Gas Exchange & Transport Flashcards
Gas exchange v. gas transport
Gas exchange = gas transfer: the movement of gases between alveolar space and blood compartment
Gas transport = movement of gases from the blood compartment in the lung to the periphery
Remember that ventilation is movement of gas from atmosphere to alveolar space
Tissue Hypoxia: definition and causes
Decreased O2 in your tissue
Causes: decreased O2 in blood (hypoxemia or Hb problem), decreased blood flow to organs, mitochondria not working
Hypoxemia
Low partial pressure of O2 in arterial blood
Normal > 90
Hypoxemia <90
What are the effects of hypoxemia?
Can cause tissue hypoxia
Dyspnea
What is one major possible cause of hypoxemia?
Impaired gas exchange
What determines the rate of gas transfer in an alveolus?
Proportional to SA, solubility of the gas, pressure gradient across alvolar/capillary membrane
Inversely proportional to thickness of capillary membrane
What is the main determinant of flow of CO2?
Solubility of CO2
It’s so soluble, that even if the other factors change (SA, pressure gradient, thickness) the flow doesn’t change very much (except in very severe lung disease)
Not a great measure of lung disease
What makes O2 a good measure of lung disease?
All the factors in the equation for flow matter: not one dominates (as opposed to CO2, where solubility dominates)
How does changing ___ affect flow of O2 (VO2)?
- Thicker capillary membrane
- Increasing PiO2
Increasing alveolar ventilation
Extracting more O2 in tissues - Decreasing alveolar ventilation
- Decreased perfusion of capillary i.e. due to clot
1. Thick capillary membrane decrease VO2
- *Increasing PiO2 increases PAO2
*Increasing alveolar ventilation increases PAO2
*Extracting more O2 in the tissues –> less O2 in the venous blood –> increases gradient –> increases VO2
*Relevant in exercise, but not in lung disease
3. Decreased alveolar ventilation –> decreased PAO2
- Decreased perfusion ultimately leads to decreased flow of O2 bc the blood can’t reach the alveolus (note that it’s slightly paradoxical bc you end up increasing PAO2, bc the O2 in the “reservoir”/alveolus can’t leave)
the bold ones are most relevant in disease states
What are the two-three major causes if impaired gas exchange? (O2 transfer)
(1) Impaired diffusion
Abnormal V/Q ratio (alters PAO2 therefore alters gas transfer) including (2a) low V/Q areas (2b) Left to Right shunt
This would be reflected in a difference in predicted PACO2 and measured PaCO2 (in other words, high AaDO2)
Why is it important to calculate PAO2?
It’s a great measure of V/Q ratio– tells you how much O2 you will get flowing across alveoli to capillary
Alveolar PO2 = measure of alveolar health, tells you if you have normal or impaired gas exchange
Alveolar gas equation: full version
(understand this equation but it’s not used clinically)
Note that alveolar PO2 is related to atmospheric O2 pressure, ventilation, and gas exchange
The first 2 are constant
Only gas exchange can change
So we know that any change in alveolar PO2 is related to a change in gas exchange
What is the respiratory exchange ratio?
Normal R = 0.8
Measure of gas exchange
Normal PAO2?
100
Low is <90
Normal PACO2?
40 (37-42)
Low = alveolar hyperventilation
High = alveolar hypoventilation
What is the alvolar gas equation?
Clinical version
This is used clinically- memorize
What is a major assumption in the alveolar gas equation?
That all the alveoli are healthy and are the same: R=8
How do you use the alvolar gas equation to assess gas exchange clinically?
-
Estimate alvolar PAO2 using the alveolar gas equation, assuming normal & homogenous gas exchange
PAO2=150-PACO2/R
PACO2 is from the blood gas & normal is around 40
R=.08 (normal), part of our assumption
So PAO2 = 100 -
Compare estimated PAO2 to measured PaO2: AaDO2
AaDO2 = PAO2 - PaO2
- If they are similar, gas exchange is normal (AaDO2<10)
- If they are different, gas exchange is impaired
What is a lung unit?
Small group of alveoli that have same physiological properties (ventilation, perfusion, and diffusion properties)
Ventilation/perfusion in the 3 zones of the lungs
How does your lung minimize V/Q mismatch?
Hypoxic pulmonary vasoconstriction (HPV): your lung directs blood flow away from under-ventilated lung to match V and Q
Hypocapneic bronchoconstriction: attempt to direct ventilation away from underperfused lung units (less efficient)
What are two major causes of low V/Q ratio?
Airway disease
Alveolus disease
Leads to decreased ventilation (V) & decreased PAO2
- low V/Q lung unit
- Right to left shunt
What is the normal PO2 in pulmonary artery? (“mixed venous”)
40 mmHg
What would the PO2 in alveolus & capillary be when V/Q ratio is zero?
Both would be 40, because air isn’t reaching the capillary so gas exchange can’t occur
What is the major cause of a V/Q ratio = zero?
Zero ventilation of the lung
Right to left shunt: mixed venous blood enters pulmonary veins or the arterial circulation
**either in heart or in lungs
How could you determine whether the V/Q ratio is zero?
The hypoxemia is not responsive to high PiO2 (supplemental oxygen)
What is the one circumsstance when the alveolar PO2 and the capillary PO2 are different?
When you have impaired diffusion
Alveolar PO2 will be normal (or a little high)
Capillary PO2 will be low
How long do you have for pulmonary capillary diffusion at rest?
0.75 seconds
But it takes less in a normal patient! About 0.25 sec for all the gas transfer to happen
Why might diffusion go down when you have impaired capillary diffusion? How would patient present?
Patient would present wtih decreased PACO2 & PaO2 during exercise & therefore increased AaDO2 (indicates worse gas exchange during exercise)
This is because during exercise, blood flows through capillary more quickly leaving less time for diffusion to occur. So in a diseased patient, where it normally takes them all 0.75 seconds or more for diffusion to occur, when you shorten the time available, less diffusion is able to occur and diffusion is “cut short”
This happens in disease that impair diffusion i.e. PCP pneumonia
What are the 5 main causes of hypoxemia?
Which ones are clinically relevant?
Which ones have pulmonary cause?
Alveolar hypoventilation, Low PiO2, Impaired diffusion, Low V/Q, Right to left shunting
All are clinically relevant except Low PiO2
High AaDO2 indicates pulmonary cause (normal = other cause)
What are the ways in which we can clinically assess gas exchange?
A-a gradient
PaO2 to FiO2 (inspired O2) ratio = P/F ratio
Exercise testing
Diffusion capacity
How do we meausre diffusion capacity of the lung?
Breathe out, then give patient a little CO, hold breath 10 s, measure how much CO out = measure the rate of transfer across the membrane; it diffuses across the membrane so changes in rate reflect changes in diffusion rate
DLCO=VCO/PACO
Diffusing capacity of CO= rate of CO transfer/partial pressure of CO in alveolar space
What is the diffusing capacity of CO related to?
(1) Alveolar capillary conductance
(2) Volume of pulmonary capillary blood (if it’s high volume, you get low CO)
What diseases can cause low DLCO?
Anything that affects the alveoli- emphysema, interstitial lung disease, pneumonia, pulm edema. NOT pure airway diseases i.e. asthma
What disease have a normal DLCO but have abnormal spirometry and/or lung volumes
Anemia (low Hb conc)
CO that’s already in the blood i.e. smoker
Pulmonary vascular diseases
Early lung disease: DLCO can decrease before other things are abnormal
What can cause an increased DLCO?
(1) more volume in your lungs (obesity, supine position, L to R shunt, early CHF, alveolar hemorrhage)
(2) Asthma: normal or high DLCO
What would cause a high V/Q ratio?
Blood clot that blocks blood flow to capillary
Leads to high PAO2 & high PCO2 but not much blood gets through to pick up the O2
Why would arterial PO2 be normal in a patient with a high V/Q ratio?
Because of the O2 dissociaton curve from Hb: O2 is maximally saturated at around 90-100, so increasing arterial PO2 more than this will not increase your O2 content in blood bc the Hb is maximally saturated
How can you measure arterial oxyhemoglobin saturation?
SaO2: calculated from arterial blood gas (ABG)
SpO2: measured with a pulse oximiter directly
Why is high V/Q not a cause of hypoxemia or hyperoxemia?
High V/Q doesn’t balance out low V/Q because mixing high & low PO2 blood is not additive bc the amount of blood flow to high V/Q areas is very low: wasted ventilation/ “dead space”
What factors lead to a “right shift” of the oxyhemoglobin dissociation curve?
Think exercise/ factors that help unload O2 in metabolically active tissue
Increased PCO2
Decreased pH
Increased temp
Increased 2,3-DPG (glycolysis byproduct)
Note that the opposite would lead to a left shift: this would occur in non-metabolically active areas i.e. the lungs
How is CO2 transported in the blood?
Most as bicarbonate
3% bound to Hb, 5% dissolved in plasma
What is the formula for oxygen delivery to tissues?
Directly related to cardiac output and arterial O2 content, which is related to Hb
How do you manage hypoxemia?
Treat underlying cause
Administer O2
Which noninvasive masks deliver the most to the least O2 flow?
(1) Nonrebreather 15 L/m
(2) Normal face mask 10 L/m
(3) Venturi mask: approximates FiO2 = more precise
(4) Nasal canula 6 L/min
When is long term oxygen therapy (LTOT) indicated?
Chronic hypoxemia: PaO2<55mmHg or SpO2<88%
OR
PaO2 56-59 mmHg or SpO2=89% with hematocrit >55%, cor pulmonale, dependent edema
COPD
What are the risks of O2 therapy?
Retinopathy of prematurity (when you give high O2 to preemies)
Oxidative lung injury (high FiO2 for more than a few days)
Fire risk
Supplemental oxygen-induced hypercapnia: in patients who already have hypercapnia
Why does supplemental O2 make hypercapnia worse?
Increased O2 –> Increased alveolar PAO2 –> relieves hypoxic pulmonary vasoconstriction –> worsening of V/Q matching: bc you increase flow but there’s still low Q!!
This increase in V/Q mismatch leads to a sudden rise in PaCO2 which is very dangerous/can be fatal
Therefore: in chronic hypercapnia+chronic hypoxemia: aim to keep SpO2 low
