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Applied Sciences Lecture Course. Ventilatory Failure & Hypoxia. Mahesh Nirmalan MD, FRCA, PhD Consultant, Critical Care Medicine Manchester Royal Infirmary. Objectives. Respiratory failure is one of the commonest manifestations of acute illness Hypoxia and CO 2 retention

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ventilatory failure hypoxia
Applied Sciences Lecture Course

Ventilatory Failure & Hypoxia

Mahesh Nirmalan MD, FRCA, PhD

Consultant, Critical Care Medicine

Manchester Royal Infirmary

objectives
Objectives
  • Respiratory failure is one of the commonest manifestations of acute illness
  • Hypoxia and CO2 retention
  • Failure of oxygen transfer
  • Failure of effective alveolar ventilation
  • Pathophysiology
  • Differences in management approach
respiration or breathing
Ventilation

Moving an adequate volume of air

Minute ventilation

Alveolar ventilation

Oxygenation

Transfer of O2 across the alveoli

Dusky colour

Cyanosis

Low SpO2

Low arterial PaO2

Respiratory rate

Tidal volume or chest expansion

Arterial PaCO2

Respiration or Breathing
respiratory failure
Type 2

Type 1

Mixed

Hypoxia

&

Hypercarbia

Hypercarbia

PaCO2>7kPa

Hypoxia

PaO2<8kPa

Respiratory Failure
treatment of respiratory failure
Treatment of Respiratory failure
  • Type 1
    • Cause
    • O2 supplementation
    • PEEP
  • Type 2
    • Cause
    • Ventilatory assistance
      • Pharmacological
      • Mechanical: IPPV
  • Mixed
lung volumes
Lung volumes

FRC is a balance between two forces

Reduced compliance

Reduced FRC

Increased compliance

Increase in FRC

slide9
Hepatisation

Fibrinous exudate

H’ge

histological changes reduced lung compliance
Hyaline.membrane

Normal lung

Interstitial oedema

Organising oedema

Alveolar oedema

Haemorrhage

Neutrophil infiltartion

Histological changes: reduced lung compliance
reduced compliance
Reduced compliance
  • Pulmonary oedema
  • Pneumonia
  • ARDS and ALI
  • Fibrosis

Tachypnoea

Increased work of breathing

Hypoxia

decreased lung compliance
Decreased lung compliance
  • Early stages: Interstitial oed
  • Tendency for the alveoli to collapse
  • May involve large parts of the lung
  • Reduction in FRC is an important factor
  • Alveolar oedema & consolidation
  • Increased work of breathing
  • Common cause for failure in oxygenation
  • Type 1 respiratory failure
increased lung compliance increased frc
Increased lung compliance: Increased FRC

Hyper-inflation

Low set diaphram

Reduced lung markings

hypoxia failure of tissue oxygenation
Hypoxia: failure of tissue oxygenation
  • Hypoxic hypoxia: Pulmonary oxygen transfer
  • Stagnant hypoxia: Poor blood flow
  • Anaemic hypoxia: poor oxygen carriage
  • Histotoxic hypoxia: Sepsis, Cyanide
oxygen cascade in an ideal lung
Oxygen cascade in an ideal lung

Diffusion, shunt, ventilation perfusion mismatch

High Altitude

Hypoventilation

pathophysiology of hypoxia
Pathophysiology of hypoxia

Venous blood

Oxygenated blood

pathophysiology of hypoxia1
Pathophysiology of hypoxia

Venous blood

Venous blood

ventilation perfusion or v q mismatch
Ventilation/perfusion or V/Q mismatch

Partially oxygenated

blood

Venous blood

shunt and v q mismatch
Shunt and V/Q mismatch

Alveolar oedema

Shunt: blood that goes through unventilated lung units

V/Q mismatch: Blood going through poorly ventilated units

causes of hypoxia
Causes of Hypoxia

Clinically how does one distinguish between shunt and V/Q mismatch?

Effect of increasing FiO2

Hypoventilation

Diffusion defects

Ventilation-perfusion mismatch

Shunts

45 years old male breathless pyrexial unwell breathing 50 o 2 pulse oximetry 90 saturation
45 years old male: Breathless, pyrexial, unwell, (breathing 50% O2)Pulse oximetry: 90% saturation
  • pH=:7.15
  • PCO2: 3.3 kPa
  • PO2: 13.47kPa
  • HCO3-: 17 mmol.l-1
  • Hb: 10.8 g.dl-1
  • Glucose: 12.8mmol.l-1
  • Lactate: 0.9mmol.l-1

Shunt and V/Q mismatch

physiological dead space
Physiological dead space

Wasted ventilation

Extension of dead space

Ventilated but not perfused alveolar units

Physiological dead space

Dead space ventilation does not clear CO2

Extension of dead space will lead to CO2 retention

pulmonary embolism
Pulmonary embolism:

Typically increase in Physiological dead space

When large also causes significant V/Q mismatch

Hypoxia and CO2 retention

slide32
Most organic parenchymal diseases:Increase in V/QSome shuntingIncrease in physiological dead space
ventilatory failure
Ventilatory Failure
  • Hypoventilation
    • Depression of respiratory centre: opiates
    • Pain: upper abdominal surgery, Rib fractures
    • Prolonged increase in work of breathing
        • Tachypnoea
        • Reduced lung compliance
        • Severe asthma
  • Extension of physiological dead space
    • COPD
copd 25 o 2
COPD: 25% O2

pH=:7.15

PCO2: 12.3 kPa

PO2: 13.47 kPa

HCO3-: 32mmol.l-1

Hb: 18.8 g.dl-1

Glucose: 9.8mmol.l-1

Lactate: 0.9mmol.l-1

treatment of respiratory failure1
CO2 retention: Ventilatory failure

Treat the cause: Opiates, pain, airway obstruction

Ventilatory support:

Non-Invasive: BiPAP

Invasive: Mechanical ventilation

OXYGENATION: HYPOXIA

Treat the cause: Infection, oedema

↑FiO2

PEEP

Treatment of respiratory failure
summary
Summary

Failure of oxygenation

    • Hypoventilation
    • Diffusion
    • Shunt and V/Q mismatch
  • Treat the cause
  • Supplemental oxygenation & PEEP

Failure of ventilation

    • Respiratory depression
    • Increase in physiological dead space
  • Treat the cause
  • Ventilatory assistance
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