Mechanical Dead Space Research Articles

Dead space washout by intentional leakage flow during conventional ventilation of premature infants-an experimental study.

ObjectiveInvasive mechanical ventilation poses a strong risk factor for the development of chronic lung disease in preterm infants. A reduction of the dead space as part of the total breathing volume would reduce the ventilation effort and thereby lower the risk of ventilator‐induced lung injuries. In this experimental study, we compared the efficacy of mechanical dead space washout via uncontrolled and controlled leakage flow in their ability to eliminate CO2 during conventional ventilation in preterm infants.MethodsThree frequently used neonatal ventilators, operating under standard conventional ventilating parameters, were individually connected to a test lung. To maintain a constant physiological end‐expiratory pCO2 level during ventilation, the test lung was continuously flooded with CO2. A side port in the area of the connector between the endotracheal tube and the flow sensor allowed breathing gas to escape passively or in a second experimental setup, regulated by a pump. Measurements of end‐expiratory pCO2 were taken in both experiments and compared to end‐expiratory pCO2 levels of ventilation without active dead space leakage.ResultsFollowing dead space washout, a significant reduction of end‐expiratory pCO2 was attained. Under conditions of uncontrolled leakage, the mean decrease was 14.1% while controlled leakage saw a mean reduction of 16.1%.ConclusionWashout of dead space by way of leakage flow is an effective method to reduce end‐expiratory pCO2. Both controlled and uncontrolled leakage provide comparable results, but precise regulation of leakage allows for a more stable ventilation by preventing uncontrolled loss of tidal volume during inspiration.

Removal of a catheter mount and heat-and-moisture exchanger improves hypercapnia in patients with acute respiratory distress syndrome: A retrospective observational study.

To avoid ventilator-associated lung injury in acute respiratory distress syndrome (ARDS) treatment, respiratory management should be performed at a low tidal volume of 6 to 8 mL/kg and plateau pressure of ≤30 cmH2O. However, such lung-protective ventilation often results in hypercapnia, which is a risk factor for poor outcomes. The purpose of this study was to retrospectively evaluate the effectiveness and safety of the removal of a catheter mount (CM) and using heated humidifiers (HH) instead of a heat-and-moisture exchanger (HME) for reducing the mechanical dead space created by the CM and HME, which may improve hypercapnia in patients with ARDS.This retrospective observational study included adult patients with ARDS, who developed hypercapnia (PaCO2 > 45 mm Hg) during mechanical ventilation, with target tidal volumes between 6 and 8 mL/kg and a plateau pressure of ≤30 cmH2O, and underwent stepwise removal of CM and HME (replaced with HH). The PaCO2 values were measured at 3 points: ventilator circuit with CM and HME (CM + HME) use, with HME (HME), and with HH (HH), and the overall number of accidental extubations was evaluated. Ventilator values (tidal volume, respiratory rate, minutes volume) were evaluated at the same points.A total of 21 patients with mild-to-moderate ARDS who were treated under deep sedation were included. The values of PaCO2 at HME (52.7 ± 7.4 mm Hg, P < .0001) and HH (46.3 ± 6.8 mm Hg, P < .0001) were significantly lower than those at CM + HME (55.9 ± 7.9 mm Hg). Measured ventilator values were similar at CM + HME, HME, and HH. There were no cases of reintubation due to accidental extubation after the removal of CM.The removal of CM and HME reduced PaCO2 values without changing the ventilator settings in deeply sedated patients with mild-to-moderate ARDS on lung-protective ventilation. Caution should be exercised, as the removal of a CM may result in circuit disconnection or accidental extubation. Nevertheless, this intervention may improve hypercapnia and promote lung-protective ventilation.

Abstract 16698: Cardiopulmonary Exercise Testing With an In-Line Filter During the COVID-19 Pandemic

Introduction: During maximum incremental exercise expiratory flow rates increase &gt; 10-fold and minute ventilation can exceed 100L/min, raising concern for possible spread of COVID-19 in asymptomatic patients undergoing exercise testing. Moreover, use of surgical or N95 masks that limit airflow are recognized to limit the ability to perform maximum exercise. Hypothesis: Use of an in-line filter during cardiopulmonary exercise testing is feasible and will not adversely impact measurements of exercise capacity. Methods: We conducted a proof-of-principle study in which a commercially available electrostat filter (Figure 1A), which has &gt;99.9% viral efficiency without affecting spirometry measurements during pulmonary function testing, was placed in-line, upstream of the flow meter and gas analyzer sample line for use during cardiopulmonary exercise testing. A single healthy subject completed incremental exercise with a 3 min period of unloaded exercise followed by 4-min stages of exercise at 50, 100, 150, and 200W with and without the filter in place on the same day. Mechanical dead space was 53 ml with the filter and 45 ml without. Results: In comparison to no internal filter, use of an in-line filter resulted in VO 2 measurements of 99%, 97%, 98%, and 97% during 50W, 100W, 150W, and 200W, respectively (Figure 1A). VO 2 /work slope measurements and measurements of minute ventilation were also highly consistent throughout exercise with and without use of an in-line filter (Figure 1B). Conclusions: Exercise testing is an integral part of cardiovascular care delivery. Our findings require further validation but suggest that an in-line filtration system can be utilized in an effort to reduce droplet and viral dissemination without impacting measures of cardiopulmonary performance.

External dead space explains sex-differences in the ventilatory response to submaximal exercise in children with and without obesity

We compared the exercise ventilatory response (slope of the ventilation, V̇E and carbon dioxide production, V̇CO2 relationship) in boys and girls with and without obesity. 46 children with obesity (BMI percentile: 97.7 ± 1.4) and 27 children without obesity (BMI percentile: 55.1 ± 22.2) were included and divided into groups by sex (with obesity: 17 girls and 29 boys; without obesity: 13 girls and 14 boys). A 6 min constant load cycling test at 45 % of peak work rate was performed. The V̇E/V̇CO2 slope was similar (p = 0.67) between children with (32.7 ± 4.3) and without (32.2 ± 6.1) obesity; however, it was higher (p = 0.02) in girls (35.4 ± 5.6) than boys (32.6 ± 4.9). We also examined a corrected V̇E/V̇CO2 slope for the effects of mechanical dead space (VDM), by subtracting V̇DM from V̇E (V̇Ecorr/V̇CO2 slope). The V̇Ecorr/V̇CO2 slope remained similar (p = 0.37) between children with (26.8 ± 3.2) and without obesity (26.1 ± 3.1); however, no sex differences were observed (p = 0.13). Therefore, VDM should be accounted for before evaluating the V̇E/V̇CO2 slope, particularly when making between-sex comparisons.

Tracheal gas insufflation during late exhalation efficiently reduces PaCO(2) in experimental acute lung injury.

Tracheal gas insufflation (TGI) reduces PaCO(2) by flushing the tracheal and mechanical deadspace, and may have its maximum benefit when TGI gas is unopposed by significant expiratory gas flow. Thus, limiting TGI to the late expiratory period may diminish tracheal exposure to TGI gas while preserving the efficacy of TGI. This study examined the gas exchange consequences of such late-expiratory TGI. Randomized controlled trial, animal study. Eleven pigs. After stable lung injury was established using oleic acid 11 pigs were ventilated using a standardized lung protective strategy. Phasic expiratory TGI was applied for 30 min stages during the last 20%, 40%, 60%, and 100% of expiration in random sequence. PaCO(2) was continuously measured via an indwelling blood gas analysis system. PaCO(2) at baseline was 86.1+/-4.7 mmHg, and decreased progressively with increasing TGI duration of 20%, 40%, and 60%, but not 100%, of expiration (PaCO(2)=75.7+/-5.2, 68.8+/-3.6, 65.1+/-5.3 and 65.2+/-5.2 mmHg, respectively). For all stages the reduction in PaCO(2) relative to baseline was significant. Trends of increasing PaO(2) and airway pressure with increasing TGI duration were noted and most likely associated with a TGI-induced increase in lung volume. Under these conditions confining TGI to the final 60% of expiration achieved effective PaCO(2) reduction, not significantly different from panexpiratory TGI, while limiting exposure of the trachea to TGI gas, and reducing the potential for TGI-induced hyperinflation. These findings suggest that TGI is most effectively applied in a phasic manner in late expiration, with its duration titrated to effect.

Accumulation of CO(2) in reservoir devices during simulated neonatal mechanical ventilation.

Aerosolized albuterol is frequently administered to mechanically ventilated neonates by metered dose inhaler (MDI) and a reservoir device. These reservoirs are often placed between the Y-piece and endotracheal tube, thereby creating mechanical dead space and increasing the risk of rebreathing carbon dioxide (CO(2)). The objectives of this study were: 1) to quantify CO(2) accumulation in two commonly used reservoirs (ACE(R), Aerochamber(R)-MV) and a bidirectional nonreservoir actuator (Airlife(R) Minispacer) during mechanical ventilation of a neonatal lung model; and 2) to determine the effect of tidal volume (V(T)) on CO(2) accumulation. We hypothesized that the accumulation of CO(2) in these devices is clinically insignificant at the small tidal volumes used in mechanically ventilated premature neonates. The model was constructed to simulate CO(2) exhalation by a ventilated neonate and consisted of a neonatal ventilator circuit (rate = 40/min; peak inspiratory pressure (PIP) = 20 cm H(2)0) attached to a reservoir/actuator and neonatal test lung. The ventilator delivered inspiratory gas (room air) to the test lung, which was vented into the atmosphere by a small adjustable leak. Expiration was simulated by manually ventilating 7.1% CO(2) (partial pressure of CO(2) (PCO(2)) = 48 mm Hg) back through the model. Accumulation of CO(2) within the reservoir/actuator was measured using an end-tidal CO(2) monitor. Each 4-min experiment was conducted at three V(T) (7.5 mL, 15 mL, and 25 mL), and the median PCO(2) was calculated in 0.5-min increments. For V(T) = 7.5 mL, CO(2) accumulated slowly in the ACE(R) and Minispacer(R) and reached a maximum at 4.0 min (PCO(2) = 2.3 mm Hg and 7.3 mm Hg, respectively). In contrast, the Aerochamber(R)-MV rapidly reached a PCO(2) of 9.5-10.0 mm Hg by 1-1. 5 min. A similar trend occurred with V(T) = 15 mL; however, higher partial pressures (approximately 10-12 mm Hg) were achieved with all devices. At V(T) = 25 mL, PCO(2) rose rapidly with the ACE(R), Aerochamber(R)-MV, and Minispacer(R), reaching peaks of 17.2, 12.3, and 20.3 mm Hg, respectively (P < 0.05). In conclusion, accumulation of CO(2) in reservoir/actuator depends on V(T) as well as the chamber design and internal volume. Due to the short duration of use when administering drugs via MDI, accumulation of CO(2) in these devices is not likely to be clinically relevant for the majority of ventilated newborns.

Effects of the high-flow modified to-and-fro anesthestic system on blood gas and respiratory rate in halothane anesthetized horses

Ten healthy adult horses male or female, mean body weight of 424±44.1kg, were anesthetized with romifidine, tiletamine/zolazepam and halothane for 60 minutes using a modified to-and-fro rebreathing anesthetic system, added of 1 liter mechanical dead space. The gas flow rate was 10 liters oxygen/minute during all inhalation anesthetic time. Variables analysed were arterial blood pH, carbon dioxide partial pressure (PaCO2) and oxygen partial pressure (PaO2), and respiratory rate (RR). The horses were allowed to breath spontaneously, and were positioned in right lateral recumbency the arterial O2 values were significantly higher during halothane anesthesia when compared to the baseline values, and significantly lower after induction with tiletamine/zolazepam although arterial hypoxemia were not present. The arterial PaCO2 values were significantly higher from baseline values during halothane anesthesia occurring arterial hypercapnia and mild respiratory acidosis. The arterial pH changes paralleled the changes in PaCO2. Respiratory rate values were significantly lower during halothane anesthesia when compared to baseline values. All values remained within accepted range for lateral recumbent spontaneously breathing anesthetized horses.

The parallel Lack anaesthetic breathing system.

The parallel Lack system is a new modification of the Mapleson A system comprising separate inspiratory and expiratory tubes. To determine that the function of the system was that anticipated of a Mapleson A, the fresh gas flow requirements to prevent rebreathing during spontaneous ventilation were assessed in three situations: (1) a lung model (2) conscious volunteers and (3) anaesthetised patients. Two sets of criteria to define rebreathing were used; (A) those based on changes in ventilation or end-expired carbon dioxide tension and (B) minimum inspired carbon dioxide tension. Using A, rebreathing occurred at a fresh gas flow to minute ventilation ratio (VF/VE) of 0.75 for the lung model, and 0.73 for conscious volunteers. These results were comparable to those obtained for a Magill attachment. They were also close to the point at which mechanical dead space began to increase in the lung model. Criteria B gave much lower values for the onset of rebreathing. Rebreathing was present by criteria A in five of the six anaesthetised patients at a fresh gas flow of 60 ml.kg-1.min-1 (VF/VF of 0.78). The results confirm that the parallel Lack behaves as a Mapleson A system. The resistance to breathing posed by the parallel Lack was also comparable to the Magill system.

The Case for Rebreathing Circuits for Very Small Animals

The objections to using adult circle systems on very small patients include increased resistance to breathing, mechanical dead space, and slow equilibration times. These objections warrant consideration before assuming that nonrebreathing systems have an inherent advantage for patients between 3 and 10 kg. The cost of anesthesia and the time taken to establish a desired anesthetic level are as important in determining which system to use for small animal patients. Based on the current evidence, it is acceptable to use adult circle rebreathing systems on healthy patients as small as 3 kg.

On-line blood and respiratory gas analysis.

Data from a patient receiving ventilatory assistance are processed by computer to calculate pulmonary shunt, dead space/tidal volume ratio, oxygen uptake and delivery, and carbon dioxide elimination and delivery. The computations are based on routines described by Kelman and by Severinghaus, but modified to match limitations of testing imposed by the requirements for ventilatory assistance. Analyses are performed sequentially on arterial and venous blood samples and on respiratory gas samples. The output of the blood gas analyzers is fed on-line to a computer together with other data, such as patient identification, which are manually entered at a keyboard and with thumb-wheel switches. The computer processing begins with determining the concentration of oxygen and carbon dioxide in whole blood and of bicarbonate in plasma. The shunt equation is used to calculate a virtual shunt at therapeutic concentrations of inspired oxygen. Dead space/tidal volume ratios are corrected for mechanical dead space in the respiratory circuit. The analyzed results are returned to the operator within seconds via a video display. Since the data include blood samples from multiple patient sites, a cross-comparison is made by the computer and the operator is informed of unusually large differences in values.

INFLUENCE OF SIMULTANEOUS AND EQUAL INCREASE IN EXTERNAL DEAD SPACE AND TIDAL VOLUME ON ARTERIAL BLOOD GASES IN ARTIFICIALLY VENTILATED PATIENTS

Comment: This report confirms the importance of using tidal volumes between 10 to 15 ml. per kg. during artificial ventilation to prevent atelectasis. The partial pressure of CO2 can be normalized by increasing the mechanical dead space. The tachypnea associated with weaning is probably related to the difference in lung volumes when the patient is breathing spontaneously as against controlled ventilation.

Normalizing Low Arterial CO2 Tension During Mechanical Ventilation

In ten patients with progressive pulmonary consolidation (PPC) during controlled mechanical ventilation with or without positive end expiratory pressure (PEEP) and in five patients with decompensated chronic obstructive lung disease (COLD) during patient triggered assisted respiration, low PaCO 2 was normalized by adding 1 percent to 3 percent CO 2 to the inhaled gas or by adding 200 to 300 milliliters of mechanical dead space to the ventilator tubing. As low arterial P co 2 and high pH were normalized, significant increases occurred in arterial P o 2 , cardiac output and arterial O 2 transport, while both O 2 utilization coefficient and systemic vascular resistance (SYR) decreased. Venous admixture ( Q ˙ s / Q ˙ T ) increased in seven of ten patients and decreased in three of ten with PPC. This variable decreased in the three COLD patients in whom it was measured. The total amount of blood flowing through ventilated areas of the lungs ( Q ˙ T − Q ˙ S ) increased in all patients. The venous O 2 content also increased in all and thereby shunted less desaturated blood to the arterial side. The beneficial circulatory effects of normalizing low Pa co 2 values in part offset the circulatory depressant effects of PEEP. The increase in Pa o 2 resulting from normalizing Pa co 2 allowed lowering of inspired O 2 concentrations from toxic to nontoxic levels even when this was not possible with PEEP alone. Controlling Pa co 2 by regulating FI co 2 during controlled and assisted ventilation with use of a prototype CO 2 mixer (attached to a commercially available air-O 2 mixer) seems more predictable and easier to adjust than the use of mechanical dead space.

Correction for mechanical dead space in the calculation of physiological dead space.

When physiological dead space (Vd(p)) is calculated for a patient who has alveolar dead space, e.g., after pulmonary vascular occlusion, less than the full volume of attached mechanical dead space (Vd(m)) appears in the measured dead space (Vd(n)). Under these conditions the traditional subtraction of Vd(m) from Vd(n) leads to underestimation of Vd(p) and can give a falsely small ratio of Vd(p) to tidal volume (Vt) when, in fact, an abnormally large Vd(p)/Vt exists. To make the proper correction for Vd(m), two equations have been derived and validated with seven subjects having Vd(p)/Vt from 0.29 to 0.87, using Vd(m)'s from 120 to 322 ml. With only a small modification, these equations are suitable for routine clinical use and give Vd(p)/Vt within 0.02 of that by the validated equations (32 of 33 comparisons). The fraction of Vd(m) subtracted from Vd(n) is the square of the ratio of effective alveolar to total alveolar ventilation and is never > 1. This fraction is (Pa(CO2)/Pa(CO2))(2), where Pa(CO2) and Pa(CO2) are the mean partial pressures of expired alveolar and of arterial CO(2); in the other equation this fraction is [Pe(CO2)/Pa(CO2) (Vt - Vd(an) - Vd(m))](2) where Pe(CO2) is mixed expired Pco(2) and Vd(an) is anatomical dead space. The second equation requires an estimated Vd(an) and is applicable when Pa(CO2) is not measured or does not plateau (as in exercise).

A study of intermittent positive pressure ventilation.

Using one degree of freedom RC lung model a respirator design criterion minimising the harmful effects of positive pressure ventilation, has been developed. To suppress the ill effects of long-term mechanical ventilation a mechanical dead space has been inserted in the breathing circuit. It is shown that by adding additional dead space the optimum design does not change except for alteration in respiratory rate. Respiratory parameter variation has also been considered and designs have been presented for discrete values of respiratory mechanical parameters.

Ventilatory reserve in the dog during partial curarization.

In dogs respiratory workloads were increased by partial airway obstruction or strapping the chest and by addition of a mechanical deadspace of 200 ml. The ventilatory responses and blood-gas values were within normal ranges during the respiratory challenge. When partial curarization was induced, ventilatory reserve diminished; with the addition of deadspace and either airway obstruction or decreased compliance induced by strapping respiratory arrest occurred when the dogs breathed room air. When the dogs breathed 100 per cent oxygen, respiratory arrest did not occur in response to the same respiratory challenges. It is suggested that hypoxia plays a role in initiating postoperative respiratory failure following anesthesia produced with neuromuscular blockers.

The reliability and usefulness of the suwa nomogram in patients in respiratory failure

The Suwa nomogram was devised to predict the amount of mechanical dead space which must be added to a ventilated patient’s breathing circuit to achieve a normal arterial carbon dioxide tension of 40 mm Hg from a hypocapnoeiac level. The reliability of the mathematical analysis from which the nomogram was derived, together with the Suwa nomogram itself, were assessed in nine patients in respiratory failure. The results from 26 samples verified the mathematical analysis with a difference of ± 1 mm Hg from the predicted value of 40 mm Hg for arterial carbon dioxide tension when mechanical dead space was added. The mechanical dead space predicted by the Suwa nomogram to achieve an arterial carbon dioxide tension of 40 mm Hg was shown to have a potential error of ± 3.23 mm Hg. It was shown that the mathematical analysis warranted more use than the Suwa nomogram because of superior accuracy.

Dead space during artificial ventilation: gas compression and mechanical dead space.

Dead space during artificial ventilation: gas compression and mechanical dead space.

Change in PaCO2 with mechanical dead space during artificial ventilation.

Change in PaCO2 with mechanical dead space during artificial ventilation.

A circulator to eliminate mechanical dead space in circle absorption systems.

A description is given of an original apparatus for the removal of the undermask dead space in paediatric anaesthesia. Its application to adult anaesthesia is also suggested. The apparatus may be used in conjunction with any circle closed or semi-closed absorption technique. The principle of operation is the forcing of carbon dioxide free gases through the under-mask space in order to displace the exhaled atmosphere before tie next inhalation takes place. The technique has been used in all the writer’s paediatric cases since 1947 and in those of his associates in the last five years.