Measured using a metabolic cart (measures expired CO2)
VE = Minute Ventilation (Respiratory Rate x VT)
VD/VT Ratio = Dead Space/Tidal Volume Ratio
Simplified Alveolar Gas Equation
Terms
PAO2: alveolar PO2 (alveolar oxygen tension)
Assumptions
FIO2: room air
Altitude: sea level
Note: arterial PaCO2 (pCO2) is assumed to be nearly the same as alveolar PACO2 in this equation
Respiratory Exchange Ratio = 0.8
Inverse Relationship Between Arterial pCO2 and pO2
Assumptions
A-a gradient remains the same (in this case, A-a gradient = 10)
Respiratory Exchange Ratio = 0.8
Increased CO2 Production Results in an Increase in Alveolar Ventilation
At a constant alveolar (minute) ventilation, increased CO2 production would thoretically increase the pCO2
Normal Patient: increased CO2 production leads to an increase in alveolar (minute) ventilation -> therefore, the patient is able to maintain normal pCO2
Patient with Moderate-Severe Lung Disease: patient may be unable to generate an increased alveolar (minute) ventilation to compensate for the increased CO2 production -> pCO2 may rise, possibly resulting in respiratory failure
Alveolar Ventilation is Inversely (But Not Linearly) Related to pCO2 (with varying CO2 production)
Patient with Acute/Chronic Hypocapnia: assuming a constant CO2 production (VCO2), a significant increase in minute ventilation (VE) must be present to maintain the low pCO2
Example: DKA patient with pH 7.40 and pCO2 30 must maintain a significanty increased VE to maintain the pCO2 at that level -> despite a normal pH, rapid respiratory failure can occur if, for any reason, patient cannot maintain that high VE
Patient with Acute/Chronic Hypercapnia: assuming a constant CO2 production (VCO2), a relatively small decrease in VE can produce a significant increase in pCO2
Example: chronically hypercapnic COPD with pCO2 60 can experience a significant increase in pCO2 with even a small decrease in VE (due to minimal sedation, etc)
Minute Ventilation (VE) is Inversely (But Not Linearly) Related to pCO2 (with varying VD/VT ratio)
Key Point: VD/VT Ratio determines how efficiently the lungs excrete CO2 per breath
Assumptions
Graph Assumes a Constant CO2 Production (VCO2) of 200 ml/min
VCO2 = VA x (PaCO2/PB)
VE = VA x 1.21/(1-VD/VT)
At Low VD/VT Ratio: a relatively low minute ventilation (VE) must be maintained to keep pCO2 constant at 40
At High VD/VT Ratio: a high minute ventilation (VE) must be maintained to keep pCO2 constant at 40
If this cannot be maintained, pt will develop hypercapnic respiratory failure
Impact on Shunt Fraction on Arterial pO2 and pCO2
Impact of Shunt Fraction on Arterial pO2: pO2 declines linearly with increasing shunt fraction -> the more shunt that exists, the more hypoxemia occurs
Impact of Shunt Fraction on Arterial pCO2: pCO2 remains relatively constant over a range of shunt fractions
Note: pCO2 only rises after shunt fractions exceeds 50% -> therefore shunt does not typically cause hypercapnia
Etiology of Hypercapnia
Respiratory Compensation for Metabolic Alkalosis (see Metabolic Alkalosis, [[Metabolic Alkalosis]])
Mechanism: elevated pH results in hypoventilation with a compensatory increase in pCO2
However, the degree of hypoventilation is limited by the hypoxic drive to breathe
The predicted compensatory increase in pCO2 in response to a primary metabolic alkalosis obeys the acid-base rules: expect 7 increase in pCO2 for each 10 increase in HCO3 or Expected pCO2 = (bicarb x 0.7) + 21 + 1.5
Clinical Pearl: ALL cases of subacute or chronic hypercapnia are accompanied by elevated serum bicarbonate (on serum chemistry or ABG)
Presence of elevated serum CO2 should raise the suspicion for presence of either a primary metabolic alkalosis OR a primary respiratory acidosis with compensatory metabolic alkalosis
Order an ABG to differentiate these conditions
Increased CO2 Production: occurs with overfeeding (with tube feedings or TPN)
Only causes hypercapnia when alveolar ventilation (VE) is inadequate (ie: in the presence of significant lung disease)
Acute Hypoventilation (see Acute Hypoventilation, [[Acute Hypoventilation]]): with acutely decreased VE
Chronic Hypoventilation (see Chronic Hypoventilation, [[Chronic Hypoventilation]]): with chronically decreased VE
Increased Dead Space Ventilation: with increased VD/VT Ratio
Note: hypercapnia only occurs when VD/VT ratio exceeds 50%
Clinical Evaluation of Hypercapnia
Increased A-a Gradient
Normal VCO2 (Normal CO2 Production)
V/Q Mismatch (V/Q ratio >1, dead space ventilation): hypercapnia only occurs when VD/VT ratio >50%
COPD: hypercapnia in COPD is multifactorial (due to hypoventilation, V/Q mismatch, etc)
Increased VCO2 (Increased CO2 Production): these conditions usually cause hypercapnia only in the setting of underlying lung disease (with inability to excrete CO2)
Hypermetabolism
Overfeeding: especially wtih excessive carbohydrate, whch generates more CO2 per calorie than do fats
