predicted alveolar po2 equation using only respiration rate, tidal volume and dead space volume

Mathematically, this relationship is determined as: Essentially, unless there is a significant loss of pulmonary ventilation metabolic processes will not induce hypercapnia. The human body is very adapted and capable of eliminating CO2 from the body as excesses are produced. Alveolar ventilation is the removal of alveolar air into the environment, defined as the expired minute volume that reaches the alveoli and is determined by minute ventilation and the ratio of dead space to tidal volume. As such, the CO2 gradients are developed and maintained where PaCO2 in arterial blood is directly proportional to the rate of CO2 metabolic production and inversely related to the rate of CO2 elimination by the lung via increased alveolar ventilation. This requires a diffusion gradient from the high concentration arteriolar blood into the relatively low concentration environmental air. One of the purposes of the pulmonary system is to remove CO2 from the body through gas diffusion. It is also to have an acute-on-chronic etiology that creates a combined picture with elevated PaCO2 and elevated HCO3 with an abnormal, decreased pH below 7.35. As a result, PaCO2 will be elevated above the normal reference range of 45 mm Hg and the HCO3 level will also be elevated proportionally resulting in a less severe pH imbalance in the low-normal range. Chronic hypercapnia allows for renal compensation to the elevated CO2 levels within the blood. Acute hypercapnia will have PaCO2 elevated above the normal reference range of 45 mm Hg, and the HCO3 level will be within normal limits at approximately 30 mm Hg with a resulting proportional decrease in pH on blood gas evaluation below 7.35.

These can be distinguished through evaluation of the pH.

Depending on the etiology, hypercapnia can be an acute process or a chronic process.

It is also technically possible to develop hypercapnia through exposure and inhalation of environmental air rich in CO2. This is from decreased central nervous system respiratory drive, anatomical defects, decreased neuromuscular response, or increased dead space within the lung. Respiratory failure in this pathology is a failure to eliminate CO2 from the pulmonary system, which is synonymous with hypoventilation secondary to decreased respiratory rate or decreased tidal volume.

Metabolic processes that increase CO2 production may include fever, thyrotoxicosis, increased catabolism seen in sepsis or steroid use, overfeeding, metabolic acidosis, and exercise. At its root, hypercapnia is caused by either increased CO2 production metabolically or Respiratory failure.

Predicted alveolar po2 equation using only respiration rate, tidal volume and dead space volume