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‫االسراء اية ‪58‬‬
‫‪Dr abdelaziz Hussein, Mansoura‬‬
‫‪Faculty of Medicine‬‬
By
Dr. Abdel Aziz M. Hussein
Lecturer of Medical Physiology
Member of American Society of Physiology
Dr abdelaziz Hussein, Mansoura
Faculty of Medicine
Dr abdelaziz Hussein, Mansoura
Faculty of Medicine
◊ Def,
• Shock means inadequate tissue perfusion.
◊ Types of shock:
1.Spinal shock.
2.Electric shock.
3.Thermal shock caused by severe cold or
severe heat.
4.Metabolic shock, e.g.:
• Hepatic failure.
• Renal failure.
• Diabetic coma.
• Toxic shock.
Dr abdelaziz Hussein, Mansoura
Faculty of Medicine
◊ Types of shock:
5. Circulatory shock, e.g.:
• Hypovolemic shock.
• Low-resistance shock.
• Cardiogenic shock.
Dr abdelaziz Hussein, Mansoura
Faculty of Medicine
Dr abdelaziz Hussein, Mansoura
Faculty of Medicine
Dr abdelaziz Hussein, Mansoura
Faculty of Medicine
◊ Manifestation:
• Hypovolemic shock is characterized by:
1. Hypotension.
2. Rapid weak pulse.
3. Pale, cold, sweaty skin.
4. Rapid respiration.
5. Intense sense of thirst.
6. Anxiety and restlessness.
Dr abdelaziz Hussein, Mansoura
Faculty of Medicine
◊ Causes :
•1. Haemorhagic shock:
•It is a hypovolemic shock caused by blood loss.
•Haemorrhage ↓es the mean systemic filling pressure
→↓es the VR→ ↓es COP below normal, and shock
occurs.
Dr abdelaziz Hussein, Mansoura
Faculty of Medicine
2. Hypovolemic shock caused by plasma
loss:
• It is due to severe loss of plasma without
loss of whole blood.
• This occurs in the following conditions:
a. Intestinal obstruction:
• Distension of the intestine causes fluid to
leak from the intestinal capillaries into the
intestinal walls and intestinal lumen→
marked ↓ of plasma volume.
Dr abdelaziz Hussein, Mansoura
Faculty of Medicine
2. Hypovolemic shock caused by plasma loss:
b. Severe burns:
• Extensive burns cause severe loss of plasma through
the burned areas→ marked ↓ of plasma volume.
c. Trauma
• Trauma or contusion to the body causes damage the
capillaries → excessive loss of plasma into the tissues.
d. Dehydration:
• Dehydration means loss of fluid from all fluid
compartments of the body e.g. in:
1. Excessive sweating.
2. Severe diarrhea or vomiting.
3. Nephrotic kidney. Dr abdelaziz Hussein, Mansoura
Faculty of Medicine
Dr abdelaziz Hussein, Mansoura
Faculty of Medicine
• It is caused by widespread VD which
markedly ↑es the capacity of the CVS.
• The blood volume is normal but, the mean
circulatory pressure is ↓ed→ ↓ VR, the COP
and the ABP → shock.
• High blood flow in the skin and makes it
warm, so it is called warm shock.
◊ Manifestation:
• The same manifestations of hypovolemic shock
except the skin is warm
Dr abdelaziz Hussein, Mansoura
Faculty of Medicine
◊Types of low-resistance shock:
• a) Neurogenic shock:
• It occurs by strong emotions, severe pain and
irritation of the trigger zones which leads to:
1. Inhibition of VCC → VD and ↓ ABP.
2. Inhibition of CAC → tachycardia.
3. VD of blood vessels of skeletal ms and diffuse
discharge of the symp VD fibers and
generalized VD.
4. ↓ed COP, ABP and fainting due to ↓ed cerebral
blood flow which worsen shock.
Dr abdelaziz Hussein, Mansoura
Faculty of Medicine
◊Types of low-resistance shock:
b) Anaphylactic shock:
• It is a severe allergic reaction which releases
large amounts of histamine → causes
massive VD.
c) Septic (endotoxin) shock:
• It is due to invasion of the blood by bacteria or
their toxins (endotoxin).
• The infection may be transmitted to the blood
from, e.g. peritonitis, generalized skin infection,
gangrenous area or from kidney, urinary
tract, or GIT infection.
Dr Abdelaziz Hussein, Mansoura
Faculty of Medicine
◊Types of low-resistance shock:
c) Septic (endotoxin) shock: manifested by;
1. High fever
2. Marked VD throughout the body due to excessive
release of nitric oxide (NO) (in infected tissues)
3. Development of microclots in widespread areas
of the body→ disseminated intravascular
coagulation.
Dr Abdelaziz Hussein, Mansoura
Faculty of Medicine
Dr abdelaziz Hussein, Mansoura
Faculty of Medicine
• This shock is caused by severe depression
of the pumping action of the heart as in
myocardial infarction → marked ↓ of COP and
ABP.
• It is suggested that certain chemical agents
(e.g. serotonin) released from the diseased
myocardium stimulates the ventricular
baroreceptors causing reflex inhibition of the
VMC leading to VD which worsens the
shock.
Dr Abdelaziz Hussein, Mansoura
Faculty of Medicine
◊ Manifestations:
• As hypovolemic shock plus the manifestations
of acute heart failure and congestion of the
lungs (congested shock).
Dr Abdelaziz Hussein, Mansoura
Faculty of Medicine
Dr abdelaziz Hussein, Mansoura
Faculty of Medicine
◊ Def,
• It is a type of hypovolemic shock due to blood loss.
◊ Manifestations:
• See before
◊ Stages:
• Its severity depends off the amount and the rate of
blood loss.
• It may be either:
Dr Abdelaziz Hussein, Mansoura
Faculty of Medicine
◊ Stages:
1) Reversible shock:
• It occurs if the amount of blood loss is less than
20% of total blood volume.
• The compensatory mechanisms succeed to
restore the ABP to its normal level with the help
of appropriate treatment by vasopressors and
blood transfusion.
Dr Abdelaziz Hussein, Mansoura
Faculty of Medicine
◊ Stages:
2) Irreversible shock:
• It occurs if the amount of blood loss is more than 30%
of total blood volume.
• The compensatory mechanisms failed to restore the
ABP to its normal level.
• The patient may:
1. Die soon after haemorrhage.
2. Recover with treatment.
3. Persist shock for 3-5 h and can't respond to
vasopressor drugs, so COP and ABP ↓→ this state is
called irreversible shock which usually ends with death.
Dr Abdelaziz Hussein, Mansoura
Faculty of Medicine
◊ Mechanisms:
A) +ve feed-back death cycles:
• These are dangerous cycles that eventually lead to
circulatory failure and death → death cycle:
Dr Abdelaziz Hussein, Mansoura
Faculty of Medicine
◊ Mechanisms:
A) +ve feed-back death cycles:
a. Cerebral ischemia:
• Hge → results in hypotension and cerebral ischemia
→ results in depression of the VMC and cardiac
centers→ bradycardia and VD→ further drop of ABP
that leads to more ischemia with more depression and
so on.
Dr Abdelaziz Hussein, Mansoura
Faculty of Medicine
◊ Mechanisms:
A) +ve feed-back death cycles:
•b. Myocardial depression:
•Hge → results in hypotension, tachycardia, ↓ed coronary
blood flow→ myocardial ischemia→ ↓ed force of
contraction, ↓ed COP, and hypotension and so on.
Dr Abdelaziz Hussein, Mansoura
Faculty of Medicine
◊ Mechanisms:
A) +ve feed-back death cycles:
•c. Ischemia to the GIT;
•When the blood flow to the GIT mucosa is inadequate→
injury and subsequent breakdown of the gut mucosal
barrier.
•This allows translocation of bacteria and endotoxin to enter
the systemic circulation. Endotoxin stimulates nitric oxide
(NO) synthesis→ VD and drop of ABP.
•This worsens the condition and so on.
Dr Abdelaziz Hussein, Mansoura
Faculty of Medicine
◊ Mechanisms:
• B) Relaxation of the precapillary sphincter:
• At the beginning of shock there is spasm in the
precapillary sphincter and venules especially in the
splanchnic area.
• This leads to hypoxia and tissue damage within 3-5
hours.
• The
precapillary
sphincters
then
dilatation of the venules leading to:
Dr Abdelaziz Hussein, Mansoura
Faculty of Medicine
dilate
without
Dr abdelaziz Hussein, Mansoura
Faculty of Medicine
◊ Mechanisms:
• B) Relaxation of the precapillary sphincter:
• 1. Stagnation of blood in the capillaries
(stagnant hypoxia) → more tissue damage
occurs including the capillary walls→ marked ↓ in
VR, COP and ABP.
• 2. Damage of the capillary wall leads to
escape of plasma protein and of the whole blood
out of the vascular system.
• At this stage the shock becomes irreversible
and administration of fluid or blood is useless.
Dr Abdelaziz Hussein, Mansoura
Faculty of Medicine
Dr abdelaziz Hussein, Mansoura
Faculty of Medicine
• 1. Treatment of the cause of shock.
• 2. General measures:
• a. Warming the patient, but avoid over-heating
as it causes VD → further drop of ABP.
• b. Raising the foot of the bed to help the VR
and improves the cerebral blood flow.
• 3. Restoration of adequate level of tissue
perfusion by transfusion of blood, plasma
or
saline as early and rapidly as possible to provide
adequate blood flow to the vital organs i.e. brain,
heart.
Dr Abdelaziz Hussein, Mansoura
Faculty of Medicine
• 4. Drugs used in the treatment of shock:
• - Adrenaline and noradrenaline to produce
arterial VC and to ↑ the force of ventricular
contraction.
• - Glucocorticoids as they decrease the
permeability of the capillaries.
• -Sedatives should be given in small doses as
they inhibit the VC and CAC.
Dr Abdelaziz Hussein, Mansoura
Faculty of Medicine
THANKS
Dr abdelaziz Hussein, Mansoura
Faculty of Medicine