Circulatory Shock - Review Article
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review article
T h e n e w e ng l a n d j o u r na l o f m e dic i n e
n engl j med 369;18 nejm.org october 31, 20131726
critical care medicine
Simon R. Finfer, M.D., and Jean-Louis Vincent, M.D., Ph.D., Editors
Circulatory Shock
Jean-Louis Vincent, M.D., Ph.D., and Daniel De Backer, M.D., Ph.D.
From the Department of Intensive Care,
Erasme Hospital, Université Libre de Brux-
elles, Brussels. Address reprint requests to
Dr. Vincent at the Department of Intensive
Care, Erasme University Hospital, Rte. de
Lennik 808, B-1070 Brussels, Belgium, or
at jlvincen@ulb.ac.be.
N Engl J Med 2013;369:1726-34.
DOI: 10.1056/NEJMra1208943
Copyright © 2013 Massachusetts Medical Society.
Shock is the clinical expression of circulatory failure that
results in inadequate cellular oxygen utilization. Shock is a common condi-
tion in critical care, affecting about one third of patients in the intensive care
unit (ICU).1 A diagnosis of shock is based on clinical, hemodynamic, and bio-
chemical signs, which can broadly be summarized into three components. First,
systemic arterial hypotension is usually present, but the magnitude of the hypoten-
sion may be only moderate, especially in patients with chronic hypertension. Typi-
cally, in adults, the systolic arterial pressure is less than 90 mm Hg or the mean
arterial pressure is less than 70 mm Hg, with associated tachycardia. Second, there
are clinical signs of tissue hypoperfusion, which are apparent through the three
“windows” of the body2: cutaneous (skin that is cold and clammy, with vasocon-
striction and cyanosis, findings that are most evident in low-flow states), renal
(urine output of <0.5 ml per kilogram of body weight per hour), and neurologic
(altered mental state, which typically includes obtundation, disorientation, and
confusion). Third, hyperlactatemia is typically present, indicating abnormal cellular
oxygen metabolism. The normal blood lactate level is approximately 1 mmol per liter,
but the level is increased (>1.5 mmol per liter) in acute circulatory failure.
Pathoph ysiol o gic a l Mech a nisms
Shock results from four potential, and not necessarily exclusive, pathophysiological
mechanisms3: hypovolemia (from internal or external fluid loss), cardiogenic fac-
tors (e.g., acute myocardial infarction, end-stage cardiomyopathy, advanced valvular
heart disease, myocarditis, or cardiac arrhythmias), obstruction (e.g., pulmonary
embolism, cardiac tamponade, or tension pneumothorax), or distributive factors
(e.g., severe sepsis or anaphylaxis from the release of inflammatory mediators)
(Fig. 1A and the interactive graphic, available at NEJM.org). The first three mech-
anisms are characterized by low cardiac output and, hence, inadequate oxygen trans-
port. In distributive shock, the main deficit lies in the periphery, with decreased
systemic vascular resistance and altered oxygen extraction. Typically, in such cases
cardiac output is high, although it may be low as a result of associated myocardial
depression. Patients with acute circulatory failure often have a combination of these
mechanisms. For example, a patient with distributive shock from severe pancreatitis,
anaphylaxis, or sepsis may also have hypovolemia and cardiogenic shock from
myocardial depression.
Differ en ti a l Di agnosis
Septic shock, a form of distributive shock, is the most common form of shock
among patients in the ICU, followed by cardiogenic and hypovolemic shock;
obstructive shock is relatively rare (Fig. 1B and 1C). In a trial involving more than
An interactive
graphic showing
initial assessment of
shock is available
at NEJM.orgThe New England Journal of MedicineDownloaded from nejm.org by Marcos Nunez on November 5, 2013. For personal use only. No other uses without permission.Copyright © 2013 Massachusetts Medical Society. All rights reserved.
T h e n e w e ng l a n d j o u r na l o f m e dic i n e
n engl j med 369;18 nejm.org october 31, 20131726
critical care medicine
Simon R. Finfer, M.D., and Jean-Louis Vincent, M.D., Ph.D., Editors
Circulatory Shock
Jean-Louis Vincent, M.D., Ph.D., and Daniel De Backer, M.D., Ph.D.
From the Department of Intensive Care,
Erasme Hospital, Université Libre de Brux-
elles, Brussels. Address reprint requests to
Dr. Vincent at the Department of Intensive
Care, Erasme University Hospital, Rte. de
Lennik 808, B-1070 Brussels, Belgium, or
at jlvincen@ulb.ac.be.
N Engl J Med 2013;369:1726-34.
DOI: 10.1056/NEJMra1208943
Copyright © 2013 Massachusetts Medical Society.
Shock is the clinical expression of circulatory failure that
results in inadequate cellular oxygen utilization. Shock is a common condi-
tion in critical care, affecting about one third of patients in the intensive care
unit (ICU).1 A diagnosis of shock is based on clinical, hemodynamic, and bio-
chemical signs, which can broadly be summarized into three components. First,
systemic arterial hypotension is usually present, but the magnitude of the hypoten-
sion may be only moderate, especially in patients with chronic hypertension. Typi-
cally, in adults, the systolic arterial pressure is less than 90 mm Hg or the mean
arterial pressure is less than 70 mm Hg, with associated tachycardia. Second, there
are clinical signs of tissue hypoperfusion, which are apparent through the three
“windows” of the body2: cutaneous (skin that is cold and clammy, with vasocon-
striction and cyanosis, findings that are most evident in low-flow states), renal
(urine output of <0.5 ml per kilogram of body weight per hour), and neurologic
(altered mental state, which typically includes obtundation, disorientation, and
confusion). Third, hyperlactatemia is typically present, indicating abnormal cellular
oxygen metabolism. The normal blood lactate level is approximately 1 mmol per liter,
but the level is increased (>1.5 mmol per liter) in acute circulatory failure.
Pathoph ysiol o gic a l Mech a nisms
Shock results from four potential, and not necessarily exclusive, pathophysiological
mechanisms3: hypovolemia (from internal or external fluid loss), cardiogenic fac-
tors (e.g., acute myocardial infarction, end-stage cardiomyopathy, advanced valvular
heart disease, myocarditis, or cardiac arrhythmias), obstruction (e.g., pulmonary
embolism, cardiac tamponade, or tension pneumothorax), or distributive factors
(e.g., severe sepsis or anaphylaxis from the release of inflammatory mediators)
(Fig. 1A and the interactive graphic, available at NEJM.org). The first three mech-
anisms are characterized by low cardiac output and, hence, inadequate oxygen trans-
port. In distributive shock, the main deficit lies in the periphery, with decreased
systemic vascular resistance and altered oxygen extraction. Typically, in such cases
cardiac output is high, although it may be low as a result of associated myocardial
depression. Patients with acute circulatory failure often have a combination of these
mechanisms. For example, a patient with distributive shock from severe pancreatitis,
anaphylaxis, or sepsis may also have hypovolemia and cardiogenic shock from
myocardial depression.
Differ en ti a l Di agnosis
Septic shock, a form of distributive shock, is the most common form of shock
among patients in the ICU, followed by cardiogenic and hypovolemic shock;
obstructive shock is relatively rare (Fig. 1B and 1C). In a trial involving more than
An interactive
graphic showing
initial assessment of
shock is available
at NEJM.orgThe New England Journal of MedicineDownloaded from nejm.org by Marcos Nunez on November 5, 2013. For personal use only. No other uses without permission.Copyright © 2013 Massachusetts Medical Society. All rights reserved.
Critical Care Medicine
n engl j med 369;18 nejm.org october 31, 20131727
1600 patients with shock who were randomly as-
signed to receive either dopamine or norepineph-
rine, septic shock occurred in 62% of the patients,
cardiogenic shock in 16%, hypovolemic shock in
16%, other types of distributive shock in 4%, and
obstructive shock in 2%.4
The type and cause of shock may be obvious
from the medical history, physical examination,
or clinical investigations. For example, shock
after traumatic injury is likely to be hypovolemic
(due to blood loss), but cardiogenic shock or
distributive shock may also occur, alone or in
combination, caused by such conditions as car-
diac tamponade or spinal cord injury. A full clini-
cal examination should include assessment of
skin color and temperature, jugular venous dis-
tention, and peripheral edema. The diagnosis
can be refined with point-of-care echocardio-
graphic evaluation, which includes assessment
for pericardial effusion, measurement of left and
right ventricular size and function, assessment for
respiratory variations in vena cava dimensions,
and calculation of the aortic velocity–time inte-
gral, a measure of stroke volume. Whenever pos-
sible, focused echocardiography should be per-
formed as soon as possible in any patient
presenting with shock (Fig. 1A).5,6
Ini ti a l A pproach
t o the Patien t in Sho ck
Early, adequate hemodynamic support of patients
in shock is crucial to prevent worsening organ
dysfunction and failure. Resuscitation should be
started even while investigation of the cause is
ongoing. Once identified, the cause must be cor-
rected rapidly (e.g., control of bleeding, percuta-
neous coronary intervention for coronary syn-
dromes, thrombolysis or embolectomy for massive
pulmonary embolism, and administration of anti-
biotics and source control for septic shock).
Unless the condition is rapidly reversed, an
arterial catheter should be inserted for monitor-
ing of arterial blood pressure and blood sam-
pling, plus a central venous catheter for the infu-
sion of fluids and vasoactive agents and to guide
fluid therapy. The initial management of shock
is problem-oriented, and the goals are therefore
the same, regardless of the cause, although the
exact treatments that are used to reach those
goals may differ. A useful mnemonic to describe
the important components of resuscitation is the
VIP rule7: ventilate (oxygen administration), in-
fuse (fluid resuscitation), and pump (administra-
tion of vasoactive agents).
Ventilatory Support
The administration of oxygen should be started im-
mediately to increase oxygen delivery and prevent
pulmonary hypertension. Pulse oximetry is often
unreliable as a result of peripheral vasoconstric-
tion, and precise determination of oxygen require-
ments will often require blood gas monitoring.
Mechanical ventilation by means of a mask
rather than endotracheal intubation has a lim-
ited place in the treatment of shock because
technical failure can rapidly result in respiratory
and cardiac arrest. Hence, endotracheal intuba-
tion should be performed to provide invasive
mechanical ventilation in nearly all patients with
severe dyspnea, hypoxemia, or persistent or wors-
ening acidemia (pH, <7.30). Invasive mechanical
ventilation has the additional benefits of reduc-
ing the oxygen demand of respiratory muscles
and decreasing left ventricular afterload by in-
creasing intrathoracic pressure. An abrupt de-
crease in arterial pressure after the initiation of
invasive mechanical ventilation strongly suggests
hypovolemia and a decrease in venous return.
The use of sedative agents should be kept to a
minimum to avoid further decreases in arterial
pressure and cardiac output.
Fluid Resuscitation
Fluid therapy to improve microvascular blood
flow and increase cardiac output is an essential
part of the treatment of any form of shock. Even
patients with cardiogenic shock may benefit
from fluids, since acute edema can result in a
decrease in the effective intravascular volume.
However, fluid administration should be closely
monitored, since too much fluid carries the risk
of edema with its unwanted consequences.
Pragmatic end points for fluid resuscitation
are difficult to define. In general, the objective is
for cardiac output to become preload-indepen-
dent (i.e., on the plateau portion of the Frank–
Starling curve), but this is difficult to assess
clinically. In patients receiving mechanical ventila-
tion, signs of fluid responsiveness may be identi-
fied either directly from beat-by-beat stroke-volume
measurements with the use of cardiac-output
monitors or indirectly from observed variations
in pulse pressure on the arterial-pressure tracing
during the ventilator cycle. However, such bedside
inferences have some limitations8 — notably,The New England Journal of MedicineDownloaded from nejm.org by Marcos Nunez on November 5, 2013. For personal use only. No other uses without permission.Copyright © 2013 Massachusetts Medical Society. All rights reserved.
n engl j med 369;18 nejm.org october 31, 20131727
1600 patients with shock who were randomly as-
signed to receive either dopamine or norepineph-
rine, septic shock occurred in 62% of the patients,
cardiogenic shock in 16%, hypovolemic shock in
16%, other types of distributive shock in 4%, and
obstructive shock in 2%.4
The type and cause of shock may be obvious
from the medical history, physical examination,
or clinical investigations. For example, shock
after traumatic injury is likely to be hypovolemic
(due to blood loss), but cardiogenic shock or
distributive shock may also occur, alone or in
combination, caused by such conditions as car-
diac tamponade or spinal cord injury. A full clini-
cal examination should include assessment of
skin color and temperature, jugular venous dis-
tention, and peripheral edema. The diagnosis
can be refined with point-of-care echocardio-
graphic evaluation, which includes assessment
for pericardial effusion, measurement of left and
right ventricular size and function, assessment for
respiratory variations in vena cava dimensions,
and calculation of the aortic velocity–time inte-
gral, a measure of stroke volume. Whenever pos-
sible, focused echocardiography should be per-
formed as soon as possible in any patient
presenting with shock (Fig. 1A).5,6
Ini ti a l A pproach
t o the Patien t in Sho ck
Early, adequate hemodynamic support of patients
in shock is crucial to prevent worsening organ
dysfunction and failure. Resuscitation should be
started even while investigation of the cause is
ongoing. Once identified, the cause must be cor-
rected rapidly (e.g., control of bleeding, percuta-
neous coronary intervention for coronary syn-
dromes, thrombolysis or embolectomy for massive
pulmonary embolism, and administration of anti-
biotics and source control for septic shock).
Unless the condition is rapidly reversed, an
arterial catheter should be inserted for monitor-
ing of arterial blood pressure and blood sam-
pling, plus a central venous catheter for the infu-
sion of fluids and vasoactive agents and to guide
fluid therapy. The initial management of shock
is problem-oriented, and the goals are therefore
the same, regardless of the cause, although the
exact treatments that are used to reach those
goals may differ. A useful mnemonic to describe
the important components of resuscitation is the
VIP rule7: ventilate (oxygen administration), in-
fuse (fluid resuscitation), and pump (administra-
tion of vasoactive agents).
Ventilatory Support
The administration of oxygen should be started im-
mediately to increase oxygen delivery and prevent
pulmonary hypertension. Pulse oximetry is often
unreliable as a result of peripheral vasoconstric-
tion, and precise determination of oxygen require-
ments will often require blood gas monitoring.
Mechanical ventilation by means of a mask
rather than endotracheal intubation has a lim-
ited place in the treatment of shock because
technical failure can rapidly result in respiratory
and cardiac arrest. Hence, endotracheal intuba-
tion should be performed to provide invasive
mechanical ventilation in nearly all patients with
severe dyspnea, hypoxemia, or persistent or wors-
ening acidemia (pH, <7.30). Invasive mechanical
ventilation has the additional benefits of reduc-
ing the oxygen demand of respiratory muscles
and decreasing left ventricular afterload by in-
creasing intrathoracic pressure. An abrupt de-
crease in arterial pressure after the initiation of
invasive mechanical ventilation strongly suggests
hypovolemia and a decrease in venous return.
The use of sedative agents should be kept to a
minimum to avoid further decreases in arterial
pressure and cardiac output.
Fluid Resuscitation
Fluid therapy to improve microvascular blood
flow and increase cardiac output is an essential
part of the treatment of any form of shock. Even
patients with cardiogenic shock may benefit
from fluids, since acute edema can result in a
decrease in the effective intravascular volume.
However, fluid administration should be closely
monitored, since too much fluid carries the risk
of edema with its unwanted consequences.
Pragmatic end points for fluid resuscitation
are difficult to define. In general, the objective is
for cardiac output to become preload-indepen-
dent (i.e., on the plateau portion of the Frank–
Starling curve), but this is difficult to assess
clinically. In patients receiving mechanical ventila-
tion, signs of fluid responsiveness may be identi-
fied either directly from beat-by-beat stroke-volume
measurements with the use of cardiac-output
monitors or indirectly from observed variations
in pulse pressure on the arterial-pressure tracing
during the ventilator cycle. However, such bedside
inferences have some limitations8 — notably,The New England Journal of MedicineDownloaded from nejm.org by Marcos Nunez on November 5, 2013. For personal use only. No other uses without permission.Copyright © 2013 Massachusetts Medical Society. All rights reserved.
T h e n e w e ng l a n d j o u r na l o f m e dic i n e
n engl j med 369;18 nejm.org october 31, 20131728
1
Drazen
10/10/13
10/31/13
AUTHOR PLEASE NOTE:
Figure has been redrawn and type has been reset
Please check carefully
Author
Fig #
Title
ME
DE
Artist
Issue date
COLOR FIGURE
Draft 9
Vincent
Knoper
Signs of tissue hypoperfusion
Chronic
hypotension?
Syncope
(if transient)
PresentAbsent
Normal
or high
Low
CVP
Distributive shock Hypovolemic shock
Small cardiac
chambers and normal
or high contractility
Normal cardiac
chambers and (usually)
preserved contractility
Cardiogenic shock
Large ventricles and
poor contractility
In tamponade: pericardial
effusion, small right and
left ventricles, dilated
inferior vena cava; in
pulmonary embolism or
pneumothorax: dilated right
ventricle, small left ventricle
Obstructive shock
Distributive shock Hypovolemic shock Cardiogenic shock Obstructive shock
HighLow
Obstruction
Pericardial
tamponade
Loss of
plasma or
blood
volume
Vasodilatation
Ventricular
failure
C
A
Estimate cardiac
output or SvO2
Arterial hypotension
Circulatory
shock
Echocardiography
Brain
Altered mental
state
Skin
Kidney
Mottled,
clammy
Oliguria
Tachycardia
Elevated
blood
lactate
B Types of shock
ObstructiveDistributive
(nonseptic)
4% 2%
Hypovolemic
16%
62%
Distributive (septic)
Cardiogenic
16%
Figure 1. Initial Assessment of Shock States.
Shown is an algorithm for the initial assessment of a patient in shock (Panel A), relative frequencies of the main types of shock (Panel B),
and schematic representations of the four main types of shock (Panel C). The algorithm starts with the most common presentation
(i.e., arterial hypotension), but hypotension is sometimes minimal or absent. CVP denotes central venous pressure, and SvO2 mixed
venous oxygen saturation.The New England Journal of MedicineDownloaded from nejm.org by Marcos Nunez on November 5, 2013. For personal use only. No other uses without permission.Copyright © 2013 Massachusetts Medical Society. All rights reserved.
n engl j med 369;18 nejm.org october 31, 20131728
1
Drazen
10/10/13
10/31/13
AUTHOR PLEASE NOTE:
Figure has been redrawn and type has been reset
Please check carefully
Author
Fig #
Title
ME
DE
Artist
Issue date
COLOR FIGURE
Draft 9
Vincent
Knoper
Signs of tissue hypoperfusion
Chronic
hypotension?
Syncope
(if transient)
PresentAbsent
Normal
or high
Low
CVP
Distributive shock Hypovolemic shock
Small cardiac
chambers and normal
or high contractility
Normal cardiac
chambers and (usually)
preserved contractility
Cardiogenic shock
Large ventricles and
poor contractility
In tamponade: pericardial
effusion, small right and
left ventricles, dilated
inferior vena cava; in
pulmonary embolism or
pneumothorax: dilated right
ventricle, small left ventricle
Obstructive shock
Distributive shock Hypovolemic shock Cardiogenic shock Obstructive shock
HighLow
Obstruction
Pericardial
tamponade
Loss of
plasma or
blood
volume
Vasodilatation
Ventricular
failure
C
A
Estimate cardiac
output or SvO2
Arterial hypotension
Circulatory
shock
Echocardiography
Brain
Altered mental
state
Skin
Kidney
Mottled,
clammy
Oliguria
Tachycardia
Elevated
blood
lactate
B Types of shock
ObstructiveDistributive
(nonseptic)
4% 2%
Hypovolemic
16%
62%
Distributive (septic)
Cardiogenic
16%
Figure 1. Initial Assessment of Shock States.
Shown is an algorithm for the initial assessment of a patient in shock (Panel A), relative frequencies of the main types of shock (Panel B),
and schematic representations of the four main types of shock (Panel C). The algorithm starts with the most common presentation
(i.e., arterial hypotension), but hypotension is sometimes minimal or absent. CVP denotes central venous pressure, and SvO2 mixed
venous oxygen saturation.The New England Journal of MedicineDownloaded from nejm.org by Marcos Nunez on November 5, 2013. For personal use only. No other uses without permission.Copyright © 2013 Massachusetts Medical Society. All rights reserved.
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