Pulmonary Physiology Flashcards
Normal measurement of
PAO2.
100 mm Hg ~ Alveolar O2
*Differs from atmospheric pO2 because some O2 is lost in the conduction system of the lungs
Normal measurement of
PaO2.
95-98 mm Hg ~ dissolved O2 (unbound in plasma)
Define CaO2.
CaO2 = Total content in blood = [PaO2] + [SaO2]
Normal measurement of
PvO2.
40-45 mm Hg
Normal measurement of
Atmospheric O2
150 mm Hg = (760 - 47[water]) * 21%
Normal measurement of
PACO2.
40 mm Hg ~ no change in pressure between alveolus and pulmonary artery therefore CO2 diffuses passively in alveoli during gas exchange.
Describe the processes that occur during inspiration.
- Diaphragm contracts (flattens) and lungs expand.
- Negative pressure builds in the lungs. Higher atmospheric pressure rushes into lower lung pressure.
- EXTERNAL INTERCOSTAL muscles pull outward, if accessory muscles are needed to create.
Describe the processes that occur during expiration.
- Diaphragm relaxes and bulges upward reducing lung volume thus building lung pressure.
- Higher alveolar pressure rushes air out of lungs and into atmosphere.
- INTERNAL INTERCOSTAL muscles pull chest wall inward, thus aiding to push air out.
What are the 2 opposing forces in the thorax and what are their causes.
- Inward Elastic recoil provided by the LUNGS.
2. Outward Elastic recoil provided by the CHEST WALL.
What is the significance of Transpulmonary Pressure and what are its components.
- Transpulm P = Alveolar P - Intrapleural P
- Transpulmonary P is negative to have alveoli expand in INSPIRATION.
- If Transpulm P is less negative, alveoli tend collapse in EXPIRATION.
Describe surfactant’s effect on alveolar tension and relationship with alveolar size. What is the significance of LaPlace’s Formula related to surface tension?
Surfactant, secreted by Type II cells:
- Reduces Surface tension AND has a Greater Effect on smaller alveoli.
- P = 2T/r, shows that the smaller the radius (alveolar volume), the more pressure it has exerted on it to collapse so air will move to the larger alveoli (atelectasis).
Describe the difference between Simple Pneumothorax and Tension Pneumothorax.
- Simple: chest wall perforation leads to an equilibrium btw. Intrapleural Pressure and Atmospheric pressure. The lung collapses due to equal pressures.
- Tension: a tissue of the lung is injured leading to a “One-way valve”, as air enters the pleural space it can’t exit so the lung w/o air collapses and the one with expands to push the heart. this leads to less CO and VR. Symptom is Hypotension.
Why is tension Pneumothorax linked to hypotension?
- One collapsed lung would cause the other lung to over-inflate.
- This mediastinal shift compresses the inferior vena cava and atria.
- This reduces venous return and cardiac output, respectively leading to HYPOTENSION [BP = CO * TPR]
Describe the 3 respiratory control centers that regulate ventilation.
- Dorsal root ganglion of medulla - controls inspiration
- Ventral root ganglion of medulla - controls expiration (and inspiration)
- Pre-Botzinger complex - controls Rhythm (Respiratory Rate)
Describe the FRC and its relationship with RV.
FRC = RV + ERV
Functional Residual Capacity indicates the amount of air left in lungs after “quiet” expiration. This DOES NOT EQUAL Residual Volume because FRC includes air that’s “not forced” out of the lungs.
*In other words, FRC includes some expiratory reserve.
What is the equation for total ventilation and how might it change for Kussmaul breathing?
- Respiration Rate * Tidal Volume = Total ventilation
2. This will increase in Kussmaul breathes (which involves DEEP gasps to BLOW OUT CO2).
Explain the significant of the FEV1 and how it relates to FVC. What is the significance of FEV/FVC?
- The “Forced Expiratory Volume-1” is how much air the person can FORCEFULLY get OUT of their lungs in ONE second. This relates to Functional vital capacity (FVC), which is how quickly AND forcefully the VC can be moved.
- The Higher the FEV1/FVC ratio, the more efficient the lungs are at expelling air.
* FEV/FVC is evaluated to check for obstructive/restrictive lung diseases.
What is the normal value of FEV/FVC, regarding pulmonary function.
Normal value is >80%.
A value < 80% indicates an expiration-related lung disease.
Describe the importance of the Second heart sound (S2) during inspiration.
- “Widened Physiologic Splitting” of S2 occurs
- This is because NEGATIVE pressures in the intrapleural pressure causes…
- Pulmonary vessel expansion > RAP decreases > Venous Return inc. > Pulmonary vessel takes LONGER to close.
- Also, increased Pulmonary blood volume reduces amount of blood returning to the heart via pulm. Vein > LV output is reduced > aortic valve closes EARLIER.
Define Critical Opening Pressure and what it means to be reached.
- Critical opening pressure is the required BP needed to open the intrapulmonary shunts to increase blood flow to normally under-perfused areas such as the lung apex.
- It’s achieved where there is the highest perfusion of blood in alveoli through pulmonary capillaries, occurring mainly at the base due to gravity.
Describe how pulmonary capillaries and larger pulmonary vessels are affected during Inspiration.
- Pulmonary capillaries (CONSTRICT) have increased resistance due to expanded alveoli during inspiration. This allows more time for gas exchange.
“Slow down to saturate with O2” - Larger Pulmonary vessels such as pulmonary veins DILATE to have blood return faster to the heart.
“Speed up flow on the way out”
What is “HYPOXIC vasoconstriction”.
Lung vessels vasoconstrict in low O2 parts of the lung to SHUNT blood away and redirect it to better ventilated areas.
Biochemically, Hypoxia impedes K+ current, depolarizing, causing Ca influx then contracting the VSM of the shunt.
What is an Absolute Intrapulmonary Shunt and what does it mean for gas exchange?
This infers perfused alveoli will not be ventilated due to an absolute shunt. NO gas exchange.
Describe a Shunt-like state and what it means for the V/Q ratio.
The shunt like state allows for some V/Q (ventilation per perfusion). However, V/Q «_space;0.8, which implies a MISMATCH.
State which part of the lungs has the greatest value for the following.
- Ventilation
- Gas Exchange
- Resistance to Perfusion
- Size of Alveoli
- V/Q ratio
- Base - ventilation
- Base - gas exchange
- Apex - more intrapulmonary shunts
- Apex - has LARGER alveoli
- Apex - V/Q ratio exceeds normal 0.8, counterproductive
Describe the importance of Fick’s Law in respect to pulm phys.
Fick’s Law explains that diffusion/ gas exchange is IMPROVED with…
- Greater Surface Area of Tissue Layer
- Inc. Difference in Partial Pressure
- Thinner Wall (less diffusion barrier)
Define Diffusing Capacity of Carbon Monoxide (DLCO).
DLCO is a marker for how well the diffusion for gas exchange is in the lungs. The higher this capacity, the better: as seen in exercise. CO diffusion is hindered in lung diseases such as COPD and Fibrosis.
Define the alveolar-to-arterial O2 Difference and the standard. Explain how this aids in showing the cause of hypoxemia.
- (A-a)DO2 is the relationship between alveoli and arterial O2 to show if there is an impediment that slows gas exchange. Normally, this value should < 5 mm Hg, since PAO2 and PaO2 have to be matched.
- An abnormally high value»_space;> 0 indicates a limitation leading to hypoxemia, possibly caused by pulmonary edema or chronic smoking.
* A-a gradient is normally increased with age due to inc. V/Q mismatching
Explain whether perfusion limitation or diffusion limitation is normal. Why?
- Perfusion limitation is NORMAL, because even with More RBCs passing per unit time O2 saturation STILL MAXES out instantaneously (0.25 seconds).
- Diffusion Limitation is PATHOLOGIC, since this shows a diffusion barrier, where saturation is not sufficient(pneumonia).
Describe the shifts in the O2 Dissociation curve: causes.
O2 Dissociation..
- Shifts right BOHR EFFECT, with lower pH, inc. Temp, inc BPG (at sites with high metabolism), inc. CO2, inc. Elevation
- Shifts left: Higher Hb-O2 affinity, seen in Fetal circulation with HbF. Enables fetus to take O2 from the Mom’s blood.
Why isn’t PaO2 (or even SaO2) affected in a blood test for CO poisoning?
The change in Hb does not alter SaO2 (as read on a pulse oximeter) even as Hb is binding to what its not supposed to. It’s still “saturated” with higher affinity CO.
*PaO2 does not change either, although what’s happening molecularly is abnormal.
What 3 forms is Total CO2 present in the blood?
- Dissolved PaCO2
- HCO3-
- Carbamino Compounds (CO2 attached to amino acids in the blood)
In what 3 ways does the Medulla Respiratory Center help to offset elevated CO2?
- Hypernea and Kussmaul breathing (deep and fast)
- Dilation of upper airways
- Increased BP (SNS effect increases perfusion)
Why wouldn’t CO poisoning cause hyperventilation?
Partial Pressure of O2 has not changed with CO poisoning. Even so, hyperventilation would be an effect of Elevated CO2 levels.
Name at least 3 causes of hyperventilation.
- Increased CO2 Levels
- Anxiety, panic attacks
- Diffusion barriers
* This is also a compensatory action for Metabolic Acidosis
Describe what occurs after breathing for a few days in High Altitude
- High Altitude equates to low PO2
- This drive HYPOXIC DRIVE that contributes to Respiratory Alkalosis (via hyperventilation)
- Renal Acclimatization occurs where kidneys EXCRETE HCO3
- pH is lowered which compensates for chronic respiratory alkalosis.
- Erythropoietin levels build up, increasing RBC production. This increases O2 Carrying Capacity.
Describe what parameters should be seen in blood as one does Sustained Vigorous Exercise.
- HR increases A LOT
- Systolic BP increases due to inc. CO
- Diastolic BP remains STABLE b/c of the drop in systemic resistance (due to vasodilator metabolites)
- PvCO2 is “slightly” increases, body is wary of acidosis; PaCO2 is not changed, due to inc. ventilation.
- Lactic acid -> mild acidemia -> increases VENTILATION
If Cardiac Output increases 5-fold (in exercise), why doesn’t BP increase just as much?
- Critical Opening Pressure is achieved for Pulmonary Capillaries to open
- Capillary pressure increases EXPONENTIALLY due to a drop in pulmonary resistance.
- Rest of the body does not see increased pressure since Systemic resistance also decreases (vasodilation).
Why would Oxygen Therapy worsen the condition of a patient with Respiratory Acidosis?
- Increasing PO2 would Reduce HYPOXIC Drive.
- The reduction in HYPOXIC Drive leads to Hypoventilation.
- Hypoventilation goes increases PCO2, worsening hypercapnia and acidosis.
