2.  Definition :- shock is a syndrome in which
there is inadequate tissue perfusion
associated with reduction of cardiac
output (absolute or relative )

3.  Inadequate perfusion and oxygenation
and supply of nutrients to cells vital
organs
› Cellular dysfunction and damage
› Organ dysfunction and damage
› High mortality - 20-90%
› Early intervention reduces mortality

4.  Tissue perfusion is determined by Mean Arterial
Pressure (MAP)
MAP = CO x SVR
Heart rate Stroke Volume

5.  Four categories depending on cause of
reduced CO
1. Hypovolaemic shock
2. Cardiogenic shock
3. Distributive shock
4. Obstructive shock

6.  Reduced CO is due to low blood volume
 AKA cold shock
Causes
1. Hemorrhagic shock
2. Surgical shock
3. Burns shock
4. Dehydration shock
5. Traumatic shock

7.  Excessive vasodilatation due to toxic
substances or neural regulation
 Increased in capacitance of vessels
 CO decreases in spite of normal blood
volume
 AKA warm shock

8.  four types:-
I. Neurogenic shock
II. Anaphylactic shock
III. Septicaemic shock
IV. Endotoxic shock

9.  Causes :-two types
1. Marked reduction in sympathetic
vasomotor tone
a) Deep general anesthesia
b) Spinal anesthesia
c) Brain damage
2. Increased vagal tone :- vasovagal
syncope , emotional fainting

10.  Acute allergic reaction
 Large quantities of histamine
 Widespread vasodilatation
 Reducing peripheral resistance
 Increased capillary permeability
 Reduction in blood volume
 Leading to shock

11.  Septicaemia ?
 Bowel perforation , peritonitis
 Toxins produced by bacteria

13.  Heart’s pumping ability is reduced
 Severe systolic dysfunction
 Venous return is not pumped out
 So reduced CO
 Congestion of lungs and vicera
 AKA congested shock

14. 1. Myocardial infarction
2. Cardiac arrhythmias
3. Congestive heart failure

15.  External pressure on the heart which
reduces CO
 Reduces ventricular filling
› Pericardial tamponade
› Tension pneumothorax
› Constrictive pericarditis

18. 1. Non –progressive shock
2. Progressive shock
3. Refractory shock

19.  AKA compensated shock
 Moderate reduction in CO
 Occurs after loss of 10-15% of blood vol
 Leading to compensatory mechanisms
1. Immediate compensatory mechanisms
2. Long term compensatory mechanisms

20.  Includes three nervous reflexes
› Baroreceptor reflex
› Chemoreceptor reflex
› CNS ischemic response
› Others responses

21.  Baroreceptors – stretch receptors which
sense change in pressure
 Chemoreceptor – detects change in
chemical composition of blood

22.  Carotid body (chemoreceptor )
 Carotid sinus ( baroreceptor)
 Aortic arch contains both baro&
chemoreceptor

25.  Carotid sinus – glossopharyngeal nerve
corotid body
 Aortic arch – vagus nerve
Aaorti sinus

27.  When the BP falls
 Barorecptors gets inactivated
 They reduce their inhibitory effect on
VMC
 so increase in BP and HR

28.  Due to hypoxia
 When the blood pressure fall below
70mm/hg

29.  When the BP falls below 40mm/hg
 Ischemia of VMC
 Activation of VMC
 Increases symp dischrage
 Increases BP , HR , CO

31.  Occurs in all vessels except cerebral and
coronary vessels
 So it increases venous return
 In turn increases CO
 Skin becomes pale and cold
 Vasoconstriction of kidney reduces gfr
 Vasoconstriction of skeletal muscle
 So bypassing of blood to vital organs

32.  Due to chemoreceptor reflex
 Also because of hypoxia
 And by increasing thoracic pumping
action
 Increases CO

33.  Person becomes restless
 Increases pumping
 Increases venous return

34.  From adrenal medulla
 Increases symp drive
 i.e. vasoconstriction and increased HR
 Stimulates RAS

35.  ADH from posterior pituitary
 Increases water absorption
 Pressor action of vessels

36.  Increased glucocortioids
 Increases sensitivity of vessels to
catecholamines

37.  RAAS
 Reverse stress relaxation
 Capillary fluid shift mechanism

39.  Restoration of plasma volume and
proteins
› Plasma volume by 12 – 72 hours
› Proteins by 3-4 days by liver
 Restoration of red cell mass – will occur
within 10 days and fully restored by 4-8
wks

40.  Occurs after 15-25% loss of blood volume
 Compensatory mechanisms are not
effective
 Despite Intense vasoconstriction
 Not able to maintain BP , CO
 CVS begins to deteriorate
 Due to positive feedback cycles
 Timely intervention is needed
 Or will progress to refractory shock

41.  Cardiac failure
 Due to severe dec in BP
 Diastolic BP falls
 Blood supply to heart falls
 Weakens myocardium
 Leading to heart failure
 Acts as positive cycle

42.  There occurs a point where body fails to
circulate the vital organs
 Failure of VMC will produce widespread
vasodilatation
 So CO and BP are further decreased

43.  Due to hypoxia and metabolites
accumulation vasodilatation occurs
 Capillary permeability increases
 Pooling and sluggish blood flow
 Intravascular clotting occurs

44.  Hypoxia in GIT
 Damage to mucosal barrier
 Leading to entry of bacteria thro’ portal
circulation
 Damage liver and reaches systemic
circulation
 Systemic toxemia and septicemia
 Leading to irreversible shock

45.  Widespread tissue damage
 Liver (first) , heart , lung
 Failure of Na-K pump
 Reduced mitochondrial activity
 Activation of lysosomes
 Depleted nutrients (glucose mainly)
 Depleted action of hormones (insulin)
 Hypoxia – anaerobic metabolism – lactic
acid accumulation – Pco2 increase –
acidosis – vasodilatation (vicious cycle )

46.  Therapeutic interventions are ineffective
and patient dies eventually
 Point of no return – severe depletion of
ATP
 Leading to necrosis (death of tissues )
 Multi-organ failure
 Death

47.  Correcting a cause & helping
physiological compensatory
mechanisms
 General measures
1. Prevent sweating
2. Trendelenburg position

49.  Transfusion of whole blood
 Plasma
 Dextran
 Ringer lactate
 Normal saline

50.  Adrenaline
 Nor-adrenalin
 Dapamine
 Oxygen therapy
 Gluocorticoids

51.  Intestinal circulation
 Hepatic circulation
 Splenic circulation

52.  Normal intestinal blood flow is 20% of CO
 Which increases to 50 during digestion
 60 – 70 % of blood flow is to mucosa
 Countercurrent exchanger system in villi
noted
 Supply of oxygen to tip of the villi is
reduced
 i.e. intestinal necrosis is common in shock

53.  Gastric – 40ml/100g/min
 Intestinal – 60ml/100g/min
 Pancreatic – 80ml/100g/min

59.  Neural
 Autoregulation
 Metabolic regulation
› Adenosine
› Osmolarity
› Potassium
 By GI activity – functional hyperemia
› Due to gastric hormones

60.  28% of cardiac output
 Blood derived from two sources
› Portal – 75% (less oxygen content)
› Hepatic artery – 25% (rich in 02)
 1500ml/min or 58ml/100g/min

62.  Hepatic arterial buffer response
 Neural
 Metabolic
 Autoregulation
 Regulation by intestinal activity

63.  Filters blood
 Detoxification
 Metabolism and storage
 Reservoir of blood
 Contribute 60% of blood during shock
 Hepatomegaly
 Portal hypertension and ascitis

67.  Splenic artery
 Sympathetic vasoconstrictor fibers
 Splenic capsule contraction