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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



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



Pneumonia lung compliance
Pneumonia: ↓lung compliance


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


Ventilatory failure co 2 retention
Ventilatory failure: CO 50% O2 retention


Physiological dead space
Physiological dead space 50% O

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: 50% O

Typically increase in Physiological dead space

When large also causes significant V/Q mismatch

Hypoxia and CO2 retention


Most organic parenchymal diseases: 50% OIncrease in V/QSome shuntingIncrease in physiological dead space


Ventilatory failure
Ventilatory Failure 50% O

  • 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% O 50% 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

    CO 50% O2 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 50% O

    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


  • ?? 50% O


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