Lecture 5: Pathophysiology of resp. failure part 2

Question 1

How is COPD characterized?

Answer 1

• A disease state characterized by airflow limitation that is not fully reversible
• The airflow limitation is usually both progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases

Question 2

Whats the pathophysiology of COPD?

Answer 2

• Increased mucous production and ciliary dysfunction
• Hypertrophy of SM and CT of large airways
• Peribronchial fibrosis
• Alveolar wall destruction (destruction of elastic component of lung)
• Development of emphysema
• Development of pulmonary hypertension and cor pulmonale

Declining FEV1 (good measure of obstruction)

Question 3

What are some relevant measures that can be done in COPD patients?

Answer 3

• VO2 of resp. muscle vs ventilation, sees an increased steepness of relationship. I.e in COPD its harder work of breathing with COPD
• A decrease in alveolar ventilation because of COPD results in a decrease in PO2 which is ok but PCO2 also decreases which results in acidosis therefore an increase in HCO3 is required.

Question 4

What partial pressure of oxygen results in 90% oxygen saturation?

Answer 4

8kPa

Question 5

What type of resp. failure is COPD?

Answer 5

Type 2 because:
- Reduction in PO2 and thus saturation -> blood oxygen content.
- There is also an increase in PCO2

(ventilation rate is limited because of the increased work of breathing, therefore the ability to increase PO2 is limited)

Question 6

What happens when supplementary oxygen is giving to COPD? How can this be detrimental?

Answer 6

It rises the Partial pressure of O2 vs alveolar ventilation curve. This can depress the respiratory drive to compensate the rise in CO2 that occurs because of the reduce ventilation capacity and cause respiratory acidosis. (hypoxia can be ok, hypoxaemia not)

Question 7

What happens to the the O2&CO2 response curves in type two respiratory failure?

Answer 7

In type two resp failure the oxygen response curve shifts upwards slightly.

In type two resp failure the CO2 response curve goes from being steep to very flat. (Insert pic of slide 8)

Question 8

At what part of the oxygen cascade does supplemental oxygen assist?

Answer 8

Can only help at the point of the pulmonary capillary (diffusion)

After this, a VQ shun must be present if low saturation continues in spite of supplement.

Question 9

Check the acute on chronic resp acidosis with normoxia

Answer 9

Slide 10

Question 10

How do you calculate the effect of a shunt?

Answer 10

Q(t) x CaO2 = Q(s) x CvO2 + Qc x CcO2

Q(t) = CO
Q(s) = Shunt (10% of RV ejected blood)
Q(c) = Pulmonary
C (a,v,c) = Oxygen content of arterial, coronary venous (shunt), pulmonary oxygenated blood

i.e re-arrange to determine CaO2 (blood content of blood) and thus know thier oxygen dissociation curve withe the capacity to estimate PaO2 - saturation relationship

Same can be used for CO2

[ Weak knowledge] ask for help

Question 11

What do shunts mostly effect?

Answer 11

Oxygen, unlikely to cause acidosis.

Cant oxygenate blood that is being shunted (with supplemental oxygen)

Question 12

Whats the approximate pressures of Pip and Ptp during tidal breathing?

Answer 12

Pip: -1.5->1.5cmH2O

Ptp: -5->-8cmH2O

~500ml

Question 13

Whats the three compartment model of Ventilation:Perfusion ratio?

Answer 13

It takes into account throughout the lung that there are differences in:

Blood flow
- Gravity
- Hypoxic vasoconstriction
- AV malformations

Blood oxygen conc.
- Ventilation
- Gas exchange

Question 14

What limits oxygen diffusion?

Answer 14

The a-A gradient.

Question 15

What is the most important cause of hypoxaemia in the compartment model of the lung?

Answer 15

V/Q mismatch