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(Chest. 2005;128:1050-1057.)
© 2005 American College of Chest Physicians

Expiratory Flow Limitation Is Associated With Orthopnea and Reversed by Vasodilators and Diuretics in Left Heart Failure*

E. Boni, MD; M. Bezzi, MD; L. Carminati, MD; L. Corda, MD; V. Grassi, MD and Claudio Tantucci, MD

*From the Department of Internal Medicine, Respiratory Medicine, University of Brescia, Brescia, Italy.

Correspondence to: Claudio Tantucci, Clinica di Medicina Interna I, University of Brescia, Spedali Civili di Brescia, Piazzale Spedali Civili 1, 25100 Brescia, Italy; e-mail: tantucci{at}med.unibs.it


   Abstract
TOP
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 References
 
Background: In patients with acute left heart failure (LHF), orthopnea has also been related to the occurrence or worsening of expiratory flow limitation (EFL) in the supine position. We wished to assess whether short-term treatment with vasodilators and diuretics was able to abolish supine EFL and whether this could help to control orthopnea in patients with acute LHF.

Methods: In nine nonobese (ie, mean [± SD] body mass index, 24 ± 5 kg/m2), never-smoker patients (two men and seven women; mean age, 77 ± 7 years) with acute LHF (mean ejection fraction, 43 ± 15%), we assessed EFL by the negative expiratory pressure method and dyspnea by the Borg scale, with patients in both the seated and supine positions, before and after short-term treatment with vasodilators and diuretics until hospital discharge. Orthopnea was defined as a positive difference in the Borg score between measurements made with the patient in the supine and seated positions. Postural variations in the end-expiratory lung volume were inferred from changes in inspiratory capacity (IC) that were measured under the same circumstances.

Results: Before treatment, with the patient in the seated position the mean dyspnea score was 1.5 ± 0.5, the mean IC was 1.49 ± 0.38 L, seven patients were non-flow-limited, and two patients were flow-limited. During recumbency, the mean dyspnea score was 2.7 ± 0.5 (p < 0.01 vs seated position values), the mean IC was 1.66 ± 0.45 L, and seven patients exhibited EFL. After a mean duration of 17 ± 8 days of treatment (range, 7 to 28 days), EFL was detected in two patients only in the supine position, IC increased both in the seated position (1.65 ± 0.34 L; p < 0.01) and the supine position (1.81 ± 0.41 L; p = 0.07) position, and, although only two patients denied orthopnea, the mean dyspnea score during recumbency actually decreased to 1.9 ± 1.0 (p < 0.05).

Conclusions: Our results indicate that short-term treatment with vasodilators and diuretics is able to control orthopnea and to remove supine EFL in most patients with acute LHF, suggesting a posture-related increase in bronchial obstruction as the main mechanism of EFL, which appears to play a role in the occurrence and severity of orthopnea in these circumstances.

Key Words: diuretics • expiratory flow limitation • left heart failure • orthopnea • vasodilators


   Introduction
TOP
 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 References
 
In most patients with acute left heart failure (LHF), shortness of breath may occur or increase when lying down and typically can be relieved or reduced only after reassuming the seated position. This phenomenon is referred to as orthopnea. The frequent association of orthopnea and increased pulmonary venous congestion in patients with acute LHF has led many authors to regard posture-related vascular engorgement of the lungs as a key factor in the increase of breathlessness with recumbency.

In patients with chronic congestive heart failure (CHF), dyspnea may ensue from mechanical factors leading to decreased static and dynamic lung compliance and increased work of breathing. Indeed, a restrictive ventilatory defect depending on an increased volume of intrathoracic fluids, enlarged cardiac size, and inspiratory muscle weakness has long been recognized.1 Moreover, small airway obstruction has also been demonstrated and ascribed to lung volume reduction, swelling of the bronchial wall, peribronchial edema, and fibrosis, and to some functional modifications such as increase in vagal tone, release of neuropeptides, and airway hyperresponsiveness.2

Although these alterations tend to worsen when patients adopt the supine posture, particularly in those with acute LHF, the mechanisms by which the increase in pulmonary vascular congestion can exaggerate dyspnea during recumbency have not been completely clarified.3 A shift of blood from the lower part of the body and unfavorable hydrostatic relations within pulmonary vessels45 are believed to induce orthopnea by adversely influencing the gas exchange,6 and further reducing lung compliance7 and increasing airway resistance.8

Moreover, orthopnea in patients with acute LHF has been associated with expiratory flow limitation (EFL).9 EFL is a condition that is frequently described in patients with moderate-to-severe COPD.10 In these patients EFL hinders lung emptying and promotes the occurrence of dynamic hyperinflation and intrinsic positive end-expiratory pressure (PEEPi), contributing to dyspnea by increasing the elastic threshold load and related work of breathing and by decreasing the effectiveness of the inspiratory muscles as pressure generators. Duguet et al9 found that EFL was present in patients with acute LHF and worsened with recumbency, contributing to their orthopnea. The aim of this study was to confirm these findings and to assess whether EFL disappeared, especially with patients in the supine position, as orthopnea improved after short-term treatment with diuretics and vasodilators in patients affected by acute LHF.


   Materials and Methods
TOP
 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 References
 
Subjects
Nine white (two male), nonobese (ie, mean [± SD] body mass index, 24 ± 5 kg/m2), lifetime nonsmoker subjects, with a mean age of 77 ± 7 years (age range, 64 to 87 years), experiencing chronic heart disease of different etiologies were studied (Table 1 ). All patients had been referred to our institution because of clinical suspicion of the acute occurrence or worsening of left ventricular failure, owing to either systolic or diastolic dysfunction. Inclusion criteria were a clinical history of heart disease, symptoms, clinical and radiologic signs of acute left ventricular failure, and echocardiographic assessment of left heart dysfunction. At hospital admission, the mean echocardiographic ejection fraction (EF) was 43 ± 15%, which was computed according to the Simpson method. None of the patients received treatment with bronchodilators (including theophylline), corticosteroids, and antibiotics before or during the hospitalization period. Obese subjects (ie, BMI, > 30 kg/m2) and patients with a history, signs, symptoms, or suspicion of COPD were excluded from the study. Patients with concomitant infectious diseases were also excluded.


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  		Table 1. Anthropometric, Clinical, and Functional Characteristics of the Patients*

 
The patients were studied as soon as possible after admission to our institution, and subsequently at discharge from the hospital, on average, after 17 ± 8 days (range, 7 to 28 days). They were treated only with vasodilators (ie, arterial, angiotensin-converting enzyme inhibitors; and/or venous, nitrates) and diuretics (ie, furosemide or thiazides) on the decision of the primary physician, who was not involved in the study and took care of the patients until hospital discharge established by the achievement of stable clinical conditions. Oxygen-enriched air was administered if necessary, but all measurements were performed while the patient was breathing room air; care was taken to maintain a level of hemoglobin oxygen saturation of > 90% throughout the experiments. The study was approved by the local ethics committee, and informed consent was obtained from each patient.

Experimental Set-Up
In each experimental condition, the patients, wearing nose clips, breathed room air spontaneously through a flanged mouthpiece and a heated pneumotachograph (series 3700; Hans Rudolph; Kansas City, MO) that was connected to a differential pressure transducer (Raytech DP55 ± 3 cm H2O; Raytech Instruments; Vancouver, BC, Canada) to measure the flow. The pneumotachograph was linear over the experimental flow range. Volume was obtained by electrical time integration of the flow signal. Pressure was measured at the mouth using a rigid polyethylene catheter (internal diameter, 1.7 mm) that was connected to a differential pressure transducer (Raytech DP55 ± 100 cm H2O; Raytech Instruments).

The pneumotachograph was assembled in series with a Venturi device that created in the circuit a negative pressure, the magnitude of which could be precisely fixed. The Venturi device was connected to a solenoid valve (electrical valve model 8262G208; Ascoelectric; Brantford, ON, Canada) controlled by a computer and activated automatically when the expiratory flow reached a preset threshold value and after a preset time delay in order to apply negative expiratory pressure (NEP) immediately after the peak of the tidal expiratory flow.11 In all instances, the NEP application was timed to last until the lung volume corresponding to the end-expiratory lung volume of the previous control breath was reached. The flow and pressure signals were amplified (AC bridge Amplifier-ABC module; Raytech Instruments), filtered through a low-pass filter at 50 Hz, sent to an A/D converter (Direc Physiologic Recording System; Raytech Instruments) connected to a personal computer, and sampled at 200 Hz. Both digitized signals were displayed in real time on the computer screen together with the volume signal. The tracings were monitored continuously with respect to time and as flow-volume curves. All signals were calibrated independently and recorded simultaneously on the hard drive of the computer and were used for subsequent analysis. Data analysis was performed using data analysis software (Direc NEP, version 9; Raytech Instruments; or Anadat, version 5.2; RHT-InfoDat; Montreal, QC, Canada). The NEP method is particularly useful as it can detect EFL during tidal breathing without the subject’s cooperation, avoiding errors due to time and volume history and gas compression artifacts that can invalidate the results obtained with other methods.11

Design of the Study
Before and after treatment, dyspnea, breathing pattern, inspiratory capacity (IC), and EFL were evaluated, always in this sequence. Initially, the patients sat down comfortably, abdomen unbound, on a reclined bed with the back, neck, and head comfortably supported, and subsequently they adopted the supine position (ie, with head 15° above the horizontal plane) for 10 min or less if they could not stand this position for the predetermined time. Only at baseline was the same procedure repeated 5 and 15 min after resuming the sitting position under the conditions previously described.

Orthopnea:
At each step, the patients were asked to score the degree of dyspnea using the modified Borg scale.12 Hence, dyspnea was assessed in the seated and supine positions. The presence of orthopnea, which was defined as a worsening of the dyspnea when assuming the lying position, was documented by the positive difference in dyspnea score between the supine and seated positions ({Delta}Borg), and its severity was quantified by the dyspnea score measured with the patient in the supine position.

Breathing Pattern:
After connecting to the experimental set-up, the patients were asked to breathe as normally as possible. Following a period of regular breathing, the breathing pattern was registered for 1 min and the average spirogram (volume over time) was obtained at each step by computing the mean tidal volume (VT), inspiratory time, and expiratory time.

IC:
The slow inspiratory maneuver from dynamic functional residual capacity to total lung capacity to obtain the IC was performed twice after a period of regular breathing with a stable end-expiratory level. The highest IC value (corrected for body temperature pressure saturated water vapor [BTPS]) was used for analysis. Its changes with posture and treatment were assumed to reflect the corresponding variations in the end-expiratory lung volume (EELV).

EFL:
EFL was assessed by the NEP method using the above-mentioned set-up. NEP was applied usually 0.2 s after the onset of tidal expiration and was maintained throughout the whole expiration, at a level of –5 cm H2O. Two NEP breath tests were performed every 5 to 10 respiratory cycles, always when the patient had resumed regular breathing. When the NEP application increased expiratory flow above the flow of the control tidal expiration, EFL was excluded; on the contrary, EFL was present if expiratory flow during NEP impinged entirely or partially on the flow of the control tidal expiration.11

Pulmonary Function Testing:
Before hospital discharge when in a stable condition, the patients underwent spirometric measurements using a computerized system (MedGraphics 1070; Medical Graphics; St. Paul, MN) in the seated position. Slow vital capacity and three acceptable and reproducible maximal full flow-volume curves were obtained.13 Subjects inspired to total lung capacity and then expired forcefully without an end-expiratory pause to obtain FVC. The predicted values for volumes and flows were those proposed by the European Community for Coal and Steel.14

Statistical Analysis
The data are presented as the mean ± SD. To compare data for measurements made in the seated and supine positions as well as those obtained before and after treatment, the Wilcoxon matched paired test was used.

To assess the difference in supine EFL before and after treatment, the Fisher exact test was adopted. Correlations between quantitative variables were performed by calculating the nonparametric Spearman correlation coefficient (rs). A p value of < 0.05 was considered to be statistically significant.


   Results
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 References
 
Orthopnea
Before treatment, the mean dyspnea score in the seated position was 1.5 ± 0.5, while during recumbency it increased to 2.7 ± 0.5 (p < 0.01 vs seated position values). Indeed, all patients were orthopneic, with the change in Borg score being 1.1 ± 0.3. On resumption of the seated position, the mean dyspnea score reverted to the initial sitting values, amounting to 1.5 ± 0.6 and 1.4 ± 0.6 after 5 and 15 min, respectively (Fig 1 ).



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  		Figure 1. Individual dyspnea scores at baseline and after short-term treatment with vasodilators and diuretics (post) in the seated and supine position in nine patients with acute LHF. ** = p < 0.01 vs seated position values; * = p < 0.05 vs seated position values; § = p < 0.05 vs respective baseline values. Patients without tidal EFL (open symbols), non-flow-limited; patients with tidal EFL (closed symbols), flow-limited.

 
After a mean duration of 17 ± 8 days of treatment (range, 7 to 28 days), the mean dyspnea scores were 0.8 ± 0.7 in the seated position and 1.9 ± 1.0 in the supine position (p < 0.02 vs seated position values). Although two patients denied having orthopnea, in seven patients dyspnea was still greater with recumbency (change in Borg score, 1.1 ± 0.9). The severity of orthopnea, however, decreased from 2.7 ± 0.5 to 1.9 ± 1.0 (p < 0.05) after treatment (Fig 1).

Breathing Pattern
Breathing pattern parameters were substantially unchanged between measurements made in the seated and supine positions, both before and after treatment (Table 2 ).


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  		Table 2. Parameters of Breathing Pattern in Seated and Supine Positions*

 
IC
Before treatment, the mean IC was 1.49 ± 0.38 L in the seated position, increasing to 1.66 ± 0.45 L in the supine position (p < 0.05 vs seated position values). When the seated position was resumed, the mean IC values were 1.50 ± 0.39 and 1.52 ± 0.39 L after 5 and 15 min, respectively (difference not significant vs pre-seated position values).

After treatment, the IC increased both in the seated position (to 1.65 ± 0.34 L; p < 0.01) and the supine position (1.81 ± 0.41 L; p = 0.07; p < 0.01 vs seated position values). An inverse correlation was observed between the severity of orthopnea (ie, dyspnea score in the supine position) and the increase in IC with recumbency (rs = –0.65; rs2 = 0.43; p < 0.01) [Fig 2 ].



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  		Figure 2. Correlation between recumbent dyspnea (Borg scale score) and change in IC on adopting the supine posture ({Delta}IC) before treatment (•) and after treatment ({circ}) in nine patients with acute LHF. The dashed lines connect the same patient.

 
EFL
Before treatment, in the seated position seven patients were non-flow-limited and two patients (No. 3 and No. 4) were flow-limited (Fig 1). During recumbency, seven patients exhibited EFL (78%) [Fig 1]. On resumption of the seated position, EFL was detected in two patients (No. 3 and No. 4) after 5 min and persisted in only one patient (No. 4) after 15 min (Fig 1). The time course of such a phenomenon is shown in a representative subject (No. 7) in Figure 3 . After treatment, no patient exhibited EFL in the seated position, whereas EFL in the supine position was present in only two subjects (No. 5 and No. 8; p = 0.05 vs baseline values) [Fig 1].



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  		Figure 3. Baseline tidal flow-volume curves, in control condition and during the application of NEP, obtained with the patient in the seated and supine position and at different times after reassuming the seated position in a representative patient with acute LHF (No. 7). Top: the corresponding dyspnea scores. Note that during recumbency EFL develops and dyspnea increases. On resumption of the seated position, EFL progressively disappears and dyspnea decreases.

 

   Discussion
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
References
 
These data are consistent with the previous observation that orthopnea in patients with acute LHF is associated with supine EFL9 and show for the first time that the administration of diuretics and vasodilators is able to reverse supine EFL in most patients while decreasing orthopnea. These findings support the view that a posture-related increase in airflow obstruction induces EFL in patients with acute LHF, that treatment with diuretics and vasodilators also acts by decreasing airway narrowing, and that EFL contributes to acute LHF-related orthopnea, mostly influencing its severity.

A vigorous effort was made to select lifetime nonsmoker, nonobese patients with no comorbidities, namely, COPD, which is known to promote per se the occurrence of EFL especially in the supine position in elderly people. Great care was taken either to exclude patients who for any reason had received bronchodilators and/or systemic and inhaled corticosteroids or to avoid the administration of these drugs after enrollment in the study until hospital discharge. Moreover, we had to choose patients who were able to collaborate and sustain the study protocol who presumably could be treated only with diuretics and vasodilators. Our patients had both systolic and diastolic dysfunction, as shown by the EF values. Since EF does not accurately reflect left ventricular stroke volume and cardiac output, acute left ventricular failure with normal EF (ie, acute diastolic heart failure) should not be seen as a surprising phenomenon.15 In addition, it must also be stressed that even patients with diastolic heart failure may have systolic dysfunction if studied by a sensitive method like tissue Doppler echocardiography imaging.16 It is important to recognize that we investigated patients with acutely increasing (ie, over days) exertional dyspnea and the presence of dyspnea at rest due to moderate-to-severe pulmonary congestion, but without obvious signs of "cardiac" asthma or acute pulmonary edema.

In patients experiencing chronic CHF, besides the presence of a restrictive ventilatory defect due to enlarged heart size, increased intrathoracic fluids,1 and impaired inspiratory muscle strength,17 the occurrence of airway narrowing caused by different mechanisms has been demonstrated,2181920 mainly during episodes of acute decompensation2122 and on adopting the supine posture.823 The consequent rise in elastic and resistive loads imposed on the inspiratory muscles when lying down has been related to increased breathlessness in recumbent CHF patients.78 However, both the presence of airflow obstruction and breathing at a reduced lung volume, because of decreased lung compliance,22 may favor the development of EFL by implying lower maximal expiratory flow rates in the VT range. This is more likely to occur with recumbency when the posture-related decrease in the EELV and/or increase in bronchial obstruction following intrathoracic blood shift from the abdomen and legs occur.8 The development or worsening of EFL with recumbency promotes dynamic hyperinflation and PEEPi in the supine position, further increasing the inspiratory muscle load and work, which are already augmented by the postural decrease in lung compliance and increase in airway resistance,7 thus contributing to orthopnea.

In a previous study,9 9 of 12 patients with acute left ventricular failure exhibited EFL when lying down, and all those claiming orthopnea (n = 7) showed supine EFL. By contrast, only one of those who denied orthopnea (n = 5) had supine EFL.

This observation was confirmed by our results. Under baseline conditions, EFL was present in two of nine patients in the seated position, while seven patients became flow-limited when in the supine position (78%). Since the breathing pattern was unchanged in the supine position, a posture-related decrease in maximal expiratory flow, which was likely due to an increase in airway resistance with recumbency,78 appears to be the main mechanism leading to supine EFL in patients with acute LHF. The high frequency of EFL in these patients when lying down may well explain the poor increase in supine IC, reflecting a postural reduction in EELV that appears to be abnormally low.2425 In fact, the small increase measured in the recumbent IC (on average, < 200 mL) may reasonably be ascribed to the development of supine EFL that prevents a normal decrease in the EELV.2425 Hence, dynamic pulmonary hyperinflation (ie, an EELV greater than the relaxation volume of the respiratory system) and PEEPi must develop in these patients when lying down, inducing a greater elastic work of breathing in the presence of less efficient inspiratory muscles and thus increasing dyspnea in the supine position. In line with this reasoning, in stable CHF patients with orthopnea breathing spontaneously the dynamic PEEPi was significantly increased in the supine position, although the mean value of 1.64 ± 1.35 cm H2O was not particularly elevated.7 In those patients, EFL was not assessed, but it is highly probable that in our patients with acute LHF, about 80% of whom had EFL when lying down, the recumbent PEEPi values were markedly higher.

Treatment with diuretics and vasodilators is widely used in patients with acute LHF to improve left ventricular function by adequately decreasing both preload and afterload.2627 The following reduction of either pulmonary (and bronchial wall) vascular congestion or pulmonary (peribronchial and interstitial) edema and airway intraluminal fluid is expected to increase lung compliance and to decrease peripheral airway resistance, particularly in the supine position, thus reducing breathlessness and orthopnea.

The results of the present study, however, indicate that the use of these drugs was associated with the abolition of EFL during recumbency in a significant percentage of patients with acute LHF, suggesting that the concurrent reduction of dyspnea in the supine position (ie, less severe orthopnea) might also be achieved by eliminating or decreasing postural dynamic pulmonary hyperinflation and PEEPi, thus improving breathlessness related to neuromechanical dissociation28 and downstream airway compression.29

On the other hand, because of the multifactorial origin of orthopnea in these conditions it is not surprising that some patients have greater dyspnea on adopting the supine posture without exhibiting EFL either before or after receiving medical treatment. In this respect, it should be underlined that the presence of supine EFL is not necessary to develop orthopnea in patients with acute LHF even if its presence seems to aggravate it and vice versa. In fact, orthopnea, although significantly reduced, was claimed after treatment by the majority of patients, even in the absence of EFL, with an increase in supine IC that was surprisingly small (ie, < 200 mL) and was not dissimilar on average from that observed in the baseline condition. This small increment of IC on adopting the supine posture, however, has been shown in pioneering work330 performed in stable CHF patients, compared to matched controls, and also has been consistently described in the most recent works.78 The reason is not clear, but active mechanisms such as expiratory narrowing of the glottis or prolonged postinspiratory activity of the inspiratory muscles may antagonize the normal decrease in the functional residual capacity (or increase in the IC) when lying down, perhaps to avoid breathing at an excessively low lung volume. Data on dogs and healthy subjects3132 have suggested that breathing tidally at a small lung volume may markedly increase both resistive and elastic work of breathing and bronchial responsiveness. In any case, this strategy would again imply a certain degree of postural dynamic pulmonary hyperinflation and PEEPi, as previously shown in stable CHF patients.7 It must be noted, indeed, that orthopnea was still present, albeit less severely in our patients after > 2 weeks of adequate therapy with diuretics and vasodilators, indicating that underlying mechanisms other than supine EFL appear more difficult to eliminate or control adequately during short-term treatment with these drugs.

In summary, in patients with acute LHF orthopnea is associated with supine EFL, which is largely reversed by reassuming the seated position. Since the breathing pattern is unchanged and EELV is only slightly reduced with recumbency, a posture-related increase in airway resistance is likely to be the main cause of supine EFL, which seems to play a relevant role mostly in the severity of acute LHF-related orthopnea. Short-term treatment with diuretics and vasodilators, while decreasing orthopnea, is able to remove supine EFL in most patients with acute LHF, probably through a significant reduction of the airway obstruction. This finding suggests that in such circumstances the effectiveness of these drugs in controlling orthopnea may be partly explained by this mechanism.


   Acknowledgements
 
The authors are grateful to Michele Guerini for his invaluable technical support.


   Footnotes
 
Abbreviations: CHF = congestive heart failure; EELV = end-expiratory lung volume; EF = ejection fraction; EFL = expiratory flow limitation; IC = inspiratory capacity; LHF = left heart failure; NEP = negative expiratory pressure; PEEPi = intrinsic positive end-expiratory pressure; VT = tidal volume

Received for publication May 7, 2004. Accepted for publication March 13, 2005.


   References
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 References
 

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