B4.055 - Hypoxia Flashcards
A young male is brought unconscious to the E.D. at KUMC. An arterial blood sample with the patient breathing room air shows the following data:
PaO2 = 63 mm Hg
PaCO2 = 66 mm Hg
pH = 7.20
[HCO3 -]= 26 mM
Hb = 15 g/dL
These data are most consistent with which of the following conditions?
Alveolar hypoventilation of short duration in a person with normal lungs.
pH is low, PaCO2 high, HCO3 moderately high. (∆HCO3/∆pH -10 mM / pH). This is non-compensated respiratory acidosis (i.e. short term hypoventilation). PaO2 is low, but the (A-a)PO2 gradient is ~ 5 mm Hg (normal is 5 to 10 mm Hg), so the low PaO2 can be explained exclusively by the hypoventilation without the contribution of a shunt or low DLCO. An additional factor to rule out COPD is that hemoglobin is a normal level (it would be increased in COPD).
Acute obstruction of large bronchus.
Arterial PO2 is markedly decreased (40 mm Hg) and arterial O2 content is low (15 ml O2/ dL). However, this O2 content is what would be expected a PO2 of 40 mm Hg (as normally seen in veins). This indicates that this is a short term hypoxia and that there has not been time to increase hemoglobin as would occur in chronic hypoxia such as COPD (which would increase O2 content above what is expected). Shunts would produce marked decreases in PaO2. Hypovolumic shock would not decrease PaO2.
Which of these patients has normal lungs but has been hypoventilating for a short time?
Patient 4.
A decrease in alveolar ventilation would increase PaCO2 and decrease PaO2. An acute increase in PaCO2 of about 20 mm Hg would decrease pH by about 0.16, so D (patient 4) is the correct answer.
A young man with normal lung function changes tidal volume from a normal of 600 ml to 300 ml. He raises respiratory frequency from a normal of 12 to 24 breaths per min. Once a new steady state is reached, you would expect that the change in ventilatory pattern would produce what?
A decrease in PaO2 and an increase in PaCO2.
Assuming normal VD/VT of 0.25, so dead space is 150 ml.
Alveolar ventilation (VA) equals respiratory rate times (tidal volume minus dead space).
VA changes from (600-150) * 12 = 5400 ml/min to (300-150) * 24 = 3600 ml/min. VA decreases by ~ 33%. This should an increase in PaCO2 of 10-12 mm Hg, and decrease PaO2 by 12-15 mm Hg.
Patient 3.
Hyperventilation would increase PaO2 and decrease PaCO2. The only person that shows these values is patient 3.
A young man is brought unconscious to the ED at KUMC. An arterial blood sample with the patient breathing air shows the following data:
PaO2 = 76 mm Hg
PaCO2 = 55 mmHg
pH = 7.25
[HCO3-] = 25.5 mM
Hb = 15 g/dl
Based on the data above, you would say that this is a case of what?
Alveolar hypoventilation of short duration (minutes to hours) in a person with normal lungs.
Hemoglobin is a normal value, so this cannot be chronic hypoxia. This is a short-term respiratory acidosis: low pH, high PaCO2, mildly elevated HCO3 (∆ HCO3/∆pH = -10 mM/pH). It has not been long enough for compensation to become apparent. The PaO2 is low, but the (A-a)PO2 is normal: 81-76 = 5 mm Hg; this suggests hypoventilation with otherwise normal pulmonary gas exchange.
Patient 2.
An increase in dead space due to a pulmonary embolism will markedly decrease mixed expired PCO2 relative to PaCO2 (because PCO2 in the dead space is zero). Patient 2 (choice B) has increased dead space: VD/VT = (PaCO2 – PECO2) / PaCO2, = (39 mm Hg – 15 mm Hg) / 39 mm Hg, or 0.62 (normal is 0.25 to 0.35).
Hypovolumic shock and normal pulmonary function.
Under normal conditions with a normal cardiac output, the difference in systemic arterial and venous O2 content is 5 ml O2/ dL. In this person, although arterial O2 content is normal, venous O2 content is markedly decreased (6 versus the normal 15 ml O2/ dL). This would occur in someone with decreased blood flow to systemic organs, which would result in greater extraction of O2 from the blood, and so decrease venous O2 content.
A 52-year-old woman is admitted to the ER. She complains of shortness of breath, pain in the right hemithorax that worsens with deep inspiration, and lightheadedness. The symptoms appeared suddenly. Her skin is clammy with excessive sweating. Heart rate is 115 b/m, chest auscultation reveals irregular heartbeat and bronchial wheezing. The following data are obtained while the patient breathes air:
PaO2 = 87 mmHg
PaCO2 = 43 mm Hg
pH = 7.35
PECO2 = 20 mm Hg
Hb= 14 g/dL
Respiratory frequency = 26 breaths /min (~ 200% of normal)
Tidal volume = 700 ml (180% of normal)
Based on these data, which of the following is most likely occurring in this patient?
Pulmonary embolism.
The key variable here is the increased VD/VT: (37-20)/37= 0.46 (normal 0.25-0.35). The embolism stops blood flow to an area of the lung that still receives airflow. The air leaving these alveoli has no CO2 and dilutes the air coming from ventilated, perfused alveoli, so PECO2 goes down with respect to PaCO2. PaO2 tends to decrease because since all the cardiac output is diverted to a smaller number of capillaries, transit time decreases and equilibration is not complete. There is usually no CO2 retention.
COPD.
Arterial PO2 is very low (40 mm Hg) yet arterial blood O2 content is much higher than what would be expected if this was a short term hypoxia. This higher O2 content can only be due to increased hemoglobin level during chronic hypoxia. Also, arterial pH is closer to 7.4 than what would be expected at this level of PaCO2 if this were an acute decrease in alveolar ventilation.
Which set of data best represents the pulmonary gas exchange in a patient with chronic obstructive pulmonary disease (COPD)?
Patient A.
A person with COPD would have alveolar hypoventilation so PaCO2 would be increased, and also have abnormal pulmonary gas exchange: PaO2 would be low and (A-a)PO2 would be greater than normal (venous admixture or shunt, and/or low diffusing capacity). Long-standing condition: Compensated respiratory acidosis: high PaCO2, nearly normal pH; high HCO3; ∆ HCO3/∆pH = - 100 mM pH. High Hb and fairly normal CaO2 even though PaO2 is low.
A patient is admitted to the emergency room at KUMC. The following values are obtained (patient breathing room air):
[Hb]= 20 g/dl
PaO2 = 40 mmHg
PaCO2 = 62 mmHg
pH= 7.33
Plasma HCO3- = 33 mM
Forced vital capacity = 4 L
Volume exhaled in the first second of FVC (FEV1 ) = 2 L
Residual volume = 50% of total lung capacity
Pleural pressure at functional residual capacity (no air flow) = -1 cm H2O
Chronic hypoventilation in a person with pulmonary disease (areas of low VA/Q, diffusion impairment).
Hemoglobin is greater than normal so this is a situation of chronic hypoxia.
PaCO2 is increased so alveolar ventilation is lower than normal.
∆HCO3/∆pH >>> -10 mM /pH which indicates metabolic compensation has occurred (long duration).
which of these patients has anemia and normal lung function?
Anemia would decrease arterial O2 content (CaO2) but would not decrease PaO2 in someone with normal lung function (so C and D are incorrect). Patient 2 has a normal arterial O2 content at a normal PaO2, which indicates that hemoglobin level is normal in this person. Patient 1 (choice A) has normal PaO2 but reduced arterial content of O2 due to decreased hemoglobin due to anemia.
The following data are obtained in a patient admitted to KUMC:
PaO2 = 40 mm Hg
PaCO2 = 57 mm Hg
pH = 7.35
TLC = 8 L
FVC = 4 L
FEV1 = 2 L
PPL at FRC = -1 cm H2O
what is going on here?
Alveolar ventilation is decreased.
PaCO2 is high = alveolar hypoventilation.
(A-a)PO2 is ~39 mm Hg (normal 5 - 10 mm Hg).
Airway resistance is high (FEV1/FVC < 0.70).
Lung compliance is increased = PTP = 1 cm H2O at FRC; normal ~ 5 cm H2O.
pH is close to normal, but PaCO2 is high, so HCO3 has to be high.
RV = TLC – FVC = 4 L, or 50% of TLC; normal ~ 20-30%.
Patient 4.
Hypoventilation will increase PaCO2 and decrease PaO2. Increased PaCO2 is only seen in patient 4.
Acute pulmonary embolism.
Mixed expired PCO2 is markedly lower than PaCO2. VD/VT is increased compared to normal, (42 mm Hg – 20 mm Hg)/42 mm Hg, or 0.52, which is greater than normal. This indicates that deadspace is increased which is consistent with a pulmonary embolism.
