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(Chest. 1999;116:1826-1832.)
© 1999 American College of Chest Physicians

Exacerbation of Acute Pulmonary Edema During Assisted Mechanical Ventilation Using a Low-Tidal Volume, Lung-Protective Ventilator Strategy*

Richard H. Kallet, MS, RRT; James A. Alonso, RRT; John M. Luce, MD, FCCP and Michael A. Matthay, MD, FCCP

* From the Departments of Anesthesia (Drs. Luce and Matthay, Mr. Kallet, and Mr. Alonso) and Medicine (Drs. Luce and Matthay), University of California, San Francisco, at San Francisco General Hospital, San Francisco, CA; and Cardiovascular Research Insitute (Mr. Kallet, Mr. Alonso, and Dr. Matthay), University of California, San Francisco, San Francisco, CA.

Correspondence to: Richard H. Kallet, MS, RRT, Clinical Research Coordinator, Department of Anesthesia, San Francisco General Hospital Room NH:GA-2, 1001 Potrero Ave, San Francisco, CA 94110; e-mail: rkallet{at}sfghsom.ucsf.edu


   Abstract
TOP
 Abstract
Introduction
 Case Report
 Materials and Methods
 Results
 Discussion
 References
 
Study objectives: To assess the magnitude of negative intrathoracic pressure development in a patient whose pulmonary edema acutely worsened immediately following the institution of a low-tidal volume (VT) strategy.

Design: Mechanical lung modeling of patient-ventilator interactions based on data from a case report.

Setting: Medical ICU and laboratory.

Patient: A patient with suspected ARDS and frank pulmonary edema.

Interventions: The patient’s pulmonary mechanics and spontaneous breathing pattern were measured. Samples of arterial blood and pulmonary edema fluid were obtained.

Measurements: A standard work-of-breathing lung model was used to mimic the ventilator settings, pulmonary mechanics, and spontaneous breathing pattern observed when pulmonary edema worsened. Comparison of the pulmonary edema fluid-to-plasma total protein concentration ratio was made.

Results: The patient’s spontaneous VT demand was greater than preset. The lung model revealed simulated intrathoracic pressure changes consistent with levels believed necessary to produce pulmonary edema during obstructed breathing. A high degree of imposed circuit-resistive work was found. The pulmonary edema fluid-to-plasma total protein concentration ratio was 0.47, which suggested a hydrostatic mechanism.

Conclusion: Ventilator adjustments that greatly increase negative intrathoracic pressure during the acute phase of ARDS may worsen pulmonary edema by increasing the transvascular pressure gradient. Therefore, whenever sedation cannot adequately suppress spontaneous breathing (and muscle relaxants are contraindicated), a low-VT strategy should be modified by using a pressure-regulated mode of ventilation, so that imposed circuit-resistive work does not contribute to the deterioration of the patient’s hemodynamic and respiratory status.

Key Words: acute pulmonary edema • assisted mechanical ventilation • lung model • lung-protective ventilation strategy • work of breathing


   Introduction
TOP
 Abstract
 Introduction
Case Report
 Materials and Methods
 Results
 Discussion
 References
 
Some have suggested limiting tidal volume (VT) delivery to 6 mL/kg to avoid ventilator-induced lung injury in patients with ARDS.1 2 3 However, during assisted mechanical ventilation (AMV), a low-VT strategy limits both the peak and mean inspiratory flow rates (I), which can lead to patient-ventilator dyssynchrony.4 Inappropriate I settings that do not meet or exceed patient I demand cause an increased breathing effort and more negative swings of intrathoracic pressure.5

Limiting pulmonary edema is another therapeutic objective in the treatment of ARDS. Damage to the capillary endothelium and alveolar epithelium in ARDS results in a permeability pulmonary edema from leakage of protein-rich plasma into the interstitial and alveolar spaces, thus reducing the protein osmotic gradient opposing edema formation.6 Subsequently, the magnitude of pulmonary edema formation depends primarily on the pressure gradient between the microvascular and perimicrovascular space.7 Excessive fluid administration in ARDS will aggravate pulmonary edema by increasing the pulmonary microvascular pressure and the transvascular pressure gradient.8 9 Likewise, high negative intrathoracic pressure swings, associated with upper airway obstruction, may lead to hydrostatic pulmonary edema by raising the transvascular pressure gradient.10

During AMV in the volume control mode, I and VT settings that do not exceed patient I and VT demand results in imposed resistive work of breathing (WOB).4 This may mimic the cardiothoracic relationships present during partial upper airway obstruction, and result in a widening hydrostatic pressure gradient. Therefore, patient-ventilator dyssynchrony could aggravate pulmonary edema and gas exchange dysfunction in patients with ARDS. We encountered a patient with suspected ARDS in whom pulmonary edema was exacerbated by the institution of a low-VT ventilation strategy during AMV. We measured the pulmonary mechanics and breathing pattern of the patient, and collected a sample of pulmonary edema fluid. By using a standard WOB lung model, we provide evidence that using a set VT slightly lower than patient demand during AMV can result in negative intrathoracic pressure swings sufficient to account for the exacerbation of pulmonary edema in this case.


   Case Report
TOP
 Abstract
 Introduction
 Case Report
Materials and Methods
 Results
 Discussion
 References
 
A 26-year-old man presented to the emergency department with severe tonsillitis and a temperature of 103°F. His previous medical history was significant only for adrenal insufficiency, for which he had been noncompliant with glucocorticoid therapy. The patient was in severe respiratory distress with a BP of 70/30 mm Hg (mean, 43 mm Hg). A chest radiograph revealed bilateral infiltrates. During emergent endotracheal intubation, the patient suffered cardiovascular collapse and required high doses of dopamine, phenylephrine, and epinephrine to maintain a systolic BP of 70 mm Hg. Within a 1-h period, the patient also received 7 L of normal saline. Treatment with clindamycin and cefuroxime, in addition to dexamethasone and methylprednisolone, was initiated.

On arrival in the ICU, the patient was placed on a Dräger E-1 ventilator (Dräger, Inc/Critical Care Systems; Telford, PA) in the pressure control mode, with a fraction of inspired oxygen (FIO2) of 1.0 and a positive end-expiratory pressure (PEEP) of 10 cm H2O. Fentanyl, midazolam, and propofol drips were required to maintain patient-ventilator synchrony. A repeat chest radiograph showed progressive, diffuse bilateral infiltrates, and moderate amounts of pulmonary edema fluid were aspirated during suctioning. Diuretics were administered; fluid balance 10 h later was positive 5 L. By this time, the PaO2/FIO2 had improved from 141 to 322, respiratory system compliance (CRS) increased from 17 to 67 mL/cm H2O, and pulmonary edema fluid was no longer present in the endotracheal tube aspirate. The patient was ventilated in the volume control (VC) mode because of his improving pulmonary status.

However, the patient’s pulmonary status again deteriorated despite relative cardiovascular stability and no change in total fluid balance. The PaO2/FIO2 fell to 128, and CRS decreased to 36 mL/cm H2O. This coincided with a temperature elevation to 39°C. Concurrently, the patient was enrolled into the National Institutes of Health ARDS Network study of mechanical ventilation and randomized to a lung-protective strategy requiring use of the VC mode. An attempt was made to reduce the VT from 580 mL (11.1 mL/kg) to 450 mL (7.4 mL/kg). As the patient was triggering the ventilator, the respiratory frequency (f) was increased to 35 breaths/min and the peak I was raised to 110 L/min to compensate for the decrease in VT. Trigger sensitivity was increased from -2 to -1 cm H2O.

Within 10 min, the pulse oximeter estimate of arterial oxygen saturation (SpO2) had decreased from 94% on an FIO2 of 0.50 and a PEEP of 10 cm H2O to 79% on an FIO2 of 0.70 and a PEEP of 10 cm H2O. The patient was triggering the ventilator at an f of 40 breaths/min, and dyssynchrony was apparent by a "saw-tooth" airway pressure waveform (ie, during inspiration, the airway pressure waveform had alternating negative deflections and positive inflections). Physical examination of the patient’s ventilatory pattern revealed pronounced inspiratory effort throughout the inspiratory phase. Despite 10 cm H2O PEEP, copious amounts of frothy, serosanguineous, pulmonary edema fluid suddenly filled the ventilator tubing. The heart rate rose to 128 beats/min, and the mean BP decreased to 56 mm Hg. The VT was increased to 600 at an f of 35 breaths/min. The patient quickly became synchronous with the ventilator and ceased triggering breaths within a few minutes. Within 10 min, the SpO2 rose to 100% and pulmonary edema fluid no longer accumulated in the ventilator tubing. A sample of pulmonary edema fluid was obtained using the method described below.

After 30 min of stabilization, the patient’s pulmonary mechanics and spontaneous breathing pattern were measured in order to assess the prudence of pursuing a lung-protective ventilator strategy. During a period of controlled ventilation, CRS was found to be 33 mL/cm H2O and the airways resistance was 13 cm H2O/L/s (measured at 60 L/min square-wave inspiratory flow pattern). The ventilator then was set at an FIO2 of 1.0 for 10 min, followed by a brief period (approximately 30 s) of continuous positive airway pressure (CPAP) at 10 cm H2O. The patient immediately began to breathe at an f of 35 breaths/min and a VT of 500 mL. The flow waveform graphics on the ventilator displayed the patient’s flow pattern as a fast rising half sine, with a peak I of approximately 60 L/min and an inspiratory:expiratory ratio of approximately 1:1. SpO2 remained stable at 98% during spontaneous breathing.

The VC mode was reinstituted, and oxygenation remained stable. On the next day, the patient’s BP improved so that the level of sedation could be increased, allowing the VT to be decreased to 6 mL/kg without provoking spontaneous inspiratory efforts. Over the next several days, fluid intake and output were balanced, and the patient’s pulmonary gas exchange function markedly improved. The patient was weaned to CPAP 6 days after intubation, and was successfully extubated 2 days later. Hospital discharge followed 5 days later.


   Materials and Methods
TOP
 Abstract
 Introduction
 Case Report
 Materials and Methods
Results
 Discussion
 References
 
Pulmonary Edema Fluid Collection and Analysis
Once the patient’s SpO2 had stabilized at a VT of 600 mL, the airway was suctioned for pulmonary edema fluid using a previously described method.10 Arterial blood was obtained for comparison of pulmonary edema fluid protein concentration to plasma protein concentration. Measurement of the total protein in the pulmonary edema fluid and plasma samples was done by the biuret and bromcresol green dye-binding technique.11 Measurement of the total protein concentration in the edema fluid and the plasma correctly characterizes the type of pulmonary edema that results from either hydrostatic or increased permeability.12

Lung Model Study
Because an esophageal balloon was not in place at the time pulmonary edema developed, we reproduced the ventilator settings, pulmonary mechanics, and spontaneous breathing pattern of the patient with a lung model to estimate the intrathoracic pressure swings that may have occurred. A standard WOB lung model based on the design of Katz and colleagues13 was used to recreate the observed patient-ventilator interactions (Fig 1 ). A Dräger E-1 ventilator and a Hamilton Veolar (Hamilton Medical, Inc; Reno, NV) ventilator were attached to separate ports of a Vent AID Training Test Lung (Michigan Instruments, Inc; Grand Rapids, MI). Two 32-cm long, 7.0-mm inner-diameter endotracheal tubes with 15-mm adapters at both ends were used to connect each ventilator to the lung compartment of the model (Fig 1) . Both compartments were connected by a bar so that one ventilator acted as the patient’s inspiratory muscles and the other as the patient’s thorax. The positive pressure created during inflation of the muscle pump created a corresponding negative pressure in the thorax. The rate of change in pressure, flow, and displacement of the thoracic unit was used as an analog for the performance of the inspiratory muscles.



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  		Figure 1.. Standard WOB lung model based on the design of Katz and colleagues.13

 
The Dräger E-1 was adjusted to the ventilator settings that were used when pulmonary edema developed. The Veolar ventilator was used to reproduce the spontaneous breathing pattern documented shortly after the incident of alveolar pulmonary edema. The Veolar was set in the VC mode incorporating a modified sine wave that approximated the inspiratory flow waveform profile and rise time percentages documented both in normal humans and in those with diseases characterized by increased elastic recoil.14 15 Measurements made from scalar tracings of the modified sine flow waveform revealed that peak I occurred at approximately 25% of the inspiratory phase. An inspiratory resistor (Rp5; Michigan Instruments, Inc; Grand Rapids, MI) was added to both endotracheal tubes in order to achieve an airways resistance of 13 cm H2O/L/s (measured at 60 L/min square-wave inspiratory flow pattern). The f on the Veolar was set at 40 breaths/min with an inspiratory duty cycle of 0.40. Preset VT was adjusted to created a VT demand of 500 mL and a peak I of 60 L/min on the thoracic compartment. Inspiratory time was confirmed by measurement of the inspiratory flow profile from a calibrated scalar tracing. Both ventilators were set at a PEEP of 10 cm H2O so that the end-expiratory compartment volumes were equal.

Changes in simulated thoracic pressure and airway pressure (Paw) were measured using an automated pulmonary mechanics monitor (Bicore CP-100; Allied Healthcare Products, Inc—Ventilation Products; Riverside, CA). Validation of this monitor has been previously documented.16 17 The monitor and sensors were electronically calibrated prior to the study. Both Paw and I were measured at the wye-adapter with the VarFlex flow transducer. The imposed WOB from the inspiratory valve of the ventilator was measured at the wye-adapter with a SmartCath neonatal extension attached to the patient pressure monitoring port of the Bicore. The maximal negative pressure developed in the thoracic compartment ({Delta}Pt) was used as an approximation of the peak effort of the inspiratory muscles. {Delta}Pt was measured with a SmartCath neonatal extension tube connected to a pressure tap into the thoracic compartment of the model.

The pulmonary mechanics monitor calculated VT from flow and time measurements and excluded circuit compression volume. Because we were primarily interested in the effects of patient-ventilator interactions on intrathoracic pressure changes, we expressed WOB as the pressure-time product (PTP). The pulmonary mechanics monitor calculated PTP as the integral of the negative changes in Pt during inspiration, taking into account inspiratory time and assuming normal chest wall compliance. {Delta}Pt, or peak inspiratory effort, was measured by the pulmonary mechanics monitor as the negative change in pressure from the end-expiratory pressure plateau to the minimum value. The data from 10 consecutive breaths were averaged and used for analysis.


   Results
TOP
 Abstract
 Introduction
 Case Report
 Materials and Methods
 Results
Discussion
 References
 
Pulmonary Edema Fluid Analysis
The pulmonary edema fluid-to-plasma total protein concentration ratio was 0.47. Initial ratios < 0.65 are characteristic of hydrostatic pulmonary edema, whereas initial ratios between 0.75 and 1.0 are characteristic of increased-permeability pulmonary edema.12 The pulmonary edema fluid-to-plasma total protein ratio found in this case was in the range recently reported during postobstructive pulmonary edema.10

Lung Model
Re-creation of the patient-ventilator interactions with the lung model resulted in a mean ± SD {Delta}Pt of 35 ± 0 cm H2O per breath with a PTP of 535 ± 12 cm H2O/s/min. The mean inspiratory pressure per breath (PTP ÷ f) was 12.4 ± 0.3 cm H2O. Inspection of the scalar Paw tracings revealed the same saw-tooth pattern seen during the episode of alveolar pulmonary edema (Fig 2 ). The contribution of imposed work from the inspiratory valve was assessed from measurements of the negative {Delta} Paw and PTP taken at the wye-adapter. These results were a {Delta}Paw of 22 ± 0 cm H2O with an imposed PTP of 130.6 ± 4.5 cm H2O/s/min. To put this in perspective, a mean total PTP of 150 cm H2O/L/s has been reported in patients recovering from acute respiratory failure and breathing on CPAP.18 An imposed PTP value that is 87% of the total value for patients being weaned from mechanical ventilation represents a high degree of imposed WOB.



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  		Figure 2.. Scalar tracings of I (flow), VT, Paw, and simulated intrathoracic pressure recorded from the lung model using the patient’s spontaneous breathing pattern and the ventilator settings measured around the time that pulmonary edema developed. The saw-tooth appearance of the Paw waveform reflects the following events: a represents the initial drop in Paw associated with simulated patient effort to trigger the ventilator into inspiration; b represents the rapid rise in Paw as ventilator I delivery exceeds simulated I demand; c represents a secondary drop in Paw as simulated patient effort continues after VT delivery; and d represents the secondary rise in Paw with the cessation of simulated effort and the cycling of the ventilator into expiration. The pressure spike above PEEP reflects initial expiratory valve resistance at peak expiratory flow.

 

   Discussion
TOP
 Abstract
 Introduction
 Case Report
 Materials and Methods
 Results
 Discussion
References
 
We have reported a case in which exacerbation of acute pulmonary edema coincided with the institution of a lung-protective strategy. The fact that pulmonary edema quickly appeared and resolved with the institution and removal of a low-VT ventilation strategy led us to suspect that vigorous inspiratory efforts were responsible for the sudden deterioration in the patient’s cardiorespiratory status. This impression was supported by the fact that the patient had been consistently triggering the ventilator at a higher VT for several hours prior to the event. During that time period, there was no pulmonary edema fluid in the tracheal aspirate, nor was there further deterioration in CRS (CRS, 39 mL/cm H2O prior to the onset of pulmonary edema, and 24 mL/cm H2O in the hours following the episode).

We recently demonstrated in a lung model that imposed resistive work in the VC mode increases exponentially when VT demand equals or exceeds VT delivery.4 Conscious of this fact, we attempted to compensate by using a very high I (110 L/min) and increasing the trigger sensitivity. However, respiratory distress and pulmonary edema developed despite the fact that the patient appeared capable of generating a spontaneous peak I of only 60 L/min. We believe that if a patient’s VT demand is higher than preset VT, then high initial peak I delivery alone may not be sufficient to prevent respiratory distress because inspiratory effort will continue beyond the ventilator-delivered VT. This point was illustrated in the lung model when the I and VT waveforms for the ventilator and simulated patient are superimposed (Fig 3 ).



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  		Figure 3.. Figure 3 . Scalar tracings of I, VT, Paw, and simulated intrathoracic pressure recorded from the lung model superimposing the simulated patient’s spontaneous breathing pattern (measured on CPAP on ventilator pattern in AMV in the VC mode). The I waveforms show the continuation of simulated patient effort beyond ventilator I delivery. The slope of the rise in ventilator delivered VT exceeds that of the simulated patient VT because of the higher peak I and square-wave delivery pattern. However, by the end of inspiration, spontaneous VT exceeds the ventilator-delivered VT. The saw-tooth appearance of the Paw waveform results from the interactions of I and VT performance between the ventilator and simulated patient demand. The differences in Paw over the course of inspiration reflect the changing characteristics of imposed resistive work during AMV and the difference in trigger levels (-1 cm H2O set during AMV and a built-in trigger level of -0.2 cm H2O during CPAP). Note that the rapid rise in Paw above baseline after the onset of ventilator-delivered I was not reflected in the pressure changes in the thoracic compartment. In addition, an intrathoracic pressure plateau below baseline is noted when I demand continues past ventilator I delivery.

 
We reasoned that imposed resistive work from the inspiratory valve of the ventilator produces the same breathing conditions that occur during partial upper airway obstruction. There has been speculation regarding the transpulmonary pressure changes necessary to produce pulmonary edema during upper airway obstruction.19 20 21 22 Both Galvis et al19 and Younker et al21 speculated that negative pleural pressures of >= 30 cm H2O may occur during upper airway obstruction resulting in pulmonary edema. Newton-John20 reported mean, peak-negative, intratracheal pressure swings of 37 cm H2O in an infant with severe croup. He believed that these negative pressure swings could account for at least the development of interstitial pulmonary edema.20 Stalcup and Mellins23 reported mean negative intraesophageal pressures of 29 cm H2O during tidal breathing and 39 cm H2O during forced inspiration in children with severe asthma. However, because of the emergent nature of upper airway obstruction, there have been no reports in the literature in which intrathoracic pressures have been measured under conditions severe enough to produce pulmonary edema. To address this, Loyd and colleagues24 measured lung lymph flow and lymph-to-plasma protein concentration ratio during resistive breathing in an animal model. Inspiratory resistive loads of 20 cm H2O caused a decrease in mean central Paw of 12 cm H2O. In normal sheep lungs, this was enough to cause a twofold increase in lung lymph flow and a decrease in lymph-to-plasma protein concentration ratio.24 These results suggest that increasingly negative intrathoracic pressure resulting from mild obstructive breathing is sufficient to cause an increase in the transvascular hydrostatic pressure gradient with resulting fluid extravasation. Our lung model provided an approximation of the intrathoracic pressure swings that might have occurred during the development of pulmonary edema. Our results are similar to both the clinical20 23 and laboratory24 measurements of mean and peak transpulmonary pressure gradients suggested as being sufficient to produce fluid extravasation24 and pulmonary edema during obstructive breathing.19 21

Our patient was more susceptible to developing pulmonary edema during a low-VT ventilation strategy because of fluid overload, possible pulmonary hypertension from large infusions of phenylephrine and epinephrine, and possible sepsis-induced acute lung injury. As Stalcup and Mellins23 observed, the effects of vigorous fluid therapy on transvascular hydrostatic pressure in the development of pulmonary edema can be potentiated by more negative pleural pressure swings.

The significance of this report is that careful assessment of a patient’s spontaneous VT capacity must be taken into consideration before a low-VT strategy is employed. This becomes especially important if high sedation or neuromuscular blocking agents cannot be used to suppress spontaneous breathing efforts. We refrained from increasing sedation and using neuromuscular blockade in our patient because of persistent hypotension (despite high-dose vasopressor support) and concurrent glucocorticoid therapy. In this situation, a low-VT strategy using a pressure-regulated mode of ventilation may either have prevented or attenuated the exacerbation of pulmonary edema. Preliminary lung model results have demonstrated that both pressure-control ventilation and VC-autoflow ventilation reduce WOB compared with VC ventilation because of their ability to augment both I and VT when patient demand for both increases.25 The ability of pressure-regulated modes to augment both I and VT delivery reduces simulated negative intrathoracic pressure swings4 25 and, therefore, should reduce the pulmonary transvascular pressure gradient favoring pulmonary edema formation. Therefore, we recommend the use of a pressure-regulated mode of ventilation during use of a low-VT strategy in ARDS when spontaneous breathing efforts cannot be adequately suppressed with sedation and neuromuscular blockade must be avoided.

The fact that gross pulmonary edema occurred in this case most likely resulted from the combination of acute lung injury, fluid overload, and probable pulmonary hypertension. However, this case serves as a salient reminder that spontaneous breathing efforts during ARDS may enhance pulmonary edema and worsen gas exchange. This deterioration may be mistakenly attributed to either fluid therapy or a worsening of the patient’s disease process. Therefore, spontaneous breathing efforts during mechanical ventilation in ARDS should be evaluated clinically in the same manner as fluid therapy, because both factors are important in determining the transvascular hydrostatic pressure gradient responsible for pulmonary edema.


   Footnotes
 
Abbreviations: AMV = assisted mechanical ventilation; CPAP = continuous positive airway pressure; CRS = respiratory system compliance; f = respiratory frequency; FIO2 = fraction of inspired oxygen; Paw = airway pressure; PEEP = positive end-expiratory pressure; {Delta}Pt = maximal negative pressure developed in the thoracic compartment; PTP = pressure-time product; SpO2 = pulse oximeter estimate of arterial oxygen saturation; VC = volume control; I = inspiratory flow rate; VT = tidal volume; WOB = work of breathing

Received for publication February 17, 1999. Accepted for publication July 15, 1999.


   References
TOP
 Abstract
 Introduction
 Case Report
 Materials and Methods
 Results
 Discussion
 References
 

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