The document discusses different types of shock and their pathophysiology. It defines shock and describes classifications proposed by Blalock and others. Types include hemorrhagic, cardiogenic, obstructive, distributive, and endocrine shock. The body responds to shock through neuroendocrine and physiological changes aimed at maintaining perfusion. These include activation of the sympathetic nervous system, renin-angiotensin-aldosterone system, and antidiuretic hormone among others. Clinical assessment and management of shock are also covered.

2.  It is a patho-physiological condition
clinically recognized as a state of
inadequate tissue perfusion.
 Cerra described shock as ‘ disordered
response of organism to an inappropriate
balance of substrate supply and demand
at a cellular level’.
 Shock is a systemic disorder that disrupts
vital organs function as the eventual result

3.  Blalock in 1934 classified shock on the
basis of etiology:
1. Hematogenic
2. Neurogenic
3. Vasovegal
4. Cardiogenic.

4.  Hematogenic or traumatic shock
characterized by global hypo perfusion.
 Vasogenic and septic is associated with
hyper circulation resulting in mal-
distribution of regional or intra-organ
blood flow.

5. Hypovolumic
Cardiogenic
Obstructive
Distributive
Endocrine

6. Hematogenic
Traumatic
Neurogenic
Cardiogenic
Septic
Miscellaneous types

8.  Decrease in circulatory intravascular
volume causing hypo-perfusion and
increase adrenergic activity.
 Intravascular volume lost increase
peripheral resistance in regional arteriolar
beds (skin, gut and kidney)
decreasing blood flow in these organs.
 Clinical presentation: anxious and
restlessness and upon treatment present

9.  On examination: (on bed side)
1. Pale
2. Cool skin
3. Blanching of bowel with
4. Decreased pulses in mesentery

10.  Decrease circulatory volume
tachycardia to prevent stroke volume.
 Ortho-static test (asking patient to stand)
may unmask cardio-vascular instability
with tachycardia and hypotension in
patients who appear stable when
examined in supine position.
 (in ortho-static state there is 30% decrease in
circulating blood volume)

12. Loss of circulating intravascular volume
Increased of peripheral resistance
Redistribution of
blood in organs in heart and brain Vascular
tone resistance
In expense of cutaneous, splenchinic and renal
circulation

13.  Decrease in intravascular volume
stimulate sympathetic response activity
decrease in vagal inhibition increase
rate & force of cardiac contraction
increase cardiac contraction
Tachycardia cardiac output +
myocardial O2 consumption increases
 Blood pressure is maintained by increase

14. Loss of blood decrease in capillary
hydrostatic pressure trans-capillary
influx of extra-vascular extra cellular fluid
from interstitial space causes alteration in
starling law (increase in right ventricular
filling cause increase in force of
contraction)
Mobilization of interstitial fluid pool into
intravenous space lead to
Increase in circulatory intravascular volume

15.  Due to hemo-dilution increase O2
carrying capacity Enhance in tissue
extraction of O2 due to acidosis &
Erythrocytosis 2,3- diphosphoglycerated
hemoglobin.
Acidosis due to decrease in excretion and
accumulation of cellular substrate
anaerobic respiration and glucose
metabolism.
 It also cause right ward shift of O2
dissociation curve to decrease in

16. Hypoxia also stimulate respiratory centre
 Hyper-ventilation
 Respiratory alkalosis
 Increase in erythrocytosis (2-3 DPG).
 More rightward shift of O2 dissociation
curve.

17.  Arteriolar constriction & loss of circulating
volume
 Decrease renal blood flow
 Stimulated of afferent and efferent
arterioles causing corticomedullary shunt
to maintain
 Effective GFR
 Urine output is subsequently decrease
 Salt water & urea and uric acid retained
 Decrease in buffering capacity
 Loss of control of acid base balance

18.  Change in blood volume with afferent sensory
impulses lead to marked release of
epinephrine and non epinephrine by adrenal
gland lead to
1. Retention of water and salt in proximal
convoluted tubule.
2. Vasoconstriction and tachycardia
increase Blood pressure and cardiac output.
3. Stimulate glycogenolysis, lipolysis and
skeletal muscle breakdown & inhibition of
insulin release.
4. Promoting glucose metabolism in brain and

19. 1. Decrease blood volume
2. Decrease arterial pressure
3. Pain
4. Hypoxemia
5. Hypothermia
 Leads to release of Adreno-cortico-tropic
hormone ACTH by pituitary.
 in severe hemorrhage circulatory cortisol
provide no feed back inhibition on ACTH
release, but feedback is restored as blood
volume is restored.

20.  Cortisol potentiate the
 action of epinephrine & glucagon on
glucose metabolism
 Insulin resistance,
 Stimulate mobilization of amino acid from
skeletal muscle.
 Also causes retention of Na+ & water
retention.

21.  Insulin secretion is diminished
 Relative hypo-insulinemia: helps in
mobilization of amino acid and fats stores
by glucagon, cortisol, and growth
hormone.

22.  Anti diuretic hormone (ADH)/arginine
vasopressin(AVP) released in response of
increase serum osmolarity and hypovolemia
(potential stimulator) causes:
1. Increase water permeability &
2. Passive Na+ transport in DCT of nephrone
3. Increase water resorption
4. Potent splenchnic vasoconstrictor

23.  Activation of renin angiotensin system
(RAS) due to increased sympathetic
stimulation of juxta-glomerular cells by
1. β- adrenergic mechanism
2. Decreased renal perfusion
3. Compositional changes of tubular fluid.
 Renin release from juxta glomerular
appartatus causes increased production
of angiotensin I which convert to
angiotensin II in lungs.

24.  Angiotensin II powerful arterial and arteriolar
vasoconstrictor causes:
1. Renal prostaglandin production; PGE2 and
kallikreins dilates renal vessels
increase renal flow
2. Release of aldosterone and ACTH.
 Aldosterone
1. Increase Na+ re-absorption in DCT
2. Excretion of K+ & H+
3. Excretion of byproducts of anarobic
metabolism and cellular damage.

25.  10% blood loss: no evidence of clinical
shock
 25 % blood loss: hypotension
 18-26 % blood loss : functional
extracellular volume loss with RBC and
plasma
 35-45 to 50 % blood loss: further loss of
extracellular volume loss with RBC and
plasma.

26.  In severe shock: decrease in early
equilibrating extracellular fluid available for
intravascular influx, whole total anatomic
extracellular fluid may be normal.
 Blood reinfusion restores RBC mass and
plasma, but not extracellular fluid volume.
Which is achieved by salt solution or ringer
lactate (mortality decreased from 80 % to 30
%)

27. Ionic differences:
 In muscles and liver tissues membrane
potential gradient serves as a reliable
indicator of cellular dysfunction during
hemorrhagic shock
 During profound hemorrhagic shock:
trans-cellular potential gradient falls from -
90 to -60mV.
 Cellular swelling
 Decease ATP production
 Changes in membrane permeability due to

28.  Nitric oxide (N2O) : free radical
 Release due to endotoxin and pro
inflammatory cytokines (IL-I, TNF).
 Potent relaxant of basal blood pressure.

29. Classifications
1.According to source
a) External hemorrhage
(revealed outside/ seen externally)
b) Internal hemorrhage or concealed hemorrhage
(not seen from outside)
eg. Fracture, bleeding peptic ulcer, rupture of
spleen, liver.
Concealed bleeding can be external viz.
hematemesis/ melaena from bleeding peptic
ulcer, hematuria from rupture kidney.

31. 3. According to percentage ex-sanguination
of blood
Class I : blood loss up to 15%
Class II : 15-30%
Class III: 30-40% (need for blood)
Class IV : more than 40%

32. IN OPERATION THEATRE:
IN OUTPATIENT
DEPARTMENT
 Weighing of soaked
cotton.
 Measuring the size of
soaked gauge.
 Hematocrit.
 Hemoglobin.
 Blood pressure.
 Pulse pressure.
 Central venous pressure.

33. 1. BP
2. Respiration
3. Urine
4. CVP
5. ECG
6. Swan – ganz catheter.

34. 1. Resuscitation :
a. Clear airway
b. adequate ventilation.
2. Immediate control of bleeding :
a. Raising foot end of bed
b. Compression bandage
c. After resuscitation surgery.

35. (most important)
a. In ER – insert large gauge needle,
catheter in arm or leg.
In sophisticated centre 2 catheters are
placed, one in vein & another in sub-
clavian or jugular vein to measure CVP.
b. In initial stage give ringer lactate 1-2L in
45 min. to restore BP.
c. Grouping and cross matching of blood.

36. Sedatives: Use to alleviate pain in patients
with shock.
Morphine i.v.: adults without head injury and
acute abdominal injury.
children's : barbiturates
Head injury : largactil.
Chronotropic agents: atropine followed by
isoproterenol.
Increases heart rate with vasodilatation of
systemic arterial and capillary sphincters.

37. Inotropic agents: improves strength of
cardiac muscle contractility.
Cardiogenic, septic shock
Dopamine and dobutamine.
In low dosages, increase myocardial
contractility
selectively increase renal blood flow by
dilating renal vasculature.
Vaso-constrictive effect.

38. Pathophysioloy:
Traumatize tissue activates coagulation system
and release micro thrombi in circulation.
These may occlude or constrict parts of
pulmonary microvasculature to increase
pulmonary vascular resistance.
Increase right ventricular diastolic pressure
and right atrial pressure.
micro thrombi induce generalize permeability
in capillary permeability leads to the plasma
loss into interstitial tissues throughout the
body.
Causes decrease in vascular volume to a
greater extent.

39. Clinically similar to hypovolaemic shock.
Two differentiating features includes
1. Presence of peripheral and pulmonary
edema.
2. Inadequate volume of fluid after infusion
of large volume of fluids which was
sufficient for hypovolaemic shock.

40. 1. Resuscitation : mechanical ventilator
support is more needed.
2. Local treatment of trauma and control of
bleeding.
3. Fluid replacement:
1. More fluid needed.
2. Role of anticoagulant therapy to prevent
disseminated intravascular coagulation
(debatable:- as it can increase bleeding/
prevent large clot formation, if use at what
dose? ).

41. Bed side monitoring of circulatory efficiency:
 HR
 Arterial blood pressure
 Urinary output
 Peripheral perfusion

42.  In patients with multiple injuries: CVP
central venous pressure (0-5cm of H2O)
monitoring is useful.
Normal to depressed CVP that does not rise
with rapid administration of crystalloids
(RL,NS) indicate continuing hypo-
volumemia.
Elevated CVP or its rapid rise: indicative of
impairment of pumping mechanism.

44.  When the heart is unable to generate
sufficient cardiac output to maintain
adequate tissues perfusion.
 It has significant mortality and morbidity
when manifest with myocardial if action
and secondary end organ injuries of
pulmonary edema, oligouric renal failure.

45.  Myocardial infarction result from
1. Valvular heart disease
2. Cardio-myopathy
3. Direct myocardial contusion.
 Acute myocardial infarction is most
frequent cause, complications include
 Papillar muscle dysfunction
 Ischemic ventricular septal defect
 Massive left ventricular infarction
 Arrhythmias

46.  Initial compensatory response
 Tachycardia for decreases myocardial
infarction.
 To maintain cardiac output
 despite of decreased left ventricular
ejection fraction and
 At the expense of increasing myocardial
oxygen consumption.

47. Cardiac index: cardiac output/body surface
area.
(4-8L/min/m2)
 As cardiac index falls below 2L
hypotension produces--- reflex
sympathetic vasoconstriction.
 In attempt to maintain Central Venous
Pressure (0-5cmH2O)
 Lead to decrease in organ perfusion.

48. It requires prompt intervention as
 Increased myocardial demand
 Hypotension
 Shortened diastole
Amplifies the mismatch between coronary
artery oxygen delivery and myocardial
oxygen demand
Extends the zone of infraction

49.  Goal : Enhance ventricular performance
 Improve global hypo perfusion.
 Management:
 Fluid with inotropic drugs: maximize
ventricular performance + increase myocardial
oxygen demand.
 Including
 Limit infract size
 Protection of reversibly ischemic myocardium
 Minimize myocardial oxygen demand.
 Early reperfusion.

50.  Early :
 Supplemental oxygen
 Pain relief
 Sedation
 Continuous electrographic monitoring.
 Foleys catheter to monitor urine output.
 Cutaneous oximetery.
 Automated arterial blood pressure cuff
 blood gas estimation

51.  In critically ill patients: crucial
therapeutic decision making
done on the basis of
measurements of Swan-ganz
catheter: Cardiac output and
pulmonary arterial wedge
pressure (pressure of left
atrium).
 In cardiogenic shock Low
cardiac output & pulmonary
hypotension causes normal

52.  Small increase in left ventricular filling
pressure by volume infusion maximizes
cardiac output.
 Emphasis should be given that although
hemodynamic measurement suggest
myocardial insuffiency: mechanical
obstructions should be ruled out;
1. Cardiac temponade in injured patients
2. Pulmonary embolism in the post-operative
patients.
 These diagnosis is made on clinical grounds
in emergency with large volume infusion if

53.  Ionotrpic drugs: beta 1 adrenergic
receptors responds to exogenous
sympathomimatic drugs to increase
contractility and improve cardiac output.
 In expense of compromised myocardial perfusion.
 I.V. infusion of dopamine may promptly
reverse life threatening hypotension and
restore mean arterial pressure around
80mmHg.
 At low dose (2-5µg/kg/min): spleen and
coronary vasodilatation
 At higher dose (5-8µg/kg/min): increase
contractility, heart rate with prominent α-

54.  Side-effects of dopamine: variable
increase in HR can ppt. arrhythmias.
Therefore need to be titrated to lowest
acceptable dose.
 Dobutamine: predominate ionotropic
effect; less arrhythmiogenic & redistribute
cardiac output in coronary circulation.
 Useful in cardiopulmonary bypass and
myocardial infarction.

55.  Vasodilating agent:
 on clinical assessment pt with decrease
perfusion pressure have near normal arterial
pressure in with low cardiac output and high
filling pressures.
 The high systolic ventricular pressure can be
corrected by decreasing after-load which in
turn increases cardiac output.
 Sodium Nitropusside can be used with
extreme caution to prevent redistribution
away from the compensated coronary and
cerebral circulation causing decrease

56. Mechanical support:
 Temporary support the failing
myocardium by reducing load of left
ventricles and decreasing oxygen
demand.
 Intra- aortic balloon pulsation device:
inflates at diastole– elevates diastolic
pressure– increase pulmonary perfusion–
decreasing myocardial work by increasing
Cardiac output distal to ventricles.

57.  Arrhythmias: rapid ventricular rates
decrease cardiac output to shock levels.
 As filling time decrease ventricular end
diastolic pressure decreases– stroke
volume decreases– cardiac output
decreases.
 Digoxin is drug of choice for atrial
fibrilation.
 Electro-cardioversion should be promptly
done to prevent tachycardia (can cause

58.  Verapamil is useful in treating
tachyarrhythmia of atrial origin.
 Cardiogenic shock with loss of
consciousness: Immediate unsynchronized
direct current electric shock(cardioversion) is
mandatory for ventricular fibrillation.
 Lodocain i.v. is initial treatment for prevetion
of recurrent ventricular fibrillation after
cardioversion.
 Bretylium tosylate is useful in life threatening
ventricular tachyarrhythmia's unresponsive to
lidocaine.

59.  Ventricular bradycardia: low cardiac
output with ventricular rate 70 beats /min.
stroke volume cannot be increase due to
pathologic bradycardia (atrial fibrillation
with slow ventricular rate)
 Electrical pacing of heart at rate of 80-100
beats/min restore sufficient output.

60.  Primary shock (older classification)
 Occurs after serious interference with the
vasodilator and vasoconstrictor influence on
arterioles and venules.
 Clinically seen in syncope.
 On sudden exposure to unpleasant events,
such as
 sight of blood,
 hearing of bad news,
 sudden onset of pain

61.  Clinical manifestation:
1. Blood pressure– extremely low
2. Pulse rate– slower than normal
3. Dry , warm and even flushed skin.
 Determination of the shock:
 Decreased cardiac output with
 Decrease in resistant to arteriolar vessels and
 Decreased resistant to venous tone.
 Normo-volumic with increase reservoir
capacity in arteriole and venules – decrease
venous return to right side of heart–
decrease in cardiac output.

62. Management:
 Shock due to high spinal anesthesia –
adminstartion of fluid and vesopressor
(ephedrine/ phenylephrine).
 Increase cardiac output and elevates
systemic blood pressure by arteriolar
constriction.
 Milder form (fainting):
 remove the patient from stimuli,
 Reliving of pain,
 Elevating legs
 Till vasoconstrictor nerves regain its ability.

63.  Shock resulting from injury, as in spinal
cord tran-section from trauma leading to
significant loss of blood and extracellular
fluid around cord and vertebral column.
 Before surgical intervention hemodynamic
management should be done.
 Uncomplicated neuralgic shock: slightly
low central venous pressure and near
normal cardiac output, which decreases
upon hypovolemia.

64.  Monitoring:
 Fluid administration without vasopressor
produce– gradual rise in arterial pressure
and cardiac output without elevation of
central venous pressure (as there is increase
in filling due to increase in intravascular fluid
volume).
 Slight volume infusion has better prognosis
than to vasopressor as it decrease organ
perfusion proximal to spinal cord.
 Best balance -- from normal central venous
pressure with rise of rapid fluid administration
and use of vasopressor (phenyephrine) to

65.  Defined as continuation of human
response to infection.
 Cause
 Virus
 Parasite
 Fungi
 Most common– gram negative bacteria
and gram positive occasionally.

66.  Increase incidence of gram negative sepsis
has rises due;
1. Developing reservoir of resistant and
virulent organism.
2. Concentration of infected patients in critical
care.
3. More extensive operation in elderly and
poor risk patients.
4. Initial rescue of severely injured patients.
5. Growing population of immuno-suppresed
patients by organ transplant protocols,
radiotherapy and chemotherapy.

67.  Most common source of gram negative
organism is genitourinary system.
 Second most common cause respiratory
system.
 Third : alimentary system
 Biliary tract.

68.  Clinical manifestation:
 Onset of chills
 Temperature elevation above 101°F (38°C).
 Rapidly progressive evidence of altered organ
function (most often renal and pulmonary).
 Development of hypotension.
 Normo-volumic with hypotension despite
normal cardiac output and filling pressure.

69.  Also called ‘Warm shock’ with pink and dry
extremities due to low peripheral
resistance.
 High cardiac output with decrease oxygen
utilization and less oxygenation difference
between arteries and vein.

70. Patient who is already in hypovolumic shock ,
presents characteristic hypo dynamic pattern
which is :
 Falling cardiac output.
 Low central pressure
 Increased peripheral resistance with more
typical
 Cold
 Pale extremities seen in global hypo-perfusion.
 Early volume replacement increases cardiac
output and hyper dynamic circulation, later
patients becomes unresponsive to volume

71.  Lab investigation shows
 Elevated WBC count
 Leucopenia may be present in imuno-
compromised and debilitated patients or
patients with exhausted white cells from
sepsis.
 Thrombocytopenia early indicator of gram
negative sepsis in Pediatric and Burn
patients.
 Mild hypoxia with compensatory

72.  Septic shock is the complex interaction
between exogenous endogenous and
host response to these stimuli.(poorly
understood)
 When host response to local cell injury
and infection from cannot be contained it
progress as systemic illness.
 At organ level: cardiovascular response to
systemic infection in absence to
hypovolumenia --- hyper dynamic state

73.  Vasoregulatory mediators combine to
produce net decrease in systemic
vascular resistance .
 As cardiac index increases and arterio-
venous oxygenation deference narrowed.
 Micro vascular blood flow in capillary bed
doesn't alters
 At cellular level: no hypoxia, no defect in
metabolic pathway defect is reported.
 Depressed myocardial function with

74.  The long postulated myocardial
depressant factor, with poorly
characterized biochemicals appear to the
cause of decreased left ventricular
ejection fraction despite of acceptable
filling pressure appears to be reasonable.


75.  Pathophysiological mechanism of organ
dysfunction prior to the onset of
hypotension is associated with refractory
hypotension with tissue ischemia leading
to cell death and end stage hypo dynamic
septic shock.
.

76.  Agents causing fever were endongenous
products leading to concept of
endogenous mediators of action of
endotoxin. Which are
 Interlukin-1
 Cachectin- TNF is central and proximal
mediator to endotoxemia and bacteremia.
 Cachectin- TNF has 50% homology with
lymphotoxin, because of functional
similarity lymphotoxin is called TNF-B and
Cachectin- TNF is called TNF-A

77.  Later after protein and complimentary
DNA sequencing, Cachectin is identical to
the TNF tumor necrosis factor, which
mediate endotoxin induced tumor cyto-
toxicity.
 Circulating TNF-a can be found in
response to endotoxin in humans and its
peak level may be co-related with sepsis
and overall mortality.

78.  TNF induces synthesis and secretion of
secondary mediators;
 Cytokines
 Prostaglandins,
 Platelet activating factors
 Complement components
 Activation of clotting cascade.
 Is responsible for pathologic changes seen in
lungs liver bowel kidneys in response to
sepsis and septic shock.

79.  Management of
 Administration of anti-endotoxin
antibodies
 HA-1A Human monoclonal IgM antibody
against lipid portion of endotoxin improve
survival and organ function in presence of
gram –ve bacteremia with /out shock.
 E5 Murine monoclonal antibody against
lipid portion of endotoxin is beneficial in
absene of shock.

80. Therapy:
 Antibiotic treatment on the basis of culture and
sensitivity test
 Early surgical debridement
 Adjunctive therapy
 Fluid therapy : correction of fluid deficit should
be rapid and cardiac output and pulmonary
wedge pressure as guide.
▪ Resuscitation in exceeds of 10ml of ringer lactate is
common.
 Vasoactive drugs.

81.  Measurement of
 Arterial and venous pressure or pulmonary
wedge pressure.
 Urine output
 Arterial and venous blood gas

82.  Steroid treatment:
 Only indication is septic shock with hypo-
adrenalism for stress coverage
 in patient taking steroid or who recently
completed course of steroid for
immunosuppressant and anti inflammatory
process.

83.  Pharmacological support:
 Inotropic / vasoactive drugs:
 Dopamine is initial
 Dobutamine is often used to increase cardiac
output with less tachycardia and arrhythmia
than dopamine.
 Vasodilator drug improve cardiac output
and oxygen deliver in normo-tensive
septic shock.
 Norepinephrine (potent alpha-receptor
agonist) is effective in raising pressure for

84.  Epinephrine (potent α and β adrenergic
activity) support blood pressure which do
not respond to norepinephrine.
 Vasopressor provide transient support
while definative therapy is with antibiotic
and surgical drainage.

85. Anaphylactic shock: commonly seen after
penicillin administration or administration
of serum, dextrose, anesthetics etc.
Pathophysiology: increased release of
histamine in combination with IgE on the
mast cells and basophils.
Bronchospasm, laryngeal edema respiratory
distress which leads to hypoxia,
Aggravated by massive vasodilatation leading
to hypotension -- shock