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Dead space is the portion of each tidal volume that does not take part in gas exchange. There are two different ways to define dead space-- anatomic and physiologic. Anatomic dead space is the total volume of the conducting airways from the nose or mouth down to the level of the terminal bronchioles, and is about 150 ml on the average in humans. The anatomic dead space fills with inspired air at the end of each inspiration, but this air is exhaled unchanged. Thus, assuming a normal tidal volume of 500 ml, about 30% of this air is "wasted" in the sense that it does not participate in gas exchange.
Physiologic dead space includes all the non-respiratory parts of the bronchial tree included in anatomic dead space, but also factors in alveoli which are well-ventilated but poorly perfused and are therefore less efficient at exchanging gas with the blood. Because atmospheric PCO2 is practically zero, all the CO2 expired in a breath can be assumed to come from the communicating alveoli and none from the dead space. By measuring the PCO2 in the communicating alveoli (which is the same as that in the arterial blood) and the PCO2 in the expired air, one can use the Bohr Equation to compute the "diluting," non-CO2 containing volume, the physiologic dead space. In healthy individuals, the anatomic and physiologic dead spaces are roughly equivalent, since all areas of the lung are well perfused. However, in disease states where portions of the lung are poorly perfused, the physiologic dead space may be considerably larger than the anatomic dead space. Hence, physiologic dead space is a more clinically useful concept than is anatomic dead space. Mini Clinic
Minute Ventilation, Dead Space, and PaCO2
Problem A patient breathing at a rate of 12 breaths/min has a tidal volume of 600 mL and a measured physiological dead space (VDphy) of 200 mL. This ventilatory pattern produces a PaCO2 of 40 mmHg. Several hours later, the patient has a breathing rate of 24 breaths/min, but the minute ventilation (VE) has remained the same as before. Arterial blood gas analysis reveals a PaCO2 of 72 mmHg. Why has the PaCO2 increased even though the VE remained constant? Discussion The initial minute ventilation (VE) and alveolar ventilation (VA) were as follows: VE = 600 x 12 = 7200 mL/min
VA = (600 – 200) x 12 = 4800 mL/min This VA of 4800 mL/min was responsible for maintaining a PaCO2 of 40 mmHg. When respiratory rate increased to 24 breaths/min and VE remained at 7200 mL/min, tidal volume (VT) must have decreased: VT = 7200 ÷ 24 = 300 mL However, if dead space remained at 200 mL, then alveolar ventilation subsequently decreased: VA = (300 – 200) x 24 = 2400 mL/min The reduction in VA (from 4800 mL/min to 2400 mL/min) explains the increase in PaCO2 from 40 mmHg to 72 mmHg. PaCO2 is inversely proportional to alveolar ventilation. Because VA was reduced by half, PaCO2 should have doubled. This approximates the data actually observed. Normally, increased CO2 tension in the blood causes academia and results in increased alveolar ventilation. This patient, although tachypneic, is hypoventilating.
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