Why hyperinflation in copd

If you have a chronic lung disease, your medical team is likely to look for signs of lung hyperinflation on your diagnostic tests. Be sure to avoid exacerbating factors, such as smoking and exposure to pollutants. Sign up for our Health Tip of the Day newsletter, and receive daily tips that will help you live your healthiest life.

Hyperinflated lungs compress the heart during expiration in COPD patients: a new finding on dynamic-ventilation computed tomography. Does this patient really have chronic obstructive pulmonary disease? Singapore Med J.

Pompeo E. ISRN Pulmonol. Pursed lip breathing improves exercise tolerance in COPD: a randomized crossover study. Eur J Phys Rehabil Med. Pathogenesis of hyperinflation in chronic obstructive pulmonary disease. Review of lung sealant technologies for lung volume reduction in pulmonary disease. Med Devices Auckl. Mechanisms, assessment and therapeutic implications of lung hyperinflation in COPD.

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Related Articles. Understanding Total Lung Capacity. The IC is diminished in the presence of significant inspiratory muscle weakness [ 30 ]. Constructed with data from: [ 96 ]. Insufficient data from longitudinal studies are available to precisely chart the natural history of lung hyperinflation in COPD. Clinical experience indicates this is an insidious process that occurs over decades. It is acknowledged that such factors as genetic susceptibility, burden of tobacco smoke, frequency and severity of exacerbations, and pathophysiological phenotype collectively dictate the rate of progression of hyperinflation.

In that study, patients with the lowest baseline IC were those with the greatest rates of exacerbation and death [ 32 ]. A cross-sectional study in patients found progressive increases in pulmonary gas trapping and lung hyperinflation measured by RV and FRC and a corresponding decline of IC across the continuum of COPD severity [ 25 ].

Lung volume increases were shown to occur even in the earliest stages of COPD i. Small studies in mild COPD have reported increased static lung compliance, and quantitative computed tomography CT scans have shown emphysema and gas trapping [ 35 — 37 ].

Gas trapping, as assessed by expiratory CT scans, can exist in the absence of structural emphysema and is believed to indirectly reflect small airway dysfunction in mild COPD [ 35 ]. The presence of lung hyperinflation assessed by quantitative CT scans was found to predict a rapid annual decline in FEV 1 in smokers with a normal FEV 1 [ 36 ]. Corbin and coworkers [ 37 ], in a 4-year longitudinal study of smokers with chronic bronchitis, reported a progressive increase in lung compliance.

From cross-sectional studies, it would appear that RV and FRC increase exponentially as airway obstruction worsens [ 25 ]. In the presence of lung hyperinflation, functional muscle weakness is mitigated, to some extent, by long term adaptations such as shortening of diaphragmatic sarcomeres and reduction in sarcomere number which cause a leftward shift of the length-tension relationship; thus improving the ability of the muscles to generate force at higher lung volumes [ 11 , 38 ].

In patients with chronic lung hyperinflation, adaptive alterations in muscle fiber composition an increase in the relative proportion of slow-twitch, fatigue resistant, type I fibers and oxidative capacity an increase in mitochondrial concentration and efficiency of the electron transport chain are believed to preserve the functional strength of the overburdened diaphragm and make it more resistant to fatigue [ 39 , 40 ].

In this regard, Similowski et al. A mild increase in EELV at rest might be advantageous as it improves airway conductance and attenuates expiratory flow limitation to a variable degree. However, lung hyperinflation in moderate to severe COPD places the inspiratory muscles, especially the diaphragm, at a significant mechanical disadvantage by shortening its fibers, thereby compromising its force generating capacity [ 42 ].

Lung hyperinflation also affects the capacity of the parasternal intercostals and scalenes to shorten with potential negative consequences [ 43 ]. Known mechanisms of compromised diaphragmatic function secondary to hyperinflation can be summarized as follows [ 44 , 45 ]:.

Lung hyperinflation decreases the resting length of the diaphragm and, less so, the rib cage muscles. The shortening of the diaphragm is due to a decrease in the length of its zone of apposition, which causes a decrease in its pressure generating capacity [ 43 , 44 ]. The change in fiber orientation with lung hyperinflation decreases the ability of the diaphragm to generate force, and this muscle has an expiratory rather than inspiratory action on the rib cage [ 39 , 40 , 44 , 45 ].

The net effect is a pronounced increase in the work and oxygen O 2 cost of breathing at rest in patients with severe COPD [ 46 ]. Severe lung hyperinflation has been linked to a reduced intra-thoracic blood volume and reduced LV end-diastolic volume as assessed by magnetic resonance imaging MRI [ 49 ].

Barr et al. Lung hyperinflation has also the potential to impair cardiac function by increasing pulmonary vascular resistance [ 50 ]. Increased intrathoracic pressure swings linked to the increased mechanical loading of hyperinflation may result in increased LV afterload as a result of the increased LV transmural pressure gradient Fig.

Reductions in venous return, right and left ventricular volumes, and LV stroke volume are additional consequences of the altered intra-thoracic pressure gradients [ 6 , 15 ]. A schematic diagram showing the potential deleterious effects of lung hyperinflation on cardio-pulmonary interactions in patients with COPD.

These interactions may vary according to phase alignment between the respiratory and cardiac cycles. There are also important modulating effects of volemic status, sympathetic nervous system activation, ventilation-related vagal reflexes and comorbidities e. From: [ 15 ]. However, patients with COPD, especially those with more severe airway obstruction, are more likely to have significant baseline abnormalities of both lung mechanics and pulmonary gas exchange [ 5 ] Fig.

Thus, the consequences of acute-on-chronic lung hyperinflation in such individuals may be serious and even life-threatening.

During AECOPD, airway resistance is abruptly increased due to a combination of bronchospasm, mucosal edema and sputum inspissation; which worsens expiratory flow limitation and compromises effective lung emptying [ 5 ]. The increased respiratory neural drive RND , secondary to attendant ventilation-perfusion abnormalities in the face of increasing lung hyperinflation, means that patients tend to adopt a rapid, shallow breathing pattern during an exacerbation.

This further limits the time available for lung emptying, thus promoting greater DH in a vicious cycle. Moreover, subjective fear, anxiety or overt panic related to distressing dyspnea, with attendant increased sympathetic nervous system activation, also powerfully influence breathing pattern to worsen DH and perceived respiratory discomfort [ 5 ]. The negative consequences of dynamic hyperinflation during an acute exacerbation of COPD. Dynamic hyperinflation develops as a consequence of worsening expiratory flow limitation.

During AECOPD, the respiratory muscles already burdened by increased resistive loading become subjected to increased elastic loading, decreased dynamic lung compliance and functional muscle weakness. Intrapulmonary pressures are positive at the end of expiration i.

PEEP i essentially acts as an inspiratory threshold load and may be as high as 6—9 cm H 2 O during quiet breathing at rest in clinically stable patients with severe resting lung hyperinflation. During acute-on-chronic hyperinflation, PEEPi may rise precipitously and, together with the increased elastic related to breathing at a less compliant part the pressure-volume relationship Fig. During AECOPD, the mechanical output of the flow-limited and hyperinflated respiratory system may not increase in proportion to increasing respiratory neural drive, resulting in critical neuromechanical dissociation of the respiratory system which may explain the worsening dyspnea [ 5 , 6 ].

In fact, dyspnea and functional indices of hyperinflation have been found to improve in parallel in the recovery phase of acute AECOPD [ 54 ].

The major goal in AECOPD is lung deflation by intensive bronchodilator therapy to restore neuromechanical coupling and relieve dyspnea. Non-invasive mechanical ventilation with continuous positive airway pressure or bi-level support can also effectively counterbalance the negative effects of increased lung hyperinflation on the inspiratory muscles and provide important dyspnea relief [ 55 ].

Dynamic increases in EELV are inevitable during exercise in patients with significant EFL in the setting of high ventilatory demand [ 17 ]. RND is increased for any given ventilation in COPD compared with healthy controls reflecting the increased intrinsic mechanical loads on the inspiratory muscles and the attendant functional muscle weakness caused by breathing at high lung volumes.

In early exercise, mean inspiratory flow rates and tidal volume increase substantially but expiratory time is often too short to allow complete gas emptying resulting in DH. Increases in EELV above resting values by 0. Thus, in patients with a low resting IC due to severe resting hyperinflation, V T quickly expands during exercise even in the absence of DH to reach a critical minimal IRV — a true mechanical limit where further increases in ventilation soon become impossible [ 60 , 61 ].

DH during exercise is even present in many individuals with mild airway obstruction and dominant peripheral airways disease as a result of the combined effects of higher ventilatory inefficiency and dynamic expiratory flow limitation [ 34 , 62 ].

Guenette et al. These results suggest that dyspnea intensity was related to the constraints on V T expansion reduction in IRV and not the magnitude of acute DH during exercise [ 64 ]. The inability to further expand V T is associated with tachypnea — the only remaining strategy available in response to the increasing ventilatory drive. As explained above, increased breathing frequency results in increased elastic loading due to further DH and the increased velocity of shortening of the inspiratory muscles, with associated functional weakness and decreased dynamic lung compliance.

These collective derangements can predispose to critical inspiratory muscle functional weakness, fatigue or even overt respiratory insufficiency with carbon dioxide CO 2 retention [ 21 , 67 ]. The upper through to lower quartiles Q1-Q4 represent the mildest to most severe groups, respectively. Data plotted are mean values at steady-state rest, isotime i. Modified from: [ 29 ]. DH adversely affects dynamic cardiac function by contributing to pulmonary hypertension intra-alveolar vessel compression , by reducing right ventricular pre-load reduced venous return and, in some cases, by increasing left ventricular afterload [ 6 , 51 ].

In the absence of cardiac disease, cardiac output has been found to increase normally as a function of oxygen uptake during submaximal exercise in COPD, although stroke volume is generally smaller and heart rate correspondingly higher than in health [ 68 , 69 ]. Of note, peak cardiac output reaches a lower maximal value during exercise in COPD, which may be due, in part, to abnormal ventilatory mechanics [ 6 ].

There is also evidence that impaired cardiac output response in the rest-to-exercise transition in non-hypoxemic patients with moderate-to-severe COPD is associated with increased muscle deoxygenation thereby suggesting reduced muscle perfusion [ 59 ]. Of note, reducing resting hyperinflation with bronchodilators improved muscle oxygenation during exercise [ 70 , 71 ], a finding related to a faster cardiac output adjustment to exercise [ 71 ].

It has also been postulated that competition between the overworked ventilatory muscles and the active peripheral muscles for a reduced cardiac output may compromise blood flow and oxygen delivery to the latter, with negative consequences for exercise performance [ 72 — 74 ]. Dyspnea is a common symptom in patients with COPD across the continuum of the disease and is often the proximate cause of exercise limitation. The increase in dyspnea intensity at any given ventilation as COPD severity increases compared to health , reflects the progressively increasing intrinsic mechanical loading of the respiratory muscles [ 7 , 75 ].

The rise in dyspnea intensity ratings during exercise correlates strongly with indirect indices of increased respiratory neural drive central motor command output such as tidal electromyographic activation of the diaphragm relative to maximum, tidal esophageal pressure swings relative to maximum, and ventilation relative to peak ventilatory capacity [ 66 , 76 ].

It is postulated that the amplitude of central neural drive originating from motor cortical and medullary centers in the brain to the respiratory muscles is sensed via neural inter-connections i. In advanced COPD, the ratio of respired effort and presumably neural drive to V T increases steeply from rest to peak exercise, reflecting progressive neuromechanical dissociation of the respiratory system [ 67 ].

Exertional dyspnea intensity closely correlates with indices of effort-volume displacement dissociation e. The corollary is that effective relief of dyspnea in COPD following bronchodilators [ 78 , 79 ] or lung volume reduction surgery [ 80 ] are largely explained by partial restoration of effort-displacement ratios and reduced neuromechanical dissociation.

From: [ 29 ]. Bronchodilators reduce airway smooth muscle tone and airway resistance, improve airflow, and accelerate the mechanical time constants for lung emptying [ 81 ]. In this way, inhaled bronchodilators favorably alter the dynamically-determined components of resting lung hyperinflation and help deflate the overinflated lung.

Bronchodilators of all classes and duration of action have consistently been shown to decrease lung hyperinflation and pulmonary gas trapping, with reciprocal increases in IC and VC in patients with COPD [ 82 , 83 ].

Since spirometric measurements are simple to perform, changes in IC have often been used to track changes in EELV both at rest and throughout exercise. The largest post-bronchodilator improvements in IC are seen in patients with the greatest resting lung hyperinflation e.

Decreases in lung volume of the magnitude seen in response to bronchodilators are associated with reduced intrinsic mechanical loading and increased functional strength of the respiratory muscles [ 15 ]. Such mechanical improvements are particularly important in dyspneic patients with more severe COPD who gain the greatest subjective benefit [ 75 ].

This pattern of lung volume recruitment is noted particularly in patients with more severe lung hyperinflation [ 81 , 84 ]. Moreover, a lack of change in FEV 1 after bronchodilator treatment does not necessarily reflect a lack of change in lung hyperinflation or associated subjective benefits for the patient [ 81 , 84 ]. Van Noord et al. After the 2-week treatment periods, they confirmed additive effects on lung deflation with significant increases in average daily IC and daytime peak IC with the combination treatment versus tiotropium alone.

Importantly, the mechanical benefits were also evident throughout the night. There has recently been interest in measuring increases in IC as a surrogate measure of lung deflation during exercise in response to bronchodilator treatment in COPD [ 28 , 81 ]. Thus, throughout exercise, less respiratory muscle effort is required to achieve greater tidal volume expansion: the dissociation between central respiratory drive and the mechanical response of the respiratory system is partially reversed.

Improvements in dyspnea and exercise tolerance after bronchodilators are closely related to this release of V T restriction and enhanced neuromechanical coupling of the respiratory system [ 65 ]. Bronchodilator-induced improvements in perceived dyspnea intensity during constant work rate cycle exercise are variable, possibly due to measurement variability in this outcome as well as the modest numbers of patients in many of these studies.

Despite variability in improvements in exertional dyspnea, increases in IC at a standardized time near end-exercise isotime and in exercise endurance time with long-acting bronchodilators compared with placebo appear to be more consistent Fig.

Such increases in cycling endurance time are typically within the range that is thought to be clinically important, i. Our understanding of the cause and consequences of lung hyperinflation in patients with COPD has considerably advanced in the last decade. It is now well established that lung hyperinflation and its effects provide a compelling physiological basis for the subjective experience of breathing discomfort during both exacerbations and physical activity in patients with COPD.

It is now understood how acute-on-chronic lung hyperinflation in these clinical settings can abruptly undermine the normal functioning of the respiratory and cardio-circulatory systems with consequent negative clinical consequences. The corollary is that partial reversal of lung hyperinflation by pharmacotherapy and other interventions can effectively mitigate such negative effects.

Thus, a persuasive case can be made to support the inclusion of indices of lung hyperinflation as valid physiological markers of disease severity that link to important clinical outcomes such as mortality, risk of exacerbation, activity-related dyspnea and exercise intolerance.

Ideally, comprehensive characterization of physiological impairment in individual symptomatic patients with COPD should incorporate measures of lung hyperinflation.

The exclusive reliance of spirometric forced expiratory flow rates to evaluate efficacy of bronchodilators in clinical trials in the past has led to underestimation of their clinical benefits, particularly in patients with more advanced COPD.

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