L7 Respiratory failure 2

Question 1

Define COPD, time course,

Answer 1

Disease state characterised by worsening airflow limitation, not fully reversible,

Associated with abnormal inflammatory response of the lungs to noxious particles/gases.
eg. smoking.

Question 2

What are the changes in proximal (cartilaginous) vs peripheral (non-cartilaginous) airways in COPD: blood cells, airway structure

Answer 2

Both:
- decrease in neutrophils/eosinophils

• Increased mucous secretions

Proximal
- increase in macrophages, T lymphocytes

• ciliary dysfunction
• Hypertrophy of SM and CT- increased responsiveness

Peripheral
- increase in B lymphocytes

• Bronchiolitis at early stage, luminal inflam
• Peribronchial fibrosis and airway narrowing (irreversible)

Question 3

What are the changes in respiratory bronchioles and alveoli airways vs Pulmonary vasculature in COPD: blood cells, airway structure, disease states

Answer 3

Both
- Increase macrophages and T lymphocytes

Resp B & A
-Alveolar wall destruction

-Development of emphysema - macro/micro by breaking alveolar septum

Pulmonary vasculature

• Intimal thickening, endothelial dysfunction
• Hypertrophy of vascular SM. and collagen deposition
• Destruction of capillary beds leading to pulmonary hypertension

Question 4

What is the effect of smoking cessation on someone with COPD

Answer 4

Stopping smoking at any age confers extra time before death at any age, as the curve’s slope will mirror the never smoked curve, (however start at a lower starting point)

Question 5

Why in the case of hypercapnic respiratory failure (COPD exacerbation) is it better to take off the O2 mask once the O2 saturation is up and then try to treat the underlying cause of exacerbation ?

Answer 5

In COPD the respiratory muscles require more oxygen to ventilate than a normal person to overcome the inefficiencies in their lung.

To reduce the work of breathing, they can compensate in pH for increased amount of CO2,

so the primary respiratory drive is left to pO2, (only a very flat curve of increase in ventilation in response to increases of pCO2)

Therefore whilst managing her O2 saturation, its better to increase her respiratory rate.

Question 6

What could be the main causes of acute big drops in O2 saturation

Answer 6

1. V/Q shunt: An increase in the A-A gradient
   - Could happen by complete stenosis of a mainstem bronchus due to bleeding/mucus = no ventilation of a lung but continued perfusion.

Question 7

Why does shunt affect O2 content greater than CO2,

Answer 7

The shape of the O2 dissociation curve for saturation at a given PO2 has a steep gradient causing large drops in O2 saturation with small decreases in PO2

Compared to CO2 dissociation curve which is relatively flat.

Question 8

What is the distribution of perfusion vs possibility of ventilation from the bottom of the lung to the top

Answer 8

At the top
1. lower perfusion pressure so therefore less blood flow

2. Pleural pressure is more negative, potential to change volume with the same force

Less ventilation possible

At the bottom

1. higher pressure of perfusion so more blood flow
2. Pressure is less negative so there is more ventilation possible.

Question 9

What are the factors that affect the change in O2 content along the lung (ventilation)

and the change in blood flow (perfusion) along the lung

Answer 9

Change in O2 content

• Rate of ventilation
• Gas exchange

Blood flow

• Gravity,
• Hypoxic vasoconstriction
• AV malformations

Question 10

What happens when you give someone with a 50% shunt 100% saturated FiO2 compared to someone with 20% shunt

(This doesn’t happen if someone doesn’t have a shunt.)

Answer 10

Giving 100% saturated O2 will not increase the O2 content in arterial blood of 50% shunt because at high ends of the curve, the Hb is saturated. It will increase the A-a gradient tho.

20% and less shunts will increase the arterial PO2 with 70% inspired O2