Peak Alveolar Pressure Research Articles

Peak pressures or plateau pressures in acute asthma

Sir: We read with interest the article “Isoflurane therapy for severe refractory status asthmaticus in children” wherein the authors describe the use of inhaled isoflurane in a series of children with lifethreatening asthma [1]. However, it was surprising to note that in the algorithm the authors used the peak inspiratory pressure rather than plateau pressure for titration of tidal volumes and as a surrogate for lung hyperinflation. Peak inspiratory pressure does not reflect peak alveolar pressure or the degree of overdistension of alveolar structures, as the high pressures are encountered largely by robust proximal airways. On the other hand, plateau pressures (measured after an inspiratory hold of 0.5–1.5 s) are most reflective of the peak alveolar pressure (also used in calculation of transpulmonary pressure and static lung compliance). Plateau pressures of more than 30–35 cmH2O risk barotrauma and hemodynamic compromise without tangible benefit to gas exchange or oxygen delivery [2]. Ina classical case of acute asthma requiring mechanical ventilation, the peak inspiratory pressures and plateau pressures are in the range of 75–100 cmH2O and 25–35 cmH2O respectively [3]. Therefore high peak pressures are generally accepted, and in fact recent data have failed to show a relationship between peak pressures and complications of mechanical ventilation [4]. Also, a strategy aimed at reducing inspiratory time with fast inspiratory flow rates and the square inspiratory flow waveform is usually associated with high peak inspiratory pressures. The importance of recognizing high peak inspiratory pressures lies in setting the alarms to a level higher than the peak pressure, otherwise the ventilator would cycle with every breath and would not deliver the set tidal volume, leading to hypoventilation and worsening gas exchange [5]. In addition, the difference between the peak and plateau pressure represents the contribution from airway resistance to the value of the peak pressure [6]. In conclusion, the measurement of peak pressures has limited clinical relevance; because of their important resistive component, the peak pressures do not reflect the alveolar distension pressure in most of the lung.

Pressure Increase Due to Hydrostatic Pressure of Perfluorocarbon

With great interest we read the recent article by Kacmarek and colleagues (1). In the trial reported therein, the authors conclude that partial liquid ventilation (PLV) results in a greater number of serious adverse effects and does not improve outcome compared with conventional ventilation in patients with severe ARDS. As one of the reasons for a higher complication rate, the authors suggest the high peak alveolar pressure due to the additional hydrostatic pressure exerted by the perfluorocarbon (PFC), which has to be added to the measured airway pressure. It is obvious that a measurement of the hydrostatic pressure is associated with technical difficulties, though it is possible to estimate it. In this study the PFC was instilled to the carina in the supine position. Therefore, the maximal hydrostatic pressure (cm H2O) can be calculated by multiplying the distance between the liquid surface and the deepest point in the thorax, the dorsovisceral pleura (in cm), and the specific density of the PFC, which is 1.92. To evaluate the effective additional hydrostatic pressure, we measured 40 patients, ages between 18 and 60 yr, median 44.6 12.8 yr, 60% male sex, who had a thoracic CT in the supine position. On the Diagnostic Workstation (Diagnostic DICOM 3.0 Workstation; Agfa-Gevaert Group, Morstel, Belgium), the distance between the level of the carina and the lowest point of the dorsovisceral pleura was measured with the on-screen tool. The median distance retrieved was 7.5 cm 1.2 cm. Using these findings for estimating the actual resulting airway pressure, the distance was multiplied by 1.92. Therefore in the “low-dose” group, the hydrostatic pressure of 14.4 2.36 cm H2O has to be added to the measured plateau pressure as well as to the measured PEEP. Following this estimation, the median plateau pressure would be as high as 45.8 cm H2O with a PEEP of 28.7 cm H2O. These excessively high pressures could explain the higher rate of adverse effects in the “low-dose” group. For the “high-dose” group the resulting pressure would even exceed these findings. As is known from the literature (2), increased airway pressures lead to a worse outcome. Therefore, to avoid barotrauma to the lung during PLV, which probably contributes to a worse outcome, the measured pressure levels during PLV should have been significantly reduced. Therefore, the conclusion based on the findings of this study should be reconsidered.

Pressure Increase Due to Hydrostatic Pressure of Perfluorocarbon

With great interest we read the recent article by Kacmarek and colleagues (1). In the trial reported therein, the authors conclude that partial liquid ventilation (PLV) results in a greater number of serious adverse effects and does not improve outcome compared with conventional ventilation in patients with severe ARDS. As one of the reasons for a higher complication rate, the authors suggest the high peak alveolar pressure due to the additional hydrostatic pressure exerted by the perfluorocarbon (PFC), which has to be added to the measured airway pressure. It is obvious that a measurement of the hydrostatic pressure is associated with technical difficulties, though it is possible to estimate it. In this study the PFC was instilled to the carina in the supine position. Therefore, the maximal hydrostatic pressure (cm H2O) can be calculated by multiplying the distance between the liquid surface and the deepest point in the thorax, the dorsovisceral pleura (in cm), and the specific density of the PFC, which is 1.92. To evaluate the effective additional hydrostatic pressure, we measured 40 patients, ages between 18 and 60 yr, median 44.6 12.8 yr, 60% male sex, who had a thoracic CT in the supine position. On the Diagnostic Workstation (Diagnostic DICOM 3.0 Workstation; Agfa-Gevaert Group, Morstel, Belgium), the distance between the level of the carina and the lowest point of the dorsovisceral pleura was measured with the on-screen tool. The median distance retrieved was 7.5 cm 1.2 cm. Using these findings for estimating the actual resulting airway pressure, the distance was multiplied by 1.92. Therefore in the “low-dose” group, the hydrostatic pressure of 14.4 2.36 cm H2O has to be added to the measured plateau pressure as well as to the measured PEEP. Following this estimation, the median plateau pressure would be as high as 45.8 cm H2O with a PEEP of 28.7 cm H2O. These excessively high pressures could explain the higher rate of adverse effects in the “low-dose” group. For the “high-dose” group the resulting pressure would even exceed these findings. As is known from the literature (2), increased airway pressures lead to a worse outcome. Therefore, to avoid barotrauma to the lung during PLV, which probably contributes to a worse outcome, the measured pressure levels during PLV should have been significantly reduced. Therefore, the conclusion based on the findings of this study should be reconsidered.

Effects of L-NAME and inhaled nitric oxide on ventilator-induced lung injury in isolated, perfused rabbit lungs

To determine whether nitric oxide (NO) might modulate ventilator-induced lung injury. Randomized prospective animal study. Animal research laboratory in a university hospital. Isolated, perfused rabbit heart-lung preparation. Thirty-six isolated, perfused rabbit lungs were randomized into six groups (n = 6) and ventilated using pressure-controlled ventilation for two consecutive periods (T1 and T2). Peak alveolar pressure during pressure-controlled ventilation was 20 cm H2O at T1 and was subsequently (T2) either reduced to 15 cm H2O in the three low-pressure control groups (Cx) or increased to 25 cm H2O in the three high-pressure groups (Px). In the control and high-pressure groups, NO concentration was increased to approximately equal to 20 ppm (inhaled NO groups: CNO, PNO), reduced by NO synthase inhibition (L-NAME groups: CL-Name, PL-Name), or not manipulated (groups CE, PE). Changes in ultrafiltration coefficients (deltaKf [vascular permeability index: g.min(-1).cm H2O(-1).100 g(-1)]), bronchoalveolar lavage fluid 8-isoprostane, and NOx (nitrate + nitrite) concentrations were the measures examined. Neither L-NAME nor inhaled NO altered lung permeability in the setting of low peak alveolar pressure (control groups). In contrast, L-NAME virtually abolished the change in permeability (deltaKf: PL-Name (0.10 +/- 0.03) vs. PNO [1.75 +/- 1.10] and PE [0.37 +/- 0.11; p <.05]) and the increase in bronchoalveolar lavage 8-isoprostane concentration induced by high-pressure ventilation. Although inhaled NO was associated with the largest change in permeability, no significant difference between the PE and PL-NAME groups was observed. The change in permeability (deltaKf) correlated with bronchoalveolar lavage NOx (r2 =.6; p <.001). L-NAME may attenuate ventilator-induced microvascular leak and lipid peroxidation and NO may contribute to the development of ventilator-induced lung injury. Measurement of NO metabolites in the bronchoalveolar lavage may afford a means to monitor lung injury induced by mechanical stress.

The search for optimal PEEP in acute lung injury (ALI): correlation between intra-abdominal pressure (IAP) and the lower inflection point (Pflex). Results of a pilot study

It is well known that IAPs above 15-20 mmHg increase peak and plateau alveolar pressures. The rise in pressure on the diaphragm causes a pattern of restrictive lung disease with a drop in functional residual capacity and all other lung volumes. Finally this results in diminished chest wall compliance causing difficult ventilation and weaning. The respiratory system can be divided into the chest wall and the lung. Since the diaphragm is coupled to the abdominal wall any increase in IAP may therefore affect chest wall and lung compliance [1]. By calculation of static V-P curves it has been shown in animal and human studies that abdominal and subsequently chest wall compliance goes up after abdominal decompression and this correlates well with the volume recruited [1]. Recent studies looking at compliance in primary and secondary ARDS found that the latter presents with preserved lung but decreased chest wall compliance and PEEP allows to recruit lung units markedly [1,2]. In a previous study we found that in patients with secondary ARDS and raised IAP, PEEP-adjustment for IAP calculated at zero PEEP (ZEEP) resulted in significant better oxygenation at the expense of a significant increase in peak and plateau alveolar pressures but without the risk for early barotrauma [3]. In this pilot study we wanted to sort out if there is a correlation between IAP and Pflex.

Ventilator-associated lung injury.

There is injury caused in numerous animal species when overdistending airway pressure and volume are delivered. The extent of this injury is attenuated by the application of PEEP. Patient case series point to the benefit of LPVS. In randomized controlled trials, the data may appear confusing. However, based on the data from the Amato and colleagues' trial, it seems prudent to employ an LPVS based on the individual patient's lung mechanics. Based on the trials discussed it appears that many have been convinced of the detrimental effects of high peak alveolar pressure. It remains to convince clinicians of the beneficial effects of the use of higher PEEP early in ARDS based on respiratory system mechanics of the individual patient and to use recruitment maneuvers. In conclusion, I concur with Dreyfuss and Saumon and Slutsky and Tremblay that the use of an LPVS may not only attenuate the severity of ARDS by preventing VALI, but may also prevent MODS or attenuate its severity.

Expiratory phase and volume-adjusted tracheal gas insufflation: a lung model study.

To evaluate in a lung model the effects of expiratory-phase tracheal gas insufflation (expiratory-phase TGI) with both volume and pressure control ventilation, and tidal volume-adjusted continuous flow TGI (volume-adjusted TGI) on system pressures and volumes. Single-compartment lung model. Research laboratory in a university medical center. Expiratory-phase TGI was established, using a solenoid valve activated by the ventilator. Volume-adjusted TGI was applied by reducing tidal volume (VT) by the product of TGI flow and inspiratory time. Ventilation was provided with pressure control of 20 cm H2O or volume control ventilation with VT similar to that with pressure control ventilation. A rate of 15 breaths/min and positive end-expiratory pressure (PEEP) of 10 cm H2O were used throughout. Inspiratory time periods of 1.0, 1.5, 2.0, and 2.5 secs were used with TGI flows of 0, 4, 8, and 12 L/min. Lung model compliance (mL/cm H2O) and resistance (cm H2O/L/sec) combinations of 20/20, 20/5, and 50/20 were used. In expiratory-phase TGI with pressure control ventilation, peak alveolar pressure remained constant, PEEP increased (p < .01) and VT decreased (p < .01). In expiratory-phase TGI with volume control ventilation and volume-adjusted TGI, there were significant increases in peak alveolar pressure and PEEP (p < .01). Readjustment of VT in volume-adjusted TGI was impossible with longer inspiratory time (> or = 2 secs) and higher TGI flows (> or = 8 L/min). The marked increases in system pressures and volumes observed with continuous-flow TGI can be avoided with expiratory-phase TGI and volume-adjusted TGI.

HIGH-INFLATION PRESSURE AND POSITIVE END-EXPIRATORY: Injurious to the Lung? Yes

There is a growing body of evidence suggesting that high levels of inflation pressure and high levels of PEEP may be injurious to lung tissue and other organ systems. Limiting peak alveolar pressures below 35 cm H2O may help in avoiding these injuries. The findings have led to the development of a lung-protective strategy that is based on physiologic parameters. This strategy, often using permissive hypercapnia and pressure-limited modes of ventilation, may gain widespread use in the near future. If this strategy reduces barotrauma, a reduction in the length of time on mechanical ventilation and mortality rates can be anticipated. At our center we routinely initiate mechanical ventilation in patients with acute lung injury, using tidal volumes of approximately 6 mL/kg. This may be decreased further if peak alveolar pressures exceed 30 to 35 cm H2O. PEEP is added to maximize alveolar recruitment and oxygenation. Optimal PEEP is located at the inflection point of the respiratory compliance curve. Usually a PEEP of 8 to 12 cm H2O is sufficient. Although we usually initiate mechanical ventilation with a volume-cycled mode, we are not hesitant to switch rapidly to a pressure-limited mode if results are unsatisfactory. We believe that more attention to the potential harmful effects of pressure and volume on lung architecture may result in further improvement of survival in patients with acute respiratory failure.

Tracheal gas insufflation-pressure control versus volume control ventilation. A lung model study.

Tracheal gas insufflation (TGI) has been recommended as an adjunct to mechanical ventilation in the presence of elevated Pa CO2. Based on our initial clinical experience with continuous flow TGI and pressure control ventilation (PCV), we were concerned about elevation in peak airway pressure as TGI was applied. In a lung model, we evaluated the effects of continuous flow TGI during both PCV and volume control ventilation (VCV). A single compartment lung model was configured with an artificial trachea into which an 8-mm endotracheal tube was positioned. TGI was established with a 16-G catheter positioned 2 cm beyond the tip of the endotracheal tube. Ventilation was provided by a Puritan-Bennett 7200ae ventilator with PCV 20 cm H2O or VCV with a tidal volume (VTt) similar to that with PCV. A rate of 15 breaths/min and PEEP of 10 cm H2O were used throughout. Inspiratory times (TI) of 1.0, 1.5, 2.0, and 2.5 s were used with TGI of 0, 4, 8, and 12 L/min. Lung model compliance (ml/cm H2O) and resistance (cm H2O/L/s) combinations of 20/20, 20/5, and 50/20 were used. Auto-PEEP, VT, and peak alveolar and airway opening pressures increased as TGI and Ti increased, regardless of lung mechanics settings (p<0.01). All increases were greater with VCV than PCV (p<0.05). Continuous flow TGI with both PCV and VT-uncorrected VCV may result in marked increases in Vt and system pressures, especially at long TI.

Current Status of New Modes of Mechanical Ventilation

Current approaches to managing patients requiring ventilatory support have focused on a lung protective strategy. This approach limits peak alveolar pressure and tidal volume, and allows hypercapnia. Although hypercapnia is tolerated by many patients, in some the acute acidosis markedly complicates clinical management. Tracheal gas insufflation (TGI) has been designed as an adjunct to conventional ventilation to decreasePaCO2. Although no commercial TGI systems are available, TGI holds great promise and can be expected to be available comercially in the future. Pressure ventilation has become the ventilatory approach of the 1990s, whether pressure support or pressure control. However, problems associated with varying tidal volumes have resulted in manufacturers developing ventilatory modes that combine the beneficial effects of both pressure and volume ventilation.

Implications of a biphasic two-compartment model of constant flow ventilation for the clinical setting

Purpose: To investigate the theoretical effects of changing frequency (ƒ), duty cycle (D), or end-inspiratory pause length on the distribution of ventilation and compartmental pressure in a heterogeneous, two compartment pulmonary model inflated by constant flow. Methods: Differential equations governing compartmental volume changes were derived and solved. Validation was conducted in a mechanical lung analogue with two mechanically independent compartments. Model predictions were then generated over wide ranges of ƒ, D, or end-inspiratory pause. Results: Disparity of compartmental end-expiratory pressure was identified as the primary mechanism by which changes in f, D, or pause alter the distribution of ventilation. Distribution of peak pressures was less sensitive to such changes. Compartmental ventilation was much less uniform than compartmental peak pressure. Ventilation could not be made entirely uniform by changes of f, D, or pause within the usual clinical range. Conclusions: In a linear, two compartment model of the respiratory system, disparity of compartmental end-expiratory pressures is the primary mechanism by which changes of ƒ, D, or pause alter the distribution of ventilation during inflation with constant flow. Ventilation is less evenly distributed than peak alveolar pressure, and there are limits to the beneficial effects on the distribution of ventilation to be gained from manipulations of machine settings.

Tracheal tube resistance and airway and alveolar pressures during mechanical ventilation in the neonate

The relationship between peak airway pressure, alveolar pressure and respiratory frequency was calculated for the range of compliances and airway resistances which might be encountered during mechanical ventilation of a 3-kg neonate. The pressure/flow relationships of 2.5, 3.0, 3.5 and 4-mm tracheal tubes were determined at a series of flows from 0.5 to 4 litres/minute. Peak airway and alveolar pressures were then measured at various frequencies and inspiratory:expiratory ratios with the tubes incorporated in a model lung. Large differences between peak airway and alveolar pressures developed when frequency was increased or inspiratory time decreased; the differences were greatest with the smaller tubes. Shortening expiratory time by increasing the frequency or altering the inspiratory:expiratory ratio resulted in increased end-expiratory pressure because of incomplete emptying of the lung.

180 AIRWAY AND ALVEOLAR PRESSURES IN VENTILATED, ABNORMAL LUNGS

To describe the relations, during mechanical ventilation(CPPB), of airway pressure(AP) and its mean value(MAP) to alveolar pressure(ALP) and its mean value(MALP) in the diseased lung, 19 infant lambs were subjected to controlled, volume regulated CPPB at inspiratory(I) times of 25 and 50%, and at 0 to 11mmHg positive end-expiratory pressure(PEEP), under conditions of fixed inspiratory airflow. To estimate ALP, static recoil pressure was determined by airway occlusion once every 10th breath, at a time in the respiratory cycle that was varied from trial to trial. From measured occlusion times, AP and ALP, real time AP and ALP curves were generated representing one respiratory cycle; MAP and MALP were calculated by integration; and the contribution to MALP of airway resistance (MALPr) was estimated from %I, PEEP, peak ALP and MALP. After control determinations, 10 lambs received oleic acid (OA-.15 ml/kg) and 9 received propranalol and serotonin(S) all pressures mmHg, x±sem, †p<.05 vs control *p<.01 vs control Both OA and S increased airway resistance (Raw) and reduced both thoracic compliance(Ct) and arterial pO2. Proximal mean airway pressure was an accurate and precise estimator of mean alveolar pressure both in normal and in abnormal lungs, in spite of elevated airway, resistance.

179 PROXIMAL AIRWAY AND AVEOLAR PRESSURES DURING MECHANICAL VENTILATION

During continuous positive pressure breathing(CPPB), proximal airway pressure(AP) and its mean value(MAP) reflect lung distending pressure, although their relationships to alveolar pressure (ALP) and its mean value(MALP) await definition. 10 infant lambs, under chloralose anesthesia and pancuronium bromide, were subjected to volume regulated, time cycled CPPB under conditions of constant inspiratory airflow. To estimate ALP, static recoil pressure was determined by interruption of airflow once every 10th breath, at a time in the respiratory cycle that was varied from trial to trial. From determinations of occlusion time, AP and ALP, real time AP and ALP curves were generated representing one respiratory cycle; MAP and MALP were calculated by integration; and the contribution to MALP of airway resistance(MALPr) was estimated from inspiratory(I) time, positive end-expiratory pressure(PEEP), peak ALP and MALP. Curves were generated at 25 and 50%, I, and at levels of PEEP between 0 and 11 mmHg. Due to airway resistance, AP exceeded ALP in inspiration and ALP exceeded AP over much of expiration(E). Yet airway resistance contributed little to MALP. Over the range of PEEP applied, and at both %I, proximal mean airway pressure was an accurate and precise estimator of mean alveolar pressure.

Respirator design

Design of an artificial respirator involves careful selection of a number of controlling parameters and correct timing of oxygen supply. The paper reviews the significance of the various controlling parameters, such as peak alveolar pressure, dead space, input waveform and ins-piratory and expiratory times, etc., their selection and computation method. Requirements as regards the timing of oxygen supply in conformity with patient&apos;s changing condition are brought out and a scheme for fulfilling them is discussed broadly.

A theoretical study of controlled ventilation.

This paper is a theoretical study of controlled ventilation with a respirator. An electric circuit analog of the respiratory system is used with respiratory parameters of the normal adult. Deleterious effects of positive pressure ventilation are considered and related to the model. The effects considered include peak alveolar pressure and its time of occurrence, work, and average alveolar pressure. Different pressure waveforms are used as the driving source for the respirator model. These waveforms are rectangle, ramp, negative ramp, sine, and exponential.

Relation of Increased Airway Resistance to Breathing Work and Breath Velocity and Acceleration Patterns With Maximum and Near Maximum Breathing Effort

The oxygen cost of breathing, mechanical work done in breathing, efficiency of breathing and breath patterns have been studied at various resistance levels with maximum breathing effort. With the chest-lung complex considered as a machine for doing external work, it was observed that mechanical efficiencies increased with increasing airway resistance, to a point, after which they fell off. When the oxygen cost was corrected for work done on the chest-lung complex, efficiencies were observed to decrease with increasing airway resistance. Breath acceleration patterns were observed to provide a more sensitive appraisal of changes in the movement of the breath than either breath volume or velocity patterns. External work output increased with increasing external resistance only to a point, after which it decreased. At low resistance levels, work output was contraction speed limited and at high resistance levels it was contraction force limited. With maximum effort at all resistance levels oxygen consumption appeared to be constant. Data are also presented as peak alveolar pressure, breath velocity and change in functional residual capacity. Inspiratory breath phase percentage increased to more than half the cycle length with increasing airway resistance. Submitted on March 18, 1958