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Late Sciences lecture series: Lecture 1. Physiology of shock. Mahesh Nirmalan Division of Cardiovascular Sciences Intensive Care Unit, Manchester Royal Infirmary. Objectives. Definition Clinical end points Classification Stages Physiological compensation Immediate Late

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physiology of shock

Late Sciences lecture series: Lecture 1

Physiology of shock

Mahesh Nirmalan

Division of Cardiovascular Sciences

Intensive Care Unit, Manchester Royal Infirmary

  • Definition
  • Clinical end points
  • Classification
  • Stages
  • Physiological compensation
    • Immediate
    • Late
  • Treatment objectives
mcq shock is defined as
MCQ: Shock is defined as:
  • Sustained reduction in Systolic blood pressure < 80 mm Hg
  • Sustained reduction in mean arterial pressure < 80 mm Hg
  • Sustained reduction in diastolic blood pressure < 40mm Hg
  • Inadequate blood flow to the tissues to meet its metabolic requirements
  • None of the above
compensated shock

MAP= 68 mm Hg

MAP= 90 mm Hg

Compensated shock

MAP is a very poor surrogate of blood flow to the peripheral tissues

Vasoconstriction will maintain MAP at thee expense of tissue flow

Compensated shock

definition of shock
Definition of Shock

Shock is an acute clinical syndrome initiated by ineffective perfusion, resulting in severe dysfunction of organs vital to survival.

Shock is not a synonym to hypotension!

shock definition
Shock: Definition
  • Inadequate perfusion to tissues
  • Large enough to compromise the supply of nutrients and removal of metabolic waste
  • Resulting in compromised organ functions
  • Usually recognised by clinical features suggestive of reduced blood flow
  • Reduced capillary fill
  • Cold clammy hands or feet
  • Widening core-toe temperature gradient
  • Reduced urine output
  • Raised plasma [Lactate-]
  • Low blood pressure is a late sign- particularly in the young previously fit individuals
ineffective perfusion


Cardiogenic shock




Ineffective perfusion

Organ perfusion may be compromised by an overall decrease or maldistribution of cardiac output.

  • Hypovolaemic: Haemorrhage, loss of ECF
  • Cardiogenic: Tamponade, Infarction, heart failure
  • Extracardiac obstructive: Pulmonary embolism, tension pneumothorax
  • Distributive: sepsis, anaphylaxis

Blood volume

Venous tone

RA pressure

Intra-pleural pressure

Ventricular filling: preload

State of myocardium


Inotropic state

Catecholamines, sympathetic tone



Arteriolar tone


Sympathetic tone

After load


Systemic vascular resistance

Arteriolar tone


Sympathetic tone

Arterial pressure

stages of shock
Stages of shock
  • Compensated shock or occult shock
    • Normal physiological compensation will lead to complete recovery
    • External interventions not necessary
  • Progressive shock
    • Progressively worse in the absence of external interventions
  • Irreversible shock
    • Death is inevitable in spite of all forms of therapy
stages of shock1
Stages of shock
  • Compensated shock
    • Autotransfusion
  • De-compensated shock
    • Redistribution of blood
  • Irreversible shock
    • MODS/ delayed death

Post hoc groups

Irreversible shock

Plasma [Lactate]

A priori groups







Plasma[lactate] (mmol/l)






Initiation of

End of shock


shock phase



effects of prolonged shock on cardiac functions
Effects of prolonged shock on cardiac functions
  • Modified Frank- Starling curves
  • Dogs bled to a pressure of 30mm Hg
  • Maintained hypotensive for variable periods
  • Resuscitated in stages to assess ventricular functions
  • Impaired ventricular functions after 4 hours of sustained shock
  • Concept of irreversible shock





LAP mm Hg

Adapted from Crowell et al 1962

reversible vs irreversible shock
Reversible Vs Irreversible shock

Sustained shock can breed more shock

Adopted from Guyton and Hall

physiological compensatory mechanisms
Physiological compensatory mechanisms
  • Immediate
    • Fluid shifts
    • Neural reflexes: Autonomic nerves
    • Endocrine
  • Delayed
    • Renal: Renin-Aldosterone-Angiotensin
    • Hypothalamo-pituitary axis
      • ADH
      • Thirst
starling forces at the capillary bed
Starling Forces at the capillary bed

Net Filtering Pressure = +5 mmHg

Net Filtering Pressure =

- 5 mmHg

Hydrostatic Pressure= 0 mmHg

Interstitial Fluid

Venous end

Arterial end


Hydrostatic Pressure = 30 mmHg

Colloid Osmotic Pressure= 25 mmHg

Hydrostatic Pressure = 20 mmHg

In the normal microcirculation

  - At arterial end:

water moves out of the capillary

Hydrostatic pressure > COP

- At venous end:

water moves into the capillary

Oncotic pressure > Hydrostatic pressure

compensation in shock
Compensation in shock
  • In shock, the hydrostatic pressure decreases and the oncotic pressure is constant
    • The fluid loss from the capillary to the extracellular space decreases.
    • Re-absorption of fluid return from the extracellular space increases
    • Partially compensates for the loss in circulatory volume
    • Never complete
    • “Fluid shift system”
  • Re-absorption is aided by the increase in osmotically active substances in blood: Glucose
  • The amount of fluid recruited through the metabolic responses may be substantial: 20-30m Osmol: 0.5 liters of fluid
  • Hyperglycaemia is an evolutionary survival mechanism
  • When persistent may have adverse consequences
autonomic neural reflexes

Venoconstriction: autotransfusion

Vasoconstriction: redistribution


Increased rate and force of contraction

Autonomic neural reflexes
  • Baro-receptors mediated increase in sympathetic outflow
  • Chemo-receptor mediated sympathetic outflow
  • Ischaemic brain response: Late but powerful
stages of shock2

Ischaemic brain response

Stages of shock
  • Compensated shock
    • Autotransfusion
  • De-compensated shock
    • Redistribution of blood
  • Irreversible shock
    • MODS/ delayed death
autonomic reflex responses to hypovolaemia
Autonomic reflex responses to hypovolaemia
  • Baroreceptors are stimulated by stretch: MAP and pulse pressure
  • Sympathetic outflow is inhibited by baroreceptor affarents
  • Direct as well as via the vagal nucleus
  • Reduction in baroreceptor affarents therefore lead to vasoconstriction and tachycardia
  • Compensates for reduction in MAP and pulse pressure
chemo receptors
  • Central chemo-receptors: Medulla
  • Peripheral chemo-receptors: Carotid body and aortic body
  • Particularly relevant when MAP < 60
  • H+ and CO2
  • Evoke a powerful sympathetic response

Sympathetic responses to haemorrhage and shock

  • In the absence of sympathetic responses 15-20% acute haemorrhage is usually fatal.
  • In the presence of an intact sympathetic response patients may be able to tolerate 30-40% acute haemorrhage and recover completely
  • Venoconstriction is helpful in maintaining stroke volume
  • Arterial constriction maintains blood pressure at the expense of organ blood flow
  • Aimed at preserving coronary and cerebral perfusion
  • Minimal constriction of the coronary and cerebral vessels
  • Does not fall until systolic pressure is < 70 mm Hg
  • Prolonged arterial-constriction initiates secondary changes in organ function
The early compensatory mechanisms preserve arterial pressure at the expense of blood flow to key visceral organs
generalised cellular degeneration

Multiple organ failure

Generalised cellular degeneration
  • Prolonged lack of oxygen and nutrients affect the viability of organs
  • Tissues with high metabolic activity are more prone
  • Centri-lobular necrosis of the liver
  • Na+/K+ active transport→swelling
  • Mitochondrial activity depressed
  • Release of lysosomal hydrolases
  • Interruption of metabolism
  • Lungs
  • Heart
  • Gut mucosal barrier

Patients resuscitated after prolonged shock usually die of multiple organ failure

Human and Health care costs

treatment priorities in shock
Treatment priorities in shock
  • Use of inotropic agents to restore myocardial contractility
  • Use of vasoactive drugs to cause venoconstriction, vasoconstriction and thereby restore venous return and blood pressure
  • Restore circulating blood volume to optimise cardiac functions
  • Increase heart rate to increase cardiac output
  • Use of HCO3- to prevent metabolic acidosis
tachycardia though an important compensatory mechanism always comes at a price


O2 supply


O2 demand

Tachycardia, though an important compensatory mechanism always comes at a price

Heart rate

Wall tension

After load


Diastolic time


O2 content