PATHOPHYSIOLOGY

OF SHOCK
SPEAKER: DR. DEEPEN CHETTRI
MODERATOR: DR. TH BIJOY SINGH
PROF. DEPTT. OF FORENSIC
MEDICINE
 DEFINITION OF SHOCK

• Inadequate perfusion and oxygenation and supply of

nutrients to cells and vital organs.

› Cellular dysfunction and damage

› Organ dysfunction and damage

› High mortality - 20-90%

› Early intervention reduces mortality

 CIRCULATORY SHOCK

• Definition :- shock is a syndrome in which

there is inadequate tissue perfusion associated with

reduction of cardiac output (absolute or relative ) or
reduction in blood volume or redistribution of blood
resulting in a decrease of effective circulating
volume.
 PATHOPHYSIOLOGY: OVERVIEW

• Tissue perfusion is determined by Mean

Arterial Pressure (MAP)

MAP = CO(cardiac output)x SVR(systemic

vascular resistance)

Heart rate Stroke Volume

 CLASIFICATION

• Four categories depending on cause of

reduced CO
1. Hypovolaemic shock
2. Cardiogenic shock
3. Distributive shock
4. Obstructive shock
 HYPOVOLAEMIC SHOCK
• Reduced CO is due to low blood volume
• Also known as cold shock
Causes
1. Hemorrhagic shock
2. Surgical shock
3. Burns shock
4. Dehydration shock
5. Traumatic shock
 CARDIOGENIC SHOCK
• Heart’s pumping ability is reduced
• Severe systolic dysfunction
• Venous return is not pumped out
• So reduced CO
• Congestion of lungs and vicera
• Also know as congested shock
 CAUSES
1. Myocardial infarction
2. Cardiac arrhythmias
3. Congestive heart failure
 DISTRIBUTIVE SHOCK

• Excessive vasodilatation due to toxic substances or

neural regulation
• Increased in capacitance of vessels
• CO decreases in spite of normal blood

volume
• Also known as warm shock
 DISTRIBUTIVE SHOCK

Four types:-
I. Neurogenic shock
II. Anaphylactic shock
III. Septicaemic shock
IV. Endotoxic shock
 NEUROGENIC SHOCK
Causes :-Two types
1. Marked reduction in sympathetic

vasomotor tone

a) Deep general anaesthesia

b) Spinal anaesthesia

c) Brain damage

2. Increased vagal tone :- vasovagal syncope , emotional fainting

 ANAPHYLACTIC SHOCK
• Acute allergic reaction
• Large quantities of histamine
• Widespread vasodilatation
• Reducing peripheral resistance
• Increased capillary permeability
• Reduction in blood volume
• Leading to shock
 SEPTICAEMIC SHOCK

• Septicaemia ?
• Bowel perforation , peritonitis
• Toxins produced by bacteria
• Generalised increase vascular permeability
 ENDOTOXIC SHOCK
• Closely related to septic shock
• Seen in patients having gram negative
infection.
 OBSTRUCTIVE SHOCK
• External pressure on the heart which
reduces CO
• Reduces ventricular filling
› Pericardial tamponade
› Tension pneumothorax
› Constrictive pericarditis
 STAGES AND CLINICAL FEATURES OF
SHOCK

1. Non –progressive shock

2. Progressive shock
3. Refractory shock
 NON-PROGRESSIVE SHOCK
• Also known as compensated shock
• Moderate reduction in CO
• Occurs after loss of 10-15% of blood volume
• Leading to compensatory mechanisms

1. Immediate compensatory mechanisms

2. Intermediate compensatory mechanisms
3. Long term compensatory mechanisms
 IMMEDIATE COMPENSATORY
MECANISM

• Includes three nervous reflexes

› Mechanoreceptor response
› CNS ischemic response
› Others responses
 MECHANORECEPTORS

• Baroreceptors – stretch receptors which sense change

in pressure.
• Chemoreceptor – detects change in chemical
composition of blood.
 LOCATION OF RECEPTORS

• Carotid body (chemoreceptor )

• Carotid sinus ( baroreceptor)
• Aortic arch contains both baro &

chemoreceptor
RECEPTORS
 INNERVATION
• Carotid sinus
Glossopharyngeal nerve
• carotid body
• Aortic arch
Vagus nerve
• Aortic sinus
 BARORECEPTOR REFLEX

• When the BP falls

• Baroreceptors gets inactivated
• They reduce their inhibitory effect on

VMC( vasomotor center)

• so increase in BP(blood pressure) and HR( heart rate)
 CHEMORECEPTOR REFLEX

• Due to hypoxia
• When the blood pressure fall below

70mm/hg
 CNS ISCHEMIC RESPONSE

• When the BP falls below 40mm/hg

 Ischemia of VMC
 Activation of VMC
 Increases sympathetic discharge
 Increases BP , HR , CO
 OTHER RESPONSES
• TACHYCARDIA
• VASOCONSTRICTION
 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(glomerular
filtration rate)
 Vasoconstriction of skeletal muscle
 So bypassing of blood to vital organs

• INCREASED RESPIRATORY RATE

 Due to chemoreceptor reflex
 Also because of hypoxia
 And by increasing thoracic pumping

Action
 Increases CO
 INCREASED SKELETAL MUSCLE
ACTIVITY

• Person becomes restless

• Increases pumping
• Increases venous return
 INCRESED SECRETION OF
CATECHOLAMINES

• From adrenal medulla

• Increases sympathatic drive
• That is vasoconstriction and increased HR
• Stimulates RAS( renin angiotensin system)
 INCREASED SECRETION OF
VASOPRESSIN

• Anti Diuretic Hormone from posterior pituitary

• Increases water absorption
• Pressor action of vessels
 INCREASED SECRETION OF
CORTISOL

• Increased glucocorticoids
• Increases sensitivity of vessels to catecholamines
 INTERMEDIATE COMPENSOTARY
MECHANISM

• RAAS
• Reverse stress relaxation
• Capillary fluid shift mechanism
 LONG TERM COMPENSATORY
MECHANISM

• 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 4-8wks
 PROGRESSIVE SHOCK
• 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

POSITIVE FEEDBACK CYCLE
• Cardiac failure
• Due to severe decrease in BP
• Diastolic BP falls
• Blood supply to heart falls
• Weakens myocardium
• Leading to heart failure
• Acts as positive cycle
 VASOMOTOR FAILURE

• 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
 PERIPHERAL CIRCULATORY
FAILURE

• Due to hypoxia and metabolites

accumulation vasodilatation occurs

• Capillary permeability increases
• Pooling and sluggish blood flow
• Intravascular clotting occurs
 SEPTICEMIA AND TOXEMIA

• Hypoxia in GIT

• Damage to mucosal barrier

• Leading to entry of bacteria through portal

circulation
• Damage liver and reaches systemic

circulation
• Systemic toxemia and septicaemia

• Leading to irreversible shock

 EFFECT ON TISSUES LEVEL

• Widespread tissue damage

• Liver (first) , heart , lung
• Failure of Na-K pump
• Reduced mitochondrial activity
• Activation of lysosomes cycle
• Depleted nutrients (glucose mainly)
• Depleted action of hormones (insulin)
• Hypoxia – anaerobic metabolism – lactic

acid accumulation – Pco2 increase – acidosis –

vasodilatation
 REFRACTORY SHOCK

• 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
 POSTMORTEM CHANGES

• Circulatory changes ,degeneration and necrosis in

various organs.
• Circulatory changes include congestion of all the
internal organs, petechial haemorrhages in the serous
cavity and edema of the viscera.
 BRAIN
• May develop ischaemic encephalopathy
• Changes occur if the person survives for 12 to 24
hours
• At first there is swelling or shrinkage of neurons.
• Nucleus becomes pyknotic
• Later, nerve cell die and are replaced by fibrillary
gliosis.
 KIDNEY

• Changes is those of acute tubular necrosis.

• Begin within 24 hr and become marked in another 7
to 10 days
• Kidney is normal in size
• In some cases peculiar brown tubular cast are seen
 LUNGS

• Not affect in hypovolaemic shock

• Vascular collapse caused by bacterial sepsis or trauma
“ SHOCK LUNG” is seen.
• Resembles liver are dark red, firm, airless and heavy.
 HEART

• 20 % cases shows fatty changes after 18 hours

and well marked in 3 or 4 days
• Subendocardial hemorrhage and necrosis
sometimes appear in all forms of necrosis.
 GIT

• Lesion are multifocal and widely distributed

throughout the bowel.
• Patchy mucosal haemorrhages and necrosis may be
seen in 2 to 3 days.
• The intestinal tract may contain blood stained fluid.
 LIVER

• Gross appearance of liver is not altered.

• Fatty changes develop after 18 hours
 SPLEEN

• Enlargement and softening of the spleen seen in

septicaemia.
 MEDICOLEGAL IMPORTANCE

 In a person with haemorrhagic diathesis or

haemophilia, minor injury produce death from
haemorrhage.
 A trivial bruise causes loss of 20-30ml of blood loss.
So an extensive bruise without any other injury might
also cause death.
 In persons of neurotic or emotional temperament, in
deeply intoxicated, severely ill or feeble old and
young children, death from primary shock occurs
readily.
 Men withstand haemorrhage better than women.
 Examination of crime scene is important to calculate
the amount of blood loss.
• Sudden rise of BP in neurogenic shock can
precipitate serious complications like –
(a) Intracerebral hge from rupture of arteriosclerotic
cerebral vessels or of berry aneurysm.
(b) Rupture of a dissecting aneurysm of aorta.
 Under such conditions even when the deceased
received minor trauma before death, the essential
cause of death will be underlying disease process.
 Minor stimuli or injury over receptic spots may cause
sudden death from neurogenic shock.
THANK YOU