● Oliguria

● Abnormal mental status

● Tachypnea

● Cool, clammy, cyanotic skin

● Metabolic acidosis

● Hyperlactatemia

Most clinical features are neither sensitive nor specific for the diagnosis of shock. However, many of the clinical manifestations provide clues to the underlying
etiology and are primarily used to narrow the differential diagnosis so that empiric therapies can be administered in a timely fashion.

Features of shock — The typical clinical features that raise the suspicion for shock include the following:

● Hypotension – Hypotension occurs in the majority of patients with shock. Hypotension may be absolute (eg, systolic blood pressure <90 mmHg; mean
arterial pressure <65 mmHg), relative (eg, a drop in systolic blood pressure >40 mmHg), orthostatic (>20 mmHg fall in systolic pressure or >10 mmHg fall
in diastolic pressure with standing), or profound (eg, vasopressor-dependent).

Importantly, patients in the early stages of shock can be normotensive or hypertensive, such that hypotension does not have to be present for the
diagnosis. Conversely, not every patient who has hypotension has shock (eg, chronic hypotension, drug-induced hypotension, autonomic dysfunction,
vasovagal syncope, peripheral vascular disease).

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● Tachycardia – Tachycardia is an early compensatory mechanism in patients with shock. It can be isolated or occur in association with hypotension.
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shock, a compensatory feature that frequently deflects attention away from the possibility of the presence of shock in this population. Given the
frequency of beta-blocker use, awareness of concurrent medications is important to incorporate into the clinical assessment of suspected shock.

● Tachypnea – Tachypnea is an early compensatory mechanism in patients with shock and metabolic acidosis specifically. While elevations in respiratory
rate are common amongst hospitalized patients [3], it is a useful tool to identify patients at risk of clinical deterioration, as evidenced by its incorporation
into the quick Sequential (Sepsis-related) Organ Failure Assessment (qSOFA) score [4].

● Oliguria – Oliguria in shock can be due to shunting of renal blood flow to other vital organs, direct injury to the kidney (eg, aminoglycoside toxicity), or
due to intravascular volume depletion (eg, from vomiting, diarrhea, or hemorrhage).

● Mental status changes – Altered sensorium in shock is usually due to poor perfusion or metabolic encephalopathy. It is a continuum that begins with
agitation, progresses to confusion or delirium, and ends in obtundation or coma.

● Cool skin – Cool, clammy skin is due to compensatory peripheral vasoconstriction that redirects blood centrally, to maintain vital organ perfusion (ie,
coronary, cerebral, and splanchnic flow). A cyanotic, mottled appearance is a late and worrisome feature of shock. However, the appearance of cool,
clammy or cyanotic skin may also be due to, or exacerbated by, ischemia from underlying peripheral arterial vascular disease. Importantly, warm,
hyperemic skin does not ensure the absence of shock because such an appearance may be present in patients with early distributive shock (prior to the
onset of compensatory vasoconstriction) or terminal shock (due to failure of compensatory vasoconstriction).

● Metabolic acidosis – In general, the demonstration of a high anion gap metabolic acidosis should always raise the clinical suspicion for the presence of
shock. Importantly, the presence of a metabolic acidosis in states of shock is not specific and can also be due to acute kidney injury or toxin ingestion.
(See "Simple and mixed acid-base disorders".)

● Hyperlactatemia – Either in conjunction with metabolic acidosis or not, the presence of an elevated serum lactate level has been associated with
adverse outcomes, including the development of shock [5]. The relationship between hyperlactatemia and mortality has been reproduced across a
number of clinical conditions, including trauma, sepsis, and post-cardiac arrest.

Features due to the underlying cause — Due to the wide range of etiologies for shock, the presenting features can be variable and frequently overlap.
However, they facilitate the early identification of the etiology of shock as well as organ failure due to shock, details of which are provided in the sections
below.

● History and examination (see 'Differential diagnosis' below)

● Laboratory tests (see 'Laboratory evaluation' below)

● Imaging (see 'Imaging' below)

INITIAL APPROACH — The initial approach to patients with undifferentiated hypotension/shock is shown in the algorithms (algorithm 1A-B). When feasible,
a multidisciplinary, team-based approach is preferred because it allows the simultaneous evaluation and administration of therapy to patients with
hypotension and shock. In brief:

● The airway should be stabilized and adequate intravenous access secured so that patients can be immediately treated with intravenous fluids to restore
adequate tissue perfusion. Importantly, resuscitative efforts, particularly intravenous fluids, should not be delayed for a detailed clinical assessment, nor
should clinicians be conservative in terms of fluid resuscitation to patients with heart failure or kidney injury as a rule. Related to the latter point, liberal
fluid resuscitation appeared to be life-saving in septic patients with intermediate serum lactate levels, a benefit derived amongst these traditionally
underresuscitated sepsis subgroups [6]. (See 'Assess airway, breathing, circulation' below.)

● Patients should be assessed for the need for an immediate or early intervention so that lifesaving therapies can be administered promptly. (See 'Risk
stratification' below.)

● Critically ill patients who have been stabilized and patients with mild hypotension or early shock should undergo a more formal diagnostic approach while
initial resuscitative therapies are ongoing. (See 'Initial diagnostic evaluation' below and 'Hemodynamic support' below.)

Importantly, patients may become hemodynamically unstable during the evaluation and early treatment period, which may necessitate rapid redirection of the
approach to the administration of lifesaving therapies.

Assess airway, breathing, circulation — The first priorities are to stabilize the airway and breathing with oxygen and/or mechanical ventilation, when
necessary. Intravenous access should be secured so that patients can be immediately treated with intravenous fluids to restore adequate tissue perfusion.

Patients with respiratory distress and/or marked hemodynamic instability are typically intubated. The exception is those with suspected tension
pneumothorax, where the prompt drainage of air from the pleural space may quickly reverse shock and avoid intubation (mechanical ventilation can worsen
tension and precipitate cardiac arrest). Rapid sequence intubation, typically with etomidate (0.3 mg/kg intravenously) or ketamine (1 to 2 mg/kg
intravenously), and a rapidly acting neuromuscular blocker, typically utilizing succinylcholine (1 mg/kg intravenously) or rocuronium (1 to 1.5 mg/kg
intravenously), is the preferred approach; agents that worsen hypotension (eg, propofol, midazolam) should be avoided. (See "Rapid sequence intubation for
adults outside the operating room" and "Induction agents for rapid sequence intubation in adults outside the operating room".)

Peripheral venous access (14 to 18 gauge catheters) or intraosseous access is sufficient for the initial evaluation and management of many patients with
undifferentiated shock and hypotension. However, central venous access should be obtained in those in whom peripheral access cannot be obtained, in
those who need infusions of large volumes of fluids and/or blood products, or in those who need prolonged infusions of vasopressors. Central venous access
may also be useful in patients who require frequent blood draws for laboratory studies and for hemodynamic monitoring (eg, central venous pressure, central
venous oxyhemoglobin saturation). Importantly, the administration of resuscitative fluids and medications should not be delayed because central venous

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access is not available. Related, evidence suggests that the use of peripheral intravenous vasoactive medications can be used safely for hours to days,
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Risk stratification — When patients present with undifferentiated hypotension or shock, the clinician should stratify the patient according to the severity of
shock and the need for immediate or early intervention so that empiric lifesaving therapies can be administered promptly (algorithm 1A-B).

● Clinicians should obtain a brief history and examination, together with bedside telemetry monitoring and/or electrocardiography [ECG], to assess whether
an immediate or early lifesaving therapy is required. While a definitive diagnosis is preferred, many of these therapies are administered based upon a
presumed diagnosis with or without preliminary test results. (See 'Common conditions needing lifesaving interventions' below.)

● Patients with milder forms of shock/hypotension or critically ill patients who have been stabilized should undergo a thorough diagnostic evaluation while
resuscitation continues. Sufficient time is typically available in such patients to obtain laboratory studies and definitive imaging so that a diagnosis can be
made and appropriate therapy administered. However, the evaluation remains time-sensitive, as patients in this category are at risk of becoming
hemodynamically unstable, such that a rapid redirection of the diagnostic and therapeutic strategy may be necessary. (See 'Initial diagnostic evaluation'
below.)

Common conditions needing lifesaving interventions — The initial approach discussed below is often dependent upon a brief history obtained from
prehospital providers, hospital staff, family members, and the patient.

Anaphylactic shock — Patients strongly suspected of having anaphylactic shock (eg, hypotension, inspiratory stridor, oral and facial edema, hives,
history of recent exposure to common allergens [eg, bee stings]) should receive intramuscular epinephrine. Patients on mechanical ventilation may also have
a sudden elevation in peak inspiratory pressures. The typical adult dose is 0.3 mg of 1:1000 epinephrine injected into the mid-outer thigh and repeated every
5 to 15 minutes as needed (table 2). Other pharmacologic agents frequently administered following epinephrine include antihistamines (eg, diphenhydramine
25 to 50 mg and ranitidine 50 mg intravenously), nebulized albuterol (2.5 mg in 3 mL of normal saline), and methylprednisolone (1 to 2 mg/kg intravenously).
Blood for total tryptase or histamine should be drawn prior to or shortly after treatment. (See "Anaphylaxis: Emergency treatment".)

Tension pneumothorax — Tension pneumothorax should be suspected in those with tachypnea, unilateral pleuritic chest pain and diminished breath
sounds, distended neck veins, tracheal deviation away from the affected side, and risk factors for tension pneumothorax (eg, trauma, recent procedure,
mechanical ventilation, underlying cystic lung disease). Patients on mechanical ventilation may also have a sudden elevation in plateau pressures. Patients
strongly suspected to have a tension pneumothorax do not require a chest radiograph and should have an emergent tube thoracostomy (24 or 28 Fr, 36 Fr for
trauma; fifth intercostal space, midaxillary line) or needle decompression using a 14 to 16 gauge intravenous catheter (second or third intercostal space,
midclavicular line) followed by immediate tube thoracostomy; tube thoracostomy is indicated should decompression fail.

Ultrasound guidance is preferable for both diagnosis and tube placement. In addition, we prefer that drainage of a tension pneumothorax be performed before
endotracheal intubation unless the patient is already intubated or is in cardiac arrest. For those on mechanical ventilation, positive pressure ventilation should
be reduced. Radiographic confirmation of reexpansion should be performed after drainage (eg, ultrasonography, chest radiography). (See "Placement and
management of thoracostomy tubes" and "Prehospital care of the adult trauma patient", section on 'Needle chest decompression' and "Diagnosis,
management, and prevention of pulmonary barotrauma during invasive mechanical ventilation in adults", section on 'Ventilator management'.)

Pericardial tamponade — Pericardial tamponade should be suspected in patients with dyspnea, tachycardia, hypotension, elevated jugular venous
pressure, distant heart sounds, pulsus paradoxus, and known risk factors (eg, trauma, bleeding diathesis, known pericardial effusion, recent thoracic or
pericardial procedure). The demonstration of an anechoic stripe and tamponade physiology on point-of-care (POC) ultrasonography or bedside
echocardiography is preferred before pericardiocentesis. Ultrasonography also guides needle or catheter placement and examines the response to drainage
of fluid from the pericardial sac. In rare cases, an emergency thoracotomy may be performed in those who are unresponsive to catheter drainage or in those
who develop a cardiac arrest during resuscitation. (See "Cardiac tamponade", section on 'Treatment' and "Emergency pericardiocentesis" and "Initial
evaluation and management of blunt thoracic trauma in adults", section on 'Emergency thoracotomy'.)

Importantly, pericardiocentesis should not be attempted in patients with a pericardial effusion due to aortic dissection or myocardial rupture, as relief of
cardiac tamponade may worsen bleeding. Such patients require emergent surgical intervention. In instances where tamponade remains on the differential
diagnosis, but additional data are required, hemodynamic measurements via pulmonary artery catheterization are frequently required. (See "Management of
acute aortic dissection" and "Mechanical complications of acute myocardial infarction", section on 'Rupture of the left ventricular free wall'.)

Hemodynamically significant hemorrhage — Patients with suspected hemorrhagic shock should be identified as having traumatic or nontraumatic
shock:

● Traumatic – Patients with a history of blunt or penetrating trauma benefit from rapid multiorgan bedside ultrasonography to locate the source of
hemorrhage, as well as for the evaluation of other body injuries (also known as focused assessment with sonography for trauma [FAST]). This population
may also benefit from drainage (eg, hemothorax, peritoneal lavage) or surgical intervention (eg, ruptured spleen) (algorithm 2 and table 3). (See "Initial
evaluation and management of penetrating thoracic trauma in adults" and "Initial evaluation and management of blunt thoracic trauma in adults" and
"Initial evaluation of shock in the adult trauma patient and management of NON-hemorrhagic shock" and "Emergency ultrasound in adults with abdominal
and thoracic trauma".)

● Nontraumatic – Patients suspected of having a ruptured abdominal aortic aneurysm (eg, hypotension, abdominal or back pain, pulsatile abdominal
mass, known history of abdominal aneurysm) should be preferably evaluated by contrast-enhanced computed tomography (CT) prior to surgical
intervention; however, patients are often too unstable to safely obtain a CT scan, and management must occur empirically. POC ultrasonography that
demonstrates peritoneal hemorrhage and an aneurysm may be performed when CT is unsafe or not available. For patients with the manifestations of
upper or lower gastrointestinal hemorrhage (eg, hematemesis, hematochezia, anemia, bleeding diathesis), endoscopic intervention, embolization, or
surgery may be indicated (table 4 and algorithm 3 and algorithm 4). (See "Management of symptomatic (non-ruptured) and ruptured abdominal aortic
aneurysm" and "Overview of the treatment of bleeding peptic ulcers", section on 'Treatment of persistent and recurrent bleeding' and "General principles
of the management of variceal hemorrhage".)

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This population typically requires large volumes of blood products, and vasopressors are avoided. Adequate peripheral access (two 14 to 18 gauge IVs)
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Life-threatening arrhythmias — Patients with rhythm disturbances resulting in shock can be cardioverted (tachyarrhythmias) (algorithm 5), receive
atropine or infusions of vasoactive agents, or undergo temporary or permanent pacemaker placement (bradyarrhythmias) (algorithm 6) as part of the
advanced cardiac life support (ACLS) protocol. Arrhythmias can be the primary cause of, or contribute to, shock, such that immediate treatment is important
and potentially lifesaving. Additionally, arrhythmias can be secondary to the metabolic disturbances associated with shock (eg, hypokalemia, acidosis) or the
underlying cause of shock (eg, sepsis [8], pulmonary embolism, myocardial infarction). Thus, their presence should prompt additional investigations (eg,
serum chemistries, arterial blood gas analysis, toxicology screen, bedside cardiac ultrasound, and cultures in those with suspected infection). (See
"Advanced cardiac life support (ACLS) in adults" and "Supportive data for advanced cardiac life support in adults with sudden cardiac arrest".)

Septic shock — Patients with suspected infection (eg, fever, hypotension, and a suspected septic source) benefit from the early administration of
intravenous antibiotics, the choice of which is determined by the suspected source, and intravenous fluid resuscitation. If the source is unknown and
Pseudomonas is unlikely, we favor combining vancomycin with a third- or fourth-generation cephalosporin (eg, ceftriaxone or cefotaxime, cefepime) or a
beta-lactam/beta-lactamase inhibitor (eg, piperacillin-tazobactam, ticarcillin-clavulanate) or a carbapenem (eg, imipenem or meropenem). If Pseudomonas is
likely, vancomycin should be combined with an antipseudomonal agent (eg, fluoroquinolone, aminoglycoside). A leukocytosis and, in particular, a bandemia,
as well as laboratory and imaging findings suggestive of a source, all support the presence of sepsis as a cause of shock. Blood and other appropriate body
fluid cultures should be obtained, preferably prior to the administration of antibiotics, in addition to imaging when necessary to facilitate timely source control.
Serial vital signs, and serum lactate measures, can be used to risk-stratify the septic patient. (See "Evaluation and management of suspected sepsis and
septic shock in adults", section on 'Choosing a regimen'.)

Cardiogenic shock from myocardial infarction — Patients who present with hypotension associated with anterior crushing chest pain, respiratory
distress, and the ECG changes consistent with ST elevation myocardial infarction (STEMI) benefit from early intervention. Elevated troponin or creatine
phosphokinase levels and pulmonary edema on chest radiography are supportive of the diagnosis. Interventions include the administration of pharmacologic
agents (eg, antiplatelet agents, heparin), coronary revascularization procedures (eg, balloon angioplasty), and/or an intraaortic balloon pump. Those with non-
STEMI may additionally benefit from the administration of glycoprotein IIb/IIIa inhibitors (table 5). (See "Prognosis and treatment of cardiogenic shock
complicating acute myocardial infarction".)

Cardiogenic shock from acute aortic or mitral valve insufficiency — Patients with chest pain, hypotension, and new low-pitched early diastolic
murmur consistent with aortic insufficiency should undergo POC ultrasonography or echocardiography prior to surgical intervention. Additional laboratory or
imaging studies aimed at discovering the etiology of rupture (eg, CT chest for aortic dissection, blood cultures and transesophageal echocardiography for
aortic root abscess) may be required in this population. Patients with acute respiratory distress and new systolic murmur following an acute myocardial
infarction (MI) should preferably undergo urgent echocardiography to look for mitral valve insufficiency or ventricular septal defect, which also typically needs
urgent surgical intervention. (See "Acute aortic regurgitation in adults" and "Acute mitral regurgitation in adults" and "Ventricular septal defect in adults",
section on 'Surgical repair'.)

Dissection of the ascending aorta — Patients with aortic dissection typically present with hypertension and tearing chest or back pain. However,
hypotension and shock occur with retrograde dissection that results in acute aortic insufficiency, pericardial tamponade, or myocardial infarction. Patients with
suspected dissection should undergo diagnostic contrast-enhanced CT, transesophageal echocardiography, or magnetic resonance imaging (MRI), as
available. When such imaging is unsafe, transthoracic echocardiography or POC ultrasonography that demonstrates aortic root dilatation and an intimal flap
may be supportive diagnostically (table 6). (See "Clinical features and diagnosis of acute aortic dissection" and "Management of acute aortic dissection".)

Hemodynamically significant pulmonary embolism — Patients with hypotension, acute dyspnea, and hypoxemia who are strongly suspected of
having a pulmonary embolism (PE) may benefit from the administration of systemic thrombolytic therapy (algorithm 7). Normal chest radiography and
elevated D-dimer, troponin, and natriuretic peptide levels are supportive diagnostically. Computed tomographic pulmonary angiography is the preferred
diagnostic modality in this population. However, for those in whom CT is unsafe, a presumptive diagnosis may be obtained by POC cardiac ultrasonography
or echocardiography (eg, right ventricle enlargement, thrombus) to justify the administration of a thrombolytic agent, provided no contraindications are
present. The indications for thrombolysis, dosing, and choice of agent, as well as alternative therapies in patients with hemodynamically unstable PE, are
discussed separately. (See "Treatment, prognosis, and follow-up of acute pulmonary embolism in adults", section on 'Hemodynamically unstable' and
"Thrombolytic (fibrinolytic) therapy in acute pulmonary embolism and lower extremity deep vein thrombosis".)

Adrenal crisis — Patients suspected of having an adrenal crisis (eg, hypotension, volume depletion, history of glucocorticoid deficiency or withdrawal)
should receive judicious fluid resuscitation and dexamethasone 4 mg intravenously. The selection of dexamethasone is based on the ability to interpret serum
cortisol measurements as part of the evaluation. Blood for serum cortisol, corticotropin (ACTH), aldosterone, renin, and serum chemistries should be drawn to
confirm the diagnosis (table 7). (See "Treatment of adrenal insufficiency in adults", section on 'Adrenal crisis'.)

Insect or animal bites — Some insect and animal bites require antivenom to reverse shock, the details of which are discussed separately. (See
"Approach to the patient with a suspected spider bite: An overview" and "Treatment of rabies" and "Snakebites worldwide: Management".)

Initial diagnostic evaluation

Clinical bedside evaluation — A high clinical suspicion for the presence of shock is critical for diagnosis. An initial efficient and targeted history from
prehospital or hospital providers, the patient, their relatives, and/or the medical record should provide ample information on a patient’s risk for shock, as well
as the potential etiology (algorithm 1A-B). Physical examination including electrocardiography should be directed towards uncovering the type, severity, and
cause of shock. With diagnostic data, the cause of shock can usually be determined or narrowed to a few possibilities, and subsequent therapy can be
appropriately tailored. (See 'Differential diagnosis' below and 'Reverse the etiology' below.)

Typically, we perform the following:

● General assessment – The evaluation should include a thorough history and assessment of sensorium, mucous membranes, lips and tongue, neck
veins, lungs, heart, and abdomen, as well as skin and joints. Hypotension, oliguria, mental status changes, and cool, clammy skin are sentinel clinical
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findings that should raise the suspicion of shock and prompt immediate treatment with intravenous fluids and further evaluation with laboratory studies
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● Electrocardiogram – Bedside telemetry and/or electrocardiogram (ECG) should be performed in patients with undifferentiated hypotension and shock.
ECG may reveal an arrhythmia or ST segment changes consistent with ischemia or pericarditis. A low-voltage ECG may be suggestive of a pericardial
effusion. The classic signs of pulmonary embolism (S1, Q3, T3) or right ventricular strain may also be evident. (See "ECG tutorial: Basic principles of
ECG analysis".)

● Assessment for the etiology – A comprehensive assessment for the underlying etiology of shock should be performed after stabilization. A more
detailed discussion of the clinical presentation and diagnostic evaluation of specific types of shock is provided below. (See 'Differential diagnosis' below.)

Laboratory evaluation — Laboratory tests should be performed early in the evaluation of patients with undifferentiated hypotension/shock to identify the
cause of shock and/or early organ failure (algorithm 1A-B). An elevated serum lactate (>2 mmol/L, depending upon the institutional laboratory normal) is an
early indicator of shock and is particularly useful in those who are normotensive or hypertensive (ie, those in whom shock is less likely to be suspected).

We suggest the following basic laboratory tests be obtained in most patients with undifferentiated hypotension or shock, recognizing that testing should be
tailored according to the suspected etiology (see 'Common conditions needing lifesaving interventions' above and 'Differential diagnosis' below):

● Serum lactate

● Renal and liver function tests

● Cardiac enzymes and natriuretic peptides

● Complete blood count and differential

● Coagulation studies and D-dimer level

● Blood gas analysis

The rationale for obtaining these tests is described below:

● Serum lactate level – Elevated lactate levels in states of shock are reflective of poor tissue perfusion (type A lactic acidosis) and are due to increased
production from anaerobic metabolism, aerobic metabolism, and decreased clearance by the liver, kidneys, and skeletal muscle [5,9]. However, although
elevated lactate is a sensitive tool for the diagnosis of shock, it is not specific and can also be found in conditions including metformin toxicity, diabetic
ketoacidosis, and alcoholism (type B lactic acidosis). (See "Causes of lactic acidosis".)

Lactate has been best studied in patients with septic shock where elevated levels >2 mmol/L, and in particular those >4 mmol/L are associated with
increased mortality independent of organ dysfunction or hypotension. However, studies performed in other populations also suggest that elevated lactate
is similarly associated with increased mortality [10]. Details regarding the role of lactate in sepsis are discussed separately. (See "Evaluation and
management of suspected sepsis and septic shock in adults".)

In addition, lactate levels can be serially measured to follow the response to therapies. (See 'Reverse the etiology' below.)

● Renal and liver function tests – Elevated blood urea nitrogen (BUN), creatine, and transaminases are usually due to shock-induced end-organ damage
(eg, acute kidney injury, shock liver) but may also explain the etiology of shock (eg, renal abscess, acute hepatitis, chronic cirrhosis). Serum and urinary
electrolytes including hypo- or hypernatremia, hypo- or hyperkalemia, low urinary sodium concentration, or fractional excretion of sodium <1 percent may
indicate hypovolemia. (See "Etiology, clinical manifestations, and diagnosis of volume depletion in adults", section on 'Laboratory abnormalities'.)

● Cardiac enzymes and natriuretic peptides – Elevated troponin-I or -T levels, creatine phosphokinase, brain natriuretic peptide, or N-terminal pro-brain
natriuretic peptide may indicate cardiogenic shock from ischemia but can also be due to demand ischemia or to pulmonary embolism (PE). (See
"Troponin testing: Clinical use" and "Natriuretic peptide measurement in heart failure" and "Clinical presentation, evaluation, and diagnosis of the
nonpregnant adult with suspected acute pulmonary embolism", section on 'Laboratory tests'.)

● Complete blood count and differential – A high hematocrit may suggest hemoconcentration from hypovolemia. Anemia in the setting of bleeding
supports hemorrhagic shock, and concurrent thrombocytopenia may suggest an etiology for hemorrhage. An elevated eosinophil count may suggest an
allergy to support anaphylaxis.

Although a leukocytosis may suggest septic shock, it is not specific for the diagnosis and may simply indicate a stress response. A low white blood cell
count and especially a bandemia are more worrisome for sepsis in the setting of undifferentiated shock. As an example, in one observational study of
145 patients admitted to the intensive care unit with undifferentiated shock, infection was significantly more common among those with a band count
greater than 10 percent than among those with a lower band count (odds ratio [OR] 8.7, 95% CI 3.4-22.4) [11].

● Coagulation studies and D-dimer level – Elevations in the prothrombin time or international normalized ratio as well as activated partial thromboplastin
time may suggest a cause for underlying hemorrhagic shock but are also frequently elevated in patients with sepsis, systemic inflammatory response
syndrome due to nonspecific activation of the coagulation cascade, and liver disease. Evidence of disseminated intravascular coagulation (elevated fibrin
split products and D-dimer level with low fibrinogen level) can also be found in patients with severe shock. Elevated D-dimer levels are not specific for the
diagnosis of PE but, when normal, can significantly reduce the probability of PE. (See "Clinical features, diagnosis, and treatment of disseminated
intravascular coagulation in adults".)

● Venous blood gas (VBG) and arterial blood gas analysis (ABG) – An ABG should be performed in most patients with undifferentiated shock if
accurate estimates of gas exchange and acid–base disturbance are needed to help with diagnosis and treatment (eg, pulse oximetry may be unreliable
due to poor tissue perfusion). Alternatively, a VBG may be obtained in any patient presenting with unstable blood pressure and concern for shock. The

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advantage of a VBG is that it can be obtained when the initial labs are drawn and will rapidly provide extensive data on the patient’s pH, CO2,
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Hypoxemia can be due to obstructive shock from pulmonary embolism, cardiogenic shock from myocardial infarction, septic shock from pneumonia, or
acute respiratory distress syndrome (ARDS) resulting from shock. Compensatory hypocapnia can be seen in those with a metabolic acidosis.
Hypercapnia may occur in patients with encephalopathy, brain injury, or increased dead space ventilation in patients with severe ARDS. Metabolic
acidosis may be due to hyperlactatemia, acute kidney injury, or toxin ingestion. Additionally, a respiratory acidosis may occur in those obtunded from end-
stage shock. (See "Arterial blood gases", section on 'Interpretation'.)

Additional laboratory tests include those directed at specific etiologies or sequelae of shock. As examples, a toxicology screen may be useful in those
suspected of having shock from drug intoxication, a type and crossmatch should be obtained in those with hemorrhage, and an amylase and lipase should be
obtained in those with suspected pancreatitis. Urinalysis and gram stain of material from sites of possible infection (eg, blood, sputum, urine, wounds) or
known organisms from prior cultures (eg, Pseudomonas in urine, clostridium difficile in stool) may provide a supportive clue to a possible source of sepsis.
Tryptase and histamine levels are useful in those with suspected anaphylaxis. Urine electrolytes (sodium and creatine) should be obtained in those with
hypovolemia. A peripheral smear may be useful in those suspected of having malaria, and fibrinogen levels and fibrin degradation products may be useful in
those thought to have disseminated intravascular coagulation. A cortisol level or corticotrophin stimulation test may be helpful in those suspected to have an
adrenal crisis, and thyroid function tests may identify those with suspected myxedema coma. (See 'Differential diagnosis' below.)

Imaging — We perform the following in patients with undifferentiated shock and hypotension:

● Chest radiography – A portable chest radiograph is typically performed in most patients with suspected shock to detect common causes (eg,
pneumonia) or complications of shock (eg, ARDS). A chest radiograph may be clear in hypovolemic shock or obstructive shock from PE. Alternatively, it
may demonstrate a pneumonia, pneumothorax, pulmonary edema, or widened mediastinum to support an etiology for septic shock, obstructive shock,
cardiogenic shock, or aortic dissection, respectively. Chest radiography may also reveal free air under the diaphragm to suggest viscus perforation, which
should prompt emergent surgical consultation and additional testing, usually computed tomography (CT) of the abdomen and pelvis if the patient is
stable, or immediate laparotomy if the patient is unstable.

● Other imaging directed at the etiology of shock – Other imaging tests should be directed at the etiology of shock. These include abdominal
radiography (intestinal obstruction, perforation), CT of the head (traumatic brain injury, stroke), spine (spinal injury), chest (pneumonia, pneumothorax,
ruptured aneurysm, dissection), abdomen and pelvis (intestinal obstruction, perforation, abscess), and pulmonary artery (pulmonary embolism), as well
as nuclear bleeding scans (gastrointestinal hemorrhage).

● Point-of-care (POC) ultrasonography – The indications for and value of POC ultrasonography are discussed in the section below. (See 'Point-of-care
ultrasonography' below and "Indications for bedside ultrasonography in the critically-ill adult patient".)

Point-of-care ultrasonography — POC ultrasonography algorithms, including rapid ultrasound in shock (RUSH), focused cardiac ultrasound
(FOCUS), or abdominal and cardiac evaluation with sonography in shock (ACES), are more frequently used as portable, bedside diagnostic tools in patients
with undifferentiated shock and hypotension [12-15]. When available, POC ultrasonography is typically used in patients in whom an empiric diagnosis has not
been achieved with clinical and laboratory evaluation or in those in whom definitive imaging is unsafe (algorithm 1A-B), and as a complementary tool to
examine fluid responsiveness. Although POC ultrasonography is not definitively diagnostic, we believe that, when performed by trained personnel as a time-
sensitive diagnostic tool in critically ill patients with undifferentiated shock or hypotension, valuable information can be obtained that can be lifesaving.

Multiorgan ultrasonography (RUSH, ACES) examines the heart first, followed by ultrasound of the chest and abdomen and major blood vessels; focused
cardiac ultrasound (FOCUS) examines the heart only. The technical views employed for POC ultrasonography in patients with undifferentiated shock are
similar to those used in trauma patients (focused assessment with sonography for trauma [FAST]), the details of which are discussed separately. (See
"Emergency ultrasound in adults with abdominal and thoracic trauma".)

The components of POC ultrasonography examination are described in brief below:

● First, limited views of the heart should be performed to examine the following:

• Pericardium – Cardiac ultrasound may detect a pericardial effusion (anechoic stripe); chamber collapse and reciprocal changes in right and left
ventricle volume during respiration may support tamponade as a cause of shock (movie 1 and movie 2 and movie 3). Cardiac ultrasound may also
be used to guide pericardiocentesis and to examine the response to drainage. (See "Emergency ultrasound in adults with abdominal and thoracic
trauma", section on 'Pericardial and limited cardiac examination' and "Cardiac tamponade", section on 'Echocardiography'.)

• Left ventricle – A large left ventricle (LV) with reduced contractility may suggest primary pump failure and prompt referral for appropriate
intervention (eg, cardiac catheterization) (image 1 and image 2 and image 3 and figure 1 and image 4). In contrast, small cardiac chambers and a
hyperdynamic LV may indicate distributive shock from sepsis or hypovolemia, which may prompt further evaluation for a septic source or for
hemorrhage, respectively. Imaging of the LV may also be used to confirm ventricular contraction or ventricle wall perforation with pacemaker
placement (transcutaneous or transvenous), or aneurysm rupture [16,17]. (See "Emergency ultrasound in adults with abdominal and thoracic
trauma", section on 'Pericardial and limited cardiac examination' and "Echocardiographic recognition of cardiomyopathies".)

• Right ventricle – Reduced right ventricle (RV) contractility may suggest RV myocardial infarction; increased size of the RV (eg, >1:1 RV/LV ratio)
may suggest a large pulmonary embolism (PE) or pulmonary hypertension (image 5 and movie 4); a floating thrombus in the right atrium/ventricle or
clot in transit also support PE. (See "Right ventricular myocardial infarction", section on 'Echocardiography' and "Clinical presentation, evaluation,
and diagnosis of the nonpregnant adult with suspected acute pulmonary embolism", section on 'Echocardiography'.)

• Inferior vena cava – A collapsing inferior vena cava (IVC) at the end of expiration suggests hypovolemia from hemorrhagic or nonhemorrhagic
causes. A dilated IVC may support cardiac tamponade or PE. (See "Emergency ultrasound in adults with abdominal and thoracic trauma", section
on 'IVC evaluation and fluid status'.)

● Second, brief imaging of the chest and abdomen should be performed to examine the following:
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• Lung and pleural space – The absence of lung sliding (movie 5) supports the presence of a pneumothorax. (See "Thoracic ultrasound: Indications,
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technique".)

Pulmonary edema as evidenced by the presence of B lines may support primary pump failure or volume overload subsequent to fluid resuscitation
(image 6). (See "Thoracic ultrasound: Indications, advantages, and technique".)

A pleural effusion (anechoic stripe or septations) may support empyema or hemothorax and guide thoracentesis (movie 6). (See "Thoracic
ultrasound: Indications, advantages, and technique".)

• Peritoneal cavity – Evidence of significant peritoneal fluid accumulation may suggest a source of blood loss in trauma or a potential source of
infection (ie, spontaneous bacterial peritonitis in the patient with cirrhosis). (See "Emergency ultrasound in adults with abdominal and thoracic
trauma", section on 'Abdominal examination'.)

● Third, brief imaging of the major arteries and veins should be performed to examine the following:

• Aorta – Although computed tomography (CT) of the chest or transesophageal echocardiography is preferred, POC ultrasonography may detect a
thoracic or abdominal aneurysm or an intimal flap consistent with dissection of the aorta. Alternatively, visualization of free fluid or of a pericardial or
pleural effusion may also provide indirect evidence of rupture or dissection. (See "Clinical manifestations and diagnosis of thoracic aortic aneurysm",
section on 'Imaging symptomatic patients'.)

• Proximal lower extremity veins – Lack of compressibility of thigh veins may be indicative of deep venous thrombosis, thereby raising the suspicion
for PE. (See "Clinical presentation and diagnosis of the nonpregnant adult with suspected deep vein thrombosis of the lower extremity", section on
'Diagnostic ultrasonography suspected first DVT'.)

Should POC ultrasonography be nondiagnostic or unavailable, definitive imaging modalities should be used when feasible, of which comprehensive
echocardiography is the most useful. Similarly, in the event of successful resuscitation from shock, follow-up testing with standard imaging is also prudent to
confirm the diagnosis that was obtained by rapid bedside ultrasound.

Advantages and disadvantages of POC ultrasonography in patients with undifferentiated shock include the following:

● Advantages – POC ultrasonography is portable, inexpensive, and does not expose the patient to ionizing radiation. Its major advantage is the rapid
examination of multiple organs, particularly the heart, to narrow the differential diagnosis and identify a potential etiology for shock. This feature is
particularly valuable for patients in whom routine imaging is unsafe. Observational studies report that empiric diagnoses can be obtained within minutes
when compared with standard imaging modalities. As an example, several studies have shown ultrasonography is more sensitive than portable chest
radiography for the detection of pneumothorax, with sensitivity and specificity ranging from 86 to 100 and 92 to 100 percent, respectively [18-21]. The
same studies also show reduced time spent obtaining imaging with ultrasonography (2 to 3 versus 20 to 30 minutes). (See "Thoracic ultrasound:
Indications, advantages, and technique".)

Additional advantages include the targeted application of lifesaving therapies (eg, pericardial drainage, chest tube insertion, thrombolytic therapy,
peritoneal drainage, or lavage), and the safe performance of vascular access procedures (eg, central venous catheter insertion). Serial imaging can also
follow the therapeutic response to interventions (eg, improved ventricle contractility following pericardiocentesis) and detect procedural complications (eg,
ventricle perforation following pacemaker placement, pneumothorax following central venous catheter placement).

● Disadvantages – When compared with definitive imaging modalities performed by fully-trained providers, the major disadvantage of POC
ultrasonography is its limited sensitivity for many of the etiologies associated with shock. Limited sensitivity may be partially explained by the lack of
standards regarding the training, performance, and indications for bedside ultrasonography.

As an example, while POC ultrasonography is sensitive and specific for the detection of pericardial effusions [22,23], comprehensive echocardiography
with additional views may be required for definitive diagnosis of tamponade, particularly when effusions are complex, loculated, or small. Additionally,
regional wall motion abnormalities, valvular dysfunction, ventricular septal wall perforation, ruptured aortic aneurysms, and aortic dissection cannot be
readily detected using limited bedside views.

The advantages and disadvantages of FAST in adults with abdominal and thoracic trauma (eg, poor sensitivity for distinguishing blood from other body
fluids) are discussed separately. (See "Emergency ultrasound in adults with abdominal and thoracic trauma", section on 'Limitations of FAST'.)

Most of the data that support the use of POC ultrasonography in patients with undifferentiated shock are extrapolated from patients with traumatic shock (see
"Emergency ultrasound in adults with abdominal and thoracic trauma"). However, limited data from small observational studies suggest similar utility in
patients with undifferentiated shock or hypotension. In general, these data demonstrate the identification of imaging abnormalities that narrow the differential
diagnosis, confirm a clinically suspected diagnosis, prompt a change in management, and/or detect a complication from a therapeutic procedure rather than
demonstrate a conclusive improvement in survival [14,24-33]. As examples:

● In a prospective observational study of 110 critically ill patients with undifferentiated shock, outcomes in patients who underwent bedside cardiac
ultrasound were compared with historical controls who underwent standard clinical evaluation [25]. The use of ultrasound was associated with reduced
infusion of intravenous fluids (49 versus 66 mL/kg), increased administration of vasopressors (22 versus 12 percent), and improved 28-day survival (66
versus 56 percent), as well as more days alive free of renal support (28 versus 25 days).

● In a prospective observational study of 108 patients with nontraumatic, undifferentiated hypotension, multiorgan ultrasonography performed in the
emergency department reported good agreement between the ultrasonography diagnosis and the final clinical diagnosis [26].

● In a post-hoc analysis of a randomized study of 103 emergency department patients who presented with nontraumatic undifferentiated shock, the
presence of a hyperdynamic LV was an independent predictor of sepsis (OR 5.5; 95% CI 1.1-45) [27]. The sensitivity and specificity of a hyperdynamic
LV for predicting sepsis were 33 and 94 percent, respectively.

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● In a retrospective study of 411 patients who had chest pain, dyspnea, or hypotension, a moderate agreement was reported between POC
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Details regarding standard techniques and diagnostic findings in comprehensive cardiac, thoracic, abdominal, and vascular ultrasound are discussed
separately. (See "Echocardiographic recognition of cardiomyopathies" and "Echocardiographic assessment of the right heart" and "Echocardiographic
evaluation of the pericardium" and "Cardiac tamponade", section on 'Echocardiography' and "Echocardiographic evaluation of the thoracic and proximal
abdominal aorta" and "Thoracic ultrasound: Indications, advantages, and technique" and "Clinical presentation and diagnosis of the nonpregnant adult with
suspected deep vein thrombosis of the lower extremity", section on 'Diagnostic ultrasonography suspected first DVT'.)

Pulmonary artery catheterization — Pulmonary arterial catheterization (PAC) has never been shown to improve patient-important outcomes, such that
the routine insertion of Swan-Ganz catheters has fallen out of favor [34-36]. However, when the diagnosis or the type of shock remains undetermined or
mixed, hemodynamic measurements obtained by PAC can be helpful (table 8 and table 9). Additional patients that may benefit from PAC are those with
unknown volume status despite adequate fluid resuscitation, those with severe cardiogenic shock (eg, acute valvular disease), or those suspected to have
severe underlying pulmonary artery hypertension or cardiac tamponade.

The major hemodynamic indices measured on PAC are cardiac output (ie, cardiac index), systemic vascular resistance, pulmonary artery occlusion pressure
(ie, pulmonary capillary wedge pressure), right atrial pressure, and mixed venous oxyhemoglobin saturation (SvO2). These measurements are most useful
diagnostically but can also be used to guide fluid resuscitation, titrate vasopressors, and assess the hemodynamic effects of changes in mechanical ventilator
settings [37]. Normal hemodynamic values and values consistent with the various classes of shock are listed in the tables (table 8 and table 10). The insertion
technique, indications for, and complications of PAC, as well as the interpretation of PAC tracings, are discussed separately. (See "Pulmonary artery
catheterization: Indications, contraindications, and complications in adults" and "Pulmonary artery catheters: Insertion technique in adults" and "Pulmonary
artery catheterization: Interpretation of hemodynamic values and waveforms in adults".)

Hemodynamic support — Because shock can be present when patients are hypotensive, hypertensive, or normotensive, the precise threshold that warrants
hemodynamic support is unknown. In general, those with suspected shock who are hypotensive and/or have clinical or laboratory evidence of hypoperfusion
(eg, change in mental status, clammy skin, diminished urine output, elevated lactate) should receive hemodynamic support with intravenous fluids (IVFs),
followed by vasopressors, should IVFs fail to restore adequate tissue perfusion; the exception is hypovolemic shock where more fluids is preferred. While the
optimal end-organ perfusion pressure is unclear, in general, we suggest maintaining the mean arterial pressure greater than 65 to 70 mmHg, since higher
targets (eg, >70 mmHg) do not appear to be associated with a mortality benefit and may be associated with increased risk of cardiac arrhythmias [38]. (See
"Treatment of hypovolemia or hypovolemic shock in adults" and "Initial evaluation of shock in the adult trauma patient and management of NON-hemorrhagic
shock".)

Intravenous fluids — IVFs are first-line agents in the treatment of patients with undifferentiated hypotension and shock. We prefer to administer IVFs in
well-defined boluses (eg, 500 to 1000 mL) that can be repeated until blood pressure and tissue perfusion are acceptable, pulmonary edema or intraabdominal
hypertension ensues, or fluid fails to augment perfusion.

The total volume infused is determined by the etiology of shock. As an example, patients with obstructive shock from pulmonary embolism or cardiogenic
shock from LV myocardial infarction usually require small volumes of IVF (500 to 1000 mL), while those with RV infarction or sepsis often need 2 to 5 L, and
those with hemorrhagic shock frequently require volumes >3 to 5 L (often inclusive of blood products). The administration of diuretic therapy should be
avoided in hypotensive patients with pulmonary edema until the need for hemodynamic support has been weaned.

The optimal choice of fluid is unknown. However, extrapolating from patients with septic shock, most patients are treated with crystalloids (eg, Ringer’s lactate
or normal saline), and those with hemorrhagic shock should be preferentially treated with blood products. We recommend avoiding the administration of
pentastarch or hydroxyethyl starch because randomized trials of patients with shock have identified potential harm from their use, the details of which are
discussed separately. (See "Treatment of hypovolemia or hypovolemic shock in adults", section on 'Hyperoncotic starch'.)

Vasopressors — Vasopressors are frequently required in the treatment of patients with suspected/undifferentiated shock to restore adequate tissue
perfusion. Importantly, the use of vasopressors in patients with hemorrhagic or hypovolemic shock may be harmful, such that vasopressors should only be
used as an additional form of hemodynamic support when aggressive resuscitation has failed to restore adequate tissue perfusion, or as a last resort for
patients in extremis. (See "Initial evaluation of shock in the adult trauma patient and management of NON-hemorrhagic shock", section on 'Vasopressors'.)

The optimal initial vasopressor is unknown, as is the optimal target mean arterial pressure [39]. However, among available agents, we prefer the following
(table 11):

● Adrenergic agonists – Norepinephrine (Levophed; initial dosing 8 to 12 mcg/minute intravenously) is the most commonly used agent in this population.
Phenylephrine (Neo-synephrine; initial dosing 100 to 200 mcg/minute intravenously) is used when tachyarrhythmias preclude the use of agents with
excessive beta-adrenergic activity (eg, norepinephrine, dopamine).

● Inotropic agents – Dobutamine (initial dose 0.5 to 1 mcg/kg/minute but frequently 2.5 mcg/kg/minute when cardiac decompensation is severe) is the
most commonly used inotropic agent in patients who have cardiogenic shock. Dobutamine is often administered together with norepinephrine to offset
the fall in peripheral vascular resistance that occurs when low doses of dobutamine are used.

Vasopressor support should be titrated according to the response (ie, indices of tissue perfusion including blood pressure, urine output, mental status, and
skin color) and limiting side effects (eg, tachycardia). In general, mean arterial pressure goals are targeted to 65 or greater, recognizing the importance of
individualizing care. While targeting higher mean arterial pressures resulted in increased arrhythmia in patients with chronic hypertension, this complication
was offset by reduced need for renal replacement therapy [40]. Additional details on the use and dosing of vasopressors are discussed separately. (See "Use
of vasopressors and inotropes" and "Evaluation and management of suspected sepsis and septic shock in adults", section on 'Vasopressors' and "Prognosis
and treatment of cardiogenic shock complicating acute myocardial infarction", section on 'Vasopressors and inotropes' and "Treatment, prognosis, and follow-
up of acute pulmonary embolism in adults", section on 'Hemodynamically unstable' and "Initial management of trauma in adults", section on 'Circulation'.)

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DIAGNOSIS — A diagnosis of shock is based upon a constellation of clinical, biochemical, and hemodynamic features. Most patients have hypotension
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saturation are not diagnostic but help to classify shock into one or more of the four main classes (distributive, cardiogenic, hypovolemic, obstructive) (table
10).

Importantly, the diagnosis is dependent upon the clinical suspicion for shock. Shock should always be suspected in those with hypotension and
hyperlactatemia, particularly in those with risk factors for specific forms of shock. Additionally, it should be suspected in those who present with normal blood
pressure who have signs of compensatory tachycardia and/or peripheral vasoconstriction. (See 'When to suspect shock' above.)

DIFFERENTIAL DIAGNOSIS — Each class of shock (distributive, cardiogenic, hypovolemic, obstructive) is distinguished from the other by a collection of
clinical features supported by laboratory, imaging, and hemodynamic findings, which are discussed in the sections below. The classification and etiology of
shock are discussed in detail separately (table 1). (See "Definition, classification, etiology, and pathophysiology of shock in adults", section on 'Classification
and etiology'.)

Distributive shock

● General clinical manifestations – Patients presenting with distributive shock typically have hypotension without the clinical and hemodynamic signs of
reduced preload (eg, normal skin turgor, moist mucous membranes, normal inferior vena cava [IVC] on imaging) or fluid overload (eg, no peripheral
edema or distended neck veins, normal central venous pressure [CVP] [8 to 12 mmHg] and mixed venous oxyhemoglobin saturation [SvO2] >70 percent
measured on central venous catheterization]). A preserved or hyperdynamic left ventricle is typically observed on echocardiography.

● Etiologic manifestations – The clinical features that distinguish one cause of distributive shock from the other depend upon the etiology. As an
example, patients may present with hypotension in association with the clinical manifestations of pneumonia (septic shock), brain or spinal trauma
(neurogenic shock), anaphylaxis (anaphylactic shock), a history of toxin exposure (toxic shock), steroid withdrawal (adrenal crisis), or hypothyroidism
(myxedema coma). Details regarding the clinical presentation and diagnosis of the causes of distributive shock are provided separately:

• Sepsis and systemic inflammatory response syndrome (see "Evaluation and management of suspected sepsis and septic shock in adults" and
"Sepsis syndromes in adults: Epidemiology, definitions, clinical presentation, diagnosis, and prognosis")

• Spinal cord trauma (see "Acute traumatic spinal cord injury")

• Anaphylaxis (see "Anaphylaxis: Emergency treatment")

• Toxic shock (see "Streptococcal toxic shock syndrome: Epidemiology, clinical manifestations, and diagnosis")

• Adrenal crisis (see "Clinical manifestations of adrenal insufficiency in adults" and "Diagnosis of adrenal insufficiency in adults" and "Treatment of
adrenal insufficiency in adults")

• Myxedema coma (see "Myxedema coma")

● Pulmonary artery catheterization findings – Physiologically, on pulmonary artery catheterization (PAC), distributive shock is primarily distinguished
from other forms of shock on the basis of low systemic vascular resistance (SVR) (<900 dynes per second/cm5) and normal or high cardiac output (CO)
(cardiac index [CI] >4.2 L/min/m2) (table 10). The pulmonary capillary wedge pressure (pcwp) is typically normal or low (<15 mmHg). SvO2 is typically
>65 percent and elevations in mixed central venous saturation (hyperoxia ≥90 percent) is associated with worse outcomes [41].

Cardiogenic shock

● General clinical manifestations – Patients with cardiogenic shock generally present with hypotension in association with the clinical and radiologic
manifestations of pulmonary edema (eg, diffuse lung crackles, distended neck veins), an elevated CVP (>12 mmHg) and low SvO2 (<70 percent) on
hemodynamic monitoring from a triple-lumen catheter, large dilated ventricle(s) and poor left ventricle function, or valvular or septal abnormalities on
echocardiography.

● Etiologic manifestations – Distinguishing the etiologies of cardiogenic shock depends upon the cause. Patients with cardiogenic shock from myocardial
infarction (MI) may have crushing substernal chest pain, acute dyspnea with elevated cardiac isoenzymes, and electrocardiographic (ECG) findings of
MI. Cardiogenic shock from arrhythmias may be sudden in onset with palpitations or syncope and may be evident on telemetry or ECG. A ruptured valve
or septal defect may present with the manifestations of acute pulmonary edema and a new murmur in the setting of a recent MI. Patients with myocarditis
may present with pleuritic chest pain and a pericardial rub. Additional details regarding the clinical presentation and diagnosis of the causes of
cardiogenic shock are provided separately:

• Myocardial infarction (see "Clinical manifestations and diagnosis of cardiogenic shock in acute myocardial infarction" and "Prognosis and treatment
of cardiogenic shock complicating acute myocardial infarction")

• Severe cardiomyopathy (see "Approach to acute decompensated heart failure in adults" and "Treatment of acute decompensated heart failure:
Components of therapy")

• Arrhythmia (see "Advanced cardiac life support (ACLS) in adults")

• Acute valve rupture or ventricular septal defect (see "Acute mitral regurgitation in adults" and "Acute aortic regurgitation in adults" and "Ventricular
septal defect in adults")

• Myocarditis or blunt cardiac trauma (see "Clinical manifestations and diagnosis of myocarditis in adults" and "Treatment and prognosis of
myocarditis in adults" and "Cardiac injury from blunt trauma")

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● Pulmonary artery catheterization findings – On PAC, typically, a high pcwp (>15 mmHg) distinguishes cardiogenic shock from other forms of shock,
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Hypovolemic shock

● General clinical manifestations – Hypovolemic shock can be distinguished from other types of shock by the characteristic presence of reduced preload
in the context of a suspected or known cause. Thus, patients with hypovolemia may display signs of reduced skin turgor, dry mucous membranes, a
collapsible IVC on imaging, and low CVP (<8 mmHg) on hemodynamic monitoring through a triple-lumen catheter.

● Etiologic manifestations – Patients with hypovolemic shock may present variably depending upon the etiology of fluid loss. As examples, patients may
present with a history of heat exposure, vomiting, diarrhea, hematemesis, hematochezia, traumatic hemorrhage, or back pain from a ruptured abdominal
aortic aneurysm. Additional details regarding the clinical presentation and diagnosis of the causes of hypovolemic shock are provided separately:

• Hemorrhage due to:

- Trauma-related blood loss (see "Initial evaluation of shock in the adult trauma patient and management of NON-hemorrhagic shock" and "Initial
management of trauma in adults")

- Nontraumatic blood loss (see "Management of symptomatic (non-ruptured) and ruptured abdominal aortic aneurysm" and "Management of
thoracic aortic aneurysm in adults" and "Peptic ulcer disease: Clinical manifestations and diagnosis" and "Methods to achieve hemostasis in
patients with acute variceal hemorrhage" and "Approach to acute lower gastrointestinal bleeding in adults" and "Approach to acute upper
gastrointestinal bleeding in adults")

• Nonhemorrhagic fluid loss (see "Etiology, clinical manifestations, and diagnosis of volume depletion in adults")

● Pulmonary artery catheterization findings – PAC findings are variable depending upon the degree of hypovolemia (table 10). Initially, the CO is normal
(CI 2.8 to 4.2 L/min/m2), the SVR is high (>1400 dynes per second/cm5), and the pcwp is preserved (6 to 15 mmHg). However, with increasing severity,
both the CO and pcwp may become reduced.

Obstructive shock

● General clinical manifestations – Patients with obstructive shock usually have hypotension associated with distended neck veins but usually without
the clinical signs of fluid overload or reduced preload. The exceptions are patients with subacute cardiac tamponade who often have evidence of fluid
overload on examination. On bedside ultrasonography or echocardiography, an effusion with a small right and left ventricle and a dilated IVC may be
seen in patients with pericardial tamponade; a dilated right ventricle and small left ventricle may be seen in patients with PE or pneumothorax.

● Etiologic manifestations – Depending upon the cause of obstructive shock, patients may present with pleuritic chest pain and acute dyspnea (from
pulmonary embolism [PE]), chronic dyspnea and a loud pulmonic component of the second heart sound (pulmonary hypertension), chest pain, tracheal
deviation, unilateral reduced breath sounds, and elevated plateau pressures on mechanical ventilation (tension pneumothorax), or quiet heart sounds,
pulsus paradoxus, and distended neck veins (cardiac tamponade). Additional details regarding the clinical presentation and diagnosis of the causes of
obstructive shock are provided separately:

• Pulmonary embolism (see "Clinical presentation, evaluation, and diagnosis of the nonpregnant adult with suspected acute pulmonary embolism" and
"Treatment, prognosis, and follow-up of acute pulmonary embolism in adults")

• Tension pneumothorax (see "Placement and management of thoracostomy tubes", section on 'Tension pneumothorax' and "Primary spontaneous
pneumothorax in adults")

• Cardiac tamponade (see "Cardiac tamponade")

• Constrictive pericarditis (see "Constrictive pericarditis")

• Restrictive cardiomyopathy (see "Idiopathic restrictive cardiomyopathy")

● Pulmonary artery catheterization findings – On PAC, CO is initially normal (CI 2.8 to 4.2 L/min/m2) and reduces as severity progresses, SVR is
increased (>1400 dynes per second/cm5), and pcwp is normal (6 to 15 mmHg) or reduced (table 10). Cardiac tamponade, constrictive pericardial
disease, and restrictive cardiomyopathy present similarly to cardiogenic shock, but are distinguished from the latter by equalization of the right atrial, right
ventricular end-diastolic, and pulmonary artery wedge pressures (waveform 1).

Combined — Importantly, many forms of shock coexist. As an example, hypovolemia may induce or coexist with cardiogenic shock and may result in
discordant clinical, biochemical, imaging, and hemodynamic features (eg, low ejection fraction with dry mucous membranes and a collapsible IVC). In such
cases, following the response to empiric therapies targeted at the suspected causes of shock may allow the clinician to determine which form of shock is
predominant.

REVERSE THE ETIOLOGY — Every attempt should be made to treat the underlying cause of shock. In some cases the etiology is clear (eg, hemorrhagic
shock from a gunshot wound to the abdomen), but in other cases the etiology is less obvious (eg, obstructive shock from massive pulmonary embolism).
Once the diagnosis is known, specific therapies should be refined, and the response to therapy monitored (eg, mean arterial blood pressure, urine output,
mental status, serum lactate level). Further details regarding the treatment and follow-up of patients with specific forms of shock are discussed separately.
(See 'Differential diagnosis' above.)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided
separately. (See "Society guideline links: Use of echocardiography as a monitor for therapeutic intervention in adults".)

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INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, “The Basics” and “Beyond the Basics.” The Basics patient
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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. There are four classes of shock; distributive, cardiogenic, hypovolemic, and obstructive. The term “undifferentiated shock” refers to that where
the state of shock is recognized but the cause is unknown. (See "Definition, classification, etiology, and pathophysiology of shock in adults" and
'Definition and classification' above.)

● The clinical manifestations of undifferentiated shock vary according to the etiology and stage of presentation. Features that are highly suspicious for
shock include hypotension; oliguria; abnormal mental status; tachypnea; cool, clammy skin; and metabolic acidosis (usually hyperlactatemia). Most
clinical features are neither sensitive nor specific for the diagnosis of shock and are primarily used to narrow the differential diagnosis so that empiric
therapies can be administered in a timely fashion. (See 'When to suspect shock' above.)

● In patients with undifferentiated hypotension or shock, the airway and breathing should be stabilized with oxygen and/or mechanical ventilation, when
necessary. Intravenous access should be secured so that patients can be immediately treated with intravenous fluids (IVF) to restore adequate tissue
perfusion. Resuscitative efforts should not be delayed for diagnostic evaluation or for central venous catheterization (algorithm 1A-B). (See 'Assess
airway, breathing, circulation' above.)

● In patients with undifferentiated hypotension or shock, the clinician should stratify the patient according to the severity of shock and the need for
immediate or early intervention so that empiric lifesaving therapies can be administered promptly. Such therapies include intramuscular epinephrine
(anaphylaxis), pericardiocentesis (pericardial tamponade), chest tube insertion (tension pneumothorax), surgical intervention (hemorrhagic shock, valve
rupture, aortic dissection), cardioversion or pacemaker placement (life-threatening arrhythmias), intravenous antibiotics (sepsis), revascularization
procedures (myocardial infarction), systemic thrombolysis (massive pulmonary embolism), and intravenous glucocorticoids (adrenal crisis). (See 'Risk
stratification' above.)

● For patients with undifferentiated hypotension and shock who have been stabilized or those who present with milder forms of shock, we suggest the
following diagnostic evaluation (see 'Initial diagnostic evaluation' above):

• Clinicians should take a thorough history and assess sensorium, mucous membranes, lips and tongue, neck veins, lungs, heart, and abdomen, as
well as skin and joints. Bedside telemetry and/or electrocardiography should also be performed.

• Basic laboratory tests should be performed, including serum lactate level, renal and liver function tests, troponin-I or -T level and/or creatine
phosphokinase isoenzymes, brain natriuretic peptide or N-terminal pro-brain natriuretic peptide level, complete blood count and differential,
prothrombin time, international normalized ratio, activated partial thromboplastin time, D-dimer level, and blood gas analysis. Additional laboratory
tests include those directed at specific etiologies or sequelae of shock (eg, urinalysis, blood cultures).

• Portable chest radiography should be performed in most patients with undifferentiated shock. Point-of-care ultrasonography is typically used in
patients in whom the diagnosis remains unclear after clinical assessment, in those in whom definitive imaging is unsafe, and to guide resuscitative
efforts. Additional imaging modalities are targeted at discovering the etiology of shock (eg, computed tomography of the chest).

• Hemodynamic measurements obtained by pulmonary artery catheter can be helpful when the diagnosis or the type of shock remains undetermined
(table 8 and table 9), as well as in patients with unknown volume status, severe cardiogenic shock, or in those suspected to have severe underlying
pulmonary artery hypertension.

● Patients with suspected shock should receive hemodynamic support with IVF (usually crystalloids in well-defined boluses of 500 to 1000 mL), followed by
vasopressors (table 11), should IVF fail to restore adequate tissue perfusion. However, in patients with hypovolemic shock, we prefer to continue to
administer fluids. While the optimal end-organ perfusion pressure is unclear, in general, we suggest maintaining the mean arterial pressure greater than
65 to 70 mmHg since higher targets may be associated with harm. (See 'Hemodynamic support' above.)

● A diagnosis of shock is based upon a constellation of clinical, biochemical, and hemodynamic features. Using data derived from the diagnostic
evaluation, shock can typically be classified and the etiology narrowed to a few possibilities. (See 'Diagnosis' above and 'Differential diagnosis' above.)

● Empiric therapies should be administered early (eg, antibiotics). The response should be monitored and therapies refined once the diagnosis is clear.
(See 'Reverse the etiology' above.)

Use of UpToDate is subject to the Subscription and License Agreement.

REFERENCES

1. Vincent JL, De Backer D. Circulatory shock. N Engl J Med 2013; 369:1726.


2. Rodgers KG. Cardiovascular shock. Emerg Med Clin North Am 1995; 13:793.

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3. Churpek MM, Zadravecz FJ, Winslow C, et al. Incidence and Prognostic Value of the Systemic Inflammatory Response Syndrome and Organ
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4. Seymour CW, Liu VX, Iwashyna TJ, et al. Assessment of Clinical Criteria for Sepsis: For the Third International Consensus Definitions for Sepsis and
Septic Shock (Sepsis-3). JAMA 2016; 315:762.
5. Kraut JA, Madias NE. Lactic acidosis. N Engl J Med 2014; 371:2309.
6. Liu VX, Morehouse JW, Marelich GP, et al. Multicenter Implementation of a Treatment Bundle for Patients with Sepsis and Intermediate Lactate Values.
Am J Respir Crit Care Med 2016; 193:1264.
7. Cardenas-Garcia J, Schaub KF, Belchikov YG, et al. Safety of peripheral intravenous administration of vasoactive medication. J Hosp Med 2015;
10:581.
8. Walkey AJ, Wiener RS, Ghobrial JM, et al. Incident stroke and mortality associated with new-onset atrial fibrillation in patients hospitalized with severe
sepsis. JAMA 2011; 306:2248.
9. Levraut J, Ciebiera JP, Chave S, et al. Mild hyperlactatemia in stable septic patients is due to impaired lactate clearance rather than overproduction. Am
J Respir Crit Care Med 1998; 157:1021.
10. del Portal DA, Shofer F, Mikkelsen ME, et al. Emergency department lactate is associated with mortality in older adults admitted with and without
infections. Acad Emerg Med 2010; 17:260.
11. Cavallazzi R, Bennin CL, Hirani A, et al. Is the band count useful in the diagnosis of infection? An accuracy study in critically ill patients. J Intensive Care
Med 2010; 25:353.
12. Perera P, Mailhot T, Riley D, Mandavia D. The RUSH exam: Rapid Ultrasound in SHock in the evaluation of the critically lll. Emerg Med Clin North Am
2010; 28:29.
13. Labovitz AJ, Noble VE, Bierig M, et al. Focused cardiac ultrasound in the emergent setting: a consensus statement of the American Society of
Echocardiography and American College of Emergency Physicians. J Am Soc Echocardiogr 2010; 23:1225.
14. Atkinson PR, McAuley DJ, Kendall RJ, et al. Abdominal and Cardiac Evaluation with Sonography in Shock (ACES): an approach by emergency
physicians for the use of ultrasound in patients with undifferentiated hypotension. Emerg Med J 2009; 26:87.
15. Shokoohi H, Boniface KS, Pourmand A, et al. Bedside Ultrasound Reduces Diagnostic Uncertainty and Guides Resuscitation in Patients With
Undifferentiated Hypotension. Crit Care Med 2015; 43:2562.
16. Ettin D, Cook T. Using ultrasound to determine external pacer capture. J Emerg Med 1999; 17:1007.
17. Macedo W Jr, Sturmann K, Kim JM, Kang J. Ultrasonographic guidance of transvenous pacemaker insertion in the emergency department: a report of
three cases. J Emerg Med 1999; 17:491.
18. Soldati G, Testa A, Sher S, et al. Occult traumatic pneumothorax: diagnostic accuracy of lung ultrasonography in the emergency department. Chest
2008; 133:204.
19. Zhang M, Liu ZH, Yang JX, et al. Rapid detection of pneumothorax by ultrasonography in patients with multiple trauma. Crit Care 2006; 10:R112.
20. Knudtson JL, Dort JM, Helmer SD, Smith RS. Surgeon-performed ultrasound for pneumothorax in the trauma suite. J Trauma 2004; 56:527.
21. Sartori S, Tombesi P, Trevisani L, et al. Accuracy of transthoracic sonography in detection of pneumothorax after sonographically guided lung biopsy:
prospective comparison with chest radiography. AJR Am J Roentgenol 2007; 188:37.
22. Rozycki GS, Feliciano DV, Ochsner MG, et al. The role of ultrasound in patients with possible penetrating cardiac wounds: a prospective multicenter
study. J Trauma 1999; 46:543.
23. Mandavia DP, Hoffner RJ, Mahaney K, Henderson SO. Bedside echocardiography by emergency physicians. Ann Emerg Med 2001; 38:377.
24. Tayal VS, Kline JA. Emergency echocardiography to detect pericardial effusion in patients in PEA and near-PEA states. Resuscitation 2003; 59:315.
25. Kanji HD, McCallum J, Sirounis D, et al. Limited echocardiography-guided therapy in subacute shock is associated with change in management and
improved outcomes. J Crit Care 2014; 29:700.
26. Volpicelli G, Lamorte A, Tullio M, et al. Point-of-care multiorgan ultrasonography for the evaluation of undifferentiated hypotension in the emergency
department. Intensive Care Med 2013; 39:1290.
27. 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.
28. Taylor RA, Moore CL. Accuracy of emergency physician-performed limited echocardiography for right ventricular strain. Am J Emerg Med 2014; 32:371.
29. Jones AE, Tayal VS, Sullivan DM, Kline JA. Randomized, controlled trial of immediate versus delayed goal-directed ultrasound to identify the cause of
nontraumatic hypotension in emergency department patients. Crit Care Med 2004; 32:1703.
30. Derr C, Drake JM. Esophageal rupture diagnosed with bedside ultrasound. Am J Emerg Med 2012; 30:2093.e1.
31. Moore CL, Rose GA, Tayal VS, et al. Determination of left ventricular function by emergency physician echocardiography of hypotensive patients. Acad
Emerg Med 2002; 9:186.
32. Sabia P, Abbott RD, Afrookteh A, et al. Importance of two-dimensional echocardiographic assessment of left ventricular systolic function in patients
presenting to the emergency room with cardiac-related symptoms. Circulation 1991; 84:1615.
33. Haydar SA, Moore ET, Higgins GL 3rd, et al. Effect of bedside ultrasonography on the certainty of physician clinical decisionmaking for septic patients in
the emergency department. Ann Emerg Med 2012; 60:346.
34. Connors AF Jr, Speroff T, Dawson NV, et al. The effectiveness of right heart catheterization in the initial care of critically ill patients. SUPPORT
Investigators. JAMA 1996; 276:889.
35. Harvey S, Harrison DA, Singer M, et al. Assessment of the clinical effectiveness of pulmonary artery catheters in management of patients in intensive
care (PAC-Man): a randomised controlled trial. Lancet 2005; 366:472.
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36. Shah MR, Hasselblad V, Stevenson LW, et al. Impact of the pulmonary artery catheter in critically ill patients: meta-analysis of randomized clinical trials.
JAMAThis site
2005; uses cookies. By continuing to browse this site you are agreeing to our use of cookies. Continue or find out more.
294:1664.
37. Mimoz O, Rauss A, Rekik N, et al. Pulmonary artery catheterization in critically ill patients: a prospective analysis of outcome changes associated with
catheter-prompted changes in therapy. Crit Care Med 1994; 22:573.
38. Hylands M, Moller MH, Asfar P, et al. A systematic review of vasopressor blood pressure targets in critically ill adults with hypotension. Can J Anaesth
2017; 64:703.
39. Gamper G, Havel C, Arrich J, et al. Vasopressors for hypotensive shock. Cochrane Database Syst Rev 2016; 2:CD003709.
40. Asfar P, Meziani F, Hamel JF, et al. High versus low blood-pressure target in patients with septic shock. N Engl J Med 2014; 370:1583.
41. Pope JV, Jones AE, Gaieski DF, et al. Multicenter study of central venous oxygen saturation (ScvO(2)) as a predictor of mortality in patients with sepsis.
Ann Emerg Med 2010; 55:40.

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GRAPHICS
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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)

Distributive Non-septic Inflammatory shock (systemic inflammatory response syndrome) – 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
Cardiogenic Myocardial contusion
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

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
hemorrhage from bleeding diathesis
Hypovolemic
Non- Gastrointestinal losses (eg, diarrhea, vomiting, external drainage); skin losses (eg, heat stroke, burns, dermatologic
hemorrhagic 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 pulmonary hypertension, severe or acute obstruction of the
vascular pulmonic or tricuspid valve, venous air embolus

Obstructive Mechanical Tension pneumothorax or hemothorax (eg, trauma, iatrogenic), 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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Approach
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shock: Initial approach

The shaded boxes indicate the points in the process at which no further action needs to be
taken, a diagnosis has been made, or continued resuscitation is required.

IV: intravascular; ACLS: advanced cardiac life support; MI: myocardial infarction; PE: pulmonary
embolus.
* The first priority is to stabilize the airway with oxygen and/or mechanical ventilation. Although most
patients are intubated, not every patient requires mechanical ventilation (eg, those with a tension
pneumothorax).
¶ Aggressive fluids and blood products may be required for those with hemorrhage.

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Approach
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The shaded boxes indicate the points in the process at which no further action needs to be taken, a diagnosis has been made, or continued resuscitation is required.

JVD: jugular venous distension; PE: pulmonary embolus; P2: pulmonic second heart sound; ABG: arterial blood gas; CBC: complete blood count; CXR: chest radiograph; ECG:
electrocardiography; DIC: disseminated intravascular coagulation; CT: computed tomography; CTPA: computed tomographic pulmonary angiography; PAC: pulmonary artery
catheter; RV: right ventricle; LV: left ventricle; IVC: inferior vena cava; Pcwp: pulmonary capillary wedge pressure; CO: cardiac output; SVR: systemic vascular resistance; SvO 2 :
mixed venous oxyhemoglobin saturation.
* Timing and availability depends on institutional resources. Point-of-care ultrasonography may also be used in those in whom routine imaging is unsafe.
¶ Myocardial contractility may be depressed in some forms of distributive shock.
Δ The presence of B lines on lung ultrasound may suggest pulmonary edema to support cardiogenic shock.
◊ Detection of fluid in the peritoneal cavity and an aortic aneurysm may support hemorrhagic shock from aneurysm rupture.
§ Absence of lung sliding may support obstructive shock from tension pneumothorax.
¥ These findings are typical of PE, pulmonary hypertension, and tension pneumothorax. In cardiac tamponade, PAC reading are similar to those in cardiogenic shock; however, right
atrial, right ventricular end-diastolic, and pulmonary artery wedge pressures are equal.

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Rapid This
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Diagnosis is made clinically:
The most common signs and symptoms are cutaneous (eg, sudden onset of generalized urticaria, angioedema, flushing, pruritus). However, 10 to 20% of patients have no
skin findings.

Danger signs: Rapid progression of symptoms, respiratory distress (eg, stridor, wheezing, dyspnea, increased work of breathing, persistent cough,
cyanosis), vomiting, abdominal pain, hypotension, dysrhythmia, chest pain, collapse.

Acute management:
The first and most important treatment in anaphylaxis is epinephrine. There are NO absolute contraindications to epinephrine in the setting of anaphylaxis.

Airway: Immediate intubation if evidence of impending airway obstruction from angioedema. Delay may lead to complete obstruction. Intubation can be difficult and
should be performed by the most experienced clinician available. Cricothyrotomy may be necessary.

Promptly and simultaneously, give:

IM epinephrine (1 mg/mL preparation): Give epinephrine 0.3 to 0.5 mg intramuscularly, preferably in the mid-outer thigh. Can repeat every 5 to 15 minutes (or
more frequently), as needed. If epinephrine is injected promptly IM, most patients respond to one, two, or at most, three doses. If symptoms are not responding to
epinephrine injections, prepare IV epinephrine for infusion.

Place patient in recumbent position, if tolerated, and elevate lower extremities.

Oxygen: Give 8 to 10 L/minute via facemask or up to 100% oxygen, as needed.

Normal saline rapid bolus: Treat hypotension with rapid infusion of 1 to 2 liters IV. Repeat, as needed. Massive fluid shifts with severe loss of intravascular volume can
occur.

Albuterol (salbutamol): For bronchospasm resistant to IM epinephrine, give 2.5 to 5 mg in 3 mL saline via nebulizer. Repeat, as needed.

Adjunctive therapies:

H1 antihistamine*: Consider giving diphenhydramine 25 to 50 mg IV (for relief of urticaria and itching only).

H2 antihistamine*: Consider giving ranitidine 50 mg IV.

Glucocorticoid*: Consider giving methylprednisolone 125 mg IV.

Monitoring: Continuous noninvasive hemodynamic monitoring and pulse oximetry monitoring should be performed. Urine output should be monitored in patients
receiving IV fluid resuscitation for severe hypotension or shock.

Treatment of refractory symptoms:


Epinephrine infusion ¶: For patients with inadequate response to IM epinephrine and IV saline, give epinephrine continuous infusion, beginning at 0.1
mcg/kg/minute by infusion pump Δ. Titrate the dose continuously according to blood pressure, cardiac rate and function, and oxygenation.
Vasopressors ¶: Some patients may require a second vasopressor (in addition to epinephrine). All vasopressors should be given by infusion pump, with the doses titrated
continuously according to blood pressure and cardiac rate/function and oxygenation monitored by pulse oximetry.

Glucagon: Patients on beta-blockers may not respond to epinephrine and can be given glucagon 1 to 5 mg IV over 5 minutes, followed by infusion of 5 to 15 mcg/minute.
Rapid administration of glucagon can cause vomiting.

Instructions on how to prepare and administer epinephrine for IV continuous infusions are available as separate tables in UpToDate.

IM: intramuscular; IV: intravenous.


* These medications should not be used as initial or sole treatment.
¶ All patients receiving an infusion of epinephrine and another vasopressor require continuous noninvasive monitoring of blood pressure, heart rate and function, and oxygen
saturation.
Δ For example, the initial infusion rate for a 70 kg patient would be 7 mcg/minute. This is consistent with the recommended range for non-weight-based dosing for adults, which
is 2 to 10 mcg/minute. Non-weight-based dosing can be used if the patient's weight is not known and cannot be estimated.

Adapted from: Simons FER. Anaphylaxis. J Allergy Clin Immunol 2010; 125:S161.

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Traumatic shock:
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IV: intravenous; IO: intraosseous; FAST: Focused Assessment with Sonography in


Trauma; CXR: chest x-ray; C-spine: cervical spine.

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Differential diagnosis
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I. Low CVP
A. Hypovolemia

1. Hemorrhage
a. External (compressible)
i. Lacerations
ii. Contusions
iii. Fractures (partly compressible)
b. Internal (noncompressible)
i. Intrathoracic
ii. Intraperitoneal
iii. Retroperitoneal (partly compressible)
c. Fractures (partly compressible)

2. Third spacing (eg, burns)

B. Neurogenic (high cervical cord injury)

II. High CVP


A. Pericardial tamponade

B. Tension pneumothorax

C. Myocardial contusion

III. Other diagnoses to consider


A. Pharmacologic or toxicologic agents

B. Myocardial infarction (severe)

C. Diaphragmatic rupture with herniation

D. Fat or air embolism

CVP: central venous pressure.

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Acute This
management of severe
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1. Resuscitation and stabilization, initiation of medical therapy with an intravenous proton pump inhibitor

2. Assessment of onset and severity of bleeding

3. Risk stratification using validated prognostic scale

4. Diagnostic endoscopy
Preparation for emergent upper endoscopy
Localization and identification of the bleeding site
Idenification of stigmata of recent hemorrhage
Stratification of the risk for rebleeding

4. Therapeutic endoscopy
Control of active bleeding or high-risk lesions
Minimization of treatment-related complications
Treatment of persistent or recurrent bleeding

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Evaluation of patients
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bleeding)

IDA: iron deficiency anemia; CTA: computed tomographic angiography; CT: computed tomographic; GI: gastrointestinal; MR: magnetic
resonance.
* If hematemesis or melena is present the patient should be evaluated for upper GI bleeding. Refer to UpToDate topics on the
evaluation of upper GI bleeding for details.
¶ Bleeding associated with signs such as hypotension, tachycardia, or orthostatic hypotension.
Δ Colonoscopy should be performed once the patient has been resuscitated and an adequate bowel preparation has been given (typically
4 to 6 L of polyethylene glycol). If the initial colonoscopy was inadequate (eg, inadequate visualization, failure to reach the cecum),
repeat colonoscopy should be considered.
◊ Consider evaluation with a side-viewing duodenoscope in patients with risk factors for hemobilia or hemosuccus pancreaticus or CT
angiography (followed by push enteroscopy if the CT angiography is negative) in patients at risk for an aortoenteric fistula. Conventional
transvenous angiography is typically performed if the patient remains hemodynamically unstable despite attempts at resuscitation. If the
suspicion for an upper GI source is moderate (rather than high), nasogastric lavage can be performed to look for evidence to support an
upper GI source. Refer to UpToDate topics on lower GI bleeding in adults for additional details.
§ CTA is an alternative but lacks therapeutic capacity. A tagged red blood cell scan may aid with localization prior to angiography.
¥ Refer to UpToDate topic review on suspected small bowel bleeding for details.
‡ A Meckel's scan should be performed in younger patients with overt bleeding. Surgical exploration is appropriate if no other studies
have revealed a source and significant bleeding continues or if there is high suspicion for a small bowel neoplasm.

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† If the deep small bowel enteroscopy was incomplete, a video capsule endoscopy study should be obtained, followed by CT or MR
enterography if the capsule endoscopy is negative.
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Evaluation of suspected
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GI: gastrointestinal; CT: computed tomographic; CTA: computed tomographic angiography; MR:
magnetic resonance.
* The presence of both hematemesis and melena suggests that brisk bleeding is present.
¶ Bleeding associated with signs such as hypotension, tachycardia, or orthostatic hypotension.
Δ Consider evaluation with a side-viewing duodenoscope if there are risk factors for hemobilia or
hemosuccus pancreaticus; consider CTA (followed by push enteroscopy if the CTA is negative) in
patients at risk for an aortoenteric fistula. Conventional angiography is typically performed if the patient
remains hemodynamically unstable despite attempts at resuscitation.
◊ Patients who present with hematemesis do not need to undergo colonoscopy, since hematemesis
suggests the bleeding is proximal to the ligament of Treitz. They should proceed directly to an
evaluation for small bowel bleeding.
§ If the patient becomes hemodynamically unstable following initial resuscitation, conventional
angiography can be performed. Patients who present with hematemesis do not need to undergo
colonoscopy and can skip this step in the evaluation because hematemesis suggests the bleeding is
proximal to the ligament of Treitz.
¥ If the initial endoscopic evaluation was inadequate (eg, fair or poor visualization, failure to reach the

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cecum), repeat examination should be considered before initiating an evaluation for small bowel
bleeding. Refer to UpToDate topic review on suspected small bowel bleeding for details.
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‡ If not already done. If the patient remains hemodynamically stable and does not have evidence of
aggressive bleeding (eg, ongoing hematochezia), perform a CTA or push enteroscopy (CTA is the initial
test of choice if there is concern for an aortoenteric fistula). If the patient becomes hemodynamically
unstable following initial resuscitation or has signs of aggressive bleeding, perform conventional
angiography.
† If not already done, angiography or CTA may be obtained. If angiography or CTA has been performed
and no source is identified, a Meckel's scan should be obtained in younger patients with overt bleeding,
unless the only manifestation of bleeding was hematemesis. Surgical exploration is appropriate if no
other studies have revealed a source and significant bleeding continues or if there is high suspicion for a
small bowel neoplasm.
** If the deep small bowel enteroscopy was incomplete, a video capsule endoscopy study should be
obtained, followed by CT enterography or MR enterography if the capsule endoscopy is negative.

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Adult tachycardia
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The algorithm presented above has been modified to make it more consistent with the 2015
update to the ACLS Guidelines while we await permission from the AHA to reproduce the latest
version.

CHF: congestive heart failure; ECG: electrocardiogram; IV: intravenous; J: joules; NS: normal
(isotonic) saline; VT: ventricular tachycardia.

Reprinted with permission. Adult Advanced Cardiovascular Life Support: 2010. American Heart
Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. ©
2010 American Heart Association, Inc.

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Adult bradycardia
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The algorithm presented above has been modified to make it more consistent with the 2015
update to the ACLS Guidelines while we await permission from the AHA to reproduce the latest
version.

ECG: electrocardiogram; IV: intravenous; mcg: microgram.

Reprinted with permission. Adult Advanced Cardiovascular Life Support: 2010. American Heart
Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. ©
2010 American Heart Association, Inc.

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Treatment options
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General measures
Ventilation support to correct hypoxemia and, in part, acidosis

Optimize intravascular volume

Sodium bicarbonate only for severe metabolic acidosis (arterial pH less than 7.10 to 7.15)

Aspirin

Intravenous heparin

Possible glycoprotein IIb/IIIa inhibitor with NSTEMI

Insertion of pulmonary artery catheter

Specific measures
Pharmacologic support
Sympathomimetic inotropes (eg, dopamine)
Norepinephrine (for refractory hypotension)

Mechanical support
IABP, usually combined with percutaneous coronary intervention or coronary artery bypass graft surgery or possible thrombolytic therapy

Newer devices
Left ventricular or biventricular assist devices
Percutaneous cardiopulmonary bypass

Reperfusion/revascularization
Primary percutaneous coronary intervention
Coronary artery bypass graft
Thrombolytic therapy for patients not receiving PCI in a timely manner

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Acute This
aortic
sitedissection: Rapid
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By continuing
Treatment of acute aortic dissection depends on the type/location. Aortic dissection involving the ascending aorta is a cardiac surgical emergency. Aortic dissection
limited to the descending thoracic and/or the abdominal aorta can often be managed medically, unless there is evidence of end-organ ischemia or rupture.

Clinical features and evaluation


Acute onset of severe, sharp, or knife-like pain in the anterior chest, with radiation to the neck, back, or abdomen. Pain may be migratory.

Assess risk factors for TAAD*.

Palpate carotid, subclavian, and femoral pulses; note any significant differences between sides. Obtain blood pressure in both arms.

Auscultate for diastolic cardiac murmur of aortic regurgitation; assess for tamponade (muffled heart sounds, jugular venous distention, pulsus paradoxus).

Evaluate for signs of ischemic stroke, spinal cord ischemia, ischemic neuropathy, hypoxic encephalopathy.
Findings suggesting involvement of the ascending aorta include back pain, anterior chest pain, hemodynamic instability, diastolic cardiac murmur, tamponade, syncope or stroke
(persistent or transient ¶; right hemispheric stroke is most common, but bilateral can occur), Horner syndrome (typically partial with ptosis/miosis), weak or absent carotid or subclavian
pulse, upper extremity pain/paresthesia/motor deficit.
Findings suggesting involvement of the descending aorta include back pain, chest pain, abdominal pain, weak or absent femoral pulses, lower extremity pain/paresthesia/motor
deficit, acute paraplegia.

Findings on initial studies


Obtain ECG. Look for signs of ACS; extension of type A dissection to coronary ostia can cause coronary ischemia (right coronary artery most commonly affected).

Obtain D-dimer, CBC, basic electrolytes, LDH, cardiac markers, coagulation parameters, and type and crossmatch. D-dimer <500 ng/dL is less likely to be aortic
dissection.

Chest radiograph: Widened mediastinum and/or unexplained pleural effusion are consistent with dissection, particularly if unilateral.

Vascular imaging
For hemodynamically stable patient without suspicion for ascending aortic involvement: Obtain thoracic CT angiography or MR angiography, depending upon resources
and speed of acquisition. Dissection is confirmed by presence of intimal flap separating true and false lumen. If these are not readily available or there is a
contraindication, obtain transesophageal echocardiogram.

For hemodynamically unstable patient or for strong suspicion of ascending aortic involvement: Obtain transesophageal echocardiogram. If not immediately available,
obtain CT angiography. Transthoracic echocardiography may be useful for identifying complications of ascending aortic dissection (eg, aortic valve
regurgitation, hemopericardium, inferior ischemia) but is not sensitive for identification of dissection.

Management
Place two large bore IVs; monitor heart rate and blood pressure continuously, preferably using an arterial line.

Control heart rate and blood pressure Δ. Maintain heart rate <60 BPM and systolic blood pressure between 100 and 120 mmHg.
Administer esmolol (250 to 500 mcg/kg IV loading dose, then infuse at 25 to 50 mcg/kg/minute; titrate to maximum dose of 300 mcg/kg/minute) or labetalol (20 mg IV initially,
followed by either 20 to 80 mg IV boluses every 10 minutes to a maximal dose of 300 mg, or an infusion of 0.5 to 2 mg/minute IV). If beta blockers are not tolerated, alternatives are
verapamil, diltiazem, or nicardipine.
Once heart rate is consistently <60 BPM, give vasodilator therapy. IF the systolic blood pressure remains above 120 mmHg, initiate nitroprusside infusion (0.25 to 0.5 mcg/kg/minute
titrated to a maximum of 10 mcg/kg/minute) or nicardipine infusion (2.5 to 5 mg/hour titrated to a maximum of 15 mg/hour). Vasodilator therapy (eg, nitroprusside, nicardipine) should
not be used without first controlling heart rate with beta blockade.

Give IV opioids for analgesia (eg, fentanyl).

Place Foley catheter for assessment of urine output and kidney perfusion.

Surgical consultation
Obtain immediate surgical consultation (cardiothoracic surgery, vascular surgery) as soon as the diagnosis is strongly suspected (particularly for involvement of the
ascending aorta) or confirmed.
Aortic dissection involving the ascending aorta is a cardiac surgical emergency. Transesophageal echocardiography should be routinely performed in the operating room to
assess aortic valve function, left ventricular function, aortic root and ascending aortic diameter, and evidence of hemopericardium/tamponade.
Aortic dissection involving only the descending thoracic aorta or abdominal aorta and with evidence of malperfusion is treated with urgent aortic stent-grafting or surgery.
Aortic dissection involving only the descending thoracic aorta or abdominal aorta without evidence for ischemia is admitted to the ICU for medical management of hemodynamics and
serial aortic imaging.

If appropriate surgical services ◊ are not available, initiate emergent transfer to nearest available cardiovascular center.

TAAD: thoracic aortic aneurysm/dissection; ECG: electrocardiogram; ACS: acute coronary syndrome; CBC: complete blood count; LDH: lactate dehydrogenase; CT: computed
tomography; MR: magnetic resonance; IV: intravenous; BPM: beats per minute; ICU: intensive care unit; AAA: abdominal aortic aneurysm.
* Known history of TAAD, AAA, aortic intramural hematoma, penetrating aortic ulcer, family history of TAAD or AAA, recent aortic instrumentation, known bicuspid aortic valve,
known aortic coarctation, known syndrome associated with TAAD (eg, Marfan, vascular Ehlers-Danlos, Loeys-Dietz, or Turner syndromes).
¶ Amaurosis fugax has been reported.
Δ Patients should be admitted to an intensive care unit as rapidly as possible. Intravenous short-acting agents for control of heart rate and blood pressure should be administered
immediately by clinicians who are trained and experienced in their titration using continuous noninvasive electronic monitoring of blood pressure, heart rate, and ECG. The use of
non-selective beta blockers alone in patients with acute cocaine intoxication may lead to unopposed alpha stimulation worsening hypertension.
◊Surgical services should include cardiothoracic/vascular surgery by surgeons experienced in the treatment of aortic dissection, equipment and technical support for
cardiopulmonary bypass, and endovascular stent-graft capability.

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Treatment algorithm
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patients with suspected pulmonary embolism (PE)

Hemodynamically unstable refers to the presence of overt shock from "massive"


PE that is imminently life-threatening (please refer to the topic text for more
details).

RV: right ventricle.


* Resuscitation involves any combination of respiratory (oxygen, noninvasive or
invasive mechanical ventilation) and hemodynamic support (intravenous fluids,
vasopressors).
¶ The use of portable perfusion scanning is dependent upon institutional availability,
but has a higher sensitivity for the diagnosis of PE than transthoracic
echocardiography. Other alternative testing that may help the clinician make a
presumptive diagnosis of PE and guide management decisions include
transesophageal echocardiography and compressive ultrasound of the lower
extremities, none of which are diagnostic of PE. Please refer to the UpToDate topic
text for more details.
Δ Evidence of RV overload on echocardiography is supportive but not diagnostic of PE.
Some experts may look for additional supportive evidence of PE (eg, deep venous
thrombosis, thrombus in the right ventricle or main pulmonary artery). Please refer to
the UpToDate topic text for more details.
◊ The decision to empirically anticoagulate this population depends upon the clinical
suspicion for PE.
§ In this population, it is assumed that the suspicion for PE remains high and that PE
is the likely cause of hemodynamic instability.
¥ Patients not already on intravenous unfractionated heparin can proceed directly to
thrombolysis, followed by anticoagulation. However, it is acceptable to proceed with
thrombolytic therapy even while anticoagulated, particularly if the bleeding risk is
deemed low and the patient is severely compromised.
‡ Combined catheter-directed embolectomy and thrombolysis is considered
investigational and should be reserved for use in institutions with expertise.

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Treatment of acute
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Emergency measures
1. Establish intravenous access with a large-gauge needle.

2. Draw blood for immediate serum electrolytes and glucose and routine measurement of plasma cortisol and ACTH. Do not wait for lab results.

3. Infuse 2 to 3 liters of isotonic saline or 5 percent dextrose in isotonic saline as quickly as possible. Frequent hemodynamic monitoring and measurement of serum
electrolytes should be performed to avoid iatrogenic fluid overload.

4. Give 4 mg dexamethasone as intravenous bolus over one to five minutes and every 12 hours thereafter. Dexamethasone is the drug of choice because it does not
interfere with the measurement of plasma cortisol. If dexamethasone is unavailable, intravenous hydrocortisone, 100 mg immediately and every six hours thereafter, may
be used.

5. Use supportive measures as needed.*

Subacute measures after stabilization of the patient


1. Continue intravenous isotonic saline at a slower rate for next 24 to 48 hours.

2. Search for and treat possible infectious precipitating causes of the adrenal crisis.

3. Perform a short ACTH stimulation test to confirm the diagnosis of adrenal insufficiency, if patient does not have known adrenal insufficiency.

4. Determine the type of adrenal insufficiency and its cause if not already known.

5. Taper parenteral glucocorticoid over one to three days, if precipitating or complicating illness permits, to oral glucocorticoid maintenance dose.

6. Begin mineralocorticoid replacement with fludrocortisone, 0.1 mg by mouth daily, when saline infusion is stopped.

* Electrolyte abnormalities may include hyponatremia, hyperkalemia or rarely hypercalcemia. Hyponatremia is rapidly corrected by cortisol and volume repletion.

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Long axis
This echocardiogram in continuing
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The long axis echocardiogram from a patient with a dilated cardiomyopathy


demonstrates spherical or globular dilation. The long and short axis dimensions
now appear to have a nearly 1:1 ratio (normal 2:1), although are unable to
confirm the long-axis dimension from this image alone since the apex is not
visualized.

AV: aortic valve; LV: left ventricle; MV: mitral valve; LA: left atrium; dAo: descending
aorta.

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Echocardiogram ofcookies.
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cardiomyopathy

A four-chamber view from the two-dimensional echocardiogram of a normal


heart is shown in the panel A. In panel B, the echocardiogram from a patient
with dilated cardiomyopathy is shown and diagrammed. Note the dilated
cardiomyopathy heart is more spherical than its normal counterpart.

LV: left ventricle; RV: right ventricle; RA: right atrium; LA: left atrium; aML: anterior
mitral leaflet; pML: posterior mitral leaflet.

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Dilated cardiomyopathy
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Shown are the precordial long axis (panel A) and apical four-chamber views (panel B) from a
patient with dilated cardiomyopathy. The long axis view demonstrates increased sphericity of
the left ventricle (LV) and the long axis and short axis ratio approaches unity (normal 2:1).
There is left atrial (LA) enlargment and a very large "residual" left ventricular end-systolic
volume (ie, at end-systole there is a large unejected volume remaining in a dilated LV). The
impression of increased sphericity is reinforced in the four-chamber view. In addition, there is
also dilation of the right atrium (RA) and right ventricle (RV) four chamber dilation, connoting
a poor prognosis.

MV: mitral valve; AV: aortic valve; Ao: aorta; TV: tricuspid valve; IVS: interventricular septum; IAS:
interatrial septum.

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M-mode echocardiogram
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The M-mode echocardiogram (left panel) and the left ventriculogram (right
panel) are from a patient with a cardiomyopathy. The ventriculogram shows
global hypokinesis, large end-diastolic (EDV) and end-systolic volumes (ESV),
and an ejection fraction (EF) of 32 percent. The M-mode echocardiogram shows
reduced septal (Sept) motion, a large left (LV) and right ventricle (RV), and an
EPSS of 20 mm.

Dia: diastole; Sys: systole.

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M-mode echocardiogram
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compared with normal

Normal M-modes of the minor axis of the left ventricle are taken along the line
(Mp) superimposed on the anatomical diagram in panel A. Panel B is from a
normal patient and panel C is from a patient with cardiomyopathy. The minor
axis dimension of the normal left ventricle (LV) at the end of systole (LVESd) is
5.2 cm compared with 6.3 cm in the patient with cardiomyopathy; the LV end
diastolic dimensions (LVEDd) are 3.4 and 5.3 cm, respectively. The fractional
shortening of the normal heart (LVEDd - LVESd / LVEDd) is 35 percent) is
compared with 16 percent for that of the heart with cardiomyopathy. Panels D
and E are M-mode echocardiograms obtained from a level nearer to the LV
base, and the beam is passed through the mitral valve. In the normal heart
(panel D), the mitral valve (MV) opens widely, very near to the septum (S); in
the cardiomyopathic heart, MV opening is reduced, due to a low stroke volume,
and it is separated from the septum by nearly 2 cm; this separation is called E
point mitral-septal separation, or EPSS.

RV: right ventricle; IVS: interventricular septum; PM: papillary muscle; PML:
posterior mitral valve leafet; AML: anterior mitral valve leaflet; Ao: aorta; LVW: left
ventricular posterior wall.

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Changes
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interventricular
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(RV) pressure or volume overload

Serial stop-frame short-axis two-dimensional echocardiographic images of the


left ventricle at the mitral chordal level with diagrams from a patient with
isolated right ventricular (RV) pressure overload due to primary pulmonary
hypertension (A) and from a patient with isolated RV volume overload due to
tricuspid valve resection (B). Whereas the left ventricular (LV) cavity maintains
a circular profile throughout the cardiac cycle in normal subjects, in RV pressure
overload, there is leftward ventricular septal (VS) shift and reversal of septal
curvature present throughout the cardiac cycle with most marked distortion of
the left ventricle at end-systole. In the patient with RV volume overload, the
septal shift and flattening of VS curvature occurs predominantly in mid to late
diastole with relative sparing of LV deformation at end-systole.

Reproduced from: Louie EK, Rich S, Levitsky, et al. Doppler echocardiographic


demonstration of the differential effects of right ventricular pressure and volume
overload on left ventricular geometry and filling. J Am Coll Cardiol 1992; 19:84.
Illustration used with the permission of Elsevier Inc. All rights reserved.

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B linesThis
on site
thoracic ultrasound
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Pleural ultrasound image depicting B lines ("comet tail artifact"), which are seen
in acute pulmonary edema and acute respiratory distress syndrome. The
presence of B lines would provide an alternate explanation for increased density
seen on the chest radiograph, other than pleural fluid.

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Hemodynamic values
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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, dyn•s/cm 5
Total systemic 1150 900-1400
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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Clinical use
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Diagnosis
Differentiation among causes of shock
Cardiogenic
Hypovolemic
Distributive (sepsis)
Obstructive (massive pulmonary embolism)

Differentiation between mechanisms of pulmonary edema


Cardiogenic
Noncardiogenic

Evaluation of pulmonary hypertension

Diagnosis of pericardial tamponade

Diagnosis of left-to-right intracardiac shunt

Diagnosis of lymphangitic spread of tumor and fat embolism (case reports based on blood aspirated from wedge position)

Unexplained dyspnea*

Therapy
Management of perioperative patient with unstable cardiac status

Management of complicated myocardial infarction

Management of patients following cardiac surgery

Management of severe preeclampsia

Guide to pharmacologic therapy


Vasopressors
Inotropes
Vasodilators (for patients with pulmonary hypertension)

Guide to nonpharmacologic therapy


Fluid management
Gastrointestinal bleed
Traumatic exsanguination
Burns
Renal failure
Sepsis
Heart failure
Decompensated cirrhosis

Ventilator management (assessment of best PEEP for O 2 delivery)

Assess response to pulmonary hypertension specific therapy

* Pulmonary artery catheters can be placed at rest or during exercise for the evaluation of patients with unexplained dyspnea.

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Hemodynamic profiles
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agreeing
Physiologic variable Preload Pump function Afterload Tissue perfusion

Pulmonary capillary wedge Mixed venous


Clinical measurement Cardiac output* Systemic vascular resistance
pressure oxyhemoglobin 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, tension ↔ (early) or ↓ (late) ↔ (early) or ↓ (late) ↑ >65%


pneumothorax

Pericardial tamponade Δ ↑ ↓ ↑ <65%

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.

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Vasopressors and inotropes


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characteristics

Range of
Usual maximum
US trade
Agent Initial dose maintenance doses used Role in therapy and selected characteristics
name
dose range in refractory
shock

Vasopressors (alpha-1 adrenergic)

Norepinephrine Levophed 8 to 12 2 to 4 35 to 100 Initial vasopressor of choice in septic, cardiogenic, and


(noradrenaline) mcg/minute (0.1 mcg/minute mcg/minute (0.5 hypovolemic shock.
to 0.15 (0.025 to 0.05 to 0.75 Wide range of doses utilized clinically.
mcg/kg/minute) mcg/kg/minute) mcg/kg/minute; Must be diluted; eg, a usual concentration is 4 mg in 250 mL of
A lower initial up to 3.3 D5W or NS (16 micrograms/mL).
dose of 5 mcg/kg/minute
mcg/minute may has been needed
be used, eg, in rarely)
older adults

Epinephrine Adrenalin 1 mcg/minute 1 to 10 10 to 35 Initial vasopressor of choice in anaphylactic shock.


(adrenaline) (0.014 mcg/minute mcg/minute (0.14 Typically an add-on agent to norepinephrine in septic shock
mcg/kg/minute) (0.014 to 0.14 to 0.5 when an additional agent is required to raise MAP to target and
mcg/kg/minute) mcg/kg/minute) occasionally an alternative first-line agent if norepinephrine is
contraindicated.
Increases heart rate; may induce tachyarrhythmias and
ischemia.
Elevates lactate concentrations during initial administration (ie,
may preclude use of lactate clearance goal); may decrease
mesenteric perfusion.
Must be diluted; eg, a usual concentration is 1 mg in 250 mL
D5W (4 micrograms/mL).

Phenylephrine Neo-Synephrine, 100 to 180 20 to 80 80 to 360 Pure alpha-adrenergic vasoconstrictor.


Vazculep mcg/minute until mcg/minute (0.25 mcg/minute (1.1 Initial vasopressor when tachyarrhythmias preclude use of
stabilized to 1.1 to 6 norepinephrine.
(alternatively, 0.5 mcg/kg/minute) mcg/kg/minute); Alternative vasopressor for patients with septic shock who: (1)
to 2 Doses >6 develop tachyarrhythmias on norepinephrine, epinephrine, or
mcg/kg/minute) mcg/kg/minute dopamine, (2) have persistent shock despite use of two or more
do not increase vasopressor/inotropic agents including vasopressin (salvage
efficacy according therapy), or (3) high cardiac output with persistent
to product hypotension.
information in the May decrease stroke volume and cardiac output in patients with
United States cardiac dysfunction.
May be given as bolus dose of 50 to100 micrograms to support
blood pressure during rapid sequence intubation.
Must be diluted; eg, a usual concentration is 10 mg in 250 mL
D5W or NS (40 micrograms/mL).

Dopamine Inotropin 2 to 5 5 to 20 20 to >50 An alternative to norepinephrine in septic shock in highly


mcg/kg/minute mcg/kg/minute mcg/kg/minute selected patients (eg, with compromised systolic function or
absolute or relative bradycardia and a low risk of
tachyarrhythmias).
More adverse effects (eg, tachycardia, arrhythmias particularly
at doses ≥20 mcg/kg/minute) and less effective than
norepinephrine for reversing hypotension in septic shock.
Lower doses (eg, 1 to 3 mcg/kg/minute) should not be used for
renal protective effect and can cause hypotension during
weaning.
Must be diluted; eg, a usual concentration is 400 mg in 250 mL
D5W (1.6 mg/mL); use of a commercially available pre-diluted
solution is preferred.

Antidiuretic hormone

Vasopressin Pitressin, 0.03 units per 0.03 to 0.04 units 0.04 to 0.07 Add-on to norepinephrine to raise blood pressure to target MAP
(arginine- Vasostrict minute per minute (not units/minute; or decrease norepinephrine requirement. Not recommended as
vasopressin) (alternatively 0.01 titrated) Doses >0.04 a replacement for a first-line vasopressor.
to 0.03 units/minute can Pure vasoconstrictor; may decrease stroke volume and cardiac
units/minute cause cardiac output in myocardial dysfunction or precipitate ischemia in
initially) ischemia and coronary artery disease.
should be Must be diluted; eg, a usual concentration is 25 units in 250 mL
reserved for D5W or NS (0.1 units/mL).
salvage therapy

Inotrope (beta 1 adrenergic)

Dobutamine Dobutrex 0.5 to 1 2 to 20 20 to 40 Initial agent of choice in cardiogenic shock with low cardiac
mcg/kg/minute mcg/kg/minute mcg/kg/minute; output and maintained blood pressure.
(alternatively, 2.5 Doses >20 Add-on to norepinephrine for cardiac output augmentation in
mcg/kg/minute in mcg/kg/minute septic shock with myocardial dysfunction (eg, in elevated left
more severe are not ventricular filling pressures and adequate MAP) or ongoing

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cardiac recommended in hypoperfusion despite adequate intravascular volume and use of
decompensation)
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vasopressor agents. Continue or find out more.
should be
Increases cardiac contractility and rate; may cause hypotension
reserved for
and tachyarrhythmias.
salvage therapy
Must be diluted; a usual concentration is 250 mg in 500 mL
D5W or NS (0.5 mg/mL); use of a commercially available pre-
diluted solution is preferred.

Inotrope (nonadrenergic, PDE 3 inhibitor)

Milrinone Primacor Optional loading 0.125 to 0.75 Alternative for short-term cardiac output augmentation to
dose: 50 mcg/kg mcg/kg/minute maintain organ perfusion in cardiogenic shock refractory to
over 10 minutes other agents.
(usually not Increases cardiac contractility and modestly increases heart rate
given) at high doses; may cause peripheral vasodilation, hypotension,
and/or ventricular arrhythmia.
Renally cleared; dose adjustment in renal impairment needed.
Must be diluted; eg, a usual concentration is 40 mg in 200 mL
D5W (200 micrograms/mL); use of a commercially available
pre-diluted solution is preferred.

All doses shown are for intravenous (IV) administration in adult patients. The initial doses shown in this table may differ from those recommended in immediate
post-cardiac arrest management (ie, advanced cardiac life support). For details, refer to the UpToDate topic review of post-cardiac arrest management in adults,
section on hemodynamic considerations.
Vasopressors can cause life-threatening hypotension and hypertension, dysrhythmias, and myocardial ischemia. They should be administered by use of an infusion
pump adjusted by clinicians trained and experienced in dose titration of intravenous vasopressors using continuous noninvasive electronic monitoring of blood
pressure, heart rate, rhythm, and function. Hypovolemia should be corrected prior to the institution of vasopressor therapy. Reduce infusion rate gradually; avoid
sudden discontinuation.
Vasopressors can cause severe local tissue ischemia; central line administration is preferred. When a patient does not have a central venous catheter, vasopressors
can be temporarily administered in a low concentration through an appropriately positioned peripheral venous catheter (ie, in a large vein) until a central venous
catheter is inserted. The examples of concentrations shown in this table are useful for peripheral (short-term) or central line administration. Closely monitor
catheter site throughout infusion to avoid extravasation injury. In event of extravasation, prompt local infiltration of an antidote (eg, phentolamine) may be useful
for limiting tissue ischemia. Stop infusion and refer to extravasation management protocol.
Vasopressor infusions are high-risk medications requiring caution to prevent a medication error and patient harm. To reduce the risk of making a medication error,
we suggest that centers have available protocols that include steps on how to prepare and administer vasopressor infusions using a limited number of standardized
concentrations. Examples of concentrations and other detail are based on recommendations used at experienced centers; protocols can vary by institution.

D5W: 5% dextrose water; MAP: mean arterial pressure; NS: 0.9% saline.

Prepared with data from:


1. Rhodes A, Evans LE, Alhazzani W, et al. Surviving sepsis campaign: International guidelines for management of sepsis and septic shock: 2016. Crit Care Med 2017;
45:486.
2. Hollenberg SM. Vasoactive drugs in circulatory shock. Am J Respir Crit Care Med 2011; 183:847.
3. Lexicomp Online. Copyright © 1978-2018 Lexicomp, Inc. All Rights Reserved.

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Pressure
Thistracings
site uses in constrictive
cookies. pericarditis
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Abnormal right atrial and ventricular pressure waveforms in a patient with


constrictive pericarditis. Note the elevation and equalization of end-diastolic
pressures, with a characteristic "dip and plateau" (or "square-root sign"). The
steep Y descent reflects rapid early ventricular filling as right atrial emptying is
rapid and unimpeded. The nadir of the Y descent reflects abrupt cessation of
early diastolic ventricular filling. A similar pattern may be seen in cardiac
tamponade or restrictive cardiomyopathy.

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Contributor
This Disclosures
site uses cookies. By continuing to browse this site you are agreeing to our use of cookies. Continue or find out more.
David F Gaieski, MD Nothing to disclose Mark E Mikkelsen, MD, MSCE Nothing to disclose Polly E Parsons, MD Nothing to disclose Robert S
Hockberger, MD, FACEP 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.

Conflict of interest policy

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