This document discusses the pathophysiology of acute respiratory failure, including different types and underlying mechanisms. It presents a case study of a patient named John admitted with worsening asthma symptoms and hypoxemia. Key factors affecting John's condition are decreased lung compliance, increased airway resistance and dead space, and ventilation/perfusion mismatch leading to hypoxia. Mechanical ventilation aims to improve oxygenation by reducing the work of breathing and improving lung mechanics, but edema remains a risk that can counter these benefits.

1. Pathophysiology of acute
respiratory failure
CT1 Education Series (Intro)

2. Respiratory Physiology Syllabus
• B:18.1.44 Gaseous exchange: O2 and CO2 transport, hypoxia and hyper-
and hypocapnia, hyper- and hypobaric pressures
• B:18.1.45 Functions of haemoglobin in oxygen carriage and acid-base
equilibrium
• B:18.1.46 Pulmonary ventilation: volumes, flows, dead space
• B:18.1.47 Effect of IPPV on lungs
• B:18.1.48 Mechanics of ventilation: ventilation/perfusion
abnormalities
• B:18.1.49 Control of breathing, acute and chronic ventilatory failure,
effect of oxygen therapy
• B:18.1.50 Non-respiratory functions of the lungs

3. Acute Respiratory Failure
• Type I – Hypoxaemia
• Type II – Hypercapnia
• Type III – Perioperative (Atelectasis)
• Type IV – Shock (Hypoperfusion)

4. Pathophysiological Issues
• Work of breathing
• Mechanisms of hypoxia
• Defenses against hypoxia & pulmonary oedema
• Oxygen transport issues
• Lung compliance
• Altered lung volumes & recruitment
• Impact of mechanical ventilation
• Impact of anaesthesia/sedation/position

5. Case scenario
• John is a 24 year old with mild asthma, admitted
with a 2 day history of increasing shortness of
breath and wheeze, preceded by 48 hours of
generalized aches and pains and fever.
• His room air oxygen saturation is 86% and his
respiratory rate is 35 per minute. He has bilateral
wheeze and also crepitations at the right base. He
looks exhausted.....
• ABG shows pH 7.37, pCO2 5.6, pO2 7.6 on air
• On 10L O2 his pO2 increases to 8.8 kPa

6. Questions
• What are the factors affecting John’s work of
breathing?
• What the mechanisms behind John’s hypoxia?
• Why is John’s pCO2 not lower?
• Why has the marked rise in FiO2 not translated
into a big change in pO2?

7. Areas of relevance
• Work of breathing
– Decreased lung compliance
– Increased deadspace
– Increased resistance to airflow
– Need for active exhalation
• Mechanisms of hypoxia
– Hypoventilation
– V/Q mismatch
– Shunt
• Higher than expected pCO2 given RR
– Increased dead space
– Increased respiratory muscle activity -> CO2 production
– V/Q mismatch
• Lack of response to oxygen
– Shunt fraction
– Alveolar ventilation

8. Poor John...
• John is admitted to the ICU and you decide to
intubate and ventilate him
• He is anaesthetised with propofol and paralysed with
rocuronium, and you successfully get the ETT in on
the first attempt
• You ventilate him with 100% oxygen, PEEP 8, rate
12/minute, inspiratory pressure 25
• ABG shows pH 7.28, pCO2 6.3, pO2 10.6
• How would you recognise improved compliance?

9. More food for thought...
• What have you done to John’s work of breathing?
• What is happening to John’s lung compliance?
• What factors affect John’s tissue oxygenation?
• What law determines intra-alveolar pressure...and how
does the body beat it?
• What are alveolar time constants...why should you care?
• How does the body minimise the effect of local changes
in V/Q on oxygenation?
• What effects does anaesthesia/sedation have on lung
volumes and defense mechanisms?
• What effects does body position have on lung volumes
and oxygenation

12. John hangs in....
• Overnight John received 2.5 L of fluid for a
dippy blood pressure. In total he is now 4.6 L
positive. His albumin is 30.
• What are John’s defense mechanisms against
pulmonary oedema?
• If his oxygenation worsens, what else can we
do to improve things...and how do your
interventions work?