Lung physiology and disorders Flashcards
Describe the basic structure.
Upper and lower lobes.
Lungs are contain an intricate system of vessels to allow air passage into them from the trachae. The trachae branches off into bronchi, then bronchioles and finally alveoli.
Where does gas exchange occur?
Alveoli and the capillary surrounding them
Function of lung
Gas exchange and acid base regulation (through PCO2)
What controls respiration? A. Cerebellar cortex B. Medulla C. Hypothalamus D. Temporal lobe
B - respiratory centre in medulla controlling rate and depth of breathing
What drives the regulation of breathing?
PCO2
Is PO2 a good measure of saturation?
No, because most oxygen is bound to haemoglobin. So SO2 describes the Hb saturation with O2. However, PO2 act as driving force for SO2. So higher PO2= greater saturation. At 13kPa the saturation plataues
What is PCO2 determined by?
Its a reflection of ventilation (amount of air reaching alveoli)
What is the Bohr effect?
Oxygens binding affinity is inversily related to acidity and concentraiton of CO2 (PCO2). Thus, oxygen dissociation curve shifts in accordance with changes in these
What is PO2 levels determined by?
A. Conc of O2 in inspired air B. Ventilation C. Perfusion of lung D. AC E. AB F. ABC
F
What is a normal V/Q?
A. 0.4
B. 0.6
C. 0.8
D. 1
C
What is V/Q mismatching? and how does changes in V/Q affect pCO2 and pO2?
This is when either V or Q is poor incomparison to other parts.
decreased V/Q = alveolar decreased pO2/increased pCO2
increased V/Q = alveolar increased pO2/decreased pCO2
In V/Q mismatching, can areas of poor ventilation be compensated for?
Yes, any alveoli can compensate for poor alveoli by hyperventilation
In V/Qmismatching, can areas of poor perfusion be compensated for?
Areas of good perfusion cannot compensate for areas of poor, Hb is already max saturated
V/Q mismatched example of poor perfusion
In a V/Q mismatch
- PO2 and SO2 in the arterial blood falls, but the PCO2 can remain normal due to hyperventilation
How is lung function monitored in the lab?
Arterial blood gases (ABG)
- Blood gases; PCO2 and PO2 - gas exchange
- Acid base: pH, PCO2, HCO3 - acid base balance
- Cooximetry: THb, O2Hb,SO2- haemoglobin saturation.
Match the following: A. Inadequate O2 reaching cells B. Decrease in PCO2 C. Decrease in SO2 D. Not enough blood E. Increase in PCO2
- Hypercapnia
- Hypoxia
- Hypocapnia
- Hypoxaemia
- Ischaemia
A2, B3, C4, D5, E1
What describes type 1 disorders of respiration best?
A. Decrease in PO2 and increase in PCO2
B. Decrease in PCO2, with normal O2
C. Decrease in PO2, unchanged PCO2
C. Type 1 - Adequate ventilation - Defective oxygenation - Hypoxaemia - Caused by pneumonia, pulmonary embolism, COPD, ARDS
What describes type 2 disorders of respiration best?
A. Decrease in PO2 and increase in PCO2
B. Decrease in PCO2, with normal O2
C. Decrease in PO2, unchanged PCO2
A. Type II - inadequate ventilation - hypercapnia and hypoxaemia - Caused by COPD, exhaustion, opiates (act directly on the respiratory centre in the brain - negatively)
What describes hyperventilation best?
A. Decrease in PO2 and increase in PCO2
B. Decrease in PCO2, with normal O2
C. Decrease in PO2, unchanged PCO2
B.
Hyperventilation
- Hypocapnia
- Causes rise in blood pH
Treatment of hypoxaemia needs to be as rapid as possible to treat the patient.
No, trying to treat hypoxaemia to rapidly by giving oxygen you can prevent the hypoxic drive and cause acute complete respiratory failure
How does type I disorders develop to type II?
Type I can develop type II because of consistent hyperventilation. The consistent hyperventilation to maintain normal PCO2 levels which can cause exhaustion. The exhaustion from hyperventilation means that the necessary ventilation cannot be kept up with normal PCO2 levels – hypercapnia
What is alpha1-AT deficiency?
There is no inhibition of neutrophil elastase
- causing emphysema as the elastase break down normal/healthy tissue such as alveoli cell wall
- can affect liver or lungs
- A1T1 measured in the lung
