During mechanical ventilation, capnography is used this records the volume of expired CO2, a value used to determine the physiologic dead space in patients. Even in a healthy patient, ventilation via an endotracheal tube will increase the dead space volume because the breathing circuit does not participate in gas exchange. Ĭlinicians use the understanding of dead space to manage mechanically ventilated patients. The strongest association of an increased volume of dead space with mortality risk is seen in patients with ARDS. Studies looking at the causes of death in this disease have shown an increase in dead space in the non-survivors versus survivors. This results in the formation of intra-alveolar hyaline membranes, which decrease the exchange of CO2 and O2 in the lung contributing to a larger dead space. Emphysema results in the enlargement of air spaces and decreases in the diffusing capacity of the alveolar membrane due to the destruction of alveolar walls. In ARDS there is endothelial damage leading to an increase in the alveolar-capillary permeability, thereby leading to leakage of protein-rich fluid into the alveolar. Increases in dead space can be seen in lung disease states including emphysema, pneumonia, and acute respiratory distress syndrome (ARDS). Ĭlinically, disease states and environmental factors, such as smoking, all play a major role in the increase of dead space. When an area of the lung is properly ventilated, but poorly perfused, there is an increase in physiologic dead space. Looking back at the equation, a lower PeCO2 will result in an increase in the physiologic dead space value for that individual. 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. This is usually seen in an abrupt decrease in cardiac output, hypotension, or pulmonary embolism, due to fat, air, or amniotic fluid. This can be seen most rapidly with sudden decreases in perfused to ventilated alveoli. In disease states where alveoli have lost function, there will be a decrease in gas exchange and an increase in alveolar dead space. Until now, clinicians have assumed the patient is a healthy individual with properly functioning alveoli. Multiply that value by the normal amount of air inspired (VT) you achieve a value for physiologic dead space. Thus, by subtracting PeCO2 from PaCO2 and dividing by the PaCO2 one has you have determined a fractional equivalent of the lung is not contributing to gas exchange.
DEAD SPACE 2 ENDING FREE
PeCO2 will always have a smaller value than arterial CO2 due to the mixture and dilution of CO2 gases with the 150 mL of anatomical dead space sitting in the conductive airway that is assumed to be free of CO2. The exchange of gases through the respiratory membrane is so rapid that we can assume the arterial CO2 partial pressure is equal to that in the alveoli. Simply translating to the amount of carbon dioxide (CO2) exchanged for oxygen (O2). The second half of the equation is representative of the fractional amount of dead space. This inspired air is assumed to contain a relatively zero amount of carbon dioxide. The equation states VD is equal to VT multiplied by the partial pressure of arterial carbon dioxide (PaCO2) minus partial pressure of expired carbon dioxide (PeCO2) divided by PaCO2.īreaking down this equation, there is the tidal volume which is the normal amount of inspired and expired gas equivalent to 500 mL. Understanding the equation will simplify the concept of dead space greatly. The Bohr equation can be used to calculate the amount of dead space in a lung. One can see an increase in the value of physiologic dead space in lung disease states where the diffusion membrane of alveoli does not function properly or when there are ventilation/perfusion mismatch defects. Therefore, physiologic dead space is equivalent to anatomical. In a healthy adult, alveolar dead space can be considered negligible. The respiratory zone is comprised of respiratory bronchioles, alveolar duct, alveolar sac, and alveoli.
DEAD SPACE 2 ENDING PLUS
Physiologic or total dead space is equal to anatomic plus alveolar dead space which is the volume of air in the respiratory zone that does not take part in gas exchange. This volume is considered to be 30% of normal tidal volume (500 mL) therefore, the value of anatomic dead space is 150 mL. Anatomical dead space is represented by the volume of air that fills the conducting zone of respiration made up by the nose, trachea, and bronchi. The two types of dead space are anatomical dead space and physiologic dead space. Dead space represents the volume of ventilated air that does not participate in gas exchange.
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