Pathophysiology - Sinclair Flashcards
How much Oxygen and Nitrogen is there in inspired air?
21% Oxygen
78% Nitrogen
How does ambient air differ once it enters the respiratory tract and becomes inspired air?
• how does this change calculations for PO2?
Ambient air is Rapidly warmed and saturated with 47mmHg of H2O
PO2 inspired = (Pb - Ph2o) x Fgas
*You must subtract 47mmHg from whatever the barometic pressure is
What is the formula for minute ventilation?
Ve = tidal volume x respiratory rate = Vt x f
If you take in 500mL of fresh air in a tidal breath, what is the volume of fresh air delivered to the alveoli?
• Why must we account for this?
Fresh Delivered air = 500mL - anatomic dead space
•Must account for this because alveolar gas remains in the anatomic dead space and re-enters the alveoli with the next breath
What causes Alveolar Dead Space?
• Alveoli that are ventilated but NOT perfused are useless in gas exchange
What is the physiologic dead space?
Vphysio = Vanatom + Valv
Differentiate Minute Ventilation and Alveolar Ventilation.
• what is Alveolar ventilation AKA?
Minute Ventilation:
• Vt•f
Alveolar Ventilation:
• (Vt - Vdphysio)•f
Alveolar Ventilation aka Effective Ventilation
What percentage of the Tidal Volume is physiologic dead space?
25-30% of Vt = dead space
typically this is 150-180mL
T or F: INCREASED Vdalv (alveolar dead space) is always pathologic
TRUE - paradigm example = pulmonary embolism
What happens to the alveolar dead space when you excercise and why?
- Increased Tidal Volume
* massively INCREASED perfusion
What does alveolar gas equation tell us?
• what is the equation?
Tells us the PAO2 (we normally just estimate this as PaO2, but this may not be the case in lung pathology)
• Tells you if lung disease is due to hypoxemia or not
What is the only way we can remove CO2 from the body?
Ventillation
What is the Tissue O2 consumption?
~250ml/min
- ***what is the COMPLETE ALVEOLAR GAS EQ?
* **What are the typical values in this equation?
PAO2 = PIO2 - (PaCO2/R)
OR
PAO2 = (Pb - Ph2o)•FiO2 - (PaCO2/R)
Typically:
• Alveolar O2 = 100mmHg
• Respiratory Exchange ratio is typically = 0.8
•Arterial CO2 = 40 mmHg
What defines Hyperventilation?
• how does this affect PAO2?
- Breathing in O2 in excess of metabolic needs
* Increased Breathing increases PAO2
What is the A - a difference?
• how would you go about calculating this on the basis of obtainable values?
**What is a normal A-a difference
A - a difference = difference in O2 saturation in alveoli and in the blood
• Should be close to 0 if diffusion is happening efficiently
How to obtain:
• PaO2 obtained by direct measure
• Calculate PAO2 with eqn. = PAO2 = PiO2 - (PaCO2/R)
***A-a difference should usually be (Age+4)/4
WHAT ARE THE 5 CAUSES OF HYPOXEMIA?
• break these down into categories
• what is the importance of this categorization?
- NORMAL A-a DIFFERENCE => No Lung Disease
• Decreased PiO2
• Hypoventilation - WIDENED A-a DIFFERENCE => Lung Disease
• Diffusion Limitation
• R to L Shunt
• Ventilation/Perfusion (V/Q) mismatch
How does the A-a gradient change as you climb in altitude?
It’s unchanged because there is no lung disease, both the alveolar and arterial PO2 will decrease proportionally
T or F: in someone who has overdosed on heroin, their arterial PO2 is a good predictor of alveolar PO2.
True, since there is no intrinsic lung disease PAO2 and PaO2 should be similar
What is the least common cause of hypoxemia with increased A-a gradient?
• Can an abnormal Diffusion Capacity Test differentiate between the mechanisms of this disease?
Diffusion Limitation => anything that affects membrane Surface Area or Thickness
NO - abnormal diffusion capacity test will not differentiate what is causing this problem
How far must the diffusion of O2 drop for it to become clinically relevant?
- 75s is the normal time an RBC spends inside a pulmonary capillary
- 25s is the normal time for equilibration
Therefore, diffusion must be decreased to 1/3 of normal for hypoxemia to result
CONVERSELY, if transit time increases by 3x you run the risk of hypoxemia
Why do people with diffusion defects get out of breath when they start walking around, but are fine at rest?
Diffusion of Oxygen is limited (greater than 0.25 seconds needed for equilibration) THEN you get up and move and DECREASE transit time of RBCs and HYPOXEMIA results
T or F: a DIFFUSION DEFECT can be corrected with 100% O2.
True
Differentiate a Pulmonary and Cardiac Shunt.
• how does supplemental O2 affect patients with these problems?
Pulmonary:
• Perfused areas are NOT VENTILATED
Cardiac:
• ASD/VSD allows mixing of Right sided oxygenated blood with Left side deoxygenated blood
SUPPLEMENTAL O2 has NO EFFECT IN PATIENTS with this issue aka the A-a gradient will STILL BE HUGE
If someone is put on 100% O2, how should their PaO2 change?
• how will this differ in a patient with shunting?
Normal:
• Low PaO2 ==> PaO2 ~ 600 mmHg
Shunting:
• Low PaO2 ==> PaO2 ~ 80 mmHg
What is the respiratory exchange ratio in a patient that is on 100% oxygen?
Respiratory Exchange Ratio:
1.0 when on supplemental O2
What Pulmonary Diseases are associated with a LOW V/Q mismatch?
- COPD (asthma)
- Pulmonary Edema
- SHUNT = extreme case = 0
What Pulmonary Diseases are associated with a HIGH V/Q mismatch?
• Pulmonary Embolism = infinity in DEAD SPACE
WHAT IS THE MOST COMMON CAUSE OF HYPOXEMIA?
• does it correct with supplemental O2?
V/Q mismatch = most common cause
• YES, this corrects with O2
