Lecture 18 - Respiratory Physiology III VA/Q matching, lung compliance and airway resistance Flashcards Preview

1060 Human form and function > Lecture 18 - Respiratory Physiology III VA/Q matching, lung compliance and airway resistance > Flashcards

Flashcards in Lecture 18 - Respiratory Physiology III VA/Q matching, lung compliance and airway resistance Deck (19):
1

What is the total alveolar ventilation in normal healthy lungs at rest ?

 

VA = 4.2 L/min

 

2

What is the total lung perfusion (Q) at rest? (same as CO)

 

 

Q = 5 L/min

 

3

In normal healthy lungs at rest, total alveolar ventilation = 4.2 L/min

VA = 4.2 L/min

 

Total lung perfusion (Q) at rest,(same as cardiac output),

= 5 L/min

Q = 5 L/min

 

Thus, on average for the whole lung at rest ??

 

VA /Q  = 4.2/5 = 0.84

 

If VA/Q differs significantly from this norm, then a reduction of blood oxygenation occurs.

 

 

4

There is some mixing of deoxygenated (right-sided) blood with

oxygenated (left-sided) blood.

What is this called?

 

This is a right-to-left shunt

 

 

5

What is teh right to left shunt ?

 

mixing of deoxygenated (right-sided) blood with oxygenated (left-sided) blood

 

A image thumb
6

L-R shunts have a disproportionate effect on PCO2 and PO2

 

 

 

 

7

Why isn’t poor ventilation in some areas of lung (low VA/Q) compensated for by increased perfusion in those areas?

 

Blood quickly absorbs all available O2 at normal perfusion rates, so increasing perfusion will only dilute that O2

->

Low VA/Q areas will always have lower than normal pulmonary capillary PO2

 

8

Why isn’t poor ventilation in some areas of lung (low VA/Q) compensated for by over-ventilation in other areas (high VA/Q)?

 

Normal O2 content is when blood is already saturated, so raising local alveolar PO2 further by hyper-ventilating will not significantly increase pulmonary capillary O2 content

->

PO2 of high VA/Q areas cannot be raised above normal

->

Most of that extra ventilation will be wasted

 

 

9

What does hypoxic vasoconstriction of pulmonary arteries help with ?

 

Hypoxic vasoconstriction of pulmonary vessels helps to reduce blood flow to poorly ventilated areas diverting it to well ventilated

areas

 

Improves ventilation - perfusion

matching and arterial oxygenation

 

But this is not helpful in global hypoxia  (altitude, hypoxic lung disease) where constriction leads to lower arterial PO2

 

[In systemic circulation hypoxia causes dilation]

 

 

10

What is resistance to airflow caused by?

 

Resistance to airflow is caused by the airways that conduct air to the alveoli

In upper airways congestion in nose, pharynx and larynx can increase resistance

In lower airways middle order bronchi contribute most resistance

Bronchioles are narrower, so individual resistances are high

but they are much more numerous so total resistance at that level is very low

Remember: multiple high resistances in parallel = low total resistance

 

 

11

What happens in your lungs when you have asthma?

 
 

Asthma:

Smooth muscle is hypersensitivity to constrictors. Smooth muscle thickening and inflammation:

Narrowing of lumen -> airway resistance increased -> airflow decreased Reduced ->VA→Low VA/Q 

 
 

12

What happens in your lungs when you have chronic bronchitis?

 

Hypertrophied glands in airways producing excess

mucus, with inflammation: 

Narrowing of lumen -> airway resistance increased -> airflow decreased Reduced ->VA→Low VA/Q 

 

13

What does Poiseuille’s Law say?

 

Resistance is directly proportional tube length (l), viscosity of flowing material (η eata) but inversely proportional to the 4th power of the radius

 

 

Tube radius is of greatest importance (as in the circulatory system)

 

 

 

 

 

 

A image thumb
14

Which factors can affect the radius of bronchi?

 

Physical, chemical and neural factors 

 

Chemical and neural factors act on airway smooth muscle:

Dilators:

Adrenalin (from circulation)

CO2

Peptides from non- adrenergic, non-cholinergic nerves (NANC)

Constrictors:

acetylcholine

from parasympathetic (vagus), stimulated by Irritant receptors

Inflammatory mediators

 

Physical factors:

During inspiration, increased trans-pulmonary pressure expands the alveoli and bronchioles

 

 

 

15

What is lung compliance?

 

Lung compliance is the ‘stretchability’ of lung tissue

Key point:

The ease at which alveoli and airways are expanded during inspiration

determines the amount of work that has to be done by respiratory muscles

 

16

What are the two major forces that inspiratory muscles have to overcome?

 

1. Resistance of tissues to stretch influenced by composition of

extracellular matrix. Elastin is stretchable, but requires work, collagen is not

2. Resistance due to Surface Tension at air/water interface in alveoli

 

 

17

Equation for lung compliance?

 

Lung Compliance (CL) =change in lung volume(∆V) / change in trans-pulmonary pressure (∆PTP)

 

Measure volumes with spirometer

Measure PIP with oesophageal balloon

Take measurements in steps as subject breathes in, from residual volume up to total lung capacity

 

18

What does abnormally high compliance suggest?

 

If compliance is abnormally high, suggests lung emphysema Tissue destruction causes alveoli to fuse forming large air-sacs Also causes bronchioles to collapse more easily upon expiration

 

 

19

Surface tension effects lung compliance, what is it and what causes it?

 
 

What is it?

The force at an air-fluid interface

What causes it?

Water molecules attract each other forming intermolecular bonds