Download Cardiovascular homeostasis in health & disease

CIRCULATORY SHOCK
Lecture by
Dr.Mohammed Sharique Ahmed Quadri
Assistant professor ,Physiology
‫بسم هللا الرحمن الرحيم‬
Objectives
• Define shock.
• Recognize types of shock – haemorrhagic,
anaphylactic, septic, and cardiogenic.
• Understand the shock by discussing changes
occurring in haemorrhagic shock.
• Explain compensatory response of body to
shock.
• Identify the concept of irreversible
(unresponsive) shock.
Circulatory shock
Is acute failure of circulatory system to supply
the peripheral tissues and organs of the body
with adequate blood supply, resulting in
cellular hypoxia.
TYPES OF SHOCK
HYPOVOLEMIC
CARDIOGENIC
OBSTRUCTIVE
DISTRIBUTIVE
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DISTRIBUTIVE
SHOCK
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Hypovolaemic
• Volume Loss
•
Blood loss
Plasma Loss
ECF Loss
-Haemorrhage
-Burns
- Vomiting & Diarrhoea
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Hypovolumic shock
• Is most widely studied shock & often used as
prototype in discussion of manifestations of shock
• Hypovolemic shock is also called "cold shock."
• It is characterized by
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–
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Hypotension;
Rapid, thready Pulse;
Cold, Pale, Clammy Skin;
Intense Thirst;
Rapid Respiration;
Restlessness .
Hemorrhagic shock
Hemorrhage
Decrease blood volume
• It illustrate the features of a major
form of hypovolemic shock and the
multiple compensatory reactions
that come into play to defend ECF
volume
Decrease venous return
Decrease stroke volume
Decrease cardiac out put
Decrease arterial pressure
Compensatory response
Compensatory reactions activated by
hemorrhage.
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–
–
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–
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Vasoconstriction
Tachycardia
Venoconstriction
Tachypnea→increased thoracic pumping
Restlessness→increased skeletal muscle pumping (in
some cases)
Increased movement of interstitial fluid into capillaries
Increased secretion of norepinephrine and epinephrine
Increased secretion of vasopressin
Increased secretion of renin and aldosterone
Increased secretion of erythropoietin
Increased plasma protein synthesis
Points to Ponder
• Goal of compensatory mechanisms
is to maintain cerebral and cardiac
perfusion
•Vasoconstriction of splanchnic, and
renal blood flow
• Compensatory mechanisms are not
effective over the long term and fails
when shock state is prolonged.
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Effect of hemorrhage on mean arterial
pressure
Stages of Shock
1. Non progressive stage or Compensated
stage: in this circulatory compensatory
mechanism cause Full recovery without
therapy
2. Progressive stage: Decreased BP AND COP.
Here without therapy ,shock gets worse.
3. Refractory shock or Irreversible stage : Here
patient does not respond to Treatment .
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Irreversible or refractory shock
Factors contributing irreversible shock
• Cerebral ischemia
– Depression of vasomotor and cardiac areas of the brain
(vasodilatation , decreased BP, decreased HR)
• Myocardial depression due to Acidosis causes decreased
COP
• Respiratory failure (ARDS)
– triggered not only by shock but also by sepsis, lung contusion,
other forms of trauma.
– Damage to capillary endothelial cells and alveolar epithelial cells,
with release of cytokines.
Cardiogenic
• Pump Failure
May be due to
– Inability of heart to Contract or
– Inability of heart to pump blood
• Myocardial damage ( M.I)
• Arrhythmias
• Valvular damage
Symptoms are those of shock and heart failure
( pulmonary oedema)
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Distributive
• Decreased Peripheral Vascular Resistance (blood
volume is normal but vascular capacity
increases, i.e. relative hypovolemia)
• Septic Shock (inflammatory mediators)
• Neurogenic Shock (loss of sympathetic control on
vascular tone)
• ANAPHYLACTIC shock (presence of vasodilator
substances like histamine)
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Anaphylactic Shock
• Systemic response to the inflammatory
mediators released in type I
hypersensitivity
– Histamine, acetylcholine, kinins, leukotrienes, and
prostaglandins all cause vasodilation and increase
capillary permeability
º What will happen when arterioles vasodilate throughout the
body?
º What will happen when there is increase vascular
permeability
– Acetylcholine, kinins, leukotrienes, and prostaglandins
all can cause bronchoconstriction
SEPTIC SHOCK
• Usually due to gram-negative bacteria
• Endotoxins released by gram-negative
Bacteria—cause VASODILATATION(Skin is
warm therefore called WARM SHOCK).
• High fever
• Increased capillary permeability with loss of
fluid in tissues
• Mortality is 30-50%
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Neurogenic shock
• In Neurogenic shock, there is decreased
sympathetic activity, therefore, increased
vascular capacity.
• Reason—Sudden loss of Vasomoter Tone
resulting in massive dilation of veins therefore
Venous pooling of blood and decreased venous
return to heart.
• Causes of Neurogenic shock
• Brain injury
• Depressant action of drugs
• General anesthesia (barbiturate)
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Fainting and Syncope
• Fainting--Feeling of dizziness due to decreased
cerebral perfusion but not sufficient to cause
loss of consciousness.
• Syncope—Temporary impairment of
consciousness due to reduction in cerebral
blood flow
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Vasovagal syncope
• Vasovagal attacks---Increased Vagal
activity,ANS Disturbance
-- It causes vasodilatation due to sympathetic
inhibition therefore pooling of blood in
extermities and Fainting.
--Bradycardia
--It is short lived and Benign.
• Causes-----overwhelming Fear, or severPain
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Fainting/ syncope
• Other forms of syncope include
– postural syncope, due to pooling of blood in the
dependent parts of the body on standing from lying
down or sitting possition .
– Micturition syncope, during urination, occurs in
patients of orthostatic hypotension It is due to the
combination of the orthostasis and reflex
bradycardia induced by voiding in these patients.
Fainting/ syncope
– Pressure on the carotid sinus, produced, for
example, by a tight collar, can cause such marked
bradycardia and vasodilation that fainting results
(carotid sinus syncope).
– Rarely, vasodilation and bradycardia may be
precipitated by swallowing (deglutition syncope).
– Cough syncope occurs when the increase in
intrathoracic pressure during straining or coughing is
sufficient to block venous return
References
• Human physiology by Lauralee Sherwood,
seventh edition
• Text book physiology by Guyton &Hall,11th
edition
• Text book of physiology by Linda .s
contanzo,third edition