Why does emphysema cause barrel chest

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Please try again. Something went wrong on our side, please try again. Show references Weaver AA, et al. Morphometric analysis of variation in the ribs with age and sex.

Journal of Anatomy. Chronic obstructive pulmonary disease COPD. Merck Manual Professional Version. However, if it moves at all, the direction is outward and upward. In some healthy individuals, at the end of maximum inspiration, they may move slightly inward. However, in COPD patients, there is a gross exaggeration of this inward movement.

The indrawing of the lateral rib cage may occur at the end of inspiration or throughout inspiration. Gilmartin and Gibson[ 32 ] described the following types of paradoxical movement: late inspiratory paradox, a combination of late inspiratory paradox at the upper level and early inspiratory paradox at the lower level or intermittent paradoxical movement. The Hoover's sign is best appreciated by placing the first and second fingers on the costal margin near the anterior axillary line.

COPD patients may also show inspiratory indrawing of the lower sternum known as anteroposterior ribcage paradox. It occurs typically in early inspiration and usually occurs along with lateral paradox. The frequency of the sign increases with the severity of airflow obstruction.

Hoover's sign has a good interobserver agreement with kappa statistics of 0. Gilmartin and Gibson[ 32 ] found a weak correlation, but Stubbing et al. Hoover's chest sign develops due to the inward pulling of the lateral rib cage by the flattened diaphragm. When the horizontally orientated fibers contract, they pull the costal margin inward. However, Gorman et al.

Therefore, the conventional theory that Hoover's sign is the result of an inward pull of the lower ribs by radially oriented diaphragm muscle fibers is probably not correct. Troyer and Wilson[ 41 ] proposed the three-compartment model to explain the chest wall mechanics. During diaphragmatic contraction, pleural pressure Ppl falls which exert a caudal and inward force on the entire rib cage. In the presence of hyperinflation, the zone of apposition is decreased, and pleural pressure becomes the dominant force on the lower ribs and rib displacement is reversed in caudal-inward direction.

The normal chest is oval shaped, with its anteroposterior diameter less than its lateral diameter. The thoracic ratio, thoracic index, or chest index[ 42 ] is the ratio of the anteroposterior to lateral diameter and is normally approximately 0. The upper normal limit is approximately 0. The ribs become more horizontal and dorsal kyphosis is present in the majority of cases. Aging can also produce barrel-shaped deformity of the chest without any lung disease.

However, the increased anteroposterior chest diameter may be an illusory finding as Kilburn and Asmundsson[ 45 ] demonstrated that the anteroposterior diameter was not different significantly between the three groups: 25 patients with emphysema, 22 patients with other diseases, and 16 normal individuals.

Hence, the authors hypothesized that the decreased abdominal diameters due to weight loss seen in COPD may be responsible for an illusory increase in the anteroposterior diameters of the chest.

Walsh et al. They reported no difference in rib cage dimensions between the COPD patients and the controls. Some patients of COPD may show recession or indrawing of the supraclavicular fossa. It is attributed to a phase lag between the generation of a large negative inspiratory Ppl and a resultant change in lung volume.

The phase leg is related to increased airway resistance and reduced FEV 1 level. Godfrey et al. COPD patients often adopt instinctively during episodes of respiratory distress dyspnea-relieving position such as tripod position.

In tripod position, the patients are in sitting and leaning forward posture with their outstretched hands on their knees. The forward-leaning position improves dyspnea by several mechanisms. The arm support in tripod position fixes and lifts the shoulder girdle and improves the length—tension relationship of other accessory muscles pectoralis major and minor that are attached between the ribs and the upper limb or shoulder girdle.

The tripod position also decreases the recruitment of sternocleidomastoid and scalene muscles. Pedal edema in patients with COPD may indicate right-sided heart failure or cor pulmonale.

Right heart failure develops as a result of pulmonary hypertension. Cohen et al. They show a significantly higher mortality and a significantly higher requirement of assisted ventilation. They also have significantly lower values for forced vital capacity VC and FEV 1 compared to patients with synchronous breathing.

The abdominal or respiratory paradox is defined by indrawing of the abdominal wall when the rib cage moves outward. Normally, during inspiration, the abdominal and thoracic wall move synchronously, both expanding in inspiration and contracting in exhalation. The diaphragm is attached to lower ribs via the zone of apposition, and its fibers are directed upward, parallel to the rib cage.

The increased abdominal pressure causes displacement of the lower rib cage via the zone of apposition. COPD patients may develop diaphragmatic fatigue due to a mechanically disadvantageous position of the diaphragm and overwork.

The pressure gradient Pdi produced by the diaphragm is zero. Therefore, with each inspiration, the fall in Ppl caused by the contraction of intercostal muscles sucks upward the fatigued diaphragm and abdomen moves inward.

This is called abdominal or respiratory paradox. The best way to demonstrate abdominal paradox is bimanual palpation with one hand over the patient's chest and one over the abdomen.

Palpation of the abdomen also helps in differentiating abdominal paradox from abdominal muscle contraction, which is present in many stable COPD patients. However, in the supine position, paradoxical movement becomes obvious. The asynchronous rib cage and abdominal movement are more common in patients with severe COPD. Tobin et al. Another sign of respiratory muscle fatigue is respiratory alternans. Patients with respiratory alternans exhibit alternate use of either the diaphragm or chest wall cyclically, so that most of the respiratory movements are abdominal for a few breaths, followed by another series of breaths that occur due to the displacement of the rib cage.

When they lean forward, the increased intra-abdominal pressure can restore the dome of the flattened diaphragm. This may improve diaphragmatic efficiency and respiratory alternans disappears. Neck veins are inspected for estimation of the jugular venous pressure and an analysis of the venous pulse. Jugular venous distension during expiration indicates that the intrathoracic pressure has become excessively positive due to airway obstruction.

During inspiration, ribs undergo pump-handle and bucket-handle movement. Due to hyperinflation and elevation of the sternum in COPD patients, there is a loss of the bucket-handle movement about the vertebrosternal axis with retention or even exaggeration of the pump-handle movement. The bucket-handle movement of the lower rib cage is lost due to two factors: loss of zone of apposition and medial orientation of the diaphragm fibers.

However, Godfrey et al. This is the distance between the top of the thyroid cartilage and suprasternal notch. The positive LR of laryngeal height is 5.

Second, the forceful diaphragmatic contraction may pull the trachea abnormally downward. Laryngeal descent is the difference between maximum and minimum laryngeal heights.

Maximum laryngeal height is measured at the end of expiration and minimum laryngeal height is measured at the end of inspiration. Laryngeal descent was not found to be useful in ruling in or out obstructive airway disease. COPD patients may also develop distortion of tracheal shape.

The ratio of the short to the long radius of trachea is a better parameter than tracheal index in detecting distortion. Patients with chronic airflow obstruction may show downward displacement of trachea during inspiration. This sign is called Campbell sign and it is different from tracheal tug seen in patients with an aortic aneurysm pulsation of aorta palpable through the trachea. Campbell sign is best felt by placing the tip of the index finger on the thyroid cartilage. However, this sign is not specific for chronic airways obstruction and can be present in respiratory distress of any cause.

Patients with COPD may present with an absent apical impulse and an impaired cardiac dullness. The cardiac apex beat in COPD may not be present at the usual location and may be shifted to the subxiphoid area. Badgett et al. The kappa statistic was 0. The positive and negative LR of absent cardiac dullness is 16 and 0. A systolic heave in the left parasternal region indicates right ventricular hypertrophy. Hyperinflation may modify this finding. The chest percussion should be done routinely in COPD patients to determine the type of percussion sounds.

The percussion sound is hyperresonant, if the sound is more hollow than normal. Oshaug et al. The diaphragmatic position and its range of movement can be demonstrated by percussion. Diaphragmatic excursion actually measures the movement of the dome as the dome moves more than the peripheral part.

However, a normal diaphragmatic movement is less likely useful in decreasing the likelihood of airflow limitation. Pardee et al. According to this system, the clinician listens sequentially over six locations on the patient's chest: bilaterally over the upper anterior portion of the chest, in the midaxillae, and at the posterior bases. At each site, the clinician grades the inspiratory sound as absent 0 points , barely audible 1 point , faint but definitely heard 2 points , normal 3 points , or louder than normal 4 points.

The patient's total score may range from 0 absent breath sounds to 24 very loud breath sounds. Best strategy would be a combination of history and physical examination. The kappa score for BSI determination is 0.

Breath sound at mouth is acoustically different from the sounds heard at chest wall. Breath sounds at mouth contain frequencies distributed widely from to Hz, whereas breath sounds heard at chest wall do not contain frequencies above Hz as they are filtered off by the alveolar air and chest wall. In contrast, emphysema patients have quiet breathing at the mouth.

This is because emphysema does not cause direct bronchial narrowing. Emphysema patients develop small airway obstruction due to the loss of elastic recoil of the lung.

Therefore, alveolar destruction and air-trapping decreases sound transmission. Ploysongsang et al. Schreur et al. Early inspiratory crackles appear at the beginning of inspiration and end before mid-inspiration. It is classically seen in COPD. Crackles are usually due to airway secretions within large airway and disappear on coughing. These crackles are scanty, gravity-independent, usually audible at the mouth, and strongly associated with severe airway obstruction.

Nath and Capel had shown that among patients with known obstructive lung disease, early inspiratory crackles imply a severe disease i. Wheezes are produced by the vibration of the narrowed walls of airway. The presence of unforced wheezing has an LR of 2. The clinical examination to detect the signs of cor pulmonale in COPD is insensitive due to the hyperinflation of the chest.

Tricuspid regurgitation may also develop in patients with right ventricular dysfunction. The murmur of tricuspid regurgitation is holosystolic, best heard in the left fourth intercostal space in the parasternal area. The intensity of the murmur increases during inspiration and is known as Carvallo's sign. The forced expiratory time FET is a simple, inexpensive, reproducible bedside test to detect airflow obstruction.

The patient is instructed to take a full breath and then exhale as fast and complete as possible with the mouth wide open. The bell of the stethoscope is placed over the trachea in the suprasternal notch. The duration of audible expiration is measured to the nearest half second with the help of a stopwatch.

The interobserver agreement is good with kappa score of 0. It is a bedside test to detect airflow obstruction. The patient is first instructed to inspire maximally and is then asked to expire rapidly and forcefully with their mouths wide open to extinguish the standard cardboard match placed at a distance of 6 inch 15 cm.

The ability to blow out the match depends on the velocity of air flow which is affected by airway obstruction. The test is positive if the patient fails to extinguish the match. This test is a simple screening test, and if positive, further pulmonary function test should be performed. The Snider's test can be positive in both obstructive and restrictive lung diseases.

This test should not be done in patients receiving supplemental oxygen therapy. It is an exaggeration of normal physiologic fall in systolic blood pressure, so the term paradoxical is a misnomer.

The cuff pressure is further reduced until the Korotkoff sounds become audible in both phases of the respiratory cycle. The difference between these two levels quantifies PP. Clubbing of the digits is not typical in COPD and when present should raise the possibilities of comorbidities such as lung cancer, interstitial lung disease, or bronchiectasis. The presence of certain physical signs in individuals with chronic airflow obstruction is related to the degree of airflow obstruction, secondary effects of the airflow obstruction e.

Stubbing et al. Eighty-five patients 76 male, 9 female; mean age, The proportion of non-smokers was higher in controls than in the COPD group. A comparison of thoracic cage dimensions between COPD patients and normal controls is presented in Table 3. COPD: chronic obstructive pulmonary disease; A: the maximal transverse diameter; B: mid-sagittal anteroposterior diameter; C and D: the maximal anteroposterior diameter of the right and left hemithorax. Table 6 summarizes the results of the univariate and multivariate regression analysis for factors related to increased ratio of AP and transverse diameter of the thoracic cage in patients with COPD.

In univariate analysis, height, BMI and smoking status were significantly associated with increased ratio of AP and transverse diameter of the thoracic cage in patients with COPD. The finding of increased AP diameter of the thoracic cage in COPD patients is consistent with results reported in previous studies 9 , 12 , 17 , 18 , 19 , 20 , 21 , However, as a measurement method, we consider that the use of CT in our study was more accurate than the simple caliper measurement of the chest wall and chest X-ray reported in previous studies 16 , 21 , If changes in the thoracic cage are reflective of the degree of hyperinflation, which is associated with more severe airflow obstruction, it is generally a more structural change in patients with COPD.

However, the AP diameter of the thoracic cage did not exhibit a difference according to the severity of COPD in our study. In addition, increased lung volume, which was assessed using TLC and RV in this study, was not associated with increased AP diameter of the thoracic cage.

These results suggest that thoracic cage changes in COPD may be associated with not only the degree of hyperinflation and lung function decline, but also various other factors including age, sex, weight, and height.

Age is an important factor in changes of the thoracic cage in the normal population. The elderly population typically exhibits a narrowing of the intervertebral disk space, which causes curvature of the spine, known as kyphosis This curvature decreases intercostal space and eventually leads to a smaller thoracic cage In this study, we also demonstrated that the overall diameter of the thoracic cage decreases with increasing age and rounding of the thoracic spine, resulting in greater decreases in AP diameter than the transverse diameter.

Because COPD is more prevalent in elderly individuals 25 , age-related changes in the thoracic cage are considered to be important contributing factors in these patients. It is also known that there are sex-related differences in the shape of the thoracic cage.

Previous studies investigating factors associated with changes in the shape of the thoracic cage have reported that sex has a greater influence on thoracic cage diameter than other factors such as BMI or age The proportion of males in the COPD group was not higher than in the normal controls in our study. Moreover, sex did not appear to be related to increased AP diameter in univariate and multivariate regression analysis in COPD patients.

BMI is also associated with the shape of the thoracic cage 12 , 16 , A previous study reported that increasing BMI may increase thoracic cage diameter in patients with emphysema, especially in the lower part of the lungs As a general concept, increased BMI can increase total thoracic cage length, which increases the AP diameter of thoracic cage.

This study revealed that height is more strongly associated with transverse—not AP—diameter of the thoracic cage. In contrast, weight is more strongly associated with AP—not transverse—diameter of the thoracic cage.

Although a relationship between increased thoracic cage diameter in COPD patients and lung volume was not documented in this study, several studies have reported changes in thoracic cage diameter according to lung volume.

Salito et al. We believe that it is necessary to evaluate these relationships in more patients with severe COPD and hyperinflation, and to assess the degree of hyperinflation than simple lung volume. We expected increased thoracic cage diameter to be associated with reduced exercise capacity in COPD patients because increased thoracic diameter may reflect more severe illness. However, the results of this study suggested that increased AP diameter of thoracic cage was positively associated with increased exercise capacity.

BMI has a greater effect on exercise capacity than thoracic cage diameter. In addition, exercise capacity in COPD patients is known to be associated not only with lung function but also various other factors, such as cardiac function, ventilator demand, and weakening and atrophy of peripheral skeletal muscles 31 , This study had some limitations, the first of which was its retrospective design.

Therefore, the number of patients with severe COPD was limited because those with more severe COPD are often unable to perform exercise tests because of dyspnea.

In addition, clinical characteristics, such as the degree of emphysema, frequency of exacerbation, and the phenotype of COPD associated with change s in the thoracic cage did not investigated in this study. In conclusion, this study demonstrated that AP diameter of thoracic cage, measured using CT, was increased in COPD patients compared with normal controls. Additional factors related to changes in the thoracic cage as COPD progresses will be investigated in the future. Conflicts of Interest: No potential conflict of interest relevant to this article was reported.

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