Respiratory failure : VQ mismatching and more Flashcards

1
Q

What are the normal arterial values?

A
  • PaO2 (11-15 kPa; 90-113mmHg)
  • PaCO2 (4.6-6.4 kPA, ~33-46mmHg)
  • Outside these ranges are abnormal. May indicate resp.failure
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2
Q

What is respiratory failure ?

A
  • Failure to maintain adequate gas exchange and is characterised by abnormalities in arterial blood gas partial pressures
  • Type 1 : hypoxaemia (< 8kPA) with a normal or low CO2
  • Type 2 : hypoxaemia with a high CO2 (>6 KPa)
  • normally breathing rate cannot keep up
  • They can co-exist
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3
Q

What are the four main pathophysiological causes of resp failure?

A
  1. Alveolar hypoventilation : reduced in minute ventilation characteristically shows an increase in PaCO2
  2. Diffusion deficit
  3. Shunts
  4. Ventilation - perfusion (VQ) mismatch
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4
Q

What is hypoventilation?

A
  • CO2 retention - reduction in minute ventilation
  • An increase in proportion of dead space ventilation
  • Causes Type II
  • E.g. respiratory muscle fatigue
  • Correctable with O2
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5
Q

What is diffusion deficit?

A
  • ## Described by Fick’s law - describes the rate of diffusion across the alveoli into the blood
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6
Q

What are shunts?

A
  • Venous blood mixing with arterial blood
  • Extra-pulmonary shunt
  • Mainly paediatric cardiac causes (ductus arteriosus. Usually reverses)
  • Intra-pulmonary shunt : blood is transported through the lungs without taking part in gas exchange
  • Commonest causes are alveolar filling (pus, oedema, blood or tumour) and atelectasis
  • Oxygen does not correct pure shunt hypoxia
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7
Q

What is ventilation-perfusion VQ matching?

A
  • Gas exchange needs good ventilation (V) and perfusion (Q) of alveolar capillaries
  • V= 5L air/min ; Q = 6L blood/min
  • Whole lung VQ = 0.8 and 1
  • ## Correlating alveolar ventilation (5L/min) and perfusion about (5L/min) Maximises gas exchange and efficiency. Ideally should be 1:! (i.e. 1.0). Regulation is needed to maximise gas exhange and maintains normal blood gas partial pressures
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8
Q

What is the most common cause of hypoxia in respiratory diseases ?

A

VQ mismatching
- increases the area that is not used for gas exchange (alveolar dead space)
- i.e physiological dead space
- PaO2 falls and then the PA-PaO2 gradient increases
- Breathing rate may increase

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9
Q

What are some causes of VQ mismatch?

A
  • Lack of inspired oxygen
  • Lack of circulation/blood flow (Shunts)
  • Respiratory dysfunctions
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10
Q

What are the consequences of VQ mismatch?

A
  • Blood leaving the relatively healthy alveoli will have an oxygen saturation of about 97% (normal) because of the flat upper portion of the oxyhaemoglobin dissociation curve
  • Blood leaving alveoli that do not have optimum V/Q ratios will have a much lower oxygen saturation and overall causes hypoxaemia , when they mix in the circulation
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11
Q

What are common respiratory dysfunctions that cause VQ mismatch and reduced PaO2?

A
  • Adult respiratory distress syndrome
  • Pneumonia
  • Asthma
  • Pulmonary oedema
  • Chronic obstructive lung disease
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12
Q

What are the type 1 respiratory failures that occur before type 2?

A

Common:
- Acute asthma
- Exacerbation COPD
- Pneumonia
- Pulmonary oedema
- Pulmonary embolism
- ALI - Adult lung injury
- Resp depression
- Opiates

Rarer :
- Lung collapse/atelectasis
- Intersitial lung disease/pulmonary fibrosis
- Pulmonary haemorrhage
- Acute resp weakness
- Upper airway obstruction
- Fat embolism
- Chest trauma
- Anaphylaxis

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13
Q

How is V/Q regulated locally?

A
  • Airflow and blood flow are governed by the same principles of flow, pressure and resistance (Poiseulle’s Law)
  • Resistance to flow is inveresly proportional to the radius
  • Bronchioles provide most resistance to airflow
  • Arterioles provide most resistance to perfusion
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14
Q

What are the continous local changes occuring relating to VQ matching?

A
  • Altering respiratory bronchiolar and pulmonary arteriolar radius changes resistance and hence flow
  • Bronchioles dilate in response to raised PaCO2 (Hypercapnia) to improve airflow
  • Pulmonary arterioles constrict to low PaO2 (hypoxia) to reduce flow and redirect blood to better perfused areas
  • Opposite to systemic circulation
  • Mechanism uncertain
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15
Q

What are the effects of local changes in o2 on the pulmonary and systemic arterioles?

A

Pulmonary arterioles - decreased O2 = vasoconstriction, Increased O2 = vasodilation
Systemic Arterioles - Vasodilation , Increased O2 = vasoconstriction

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16
Q

What is the effect of gravity on VQ ratio?

A
  • Both blood flow and ventillation vary from bottom to top of the lung
  • Result - the average arterial and alveolar partial pressures of O2 are not exactly the same. Normally, this effect is not significant but it can be in disease
17
Q

Why is there a VQ difference from the base to the apex?

A
  • The intrapleural pressure is more negative at apex than the base
  • The alveoli at the base are highly compliant so can acoomodate more air
18
Q

Discuss what happens in zone 1 of the lungs in terms of pulmonary blood flow

A
  • Changes in the surrounding areas:
  • Zone 1 = alveolar pressure is greater than both local pulmonary arterial and venous pressures. Irrespective of the normal pressure gradient from arteries to veins, the vessels are compressed by the high alveolar pressure and there is only intermittent flow if Pa increases during the breathing cycle
  • Palv > Pa> Pv
19
Q

Discuss what happens in Zone II of the lungs

A

The normal pressure gradient from arteries to veins can be disrupted by interittent high alveolar pressures
-Pulmonary arterial pressure is low
The flow is independent of the eventual venous pressure and depends only on the difference between pulmonary arterial pressure and alveolar pressure
Pa> Palv> Pv

20
Q

Discuss what happens in zone III in lungs ?

A
  • Normal pressure gradient from arteries to veins
  • Pulmonary artery pressure is greater than venous pressure and alveolar pressure ensuring perfusion
  • Pa> Pv> Palv