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1 Department of Biomedical Engineering, Boston University, Boston 02215; and 2 Pulmonary Division, 3 Department of Anesthesia, Perioperative and Pain Medicine, and 4 Division of Thoracic Surgery, Brigham and Women's Hospital, Boston, Massachusetts 02115
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
APPENDIX
REFERENCES
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Frequency-dependent characteristics of lung resistance (RL) and elastance (EL) are sensitive to different patterns of airway obstruction. We used an enhanced ventilator waveform (EVW) to measure inspiratory RL and EL spectra in ventilated patients during thoracic surgery. The EVW delivers an inspiratory flow waveform with enhanced spectral excitation from 0.156 to 8.1 Hz. Estimates of the coefficients in a trigonometric approximation of the EVW flow and transpulmonary pressure inspirations yielded inspiratory RL and EL spectra. We applied the EVW in a group with mild obstruction undergoing various thoracoscopic procedures (n = 6), and another group with severe chronic obstructive pulmonary disease undergoing lung volume reduction surgery (n = 8). Measurements were made at positive end-expiratory pressure (PEEP) of 0, 3, and 6 cmH2O. Inspiratory RL was similar in both groups despite marked differences in spirometry. The chronic obstructive pulmonary disease patients demonstrated a pronounced frequency-dependent increase in inspiratory EL consistent with severe heterogeneous peripheral airway obstruction. PEEP appears to have beneficial effects by reducing peripheral airway resistance. Lung volume reduction surgery resulted in increased inspiratory RL and EL at all frequencies and PEEPs, possibly due to loss of diseased lung tissue, pulmonary edema, increased mechanical heterogeneity, and/or an improvement in airway tethering.
positive end-expiratory pressure; chronic obstructive pulmonary disease; inspiratory lung resistance; inspiratory lung elastance; enhanced ventilator waveform
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
APPENDIX
REFERENCES
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CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD) is characterized by both intrinsic airway obstruction (bronchitis) and parenchymal tissue destruction (emphysema). The compromise in lung function in this disease is often slow and progressive. Traditional therapeutic measures for both early- and late-stage COPD consist of beta agonists and anticholinergics for the relief of bronchospasm, corticosteroids for controlling airway inflammation, antibiotics for treatment of infectious exacerbations, and supplemental oxygen to improve hypoxemia. Usually these approaches offer only mild improvement in symptoms and clinical outcomes.
Recently, several investigators have advocated the use of low-level positive end-expiratory pressure (PEEP) in patients suffering from acute exacerbations of COPD (5, 11, 14, 35), with the goal of prevention of atelectasis and/or small airway closure. Extrinsic PEEP may also counterbalance intrinsic PEEP and unload the inspiratory muscles during assisted modes of ventilation. Even more recently, there has been a resurgence of interest in the use of lung volume reduction surgery (LVRS) for the treatment of severe emphysema (1, 4, 19). Although different approaches to LVRS have been developed, their common goal is the removal of the most diseased portions of the lung, allowing less diseased areas to expand and develop greater elastic recoil pressures. In addition to an improvement in driving pressure, the decompression of healthier lung tissues results in increased radial traction on the airways, which helps maintain their caliber during expiration. As a result, LVRS can potentially increase expiratory airflow (19).
There are major limitations in quantifying the degree of functional impairment in patients with COPD, with most techniques relying on spirometric indexes or measurements of dynamic lung resistance (RL) and lung elastance (EL) at a single frequency. Such information can be misleading in patients with COPD. For example, reduced forced expiratory flows may result from either bronchitic airway obstruction or premature airway collapse due to emphysematous tissue destruction. In addition, alterations in dynamic RL and EL may reflect changes in airway caliber, alterations in parenchymal tissue integrity, or serial and parallel time-constant heterogeneity. Thus these traditional measurement indexes lack specificity in localizing disease processes or gauging the effectiveness of medical or surgical interventions.
Several studies from our group have shown that the frequency-dependent features of RL and EL over low frequencies (0.1-10 Hz) are specific to particular patterns of airway obstruction (20, 22-24). For example, when there is large and homogeneous peripheral airway obstruction, RL will be increased uniformly throughout this bandwidth. The EL will be unaffected below 1 Hz but will demonstrate positive frequency dependence above 1 Hz because of the shunting of air flow into the central airway walls (27). Thus EL at higher frequencies will reflect the mechanical properties of the airway walls (23, 24, 27, 31). With mild heterogeneous airway obstruction in which a few closed airways occur randomly throughout the lung periphery, both RL and EL will demonstrate substantial elevations in frequency dependence below 1 Hz (23).
The most direct way to determine such RL and EL spectra is through measures of pulmonary impedance (ZL), the complex ratio of transpulmonary pressure to flow at the airway opening. However, the measurement of ZL in ventilated patients is difficult, especially in patients with severe airway obstruction. For example, the measurement of ZL using forced oscillations or random noise near breathing frequencies requires the suspension of ventilatory support (30). Moreover, its physiological interpretation is difficult in the presence of highly nonlinear phenomena such as dynamic airway compression and flow limitation (34). Whereas expiratory flow limitation is a central feature of the pathophysiology in COPD and a major contributor to the functional compromise in such patients, it is nonetheless a highly nonlinear phenomenon in which flow is no longer related to the pressure drop across the airways (17, 18, 28, 34). Thus any linear description of lung mechanics in these patients (i.e., transfer function approximation) must be restricted to pressure and flow data in which such nonlinearities are known to be minimal, such as inspiration (1, 21, 28).
In a recent study (21), we introduced an enhanced
ventilator waveform (EVW) to measure inspiratory lung impedance
(Z
In the present study, we applied the EVW to anesthetized,
paralyzed patients to obtain accurate measurements of
Z
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
APPENDIX
REFERENCES
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Patients.
Measurements were made on 14 patients undergoing elective thoracic
surgery (Table 1). Patients consisted of
a control group of six patients with mild obstruction or normal lung
function [forced expiratory volume in 1 s (FEV1) = 86 ± 18% predicted] undergoing thoracoscopic surgery and
eight patients with severe COPD (FEV1 = 26 ± 9%
predicted) undergoing LVRS. The protocol was approved by the
appropriate institutional research committees, and informed consent was
obtained from each patient.
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Experimental measurements.
The details of the EVW measurements have been previously described
(21). Briefly, the flow pattern of the EVW inspiration consists of a rectified sine wave at a frequency of 0.156 Hz with superimposed lower amplitude sinusoids at frequencies of 0.391, 0.859, 1.484, 2.422, 4.609, and 8.047 Hz. The frequencies of these sinusoids
are selected to minimize the effects of harmonic distortion on
estimates of Z
) was measured
with a pneumotachograph (Hans Rudolph 4700A, Kansas City, MO) placed at
the proximal end of a single lumen endotracheal tube (ETT) and
connected to a 0 to 2 cmH2O variable-reluctance pressure
transducer (Celesco LCVR-0002, Canoga Park, CA). Esophageal pressure
was obtained with a balloon catheter inserted orally, the distal tip of
which was positioned 35-40 cm from the incisors. Tracheal pressure
was obtained with a small polyethylene catheter placed into the ETT and
allowed to extend ~2 cm into the trachea. Transpulmonary pressure
(Ptp) was estimated as the difference between tracheal and esophageal
pressures across a single 0 to 50 cmH2O variable-reluctance
pressure transducer (Celesco LCVR-0050). The flow and pressure signals
were demodulated (Celesco LCCD-110), low-pass filtered at 10 Hz
(Frequency Devices), and sampled at 40 Hz by an analog-to-digital board
(Data Translations DT-2811).
Protocol.
After induction of anesthesia and muscle paralysis, all patients
were intubated with a single-lumen ETT. The EVW measurements were made
before any surgical manipulation. After an inspiratory sigh and passive
exhalation to resting lung volume, patients were switched from
conventional ventilatory support and connected to the EVW system as
shown in Fig. 1. Each patient received at
least six EVW breaths with PEEPs of 0, 3, and 6 cmH2O in
random order. Each run lasted ~40-50 s, during which time
arterial oxygen saturation, systemic arterial pressure, central venous
pressure, and electrocardiogram were continuously monitored. At no time
during the EVW forcings did the arterial oxygen saturation of any
patient drop below 98%.
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Data analysis and statistics.
In flow-limited patients, data analysis must be restricted to the
inspiratory segments of and Ptp if any linearity assumptions are to remain valid (28). Because the frequency content of
the EVW is exactly specified during each inspiratory period
TI, our approach was to model both the and Ptp
inspiratory segments with trigonometric approximations
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(1) |
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(2) |
and Ptp at
each specified frequency fk. Note that
Eqs. 1 and 2 are not true Fourier expansions of
the inspiratory flow and pressure segments, because each
fk is not constrained to be an integer multiple
of 1/TI (21). The trigonometric coefficients were estimated by using a least squares approach with error weighting (i.e., time-domain windowing) to minimize the effects of Ptp transient responses due to stress-relaxation, pendulluft, and alveolar
recruitment (21). The Z
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(3) |
![R<SUP>insp</SUP><SUB>L</SUB>(<IT>f<SUB>k</SUB></IT>)<IT>=</IT>Re[Z<SUP>insp</SUP><SUB>L</SUB>(<IT>f<SUB>k</SUB></IT>)]](/content/vol90/issue5/fulltext/1833/img005.gif)
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(4) |
![E<SUP>insp</SUP><SUB>L</SUB>(<IT>f<SUB>k</SUB></IT>)<IT>=</IT>−<IT>2&pgr;f<SUB>k</SUB> </IT>Im [Z<SUP>insp</SUP><SUB>L</SUB>(<IT>f<SUB>k</SUB></IT>)]](/content/vol90/issue5/fulltext/1833/img006.gif)
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(5) |
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
APPENDIX
REFERENCES
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Between-group comparisons of the
R
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Because little change was observed between 0 and 3 cmH2O
PEEP for most patients, we performed within-group comparisons of R
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The impact of LVRS on R
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A summary of the impact of PEEP on R
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
APPENDIX
REFERENCES
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Several techniques are available to provide clinical assessments of pulmonary mechanics in patients maintained on artificial ventilation. Measures of peak inspiratory pressure, work of breathing, and effective dynamic resistance and elastance for a particular breathing pattern are simple indexes that can provide a rough estimate of the relative ease with which air is brought into and out of the lungs. However, none of these permit inference on the distribution or nature of obstruction in the airways. As such, they are limited in their ability to enhance our understanding of the physiological effects of interventions such as PEEP or LVRS. Although the airway occlusion technique has been used to analyze pulmonary mechanics in ventilated patients (6, 9, 13), such an approach provides only an indirect and model-based prediction of the frequency dependence in RL and EL. Moreover, the accuracy of the airway occlusion is questionable in COPD patients because of its limited bandwidth of excitation (9).
In obstructive diseases such as asthma, there may be substantial and
widespread peripheral airway constriction. Previous morphometric modeling studies have demonstrated that if this obstruction is not
inclusive of peripheral airway closure, RL will be elevated at all frequencies, whereas EL will show mild frequency
dependence below 1 Hz (23, 24). Above 1 Hz, EL
will demonstrate pronounced positive frequency dependence due to the
shunting of flow into the central airway walls (23, 27).
When the obstruction is heterogeneous and includes a few closed or
nearly closed peripheral airways, both RL and
EL will be elevated for frequencies below 1 Hz, and
EL will show sharp frequency dependence above 2 Hz. In
patients with severe COPD, additional mechanisms may also contribute to
frequency dependence in R
Our data demonstrate that despite large differences in forced
expiratory flows, both the values and frequency dependence of R
Effects of PEEP.
Recently, several studies have advocated the use of low-level PEEP in
patients suffering from acute exacerbation of COPD (5, 11, 14,
35) to prevent atelectasis, counterbalance intrinsic PEEP, and
unload the inspiratory muscles during assisted modes of ventilation.
The pattern of reduced R
Effects of LVRS. There has been a resurgence of interest in the use of LVRS for the treatment of severe emphysema. Although many different approaches of LVRS have been developed, their common goal is the surgical removal of the most diseased portions of the lung, allowing healthier portions to expand and develop greater elastic recoil pressures. In addition to an improvement in driving pressure, the decompression of healthier lung tissue can result in increased radial traction on the airways, which helps maintain their caliber during expiration. As a result, LVRS can often increase expiratory airflow.
Although the size of our group is small, our data are consistent with those of Barnas et al. (1), who reported significant increases in inspiratory RL and EL from 0.16 to 0.50 Hz immediately after LVRS. The increases we observed in R| |
APPENDIX |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
APPENDIX
REFERENCES
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Increases in E
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With this model, a central airway compartment consisting of a resistance (R1) and inertance (I) is separated from a peripheral resistance (R2) by an airway wall elastance element (Eaw). The tissues are represented by a single linear elastance element. The RL and EL spectra were simulated from the model as described previously (21). We chose model parameter values consistent with emphysematous lungs (27), except that the Eaw was varied from 0.5 to 100 times the value expected for healthy lungs. In healthy lungs, airway wall elastance has been estimated to be ~200 cmH2O/l (27), but in emphysematous lungs it may be lower because of the loss of radial traction on the airways (17).
The three-dimensional surfaces of RL and EL as a function of both frequency and Eaw are shown in Fig. 6B. Note that there is a range of increasing Eaw (100-400 cmH2O/l) for which EL actually increases, beyond which EL progressively decreases. The RL becomes progressively elevated with increasing Eaw, even though we did not alter the R1 or R2 parameters. In the limit as Eaw approaches infinity (i.e., the airways become rigid), RL will approach a constant value equal to R1 + R2. Thus the increase in RL is not due to an increase in peripheral airway obstruction per se.
It should be noted that these simulations are extremely simplified compared with the actual alterations in lung mechanics after LVRS, because they only address the impact of airway wall stiffening on RL and EL spectra. Nonetheless, they demonstrate the possibility that increasing airway wall stiffness can in fact increase both RL and EL at high frequencies, giving the appearance that peripheral airway resistance has increased.
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ACKNOWLEDGEMENTS |
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We thank Dr. Stephen H. Loring for many helpful suggestions during the course of this study.
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FOOTNOTES |
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This work was supported by National Heart, Lung, and Blood Institute Grant R01 HL-622969-02 and National Science Foundation Grant BES-9711259.
Address for reprint requests and other correspondence: D. W. Kaczka, Boston Univ., Dept. of Biomedical Engineering, 44 Cummington St., Boston, MA 02215 (E-mail: dk{at}bu.edu).
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
Received 27 June 2000; accepted in final form 1 December 2000.
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
APPENDIX
REFERENCES
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) and COPD patients (
) at all 3 positive end-expiratory pressure (PEEP) levels. Data are means ± SD. *Significant difference (P < 0.05) between groups
via two-tailed Student's t-test; **significant difference
between groups (P < 0.05) via one-tailed Student's
t-test.
) cmH2O PEEP for control
(left) and COPD (right) patients. *Significant
difference between PEEP levels (P < 0.05) via paired
t-test.
1 · s, inertance
(I) = 0.01 cmH2O · l