Physiological dead space

Distinguish among anatomical dead space, alveolar dead space, and physiological dead space... 

Dead space. Anatomical dead space is equal to the volume of the conducting airways. This is determined by the physical characteristics of the lungs because, by definition, these airways do not contain alveoli to participate in gas exchange. Alveolar dead space is the volume of air that enters unperfused alveoli. In other words, these alveoli receive airflow but no blood flow with no blood flow to the alveoli, gas exchange cannot take place. Therefore, alveolar dead space is based on functional considerations rather than anatomical factors. Healthy lungs have little or no alveolar dead space. Various pathological conditions, such as low cardiac output, may result in alveolar dead space. The anatomical dead space combined with the alveolar dead space is referred to as physiological dead space ... 

Physiological dead space is determined by measuring the amount of carbon dioxide in the expired air. Therefore, it is based on the functional characteristics of the lungs because only perfused alveoli can participate in gas exchange and eliminate carbon dioxide. 

The physiological dead space can be calculated using the Bohr equation. 

The purpose of the Bohr equation is to give a ratio of physiological dead space volume to tidal volume. Dead space volume is normally around 30% of tidal volume and so the normal ratio is quoted as 0.3. Under abnormal conditions, the ratio will tend to increase and so make ventilation inefficient. 

In doses used clinically (0,5-1.0 mg), this effect is usually confined to mild vagal excitation. The rate and occasionally the depth of breathing are increased, but this effect is probably the result of bronchlolar dilatation and the consequent Increase in physiologic "dead space." With toxic doses of atropine, central excitation becomes more pronflnent, leading to restlessness, irritability, disorientation, hallucinations, or delirium. With still larger doses, stimulation is followed by depression, coma, and medullary paralysis. The latter may be primarily responsible for a fatal outcome. Even moderate doses of atropine may depress some central motor mechanisms that control muscle tone and movement. 

United States Department of Labor, Occupational Safety and Health Administration, OSHA Training Institute, Online Course 2220c (unknown year) Respiratory Protection, Lesson 6, Medical Evaluation, Physiological Effects of Wearing a Respirator, Increased Volume in Dead Space, U.S. Department of Labor, Occupational Safety and Health Administration, OSHA Training Institute, Washington, DC. Available at http /respiration.eleaming.dol.gov/Medic/T2/P3/ (accessed September 2006). 

Harber P, Tamimie J, Bhattacharya A et al. (1982). Physiological effects of respirator dead space and resistance loading. J Occ Med, 24, 681-684. 

Lung Volumes Pulmonary Function Tests Physiologic Dead Space References... 

Measurement of physiologic dead space is based on the assumption that there is almost complete equilibrium between alveolar PCO2 and pulmonary capillary blood. Therefore, the arterial pCOj represents mean alveolar PCO2 over many breaths when an arterial blood sample is drawn for analysis of PCO2. The Bohr equation for physiologic dead space is... 

It is obvious that an elevated physiological dead space indicates lung tissue that is not perfused with blood. 

Improved alveolar ventilation may be partly compromised by an increase in the dynamic dead space (VDdyn), derived from the physiologic dead space (VDphys) plus the dead space of the apparatus (VDap). Whereas the physiologic dead space is influenced by the tidal volume, the dead space of the apparatus is a fixed consequence of the internal volume of the interface. Differences in flow pattern and pressure waveform associated with the machine and mode of ventilation, also affect the dead space of the apparatus. Saatci et al. (36) noted that during spontaneous breathing, a face mask increased VDdyn from 32% to 42% of tidal volume (VT) above VDp ys. Positive pressure during the expiratory phase reduced VDdyn close to VDphys, while inspiratory pressure support without positive end-expiratory pressure decreased VDdyn from 42% to 39% of VT, i.e., VDdyn remained higher than VDphys. When the exhalation port was placed close to the nasal bridge, VDdyn was lower than VDp ys as a consequence of a beneficial flow path that decreased VDdyn (from 42% to 28% of VT), in the presence of an expiratory positive pressure. 

Fig. 2 Nonnal capnogram. (a, b) Beginning of exhalation. Gas is exhaled from the physiological dead space, (b, c) Steep rise of the CO2 level, liom the lower airways, (c, d) Alveolar plateau. CO2 concentration of the expired alveolar gas. (d) End-tidal pC02. (d, e) Inspiration. Adapted from [1]...

---