Flashcards in Respiratory pathophysiology Deck (26):
What determines partial pressure of inspired oxygen?
Partial pressure of inspired oxygen: altitude and fractional inspired O2 (if breathing air is 0.21) ( need to account for athletes training at altitude or in hypobaric chambers)
What influences PAO2?
ventilation, particularly alveolar ventilation, measure indirectly through PaO2
What influences the gap between PAO2 and PaO2?
The gap between the alveolus and the capillaries and the width of the capillaries? (anaemic patients slightly less PaO2)
Gas exchange is
- measured by?
- Influenced by?
- A-a gradient
- V/Q mismatch
what happens to gas exchange if you have purely hypoventilation?
Any changes in ventilation should not change the A:a gradient as oxygen should be able to freely diffuse across the alveoli and into the blood stream (PaO2 equilibrates before the blood has cleared the alveoli) Likewise small changes in perfusion shouldn't change the A:a gradient as whatever oxygen is in the alveoli will equilibrate with arterial blood
What causes an increased A;a gradient? (3 things)
1. Diffusion problems: If oxygen unable to diffuse across alveolar membrane cannot enter blood resulting in high PAO2 and low PaO2 e.g. pulmonary oedema, ARDS (build up of fluid in the alveoli e.g. pneumonia), fibrosis
2. Serious perfusion problems e.g. PE resulting in increased dead space, since no blood is able to flow through the ventilated alveoli it is shunted to other regions without being adequately oxygenated before returning to the pulmonary veins
3. Shunts wishing the heart (any cause of Eisenmenger complex) resulting in R-->L shunt, deoxygenated blood enters arterial system --> PaO2 decreases (while PAO2 unaffected)
Only presents later in life
If anatomic defect exists between the two sides of the heart shunt will occur allowing blood to flow from the left to the right side. If a high index of the CO is shunted abnormally high blood flow and pressure is directed to the right heart circulation, pulmonary capillaries become replaced with scar tissue increasing pulmonary vascular resistance (this damage irreversible even if heart is corrected now), elevated pressure cause the myocardium of the right heart to hypertrophy. Onset of Eisnmengers syndrome occurs when right heart pressure exceeds that of left leading to reversal of blood flow through the shunt, so deoxygenated blood bypasses the lungs
what is the difference between partial pressure of O2, O2 content and O2 saturation
partial pressure of oxygen in arterial blood (PaO2) the portion of total blood gas pressure exerted by oxygen.
The arterial oxygen content (CaO2) is the amount of oxygen bound to hemoglobin plus the amount of oxygen dissolved in arterial blood
Oxygen saturation is a term referring to the fraction of oxygen-saturated hemoglobin relative to total hemoglobin (unsaturated + saturated) in the blood.
How doe drug use cause hypercapnia?
If makes you unconscious can cause enough cerebral depression to reduce respiratory drive
What is the definition of respiratory failure?
when the lungs fail to oxygenate the arterial blood adequately and / or fails to prevent undue CO2 retention
Pa thesholds for respiratory failure
PaO2 < 60mmHg (8.0kPa) = hypoxic/type I
PaCO2 > 50mmHg (6.6Kpa) = hypercapnic /type II
The difference between alveolar ventilation and minute ventilation
minute ventilation is the sum of alveolar and dead space ventilation
It is possible to increase minute ventilation with decrease in alveolar ventilation and increase in dead
PaCO2 is inversie proportional to?
What are the 3 causes of hypoventilation --> hypercapnia?
1. Decreased respiratory drive
2. Neuromuscular competence
- Decreased drive
- Decreased nm transmission
- Muscle weakness / fatigue (electrolyte disturbances, malnutrition, abnormal length tension relationship)
3. Abnormal load
- Increased resistive load (e.g. weight gain)
- Increased lung elastic load
- Chest wall elastic load
- Minuete ventilation load
Why does hyperaemia often worsen as patient walks across room?
when walking across room oxygen uptake increases 3-4x, to manage this increase uptake and get good delivery to tissues needs to increase CO and therefore decrease time the RBCs are exposed to oxygen in the capillary --> hypoxaemia unmasked on exercise
How do you distinguish between pure hypo and hyperventilation and intrinsic lung disease?
Viz A:a gradient
characterised by airflow obstruction,not fully reversible, due to inflammatory response from inhaled particles
In developed countries from cigarette smoke and in underdeveloped countries from burning of biomass (often inside their houses with poor ventilation)
Lung function with smoking and not
Lung function on steady decline after about 25 years, once you stop smoking the rate of decline goes back to that of a non-smoker (lines parallel) but a continuing smoker will have a steeper gradient of decline
The 3 components of COPD?
1. chronic mucous hypersecretion - hyperplasia of goblet cells and hypertrophy of mucous glands so that you produce more mucous this leads to chronic coughing sputum production
2. Emphysema = destruction of alveoli walls
3. Small airway inflammation
2 and 3 cause airflow obstruction in this condition
The 3 possibilities of V/Q mismatch?
Lung that is ventilated but not perfused
Lung that is ventilated and perfused
Lung that is perfused but not ventilated
V/Q = 00 dead space
V/Q = 1 ideal
V/Q = 0 shunt, venous mixture
How does a patient who smokes and has bad lungs progress to having chronic respiratory acidosis?
Because of COPD say emphysema we have part of the lung that is ventilated but not perfused, so when the capillaries anastomose we get half oxygenated blood and half deoxygenated (mixed venous) blood. patient hypercapnia and because Co2 levels drive ventilation patient will start to hyperventilate
CO2 levels will come back to normal
However oxygen content won't normalise because you can still only hyperventilate your ventilate able compartments and the blood in the ventilateable and perfused compartments will already have been saturated with oxygen at the previous rate of ventilation
This all results in a normal PaCO2 and a normal pH.
As patient continues to smoke her V/Q becomes worse so she becomes hypercapnia and hyperaemic, she then hyperventilates again to normalise her CO2. She continues to do this till she can maintain her this level of hyperventilation, then she'll let her CO2 climb and reset her chemoreceptors. The body can live with high CO2 but it doesn't like acidosis. H+ excreted by kidneys so we're left with raised blood bicarbonate.
What is the normal A-a gradient range?
Dangers of administering high (as opposed to low) inspired O2 to patients with chronic respiratory acidosis?
Patients sensitivity to their raised PaCO2 levels is decreased, become dependant on their hypoxic drive to stay ventilated. If you administer high inspired oxygen the body will think it doesnt need to breathe as fast and slowly the stop breathing but don't realise theyre become hypoxic, because their A:a gradients are still terrible
using the A:a gradient to determine whether patient is breathing properly or needs help
PaCO2/0.8 + PaO2 < 20
equation must come out to be less than 20 if they're to be breathing air properly at sea level. But if you add up sick patients PaO2 and PaCO2 and they come out to be greater than 20 they should be on supplemental oxygen
How to distinguish shunts from V/Q mismatch
Admin 100% oxygen to patient and measure their PaO2