CIRCULATORY SHOCK

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CIRCULATORY SHOCK

• Lecture by
• Dr.Mohammed Sharique Ahmed Quadri
• Assistant professor ,Physiology

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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.

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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.

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TYPES OF SHOCK

• HYPOVOLEMIC
• CARDIOGENIC
• OBSTRUCTIVE
• DISTRIBUTIVE

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DISTRIBUTIVE SHOCK
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Hypovolaemic

• Volume Loss
• Blood loss -Haemorrhage
• Plasma Loss -Burns
• ECF Loss - 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
• Hypotension
• Rapid, thready Pulse
• Cold, Pale, Clammy Skin
• Intense Thirst
• Rapid Respiration
• Restlessness .

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Hemorrhagic shock

• It illustrate the features of a major form of
  hypovolemic shock and the multiple compensatory
  reactions that come into play to defend ECF volume

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Compensatory response
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Compensatory reactions activated by hemorrhage.

• 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

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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
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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.

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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
• What will happen when arterioles vasodilate
  throughout the body?
• What will happen when there is increase vascular
  permeability
• Acetylcholine, kinins, leukotrienes, and
  prostaglandins all can cause bronchoconstriction

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SEPTIC SHOCK

• Usually due to gram-negative bacteria
• Endotoxins released by gram-negative
  Bacteriacause 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.
• ReasonSudden 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.
• SyncopeTemporary 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.
  

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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

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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