1. CIRCULATORY SHOCK Lecture by Dr.Mohammed Sharique Ahmed Quadri
Assistant professor ,Physiology

2. بسم الله الرحمن الرحيم

3. 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.

4. 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.

5. TYPES OF SHOCK
HYPOVOLEMIC
CARDIOGENIC
OBSTRUCTIVE
DISTRIBUTIVE

6. DISTRIBUTIVE SHOCK

7. Hypovolaemic Volume Loss Blood loss -Haemorrhage Plasma Loss -Burns
ECF Loss - Vomiting & Diarrhoea

8. 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 .

9. Hemorrhagic shock
Hemorrhage
Decrease arterial pressure
Decrease cardiac out put
Decrease blood volume
Decrease venous return
Decrease stroke 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

10. Compensatory response

12. 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

13. 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.

14. Effect of hemorrhage on mean arterial pressure

15. Stages of Shock
Non progressive stage or Compensated stage: in this circulatory compensatory mechanism cause Full recovery without therapy
Progressive stage: Decreased BP AND COP. Here without therapy ,shock gets worse.
Refractory shock or Irreversible stage : Here patient does not respond to Treatment .

16. 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.

17. 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)

18. 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)

19. 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

20. 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%

21. 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)

22. 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

23. 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

24. Other forms of syncope include
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.

25. 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

26. 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