SHOCK

Dr vishwabharathi T
Definition

 Shock is a condition in which “circulation

fails
to meet the nutritional needs of the cells
and
fails to remove the metabolic waste
products”.
 Peripheral circulatory failure

Discrepancy in the size of vascular bed and

volume of the IVF

Cardiac output is insufficient to fill the

arterial tree with sufficient pressure to
provide all the organs and tissues with
adequate blood flow

Decreased blood flow state in the vital organs

is the main cause of shock
Types of shock
1. Haemorrhagic / hypovolaemic shock
2. Traumatic shock
3. Neurogenic shock
4. Cardiogenic shock
5. Septic shock
6. Miscellaneous type- Anaphylactic shock
Hypovolaemic shock
 Due to loss of blood, plasma/body
fluids(water and electrolytes)/loss of intra
vascular volume

Pathophysiology
 Sudden loss of blood volume / loss of fluids

from the vascular space

 Haemorrhage mostly occurs from the

systemic venules and small veins which

contain 50% of total blood volume
 Loss of blood will cause decreased filling of
right atrium
 Decrease of filling of pulmonary vasculature
 Decrease of filling of lt. atrium and lt.
ventricle
 Lt. ventricular stroke volume decreases
 Drop in arterial blood pressure
Compensatory mechanism
 Adrenergic discharge
 Hyperventillation
 Release of vasoactive hormones
 Collapse
 Resorption of fluids from the interstitial tissue
 Resorption of fluid from the intracellular space
to extra cellular space
 Renal conservation of body water and
electrolytes
Adrenergic discharge: stars within 60 secs
after blood loss
causes
 Constriction of venules and small veins
◦ Displaces blood to rt. Atrium and ventricle
◦ Increase of blood in pulmonary vasculature and in
lt. atrium and vantricle
◦ Increase of lt. ventricular stroke volume

 Increase of heart rate

 Constriction of vascular spincters in the
kidneys, splanchnic vessels and in the skin
 Selective vaso constriction improves filling
of rt. Atrium and increases cardiac output
 Diverts blood to the heart and brain
Hyperventilation
Occurs in response to metabolic acidaemia
which develops shortly after haemorrhage
 Spontaneous deep breathing sucks blood from
extra thoracic sites to the heart and lungs
 Increases filling of lt. ventricle and stroke volume
 Adrenergic discharge and hyper ventilation
occurs with in one minute of blood loss
Release of vasoactive hormones
 Low perfusion of kidneys leads to release of
hormone renin from juxtroglomerular apparatus
 Renin liberates angiotensin 1 from the liver
which converts into angiotensin 2 by lungs
 Angiotensin 2 is a potent selective
vasoconstrictor
 It selectively constricts the vasculature of
splanchnic organs, kidneys and skin
 Vasopressin: released due to stimulus from
the baroreceptors situated in the carotid
bodies and aortic arch caused by hypotension
 It acts as a systemic vasoconstrictor thus
diverting blood to the brain and heart
 Increases cardiac output
 Epinephrine: vasoactive hormone released
from the adrenal medulla
 Release takes place after 2-3 mins of
haemorrhage
Collapse
In recumbent posture due to collapse
automatically displaces blood from the
lower part of the body to the heart ,
increases cardiac output
Resorption of fluid from the interstitial tissue
 Due to adrenergic discharge the arterioles,
precapillary sphincters, post capillary
sphincters, the venules and small veins of the
skin and splanchnic organs and skeletal
muscle constrict
 Leads to decrease of capillary intravascular
hydrostatic pressure
 Leads to influx of water, sodium, chloride
from the interstitial space into the capillaries
Resorption of fluid from intracellular space to
extracellular space
 Release of epinephrine from the adrenal medulla,
cortisol from the adrenal cortex and glucagone from
the pancreas and inhibition of release of insuline all
lead to high extracellular glucose concentration
 Products of anaerobic metabolism also accumulates
in the extra cellular space
 Both these causes hyperosmolarity of the
extracellular tissue which draws water out of the
cells
 Interstitial pressure increases which forces
water, sodium, chloride across the capillary
endothelium into the vascular space
Renal conservation of body water and
electrolytes
 Adrenocorticotrophic hormone is released by
any stress including shock
 This hormone and angiotensin 2 stimulate
synthesis and release of hormone
aldosterone from the adrenal cortex
 Aldosteron is concerned with resorption of
sodium from glomerular filtration into the
vascular space
 Resorption of sodium and water by the kidney
helps to maintain the vascular volume
Clinical features
 Decreased filling pressure of the heart
 Decreased systemic arterial pressure
 Tachycardia
 Increased vascular resistance
Clinical manifestation includes
 Low cardiac output
 Tachycardia
 Low blood pressure
 Vasoconstriction leads to cold extremities
Clinical features of hypovolaemic shock

 Mild shock
 Moderate shock
 Severe shock
Mild shock
 Loss of blood less than 20%
 Feet becomes pale and cold due to collapse of
veins by adrenergic constriction of blood
vessels in the skin
 Sweat in the forehead, hand, feet due to
adrenergic discharge
 Urinary output, pulse rate, blood pressure
remains normal
 Patient feels thirsty and cold
Moderate shock
 Loss of blood volume 20-40%
 Oliguria
 Pulse rate increases, less than
100beats/min
 Initially BP remains normal
Severe shock
 Loss of blood volume more than 40%
 Pallor- skin and extremities
 Low urinary output
 Rapid pulse
 Low blood pressure
 Monitoring of shock clinically

Required to assess the degree of blood loss and

haemodynamic impairment
 Blood pressure: very essential to monitor
◦ Diastolic pressure is the main indication of the degree
of vasoconstriction
◦ Systolic pressure indicates vasoconstriction along with
stroke volume and rigidity of the main vessels
◦ Pulse pressure : systolic – diastolic pressure which
indicates stroke volume of the heart and cardiac output
 Respiration: hyperventilation is an important
indicator of shock
◦ Hyperventilation is normal in initial period
◦ If pt. is not hyperventilating means problem
in central nervous system/ respiratory
system
◦ Persistent hyperventilation is an ominous
sign and indicates improper treatment
 Urine: good indicator of shock
◦ Affected quite early in moderate shock
◦ Good index of adequacy of replacement
therapy
CVP:
Hypovolaemic shock, blood volume decreases ,
cvp decreases
Cardiogenic shock blood volume remains same
as no depletion of blood volume

 ECG:
 Treatment of shock
 Resuscitation :
◦ Clear air way
◦ Maintain adequate ventilation and oxygen
◦ Lowering the head with support of jaw to
prevent airway obstruction
◦ Administer O2 if needed
◦ Airway obstruction, intra tracheal intubation
and mechanical ventilation
◦ Abrupt increase in airway pressure expands
alveoli and displaces blood from pulmonary
vasculature to lt. heart
◦ Increases lt. ventricular output and systemic
arterial pressure
Immediate control of bleeding: haemorrhagic
shock
Along with foot end elevation, compression
bandage to tamponade external haemorrhage
Surgery may require to stop bleeding
 Extra cellular fluid replacement:
◦ Very important in hypovolaemic shock
◦ With large gauze needle is inserted to vein
◦ Fluid should be administered immediately
◦ Measure CVP
◦ Fluids: non sugar, non protein crystalloid solution
with sodium concentration in initial stage
◦ RL/RA/NS with two ampules of sodium bicarbonate
◦ RL/RA shouldn't be given in pre existing liver
disease
 Fluid administration speed: 45 mins, 1L to 2 L
 Check BP after administration
 If blood loss is severe/ haemorrhage is
continuing elevation of blood pressure is
transient
 Resuscitation should always be started with
crystalloid solution even if blood is available
 3 Lts of fluid given over 45 mins should
resuscitate pt. with arrested haemorrhage
 Need of more fluid indicates continuation of
bleeding- haemorrhage should be
controlled by surgical intervention
 Note: better to with hold administration of
blood until surgical control of bleeding/ just
before induction of anaesthesia
 Bleeding is severe blood should be given
before surgical control of haemorrhage
 Points to be remembered for fluid
replacement:
◦ Crystalloid should be given first, administered
rapidly
◦ Monitor blood pressure, pulse rate, urine output,
CVP to know how much to be infused
◦ Blood loss is replaced by blood, not by blood
substitues
 Drugs :
 Sedatives: alleviate pain
 Morphin is good administered IV route
 CI: head injury, children

◦ chronotropic drugs: increases heart rate

 Atropin: widely used drug, vosodolator

◦ Inotropic agents: inc. myocardial contractibility and

inc. renal blood flow
 Dopamine

◦ Vasodilators: septic shock, cardiogenic shock

◦ nitroglycerine
 Vasoconstrictors: beneficial in neurogenic shock
◦ Increases blood pressure and perfusion pressure for
coronary circulation
◦ Phenylephrine
 Beta blockers: cardiogenic shock with stiff
myocardium and rapid heart rate
◦ Inc. efficacy of ventricular contraction
◦ Proponolol
 Diuretics : cardiogenic shock, dec. vascular
volume and filling pressure
 Traumatic shock

 Traumatised tissues activate coagulation

system and release microthrombi into the
circulation
 Occlude / constrict parts of pulmonary
vascular resistance
 Increases rt. Ventricular diastolic pressure
 C/F: similar to that of hypovolaemic shock
◦ Two differences Presence of peripheral and pulmonary edema
◦ Infusion of large volume of fluid is inadequte

 Treatment :
1. Resuscitation: mechanical ventilator support
2. Local treatment of trauma and control of bleeding:
a) Similar to hypovolaemia
b) Surgical debridement of ischaemic and necrosed tissues
c) immobilisation

3. Fluid replacement: administered to bring back BP

1. HEPARIN 10000 iu iv
 CARDIOGENIC SHOCK
 Primary dysfunction of one ventricle / other
 Due to MI, chronic congestive heart failure,
pulmonary embolism/ syatemic arterial
hypertention
 C/F:
 Skin pale, cool
 Urine output low
 Pulse rapid, BP- decreases
 Rt. Ventricular dysfunction:
◦ Neck veins distended
◦ Liver enlarged
 Lt. ventricular dysfunction:
◦ Bronchial rales
◦ Third heart sound
◦ cardiomegaly
 Treatment :
a) airway clear with adequate O2
b) Rt. Ventricular failure due to massive
pulmonary embolus, large dose of heparine
IV
c) Lt. ventricular failure: pain is complained,
morphin, diuretic to treat fulminant
pulmonary edema
 Neurogenic shock
 Dilatation of the systemic vasculature which
lowers the systemic arterial pressure
 Blood pools in the systemic venules and small
veins
 Right heart filling and stroke volume decreases
 Compensatory mechanism like adrenergic
discharge and vasopressin, angiotensin fail to
restore the cardiac output to normal
Clinical features:
 Skin remains warm, pink Well perfused
 Urinary output normal
 Heart rate rapid and blood pressure decreases
Treatment:
 Foot end elevation- trendelenburg
position(displaces blood from systemic
venules and small veins into right heart,
increases cardiac output)
 Administration of fluids (increases filling of
right heart)
 Neurogenic shock is the only shock which can
be safely treated with a vasoconstrictor drugs
 Complication: ischaemic necrosis of fingers
 Septic shock
 Possesses high mortality rate about 50% or
more
 Causative organism:
◦ Gram positive: incidence is less as effective
antibacterial treatment is available
◦ Gram negative: E.coli, klebsiella aerobacter, proteus
pseudomonas
Gram positive sepsis and shock:
 Caused by dissemination of a potent exotoxin
liberated from gram positive bacteria without
evidence of bacteraemia
 Organism: clostridium tetani, clostridium
perfringers
 Shock is caused by massive fluid losses
 There is no or little reduction in cardiac output
even with progressive hypotension
 Urine output is normal
Gram negative sepsis and shock:
 Source of infection from genito urinary infection
 Patient had associate with operation /
instrumentation of urinary tract
 Second most frequent site – respiratory system
 Many patients have had tracheostomy done
 Diseases of gastro intestinal system, biliary tree
infection, intra abdominal abscess, peritonitis
Clinical features:
 Initially recognized by development of chills
and elevated temperature above 100℉

 Early warm shock symptoms

 Late cold shock symptoms
Early warm shock symptoms:
 Cutaneous vasodilatation
 Toxins from infected tissues increases the body
temperature
 To bring down temperature, vasculature of skin
dilates
 Cutaneous vasodilatation decreases the systemic
vascular resistence
 Arterial pressure falls, cardiac out put increases
 Adrenergic discharge further increases cardiac output
Clinical features:
 Skin warm, pink, well perfused
 Cutaneous veins remains full
 Pulse rate high
 Systemic arterial pressure low
 Intermittent fever with chills

Late cold shock:

 Increased vascular permeability due to the liberation of
toxic products into the circulation
 hypovolaemia
 Right heart filling decreases
 Decrease of flow into the pulmonary
vasculature
 Left heart filling decreases, cardiac output
decreases
 Clinically this shock is difficult to differentiate
from hypovolaemic shock/ traumatic shock
Treatment: done two groups
1) Treatment of infection: by early surgical
debridement/drainage and appropriate
antibiotic usage
2) Treatment of shock: which includes fluid
replacement, steroid administration and use
of vasoactive drugs
Treatment of infection:
 Search for the source of infection once septic shock is
diagnosed
 Debridement operation/ drainage of infection, under
local anesthesia/ general anesthesia
 Use of specific antibiotics based on appropriate c/s test
 Prior to sensitivity test, appropriate antibiotics should
be selected on the basis of suspected organism
 Gentamicin – 5mg/kg/day
 clindamycin
Fluid replacement:
 Great importance in late septic shock
 Provide sufficient blood volume to the vital
organs
 Mechanical ventilation along with
endotracheal intubation frequently needed to
treat inadequate oxygen supply
 Steroids: favorable responses with
improvement in cardiac, pulmonary and renal
function
 Better survival rate reported
 Steroids protect body cells and its contents
from effect of endotoxin
 Prednisolone/ dexamethasone 15-30
mg/kg/5 to 10 mins
 Repeated 4th hourly