Shock Uptodate

Evaluation of and initial approach to the adult patient with undifferentiat... https://www.uptodate.com/contents/evaluation-of-and-initial-approach-to...
Official reprint from UpToDate®

www.uptodate.com ©2020 UpToDate, Inc. and/or its affiliates. All Rights Reserved.
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: Feb 2020. | This topic last updated: Sep 13, 2019.
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
1 de 47 20-03-2020 16:18
● 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)
2 de 47 20-03-2020 16:18
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
3 de 47 20-03-2020 16:18
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. (See "Placement and management of thoracostomy tubes and catheters in adults and
children", section on 'Tension pneumothorax' and "Placement and management of thoracostomy tubes and catheters in adults and children",
section on 'Needle thoracostomy' and "Prehospital care of the adult trauma patient", section on 'Needle chest decompression'.)
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 "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 "Acute myocardial infarction: Mechanical complications", 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 identify blood
in the abdomen (also known as focused assessment with sonography for trauma [FAST]). A positive study indicates the need for surgical
exploration to identify and control the source of hemorrhage (algorithm 2 and table 3). (See "Emergency ultrasound in adults with
abdominal and thoracic trauma" and "Initial evaluation and management of penetrating thoracic trauma in adults" and "Initial evaluation
and management of blunt thoracic trauma in adults" and "Overview of damage control surgery and resuscitation in patients sustaining
severe injury".)
● Nontraumatic – Patients suspected of having a ruptured aorta (eg, hypotension, abdominal, chest or back pain, known history of
aneurysm or dissection) may be too unstable to safely obtain a contrast-enhanced computed tomography (CT). Other options for
4 de 47 20-03-2020 16:18
diagnosis prior to management include transesophageal echocardiography (thoracic aorta) and abdominal ultrasound (abdominal aorta),
to identify perioaortic hematoma or aneurysmal disease. (See "Management of symptomatic (non-ruptured) and ruptured abdominal aortic
aneurysm" and "Overview of acute aortic dissection and other acute aortic syndromes", section on 'Periaortic hematoma'.)
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 "Overview of the management of patients with variceal bleeding".)
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 [limited
supply]) 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, ceftazidime). 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 descending thoracic aortic dissection often present with hypertension and tearing
chest or back pain. However, patients with ascending aortic dissection are more likely to present with hypotension and shock associated with
acute aortic insufficiency, pericardial tamponade, or myocardial infarction. Hemodynamically unstable patients with suspected aortic dissection
transesophageal echocardiography, if available or contrast-enhanced CT to evaluate the ascending aorta and aortic valve (table 6). Ascending
aortic dissection is a cardiac surgical emergency and immediate consultation with a cardiac surgeon should be obtained. (See "Clinical
features and diagnosis of acute aortic dissection" and "Management of acute aortic dissection", section on 'Ascending (type A) aortic
dissection'.)
5 de 47 20-03-2020 16:18
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 "Approach to thrombolytic (fibrinolytic) therapy in
acute pulmonary embolism: Patient selection and administration".)
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
6 de 47 20-03-2020 16:18
● 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
7 de 47 20-03-2020 16:18
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
8 de 47 20-03-2020 16:18
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)
9 de 47 20-03-2020 16:18
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. A meta-analysis of nine studies that compared
FoCUS-assisted clinical assessment with clinical assessment alone reported that while FoCUS examination of the left ventricle and mitral
valve was more sensitive than clinical assessment alone (84 versus 43 percent), its specificity was similar (89 versus 81 percent) [24].
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 [14,25-34]. 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 [35].
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 [26]. 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
[27].
● 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) [28]. 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) [29]. 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 [36-38]. 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
10 de 47 20-03-2020 16:18
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 [39]. 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 [40]. (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",
section on 'Fluids to avoid: hyperoncotic starch (colloid)'.)
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 [41]. 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,
11 de 47 20-03-2020 16:18
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 [42]. 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 "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' and "Prognosis and treatment of
cardiogenic shock complicating acute myocardial infarction", section on 'Vasopressors and inotropes'.)
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
12 de 47 20-03-2020 16:18
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 [43].
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 diagnosis and evaluation of 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" and "Endovascular methods for aortic control in trauma", section on
'Resuscitative aortic occlusion')
- 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")
13 de 47 20-03-2020 16:18
• 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 and catheters in adults and children", section on
'Tension pneumothorax' and "Pneumothorax in adults: Epidemiology and etiology")
• 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 bedside echocardiography as a monitor for therapeutic intervention in critically ill adults".)
14 de 47 20-03-2020 16:18
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.
15 de 47 20-03-2020 16:18
● 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.
Topic 98976 Version 24.0
16 de 47 20-03-2020 16:18
GRAPHICS
Classification of shock
Septic Gram positive (Pneumococcus, Staphylococcus, Streptococcus, Enterococcus, Listeria)

Gram negative (Klebsiella, Pseudomonas, Escherichia, Haemophilus, Legionella, 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), neuraxial 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.
Graphic 99574 Version 6.0
17 de 47 20-03-2020 16:18
Approach to the patient with undifferentiated hypotension or

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.
18 de 47 20-03-2020 16:18
Approach to the patient with undifferentiated hypotension or shock: Ongoing resuscitation
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.
19 de 47 20-03-2020 16:18
Rapid overview: Emergency management of anaphylaxis in adults
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, or 2 to 3 puffs by metered dose inhaler. Repeat, as
needed.
Adjunctive therapies:
H1 antihistamine*: Consider giving cetirizine 10 mg IV or 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.
20 de 47 20-03-2020 16:18
Traumatic shock: Initial management
IV: intravenous; IO: intraosseous; FAST: Focused Assessment with Sonography in

Trauma; CXR: chest x-ray; C-spine: cervical spine.
21 de 47 20-03-2020 16:18
Differential diagnosis of shock in trauma
I. Low CVP
A. Hypovolemia
1. Hemorrhage
a. External (compressible)
i. Lacerations
ii. Co ntusions
iii. Fractures (partly compressible)
b. Internal (noncompressible)
i. Intrathoracic
ii. Intraperito neal
iii. Retroperitoneal (partly co mpressible)
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.
22 de 47 20-03-2020 16:18
Acute management of severe upper gastrointestinal bleeding
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
Stratificatio n of the risk for rebleeding
4. Therapeutic endoscopy
Control o f active bleeding or high-risk lesions
Minimization of treatment-related complications
Treatment of persistent or recurrent bleeding
23 de 47 20-03-2020 16:18
Evaluation of patients presenting with hematochezia (excluding those with minimal rectal
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.
† If the deep small bowel enteroscopy was incomplete, a video capsule endoscopy study should be obtained, followed by CT or MR
24 de 47 20-03-2020 16:18
enterography if the capsule endoscopy is negative.
25 de 47 20-03-2020 16:18
Evaluation of suspected upper gastrointestinal bleeding
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 upper endoscopy is negative. Colonoscopy is the next step in the
evaluation of patients with melena.
§ 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
26 de 47 20-03-2020 16:18
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.
‡ 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.
27 de 47 20-03-2020 16:18
Adult tachycardia with a pulse algorithm
IV: intravenous; ECG: electrocardiogram; NS: normal saline; CHF: congestive heart failure; VT: ventricular tachycardia.
Reprinted with permission. Web-based Integrated 2010, 2015, & 2017 American Heart Association Guidelines for Cardiopulmonary Resuscitation and
Emergency Cardiovascular Care – Part 7: Adult Advanced Cardiovascular Life Support. Copyright © 2015 American Heart Association, Inc.
28 de 47 20-03-2020 16:18
Adult bradycardia with a pulse algorithm
IV: intravenous; ECG: electrocardiogram.
Reprinted with permission. Web-based Integrated 2010, 2015, & 2017 American Heart Association Guidelines for Cardiopulmonary Resuscitation
and Emergency Cardiovascular Care – Part 7: Adult Advanced Cardiovascular Life Support. Copyright © 2015 American Heart Association, Inc.
29 de 47 20-03-2020 16:18
Treatment options for cardiogenic shock due to left ventricular dysfunction
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 po ssible thro mbolytic therapy
Newer devices
Left ventricular or biventricular assist devices
Percutaneous cardiopulmonary bypass
Reperfusion/revascularization
Primary percutaneous coronary intervention
Coro nary artery bypass graft
Thrombolytic therapy for patients not receiving PCI in a timely manner
30 de 47 20-03-2020 16:18
Acute aortic dissection: Rapid overview
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, progression, 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, diasto lic cardiac murmur, tampo nade, syncope or stroke
(persistent or transient ¶; right hemispheric stro ke 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 o f 0.5 to 2 mg/minute IV). If beta blockers are not tolerated, alternatives are
verapamil or diltiazem.
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)
sho uld not be used witho ut 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 o f 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.
31 de 47 20-03-2020 16:18
Treatment algorithm for hemodynamically unstable

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.
32 de 47 20-03-2020 16:18
Treatment of acute adrenal insufficiency (adrenal crisis) in adults
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 laboratory results.
3. Infuse 2 to 3 liters of isotonic saline or 5% 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 hydrocortisone (100 mg intravenous bolus), followed by 50 mg intravenously every 6 hours (or 200 mg/24 hours as a continuous intravenous infusion for the first 24
hours). If hydrocortisone is unavailable, alternatives include prednisolone, prednisone, and dexamethasone.
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 1 to 3 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.
33 de 47 20-03-2020 16:18
Long axis echocardiogram in dilated cardiomyopathy
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.
34 de 47 20-03-2020 16:18
Echocardiogram of a normal heart and a case of dilated

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.
35 de 47 20-03-2020 16:18
Dilated cardiomyopathy
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.
36 de 47 20-03-2020 16:18
M-mode echocardiogram in cardiomyopathy
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.
37 de 47 20-03-2020 16:18
M-mode echocardiogram of cardiomyopathy compared w

ith normal
Normal M-modes of the minor axis of the left ventricle (LV) 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 normal
LV end-diastolic dimension (LVEDD) is 5.2 cm compared with 6.3 cm in the
patient with cardiomyopathy; the LV end-systolic dimensions (LVESD) 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 inferolateral wall; PW: left ventricular posterior wall (also known as
inferolateral wall)
38 de 47 20-03-2020 16:18
Changes in interventricular septum with right ventricular

(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.
39 de 47 20-03-2020 16:18
B lines on thoracic ultrasound
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.
40 de 47 20-03-2020 16:18
Hemodynamic values of normal recumbent adults
Mean Range
Cardiac index (L/min/m 2 ) 3.4 2.8 to 4.2
Stroke volume index (mL/m 2 /beat) 47 30 to 65
Arteriovenous oxygen difference (mL per liter of blood) 38 30 to 48
Arterial saturation (%) 98 94 to 100
Pressure* (mmHg)
Left ventricle
Systolic 130 90 to 140
End-diastolic 7 4 to 12
Left atrium
Maximum 13 6 to 20
Minimum 3 –2 to +9
Mean 7 4 to 12
Pulmonary artery wedge ("PC")
Maximum 16 9 to 23
Minimum 6 1 to 12
Mean 9 6 to 15
Pulmonary artery
Diastolic 10 5 to 16
Mean 16 10 to 22
Right ventricle
End-diastolic 4 0 to 8
Right atrium
Maximum 7 2 to 14
Minimum 2 –2 to +6
Mean 4 –1 to +8
Venae cavae
Maximum 7 2 to 14
Minimum 5 0 to 8
Mean 6 1 to 10
End-diastolic volume index
Left ventricular (mL/m 2) 70 50 to 90
Resistance - Wood units (dyn×s/cm 5 )
Total systemic 14.4 (1150) 11.3 to 17.5 (900 to 1400)
Systemic arteriolar 10.6 (850) 7.5 to 11.3 (600 to 900)
Total pulmonary 2.5 (200) 1.9 to 3.1 (150 to 250)
Pulmonary arteriolar 0.9 (70) 0.6 to 1.5 (45 to 120)
* Baseline for pressure measurements one-half of anteroposterior chest diameter. 1 mmHg = 133.332 Pascal (PA) = 0.133 kPa.
Reproduced with permission from: Hurst JW, Rackley CE, Sonnenblick EH, Wenger NK. The Heart: Arteries and veins. 7th ed. McGraw-Hill, Inc, New York 1990. Copyright © 1990
McGraw-Hill Companies, Inc.
41 de 47 20-03-2020 16:18
Clinical use of the pulmonary artery catheter
Diagnosis
Differentiation among causes of shock
Cardio genic
Hypovolemic
Distributive (sepsis)
Obstructive (massive pulmonary embolism)
Differentiation between mechanisms of pulmonary edema
Cardio genic
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
Vaso pressors
Inotropes
Vaso dilators (for patients with pulmo nary hypertensio n)
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.
42 de 47 20-03-2020 16:18
Hemodynamic profiles of shock on pulmonary artery catheter in adults
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.
43 de 47 20-03-2020 16:18
Vasopressors and inotropes in treatment of acute hypotensive states and shock: Adult dose and selected characteristics
Range of
Usual maximum
United States
Agent Initial dose maintenance doses used in Role in therapy and selected characteristics
trade name
dose range refractory
shock
Vasopressors (alpha-1 adrenergic)
Norepinephrine Levophed 8 to 12 2 to 4 mcg/minute 35 to 100 Initial vasopressor of choice in septic, cardiogenic, and
(noradrenaline) mcg/minute (0.1 (0.025 to 0.05 mcg/minute (0.5 hypovolemic shock.
to 0.15 mcg/kg mcg/kg/minute) to 0.75 mcg/kg Wide range of doses utilized clinically.
/minute) /minute; up to 3.3 Must be diluted; eg, a usual concentration is 4 mg in 250 mL of
A lower initial mcg/kg/minute D5W or NS (16 micrograms/mL).
dose of 5 has been needed
mcg/minute may rarely)
be used, eg, in
older adults
Epinephrine Adrenalin 1 mcg/minute 1 to 10 10 to 35 Initial vasopressor of choice in anaphylactic shock.

(adrenaline) (0.014 mcg/kg mcg/minute mcg/minute (0.14 Typically an add-on agent to norepinephrine in septic shock
/minute) (0.014 to 0.14 to 0.5 mcg/kg when an additional agent is required to raise MAP to target and
mcg/kg/minute) /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 mcg/kg to 6 mcg/kg norepinephrine.
(alternatively, 0.5 /minute) /minute); Alternative vasopressor for patients with septic shock who: (1)
to 2 mcg/kg Doses >6 mcg/kg develop tachyarrhythmias on norepinephrine, epinephrine, or
/minute) /minute do not dopamine, (2) have persistent shock despite use of two or more
increase efficacy vasopressor/inotropic agents including vasopressin (salvage
according to therapy), or (3) high cardiac output with persistent hypotension.
product May decrease stroke volume and cardiac output in patients with
information in the cardiac dysfunction.
United States May be given as bolus dose of 50 to 100 mcg to support blood
pressure during rapid sequence intubation.
D5W or NS (40 mcg/mL).
Dopamine Inotropin 2 to 5 mcg/kg 5 to 20 mcg/kg 20 to >50 mcg/kg An alternative to norepinephrine in septic shock in highly
/minute /minute /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.
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 a
vasopressin) (alternatively 0.01 titrated) Doses >0.04 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 mcg/kg 2 to 20 mcg/kg 20 to 40 mcg/kg Initial agent of choice in cardiogenic shock with low cardiac
/minute /minute /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
cardiac recommended in hypoperfusion despite adequate intravascular volume and use of
decompensation) heart failure and vasopressor agents.
should be Increases cardiac contractility and rate; may cause hypotension
44 de 47 20-03-2020 16:18
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 other
over 10 minutes 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.
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 © 1978-2020 Lexicomp, Inc. All Rights Reserved.
45 de 47 20-03-2020 16:18
Pressure tracings in constrictive pericarditis
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.
46 de 47 20-03-2020 16:18
47 de 47 20-03-2020 16:18

Shock Uptodate

Uploaded by

Document Information

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Shock Uptodate

Uploaded by

Copyright:

Available Formats

Evaluation of and initial approach to the adult patient with undifferentiat... https://www.uptodate.com/contents/evaluation-of-and-initial-approach-to...

Official reprint from UpToDate®

Evaluation of and initial approach to the adult patient with undifferentiated

DEFINITION AND CLASSIFICATION

● Hypovolemic (eg, hemorrhagic and nonhemorrhagic fluid losses)

WHEN TO SUSPECT SHOCK

● Abnormal mental status

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

strategy may be necessary. (See 'Initial diagnostic evaluation' below.)

Initial diagnostic evaluation

Typically, we perform the following:

● Complete blood count and differential

The rationale for obtaining these tests is described below:

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

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

• Anaphylaxis (see "Anaphylaxis: Emergency treatment")

• Myxedema coma (see "Myxedema coma")

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

• Hemorrhage due to:

• Cardiac tamponade (see "Cardiac tamponade")

• Constrictive pericarditis (see "Constrictive pericarditis")

• Restrictive cardiomyopathy (see "Idiopathic restrictive cardiomyopathy")

REVERSE THE ETIOLOGY

SOCIETY GUIDELINE LINKS

INFORMATION FOR PATIENTS

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

SUMMARY AND RECOMMENDATIONS

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

Topic 98976 Version 24.0

Septic Gram positive (Pneumococcus, Staphylococcus, Streptococcus, Enterococcus, Listeria)

Endocrine (eg, adrenal insufficiency, thyrotoxicosis, myxedema coma)

PEEP: positive end-expiratory pressure.

Graphic 99574 Version 6.0

Approach to the patient with undifferentiated hypotension or

Graphic 99357 Version 2.0

Approach to the patient with undifferentiated hypotension or shock: Ongoing resuscitation

Graphic 100420 Version 1.0

Rapid overview: Emergency management of anaphylaxis in adults

Diagnosis is made clinically:

Promptly and simultaneously, give:

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.

H2 antihistamine*: Consider giving ranitidine 50 mg IV.

Glucocorticoid*: Consider giving methylprednisolone 125 mg IV.

Treatment of refractory symptoms:

IM: intramuscular; IV: intravenous.

Graphic 58346 Version 31.0

Traumatic shock: Initial management

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

Graphic 76631 Version 4.0

Differential diagnosis of shock in trauma

iii. Fractures (partly compressible)

ii. Intraperito neal

iii. Retroperitoneal (partly co mpressible)

c. Fractures (partly compressible)

2. Third spacing (eg, burns)

B. Neurogenic (high cervical cord injury)

II. High CVP

III. Other diagnoses to consider

B. Myocardial infarction (severe)

C. Diaphragmatic rupture with herniation

D. Fat or air embolism

CVP: central venous pressure.

Graphic 63698 Version 3.0