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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

slide2

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
slide3

Failure to respond

Inadequate response

Inappropriate response

Irreversible damage

Cardiac arrest

Documented deterioration

objectives
Objectives
  • 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
slide8

Injury

MODS/ALI

Reaction

Second hit

Reperfusion, Surgery, Infection

Resolution

MODS/ALI

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
slide14

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

slide15

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

15-30

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

30-50

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

slide20

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

normetepinephrine

metepinephrine

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

Hyperglycemia

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

Hypoinsulinaemia

Corticosteroids, glucagon responses

Increased glycogenolysis & gluconeogenesis

slide25

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?

BP= CO* SVR

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

Assess

Intervene

RE-assess

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

Supportive

Specific

Summary: be very familiar with……
  • Immediate management of all forms of shock
    • Hypovolaemic
    • Septic
    • Anaphylactic
    • Cardiogenic: with and without pulmonary oedema
summary
summary
  • 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