Until now, clinicians have assumed the patient is a healthy individual with properly functioning alveoli. In disease states where alveoli have lost function, there will be a decrease in gas exchange and an increase in alveolar dead space. This can be seen most rapidly with sudden decreases in perfused to ventilated alveoli. This is usually seen in an abrupt decrease in cardiac output, hypotension, or pulmonary embolism, due to fat, air, or amniotic fluid. While obstruction can cause decreased perfusion in PE, the greatest decrease in pulmonary blood flow is due to vasoconstriction caused by locally released vasoactive substances. In these situations, a lack of gas exchange at the alveolar level results in a decrease of PaCO2 gas being exchange by the remaining healthy alveoli and ultimately a lower PeCO2. Looking back at the equation, a lower PeCO2 will result in an increase in the physiologic dead space value for that individual. When an area of the lung is properly ventilated, but poorly perfused, there is an increase in physiologic dead space.[7][8]