Breath-holding Time in Normal Subjects, Snorers, and Sleep Apnea Patients

CHEST Journal ◽  
1995 ◽  
Vol 107 (4) ◽  
pp. 959-962 ◽  
Author(s):  
Varsha Taskar ◽  
Nigel Clayton ◽  
Mark Atkins ◽  
Zubair Shaheen ◽  
Patricia Stone ◽  
...  
1959 ◽  
Vol 14 (1) ◽  
pp. 105-108 ◽  
Author(s):  
Ingemar Kjellmer ◽  
Lars Sandqvist ◽  
Erik Berglund

The single breath N2 elimination test, as standardized by Comroe and Fowler, has been used in normal subjects. The N2 difference, i.e. the difference in N2 concentration between Ve = 1250 and Ve = 750 ml, showed a tendency to increase with increasing volumes of inspired O2 and with increasing inspiratory flow rates. It decreased with increasing breath-holding time and was not consistently influenced by expiratory flow rate. The findings are compared with those of Fowler and of Shephard on normal subjects; different results were obtained, largely depending on different analytical procedures. These factors must be considered when evaluating results in patients. Submitted on July 21, 1958


1971 ◽  
Vol 41 (3) ◽  
pp. 275-283 ◽  
Author(s):  
M. I. M. Noble ◽  
J. H. Eisele ◽  
H. L. Frankel ◽  
Wendy Else ◽  
A. Guz

1. Block of the phrenic nerves in three normal subjects, produced by injection of lignocaine in the neck, caused alleviation of the thoracic sensation during breath holding and prolonged breath-holding time. 2. Injection of lignocaine in the neck without nerve block had no effect on breath holding sensation or breath-holding time. 3. A patient with a spinal-cord transection at the third cervical segment with paralysed diaphragm and chest wall, had no sensation in the chest or abdomen during breath holding. 4. This patient maintained normal ventilation by using hypertrophied sternomastoid muscles. During breath holding he experienced no sensation in the neck despite the presence of sternomastoid contraction. 5. There is previous evidence that complete muscular paralysis abolishes breath-holding sensation but that paralysis of all muscles innervated from spinal segments below the eighth cervical has no effect.


2017 ◽  
Vol 38 (3-4) ◽  
pp. 85
Author(s):  
Sudigdo Sastroasmoro ◽  
Nuraini Irma Susanti

The definite diagnosis of cardiac disease in infants and children usuallycannot be made on the clinical evidence alone; in most instances supportingexaminations are required. lt is understandable, therefore, that non-cardiologists might suggest that normal subjects are thought to have cardiac problems; the reverse is also true: infants and children with cardiac disease may be ignored. This study aimed to examine the clinical and laboratory findings of normal infants and children who were initially suspected to have cardiac disease. Of 3601 patients referred to our OPD of the Division of Cardiology, Department of Child Health, Medical School, University of Indonesia, from January 1983 to December 1992; in 1782 patient (49.5%) no cardiovascular problems were detected. Most of them (66.2%) were of the age of less than 1 month. Most of the referring physicians (66.3%) were general practitioners. The referring diagnoses were congenital heart disease (286), cardiomegaly (197), rheumatic fever or rheumatic heart disease (110), and syndromes with cardiac involvement (104). The diagnoses were based on dyspnea, cyanosis on crying, chest pain, joint pains, and easy fatiguability. Murmurs found on examination were systolic in 355 patients (19. 9%), and continuous in 6 patients (0,33%). No diastolic murmurs were noted. The final diagnoses were normal (including innocent murmurs and sinus arrhythmias) in 85.8%, mild cardiomegaly in 10.4%., breath holding spells in 2.0%, sinus tachycardia in 0.9%, polyarthritis in 0.2% and other in 0.7% of all cases. More practice in cardiac physical examination is needed for medical students to reduce the unnecessary referrals.


1984 ◽  
Vol 56 (1) ◽  
pp. 52-56 ◽  
Author(s):  
T. S. Hurst ◽  
B. L. Graham ◽  
D. J. Cotton

We studied 10 symptom-free lifetime non-smokers and 17 smokers all with normal pulmonary function studies. All subjects performed single-breath N2 washout tests by either exhaling slowly (“slow maneuver”) from end inspiration (EI) to residual volume (RV) or exhaling maximally (“fast maneuver”) from EI to RV. After either maneuver, subjects then slowly inhaled 100% O2 to total lung capacity (TLC) and without breath holding, exhaled slowly back to RV. In the nonsmokers seated upright phase III slope of single-breath N2 test (delta N2/l) was lower (P less than 0.01) for the fast vs. the slow maneuver, but this difference disappeared when the subjects repeated the maneuvers in the supine position. In contrast, delta N2/l was higher for the fast vs. the slow maneuver (P less than 0.01) in smokers seated upright. For the slow maneuver, delta N2/l was similar between smokers and nonsmokers but for the fast maneuvers delta N2/l was higher in smokers than nonsmokers (P less than 0.01). We suggest that the fast exhalation to RV decreases delta N2/l in normal subjects by decreasing apex-to-base differences in regional ratio of RV to TLC (RV/TLC) but increases delta N2/l in smokers, because regional RV/TLC increases distal to sites of small airways obstruction when the expiratory flow rate is increased.


CHEST Journal ◽  
1985 ◽  
Vol 88 (5) ◽  
pp. 776-778 ◽  
Author(s):  
Christian Guilleminault ◽  
Robert Riley ◽  
Nelson Powell

1999 ◽  
Vol 87 (4) ◽  
pp. 1532-1542 ◽  
Author(s):  
Anthony P. Pietropaoli ◽  
Irene B. Perillo ◽  
Alfonso Torres ◽  
Peter T. Perkins ◽  
Lauren M. Frasier ◽  
...  

Human airways produce nitric oxide (NO), and exhaled NO increases as expiratory flow rates fall. We show that mixing during exhalation between the NO produced by the lower, alveolar airways (V˙l NO) and the upper conducting airways (V˙u NO) explains this phenomenon and permits measurement ofV˙l NO,V˙u NO, and the NO diffusing capacity of the conducting airways (Du NO). After breath holding for 10–15 s the partial pressure of alveolar NO (Pa) becomes constant, and during a subsequent exhalation at a constant expiratory flow rate the alveoli will deliver a stable amount of NO to the conducting airways. The conducting airways secrete NO into the lumen (V˙u NO), which mixes with Pa during exhalation, resulting in the observed expiratory concentration of NO (Pe). At fast exhalations, Pa makes a large contribution to Pe, and, at slow exhalations, NO from the conducting airways predominates. Simple equations describing this mixing, combined with measurements of Pe at several different expiratory flow rates, permit calculation of Pa,V˙u NO, and Du NO.V˙l NOis the product of Pa and the alveolar airway diffusion capacity for NO. In seven normal subjects, Pa = 1.6 ± 0.7 × 10−6 (SD) Torr,V˙l NO= 0.19 ± 0.07 μl/min,V˙u NO= 0.08 ± 0.05 μl/min, and Du NO = 0.4 ± 0.4 ml ⋅ min−1 ⋅ Torr−1. These quantitative measurements ofV˙l NOandV˙u NOare suitable for exploring alterations in NO production at these sites by diseases and physiological stresses.


1994 ◽  
Vol 76 (4) ◽  
pp. 1494-1501 ◽  
Author(s):  
G. R. Soparkar ◽  
J. T. Mink ◽  
B. L. Graham ◽  
D. J. Cotton

The dynamic changes in CO concentration [CO] during a single breath could be influenced by topographic inhomogeneity in the lung or by peripheral inhomogeneity due to a gas mixing resistance in the gas phase of the lung or to serial gradients in gas diffusion. Ten healthy subjects performed single-breath maneuvers by slowly inhaling test gas from functional residual capacity to one-half inspiratory capacity and slowly exhaling to residual volume with target breath-hold times of 0, 1.5, 3, 6, and 9 s. We calculated the three-equation single-breath diffusing capacity of the lung for CO (DLSBCO-3EQ) from the mean [CO] in both the entire alveolar gas sample and in four successive equal alveolar gas samples. DLSBCO-3EQ from the entire alveolar gas sample was independent of breath-hold time. However, with 0 s of breath holding, from early alveolar gas samples DLSBCO-3EQ was reduced and from late alveolar gas samples it was increased. With increasing breath-hold time, DLSBCO-3EQ from the earliest alveolar gas sample rapidly increased, whereas from the last alveolar gas sample it rapidly decreased such that all values from the small alveolar gas samples approached DLSBCO-3EQ from the entire alveolar sample. These changes correlated with ventilation inhomogeneity, as measured by the phase III He concentration slope and the mixing efficiency, and were larger for maneuvers with inspired volumes to one-half inspiratory capacity vs. total lung capacity.(ABSTRACT TRUNCATED AT 250 WORDS)


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