MEASUREMENT OF LUNG DEAD SPACE VOLUME BY CAPNOVOLUMETRY

The article provides information on the lung dead space – a part of the respiratory volume that does not participate in gas exchange. The anatomical and alveolar dead spaces jointly together form the physiological dead space. The article describes methods for determining the volume of dead spaces using the capnovolumetry. The volume of physiological dead space is calculated using the C. Bohr equation. The volume of anatomical dead space can be determined using the equal area method proposed by W.S. Fowler. The volume of the alveolar dead space is the difference of volumes of the physiological and anatomical dead spaces. In pathology, the volume of the alveolar space and, consequently, physiological dead space can increase significantly. Determination of the volume of dead space is the significant criterion for diagnostic and predicting the outcome of a number of diseases. Keywords: Physiological dead space , anatomical dead space , alveolar dead space , capnovolumetry, volumetric capnography.

Nasal high flow reduces minute ventilation during sleep through a decrease of carbon dioxide rebreathing

Nasal high flow (NHF) is an emerging therapy for respiratory support, but knowledge of the mechanisms and applications is limited. It was previously observed that NHF reduces the tidal volume but does not affect the respiratory rate during sleep. The authors hypothesized that the decrease in tidal volume during NHF is due to a reduction in carbon dioxide (CO2) rebreathing from dead space. In nine healthy males, ventilation was measured during sleep using calibrated respiratory inductance plethysmography (RIP). Carbogen gas mixture was entrained into 30 l/min of NHF to obtain three levels of inspired CO2: 0.04% (room air), 1%, and 3%. NHF with room air reduced tidal volume by 81 ml, SD 25 ( P < 0.0001) from a baseline of 415 ml, SD 114, but did not change respiratory rate; tissue CO2 and O2 remained stable, indicating that gas exchange had been maintained. CO2 entrainment increased tidal volume close to baseline with 1% CO2 and greater than baseline with 3% CO2 by 155 ml, SD 79 ( P = 0.0004), without affecting the respiratory rate. It was calculated that 30 l/min of NHF reduced the rebreathing of CO2 from anatomical dead space by 45%, which is equivalent to the 20% reduction in tidal volume that was observed. The study proves that the reduction in tidal volume in response to NHF during sleep is due to the reduced rebreathing of CO2. Entrainment of CO2 into the NHF can be used to control ventilation during sleep. NEW & NOTEWORTHY The findings in healthy volunteers during sleep show that nasal high flow (NHF) with a rate of 30 l/min reduces the rebreathing of CO2 from anatomical dead space by 45%, resulting in a reduced minute ventilation, while gas exchange is maintained. Entrainment of CO2 into the NHF can be used to control ventilation during sleep.

Satisfactory use of high flow nasal cannula in a patient with acute pulmonary embolism

High Flow Nasal Cannula (HFNC) oxygen therapy is a recent technique that delivers a high flow of heated and humidified gas to the patient.1 Compared to noninvasive ventilation (NIV), HFNC has been proved to be an effective alternative treatment for acute respiratory failure. HFNC also has a significant number of physiological advantages compared with other commonly used oxygen-based therapies, including PEEP, reduced anatomical dead space, constant FiO2 and it is better tolerated than NIV.2 After a thorough bibliographical research, only one article was found assessing the benefits of using HFNC in patients with acute pulmonary embolism.3 We present the case of an 86-year-old patient with acute pulmonary embolism and desaturation refractory to noninvasive ventilation that was successfully treated with high flow therapy.

Reductions in dead space ventilation with nasal high flow depend on physiological dead space volume: metabolic hood measurements during sleep in patients with COPD and controls

Nasal high flow (NHF) reduces minute ventilation and ventilatory loads during sleep but the mechanisms are not clear. We hypothesised NHF reduces ventilation in proportion to physiological but not anatomical dead space.11 subjects (five controls and six chronic obstructive pulmonary disease (COPD) patients) underwent polysomnography with transcutaneous carbon dioxide (CO2) monitoring under a metabolic hood. During stable non-rapid eye movement stage 2 sleep, subjects received NHF (20 L·min−1) intermittently for periods of 5–10 min. We measured CO2 production and calculated dead space ventilation.Controls and COPD patients responded similarly to NHF. NHF reduced minute ventilation (from 5.6±0.4 to 4.8±0.4 L·min−1; p<0.05) and tidal volume (from 0.34±0.03 to 0.3±0.03 L; p<0.05) without a change in energy expenditure, transcutaneous CO2 or alveolar ventilation. There was a significant decrease in dead space ventilation (from 2.5±0.4 to 1.6±0.4 L·min−1; p<0.05), but not in respiratory rate. The reduction in dead space ventilation correlated with baseline physiological dead space fraction (r2=0.36; p<0.05), but not with respiratory rate or anatomical dead space volume.During sleep, NHF decreases minute ventilation due to an overall reduction in dead space ventilation in proportion to the extent of baseline physiological dead space fraction.

Nasal high flow therapy: a novel treatment rather than a more expensive oxygen device

Nasal high flow is a promising novel oxygen delivery device, whose mechanisms of action offer some beneficial effects over conventional oxygen systems. The administration of a high flow of heated and humidified gas mixture promotes higher and more stable inspiratory oxygen fraction values, decreases anatomical dead space and generates a positive airway pressure that can reduce the work of breathing and enhance patient comfort and tolerance. Nasal high flow has been used as a prophylactic tool or as a treatment device mostly in patients with acute hypoxaemic respiratory failure, with the majority of studies showing positive results. Recently, its clinical indications have been expanded to post-extubated patients in intensive care or following surgery, for pre- and peri-oxygenation during intubation, during bronchoscopy, in immunocompromised patients and in patients with “do not intubate” status. In the present review, we differentiate studies that suggest an advantage (benefit) from other studies that do not suggest an advantage (no benefit) compared to conventional oxygen devices or noninvasive ventilation, and propose an algorithm in cases of nasal high flow application in patients with acute hypoxaemic respiratory failure of almost any cause.