A microcomputer system for on-line monitoring of pulmonary function during artificial ventilation

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.

The effect of increased apparatus dead space and tidal volumes on carbon dioxide elimination and oxygen saturations in a low-flow anesthesia system

Dead space in acute respiratory distress syndrome: more than a feeling!

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A sinusoidal forcing function inert-gas-exchange model (C. E. W. Hahn, A. M. S. Black, S. A. Barton, and I. Scott. J. Appl. Physiol. 75: 1863-1876, 1993) is modified by replacing the inspired inert gas with oxygen, which then behaves mathematically in the gas phase as if it were an inert gas. A simple perturbation theory is developed that relates the ratios of the amplitudes of the inspired, end-expired, and mixed-expired oxygen sine-wave oscillations to the airways' dead space volume and lung alveolar volume. These relationships are independent of oxygen consumption, the gas-exchange ratio, and the mean fractional inspired (FIO2) and expired oxygen partial pressures. The model also predicts that blood flow shunt fraction (Qs/QT) is directly related to the oxygen sine-wave amplitude perturbations transmitted to end-expired air and arterial and mixed-venous blood through two simple equations. When the mean FIO2 is sufficiently high for arterial hemoglobin to be fully saturated, oxygen behaves mathematically in the blood like a low-solubility inert gas, and the amplitudes of the arterial and end-expired sine-wave perturbations are directly related to Qs/QT. This relationship is independent of the mean arterial and mixed-venous oxygen partial pressures and is also free from mixed-venous perturbation effects at high forcing frequencies. When arterial blood is not fully saturated, the theory predicts that QS/QT is directly related to the ratio of the amplitudes of the induced-saturation sinusoids in arterial and mixed-venous blood. The model therefore predicts that 1) on-line calculation of airway dead space and end-expired lung volume can be made by the addition of an oxygen sine-wave perturbation component to the mean FIO2; and (2) QS/QT can be measured from the resultant oxygen perturbation sine-wave amplitudes in the expired gas and in arterial and mixed-venous blood and is independent of the mean blood oxygen partial pressure and oxyhemoglobin saturation values. These calculations can be updated at the sine-wave forcing period, typically 2-4 min.

High-Frequency Oscillatory Ventilation for Adult Patients With ARDS

Dead space volumes in cats and dogs with small body mass ventilated with a fixed tidal volume

The volumes of the dead space (anatomic and alveolar) play an important role in the physiology of external respiration and information on these volumes makes the diagnosis of different respiratory disorders easier. The volume of the anatomic dead space (the last inspiratory portions) is uninvolved in the mixing with the gas of functional residual capacity (FRC) and leaves the airways unchanged in the gas composition on expiration. Mixing of the other portion of the tidal volume with FRC gas should be regarded as preparation for an alveolar gas exchange process. The increased partial value of the anatomic dead space in the tidal volume with its decrease (tachypnea) and, accordingly, reduced alveolar ventilation volume may result in ventilation respiratory failure. The time course of changes in the volume of the alveolar dead space is easily detectable from the decrease in expiratory CO2 concentrations as compared with PaCO2. The increased alveolar dead space volume suggests impaired local blood flow (thromboembolism, acute respiratory distress syndrome) in the lesser circulation and gives grounds to diagnose shunting and venous mixing. Procedures for measuring the dead space volumes are simple and may be introduced into clinical practice. Key words: anatomic dead space, alveolar dead space, functional residual capacity, respiratory failure.

Objective To investigate the mechanism and significance of low concentration nitric oxide (NO) inhalation in the treatment of pulmonary thromboembelism in swine. Method The pulmonary thromboem-bolism(PTE) model was made in 15 healthy infantile swines which were subsequently assigned to either control group (n = 8) or NO group (n = 7). Swines of the control group were not treated with any medicine, while 10 ppm of NO was administered by continuous inhalation for 2 hours to swines of NO group. Volume of physiological dead space (VDphy), volume of alveolar dead space (VDalv), intrapulmonary shunt (Qs/Qt), mean pulmonary arterial pressure (PAP), systolic blood pressure (SBP), heart rate (HR), cardiac output (CO), arterial blood pH (pH), arterial partial pressure of carbon dioxide (PaCO2) and arterial partial pressure of oxygen (PaO2) were measured 30 min before and 0 min, 30 min, 60 min, 120 min and 180 min after establishment of VIE. Results The post-FIE VDphy, VDalv, Qs/Qt and PAP in both groups increased markedly after PTE compared with the cor-responding pre-PTE measurements (P 0.05). Both post-PTE PAP and VDalv in NO group were markedly lower(P <0.05 and P <0.01) and beth PaCO2 and PaO2 were much higher than those of the control group (P <0.05). No signi-fieant difference were found in other measurements between two groups. Conclusions Pulmonary arterial pressure may be lowered, alveoli dead space may be reduced and PaCO2 increased by low concentration NO inhalation for the treatment of PIE without decline in haemodynamic status. Key words: Pulmonary thromboembolism; Nitric oxide; Dead space; Shunt; Gas exchange; Pulmonary ar-terial pressure; Model; Arterial partial pressure of oxygen;

Forced sinusoidal oscillations in the inspired concentration of a low-solubility inert gas can be used to measure airways dead space and alveolar volume. When inspired oxygen is oscillated about its mean value in the same way, the ratio between the amplitudes of the resulting end-expired and inspired oxygen oscillations is the same as that of an inert gas such as argon. Thus, oxygen forcing oscillations can be used to measure lung volume. In nine healthy spontaneously breathing adults, the FIO2 (mean FIO2 = 0.26, mean minute volume = 8.5 L/min) was forced to sinusoidally oscillate with an amplitude of +/- 0.04. The mean airways dead space measured using FIO2 oscillations with a forcing period of 3 min was 0.17 +/- 0.04 L, and the airways dead space measured by a single-breath C02 technique was no different at 0.19 +/- 0.03 L. An oxygen oscillation of the same period measured the mean end-expired alveolar volume at 3.1 +/- 0.7 L. Adding together the airways dead space and end-expired alveolar volume, obtained by the oxygen oscillation technique, provided a measure of FRC that at 3.3 +/- 0.7 L matched the FRC of 3.3 +/- 0.8 L measured by whole-body plethysmography. A third measure of FRC using a multiple-breath nitrogen washout technique gave a smaller volume of 3.00 +/- 0.85 L. The advantage of using FIO2 oscillations is that accurate FRC measurements can be made continuously, without interfering with the subject's natural breathing rhythm.

What is the central question of this study? The goal of this study was to investigate the effect of alterations in tidal volume and alveolar volume on the elevated physiological dead space and the contribution of ventilatory constraints thereof in heart failure patients during submaximal exercise. What is the main finding and its importance? We found that physiological dead space was elevated in heart failure via reduced tidal volume and alveolar volume. Furthermore, the degree of ventilatory constraints was associated with physiological dead space and alveolar volume. Patients who have heart failure with reduced ejection fraction (HFrEF) exhibit impaired ventilatory efficiency [i.e. greater ventilatory equivalent for carbon dioxide ( ) slope] and elevated physiological dead space (VD /VT ). However, the impact of breathing strategy on VD /VT during submaximal exercise in HFrEF is unclear. The HFrEF (n= 9) and control (CTL, n= 9) participants performed constant-load cycling exercise at similar ventilation ( ). Inspiratory capacity, operating lung volumes and arterial blood gases were measured during submaximal exercise. Arterial blood gases were used to derive VD /VT , alveolar volume, dead space volume, alveolar ventilation and dead space ventilation. During submaximal exercise, HFrEF patients had greater slope and VD /VT than CTL subjects (P= 0.01). At similar , HFrEF patients had smaller tidal volumes and alveolar volumes (HFrEF 1.11± 0.33litres versus CTL 1.66± 0.37 litres; both P≤ 0.01), whereas dead space volume was not different (P= 0.47). The augmented breathing frequency in HFrEF patients resulted in greater dead space ventilation compared with CTL subjects (HFrEF 15± 4lmin-1 versus CTL 10± 5lmin-1 ; P= 0.048). The HFrEF patients exhibited greater increases in expiratory reserve volume and lower inspiratory capacity (as a percentage of predicted) than CTL subjects (both P< 0.05), which were significantly related to VD /VT and alveolar volume in HFrEF patients (all P< 0.03). In HFrEF, the reduced tidal volume and alveolar volume elevate physiological dead space during submaximal exercise, which is worsened in those with the greatest ventilatory constraints. These findings highlight the negative consequences of ventilatory constraints on physiological dead space during submaximal exercise in HFrEF.

Are New Ventilatory Modalities Really Different?

It was observed previously that end-expired carbon dioxide (P(E)CO2) decreased when immobilized black rhinoceroses (Diceros bicornis) were moved from sternal to lateral recumbency. These experiments were designed to test whether greater alveolar ventilation or greater pulmonary dead space in lateral recumbency explains this postural difference in P(E)CO2. Twenty-one (9 male, 12 female; 15 [3.5-26] yr old) wild black rhinoceroses were immobilized with etorphine and azaperone and positioned in either sternal or lateral recumbency. All rhinoceroses were hypoxemic and had lactic and respiratory acidemia. The animals in lateral recumbency were more acidemic, had higher lactate, and lower arterial oxygen that those in sternal recumbency; however, arterial carbon dioxide was similar between groups. Both P(E)CO2 and mixed expired carbon dioxide pressure were lower in lateral than sternal recumbency. Although there was no difference in tidal volume or arterial carbon dioxide, both the breathing rate and minute ventilation were greater in lateral recumbency. The physiologic dead space ratio and dead space volume were approximately two times larger in lateral recumbency; hence, the decrease in P(E)CO2 in lateral recumbency can be attributed to increased dead space ventilation not increased alveolar ventilation. Positioning immobilized rhinoceroses in lateral recumbency does not confer any advantage over sternal in terms of ventilation, and the increase in minute ventilation in lateral recumbency can be considered an energetic waste. Although arterial oxygen was superior in sternal recumbency, further studies that measure oxygen delivery (e.g., to the muscles of locomotion) are warranted before advice regarding the optimal position for immobilized rhinoceroses can be given with confidence.

BackgroundDead space is the volume not taking part in gas exchange and, if increased, could affect alveolar ventilation if there is too low a delivered volume. We determined if there were differences in dead space and alveolar ventilation in ventilated infants with pulmonary disease or no respiratory morbidity.MethodsA prospective study of mechanically ventilated infants was undertaken. Expiratory tidal volume and carbon dioxide levels were measured. Volumetric capnograms were constructed to calculate the dead space using the modified Bohr–Enghoff equation. Alveolar ventilation (VA) was also calculated.ResultsEighty-one infants with a median (range) gestational age of 28.7 (22.4–41.9) weeks were recruited. The dead space [median (IQR)] was higher in 35 infants with respiratory distress syndrome (RDS) [5.7 (5.1–7.0) ml/kg] and in 26 infants with bronchopulmonary dysplasia (BPD) [6.4 (5.1–7.5) ml/kg] than in 20 term controls with no respiratory disease [3.5 (2.8–4.2) ml/kg, p < 0.001]. Minute ventilation was higher in both infants with RDS or BPD compared to the controls. VA in infants with RDS or BPD was similar to that of the controls [p = 0.54].ConclusionPrematurely born infants with pulmonary disease have a higher dead space than term controls, which may influence the optimum level during volume-targeted ventilation.ImpactMeasurement of the dead space was feasible in ventilated newborn infants.The physiological dead space was a significant proportion of the delivered volume in ventilated infants.The dead space (per kilogram) was higher in ventilated infants with respiratory distress syndrome or evolving bronchopulmonary dysplasia compared to term controls without respiratory disease.The dead space volume should be considered when calculating the most appropriate volume during volume-targeted ventilation.

Pulmonary dead space is the volume of gas that is delivered to the lungs but does not participate in gas exchange. Knowing pulmonary dead space in patients under general anesthesia is clinically useful because it can aid in detecting disease processes such as pulmonary emboli or low cardiac output states. Dead space can be simply calculated by using the Bohr equation; however, it is difficult to measure mixed exhaled carbon dioxide (PECO(2)) with a standard anesthesia machine. Previously, a study at our institution demonstrated the carbon dioxide (CO(2)) concentration in the bellows of a standard anesthesia machine is an accurate approximation of PECO(2). In this study, we used the bellows PECO(2) measurement and arterial CO(2) (PaCO(2)) to calculate pulmonary dead space. We verified the technique by adding known apparatus dead space volumes during anesthesia. Subjects were under general endotracheal anesthesia. A sampling line was positioned inside the ventilator bellows and connected to a capnometer. Measurements of PECO(2) and PaCO(2) from an arterial catheter were taken at baseline and after adding 100 mL and 200 mL of dead space to the endotracheal tube. Dead space was calculated using the Bohr equation (alveolar dead space/tidal volume = [PaCO(2) - PECO(2)]/PaCO(2)) at baseline and after adding 100 mL and 200 mL of apparatus dead space. The dead space at baseline was 265 ± 47 mL (mean ± SD) in 10 study subjects. After adding 100 mL of dead space to the endotracheal tube, the measured dead space increased by 110 ± 46 mL. The measured dead space increased by 158 ± 39 mL after adding 200 mL. Our baseline dead space measurements were in the expected range under general anesthesia. When dead space was added, we were able to calculate that an increase in dead space occurred. Our calculation was more accurate after adding a 100-mL volume than after adding 200 mL. We present a simple way to detect trends in dead space in ventilated patients using a Narkomed GS anesthesia machine (Dräger Medical, Lübeck, Germany).