Maldistribution Of Ventilation Research Articles

Short term abstinence from smoking: its place in preoperative preparation.

Newer pulmonary function instruments make measurement of small airway function possible as a routine, inexpensive part of preoperative preparation of patients with obstructive lung disease. Patients with early stages of chronic obstructive lung disease have maldistribution of ventilation and perfusion producing an increased A-a oxygen gradient. If the disease is at a reversible stage, early diagnosis and treatment should be helpful in preventing postoperative complications. Five volunteer heavy smokers stopped smoking for one week without any improvement in small airway function. A longer period of abstinence and other therapeutic modalities for these patients is needed prior to surgery to reduce the postoperative impact of this pathology.

Pulmonary function during clinical remission of asthma. How reversible is asthma?

Summary: The frequency, range and severity of functional abnormalities during complete clinical remission of asthma were studied in 57 patients. Ninety per cent had abnormal tests, the usual pattern being impaired ventilatory capacity, hyperinflation, maldistribution of ventilation, ventilation/blood‐flow inequality and hyperventilation with norm‐al arterial oxygen tension and gas transfer. If spirometry had been used as the sole screening procedure, nearly one third of patients with abnormal function would have been missed. The measurement of lung volumes appeared to be the most practical way to detect these latter patients. Since there is a poor relation between symptoms and functional abnormalities in asthma, laboratory measurements are an important adjunct to clinical assessment. Although asthma is generally regarded as reversible airways obstruction, the extent of reversibility appears to be frequently incomplete.

Alveolar-arterial PCO2 difference during rebreathing in patients with chronic hypercapnia.

ArticleAlveolar-arterial PCO2 difference during rebreathing in patients with chronic hypercapnia.J D McEvoy, N L Jones, and E J CampbellJ D McEvoy, N L Jones, and E J CampbellPublished Online:01 Oct 1973https://doi.org/10.1152/jappl.1973.35.4.542MoreSectionsPDF (968 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByA quick and easy method of measuring the hypercapnic ventilatory response in patients with COPDRespiratory Medicine, Vol. 103, No. 2CO2 rebreathing model in COPD: blood-to-gas equilibration8 September 2006 | European Journal of Applied Physiology, Vol. 98, No. 5Mesure non invasive du débit cardiaque par réinhalation de CO2 chez le patient en ventilation contrôléeRéanimation Urgences, Vol. 2, No. 4CapnographyAutomated non-invasive measurement of cardiac output: comparison of electrical bioimpedance and carbon dioxide rebreathing techniques.Heart, Vol. 59, No. 3Blood/gas equilibrium of carbon dioxide in lungs. A critical reviewRespiration Physiology, Vol. 39, No. 1Blood–Gas Equilibration in LungsMeasurements of Cardiac Output in Seriously Ill Patients Using a CO2 Rebreathing MethodChest, Vol. 73, No. 2Symptomatic Osseous Sarcoidosis with Findings on Bone ScanChest, Vol. 73, No. 2Reproducibility of Data on Steady-State Gas Exchange and Indices of Maldistribution of Ventilation and Blood FlowChest, Vol. 71, No. 6 More from this issue > Volume 35Issue 4October 1973Pages 542-5 https://doi.org/10.1152/jappl.1973.35.4.542PubMed4743014History Published online 1 October 1973 Published in print 1 October 1973 Metrics

Serial studies of lung volume and VA-Q in hyaline membrane disease.

Extract: Twenty infants with a clinical and radiologic diagnosis of hyaline membrane disease were studied serially by measurement of functional residual capacity (FRC) and arterial and alveolar gradients for O2, CO2, and N2. Nitrogen washouts were determined as well in nine infants. The FRC, alveolar-arterial O2 gradients (AaDo2) in 100% O2, and true shunt (Qs/Qt), which are different ways of quantitating atelectasis and shunt in hyaline membrane disease, were shown to be statistically related. The FRC was below 1.0 ml/cm in all infants when sick and returned to the usual range for gestational age, generally around 15 days. Extensive cardiopulmonary shunting was recorded both at the height of illness and for a considerable time during recovery. However, during recovery, not all of the venous admixture was due to shunt. As maldistribution of ventilation was excluded, the possibility of a diffusion barrier was raised. Alveoli with a high VA/Q were identified by large arterial-alveolar CO2 gradients (aADCO2) both during illness and recovery. This indicates that maldistribution of pulmonary blood flow is an important physiologic abnormality in hyaline membrane disease. Speculation: The FRC was shown to correlate inversely with AaDo2 and Qs/Qt ratios. As a low FRC is the only true unique characteristic of hyaline membrane disease, it is suggested that in the future the disease be defined in terms of the lung volume as well as in terms of the usual clinical and biochemical parameters which appear in other forms of respiratory distress in neonates. Constant positive airway pressure is an attempt to approach treatment from this point of view.

PATHOPHYSIOLOGIC ROLE OF HYPOCARBIA IN POST-TRAUMATIC PULMONARY INSUFFICIENCY

Abstract Post-traumatic pulmonary insufficiency (PTPI) is characterized by hypoxemia, hypocarbia, and respiratory alkalosis. The roles of hypocarbia and respiratory alkalosis in aggravating pulmonary dysfunction have been investigated in five patients with PTPI by sequential volume ventilation under paralysis both with 100 per cent oxygen and with 97 per cent oxygen plus 3 per cent carbon dioxide. When normocarbia was produced by supplemental carbon dioxide, arterial oxygenation improved, alveolar-arterial gradients diminished, airways resistance reduced, and cardiac output and pulmonary perfusion pressures increased. Hypocarbia aggravates PTPI by inducing bronchoconstriction which may cause maldistribution of ventilation, heightened airways resistance, and increased work of breathing. Additionally, alkalosis unfavorably affects oxyhemoglobin dissociation and regional (pulmonary, coronary, and cerebral) blood flows. Rationale is provided for more attentive regulation of alveolar carbon dioxide tensions in such patients.

Pathophysiologic role of hypocarbia in post-traumatic pulmonary insufficiency

Post-traumatic pulmonary insufficiency (PTPI) is characterized by hypoxemia, hypocarbia, and respiratory alkalosis. The roles of hypocarbia and respiratory alkalosis in aggravating pulmonary dysfunction have been investigated in five patients with PTPI by sequential volume ventilation under paralysis both with 100 per cent oxygen and with 97 per cent oxygen plus 3 per cent carbon dioxide. When normocarbia was produced by supplemental carbon dioxide, arterial oxygenation improved, alveolar-arterial gradients diminished, airways resistance reduced, and cardiac output and pulmonary perfusion pressures increased. Hypocarbia aggravates PTPI by inducing bronchoconstriction which may cause maldistribution of ventilation, heightened airways resistance, and increased work of breathing. Additionally, alkalosis unfavorably affects oxyhemoglobin dissociation and regional (pulmonary, coronary, and cerebral) blood flows. Rationale is provided for more attentive regulation of alveolar carbon dioxide tensions in such patients.

ADJUSTMENT OF VENTILATION AND PERFUSION IN THE FULL-TERM NORMAL AND DISTRESSED NEONATE AS DETERMINED BY URINARY ALVEOLAR NITROGEN GRADIENTS

The urinary alveolar nitrogen gradient was measured serially in 20 normal and six distressed full-term newborn infants. When the gradient is small (less than 10 mm Hg) ventilation is evenly distributed throughout the lung. When a large gradient is determined this is a reflection of numbers of alveoli with low ventilation-perfusion (VA/Q) ratios. In healthy adults used as a control for the method, a gradient of less than 10 mm Hg was recorded. Healthy, nondistressed newborn infants were almost all within the normal range from the first day of life. Infants found to have distress due to meconium aspiration or transient neonatal tachypnea had large gradients throughout the first week of life. The studies indicate that the healthy, full-term infant rapidly achieves a normal distribution of pulmonary ventilation, whereas serious maldistribution of ventilation occurs in meconium aspiration pneumonia.

Adjustment of Ventilation in the Newborn

In adapting to extrauterine life, ventilation and perfusion must soon become well-matched. the time course of this process can be assessed by measurement of the urinary-alveolar nitrogen gradient (uADN2). An elevated uADN2 is an indication of the maldistribution of VA/Q, specifically the presence of areas of low VA/Q. Seventeen healthy full-term neonates were studied serially from the first day of life. Values of uADN2 within the range for normal adults were found (less than 10mm Hg). Serial studies on 3 infants with evidence of aspiration pneumonia revealed uADN2 consistently elevated above the normal. Children and adults with obstructive pulmonary disease were tested as a validation of the method and the expected elevation of uADN2 was found. Thw studies indicate that (1) ventilation is uniformly distribution in the first days of life in normal infants; (2) maldistribution of ventilation is an important cause of arterial unsaturation in aspiration pneumonia. These results will be considered in the context of other studies of extrauterine pulmonary adaptation.

Physiologic studies on infants with Wilson-Mikity syndrome: Ventilation-perfusion abnormalities and cardiac catheterization angiography

Abnormalities of ventilation and perfusion were found in infants with the Wilson-Mikity syndrome. Intrapulmonary shunting and maldistribution of ventilation and perfusion were noted. Three patients were subjected to cardiac catheterization and pulmonary hypertension was detected. The increased pulmonary vascular resistance was unresponsive to oxygen, suggesting permanent damage to the pulmonary capillary bed. Angiocardiography showed changes typical of pulmonary hypertension.

Arterial hypoxemia following acute myocardial infarction.

Arterial hypoxemia was common in 53 patients following acute myocardial infarction. It was most marked in patients with evidence of left ventricular failure. Arterial oxygen tension, however, was reduced in many of the patients who were without evidence of failure. An increase in arterial oxygen tension following three deep breaths suggested maldistribution of ventilation. Right-to-left shunting of blood was demonstrated by 100% oxygen studies. There was a significant correlation between reduced arterial oxygen tension and low pulmonary diffusing capacity, but a poor correlation between the former and a low cardiac index. We suggest that the hypoxemia following acute myocardial infarction is the result of abnormalities in small airways as well as of vascular congestion in the lungs. The patients with the lowest arterial oxygen tension at the time of study subsequently had more marked arrhythmias and a higher mortality rate.

UNIFORMITY OF VENTILATION IN THE NEWBORN INFANT: DIRECT ASSESSMENT OF THE ARTERIAL-ALVEOLAR N2 DIFFERENCE

The arterial-alveolar pressure difference for nitrogen (aADN2) was directly measured during the first 4 hours after birth in nine clinically normal infants. Transient gross elevations of the aADN2 were seen in most babies, indicating early maldistribution of ventilation. However, by 4 hours of age, the aADN2 had subsided to 6 ± 22 mm Hg, a value characteristic of normal older infants and children. These findings are in conflict with previous indirect assessments of aADN2 by analyses of urinary nitrogen pressure. It is concluded that normal infants achieve excellent uniformity of pulmonary distribution of gas and blood soon after birth.

Airway resistance and uneven ventilation in bronchial asthma

ARTICLESAirway resistance and uneven ventilation in bronchial asthmaE. R. McFadden Jr., and Harold A. LyonsE. R. McFadden Jr.Department of Medicine, State University of New York, Downstate Medical Center, Kings County Hospital Center, Brooklyn, New York 11203, and Harold A. LyonsDepartment of Medicine, State University of New York, Downstate Medical Center, Kings County Hospital Center, Brooklyn, New York 11203Published Online:01 Oct 1968https://doi.org/10.1152/jappl.1968.25.4.365MoreSectionsPDF (1 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByMorphometric changes after thermal and methacholine bronchoprovocationsChakradhar Kotaru, Albert Coreno, Mary Skowronski, Gary Muswick, Robert C. Gilkeson, and E. R. McFadden1 March 2005 | Journal of Applied Physiology, Vol. 98, No. 3Mechanical strain enhances proteoglycan message in fibroblasts from asthmatic subjectsClinical <html_ent glyph="@amp;" ascii="&"/> Experimental Allergy, Vol. 34, No. 6Acute Severe AsthmaAmerican Journal of Respiratory and Critical Care Medicine, Vol. 168, No. 7Modulation of airway caliber by deep inhalation in childrenManlio Milanese, Chiara Mondino, Mariangela Tosca, G. Walter Canonica, and Vito Brusasco1 April 2000 | Journal of Applied Physiology, Vol. 88, No. 4Status Asthmaticus30 June 2016 | Journal of Intensive Care Medicine, Vol. 4, No. 4Relationship between maldistribution of ventilation and airways obstruction in children with asthmaRespiration Physiology, Vol. 69, No. 3Glucocorticoids in acute asthmaThe American Journal of Medicine, Vol. 74, No. 5Sites of airway dilatation in asthma following inhaled versus subcutaneous terbutalineThe American Journal of Medicine, Vol. 68, No. 1The role of mucociliary dysfunction in bronchial asthmaThe American Journal of Medicine, Vol. 67, No. 3Effects of an inhaled bronchodilator on gas distribution and over-all ventilatory efficiency in patients with chronic obstructive pulmonary diseaseThe American Journal of Medicine, Vol. 61, No. 1Pulmonary function in ambulatory asthmaticsJournal of Chronic Diseases, Vol. 29, No. 4Small airway diseaseThe American Journal of Medicine, Vol. 57, No. 2A reduction in maximum mid-expiratory flow rateThe American Journal of Medicine, Vol. 52, No. 6 More from this issue > Volume 25Issue 4October 1968Pages 365-370 Copyright & PermissionsCopyright © 1968 the American Physiological Societyhttps://doi.org/10.1152/jappl.1968.25.4.365History Received 1 April 1968 Published online 1 October 1968 Published in print 1 October 1968 Metrics

Effect of oxygen breathing on distribution of pulmonary blood flow in chronic obstructive lung disease.

In chronic obstructive lung disease, a major functional disturbance lies in maldistribution of ventilation of the lungs. It has been postulated that, at least in some patients, compensatory regional pulmonary vasoconstriction may occur in the poorly ventilated portions of such lungs, thus reducing the range of ventilation-perfusion ratios and improving arterial oxygen tension. The evidence for this lies largely in the reduction of arterial oxygen tension or saturation that may follow the administration of pulmonary vasodilator drugs, such as tolazoline (1, 2) and aminophylline (3-5). It has been suggested that these drugs reverse pre-existing vasoconstriction in poorly ventilated regions of the lungs and that this leads to a worsening of ventilation-perfusion ratio distribution and a fall in arterial oxygen tension. Oxygen is a powerful, nonspecific, pulmonary vasodilator agent. Pain, Read, and Read (6) showed that in a group of patients with chronic lung disease oxygen breathing was sometimes associated with an increase of arterial carbon dioxide tension (Pac02 ) greater than that to be expected from any hypoventilation produced by the oxygen. It was suggested that these increases of Pa002, not due to diminished ventilation of the lungs, were also due to worsening of ventilationperfusion ratio distribution in the lungs. Analysis of the factors involved indicated that this, in turn, must reflect an increased blood flow through poorly ventilated regions of the lungs associated with oxygen breathing; that is, there was reversal of pre-existing regional compensatory vasoconstriction in some of these patients. These conclusions were based on comparisons of ventilation and Pa002 that were made when the subject was breathing air and after breathing oxygen for ten minutes. Some of the conclusions

Mechanical factors in distribution of pulmonary ventilation.

Mechanical factors in distribution of pulmonary ventilation.