Gas Exchange Flashcards
Hypoxemia vs. hypoxia
Hypoxemia = decrease in systemic arterial PO2
Hypoxia = decrease in oxygen tension in metabolizing tissues due to excess of O2 demand over supply
List the major causes of Hypoxemia
- Decreased inspired O2 tension (ex. With high altitude)
- Alveolar hypoventilation
- Diffusion impairment
- Ventilation-perfusion mismatch
- Anatomic or true shunt
Equation for normal PaO2
- Varies with age
- Equation (at sea level, if PaCO2 is 40 torr): predicted PaO2 = (104 -0.27 x age)
Different mechanism of hypoxemia:
decreased inspired PO2
o Ex. With increased altitude
o Reduces PIO2 → reduces PA O2 and Pa O2
o Corrected with supplemental O2
Summary:
PaCO2: decrease
P(A-a)O2: normal
Effect of exercise on PaO2: no significant change
Effect of O2 on Pa)O2: Increased
Different mechanism of hypoxemia:
Alveolar hypoventilation
o PACO2 determined by balance between tissue CO2 production and rate CO2 is removed by inspired air reaching alveoli (minute alveolar ventilation = VA)
o As decrease VA → PaCO2 rises
Alveolar hypoventilation if PaCO2 above normal of 37-42 mm Hg
o Remember: PAO2 = PIO2 – 1.25 x PaCO2 (assuming R = 0.8 and arterial PCO2 substitutes for alveolar PCO2)
• If increase PaCO2 → decrease in PAO2 (so also decrease in PaO2)
• Usually no increase in P(A-a)O2
o Supplemental O2 = corrects hypoxemia but not increased PaCO2
Summary:
PaCO2: increased
P(A-a)O2: normal
Effect of exercise on PaO2: variable
Effect of O2 on Pa)O2: increased
Different mechanisms of hypoxemia:
Diffusion Impairment
o Causes:
• Increased thickness of alveolar capillary membrane
• Decreased area for diffusion
• Decreased blood transit time
o Usually more significant in exercise → reduced blood transit time
o Less time for complete O2 transfer → decreased P(A-a)O2
o Supplemental O2 corrects hypoxemia
Summary:
PaCO2: normal or decreased
P(A-a)O2: increased
Effect of exercise on PaO2:marked decrease if capillary bed is “fixed”
Effect of O2 on Pa)O2: increased
Different Mechanisms of hypoxemia:
VA/Q mismatch
o Most common cause of hypoxemia
o Increased P(A-a)O2
o Supplemental O2 tends to correct hypoxemia = slight increase in PIO2 → increase PAO2 → increase PO2
Summary:
PaCO2: normal or decreased
P(A-a)O2:increased
Effect of exercise on PaO2: usually decreased
Effect of O2 on Pa)O2: increased
Different mechanisms of hypoxemia:
True or Anatomic shunt
o When venous deoxygenated blood reaches arterial circulation without having O2 added to it
o Causes an increased P(A-a)O2
o Supplemental O2 will not correct hypoxemia, but may give small rise in PaO2 due to added dissolved oxygen
Summary:
PaCO2: normal or decreased
P(A-a)O2: increased
Effect of exercise on PaO2: usually decreased
Effect of O2 on Pa)O2: No change or increased
Effects of altered VA/Q ratios
• Ventilation (V) and Perfusion (Q) determine PAO2 and PACO2
• Normal V/Q = 1
o There may be regional differences though
o Larger differences in disease
• Effects of altered VA/Q ratios
o Normal values:
• Inspired air: O2 = 150 mmHg; CO2 = 0
• Mixed venous blood entering unit: O2 = 40 mmHg, CO2 = 45 mmHg
• Alveolar gas: O2 = 100 mmHg; CO2 = 40 mmHg
o If obstruct ventilation
• Decrease PA O2
• Increase PA CO2
• With complete block (VA/Q = 0)
• Alveolar and capillary gases equal to mixed venous blood concentrations
o If obstruct perfusion
• Increase PA O2
• Decrease PA CO2
• With complete block (VA/Q = infinity)
• Same composition as inspired gas
VA/Q mismatch effect on overall gas exchange
o Lung will have lower PaO2 and higher PaCO2
o In lung:
• PO2 at apex is about 40 mmHg more than at base
• BUT most blood leaving lungs comes from lower regions → decreases PaO2
• A low VA/Q causing disease will cause a greater decrease in PaO2 if its in lower zones (area with higher flow)
o With low VA/Q → low O2 content in end-capillary blood
o With high VA/Q → only slight increase in O2 content in end-capillary blood
• Due to flatness of hemoglobin-O2 dissociation curve at high PO2 levels
o Result: a high VA/Q cannot compensate for decrease in PaO2 caused by units with low VA/Q
• Leads to alveolar-arterial O2 difference
• Normal lung: only about 4 mmHg P(A-a)O2
• Diseased lung: up to 50 mmHg or more due to VA/Q mismatch
VA/Q mismatch effect on CO2 transfer
o With low VA/Q → decreased CO2 transfer → increased PACO2 and PaCO2
o Units with high VA/Q (lower PACO2) = have proportionally less CO2 content
• Help offset blood with higher CO2 content (from units with low VA/Q)
• Because CO2 dissociation curve is linear = affects units with both high and low VA/Q
o With decreased PaO2 and increased PaCO2
• Stimulates central chemoreceptors → increase ventilation → lowers PCO2 to normal
• BUT not enough to raise PO2 to normal (only increases O2 uptake in units with low VA/Q due to sigmoidal O2 dissociation curve)
List what mechanisms of hypoxemia predominate in which types of lung disease.
• Decreased PIO2
o Altitude
• Alveolar hypoventilation
o Conditions involving increased PaCO2:
o In normal lungs:
• Sedative overdose
• CNS damage
• Upper airway obstruction
• Neuromuscular disease
o In abnormal lungs:
• COPD
• Advanced lung disease without respiratory muscle fatigue
• Diffusion abnormality
o Usually only important with alveolar-capillary membrane is thickened (ex. Fibrosis) PLUS exercise and a “fixed” (non-dilating) capillary bed
• Ventilation-Perfusion mismatch
o Uneven ventilation:
• Changes in elasticity: emphysema
• Partial airway obstruction: mucus, mucosal edema, bronchospasm, intrabronchial lesion, peribronchial compression (asthma, inflammation, tumors, cysts)
• Regional check valves (dynamic compression): emphysema
• Disturbances in expansion: interstitial fibrosis, chest wall restrictive diseases
o Uneven perfusion
• Embolization or thrombosis
• Partial or complete occlusion: atherosclerotic lesions, endarteritis, collagen disease, or congenital anomalies
• Compression or vessels by masses, exudates or pneumo- or hydrothorax
• Reduction of vascular bed by destruction of lung tissue
o Note: Va/Q mismatch is also increased with age and obesity
• True or anatomic shunt
o Acute Respiratory Distress syndrome (ARDS), lobar pneumonia, alveolar pulmonary edema, lobar collapse, intrapulmonary AV fistula or shunts, extrapulmonary shunts
Hypercapnea in COPD
- V/Q mismatch → areas with high V/Q ratio, wasted ventilation and increased physiologic dead space
- Higher frequency, lower tidal volume pattern of ventilation → increased VD/VT ratio even if total minute ventilation is not decreased
- Result: VE decreases → PaCO2 increases
- Usually: total minute ventilation and respiratory drive not decreased below normal
- BUT: VE and respiratory drive can be deficient relative to increased demands from airflow resistance and dead space
Alveolar ventilation: effects of gravity
• Effect of gravity on ventilation
o Creates gradient in pleural pressure from top to bottom of lung
• Most negative pleural pressure at top
• Less negative pleural pressure at bottom
o Result: alveoli at top are more expanded = operate at a flatter portion of the pressure-volume curve
• Expand less for a given unit change in pressure
o Alveoli at bottom = more ventilation than at top
• Effect of gravity on perfusion
o Blood flow decreases from base to top of lung
• Distribution of VA/Q ratio in lung
o Both VA and Q are higher at base
o Perfusion (Q) increases more rapidly from top to bottom
o Result: VA/Q ratio is higher at top of lung
Equation for alveolar ventilation (VA)
o VA = minute ventilation participating in gas exchange = minute ventilation minus dead space ventilation
PaCO2 = VCO2 / VA or PaCO2 = VCO2 / VE - (VE x VD / VT)
• VA = VE - (VE x VD / VT)
• VE = total minute ventilation
• VD = physiologic dead space
• VT = tidal volume
o If VCO2 constant = if VE decreases or if VD/VT increase > increase in VE → PaCO2 increases
o Remember: VD/VT ratio is not constant
• If VT larger → VD will be a smaller fraction of VT
• If VT smaller → VD will be a larger fraction of VT
• Result: shallow rapid breathing will increase VD/VT ratio → increase PaCO2
