scholarly journals Crackle Pitch Rises Progressively during Inspiration in Pneumonia, CHF, and IPF Patients

2012 ◽  
Vol 2012 ◽  
pp. 1-4 ◽  
Author(s):  
Andrey Vyshedskiy ◽  
Raymond Murphy
Keyword(s):  
Heart Failure ◽  
Lung Volume ◽  
Interstitial Fibrosis ◽  
Lung Sounds ◽  
Lung Sound ◽  
Lung Volumes ◽  
Alternate Explanation ◽  
40 Hz

Objective. It is generally accepted that crackles are due to sudden opening of airways and that larger airways produce crackles of lower pitch than smaller airways do. As larger airways are likely to open earlier in inspiration than smaller airways and the reverse is likely to be true in expiration, we studied crackle pitch as a function of crackle timing in inspiration and expiration. Our goal was to see if the measurement of crackle pitch was consistent with this theory.Methods. Patients with a significant number of crackles were examined using a multichannel lung sound analyzer. These patients included 34 with pneumonia, 38 with heart failure, and 28 with interstitial fibrosis.Results. Crackle pitch progressively increased during inspirations in 79% of all patients. In these patients crackle pitch increased by approximately 40 Hz from the early to midinspiration and by another 40 Hz from mid to late-inspiration. In 10% of patients, crackle pitch did not change and in 11% of patients crackle pitch decreased. During expiration crackle pitch progressively decreased in 72% of patients and did not change in 28% of patients.Conclusion. In the majority of patients, we observed progressive crackle pitch increase during inspiration and decrease during expiration. Increased crackle pitch at larger lung volumes is likely a result of recruitment of smaller diameter airways. An alternate explanation is that crackle pitch may be influenced by airway tension that increases at greater lung volume. In any case improved understanding of the mechanism of production of these common lung sounds may help improve our understanding of pathophysiology of these disorders.

Methacholine-induced bronchoconstriction in dogs: effects of lung volume and O3 exposure

1988 ◽  
Vol 65 (6) ◽  
pp. 2679-2686 ◽  
Author(s):  
S. T. Kariya ◽  
S. A. Shore ◽  
W. A. Skornik ◽  
K. Anderson ◽  
R. H. Ingram ◽  
...  
Keyword(s):  
Lung Volume ◽  
Maximal Response ◽  
Maximal Effect ◽  
Response Curves ◽  
Lung Volumes ◽  
Before And After ◽  
Residual Capacity ◽  
Induced Changes ◽  
Conducting Airways ◽  
Concentration Response Curve

The maximal effect induced by methacholine (MCh) aerosols on pulmonary resistance (RL), and the effects of altering lung volume and O3 exposure on these induced changes in RL, was studied in five anesthetized and paralyzed dogs. RL was measured at functional residual capacity (FRC), and lung volumes above and below FRC, after exposure to MCh aerosols generated from solutions of 0.1-300 mg MCh/ml. The relative site of response was examined by magnifying parenchymal [RL with large tidal volume (VT) at fast frequency (RLLS)] or airway effects [RL with small VT at fast frequency (RLSF)]. Measurements were performed on dogs before and after 2 h of exposure to 3 ppm O3. MCh concentration-response curves for both RLLS and RLSF were sigmoid shaped. Alterations in mean lung volume did not alter RLLS; however, RLSF was larger below FRC than at higher lung volumes. Although O3 exposure resulted in small leftward shifts of the concentration-response curve for RLLS, the airway dominated index of RL (RLSF) was not altered by O3 exposure, nor was the maximal response using either index of RL. These data suggest O3 exposure does not affect MCh responses in conducting airways; rather, it affects responses of peripheral contractile elements to MCh, without changing their maximal response.

scholarly journals p90 ribosomal S6 kinase 3 contributes to cardiac insufficiency in α-tropomyosin Glu180Gly transgenic mice

2013 ◽  
Vol 305 (7) ◽  
pp. H1010-H1019 ◽  
Author(s):  
Catherine L. Passariello ◽  
Marjorie Gayanilo ◽  
Michael D. Kritzer ◽  
Hrishikesh Thakur ◽  
Zoharit Cozacov ◽  
...  
Keyword(s):  
Heart Failure ◽  
Transgenic Mice ◽  
Cardiac Function ◽  
Interstitial Fibrosis ◽  
Cardiac Insufficiency ◽  
S6 Kinase ◽  
Transgenic Expression ◽  
P90 Ribosomal S6 Kinase ◽  
Ribosomal S6 Kinase

Myocardial interstitial fibrosis is an important contributor to the development of heart failure. Type 3 p90 ribosomal S6 kinase (RSK3) was recently shown to be required for concentric myocyte hypertrophy under in vivo pathological conditions. However, the role of RSK family members in myocardial fibrosis remains uninvestigated. Transgenic expression of α-tropomyosin containing a Glu180Gly mutation (TM180) in mice of a mixed C57BL/6:FVB/N background induces a cardiomyopathy characterized by a small left ventricle, interstitial fibrosis, and diminished systolic and diastolic function. Using this mouse model, we now show that RSK3 is required for the induction of interstitial fibrosis in vivo. TM180 transgenic mice were crossed to RSK3 constitutive knockout ( RSK3−/−) mice. Although RSK3 knockout did not affect myocyte growth, the decreased cardiac function and mild pulmonary edema associated with the TM180 transgene were attenuated by RSK3 knockout. The improved cardiac function was consistent with reduced interstitial fibrosis in the TM180; RSK3−/− mice as shown by histology and gene expression analysis, including the decreased expression of collagens. The specific inhibition of RSK3 should be considered as a potential novel therapeutic strategy for improving cardiac function and the prevention of sudden cardiac death in diseases in which interstitial fibrosis contributes to the development of heart failure.

Breathing at low lung volumes and chest strapping: a comparison of lung mechanics

1981 ◽  
Vol 50 (3) ◽  
pp. 650-657 ◽  
Author(s):  
N. J. Douglas ◽  
G. B. Drummond ◽  
M. F. Sudlow
Keyword(s):  
Lung Volume ◽  
Maximum Flow ◽  
Normal Subjects ◽  
Lung Mechanics ◽  
Lung Volumes ◽  
Flow Rates ◽  
Recoil Pressure ◽  
Forced Expiratory Flow ◽  
Expiratory Flow ◽  
Expiratory Flow Rates

In six normal subjects forced expiratory flow rates increased progressively with increasing degrees of chest strapping. In nine normal subjects forced expiratory flow rates increased with the time spent breathing with expiratory reserve volume 0.5 liters above residual volume, the increase being significant by 30 s (P less than 0.01), and flow rates were still increasing at 2 min, the longest time the subjects could breathe at this lung volume. The increase in flow after low lung volume breathing (LLVB) was similar to that produced by strapping. The effect of LLVB was diminished by the inhalation of the atropinelike drug ipratropium. Quasistatic recoil pressures were higher following strapping and LLVB than on partial or maximal expiration, but the rise in recoil pressure was insufficient to account for all the observed increased in maximum flow. We suggest that the effects of chest strapping are due to LLVB and that both cause bronchodilatation.

scholarly journals THE LUNG VOLUME IN HEART DISEASE

1923 ◽  
Vol 38 (4) ◽  
pp. 445-476 ◽  
Author(s):  
Carl A. L. Binger
Keyword(s):  
Heart Disease ◽  
Lung Volume ◽  
Vital Capacity ◽  
Lung Volumes ◽  
Total Lung Volume ◽  
Surface Areas ◽  
Normal Individuals ◽  
The Absolute ◽  
Total Capacity ◽  
Residual Air

The lung volumes in a group of individuals suffering from chronic cardiac disease have been studied by a method which is applicable to patients suffering from dyspnea. In a number of instances the same patients were investigated during various stages of decompensation and compensation. The values found have been compared with those determined in a group of normal subjects. Lung volumes have been considered from three points of view: (1) relative lung volumes or subdivisions of total lung volume expressed as percentage of total lung volume; (2) the absolute lung volumes of patients with heart disease have been compared with lung volumes calculated for normal individuals having similar surface areas or chest measurements; and (3) in individual cases absolute lung volumes have been measured in various stages of compensation and decompensation. (1) In patients with heart disease it has been observed that the vital capacity forms a portion of the total lung volume relatively smaller than in normal individuals, and that the mid-capacity and residual air form relatively larger portions. When the patient progresses from the compensated to the decompensated state these changes become more pronounced. (2) When the absolute lung volumes determined for patients are compared with volumes of the same sort, as calculated for normal individuals of the same surface areas and chest measurements, the following differences are found. The vital capacities are always smaller in the patients and the volumes of residual air are always larger. There is a tendency for middle capacity and total capacity to be smaller, though, when the patients are in a compensated state, these volumes may approximate normal. (3) When decompensation occurs the absolute lung volumes undergo changes as follows: (a) vital capacity, mid-capacity, and total capacity decrease in volume; and (b) the residual air may either increase or decrease according to the severity of the state of decompensation. The significance of these changes has been discussed and an explanation offered for the occurrence of a residual air of normal volume in patients with heart disease. It results from a combination of two tendencies working in opposite directions: one to increase the residual air—stiffness of the lungs (Lungenstarre); the other to decrease it—distended capillaries (Lungenschwellung), edema, round cell infiltration.

Abstract 428: Pharmacologic and Activated Fibroblast-specific Gβγ-GRK2 Inhibition is Protective Following Ischemia Reperfusion Injury

2016 ◽  
Vol 119 (suppl_1) ◽  
Author(s):  
Joshua G Travers ◽  
Fadia A Kamal ◽  
Michelle L Nieman ◽  
Michelle A Sargent ◽  
Jeffery D Molkentin ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiac Function ◽  
Reperfusion Injury ◽  
G Protein ◽  
Knockout Mice ◽  
Ischemia Reperfusion Injury ◽  
Interstitial Fibrosis ◽  
Myocardial Dysfunction ◽  
Ischemia Reperfusion ◽  
Ventricular Compliance

Heart failure is a devastating disease characterized by chamber remodeling, interstitial fibrosis and reduced ventricular compliance. Cardiac fibroblasts are responsible for extracellular matrix homeostasis, however upon injury or pathologic stimulation, these cells transform to a myofibroblast phenotype and play a fundamental role in myocardial fibrosis and remodeling. Chronic sympathetic overstimulation induces excess signaling through G protein βγ subunits and ultimately the pathologic activation of G protein-coupled receptor kinase 2 (GRK2). We hypothesized that Gβγ-GRK2 inhibition plays an important role in the cardiac fibroblast to attenuate pathologic myofibroblast activation and cardiac remodeling. To investigate this hypothesis, mice were subjected to ischemia/reperfusion (I/R) injury and treated with the small molecule Gβγ-GRK2 inhibitor gallein. While animals receiving vehicle demonstrated a reduction in overall cardiac function as measured by echocardiography, mice treated with gallein exhibited nearly complete preservation of cardiac function and reduced fibrotic scar formation. We next sought to establish the cell specificity of this compound by treating inducible cardiomyocyte- and activated fibroblast-specific GRK2 knockout mice post-I/R. Although we observed modest restoration in cardiac function in cardiomyocyte-specific GRK2 null mice, treatment of these mice with gallein resulted in further protection against myocardial dysfunction following injury, suggesting a functional role in other cardiac cell types, including fibroblasts. Activated fibroblast-specific GRK2 knockout mice were also subjected to ischemia/reperfusion injury; these animals displayed preserved myocardial function and reduced collagen deposition compared to littermate controls following injury. Furthermore, systemic Gβγ-GRK2 inhibition by gallein did not appear to confer further protection over activated fibroblast-specific GRK2 ablation alone. In summary, these findings suggest a potential therapeutic role for Gβγ-GRK2 inhibition in limiting pathologic myofibroblast activation, interstitial fibrosis and heart failure progression.

Abstract P170: Nicorandil Inhibits Gáq-Induced Chronic Heart Failure in Transgenic Mice

2011 ◽  
Vol 109 (suppl_1) ◽  
Author(s):  
Masamichi Hirose ◽  
Yasuchika Takeishi ◽  
Hisashi Shimojo ◽  
Toshihide Kashihara ◽  
Tsutomu Nakada ◽  
...  
Keyword(s):  
Heart Failure ◽  
Transgenic Mice ◽  
Structural Changes ◽  
Interstitial Fibrosis ◽  
Left Ventricular ◽  
Acute Administration ◽  
Sulfonylurea Receptor ◽  
Inhibitory Effects ◽  
Premature Ventricular Contractions ◽  
Beneficial Effects

Introduction: Beneficial effects of nicorandil on the treatment of hypertensive heart failure (HF) and ischemic heart disease have been suggested. However, whether nicorandil has inhibitory effects on HF and ventricular arrhythmias caused by the activation of G protein alpha q (Gαq) -coupled receptor (GPCR) signaling pathway still remains unknown. We examined effects of chronic and acute administration of nicorandil on the development of HF and ventricular action potential (VAP) in transgenic mice with transient cardiac expression of activated Gαq (Gαq-TG), respectively. Method and Results: Nicorandil (6 mg/kg/day) or vehicle was chronically administered in Gαq-TG mice for 24 weeks from 8 weeks of age, and then ventricular function, and electrical and structural changes were investigated in the hearts. Chronic nicorandil administration improved the reduction of left ventricular fractional shortening (p < 0.001) in Gαq-TG hearts. During 10 min of electrocardiogram recording, premature ventricular contractions (more than 20 beats/min) were observed in 7 of 10 vehicle-treated Gαq-TG but in none of 10 nicorandil-treated Gαq-TG hearts (p < 0.01). QT interval was significantly shorter in nicorandil-treated Gαq-TG than in vehicle-treated Gαq-TG hearts (p < 0.05). Chronic nicorandil administration improved the increased ventricular interstitial fibrosis (p < 0.05) but not cardiac hypertrophy in Gαq-TG left ventricles. Real time RT-PCR revealed that mRNA expression levels of s sulfonylurea receptor 2B (SUR-2B) were decreased in vehicle-treatd Gαq-TG but not in nicorandil-treated Gαq-TG. In addition, chronic nicorandil increased endotherial nitric oxide syntheses gene expression in Gαq-TG hearts (p < 0.05). Acute nicorandil administration (1 microM) significantly shortened the prolonged VAP duration and reduced the number of PVCs in vehicle treated Gαq-TG hearts. Conclusions: These findings suggest that nicorandil inhibits ventricular electrical and structural remodeling and arrhythmias through the shortening of VAP duration and the increased expression of SUR-2B and eNOS in a mouse model of HF.

Automated classification of human lung sound signals using phase space representation of intrinsic mode function

2021 ◽  
Author(s):  
Sibghatullah I. Khan ◽  
Vikram Palodiya ◽  
Lavanya Poluboyina
Keyword(s):  
Phase Space ◽  
Human Lung ◽  
Feature Space ◽  
Normal Lung ◽  
Space Representation ◽  
Support Vector ◽  
Lung Sounds ◽  
Lung Sound ◽  
Phase Space Representation

Abstract Bronchiectasis and chronic obstructive pulmonary disease (COPD) are common human lung diseases. In general, the expert pulmonologistcarries preliminary screening and detection of these lung abnormalities by listening to the adventitious lung sounds. The present paper is an attempt towards the automatic detection of adventitious lung sounds ofBronchiectasis,COPD from normal lung sounds of healthy subjects. For classification of the lung sounds into a normaland adventitious category, we obtain features from phase space representation (PSR). At first, the empirical mode decomposition (EMD) is applied to lung sound signals to obtain intrinsic mode functions (IMFs). The IMFs are then further processed to construct two dimensional (2D) and three dimensional (3D) PSR. The feature space includes the 95% confidence ellipse area and interquartile range (IQR) of Euclidian distances computed from 2D and 3D PSRs, respectively. The process is carried out for the first four IMFs correspondings to normal and adventitious lung sound signals. The computed features depicta significant ability to discriminate the two categories of lung sound signals.To perform classification, we use the least square support vector machine with two kernels, namely, polynomial and radial basis function (RBF).Simulation outcomes on ICBHI 2017 lung sound dataset show the ability of the proposed method in effectively classifying normal and adventitious lung sound signals. LS-SVM is employing RBF kernel provides the highest classification accuracy of 97.67 % over feature space constituted by first, second, and fourth IMF.

scholarly journals Assessment of the influence of lung inflation state on the quantitative parameters derived from hyperpolarized gas lung ventilation MRI in healthy volunteers

2019 ◽  
Vol 126 (1) ◽  
pp. 183-192 ◽  
Author(s):  
Paul J. C. Hughes ◽  
Laurie Smith ◽  
Ho-Fung Chan ◽  
Bilal A. Tahir ◽  
Graham Norquay ◽  
...  
Keyword(s):  
Healthy Volunteers ◽  
Lung Volume ◽  
Lung Ventilation ◽  
Lung Volumes ◽  
Lung Inflation ◽  
Longitudinal Measurements ◽  
Anatomical Images ◽  
Lower Lung ◽  
Ventilation Heterogeneity ◽  
Residual Capacity

In this study, the effect of lung volume on quantitative measures of lung ventilation was investigated using MRI with hyperpolarized 3He and 129Xe. Six volunteers were imaged with hyperpolarized 3He at five different lung volumes [residual volume (RV), RV + 1 liter (1L), functional residual capacity (FRC), FRC + 1L, and total lung capacity (TLC)], and three were also imaged with hyperpolarized 129Xe. Imaging at each of the lung volumes was repeated twice on the same day with corresponding 1H lung anatomical images. Percent lung ventilated volume (%VV) and variation of signal intensity [heterogeneity score (Hscore)] were evaluated. Increased ventilation heterogeneity, quantified by reduced %VV and increased Hscore, was observed at lower lung volumes with the least ventilation heterogeneity observed at TLC. For 3He MRI data, the coefficient of variation of %VV was <1.5% and <5.5% for Hscore at all lung volumes, while for 129Xe data the values were 4 and 10%, respectively. Generally, %VV generated from 129Xe images was lower than that seen from 3He images. The good repeatability of 3He %VV found here supports prior publications showing that percent lung-ventilated volume is a robust method for assessing global lung ventilation. The greater ventilation heterogeneity observed at lower lung volumes indicates that there may be partial airway closure in healthy lungs and that lung volume should be carefully considered for reliable longitudinal measurements of %VV and Hscore. The results suggest that imaging patients at different lung volumes may help to elucidate obstructive disease pathophysiology and progression. NEW & NOTEWORTHY We present repeatability data of quantitative metrics of lung function derived from hyperpolarized helium-3, xenon-129, and proton anatomical images acquired at five lung volumes in volunteers. Increased regional ventilation heterogeneity at lower lung inflation levels was observed in the lungs of healthy volunteers.

Lung volume specificity of inspiratory muscle training

1994 ◽  
Vol 77 (2) ◽  
pp. 789-794 ◽  
Author(s):  
G. E. Tzelepis ◽  
D. L. Vega ◽  
M. E. Cohen ◽  
F. D. McCool
Keyword(s):  
Lung Volume ◽  
Vital Capacity ◽  
Inspiratory Muscle ◽  
Control Group ◽  
Residual Volume ◽  
Maximal Inspiratory Pressure ◽  
Muscle Training ◽  
Inspiratory Capacity ◽  
Lung Volumes ◽  
Before And After

We examined the extent to which training-related increases of inspiratory muscle (IM) strength are limited to the lung volume (VL) at which the training occurs. IM strength training consisted of performing repeated static maximum inspiratory maneuvers. Three groups of normal volunteers performed these maneuvers at one of three lung volumes: residual volume (RV), relaxation volume (Vrel), or Vrel plus one-half of inspiratory capacity (Vrel + 1/2IC). A control group did not train. We constructed maximal inspiratory pressure-VL curves before and after a 6-wk training period. For each group, we found that the greatest improvements in strength occurred at the volume at which the subjects trained and were significantly greater for those who trained at low (36% for RV and 26% for Vrel) than at high volumes (13% for Vrel + 1/2IC). Smaller increments in strength were noted at volumes adjacent to the training volume. The range of vital capacity (VC) over which strength was increased was greater for those who trained at low (70% of VC) than at high VL (20% of VC). We conclude that the greatest improvements in IM strength are specific to the VL at which training occurs. However, the increase in strength, as well as the range of volume over which strength is increased, is greater for those who trained at the lower VL.

Sign in / Sign up

Export Citation Format

Share Document