Functional Dead Space Research Articles

The Functional Deadspace of Needle-free Injection Ports

This study examined six needle-free injection ports comprising three taps (Sorenson Intralock, Top type L, Viggo Connecta), a one-way valve (Braun RV 1000) and two cannulae with integral injection ports (Vasofix, Venflon 2) with regard to deadspace, protection against blood spillage, and potential difficulties in use. A conventional bung (Baxter), requiring needle use for drug administration, was included for comparison. Where necessary, ports were combined with cannulae in order to simulate clinical practice and allow fair comparison with the Vasofix and Venflon cannulae. Total deadspace was then calculated by filling with normal saline and measuring weight increase. Deadspace (0.10 to 0.43 ml) varied with injection port type and cannula size. Such volumes can contain significant amounts of drug and may be hazardous if not flushed after injection. Only the Vasofix and Venflon Cannulae and the Braun RV1000 protected adequately against blood spillage. Costs varied widely (A$0.19 to A$2.20 excluding cannula). The Vasofix and Venflon 2 cannulae were found to be nearest the ideal.

Multiple breath nitrogen dead space.

Ventilatory efficiency for eliminating CO2 is expressed by the physiological dead space, VD phys = (1-PE CO2/Pa CO2) x VT, where PE is the mixed exhaled and Pa the arterial CO2-tension and VT the tidal volume. We used data from the multiple breath N2-wash-out with oxygen for calculating a functional dead space for nitrogen. VDF N2 = (1-FEN2/FidN2) x VT.FEN2 is the mixed exhaled N2-fraction and FidN2 the calculated mean alveolar N2-fraction during a wash-out with the same number of breaths to reach 2% N2 in end tidal air, but having completely even distribution. FidN2 is shown to be 0.20 +/- 0.01 for wash-outs using 20-150 breaths. The method was applied to wash-outs from 21 healthy volunteers, 18 patients with chronic obstructive lung disease and two subjects with acute bronchospasm. VDF was well related to VD phys CO2 (r = 0.78) but higher than the latter. In subjects with lung disease VDF was inversely related to the degree of obstruction expressed by forced expiratory volume in one second per cent of vital capacity (r = 0.85). The subjects with bronchospasm had very high VD/VTF in relation to their FEV%. If airway dead space predicted from height and sex is subtracted from VDF, the resulting alveolar dead space will be a good expression for uneven gas distribution in the lungs. We also deduced a direct mathematical relation between lung clearance index and VD/VTF. The documented good reproducibility of LCI is thus also valid for VD/VTF, while the latter better expresses ventilatory efficiency.

Effects of small and large face masks and translaryngeal and tracheostomy intubation on ventilation, upper-airway dead space, and arterial blood gases

SUMMARY Pulmonary function was examined in pentobarbital-anesthetized dogs that were spontaneously breathing through a large poorly fitted face mask, a small snug-fitted face mask, an endotracheal tube, and a tracheostomy tube. Increasing upper-airway dead space volumes were associated with higher minute ventilation and faster breathing rates. Minute and tidal alveolar ventilation, calculated ideal alveolar oxygen, alveolar-arterial oxygen gradient, venous admixture, arterial pH and blood gases, cardiac output, and systemic and pulmonary arterial blood pressure were not changed. The functional dead space of each mask was considerably less than that measured by water displacement. The small mask only slightly increased, and the endotracheal tube slightly decreased, the dead space estimated for a nasally breathing healthy dog.

Determination of the alveolar dead space

The author suggests a method of finding the alveolar dead space (AIDS), i.e. the part of the functional dead space (FDS) which presents the greatest difficulties for determination. A1DS determination is based on the difference in the CO2 concentration in the venous blood flowing to the lungs for oxygenation under conditions of respiration at rest, and of CO2 concentration in the alveolar portions of expriation following 10-sex breath withholding at the level of the usual inspiration. The mean A1DS volume (VDA1) in % to the alveolar part of the tidal volume for 20 healthy persons in sitting position and in 12 of them in lying position was found: VDA1 (in sitting position)= = 8.0 +/- 1.5% (P = 0.95), sigma = 3%; VDA1 (in lying position) = = 5.0 +/- 0.7% (P = 0.95), sigma = 2.6%. It is suggested that FDS determined by this method be used to judge the efficacy of using the inspired air in the lung ventilation, to determine AIDS in the diagnosis of lung embolism, to judge the pulmonary circulation shunt by the difference between the value found according to Bohr's formula for FDS and the FDS value established according to the suggested formula.

Single-breath determination of functional dead space.

Single-breath determination of functional dead space.

Dead space and blood gases.

The determination of dead space of any kind is rarely done because it is of more interest to determine blood gases and pH which will be altered as a result of the increase in the functional dead space (anatomic and physiologic). The most frequent cause of increased dead space is an imbalance between ventilation and perfusion, and this alteration is present in any pulmonary illness

Respiratory function in recurrent pulmonary embolism.

Pulmonary arterial and right atrial pressure, cardiac output, lung volumes, blood gases, VD/VT ratio and alveoloarterial oxygen tension gradient were measured in 21 subjects with pulmonary hypertension due to recurrent pulmonary emboli. The mean pressure in pulmonary artery ranged from 19.5 to 97.0 mm Hg. Respiratory examination revealed normal spirometry and slight hypoxemia associated with an increase in alveoloarterial oxygen tension gradient. Lung transfer factor for CO was measured in nine patients; it was either normal or slightly reduced. Hyperventilation was found in the majority of patients already at rest. Pulmonary hypertension was believed to be the most important cause of alveolar hyperventilation in these patients. Total ventilation and VD/VT ratio were measured in 22 normal subjects at rest and during exercise, both with and without unilateral pulmonary artery occlusion. At rest, pulmonary artery occlusion did not lead to any change in total ventilation; during exercise, a 30-percent increase in total ventilation was observed with pulmonary artery occlusion. Pulmonary artery occlusion led to an increase in functional dead space only in those subjects in whom the tidal volume exceeded 700 ml. Whether this increase in tidal volume was associated with exercise or not did not make any difference. In patients with recurrent pulmonary embolism, the value of functional dead space was also higher only in subjects breathing with higher tidal volumes. It seems, therefore, that in the patients the same principle of unmasking the alveolar dead space by the increase in tidal volume can be demonstrated as in the model experiments with pulmonary artery occlusion

THE EFFECT OF INTUBATION ON THE DEADSPACE DURING HALOTHANE ANAESTHESIA

SUMMARY Total functional deadspace (including apparatus deadspace) was measured in anaesthetized patients while breathing from masks and after tracheal intubation. The mean VD/VT ratio was 0.18 larger during mask breathing and the mean value for the total functional deadspace was 82 ml greater than in the intubated patients. The results showed an increase in the VD/VT ratio during the inhalation of higher concentrations of halothane: the difference closely approached but did not attain the 95 per cent confidence limit. Values for VD/VT ratio and VD were uninfluenced by the duration of anaesthesia up to 120 minutes.

A NEW UNIDIRECTIONAL VALVE TO STUDY STEADY STATE GAS EXCHANGE

SUMMARY A new unidirectional valve, constructed from existing anaesthetic equipment to be used in steady state gas exchange measurements, is described. Its characteristics are equal to, or superior to, any other valve used for this purpose. A method for the measurement of functional deadspace is described.

Pulmonary-function tests.

To the Editor:— article Pulmonary-Function Tests which appeared inThe Journal( 206 :2302, 1968) contains the following statement: The level of arterial Pco 2 is governed solely by the alveolar ventilation. Elevated Pco 2 means alveolar hypoventilation, and reduced Pco 2 , alveolar hyperventilation. Such a statement ignores the ventilation to perfusion relationship in which a reduction in perfusion may commonly increase functional dead space, shuntlike effects, hypoxemia, and finally CO 2 retention. Ventilation-perfusion problems must be distinguished from alveolar hypoventilation, which caused decreased alveolar Po 2 together with increased arterial Pco 2 . While it is true that a diffusion barrier for CO 2 is for practical purposes almost nonexistent as compared to O 2 , the perfusion of alveoli has an important role in relationship to CO 2 elimination. This fact has clinical importance in the evaluation of pulmonary emboli in which the alveolar Pco 2 levels may be reduced

THE EFFECT OF INTUBATION ON THE DEADSPACE DURING HALOTHANE ANAESTHESIA

SUMMARY Total functional deadspace (including apparatus deadspace) was measured in anaesthetized patients while breathing from masks and after tracheal intubation. The mean VD/VT ratio was 0.18 larger during mask breathing and the mean value for the total functional deadspace was 82 ml greater than in the intubated patients. The results showed an increase in the VD/VT ratio during the inhalation of higher concentrations of halothane: the difference closely approached but did not attain the 95 per cent confidence limit. Values for VD/VT ratio and VD were uninfluenced by the duration of anaesthesia up to 120 minutes.

Effects of raised barometric pressures on respiration in man.

AbstractHesser, C. M. and B. Holmgren. Effects of raised barometric pressures on respiration in man. Acta physiol. scand. 1959. 47. 28—43. – The effects of raised barometric pressures (up to 4.0 atm) on various respiratory functions, hitherto largely neglected, were studied on 8 healthy subjects at rest in a recompression chamber. The independent effects of changes in inspired oxygen and nitrogen pressures were studied by comparing data obtained on air, 100 % oxygen, and 5 % oxygen in nitrogen at various ambient pressures. Breathing air with increasing ambient pressure, respiration became progressively slower and deeper, whereas at 4.0 atm the effective alveolar ventilation was slightly increased. Other observations at 4.0 atm were: Average increase of 33 % in tidal volume; average decreases in respiratory rate of 27 %, respiratory minute volume of 10 %, and functional dead space/tidal volume ratio of 9 %; no demonstrable changes in expiratory reserve volume, functional dead space and respiratory exchange ratio. Evidence is presented that the respiratory changes were caused by the combined effects of increased oxygen tension and of increased breathing resistance due to increased gas density. Thus, nitrogen at high pressures (up to 3.8 atm) exerted little, if any, depressant action on respiration.

Pulmonary function in mitral valve disease: Hemodynamic and ventilatory studies

Hemodynamic and ventilatory studies were carried out in a large series of patients who underwent mitral surgery for mitral stenosis or insufficiency. A diminution of cardiac index was found, which paralleled the narrowing of the mitral orifice. However, left ventricular failure seemed to be operative in some of the cases, even in the presence of pure, tight mitral stenosis. This hypothesis was also suggested by the observation that pulmonary artery and venous wedge pressures were significantly higher in patients with combined heart failure, independently of the size of the mitral orifice. A positive linear correlation was found between pulmonary artery pressures and pulmonary vascular resistances, when the latter were more than 200 and less than 900 dynes sec cm −5. No significant increase of pulmonary blood volume could be found in patients with mitral stenosis. Lack of correlation was found between ventilatory and hemodynamic findings studied simultaneously in 50 patients. Vital capacity was significantly impaired only in decompensated patients. Residual volume was increased in every case of mitral disease. Ventilatory dynamics were also altered in every instance, particularly when congestive heart failure was present. Functional dead space was consistently increased, in spite of an increased alveolar ventilation. These findings confirm that in mitral stenosis the ventilatory perfusion ratio is consistently impaired. Results of postcommissurotomy ventilatory studies were quite variable in spite of good clinical results. In 26 patients the hemodynamic behavior was studied before and at varying intervals (30 days to 3.5 years) after mitral commissurotomy. The hemodynamic findings in patients who underwent a successful commissurotomy are similar to those observed in subjects with anatomically and functionally mild mitral stenosis.

OBSERVATIONS ON THE PATHOLOGIC PHYSIOLOGY OF CHRONIC PULMONARY EMPHYSEMA

The object of this paper is to record the results obtained from experiments on two patients with chronic pulmonary emphysema, of the so-called large lunged type. The work was undertaken in an effort to ascertain facts which might lead to a clearer appreciation of the disturbance in respiratory physiology in emphysema. The gross and microscopic appearance of the lungs in this condition is well defined; also the impediment to the mechanics of respiration afforded by the loss of the elastic tissue of the lungs is appreciated. Further investigation, however, is necessary to show to what extent the degenerative process interferes with the aeration of the blood and the manner in which the body adapts itself to the altered conditions. The work of Siebeck,1Porges, Leimdorfer and Markovivi,2Hoover3and others established the fact that the residual air and the functional dead space are increased, while the vital capacity is much