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

Contributor Disclosures

All topics are updated as new evidence becomes available and our peer review process is
complete.
Literature review current through: Dec 2018. | This topic last updated: Oct 17, 2018.

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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).

● Tachycardia – Tachycardia is an early compensatory mechanism in patients with

shock. It can be isolated or occur in association with hypotension. Importantly,
compared with older patients, younger patients develop severe and persistent
tachycardia before becoming hypotensive late in the course of 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 access is not available.
Related, evidence suggests that the use of peripheral intravenous vasoactive medications
can be used safely for hours to days, obviating the need for central venous catheterization
in a number of patients [7].

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".)

This population typically requires large volumes of blood products, and vasopressors are
avoided. Adequate peripheral access (two 14 to 18 gauge IVs) and/or a large-bore, single-
lumen central cordis are essential. A type and crossmatch, a complete blood count, and
coagulation studies should be obtained in all patients with suspected hemorrhage.

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 two antipseudomonal agents (eg, fluoroquinolone,
aminoglycoside, piperacillin-tazobactam, cefepime, ceftazadime). 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 "Management and prognosis of 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 findings that should raise the
suspicion of shock and prompt immediate treatment with intravenous fluids and
further evaluation with laboratory studies and relevant imaging. (See 'When to suspect
shock' above.)

● 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 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, bicarbonate,
base deficit, and serum lactate, particularly when obtaining an ABG is delayed.

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 life-saving.

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:

• Lung and pleural space – The absence of lung sliding (movie 5) supports the
presence of a pneumothorax. (See "Bedside pleural ultrasonography: Equipment,
technique, and the identification of pleural effusion and pneumothorax".)

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
"Bedside pleural ultrasonography: Equipment, technique, and the identification of
pleural effusion and pneumothorax".)

A pleural effusion (anechoic stripe or septations) may support empyema or

hemothorax and guide thoracentesis (movie 6). (See "Bedside pleural
ultrasonography: Equipment, technique, and the identification of pleural effusion
and pneumothorax".)

• 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 "Bedside pleural ultrasonography: Equipment, technique, and
the identification of pleural effusion and pneumothorax".)

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, data from
one randomized trial and several small observational studies have been published 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 randomized trial of 273 patients with undifferentiated hypotension, more than half
of whom had occult sepsis, compared with standard of care, POC ultrasonography did
not alter the 30 day survival, CT scanning rate, inotrope or intravenous fluid use, or
length of stay [34]. However, this study stopped recruitment early due to slow accrual,
and had a large number of exclusion criteria which may have limited the impact of POC
ultrasonography.    

● 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.

● In a retrospective study of 411 patients who had chest pain, dyspnea, or hypotension, a
moderate agreement was reported between POC ultrasonography and comprehensive
echocardiography for the detection of right ventricle strain (RVS) [28]. The sensitivity
and specificity of ultrasound for RVS were 26 and 98 percent, respectively.

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 "Bedside pleural ultrasonography: Equipment,
technique, and the identification of pleural effusion and pneumothorax" 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 [35-37]. 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 [38]. 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 [39]. (See "Treatment of severe 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 severe hypovolemia or
hypovolemic shock in adults".)

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
[40]. 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 [41]. 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'.)
DIAGNOSIS — A diagnosis of shock is based upon a constellation of clinical, biochemical,
and hemodynamic features. Most patients have hypotension and/or clinical signs of tissue
hypoperfusion (eg, cold, clammy, mottled skin; oliguria [<0.5 mL/kg/hour]; altered mental
status) and hyperlactatemia (>1.5 mmol/L). Noninvasive imaging and/or hemodynamic
indices of low cardiac output, systemic vascular resistance, and/or mixed venous
oxyhemoglobin 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 "Invasive group A streptococcal infection and 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
[42].

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 "Clinical manifestations and
diagnosis of 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")

● Pulmonary artery catheterization findings – On PAC, typically, a high pcwp (>15

mmHg) distinguishes cardiogenic shock from other forms of shock, particularly in the
setting of a low CO (CI <2.8 L/min/m2), and a high SVR (>1400 dynes per second/cm5)
(table 10). PAC tracings can also be helpful in diagnosing certain valvular defects (eg,
large v-waves of severe tricuspid valve insufficiency). SvO2 is typically <65 percent.

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".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials,

“The Basics” and “Beyond the Basics.” The Basics patient education pieces are written in
plain language, at the 5th to 6th grade reading level, and they answer the four or five key
questions a patient might have about a given condition. These articles are best for patients
who want a general overview and who prefer short, easy-to-read materials. Beyond the
Basics patient education pieces are longer, more sophisticated, and more detailed. These
articles are written at the 10th to 12th grade reading level and are best for patients who want
in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to
print or e-mail these topics to your patients. (You can also locate patient education articles
on a variety of subjects by searching on “patient info” and the keyword(s) of interest.)

● Basics topic (see "Patient education: Shock (The Basics)")

SUMMARY AND RECOMMENDATIONS

● Shock is defined as a state of cellular and tissue hypoxia due to reduced oxygen
delivery and/or increased oxygen consumption or inadequate oxygen utilization. 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.)

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