This causes an enlargement of the ventricular wall known as hypertrophy. As the disease process continues, the heart will begin to remodel. Remodeling is the process of the heart muscle changing shape. As the heart remodels, the walls of the ventricle stretch and become thinner.
The shape of the ventricle becomes rounded and cardiac muscle weakens. EF will drop, and blood backs up. Left-ventricular failure results in blood backing into the pulmonary circulatory system. As pressure in the pulmonary blood vessels increases, fluid is pushed into the alveoli resulting in pulmonary edema.
Paroxysmal Nocturnal Dyspnea PND , a condition where the patient is short of breath while lying supine, may present in early stages. PND is a result of fluid in the lungs blocking oxygen exchange.
When the patient is in an upright position, the fluid is in the lung bases. When the patient lies supine, the fluid diffuses throughout the lung fields. This means more oxygen is blocked from exchanging in the alveoli. The patient will awaken with shortness of breath. The patient will progressively begin sleeping with more pillows and awake more frequently. Levels of B-type natriuretic peptide BNP , a protein released to help the body compensate for CHF, will elevate and be a helpful in-hospital diagnostic tool.
Class II heart failure is still classified as mild, but the patient will begin to experience dyspnea with moderate exertion. The patient is comfortable at rest but becomes short of breath while performing routine chores. The crackle transmission coefficient is lower in IPF than in pneumonia or CHF, and the combination of crackle pitch and crackle transmission coefficient separates IPF from pneumonia and CHF more clearly than either measurement alone.
We did not monitor air flow at the mouth. We chose to study the relationship of crackle characteristics to breathing maneuvers that can be performed at the bedside during routine physical examination. The patients in this study were instructed to breathe normally or more deeply by a technician who carefully observed their performance.
This can be readily done in most patients. Measuring flow at the mouth would have been difficult in many of the patients we studied. The majority of the patients with CHF and pneumonia were too ill to have their flow measured at the mouth or to be sent to a laboratory for pulmonary function testing.
In addition, devices that accurately measure flow at the mouth also alter the breathing pattern and minute ventilation. Other unexpected observations have been made in lung-sounds studies. Systematic studies of automated-auscultation recordings led to the rediscovery of the association of squawks with pneumonia. Such studies, which rapidly collect a large amount of objective acoustic information, offer the promise of uncovering other potentially useful associations of lung sounds with cardiopulmonary disorders.
The finding that crackle rate is reproducible in repeated measurements in a single automated-auscultation session shows that crackle rate can be used to follow the course of patients with CHF, pneumonia, and IPF. To further assess the clinical value of this observation, studies on whether individual practitioners using a stethoscope can be trained to reliably assess crackle rate and pitch should be done.
We have evidence that lung-sounds assessment by highly qualified pulmonary specialists compares favorably to computerized assessment. A study to determine whether less-trained clinicians can perform as well or be trained to do so is also indicated.
NOTE: We only request your email address so that the person you are recommending the page to knows that you wanted them to see it, and that it is not junk mail. We do not capture any email address. Skip to main content. Research Article Original Research. Andrey Vyshedskiy. Raymond LH Murphy Jr. Introduction Lung sounds detected over the chest reflect the underlying pulmonary pathophysiology.
All the patients performed the following sequence of breathing maneuvers: Normal breathing Deeper than normal breathing Coughing Deeper than normal breathing A vital-capacity maneuver Deeper than normal breathing Only data from maneuvers 1, 2, 4, and 6 are reported here Fig. View this table: View inline View popup Download powerpoint. Table 1. Average Tracheal Amplitude. Results Within-Maneuver Crackle Variability To compare crackle pitch ie, spectral frequency and crackle rate between breaths within each maneuver, we express the crackle pitch or rate in each breath as a percent of the crackle pitch or rate in the first breath Fig.
Table 2. Table 3. Table 4. Table 5. Between-Maneuver Crackle Variability We compared each patient's average crackle pitch during the first deeper-than-normal breathing to his or her crackle pitch during each of the other maneuvers, and we express the crackle pitch in each maneuver as a percentage of the crackle pitch during the first deeper-than-normal breathing Table 6. Table 6. Crackle Pitch in the 4 Breathing Maneuvers. Table 7. Crackles Measured on Multiple Days Our crackle rate and pitch assessment with each patient were done at a single session.
Discussion Crackles in all 3 conditions were surprisingly stable. Conclusions The finding that crackle rate is reproducible in repeated measurements in a single automated-auscultation session shows that crackle rate can be used to follow the course of patients with CHF, pneumonia, and IPF.
Dr Murphy and Dr Vyshedskiy have disclosed a relationship with Stethographics. References 1. In defense of the stethoscope. Respir Care ; 53 3 : — OpenUrl PubMed.
Clinical utility of chest auscultation in common pulmonary disease. Respiratory sounds: advances beyond the stethoscope. Gavriely N. Breath sounds methodology. CRC Press ; March 16 , State of the art: lung sounds.
Am Rev Respir Dis ; 4 : — Murphy RL Jr. Validation of an automatic crackle rale counter. Mechanism of inspiratory and expiratory crackles. Chest ; 1 : — Sound transmission in the lung as a function of lung volume. J Appl Physiology ; 93 2 : — Automated lung sound analysis in patients with pneumonia. Respir Care ; 49 12 : — Transmission of crackles in patients with interstitial pulmonary fibrosis, congestive heart failure, and pneumonia.
Chest ; 3 : — Visual lung sound characterization by time expanded wave-form analysis. N Engl J Med ; 17 : — Eur Respir Rev ; 10 : 77 ; — Gravity dependence of crackles: computers in critical care and pulmonary medicine.
Plenum Publishing ; : — Pneumonia may be mild or life-threatening. Bronchitis occurs when your bronchial tubes become inflamed. These tubes carry air to your lungs. The symptoms may include bibasilar crackles, a severe cough which brings up mucus, and wheezing.
Viruses, such as the cold or flu, or lung irritants usually cause acute bronchitis. Smoking is the main cause of chronic bronchitis. Pulmonary edema may cause crackling sounds in your lungs. People with congestive heart failure CHF often have pulmonary edema. CHF occurs when the heart cannot pump blood effectively. This results in a backup of blood, which increases blood pressure and causes fluid to collect in the air sacs in the lungs.
The interstitium is the tissue and space that surrounds the air sacs of the lung. Any lung disease that impacts this area is known as interstitial lung disease. It may be caused by:. Although not as common, bibasilar crackles may also be present if you have chronic obstructive pulmonary disease COPD or asthma.
A study showed that lung crackles may be related to age in some asymptomatic cardiovascular patients. Although more research is needed, the study found that after the age of 45, the occurrence of crackles tripled every 10 years. Your doctor uses a stethoscope listens to you breathe and to listen for bibasilar crackles. Crackles make a similar sound to rubbing your hair between your fingers, near your ear.
In severe cases, crackles may be heard without a stethoscope. If you have bibasilar crackles, your doctor will take your medical history and possibly order diagnostic tests to look for the cause. These tests can include:. Table 1 shows the number of patients in each group and in each disease.
A reverse phenomenon was observed during expiration. The progressive decrease of crackle pitch was observed during expiration in most patients, Table 2. There is considerable evidence, summarized by Forgacs [ 1 ], that inspiratory crackles are caused by airway opening.
There is also some evidence that expiratory crackles are caused by abrupt airway closing [ 2 , 3 ]. Our group recently reported that crackle rate and crackle pitch do not vary significantly from breath to breath [ 12 ]. Even when breaths were separated by cough and vital capacity maneuver crackle rate and crackle pitch did not vary significantly in a single auscultation session.
In this report, we systematically examined crackle pitch as a function of crackle timing during a single breath. We have observed that in the majority of patients crackle pitch progressively increases during inspiration and progressively decreases during expiration. This finding is consistent with the clinical observations that coarser lower-pitched crackles tend to occur in early inspiration and that finer higher-pitched crackles tend to occur in late-inspiration. Several hypotheses are consistent with this observation.
The first hypothesis proposes that crackle pitch is determined by airway diameter. Airways with progressively smaller diameter are recruited during inspiration. Therefore, crackles recorded during the beginning of inspiration are expected to be generated by larger diameter airways than the crackles generated at the end of inspiration. If crackle pitch is determined by airway diameter then crackles generated in the beginning of inspiration are expected to have lower pitch than the crackles generated at the end of inspiration.
The progressive pitch decrease during expiration is explained similarly as smaller airways close earlier in expiration than larger airways. How can we explain the association between crackle pitch and the airway diameter? When an airway collapses, the walls of the airway become flat. In this position, the airway wall tissue can be compared to a guitar string fixed at both ends. Airways opening during an inspiration sets airway walls tissue into motion. The resonant frequency of a guitar string is determined by its length, tension, and density.
Shorter lengths, higher tension, and lower density increase the resonant frequency. If the analogy with a guitar string has scientific merits, we can expect higher-pitched crackles generated by smaller airways with higher tension and lower airway wall density.
If crackle pitch is influenced by airway tension, then greater crackle pitch can be explained by increased airway tension at greater lung volume. Finally, the third hypothesis proposes that crackles are generated closer to the chest wall at larger lung volumes. According to this hypothesis, crackles generated at lower lung volume are generated deeper in the lung and are low pass filtered by the lung parenchyma to a greater extend. This hypothesis concludes that the difference in pitch is the result of the difference of sound filtering by lung parenchyma.
It is also feasible that all three mechanisms contribute to the increase of crackle pitch at greater lung volume. In summary, we observed that within a single breath crackle pitch tends to increase during inspiration and decrease during expiration. While the clinical implications of this observation are not clear, better general understanding of the mechanism of crackles production offers the promise of improving noninvasive diagnosis of lung disorders.
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