2. Shock is the most common and important
cause of the death among the surgical
patients
Death occurs rapidly as result of the
1- Profound state of the shock
2- Consequence of the organ ischemia
3- Reperfusion injury
3. Shock is the systemic state of the low tissue
perfusion, which is inadequate for the
normal cellular respiration.
With insufficient delivery of the oxygen and
glucose cells switch from aerobic to
inaerobic metabolism.
4. Pathophysiology of the shock is divided in to
three categories
1- Cellular
2- Microvascular
3- Systemic
5. Reduced tissues perfusion dec. cellular
O2 switch from aerobic to anaerobic
metabolism accumulation of the lactic
acid in the blood “Systemic Metabolic
Acidosis”.
As glucose within cells exhausted stop
respiration failure of Na+/K+ pump of
cellular membranes lysosomal enzymes
become released lyses of the cells
Potassium released into the blood stream.
6. As tissues ischemia progress change in
the internal environment of the body
activation of the immune and coagulation
systems.
Hypoxia and acidosis activate
compliment and the prime neutrophils
generation of the O2 free radicals and
release of the cytokines.
Above two mechanism leads to injury to
endothelials cells of the capillaries
damage endothelial cells become leaky
tissues edema exacerbating tissues
hypoxia
7. Systemic pathophysiology involves
1- Cardiovascular system
2- Respiratory system
3- Renal System
4- Endocrine System
8. Due to tissues edema pre-load & after –
load decrease Compensatory baro
receptor response increase sympathetic
activity release of the catecholamine
tachycardia and systemic vasoconstriction
Above mechanism not associated with the
shock result from the sepsis.
9. Metabolic acidosis and increase sympathetic
response increase respiratory rate and
minuet ventilation increase the excretion
of the CO2 Compensatory respiratory
alkalosis.
10. Due to dec. preload and afterload dec.
perfusion pressure in the kidneys reduce
filtration at glomerulus dec. urine output
activation of renin – angiotensin –
aldosterone system further vasoconstri –
-on increase water and sodium
reabsorbtion from kidneys further edema
exacerbating further ischemia.
11. In addition to adrenal and renin-angiotensin
system, vasopressin release from the
hypothalamus in response to decrease
preload vasoconstriction and reabsorbtion
of the sodium and water
12. During period of the systemic hypoperfusion
cellular and organ damage progress just because
of the direct effects of tissues hypoxia and local
activation of the inflammation.
Further injury is also occurs once restoration of
the normal circulation acid and K+ load that
has build up myocardial depression, vascular
dilatation and hypotension.
The cellular and humoral elements activated by
the hypoxia flushed back into circulation
further endothelial injury Acute lung injury,
acute renal injury, multiple organs failure and
death.
Reperfusion injury only attenuated by reducing
extent and duration of the tissue hypoxia.
13. Clinically shock is divided on the basis of the
initiating mechanism
1- Hypovolemic Shock
2- Cardiogenic Shock
3- Obstructive Shock
4- Distributive Shock
5- Endocrine Shock
14. Hypovolemic shock is caused by the reduce
circulating volume. It may be due to following
causes
1- Hemorrhage
2- Non – Hemorrhagic
Non-hemorrhagic causes includes following
1- Poor Fluid intake (dehydration)
2- Excessive loss of fluid in vomiting, diarrhea,
urinary loss as in diabetes and “third spacing” in
which fluid loss in GIT & interstitial space E.g.
bowl obstruction and pancreatitis.
Hopovolaemia is most common cause of the
shock and in some degree also component of the
all other shock.
15. Cardiogenic shock result from primary failure of the heart
to pump the blood to the tissues and causes of that shock
include followings
1- Myocardial Infarction
2- Cardiac Dysrhthemia
3- Valvular Heart Disease
4- Blunt myocardial Injury
5- Cardiomyopathy
Cardiac insufficiency may also be caused by myocardial
depression resulting from
1- Endogenous factors (Bacterial and humoral agents as in
sepsis)
2- Exogenous factors (pharmaceutical and drug abuse)
Evidence of the systemic hypertension with pulmonary or
systemic edema may co – exist with the classic signs of the
shock.
16. There is reduction in preload because of
the mechanical obstruction of the cardiac
filling.
Common causes of the obstructive causes
are followings
1- Cardiac Temponade
2- Tension Pneumothorax
3- Massive Pulmonary Embolus
In each of the above situation there is
dec. filling of the left or right ventricles
leading to reduce preload Fall In
Cardiac Output.
17. That describe the cardiovascular response
in variety of the conditions such as
1- Septic Shock
2- Anaphylaxis
3- Spinal Cord Injury
Inadequate organs perfusion accompanied
by the
1- Vascular dilatation
2- Hypotension
3- Low systemic vascular resistance
4- Inadequate afterload
18. There is vasodilatation is caused by the
release of the histamine in the systemic
circulation.
That occurs mostly in allergic reaction.
19. In high spinal cord injury there is failure of
the sympathetic outflow and that leads to
inadequate vascular tone.
20. There is release of the bacterial products
such as endotoxin and activation of the
cellular and humoral components of
immune system.
There is maldistribution of blood flow at
microvascular level with arteriovenous
shunting and dysfunction of cellular
utilization of the oxygen.
Mostly in the late phase of the septic
shock hypovolaemia result from fluid loss
into interstitial space and there may be
myocardial depression which complicate
the clinical picture.
21. Endocrine shock may present as complication
of
1- Hypovolemic Shock
2- Cardiogenic Shock
3- Distributive Shock
Causes Of Endocrine Shock
1- Hypo or Hyperthyroidism
2- Adrenal Insufficiency