Types of shock

Cardiogenic Shock

blood flow decreased due to an intrinsic defect in cardiac function either the heart
muscle, or the valves are dysfunctional

classical example is acute anterior myocardial infarction, when the amount of

damaged ischaemic muscle may be so great that the heart cannot pump anymore. The
decreased contractility causes a decrease in stroke volume

typical haemodynamic picture:

decreased cardiac output and blood pressure

high left ventricular filling pressures (backward failure)

o
increased systemic vascular resistance (from vasoconstriction, which is a
sympathetic compensatory response to the low blood pressure)
o
pressure)

increased heart rate (sympathetic compensatory response to the low blood

o
other features of cardiogenic shock such as the cool peripheries, decreased
urine output and sweating can also be explained by the sympathetic compensatory response.

Hypovolemic shock

result of intravascular blood volume depletion

common causes:

haemorrhage

vomiting

diarrhoea

dehydration

third-space losses during major operations

primary abnormality is a decrease in preload. The decreased preload causes a decrease

in stroke volume.

typical haemodynamic picture:

decreased cardiac output and blood pressure

low left ventricular filling pressures (because the ventricle is empty)

o
increased SVR (from vasoconstriction, which is a sympathetic compensatory
response to the low blood pressure)
o
pressure)

increased heart rate (sympathetic compensatory response to the low blood

Other features of hypovolaemic shock are similar to those seen in cardiogenic shock
and include cool peripheries, decreased urine output and sweating that can also be explained
by the sympathetic compensatory response.

Distributive Shock

occurs when the peripheral vascular dilatation causes a fall in SVR

most common causes:

septic shock

anaphylactic shock

acute adrenal insufficiency

neurogenic shock.

cardiac output is often increased but the perfusion of many vital organs is
compromised because the blood pressure is too low and the body loses its ability to
distribute blood properly

haemodynamic profile is usually characterised by:

normal or increased cardiac output with a low SVR

low to normal left ventricular filling pressures

low blood pressure

clinical features include:

warm peripheries

bounding pulses

tissue dysfunction despite this:

mental status changes

oliguria

lactic acidosis.

Obstructive Shock
Cardiac tamponade

extracardiac obstructive shock

mechanical obstruction to cardiac filling

pressures of the right cardiac chambers, the pulmonary artery, and the left cardiac
chambers equilibrate in diastole

always consider cardiac tamponade when the CVP is high and BP low.

pulsus paradoxus

o
exaggeration of normal physiology in which there is a decrease of >10 mm Hg
in systolic blood pressure during inspiration
important clinical finding in patients with suspected cardiac tamponade

Other forms

tension pneumothorax

massive pulmonary embolus

Principles of management

look for reversible causes such as acute valvular insufficiency, drug overdose, or
tamponade

major goal of management is to return tissue oxygen delivery to normal. The

treatment priority is therefore to increase cardiac output and blood pressure. Optimising the
oxygen content of blood can also help to improve tissue oxygen delivery. The goal of
improving cardiac output and blood pressure is usually accomplished with some combination
of adjusting preload, increasing cardiac contractility and optimising SVR. Ensuring both
good oxygenation and haemoglobin content optimises the oxygen content of the blood


occasionally, heart rate abnormalities, such as bradycardia, or tachyarrhythmias such
as ventricular tachycardia, may cause or contribute to hypotension and must be treated.

Acute Cardiogenic Shock

primary goal is to improve myocardial muscle function

elevated SVR may also impair cardiac output because it increases afterload. Often in
acute cardiogenic shock, the SVR is secondarily elevated (part of the baroreceptor response
to shock) to maintain vascular perfusion pressure

inotropes, such as dobutamine, are indicated to increase myocardial contractility in

the presence of normal or slightly decreased blood pressure and may have a secondary
beneficial effect of decreasing SVR and improving afterload.

NB driving pressure for coronary artery perfusion is aortic diastolic pressure (this is
because coronary artery perfusion occurs primarily during diastole). A low aortic diastolic
pressure is common in severe shock seen in ICU and may be gently increased with
vasopressors (agents that cause vasoconstriction and therefore increase SVR). However,
because of the increase in afterload, an agent that also increases cardiac muscle performance
must also be used, and initial therapy with a single agent that has both inotropic and
vasopressor effects (i.e. norepinephrine or high-dose dopamine) is indicated

if hypotension is not responsive to initial therapy, consultation should be obtained for

consideration of a cardiac assist device such as intra-aortic balloon counterpulsation.

Hypovolemic Shock

return intravascular volume to normal

initial resuscitation:

colloid or crystalloid fluids are effective

choice of fluid should be based on the fluid type that has been lost. For
example, blood should replace blood and crystalloid should be used for vomiting and
dehydration

because of the inherent complications of blood transfusion, mild to

moderate blood loss (less than one liter in an adult), should be replaced by colloid (1-1.5
times volume of blood lost) or crystalloid (crystalloid 2.5-3 times volume of blood lost)

crystalloid of choice is normal saline or lactated Ringers solution

because its osmolality is similar to that of the intravascular volume. In large-volume
resuscitation, however, excessive normal saline infusion may produce hyperchloremic
metabolic acidosis. Colloid solutions (5% albumin and hetastarch) offer the most efficient
intravascular volume expansion, but are expensive and no outcome benefit has been shown.

Dextrose 5% in water does not offer significant expansion of intravascular volume because it
is quickly distributed throughout body fluid compartments.
o
endpoints of therapy are to re-establish normal blood pressure, pulse, and
organ perfusion.

Distributive Shock

vasodilation, resulting in a very low SVR, and diffuse capillary leak are the major
features

because of capillary leakage, hypovolaemia contributes significantly to the shock

before resuscitation and fluid requirements may be very large

end points of fluid resuscitation are the same as for hypovolaemic shock at this stage

if the patient remains hypotensive despite adequate fluid resuscitation (high CVP,
pulmonary artery occlusion pressure, or pulmonary oedema) inotropes and/or vasopressors
are necessary

anaphylactic shock is treated with subcutaneous epinephrine (0.3-1mg) and volume

resuscitation. In circumstances of very low blood pressure and poor peripheral perfusion,
titrated intravenous epinephrine (25-50g per bolus) is indicated

acute adrenal insufficiency is treated with volume therapy, intravenous

corticosteroids, and vasopressors.

septic shock

o
combination of inotropic and vasopressor effect is optimal. Dopamine (5
g/kg/min and increased if necessary to 15-20 g/kg/min) or adrenaline (0.05 g/kg/min and
increased if necessary to 2 g/kg/min) provide both vasopressor and inotropic support
o
if g/kg/min and increased if necessary to 2 g/kg/min). The addition of
dobutamine (5-10 g/kg/min) may be beneficial if noradrenaline is used
o

Obstructive Shock

relief of the obstruction is life saving

if cardiac tamponade is present, urgent pericardiocentesis is essential

tension pneumothorax must be treated promptly with needle thoracostomy

o
removal

massive pulmonary embolism requires urgent thrombolysis or surgical

keeping preload normal is important in patients with all forms of obstructive shock.
Fluid resuscitation may improve the patients cardiac output and hypotension temporarily and
buy time for definitive intervention.

Circulatory shock, commonly known simply as shock, is a serious, life-threatening medical

condition characterized by a decrease in tissue perfusion to a point at which it is inadequate to
meet cellular metabolic needs. As the blood carries oxygen and nutrients around the body,
reduced flow hinders the delivery of these components to the tissues, and can stop the tissues
from functioning properly.[1] The process of blood entering the tissues is called perfusion, so
when perfusion is not occurring properly this is called a hypoperfusional (hypo = below)
state.
A circulatory shock should not be confused with the emotional state of shock, as the two are
not related. Medical shock is a life-threatening medical emergency and one of the most
common causes of death for critically ill people. Shock can have a variety of effects, all with
similar outcomes, but all relate to a problem with the body's circulatory system. For example,
shock may lead to hypoxemia (a lack of oxygen in arterial blood) or cardiac arrest (the heart
stopping).[2][3][4][5][6][7][8]
The essential signs of shock are seen as tachycardia/tachypnoea (compensatory mechanisms),
hypotension, and signs of poor end-organ perfusion (such as low urine output, confusion or
loss of consciousness) (failure to compensate). Other signs should be looked for to establish
the underlying cause for the shock to guide effective treatment.
Signs of severity

The severity of shock can be graded 1-4 based on the physical signs. This approximates to the
effective loss of blood volume. The blood volume does not have to actually be lost from the
circulation as an expansion in the volume of the circulatory system (e.g. in septic shock) will
render the patient proportionally hypovolaemic.

Grade 1
Up to about 15% loss of effective blood volume (~750ml in an average
adult who is assumed to have a blood volume of 5 liters). This leads to a
mild resting tachycardia and can be well tolerated in otherwise healthy
individuals. In the elderly or those with underlying conditions such as
ischaemic heart disease the additional myocardial oxygen demands may
not be tolerated so well.
Grade 2
Between 15-30% loss of blood volume (750-1500ml) will provoke a
moderate tachycardia and begin to narrow the pulse pressure. The time
taken for the capillaries to refill after 5 seconds of pressure (capillary refill
time) will be extended.
Grade 3
At 30 - 40% loss of effective blood volume (1500 - 2000 ml) the
compensatory mechanisms begin to fail and hypotension, tachycardia and
low urine output (<0.5ml/kg/hr in adults) are seen.
Grade 4
At 40-50% loss of blood volume (2000 -2500 ml) profound hypotension will
develop and if prolonged will cause end-organ damage and death.
Signs relating to different causes
Hypovolaemic shock
Direct loss of effective circulating blood volume leading to:

Anxiety, restlessness, altered mental state due to decreased cerebral

perfusion and subsequent hypoxia

Hypotension due to decrease in circulatory volume

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 respirations 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

Fatigue due to inadequate oxygenation

Cold and mottled skin (cutis marmorata), especially extremities, due to

insufficient perfusion of the skin

Distracted look in the eyes or staring into space, often with pupils dilated

Cardiogenic shock
Similar to hypovolemic shock but in addition:

Distended jugular veins due to increased jugular venous pressure

Weak or absent pulse

Arrhythmia, often tachycardic

Obstructive shock
Similar to hypovolemic shock but in addition:

Distended jugular veins due to increased jugular venous pressure

Pulsus paradoxus in case of tamponade

Septic shock
Similar to hypovolemic shock except in the first stages:

Pyrexia (fever), due to increased level of cytokines[1]

Systemic vasodilation resulting in hypotension (low blood pressure)[1]

Warm and sweaty skin due to vasodilation

Systemic leukocyte adhesion to endothelial tissue[1]

Reduced contractility of the heart[1]

Activation of the coagulation pathways, resulting in disseminated

intravascular coagulation[1]

Increased levels of neutrophils[1]

Neurogenic shock

As with hypovolemic shock but in high spinal injuries may also be

accompanied by profound bradycardia due to loss of the cardiac
accelerating nerve fibres from the sympathetic nervous system at T1-T4.

The skin is warm and dry or a clear sweat line exists, above which the skin
is diaphoretic.

Priapism due to Peripheral nervous system stimulation

Anaphylactic shock

Skin eruptions and large bumps

Localised oedema, especially around the face

Weak and rapid pulse

Breathlessness and cough due to narrowing of airways and swelling of the

throat

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.[9]
Initial
During this stage, the hypoperfusional state causes hypoxia, leading to the
mitochondria being unable to produce adenosine triphosphate (ATP). Due
to this lack of oxygen, the cell membranes become damaged, they
become leaky to extra-cellular fluid, and the cells perform anaerobic
respiration. This causes a build-up of lactic and pyruvic acid which results
in systemic metabolic acidosis. The process of removing these compounds
from the cells by the liver requires oxygen, which is absent.
Compensatory (Compensating)
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
adrenaline and noradrenaline. Noradrenaline causes predominately
vasoconstriction with a mild increase in heart rate, whereas adrenaline
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. This is known as Cushing reflex and its triad is the subjective
identifying characteristic of this stage. Renin-angiotensin axis is activated
and arginine vasopressin (Anti-diuretic hormone; ADH) is released to
conserve fluid via the kidneys. Also, 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 (Decompensating)
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[1]. 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 microcirculation. The prolonged vasoconstriction will also cause the vital organs
to be compromised due to reduced perfusion [1]. If the bowel becomes
sufficiently ischemic, bacteria may enter the blood stream, resulting in the
increased complication of endotoxic shock[1].
Refractory (Irreversible)
At this stage, the vital organs have failed and the shock can no longer be
reversed. Brain damage and cell death have occurred. Death will occur
imminently.
Types
Hinshaw and Cox classification

In 1972 Hinshaw and Cox suggested the following classification which is still used today.[2] It
names four types of shock: hypovolemic, cardiogenic, distributive and obstructive shock:[3][4]
[5][8][10]
In many patients, shock is a combination of two or more of these four types of shock.

Hypovolemic shock

This is the most common type of shock and based on insufficient circulating volume. Its
primary cause is loss of fluid from the circulation (most often "hemorrhagic shock"). Causes
may include internal bleeding, traumatic bleeding, high output fistulae or severe burns.
Cardiogenic shock

This type of shock is caused by the failure of the heart to pump effectively. This can be due to
damage to the heart muscle, most often from a large myocardial infarction. Other causes of
cardiogenic shock include arrhythmias, cardiomyopathy, congestive heart failure (CHF),
contusio cordis, or cardiac valve problems.
Distributive shock

As in hypovolaemic shock there is an insufficient intravascular volume of blood. This form of

"relative" hypovolaemia is the result of dilation of blood vessels which diminishes systemic
vascular resistance. Examples of this form of shock are:

Septic shock
o

Anaphylactic shock
o

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 release an endotoxin
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
mm Hg or a reduction of 40 mm Hg 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."

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.

Neurogenic shock
o

Neurogenic shock is the rarest form of shock. It is caused by trauma

to the spinal cord resulting in the sudden loss of autonomic and
motor reflexes below the injury level. Without stimulation by
sympathetic nervous system the vessel walls relax uncontrollably,

resulting in a sudden decrease in peripheral vascular resistance,

leading to vasodilation and hypotension. (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.)
Obstructive shock

In this situation the flow of blood is obstructed which impedes circulation and can result in
circulatory arrest. Several conditions result in this form of shock.

Cardiac tamponade
o

Tension pneumothorax
o

Through increased intrathoracic pressure, bloodflow to the heart is

prevented (venous return).

Massive pulmonary embolism

o

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.

is the result of a thromboembolic incident in the bloodvessels of the

lungs and hinders the return of blood to the heart.

Aortic stenosis
o

hinders circulation by obstructing the ventricular outflow tract

Other proposed types of shock

Revisions to the Hinshaw and Cox classification have been proposed. Several types of shock
have been proposed as a "fifth type of shock", including hypoglycemic shock, cytotoxic
shock and endocrine shock. However, each of these is actually a subtype of one of the four
types of shock in Hinshaw and Cox's original model.
For example:
Endocrine shock
Based on endocrine disturbances such as:

Hypothyroidism (Can be considered a form of Cardiogenic shock)

o

in critically ill patients, reduces cardiac output and can lead to

hypotension and respiratory insufficiency.

Thyrotoxicosis (Cardiogenic shock)

Acute adrenal insufficiency (Distributive shock)

o

may induce a reversible cardiomyopathy.

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)

o

in critically ill patients where present hormone levels are insufficient

to meet the higher demands

Treatment

Shock requires immediate interventions to preserve life. Therefore, the early recognition and
treatment is essential even before a specific diagnosis is made (As a general rule, you should
treat for a sustained wound and shock). Most forms of shock seen in trauma or sepsis respond
initially to aggressive intravenous fluids (e.g. 1 liter normal saline bolus over 10 minutes or
20ml/kg in a child). Therefore this treatment is usually instituted as the person is being
further evaluated.[11]
Re-establishing perfusion to the organs is the primary goal through restoring and maintaining
the blood circulating volume ensuring oxygenation and blood pressure are adequate,
achieving and maintaining effective cardiac function, and preventing complications. Patients
attending with the symptoms of shock will have, regardless of the type of shock, their airway
managed and oxygen therapy initiated. In case of respiratory insufficiency (i.e. diminished
levels of consciousness, hyperventilation due to acid-base disturbances or pneumonia)
intubation and mechanical ventilation may be necessary. A paramedic may intubate in
emergencies outside the hospital, whereas a patient with respiratory insufficiency in-hospital
will be intubated usually by a respiratory therapist, paramedic, or physician.
The aim of these acts is to ensure survival during the transportation to the hospital; they do
not cure the cause of the shock. Specific treatment depends on the cause.
Hypovolemic shock

In hypovolemic shock, usually hemorrhagic shock caused by traumatic injury, it is necessary

to immediately control the bleeding and restore the casualty's blood volume by giving
infusions of isotonic crystalloid solutions. Blood transfusions, packed red blood cells (RBCs),
Albumin (or other colloid solutions), or fresh-frozen plasma are necessary for loss of large
amounts of blood (e.g. greater than 20% of blood volume), but can be avoided in smaller and
slower losses. Hypovolemia due to burns, diarrhea, vomiting, etc. is treated with infusions of
electrolyte solutions that balance the nature of the fluid lost. Sodium is essential to keep the
fluid infused in the extracellular and intravascular space whilst preventing water intoxication
and brain swelling. Metabolic acidosis (mainly due to lactic acid) accumulates as a result of

poor delivery of oxygen to the tissues, and mirrors the severity of the shock. It is best treated
by rapidly restoring intravascular volume and perfusion as above. Inotropic and
vasoconstrictive drugs should be avoided, as they may interfere in knowing blood volume has
returned to normal.[2][3][4][5]
Regardless of the cause, the restoration of the circulating volume is priority. As soon as the
airway is maintained and oxygen administered the next step is to commence replacement of
fluids via the intravenous route. A size 14g intravenous in the arm will flow at twice the rate
of a 16g central venous catheter.[12]
Opinion varies on the type of fluid used in shock. The most common are:

Crystalloids Such as sodium chloride (0.9%), or Lactated Ringer's

solution (Hartmann's solution). Dextrose solutions which contain free
water are less effective at re-establishing circulating volume, and promote
hyperglycaemia.

Colloids For example, polysaccharide (Dextran), polygeline (Haemaccel),

succinylated gelatin (Gelofusine) and hetastarch (Hespan). Colloids are, in
general, much more expensive than crystalloid solutions and have not
conclusively been shown to be of any benefit in the initial treatment of
shock.

Combination Some clinicians argue that individually, colloids and

crystalloids can further exacerbate the problem and suggest the
combination of crystalloid and colloid solutions.

Blood Essential in severe hemorrhagic shock, often pre-warmed and

rapidly infused.

It is to be noted that NO plain water should be given to the patient at any point, as the
patient's low electrolyte levels would easily cause water intoxication, leading to premature
death. An isotonic or solution high in electrolytes should be administered if intravenous
delivery of recommended fluids is unavailable.
Vasoconstrictor agents have no role in the initial treatment of hemorrhagic shock, due to their
relative inefficacy in the setting of acidosis, and because the body, in the setting of
hemorrhagic shock, is in an endogenously catecholaminergic state. Definitive care and
control of the hemorrhage is absolutely necessary, and should not be delayed.
Cardiogenic shock

In cardiogenic shock, depending on the type of myocardial infarction, one can infuse fluids
such as or in shock refractory to infusing fluids, normal saline would be an example of said
fluids[clarification needed] inotropic agents. Inotropic agents, which enhance the heart's pumping
capabilities, are used to improve the contractility and correct the hypotension. Should that not
suffice, an intra-aortic balloon pump can be considered (which reduces the workload for the

heart and improves perfusion of the coronary arteries) or a left ventricular assist device
(which augments the pump-function of the heart.)[2][3][4][5]
The main goals of the treatment of cardiogenic shock are the re-establishment of circulation
to the myocardium, minimizing heart muscle damage and improving the heart's effectiveness
as a pump. This is most often performed by percutaneous coronary intervention and insertion
of a stent in the culprit coronary lesion or sometimes by cardiac bypass.
Although this is a protection reaction, the shock itself will induce problems; the circulatory
system being less efficient, the body gets "exhausted" and finally, the blood circulation and
the breathing slow down and finally stop (cardiac arrest). The main way to avoid this deadly
consequence is to make the blood pressure rise again with

Fluid replacement with intravenous infusions;

Use of vasopressing drugs (e.g. to induce vasoconstriction);

Use of Pneumatic anti-shock Garment(PASG) that compress the legs and

concentrate the blood in the vital organs (lungs, heart, brain).

Use of blankets to keep the patient warm metallic PET film emergency
blankets are used to reflect the patient's body heat back to the patient.

Distributive shock

In distributive shock caused by sepsis the infection is treated with antibiotics and supportive
care is given (i.e. inotropica, mechanical ventilation, renal function replacement).
Anaphylaxis is treated with epinephrine "adrenaline" to stimulate cardiac performance and
corticosteroids to reduce the inflammatory response. In neurogenic shock because of
vasodilation in the legs, one of the most suggested treatments is placing the patient in the
Trendelenburg position, thereby elevating the legs and shunting blood back from the
periphery to the body's core. However, since bloodvessels are highly compliant, and expand
as result of the increased volume locally, this technique does not work. More suitable would
be the use of vasopressors such as Norepinephrine to decrease vasodilatation.[2][3][4][5]
Obstructive shock

In obstructive shock, the only therapy consists of removing the obstruction. Pneumothorax or
hemothorax is treated by inserting a chest tube, pulmonary embolism requires thrombolysis
(to reduce the size of the clot), or embolectomy (removal of the thrombus), tamponade is
treated by draining fluid from the pericardial space through pericardiocentesis.[2][3][4][5]
Endocrine Shock

Endocrine shock is defined as a significant (and usually life-threatening) disturbance to an

animal's endocrine (hormone production) system. Examples of conditions which may cause
endocrine shock include hypothyroidism, hyperthyroidism (thyrotoxicosis) and acute adrenal
deficiency. The major and generally accepted modalities for treatment of hyperthyroidism in
humans involve initial temporary use of suppressive thyrostatics medication, and possibly

later use of permanent surgical or radioisotope therapy. All approaches may cause under
active thyroid function (hypothyroidism) which is easily managed with levothyroxine
supplementation. Adrenal deficiencies are often treated with application of corticosteroids.
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 and with a
mortality rate between 30% and 50%. The prognosis of cardiogenic shock is even worse.[2]
Shock is said to evolve from reversible to irreversible in experimental hemorrhagic shock
involving certain animal species (dogs, rats, mice) that develop intense vasoconstriction of
the gut. Death is due to hemorrhagic necrosis of the intestinal lining when shed blood in
reinfused. In pigs and humans 1) this is not seen and cessation of bleeding and restoration of
blood volume is usually very effective; however 2) prolonged hypovolemia and hypotension
does carry a risk of respiratory and then cardiac arrest. Perfusion of the brain may be the
greatest danger during shock. Therefore urgent treatment (cessation of bleeding, rapid
restoration of circulating blood volume and ready respiratory support) is essential for a good
prognosis in hypovolemic shock.

When performing laboratory tests to evaluate bleeding disorders, the coagulation cascade can
be thought of as having two branches: the extrinsic pathway and the intrinsic pathway. Each
of these pathways utilizes different coagulation factors, proteins that are carried in an inactive
form in the blood. These factors are sequentially activated down one pathway or the other and
come together to complete the clotting process in the common pathway.
Using this approach, bleeding disorder testing is a step-by-step investigative procedure. If
someone presents with a bleeding episode, a doctor may order a Prothrombin Time (PT),
which evaluates the extrinsic and common pathways, Partial Thromboplastin Time (PTT),
which evaluates the intrinsic and common pathways, and a CBC to see whether or not the
patient is anemic and to evaluate the number of platelets present. If the PT is prolonged,
further testing may be done to identify problems with factors involved in the extrinsic or

common pathway. If the PTT is prolonged, then the doctor may follow-up with other testing
to look for specific factor deficiencies in the intrinsic or common pathway and to see whether
or not there may be factor inhibitors.
Some of the tests that may be ordered include:

Expand TableTests for Bleeding Disorders

The tests listed here are the more common tests performed to evaluate bleeding disorders.
Abnormal Results May
Test
Measures
Ordered When/To
Indicate
Counts and
evaluates size and
Routine screen
shape of platelets,
CBC (Complete red and white blood
Decreased platelet numbers
Blood Count)
cells (WBCs), types
increase bleeding tendency
Check for any
of WBCs; measures
abnormalities
hemoglobin and
hematocrit
Individual tests to
Decreased activity of one or
Coagulation
measure the
Evaluate bleeding
more factors may increase
Factors, Activity function of specific episodes
risk of bleeding
coagulation factors
Decreased production or
Measures the
Coagulation
When factor activity is increased use of one or more
quantity of
Factors, Antigen
consistently low
factors, increased risk of
individual factors
bleeding
If elevated, indicates recent
clotting activity may be due
Evaluate blood clot
Measures a specific
to acute or chronic
formation during
D-dimer
type of cross-linked
condition, such as a
bleeding and clotting
fibrin degradation
thromboembolism or
episodes
disseminated intravascular
coagulation (DIC)
Individual tests for Evaluate excessive
If present, may cause
Factor Inhibitors coagulation factor bleeding and prolonged specific factor deficiencies
antibodies
PTT
and excessive bleeding
Fibrin
Reflection of
If increased, indicates recent
Evaluate bleeding and
degradation
clotting activity and
blood clot formation and
clotting
Products (FDP) breakdown
breakdown
If low, may indicate
decreased production or
Reflection of
Evaluate bleeding and increased use; may be
Fibrinogen
clotting ability and
clotting
elevated with infection and
activity
inflammation. It is an acute
phase reactant.
Partial
Time to clot;
Prolonged PTT suggests
Thromboplastin evaluates the
need for further tests. May
Investigate
Time (PTT)
intrinsic and
indicate:

The tests listed here are the more common tests performed to evaluate bleeding disorders.
Abnormal Results May
Test
Measures
Ordered When/To
Indicate

Coagulation factor
deficiency

Pre-surgical
screen for risk of
excessive
bleeding

Specific inhibitor
(such as Factor VIII
antibody)

Monitor heparin
anticoagulant
therapy

Nonspecific inhibitor
(such as Lupus
anticoagulant)

Patient on heparin
and/or blood sample
contaminated with
heparin

bleeding

common pathways
of coagulation
cascade

If abnormal, increases risk of

Evaluate platelets Evaluate bleeding,
excessive bleeding; may
ability to adhere and especially when platelet indicate presence of one of
form clumps
count normal
several disorders including
von Willebrands disease
An automated
Abnormal result may
method to measure
indicate acquired platelet
Sometimes used as a
platelet function
disorder or von Willebrands
Platelet Function
presurgical screen or to
(this is the most
disease. Indicates greater
Analyzer
evaluate recurrent
widely used; there
risk of excessive bleeding.
bleeding
are also other
This test has largely replaced
analyzers)
the Bleeding time test.
Platelet
aggregation
(Platelet
function test)

Prothrombin
Time (PT)

Time to clot tes;

evaluates the
extrinsic and
common pathways
of coagulation
cascade

Investigate
bleeding or
thrombotic
episode

Presurgical
screen for risk of
excessive
bleeding

Monitor warfarin
(coumadin)
anticoagulant
therapy

Most common use is

monitoring warfarin
anticoagulant therapy.
Prolonged PT may suggest
need for further tests. May
be elevated in inherited or
acquired conditions.

The tests listed here are the more common tests performed to evaluate bleeding disorders.
Abnormal Results May
Test
Measures
Ordered When/To
Indicate
vWF activity and decreased
Indirect measure of
ability for platelets to adhere
Ristocetin
von Willebrand
Evaluate bleeding
to injuries; may be due to
Cofactor
factor (vWF)
episodes
von Willebrands disease,
activity/function
increased risk of bleeding
Time to clot;
If elevated, heparin may be
thrombin activates Help evaluate bleeding
contaminating blood sample;
fibrinogen to fibrin episode; sometimes
Thrombin Time
also elevated with FDP, with
stands; TT detects when PTT prolonged;
(TT)
very low levels of
presence of
when heparin
fibrinogen, and with
inhibitors to this
contamination suspected
abnormal fibrinogen
process

von Willebrand
Quantitative
Factor (vWF)
measure of vWF
Antigen

When activity
(measured as
If low, may indicate plateletRisocetin
related acquired condition or
Cofactor) is low
von Willebrand disease,
increased risk
Evaluate
bleeding episodes