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Applied Sciences Lecture Course. Physiology of Shock. Mahesh Nirmalan MD, FRCA, PhD Consultant, Critical Care Medicine Manchester Royal Infirmary.

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physiology of shock

Applied Sciences Lecture Course

Physiology of Shock

Mahesh Nirmalan MD, FRCA, PhD

Consultant, Critical Care Medicine

Manchester Royal Infirmary


Catastrophic deterioration of patients who are already in a hospital is frequently preceded by documented deterioration of physiological parameters

  • Sax FL et al Crit Care Med 1987; 15:510-515
  • Smith AF et al. Resuscitation 1998;37:133-137

Failure to respond

Inadequate response

Inappropriate response

Irreversible damage

Cardiac arrest

Documented deterioration

  • Definition of shock
  • Classification of shock
  • Grades of shock
  • Recognition of shock……….in particular the early recognition of shock
  • Pathophysiology of shock
  • Treatment objectives in shock
definition of shock
Definition of shock

A clinical state in which the organs and tissues do not receive adequate blood flow to meet their metabolic needs.

  • Inadequate tissue perfusion
  • Decreased oxygen supply
  • Anaerobic metabolism
  • Accumulation metabolic waste
  • Cellular failure
cellular or organ failure in shock
Cellular or organ failure in shock
  • Early: Immediate effects of hypo-perfusion → direct ischaemic damage
  • Late: Indirect effects
      • Ischaemia-Reperfusion
      • Oxidative stress
      • Pro-inflammatory cytokines
      • Sepsis
  • The late effects are directly related to the severity and duration of the early insult
  • Early recognition and immediate reversal of tissue ischaemia




Second hit

Reperfusion, Surgery, Infection



Giannoudis PV. Injury, Int.J.Care Injured 2003;34;397-404

pathophysiology of shock
Pathophysiology of shock
  • Immediate hypo-perfusion→ cell damage
  • Ischaemia-reperfusion
  • Sepsis
  • Cytokine activation
  • Oxidative stress
  • Distal organ dysfunction: Kidney or liver
  • Multiple organ failure: MODS
causes or the classification of shock

Distributive shock

Causes or the classification of shock
  • Severe or sudden blood loss: Hypovolaemic shock
  • Loss of ECF: Hypovolaemic shock
  • Myocardial infarction: Cardiogenic shock
  • High spinal injuries: Neurogenic shock
  • Major infections: Septic shock
  • Anaphylaxis: Anaphylactic shock
  • Poisoning: Cytotoxic shock
classification of shock
Classification of shock
  • Hypovolemic Shock:
    • haemorrhagic
    • non haemorrhagic
  • Other causes of shock
    • Cardiogenic Shock
    • Septic Shock
    • Neurogenic Shock
    • Anaphylactic Shock
the following photograph depicts
The following photograph depicts?
  • The first world war
  • Charge of the light brigade: Crimean War
  • Battle of Gettysburg; American Civil War
  • Battle of Waterloo
  • Russian Civil War

Oxygenated arterial blood

Body tissues

Fixed oxygen demand

Constant oxygen extraction

Venous blood

Venous oxygen saturation provides a good estimate of oxygen supply-demand balance in patients with shock


Cardiac output

  • Haemoglobin content
  • Haemoglobin saturation
  • Metabolic status
  • Temperature: sepsis
  • Hormonal status

Oxygen supply

Oxygen demand

  • Metabolic acidosis
  • Lactate production
  • Low venous saturation
classical features of shock
Classical features of shock
  • Tachycardia
  • Tacypnoea
  • Impaired tissue blood flow
    • Capillary fill time
    • Cold peripheries?
  • Low blood pressure
  • Reduced UOP: <0.5ml/kg/hr
  • Increased serum [lactate]
  • Low venous saturation …….<70%
signs of acute haemorrhagic shock

% Blood loss

Clinical Signs

< 15

Slightly increased heart rate, local swelling, bleeding


Increased heart rate, increased diastolic blood pressure, prolonged capillary refill


Above findings plus: hypotension, confusion, acidosis, decreased urine output

> 50

Refractory hypotension, refractory acidosis, death

Signs of acute haemorrhagic shock
haemorrhage and blood pressure
Haemorrhage and blood pressure

Blood pressure = CO * Vascular resistance


CO, MAP and SvO2

Hypovolaemic shock in an animal model of shock

typical changes in blood gases

Metabolic acidosis

Typical changes in blood gases
  • pH: 7.19
  • PCO2: 3.1KPa
  • PO2: 28KPa
  • HCO3-: 12.3mmol.l-1
  • BE: -14.3mmol.l-1
  • Lactate: 5.6mmol.l-1

Arterial oxygen saturation: 99-100%

Venous oxygen saturation: 55%

sympathetic response to trauma shock

Post ganglionic sympathetic fibres: Norepinephrine (A diffuse response)

Adrenals: Predominantly adrenaline

Reuptake : MAO

Local metabolism : Catechol-O-methyl-transferase



Systemic splillover

Sympathetic response to trauma & shock

A nonspecific & generalized response to a variety of stressful stimuli

effects of sympathetic activation
Effects of sympathetic activation
  • Tachycardia: baroreceptors & parasympathetics
  • Vasoconstriction: arteries and veins: 1 and 2
  • MAP
  • CO: Increased inotropy (1)
  • Vasodilatation in muscle and liver vascular beds (2) at low concentrations & vasoconstriction at high concentrations (1)
  • Overall increased CO and redistribution of flow: cardiac, cerebral, hepatic and muscle vascular beds.
hyperglycaemia in injury an essential survival mechanism


Increase in plasma osmolality by 20-30mOsmol

Mobilisation of extracellular fluid : upto 500ml

Jarhult J. Acta Physiol Scand 1973;89:213-226

Hyperglycaemia in injury: an essential survival mechanism?

Sympathetic activation


Corticosteroids, glucagon responses

Increased glycogenolysis & gluconeogenesis


CO, MAP and SvO2

Ischaemia-Reperfusion injuries in shock

even when cardiac output had been restored the blood pressure remained low why
Even when cardiac output had been restored the blood pressure remained low: why?


Vasoplegia is a feature of ischaemia-reperfusion

treatment objectives
Treatment objectives
  • Early recognition
  • Accurate diagnosis
  • Optimise tissue oxygen delivery early
  • Invasive haemodynamic monitoring
  • Urinary catheter
  • Blood gas estimation: to guide metabolic status
  • Appropriate environment
  • Specific treatment will depend on the underlying cause
      • ABC approach
      • Volume replacement: Hypovolaemic or septic
      • Inotropes: Cardiogenic
      • Vasopressors: Septic
      • Adrenaline: Anaphylactic
avoid over reliance on invasive haemodynamic monitoring




Seek help

Avoid over reliance on invasive haemodynamic monitoring

Pulse rate

Capillary fill time

Core-toe temperature

Blood pressure

Level of consciousness

Blood-gas estimation

summary be very familiar with



Summary: be very familiar with……
  • Immediate management of all forms of shock
    • Hypovolaemic
    • Septic
    • Anaphylactic
    • Cardiogenic: with and without pulmonary oedema
  • Definition of shock
  • Early and late effects
  • Causes
  • Oxygen supply-demand balance
  • Early recognition of shock: Early warning scores
  • Assess, intervene, reassess and seek help