COMPENSATORY

MECHANISM OF
CIRCULATORY
SHOCK
 Compensated shock

Early stages of shock where

the body’s compensatory
mechanisms are able to
maintain normal perfusion.
•Increase in heart rate, stroke volume and
vascular smooth tone. Regulated through
sympathetic nervous system and
neurohormonal responses.

•Increase respiratory rate with greater carbon

dioxide elimination is a compensatory
response to the metabolic acidosis and
increased carbon dioxied production from
poor tissue perfusion
 Compensatory mechanism

Rapid compensatory Long term

mechanism compensatory
mechansim

•Increased venous return

•Vasoconstriction •Increased synthesis of
•Increased secretion of cortisol erythropoietin
,vasopressin ,aldosterone and
•Increased plasma
catecholamines
•Activation of Cushing’s reflex protein synthesis
•Activation of renin-angiotensin
system
The factors that can cause a person to recover from
moderate degree of shock are all the negative feedback
control mechanisms of the circulation that attempt to
return the cardiac output and arterial pressure back to
normal. They include the following:
• Baroreceptor reflexes which elicit powerful sympathetic
stimulation of the circulation.
• Central nervous system ischemic response, which elicit
even more powerful sympathetic stimulation throughout
the body but is not activated significantly until the arterial
pressure falls below 50 mm Hg.
Symptoms of compensated shock
include:
Agitation, restlessness and anxiety
Altered mental status
Tachycardia or tachypnea
Change in pallor, cyanosis around the lips, or
clammy skin
Nausea or vomiting
Thirst
Weak, thready or absent pulse
Narrowing pulse pressure
Shallow, rapid breathing
Mental status may be normal, in the early
stages
Reverse stress-relaxation of the circulatory system, which
causes the blood vessels to contract around the
diminished blood volume,so that the blood volume that is
available more adequately fills the circulation.

Formation of angiotensin by the kidneys ,which constricts

the peripheral arteries and also cause decrease output
of water and water by the kidneys, both which helps to
prevent progression of shock.
Drop in blood
pressure liver

angiotensinogen

renin

Angiotensin I
Angiotensin
converting enzyme
(ACE)
Angiotensin II

hypothalamus
aldosterone

Thirst and vasoconstriction

Sodium and water
drinking
retention

Elevated blood pressure

Formation of vasopressin by the pituitary gland which
also constricts the peripheral arteries and veins and
greatly increases water retention by kidneys.
Compensatory mechanism that return the blood
volume back to normal including absorption of fluid
into the capillaries from the interstitial space of the
body, conservation of water and salt by the kidneys,
increased thirst and appetite for salt, which makes the
person to drink water and eat salty food if able.
 COMPENSATION MECHANISMS
• Catecholamines may be secreted (I.E.
epinephrine and norepinephrine)
• The renin-angiotensin system aids in the
maintaining blood pressure.
• Endocrine response by pituitary gland results
in secretion of anti diuretic hormone (ADH).
 RENIN- ANGIOTENSIN SYSTEM

•Renin is released from the kidneys, and acts on

the specialized plasma protein called angiotensin
that produces angiotensin I.

•Angiotensin I is converted to angiotensin II by

enzymes in the lungs called angiotensin
converting enzyme (ACE).
 ANTI-DIURETIC HORMONE

Causes the kidney to

reabsorb water creating
an additive to the
aldosterone.
 FAILURE OF COMPENSATORY
MECHANISM
• Decrease blood flow to the tissues causes cellular
hypoxia.
• Anaerobic metabolism begins.
• Cell swelling, mitochondrial disruption, and
eventual cell death.
• If low perfusion state persists:

Irreversible Death imminent

• It causes permanent cellular damage and
multiple organ dysfunction syndrome
• Recovery does not even occur even with adequate
restoration of circulatory volume.
• Death occurs due to refractory acidosis,myocardial
and brain ischemia.
 DECOMPENSATED
SHOCK

Advance stage of shock that

occurs when the body’s
compensatory mechanisms
fails to maintain normal
perfusion.
Symptoms of decompensated shock
include:
•Falling blood pressure (systolic of 90 mm Hg
or lower with adults)
•Tachycardia and tachypnea
•Low urine output
•Labored and irregular breathing
•Weak, thready or absent peripheral pulses
•Ashy or cyanotic pallor
•Reduced body temperature
•Decreased mental status
•Dilated pupils
 SOME OF THE MORE IMPORTANT
FEEDBACKS ARE DESCRIBED BELOW:
Cardiac depression:
• When arterial pressure falls low enough ,coronary
blood flow decreases below that required adequate
nutrition of the myocardium.
• This weakens the heart muscle and thereby deceases
the cardiac output more. Thus a positive feedback
cycle has developed whereby the shock become
more and more severe.
Vasomotor failure
• In the early stage of shock various circulatory reflexes causes
intense activity of the sympathetic nervous system. This
activity delays the cardiac output and also helps prevent
decreased arterial pressure.
• However there comes to a point when diminished blood flow
to the brain’s vasomotor center depresses the center so much
that it too becomes progressively less active and finally
totally inactive.
• Fortunately the vasomotor center does not fail in the early
stages of shock if the arterial pressure remains above 30 mm
Hg.
Blockage of very small vessels by “sludged blood”
• Blockage occurs in many of the very small blood vessels in the
circulatory system and this blockage cause the shock to progress.
• The initiating cause of this blockage is sluggish blood flow in the
microvessels. Because tissue metabolism continues despite the low
flow,large amounts of acid ,both carbonic and lactic acid,continue
to empty into the local blood vessels and greatly increase the local
acidity of the blood.
• This acid plus other deterioration products from ischemic tisssues,
causes blood agglutination.
• Even if the vessels do not become plugged there is an
increase in tendency for the blood cells to stick too one
another makes it more difficult for the blood to flow through
the microvasculature in which gives rise to sludged blood.
Increased capillary permeability
• After many hours of hypoxia and lack of nutrients the
permeability of capillaries gradually increases and large
quantities of fluid begins to transude into the tissue.
• This decreases the blood volume, with a resultant further
decrease in the cardiac output making the shock still more
severe.
• Capillary hypoxia does not cause increase in capillary
permeability until the late stages of prolonged shock .
Release of toxins by ischemic tissue
• Shock has been suggested to cause tissues to release toxic
substances such as hiatamine, serotinin and other tissue enzymes
that cause further deterioration of the circulatory system.
Cardiac depression caused by endotoxin
• Endotoxin is released from the bodies of dead gram- negative
bacteria in the intestine. Diminished blood flow to the intestine
often causes enhanced formation and absorption of this toxic
substances.
• The circulating toxin causes increased cellular metabolism despite
inadequate nutrition of the cells, which has specific effect on the
heart muscle ,causing cardiac depression.
• Endotoxin plays a major role in septic shock.
Generalized cellular deterioration
• As shock becomes severe , many signs of
generalized cellular deterioration occur throughout
the body.
• One organ especially affected is the liver. The liver
is affected mainly because of the lack of enough
nutrients to support the normally high metabolism
in the liver cells, but also partly because of the
exposure of the liver to any vascular toxin or other
abnormal metabolic factor occurring in shock.
 AMONG THE DAMAGING CELLULAR EFFECTS
THAT ARE KNOWN TO OCCUR IN MOST
BODY TISSUES ARE FOLLOWING:
1. Active transport of sodium and potassium through cell
membrane is greatly diminished. As a result sodium and chloride
accumulate in the cells and potassium is lost from the cell and
the cells begins to swell.
2. Mitochondrial activity in the liver as well as in many other
tissues of the body, becomes severely depressed.
3. Lysosomes in the cells in widespread tissue areas begin to break
open, with intracellular release of hydrolases that causes further
intracellular deterioration.
4. Cellular metabolism of nutrients eventually becomes greatly
depressed in the last stages of shock. The actins of some
hormones are depressed as well, almost 100% depression of
actions of insulin.
 IRREVERSIBLE
SHOCK
•Stage of shock that has
progressed to the point that the
body nor medical
interventions can correct the
problem.
• The above figure shows that transfusion during the irreversible stage van
sometimes cause cardiac output to return to nearly normal.
• However the cardiac output soon begins to fall again, and subsequent
transfusion have less and less effect.
• By this time multiple deteriorative changes have occurred in the muscles
of the heart that may not necessarily affect the heart’s immediate ability to
pump blood but, over along period ,depress heart pumping is enough to
cause death.
• Beyond a certain point ,so much of tissue damage
has occurred ,so many destructive enzymes have
been released into the body fluids, so much of
acidosis has developed, so many other destructive
factors are now in progress that even a normal
cardiac output for a few minutes cannot reverse the
continuing deterioration.
• Therefore, in a severe shock a stage is eventually
reached at which the person will die even though
vigorous therapy might still return the cardiac output
to normal for short periods.
 DEPLETION OF HIGH ENERGY PHOSPHATE
RESERVE IN IRREVERSIBLE SHOCK

• The high-energy phosphate reserve in the tissues of the body,

especially in the liver and heart are greatly diminished in
sever shock.
• Essentially, all the creatine phosphate has been degraded to
adenosine diphosphate, adenosine mono phosphate and
eventually ,adenosine .
• Much of this adenosine then diffuses out of the cell into the
circulating blood and is converted into uric cid ( a substance
that cannot re-enter the cells reconstitute the adenosine
phosphate system).
• The high-energy phosphate reserve are difficult to replenish
and the store is depleted.