Circulatory Shock

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

M.D., Ph.D.
 THREE COMPONENTS SHOCK
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.

clinical signs of tissue

hypoperfusion
common condition in critical care 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

based on clinical, hemodynamic, and failure
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
cause of history, 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
evaluation and function, assessment for respiratory
Relative frequencies of variations in vena cava dimensions, and
the main types of shock calculation of the aortic velocitytime integral, a
(Panel B), measure of stroke volume.
 Schematic
representations
of the four
main types of
shock (Panel
C).

distributive factors
(e.g severe sepsis
or anaphylaxis from
obstruction (e.g., the 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
resuscitatio
n administration of oxygen started immediately
increase oxygen delivery and prevent pulmonary hypertension
ventilate
(oxygen
administration Pulse oximetry is often Unreliable
) 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
(administratio use of sedative agents
n of
vasoactive kept to a minimum to avoid further decreases in arterial pressure
agents). 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
norepinephrine first choice
Predominantly -adrenergic
properties, but its modest -
adrenergic effects help to
maintain cardiac output.
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
Inotropic
Vasodilators
Agents
increase cardiac output
without increasing
dobutamine to be the myocardial demand for
inotropic agent of choice oxygen by reducing
ventricular afterload
prudent use of nitrates and
for increasing cardiac output, possibly other vasodilators
regardless of whether may improve microvascular
norepinephrine is also being perfusion and cellular
given function
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
membrane
reversible cardiogenic shock or as a bridge to heart
oxygenation transplantation
(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 least 70% during the first 6 hours was
loss and associated coagulopathy, until the associated 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
easilyaccessible surfaces,
targeting a decrease of at least 20% in the blood lactate level such as the sublingual
over a 2-hour period in patients with shock and a blood lactate area
level of 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
characterized Near-infrared
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 Analysis of the
many of the capillaries have changes in technique that uses
tissue oxygen near-infrared light
stopped or intermittent saturation to determine tissue
flow during a brief oxygen saturation
episode of from the fractions
forearm of oxyhemoglobin
Figure 2. Sidestream Dark-Field Images of and
ischemia
Sublingual deoxyhemoglobin.
Microcirculation in a Healthy Volunteer and a
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.