Hypovolemic Shock

Hypovolemic Shock
-Pravesh Acharya
The word ‘Shock’ has Dutch origin, in which
the term ‘Schokken’ in the original language
refers to jolt or sudden jerk.
 Shock is defined as the state of diminished cardiac output

or reduced effective circulating blood volume that leads
to impaired tissue perfusion and cellular hypoxia.
 Shock is indeed a cardiovascular failure as the cellular

metabolic needs demand enough oxygen and nutrients,
which the tissues are deprived of.
Types of shock
Hypovolemic or Distributive/ Cardiogenic Obstructive

cold shock vasogenic/ low- shock shock
resistance/ warm
shock
The end result of any type of shock is hypotension.

Though initially reversible, it’s persistence implies
the fate of irreversible tissue injury; often fatal to the
shock patient.
However, other types of shocks too, do exist. This
classification is based on the causes.
 Septic shock associated with systemic inflammation
 Shock due to anesthetic accident
 Neurogenic shock- spinal cord injury
 Anaphylactic shock/ IgE mediated hypersensitivity

reactionhylactic shock/ IgE mediated hypersensitivity
reaction
Types of hypovolemic or
cold shock
Hemorrhagic Traumatic shock Surgical Dehydration

shock shock shock
Due to Due to severe Due to external Due to fluid

hemorrhage traumatic damage or internal loss by any
to muscle and bone blood loss by causes
ruptured blood
vessels during
surgery
Mention the characteristic features of hypovolemic shock.
Why is it known as cold shock?
• Rapid and thready pulse
• Systolic BP < 90 mm Hg
• Rapid, shallow breathing.
• Intense thirst as the extracellular fluid is lost.

Mention the characteristic features of
hypovolemic shock. Why is it known
as cold shock?
 Increased aldosterone and ADH levels, so decreased urine formation.
 Cerebral ischemia and acidosis so patients may either be restless

or lethargic.
 Due to sympathetic vasoconstriction, blood flow to GIT is reduced

i.e. susceptibility to vomiting increases.
 The patient is cold, pale and moist (clammy) skin with greyish
coloration (if cyanosis is present too). Hence the shock is termed
as ‘cold’ shock.
Details of hemorrhagic shock:
 A major form of hypovolemic shock, it’s effects depends on
amount and rapidity of blood loss, along with efficiency of
compensatory power of the patient.
 So, in mild to moderate hemorrhage (5-15 ml/kg body

weight), if patient is healthy, normal condition restoration is
easy via compensatory mechanisms.
 But in severe hemorrhage (30 ml/kg body weight), the

patient may suffer from circulatory collapse and even die.
Details of compensatory mechanisms:
 The compensatory mechanisms occur after hemorrhage. They are of two types, viz.
rapid and long-term compensatory mechanisms.
 The following sequence of events occur in rapid compensatory mechanism:
1. Hypotension (plus reflex tachycardia) ----------------------- Rapid thready pulse
2. Generalized vasoconstriction (but not in brain and heart) that’s most pronounced in
kidneys, skin, subcutaneous tissue, pulmonary circuit and spleen, plus generalized
venoconstriction.
3. Increased catecholamine release by stimulated adrenal medulla
4. Restlessness, apprehension, irritability due to stimulated reticular activating system
5. Rapid shallow breathing (since stimulated respiratory center)

DETAILS OF COMPENSATORY MECHANISMS:
 The generalized vasoconstriction, increased catecholamine release

and restlessness, apprehension, irritability all occur in pretext of
eventually increasing cardiac output by increasing venous return.
 Similarly, renal vasoconstriction has many effects such as:

a. Renal ischemia plus increased angiotensin II release ------ act on
subfornical region of brain ----- Intense thirst
b. Afferent arteriole constriction (decreases GFR slightly) and

efferent arteriole constriction (decreases RPF a lot) that indeed
increases filtration fraction and thus oliguria, sodium retention,
uremia and later on, acute renal failure.
 In fact, all these major compensatory reactions are a result of

increased sympathetic discharge that followed hemorrhage.
Applied aspect of short term compensatory
mechanism:
• Sympathectomized animals thus can’t tolerate a blood loss of
>30% and may die.
• Reflex warming of a shock patient either with water bottles or

providing warm environment can abolish the sympathetic
discharge, thus killing the patient.
Details of long term compensatory
reactions:
 It includes four aspects:
a. Restoration of plasma volume within 12-72 hours
b. Restoration of plasma proteins over a period of 3-4 hours
c. Restoration of RBC mass in 4-8 weeks
d. Restoration of BP over several months via kidney’s long term regulatory

mechanisms
Mechanism of plasma volume
restoration within 12-72 hours:
Increased uptake of tissue fluids by Water and electrolytes retention by kidneys
Decreased Increased Decreased Renal Decreased Increased

blood volume sympathetic right atrial ischemia tissue stress to
discharge pressure perfusion body
Decreased Stimulated
GFR and Increased
Decreased Arteriolar Decreased adrenal
release of corticotropin
venous constriction discharge from cortex
renin from releasing
pressure atrio-caval
JGA hormone
receptors Increased
aldosterone
Decreased secretion Increased
capillary Increased ACTH
pressure Increased ADH Angiotensin II
Increased Na+
secretion level Increased
reabsorption
glucocorticoid
secretion
Mechanism of plasma protein
restoration over 3-4 days
 Hemorrhage is followed by activation of liver.
 The activated liver initiates heightened protein synthesis.
 The activated liver also initiates the release of preformed

proteins increasingly.
 After hemorrhage, fibrinogen, globulin and albumin are

regenerated in that order.
Mechanism of RBC mass restoration in
4-8 weeks:
 Hemorrhage is also followed by hypoxia.
 The liver initiates erythropoietinogen synthesis in high rate,

following hypoxia.
 The kidneys simultaneously release REF i.e. Renal Erythropoietic

Factor increasingly.
 The combined interplay of liver and kidney cause increased

erythropoietin production (in fact, the peak of erythropoietin
reaches on 10th day).
What about traumatic shock then??
• Frank bleeding into injured areas of muscles and bones, results in this shock.
• If there is extensive soft tissue and muscle crushing known as crushing syndrome
then myoglobin leaks into circulation, gets precipitated in the renal tubules and clogs
them, resulting in renal damage.
• It is an interesting fact to note, that when traumatic injury targets thigh muscles, the
thigh muscles indeed can accommodate one liter of extruded blood with an increase
in only one centimeter of thigh diameter. See the body’s extent of temporarily
compensating blood loss before onset of shock!
Surgical shock: A challenge!
• Surgeons do need to have professional mastery, for the patients intended to
be saved, may induce worsening of the patient’s misery.
• Whether the error be slight or blunder, the blood vessels may rupture during
the surgical procedures.
• All thanks to the external or internal blood loss caused by vasculature rupture,
the patient may undergo surgical shock.
Dehydration shock: A vamp!
• The dehydration shock is due to fluid loss from:
• GIT due to prolonged vomiting or diarrhea.
• Kidneys due to:

a. Diabetes mellitus
b. Diabetes insipidus
c. Diuretic overdose
d. Adrenal insufficiency
• Skin due to ‘burns’, heat stress (fever, exposure to heat) that results in sweating
How does shock due to burns cause hemoconcentration?
Burn is followed by loss of protein rich fluid via the capillary wall.
Burn also causes accumulation of cellular damage products in

interstitial space.
The above combination of events result in an increase in osmotic

pressure of the tissue fluid.
This leads to a swift loss of fluid from circulation.
Hence, it leads to hemoconcentration.

Why is the skin cold, pale and moist in
hypovolemic shock?
 The decrease in blood volume is followed by peripheral
vasoconstriction, shunting the blood away from skin and towards vital
organs like lungs, heart and brain. This decreases the skin
temperature.
 The activation of sympathetic autonomic nervous system stimulates
release of catecholamines, that further provoke the peripheral
vasoconstriction, contributing to cold and pale appearance.
 The body’s response to hypovolemia and increased stress further
stimulates sympathetic autonomic nervous system to provoke excess
perspiration via sweat gland activation, thus moistening the skin.

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Hypovolemic Shock

 Shock is defined as the state of diminished cardiac output

 Shock is indeed a cardiovascular failure as the cellular

Hypovolemic or Distributive/ Cardiogenic Obstructive

The end result of any type of shock is hypotension.

 Septic shock associated with systemic inflammation

 Shock due to anesthetic accident

 Neurogenic shock- spinal cord injury

 Anaphylactic shock/ IgE mediated hypersensitivity

Hemorrhagic Traumatic shock Surgical Dehydration

Due to Due to severe Due to external Due to fluid

• Rapid, shallow breathing.

• Intense thirst as the extracellular fluid is lost.

 Cerebral ischemia and acidosis so patients may either be restless

 Due to sympathetic vasoconstriction, blood flow to GIT is reduced

 So, in mild to moderate hemorrhage (5-15 ml/kg body

 But in severe hemorrhage (30 ml/kg body weight), the

 The following sequence of events occur in rapid compensatory mechanism:

1. Hypotension (plus reflex tachycardia) ----------------------- Rapid thready pulse

3. Increased catecholamine release by stimulated adrenal medulla

4. Restlessness, apprehension, irritability due to stimulated reticular activating system

5. Rapid shallow breathing (since stimulated respiratory center)

 The generalized vasoconstriction, increased catecholamine release

 Similarly, renal vasoconstriction has many effects such as:

b. Afferent arteriole constriction (decreases GFR slightly) and

 In fact, all these major compensatory reactions are a result of

• Reflex warming of a shock patient either with water bottles or

 It includes four aspects:

a. Restoration of plasma volume within 12-72 hours

b. Restoration of plasma proteins over a period of 3-4 hours

c. Restoration of RBC mass in 4-8 weeks

d. Restoration of BP over several months via kidney’s long term regulatory

Decreased Increased Decreased Renal Decreased Increased

 The activated liver initiates heightened protein synthesis.

 The activated liver also initiates the release of preformed

 After hemorrhage, fibrinogen, globulin and albumin are

 The liver initiates erythropoietinogen synthesis in high rate,

 The kidneys simultaneously release REF i.e. Renal Erythropoietic

 The combined interplay of liver and kidney cause increased

• GIT due to prolonged vomiting or diarrhea.

• Kidneys due to:

Burn also causes accumulation of cellular damage products in

The above combination of events result in an increase in osmotic

This leads to a swift loss of fluid from circulation.

Hence, it leads to hemoconcentration.

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