Shock

Other names Circulatory shock

Specialty Critical care medicine

Symptoms Initial: Weakness, fast

heart rate, fast
breathing, sweating,
anxiety, increased
thirst[1]
Later: Confusion,
unconsciousness,
cardiac arrest[1]

Types Low volume,

cardiogenic,
obstructive,
distributive[2]

Causes Low volume: Bleeding,

vomiting, pancreatitis[1]
Cardiogenic: heart
 attack, cardiac
contusion[1]
Obstructive: Cardiac
tamponade, tension
pneumothorax[1]
Distributed: Sepsis,
spinal cord injury,
certain overdoses[1]

Diagnostic method Based on symptoms,

physical exam,
laboratory tests[2]

Treatment Based on the

underlying cause[2]

Medication Intravenous fluid,

vasopressors[2]

Prognosis Risk of death 20 to

50%[3]

Frequency 1.2 million per year

(USA)[3]
Shock is divided into four main types
based on the underlying cause: low
volume, cardiogenic, obstructive, and
distributive shock.[2] Low volume shock
may be from bleeding, diarrhea, vomiting,
or pancreatitis.[1] Cardiogenic shock may
be due to a heart attack or cardiac
contusion.[1] Obstructive shock may be
due to cardiac tamponade or a tension
pneumothorax.[1] Distributed shock may
be due to sepsis, spinal cord injury, or
certain overdoses.[1]

The diagnosis is generally based on a

combination of symptoms, physical
examination, and laboratory tests.[2] A
decreased pulse pressure (systolic blood
pressure minus diastolic blood pressure)
or a fast heart rate raises concerns.[1]
The heart rate divided by systolic blood
pressure, known as the shock index (SI),
of greater than 0.8 supports the
diagnosis more than low blood pressure
or a fast heart rate in isolation.[4][5]

Treatment of shock is based on the likely

underlying cause.[2] An open airway and
sufficient breathing should be
established.[2] Any ongoing bleeding
should be stopped, which may require
surgery or embolization.[2] Intravenous
fluid, such as Ringer's lactate or packed
red blood cells, is often given.[2] Efforts to
maintain a normal body temperature are
also important.[2] Vasopressors may be
useful in certain cases.[2] Shock is both
common and has a high risk of death.[3]
In the United States about 1.2 million
people present to the emergency room
each year with shock and their risk of
death is between 20 and 50%.[3]

Signs and symptoms

The presentation of shock is variable
with some people having only minimal
symptoms such as confusion and
weakness.[6] While the general signs for
all types of shock are low blood pressure,
decreased urine output, and confusion,
these may not always be present.[6] While
a fast heart rate is common, those on β-
blockers, those who are athletic, and in
30% of cases of those with shock due to
intra abdominal bleeding may have a
normal or slow heart rate.[7] Specific
subtypes of shock may have additional
symptoms.

Dry mucous membrane, reduced skin

turgor, prolonged capillary refill time,
weak peripheral pulses and cold
extremities can be early signs.[8]

Low volume
Hemorrhage classes[9]
Class Blood loss Response Treatment

I <15 %(0.75 l) min. fast heart rate, normal blood pressure minimal

15-30 %(0.75-
II fast heart rate, min. low blood pressure intravenous fluids
1.5 l)

very fast heart rate, low blood pressure, fluids and packed
III 30-40 %(1.5-2 l)
confusion RBCs

aggressive
IV >40 %(>2 l) critical blood pressure and heart rate
interventions

Hypovolemia is a direct loss of effective

circulating blood volume leading to:

A rapid, weak, thready pulse due to

decreased blood flow combined with
tachycardia
Cool, clammy skin due to
vasoconstriction and stimulation of
vasoconstriction
Rapid and shallow breathing due to
sympathetic nervous system
stimulation and acidosis
 Hypothermia due to decreased
perfusion and evaporation of sweat
Thirst and dry mouth, due to fluid
depletion
Cold and mottled skin (Livedo
reticularis), especially extremities, due
to insufficient perfusion of the skin

The severity of hemorrhagic shock can

be graded on a 1–4 scale on the physical
signs. This approximates to the effective
loss of blood volume. The shock index
(heart rate divided by systolic blood
pressure) is a stronger predictor of the
impact of blood loss than heart rate and
blood pressure alone.[4] This relationship
has not been well established in
pregnancy-related bleeding.[10]

Cardiogenic

Symptoms of cardiogenic shock include:

Distended jugular veins due to

increased jugular venous pressure
Weak or absent pulse
Abnormal heart rhythms, often a fast
heart rate
Pulsus paradoxus in case of
tamponade
Reduced blood pressure

Distributive
Systemic inflammatory response syndrome[11]
Finding Value

Temperature <36 °C (96.8 °F) or >38 °C (100.4 °F)

Heart rate >90/min

Respiratory rate >20/min or PaCO2<32 mmHg (4.3 kPa)

WBC <4x109/L (<4000/mm³), >12x109/L (>12,000/mm³), or 10% bands

Distributive shock is low blood pressure

due to a dilation of blood vessels within
the body. This can be caused by
systemic infection (septic shock), a
severe allergic reaction (anaphylaxis), or
spinal cord injury (neurogenic shock).
Like any type of shock, the result is the
same: inadequate perfusion pressure
resulting in inadequate cellular
oxygenation.[12][6] The SIRS features
typically occur in early septic shock.[6]

Septic shock
 Systemic leukocyte adhesion to
endothelial cells[13]
Reduced contractility of the heart[13]
Activation of the coagulation
pathways, resulting in disseminated
intravascular coagulation[13]
Increased levels of neutrophils[13]

Main manifestations are produced due to

massive release of histamine which
causes intense dilation of the blood
vessels. People with septic shock will
also likely be positive for the SIRS
criteria. The most generally accepted
treatment for these patients is early
recognition of symptoms, and early
administration of broad spectrum and
organism specific antibiotics.[14]

Cause
Causes of shock[6]
Type Cause

Low volume Fluid loss such as bleeding or diarrhea

Heart Ineffective pumping due to heart damage

Obstructive Blood flow to or from the heart is blocked

Distributive Due to abnormal flow within the small blood vessels[15]

Shock is a common end point of many

medical conditions.[16] Shock itself is a
life-threatening condition as a result of
compromised body circulation.[17] It has
been divided into four main types based
on the underlying cause: hypovolemic,
distributive, cardiogenic, and
obstructive.[18] A few additional
classifications are occasionally used
including: endocrinologic shock.[16]

Low volume

Hypovolemic shock is the most common

type of shock and is caused by
insufficient circulating volume.[6] Its
primary cause is haemorrhage (internal
or external), or loss of fluid from the
circulation. Vomiting and diarrhea are the
most common cause in children.[16]
Other causes include burns, and excess
urine loss due to diabetic ketoacidosis
and diabetes insipidus.[16]

Cardiogenic
Cardiogenic shock is caused by the
failure of the heart to pump effectively.[6]
This can be due to damage to the heart
muscle, most often from a large
myocardial infarction. Other causes of
cardiogenic shock include dysrhythmias,
cardiomyopathy/myocarditis, congestive
heart failure (CHF), contusio cordis, or
valvular heart disease problems.[16]

Obstructive

Obstructive shock is due to a physical

obstruction of the great vessels or the
heart itself.[6] Several conditions can
result in this form of shock.
Cardiac tamponade[16] in which fluid in
the pericardium prevents inflow of
blood into the heart (venous return).
Constrictive pericarditis, in which the
pericardium shrinks and hardens, is
similar in presentation.
Tension pneumothorax[16] Through
increased intrathoracic pressure,
bloodflow to the heart is prevented
(venous return).
Pulmonary embolism is the result of a
thromboembolic incident in the blood
vessels of the lungs and hinders the
return of blood to the heart.
Aortic stenosis hinders circulation by
obstructing the ventricular outflow
 tract
Hypertrophic sub-aortic stenosis is
overly thick ventricular muscle
dynamically occludes the ventricular
outflow tract.

Distributive

Distributive shock is due to loss of

muscle tone in the arteries or
inflammation and dilation of the
capillaries.[12][6] Examples of this form of
shock are:

Septic shock is the most common

cause of distributive shock.[16] Caused
by an overwhelming systemic infection
resulting in vasodilation leading to
hypotension. Septic shock can be
caused by Gram negative bacteria
such as (among others) Escherichia
coli, Proteus species, Klebsiella
pneumoniae which have an endotoxin
on their surface which produces
adverse biochemical, immunological
and occasionally neurological effects
which are harmful to the body, and
other Gram-positive cocci, such as
pneumococci and streptococci, and
certain fungi as well as Gram-positive
bacterial toxins. Septic shock also
includes some elements of
cardiogenic shock. In 1992, the
ACCP/SCCM Consensus Conference
Committee defined septic shock: ". .
.sepsis-induced hypotension (systolic
blood pressure < 90 mmHg or a
reduction of 40 mmHg from baseline)
despite adequate fluid resuscitation
along with the presence of perfusion
abnormalities that may include, but are
not limited to, lactic acidosis, oliguria,
or an acute alteration in mental status.
Patients who are receiving inotropic or
vasopressor agents may have a
normalized blood pressure at the time
that perfusion abnormalities are
identified."
Anaphylactic shock is caused by a
severe anaphylactic reaction to an
allergen, antigen, drug or foreign
protein causing the release of
 histamine which causes widespread
vasodilation, leading to hypotension
and increased capillary permeability.
High spinal injuries may cause
neurogenic shock.[19] The classic
symptoms include a slow heartrate
due to loss of cardiac sympathetic
tone and warm skin due to dilation of
the peripheral blood vessels.[19] (This
term can be confused with spinal
shock which is a recoverable loss of
function of the spinal cord after injury
and does not refer to the
haemodynamic instability per se.)

Endocrine
Based on endocrine disturbances such
as:

Hypothyroidism (can be considered a

form of cardiogenic shock) in people
who are critically ill patients, reduces
cardiac output and can lead to
hypotension and respiratory
insufficiency.
Thyrotoxicosis (cardiogenic shock)
may induce a reversible
cardiomyopathy.
Acute adrenal insufficiency
(distributive shock) is frequently the
result of discontinuing corticosteroid
treatment without tapering the dosage.
However, surgery and intercurrent
 disease in patients on corticosteroid
therapy without adjusting the dosage
to accommodate for increased
requirements may also result in this
condition.
Relative adrenal insufficiency
(distributive shock) in critically ill
patients where present hormone levels
are insufficient to meet the higher
demands

Pathophysiology
Effects of inadequate perfusion on cell function.

There are four stages of shock. As it is a

complex and continuous condition there
is no sudden transition from one stage to
the next.[20] At a cellular level, shock is
the process of oxygen demand becoming
greater than oxygen supply.[6]

One of the key dangers of shock is that it

progresses by a positive feedback
mechanism. Poor blood supply leads to
cellular damage, which results in an
inflammatory response to increase blood
flow to the affected area. This is normally
very useful to match up blood supply
level with tissue demand for nutrients.
However, if enough tissue causes this, it
will deprive vital nutrients from other
parts of the body. Additionally, the ability
of the circulatory system to meet this
increase in demand causes saturation,
and this is a major result, of which other
parts of the body begin to respond in a
similar way; thus, exacerbating the
problem. Due to this chain of events,
immediate treatment of shock is critical
for survival.[5]
Initial

During this stage, the state of

hypoperfusion causes hypoxia. Due to
the lack of oxygen, the cells perform
lactic acid fermentation. Since oxygen,
the terminal electron acceptor in the
electron transport chain, is not abundant,
this slows down entry of pyruvate into
the Krebs cycle, resulting in its
accumulation. Accumulating pyruvate is
converted to lactate by lactate
dehydrogenase and hence lactate
accumulates (causing lactic acidosis).

Compensatory
This stage is characterised by the body
employing physiological mechanisms,
including neural, hormonal and bio-
chemical mechanisms in an attempt to
reverse the condition. As a result of the
acidosis, the person will begin to
hyperventilate in order to rid the body of
carbon dioxide (CO2). CO2 indirectly acts
to acidify the blood and by removing it
the body is attempting to raise the pH of
the blood. The baroreceptors in the
arteries detect the resulting hypotension,
and cause the release of epinephrine and
norepinephrine. Norepinephrine causes
predominately vasoconstriction with a
mild increase in heart rate, whereas
epinephrine predominately causes an
increase in heart rate with a small effect
on the vascular tone; the combined effect
results in an increase in blood pressure.
The renin–angiotensin axis is activated,
and arginine vasopressin (Anti-diuretic
hormone; ADH) is released to conserve
fluid via the kidneys. These hormones
cause the vasoconstriction of the
kidneys, gastrointestinal tract, and other
organs to divert blood to the heart, lungs
and brain. The lack of blood to the renal
system causes the characteristic low
urine production. However the effects of
the renin–angiotensin axis take time and
are of little importance to the immediate
homeostatic mediation of shock.
Progressive

Should the cause of the crisis not be

successfully treated, the shock will
proceed to the progressive stage and the
compensatory mechanisms begin to fail.
Due to the decreased perfusion of the
cells, sodium ions build up within while
potassium ions leak out. As anaerobic
metabolism continues, increasing the
body's metabolic acidosis, the arteriolar
smooth muscle and precapillary
sphincters relax such that blood remains
in the capillaries.[13] Due to this, the
hydrostatic pressure will increase and,
combined with histamine release, this
will lead to leakage of fluid and protein
into the surrounding tissues. As this fluid
is lost, the blood concentration and
viscosity increase, causing sludging of
the micro-circulation. The prolonged
vasoconstriction will also cause the vital
organs to be compromised due to
reduced perfusion.[13] If the bowel
becomes sufficiently ischemic, bacteria
may enter the blood stream, resulting in
the increased complication of endotoxic
shock.[5][13]

Refractory

At this stage, the vital organs have failed

and the shock can no longer be reversed.
Brain damage and cell death are
occurring, and death will occur
imminently. One of the primary reasons
that shock is irreversible at this point is
that much cellular ATP has been
degraded into adenosine in the absence
of oxygen as an electron receptor in the
mitochondrial matrix. Adenosine easily
perfuses out of cellular membranes into
extracellular fluid, furthering capillary
vasodilation, and then is transformed
into uric acid. Because cells can only
produce adenosine at a rate of about 2%
of the cell's total need per hour, even
restoring oxygen is futile at this point
because there is no adenosine to
phosphorylate into ATP.[5]
Diagnosis
The first change seen in shock is an
increased cardiac output followed by a
decrease in mixed venous oxygen
saturation (SmvO2) as measured in the
pulmonary artery via a pulmonary artery
catheter. Central venous oxygen
saturation (ScvO2) as measured via a
central line correlates well with SmvO2
and are easier to acquire. If shock
progresses anaerobic metabolism will
begin to occur with an increased blood
lactic acid as the result. While many
laboratory tests are typically performed
there is no test that either makes or
excludes the diagnosis. A chest X-ray or
emergency department ultrasound may
be useful to determine volume state.[6][7]

Management
The best evidence exists for the
treatment of septic shock in adults and
as the pathophysiology appears similar
in children and other types of shock
treatment this has been extrapolated to
these areas.[16] Management may
include securing the airway via intubation
if necessary to decrease the work of
breathing and for guarding against
respiratory arrest. Oxygen
supplementation, intravenous fluids,
passive leg raising (not Trendelenburg
position) should be started and blood
transfusions added if blood loss is
severe.[6] It is important to keep the
person warm to avoid hypothermia [21] as
well as adequately manage pain and
anxiety as these can increase oxygen
consumption.[6]Negative impact by shock
is reversible if it's recognized and treated
early in time.[17]

Fluids

Aggressive intravenous fluids are

recommended in most types of shock
(e.g. 1–2 liter normal saline bolus over
10 minutes or 20 ml/kg in a child) which
is usually instituted as the person is
being further evaluated.[22] Which
intravenous fluid is superior, colloids or
crystalloids, remains undetermined.[6]
Thus as crystalloids are less expensive
they are recommended.[23] If the person
remains in shock after initial
resuscitation packed red blood cells
should be administered to keep the
hemoglobin greater than 100 g/l.[6]

For those with haemorrhagic shock the

current evidence supports limiting the
use of fluids for penetrating thorax and
abdominal injuries allowing mild
hypotension to persist (known as
permissive hypotension).[24] Targets
include a mean arterial pressure of
60 mmHg, a systolic blood pressure of
70–90 mmHg,[6][25] or until their
adequate mentation and peripheral
pulses.[25] Hypertonic fluid may also be
an option in this group.[26]

Medications

Vasopressors may be used if blood

pressure does not improve with fluids.
There is no evidence of substantial
superiority of one vasopressor over
another; however, using dopamine leads
to an increased risk of arrythmia when
compared with norepinephrine.[27]
Vasopressors have not been found to
improve outcomes when used for
hemorrhagic shock from trauma[28] but
may be of use in neurogenic shock.[19]
Activated protein C (Xigris) while once
aggressively promoted for the
management of septic shock has been
found not to improve survival and is
associated with a number of
complications.[29] Xigris was withdrawn
from the market in 2011, and clinical
trials were discontinued.[29] The use of
sodium bicarbonate is controversial as it
has not been shown to improve
outcomes.[30] If used at all it should only
be considered if the pH is less than
7.0.[30]

Mechanical support
 Intra-aortic balloon pump (IABP)
Ventricular assist device (VAD)
Artificial heart (TAH)
Extracorporeal membrane oxygenation
(ECMO)

Treatment goals

The goal of treatment is to achieve a

urine output of greater than 0.5 ml/kg/h,
a central venous pressure of 8–
12 mmHg and a mean arterial pressure
of 65–95 mmHg. In trauma the goal is to
stop the bleeding which in many cases
requires surgical interventions.

Epidemiology
Haemorrhagic shock occurs in about 1–
2% of trauma cases.[25] Up to one-third of
people admitted to the intensive care unit
(ICU) are in circulatory shock.[31] Of
these, cardiogenic shock accounts for
approximately 20%, hypovolemic about
20%, and septic shock about 60% of
cases.[32]

Prognosis
The prognosis of shock depends on the
underlying cause and the nature and
extent of concurrent problems.
Hypovolemic, anaphylactic and
neurogenic shock are readily treatable
and respond well to medical therapy.
Septic shock however, is a grave
condition with a mortality rate between
30% and 50%. The prognosis of
cardiogenic shock is even worse with a
mortality rate between 70% and 90%.[33]

History
In 1972 Hinshaw and Cox suggested the
classification system for shock which is
still used today.[33]

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External links
Classification ICD-10: R57 • D

ICD-9-CM: 785.50 •
MeSH: D012774
D012769, D012774 •
DiseasesDB: 12013

External resources MedlinePlus:

000039 •
eMedicine:
emerg/531 med/285
emerg/533
Retrieved from
"https://en.wikipedia.org/w/index.php?
title=Shock_(circulatory)&oldid=898258517"

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