Circulatory Shock

Jean-Louis Vincent, M.D., Ph.D., and Daniel De Backer, M.D.,

Ph.D.
 Shock THREE COMPONENTS SHOCK
the clinical expression of circulatory failure that
results in inadequate cellular oxygen utilization systemic arterial hypotension

systolic arterial pressure <90 mm Hg or the

mean arterial pressure < 70 mm Hg
associated tachycardia.

common condition in critical care clinical signs of tissue hypoperfusion

Cutaneous (skin that is cold and clammy, with

vasoconstriction and cyanosis,
affecting about one third of patients in ICU
renal (urine output of <0.5 ml per kilogram of
body weight per hour),
neurologic (altered mental state, which
typically includes obtundation, disorientation,
and confusion).

diagnosis of shock hyperlactatemia

>1.5 mmol per liter in acute circulatory failure

based on clinical, hemodynamic, and
biochemical signs
Pathophysiological Mechanisms

hypovolemia
not
necessarily distributive
exclusive factors
cardiogenic
obstruction factors

four characterized by low Decreased systemic

potentialpathophysiolo cardiac output and, vascular resistance and
gical hence, inadequate altered oxygen
mechanisms oxygen transport. extraction
Figure 1. Initial Assessment of Shock States.
Shown is an algorithm
for the initial
assessment of a
patient in shock (Panel
A)
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
Differential Diagnosis
type and may be obvious from the medical history,
cause of physical examination, or clinical
shock investigations.

A full include assessment of skin color and

clinical temperature, jugular venous
examina distention,and peripheral edema.
tion

Echocardio includes assessment for pericardial effusion,

graphic measurement of left and right ventricular size and
evaluation function, assessment for respiratory variations in
Relative frequencies of the vena cava dimensions, and calculation of the
main types of shock aortic velocitytime integral, a measure of stroke
(Panel B), volume.
 Schematic
representations
of the four main
types of shock
(Panel C).

distributive factors
(e.g severe sepsis or
anaphylaxis from the
obstruction (e.g., release of
pulmonary inflammatory
embolism, cardiac mediators)
cardiogenic factors tamponade, or
(e.g., acute myocardial tension
infarction, end-stage pneumothorax),
hypovolemia (from cardiomyopathy,
internal or external advanced valvular
fluid loss) heart disease,
myocarditis, or cardiac
arrhythmias)
Initial Approach to the Patient in Shock
VIP rule Ventilatory Support
resuscitation
administration of oxygen started immediately
increase oxygen delivery and prevent pulmonary hypertension
ventilate
(oxygen Pulse oximetry is often Unreliable
administration)
precise determination of oxygen requirements often require blood gas
monitoring
Infuse endotracheal intubation
(fluid
resuscitation) performed to provide invasive mechanical ventilation in nearly all
patients with severe dyspnea, hypoxemia, or persistent or worsening
acidemia (pH, <7.30)
pump
(administration use of sedative agents
of vasoactive
agents). kept to a minimum to avoid further decreases in arterial pressure and
cardiac output
Initial Approach to the Patient in Shock
Fluid Resuscitation
to improve microvascular blood
flow and increase cardiac output
fluid-challenge technique
used to determine a patients actual
response to fluids, while limiting the risks of
adverse effects
Fluid challenges can be repeated
as required
but must be stopped rapidly in case of
nonresponse in order to avoid fluid
overload
four elements fluid-challenge
type of fluid
Crystalloid solutions are the first choice
rate of fluid administration
Infused rapidly to induce a quick response but not o fast that an
artificial stress response develops;
typically, an infusion of 300 to 500 ml of fluid is administered
during a period of 20 to 30 minutes.
objective of the fluid challenge
In shock, the objective is usually an increase in systemic arterial
pressure,
could also be decrease heart rate
increase in urine output.
Safety limits
Pulmonary edema is the most serious complication of fluid
infusion.
a limit in central venous pressure of a few millimeters of mercury
above the baseline value is usually set to prevent fluid overload
Vasoactive Agents
Vasopressors Inotropic Agents Vasodilators

increase cardiac output

norepinephrine first choice without increasing myocardial
dobutamine to be the
inotropic agent of choice demand for oxygen by
reducing ventricular afterload
Predominantly -adrenergic
properties, but its modest -
adrenergic effects help to prudent use of nitrates and
for increasing cardiac output,
maintain cardiac output. possibly other vasodilators
regardless of whether
may improve microvascular
norepinephrine is also being
perfusion and cellular function
given
usual dose is 0.1 to 2.0 g per
kilogram of body weight per
minute

epinephrine as a second-line
agent for severe case
Mechanical Support
intraaortic reduce left ventricular afterload and increase coronary blood flow
balloon
counterpulsation
(IABC) recent randomized, controlled trial showed no beneficial effect of
IABC in patients with cardiogenic shock
its routine use in cardiogenic shock is not currently recommended

Venoarterial may be used as a temporary lifesaving measure in patients with

extracorporeal
reversible cardiogenic shock or as a bridge to heart transplantation
membrane
oxygenation
(ECMO)
Goals of Hemodynamic Support
Arterial Pressure Cardiac Output and Oxygen Delivery

a good initial goal

Restoring a mean systemic arterial pressure

of 65 to 70 mm Hg
Rivers et al
The level should be adjusted

to restore tissue perfusion, assessed on the

basis of mental status, skin appearance, and
urine output in patients presenting to the emergency
department with septic shock
mean arterial pressure lower than 65 to 70 mm
Hg
may be acceptable in a patient with acute
bleeding who has no major neurologic a treatment algorithm targeting an ScvO2 of at
problems, with the aim of limiting blood loss least 70% during the first 6 hours was associated
and associated coagulopathy, until the with decreased rates of death
bleeding is controlled
Goals of Hemodynamic Support
Blood Lactate Level
Microcirculatory Variables
increase in the blood lactate level reflects abnormal
handheld devices for
cellular function.changes in lactate take place more slowly than
changes in systemic arterial pressure or cardiac output
orthogonal polarization
spectral (OPS) imaging
and sidestream dark-
field (SDF) imaging
the blood lactate level should decrease over a period of hours
with effective therapy

directly visualizing the

microcirculation and
valuating the effects of
interventions on
reduced in-hospital mortality (Jansen et al) microcirculatory flow in
targeting a decrease of at least 20% in the blood lactate level over easilyaccessible surfaces,
a 2-hour period in patients with shock and a blood lactate level of such as the sublingual area
more than 3 mmol per liter
Goals of Hemodynamic Support
Microcirculatory Variables
(Panel A, arrows)
The microcirculation in the can be used to
quantify
healthy volunteer is microvascular Near-infrared
characterized dysfunction; such spectroscopy
by dense capillaries that are alterations are
consistently perfused associated with
worse outcomes
(Panel B, arrows)
in the patient with septicshock,
the density of the capillaries is
diminished, and
many of the capillaries have Analysis of the
stopped or intermittent changes in tissue technique that uses
flow oxygen near-infrared light to
saturation during determine tissue
a brief episode oxygen saturation
of forearm from the fractions of
Figure 2. Sidestream Dark-Field Images of Sublingual ischemia oxyhemoglobin and
Microcirculation in a Healthy Volunteer and a Patient deoxyhemoglobin.
with Septic Shock.
Therapeutic Priorities and Goals
essentially four phases in the treatment of shock, and herapeutic
goals and monitoring need to be adapted to each phase
Conclusions
Circulatory shock is associated with high morbidity and mortality.

Prompt identification is essential so that aggressive management can be started

Appropriate treatment is based on a good understanding of the underlying

pathophysiological mechanisms.

Treatment should include correction of the cause of shock and hemodynamic

stabilization, primarily through fluid infusion and administration of vasoactive agents.

The patients response can be monitored by means of careful clinical evaluation and
blood lactate measurements; microvascular evaluation may be feasible in the future.