Definition :- shock is a syndrome in which

there is inadequate tissue perfusion

associated with reduction of cardiac

output (absolute or relative )

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

Tissue perfusion is determined by Mean Arterial Pressure (MAP)

MAP = CO x SVR

Heart rate Stroke Volume

Four categories depending on cause of

reduced CO

1. Hypovolaemic shock

2. Cardiogenic shock

3. Distributive shock

4. Obstructive shock

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

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

four types:-

I. Neurogenic shock

II. Anaphylactic shock

III. Septicaemic shock

IV. Endotoxic shock

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

Acute allergic reaction

Large quantities of histamine

Widespread vasodilatation

Reducing peripheral resistance

Increased capillary permeability

Reduction in blood volume

Leading to shock

Septicaemia ?

Bowel perforation , peritonitis

Toxins produced by bacteria

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

1. Myocardial infarction

2. Cardiac arrhythmias

3. Congestive heart failure

External pressure on the heart which

reduces CO

Reduces ventricular filling

› Pericardial tamponade

› Tension pneumothorax

› Constrictive pericarditis

1. Non –progressive shock

2. Progressive shock

3. Refractory shock

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

Includes three nervous reflexes

› Baroreceptor reflex

› Chemoreceptor reflex

› CNS ischemic response

› Others responses

Baroreceptors – stretch receptors which

sense change in pressure

Chemoreceptor – detects change in

chemical composition of blood

Carotid body (chemoreceptor )

Carotid sinus ( baroreceptor)

Aortic arch contains both baro&

chemoreceptor

Carotid sinus – glossopharyngeal nerve

corotid body

Aortic arch – vagus nerve

Aaorti sinus

When the BP falls

Barorecptors gets inactivated

They reduce their inhibitory effect on

VMC

so increase in BP and HR

Due to hypoxia

When the blood pressure fall below

70mm/hg

When the BP falls below 40mm/hg

Ischemia of VMC

Activation of VMC

Increases symp dischrage

Increases BP , HR , CO

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

Due to chemoreceptor reflex

Also because of hypoxia

And by increasing thoracic pumping

action

Increases CO

Person becomes restless

Increases pumping

Increases venous return

From adrenal medulla

Increases symp drive

i.e. vasoconstriction and increased HR

Stimulates RAS

ADH from posterior pituitary

Increases water absorption

Pressor action of vessels

Increased glucocortioids

Increases sensitivity of vessels to

catecholamines

RAAS

Reverse stress relaxation

Capillary fluid shift 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 4-8

wks

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

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

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

Due to hypoxia and metabolites

accumulation vasodilatation occurs

Capillary permeability increases

Pooling and sluggish blood flow

Intravascular clotting occurs

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

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 )

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

Correcting a cause & helping

physiological compensatory

mechanisms

General measures

1. Prevent sweating

2. Trendelenburg position

Transfusion of whole blood

Plasma

Dextran

Ringer lactate

Normal saline

Adrenaline

Nor-adrenalin

Dapamine

Oxygen therapy

Gluocorticoids

Intestinal circulation

Hepatic circulation

Splenic circulation

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

Gastric – 40ml/100g/min

Intestinal – 60ml/100g/min

Pancreatic – 80ml/100g/min

Neural

Autoregulation

Metabolic regulation

› Adenosine

› Osmolarity

› Potassium

By GI activity – functional hyperemia

› Due to gastric hormones

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

Hepatic arterial buffer response

Neural

Metabolic

Autoregulation

Regulation by intestinal activity

Filters blood

Detoxification

Metabolism and storage

Reservoir of blood

Contribute 60% of blood during shock

Hepatomegaly

Portal hypertension and ascitis

Splenic artery

Sympathetic vasoconstrictor fibers

Splenic capsule contraction