The Effect of Alveolar Dead Space on the Measurement of End-Expiratory Lung Volume by Modified Nitrogen Washout/Washin in Lavage-Induced Lung Injury

2012 ◽  
Author(s):  
Rui Tang ◽  
Yingzi Huang ◽  
Qiuhua Chen ◽  
Xia Hui ◽  
Yang Li ◽  
...  
Keyword(s):  
Lung Injury ◽  
Lung Volume ◽  
Dead Space ◽  
Alveolar Dead Space ◽  
Nitrogen Washout

Spontaneous Breathing Improves Lung Aeration in Oleic Acid–induced Lung Injury

2003 ◽  
Vol 99 (2) ◽  
pp. 376-384 ◽  
Author(s):  
Hermann Wrigge ◽  
Jörg Zinserling ◽  
Peter Neumann ◽  
Jerome Defosse ◽  
Anders Magnusson ◽  
...  
Keyword(s):  
Oleic Acid ◽  
Lung Injury ◽  
Lung Volume ◽  
Spontaneous Breathing ◽  
Arterial Oxygen Tension ◽  
Carbon Dioxide Tension ◽  
Arterial Oxygen ◽  
Nitrogen Washout ◽  
Lung Aeration ◽  
Pressure Release Ventilation

Background Experimental and clinical studies have shown reduction in intrapulmonary shunt with improved oxygenation by spontaneous breathing with airway pressure release ventilation (APRV) in acute lung injury. The mechanisms of these findings are not clear. The authors hypothesized that spontaneous breathing results in better aeration of lung tissue and that improvement in oxygenation can be explained by these changes. This hypothesis was studied in a porcine model of oleic acid-induced lung injury. Methods Two hours after induction of lung injury, 24 pigs were randomly assigned to APRV with or without spontaneous breathing at a positive end-expiratory pressure of 5 cm H(2)O. Hemodynamics, spirometry, and end-expiratory lung volume by nitrogen washout were measured at baseline, after 2 h of lung injury, and after 2 and 4 h of mechanical ventilation in the specific mode. Finally, spiral computed tomography of the chest was performed at end-expiratory lung volume in 22 pigs. Results Arterial carbon dioxide tension and mean and end-inspiratory airway pressures were comparable between settings. Four hours of APRV with spontaneous breathing resulted in improved oxygenation compared with APRV without spontaneous breathing (arterial oxygen tension, 144 +/- 65 vs. 91 +/- 50 mmHg, P < 0.01 for interaction time x mode), higher end-expiratory lung volume (786 +/- 320 vs. 384 +/- 148 ml, P < 0.001), and better aeration. End-expiratory lung volume and venous admixture were both correlated with the amount of lung reaeration (r(2) = 0.62 and r(2) = 0.61, respectively). Conclusions The results support the hypothesis that spontaneous breathing during APRV improves oxygenation mainly by recruitment of nonaerated lung and improved aeration of the lungs.

scholarly journals The Use of Alveolar Dead Space Fraction to Predict Postoperative Outcomes after Pediatric Cardiac Surgery: A Retrospective Study

2021 ◽  
Author(s):  
Imran A. Sayed ◽  
Scott Hagen ◽  
Victoria Rajamanickam ◽  
Petros V. Anagnostopoulos ◽  
Marlowe Eldridge ◽  
...  
Keyword(s):  
Cardiac Surgery ◽  
Retrospective Study ◽  
Dead Space ◽  
Pediatric Cardiac Surgery ◽  
Postoperative Outcomes ◽  
Alveolar Dead Space

PULMONARY FUNCTION IN THE NEWBORN INFANT

PEDIATRICS ◽  
1962 ◽  
Vol 30 (6) ◽  
pp. 975-989
Author(s):  
N. M. Nelson ◽  
L. S. Prod'hom ◽  
R. B. Cherry ◽  
P. J. Lipsitz ◽  
C. A. Smith
Keyword(s):  
Pulmonary Function ◽  
Respiratory Distress ◽  
Newborn Infant ◽  
Dead Space ◽  
Clinical Course ◽  
Average Difference ◽  
Alveolar Dead Space ◽  
Physiological Dead Space ◽  
New Born ◽  
Pulmonary Capillary

The arterial-alveolar tension gradient for CO2 has been investigated in 17 normal new born infants and in 15 with some degree of respiratory distress. Whereas the normal infants had virtually no Pco2 gradient from pulmonary capillary to alveolus, an average difference of 13.9 mm Hg was detected in sick infants. This gradient for Pco2 is caused by increased alveolar (and total physiological dead space, the relative amount of which closely parallels the clinical course of the disease. The data obtained indicate the increase in alveolar dead space to be largely due to poor perfusion of ventilated alveoli. In severely ill infants more than 60% of ventilated alveoli appear to be under-perfused.

Postural variations in dead space and CO2 gradients breathing air and O2

1962 ◽  
Vol 17 (3) ◽  
pp. 417-420 ◽  
Author(s):  
C. P. Larson ◽  
J. W. Severinghaus
Keyword(s):  
Dead Space ◽  
Normal Limit ◽  
Healthy Adult ◽  
Sitting Position ◽  
Alveolar Dead Space ◽  
Vascular Bed ◽  
Postural Changes ◽  
Physiologic Dead Space ◽  
Pulmonary Vascular Bed

Effects of postural changes on anatomic and physiologic dead space and arterial-alveolar CO2gradients were studied in 11 healthy, adult subjects breathing air and O2. Results indicate that, on moving from the supine to the sitting position, Vads and Vpds increased by corresponding amounts (42 and 37 ml) with no increase in alveolar dead space or volume of lung which is nonperfused. Arterial-alveolar CO2 gradients were unaffected by posture, but more than doubled with O2 breathing, suggesting that O2 may relax the pulmonary vascular bed and diminish perfusion of highest lung segments. Isoproterenol aerosol (0.5%) produced significant bronchodilatation (27 ml increase in Vads), but only small and inconsistent increases in alveolar dead space and CO2 gradients. The PDS/Vt ratio in these subjects while sitting, breathing air, averaged 31 ± 6%, which is higher than the normally accepted value of 30%. As a result, the upper normal limit for PDS/Vt has been increased to 40% in our laboratories. Submitted on January 22, 1962

scholarly journals Effect of Recruitment and Body Positioning on Lung Volume and Oxygenation in Acute Lung Injury Model

2008 ◽  
Vol 36 (6) ◽  
pp. 792-797 ◽  
Author(s):  
H. G. Ryu ◽  
J.-H. Bahk ◽  
H.-J. Lee ◽  
J.-G. Im
Keyword(s):  
Acute Lung Injury ◽  
Oleic Acid ◽  
Lung Injury ◽  
Lung Volume ◽  
Supine Position ◽  
Recruitment Manoeuvre ◽  
Prone Positioning ◽  
Dependent Lung ◽  
Arterial Blood Gas ◽  
Arterial Blood

The mechanism of oxygenation improvement after recruitment manoeuvres or prone positioning in acute lung injury or acute respiratory distress syndrome is still unclear. We tried to determine the mechanism responsible for the effects of recruitment manoeuvres or prone positioning on lung aeration using a whole lung computed tomography scan in an oleic acid induced acute lung injury canine model. Twelve adult mongrel dogs were allocated into either the supine group (n=6) or the prone group (n = 6). After the establishment of acute lung injury, three recruitment manoeuvres were performed at one-hour intervals. Haemodynamic and ventilatory variables, arterial blood gas analyses and CT scans of the whole lung were obtained 90 minutes after oleic acid injection and five minutes before and after each recruitment manoeuvre. Recruitment manoeuvres in the supine position improved oxygenation (P=0.025) that correlated with increase of the poorly- and well-aerated dorsal (dependent) lung volume (r=0.436, P=0.016). Prone positioning increased oxygenation (P=0.004) that also correlated with increase of the poorly- and well-aerated dorsal (nondependent) lung volume (r=0.787, P <0.001). However, the recruitment manoeuvre in the prone position had no effect on oxygenation despite an increase in ventral (dependent) lung volume. The increase in PO2 after recruitment manoeuvres in the supine position or after prone positioning is related to the increase of the poorly- and well-aerated dorsal lung.

Ventilation-perfusion relationship in young healthy awake and anesthetized-paralyzed man

1979 ◽  
Vol 47 (4) ◽  
pp. 745-753 ◽  
Author(s):  
K. Rehder ◽  
T. J. Knopp ◽  
A. D. Sessler ◽  
E. P. Didier
Keyword(s):  
Blood Flow ◽  
Healthy Volunteers ◽  
Dead Space ◽  
Flow Distribution ◽  
Blood Flow Distribution ◽  
Alveolar Dead Space ◽  
Awake State ◽  
Lateral Decubitus ◽  
Inspired Oxygen ◽  
Ventilation And Perfusion

Distributions of ventilation and perfusion relative to Va/Q were determined in seven young healthy volunteers (24–33 yr) while they were either in the supine or right lateral decubitus position. The subjects were studied first awake and then while anesthetized-paralyzed and breathing 30% oxygen and again while breathing 100% oxygen. In the awake state, no statistically significant differences were observed in the distribution of ventilation and perfusion relative to Va/Q between the supine and right lateral decubitus positions or on changing the inspired oxygen concentrations. After induction of anesthesia-paralysis, Va/Q mismatching increased significantly but only small right-to-left intrapulmonary shunts developed. Ventilating the lungs with 100% oxygen further increased the dispersion of blood flow distribution during anesthesia-paralysis; lung units with low Va/Q or right-to-left intrapulmonary shunts (or both) developed. With induction of anesthesia-paralysis and intubation of the trachea, the anatomic dead space was decreased and the alveolar dead space increased.

Effects of altering ventilation on steady-state diffusing capacity for carbon monoxide

1963 ◽  
Vol 18 (1) ◽  
pp. 89-96 ◽  
Author(s):  
Kaye H. Kilburn ◽  
Harry A. Miller ◽  
John E. Burton ◽  
Ronald Rhodes
Keyword(s):  
Carbon Monoxide ◽  
Steady State ◽  
Tidal Volume ◽  
Lung Volume ◽  
Dead Space ◽  
Control Level ◽  
Alveolar Ventilation ◽  
Positive Pressure ◽  
Diffusing Capacity ◽  
Fixed Rate

Alterations in the steady-state diffusing capacity for carbon monoxide (Dco) by the method of Filley, MacIntosh, and Wright, produced by sequential changes in the pattern of breathing were studied in anesthetized, paralyzed, artificially ventilated dogs. The Dco of paralyzed, artificially ventilated control dogs did not differ significantly during 3 hr from values found in conscious and anesthetized controls. A fivefold increase in tidal volume without changing frequency of breathing raised alveolar ventilation and CO uptake 500% and Dco 186%. A high correlation between tidal volume and Dco was noted during reciprocal alterations of tidal volume and rate which maintained minute volume. The Dco appeared to fall when alveolar ventilation was tripled by increments of rate with a fixed-tidal volume, despite a 63% increase in CO uptake. Doubling end-expiratory lung volume by positive pressure breathing without altering tidal volume or rate did not affect Dco. The addition of 100 ml of external dead space with rate and tidal volume constant decreased Dco to 42% of control level, however, stepwise reduction of dead space from 100 ml to 0 in two dogs failed to change Dco. Added dead space equal to frac12 tidal volume (170 ml) reduced Dco to 25% of control in two dogs with a return to control with removal of dead space. Thus, in paralyzed artificially ventilated dogs, tidal volume appears to be the principal ventilatory determinant of steady-state Dco. Dco is minimally affected by increases in alveolar ventilation with a constant tidal volume effected by increasing the frequency of breathing. Prolonged ventilation, at fixed rate and volume, and increased dead space either did not effect, or they reduced Dco, perhaps by rendering less uniform the distribution of gas, and blood in the lungs. Although lung volume was doubled by positive-pressure breathing, pulmonary capillary blood volume was probably reduced to produce opposing effects on diffusing capacity and no net change. Submitted on March 14, 1962

Distal effects of tracheal gas insufflation: changes with catheter position and oleic acid lung injury

1996 ◽  
Vol 81 (3) ◽  
pp. 1121-1127 ◽  
Author(s):  
A. Nahum ◽  
S. A. Ravenscraft ◽  
A. B. Adams ◽  
J. J. Marini
Keyword(s):  
Oleic Acid ◽  
Lung Injury ◽  
Dead Space ◽  
Minute Ventilation ◽  
Catheter Position ◽  
Tracheal Gas Insufflation ◽  
Before And After ◽  
Dead Space Volume ◽  
Catheter Tip ◽  
Conducting Airways

We separated distal (turbulence-related) and proximal (dead space washout-related) effects of tracheal gas insufflation (TGI) by comparing the effects of straight and inverted catheters. We reasoned that the inverted catheter was unlikely to remove CO2 from conducting airways distal to its orifice. In six normal dogs during TGI at 10 l/min, advancing the catheters from 10 to 1 cm above the main carina decreased dead space volume by 29 +/- 12 and 12 +/- 6 ml (P < 0.04) with the straight and inverted catheters, respectively. By comparison, the tracheal volume between 10 and 1 cm above the carina was 15 +/- 2 ml. In another set of dogs (n = 5), we examined the distal effects of TGI before and after oleic acid-induced lung injury. During TGI at 10 l/min before and after oleic acid injury, the differences in arterial PCO2 between the straight and inverted catheters were 5 +/- and 9 +/- 6 Torr (P < 0.18), respectively. Our data suggest that distal effects of TGI become more pronounced as the catheter tip is positioned closer to the main carina. The distal effects of TGI were not diminished after oleic acid injury when minute ventilation was maintained constant.

Effect of inhaled nitric oxide on pulmonary hemodynamics after acute lung injury in dogs

1994 ◽  
Vol 76 (3) ◽  
pp. 1356-1362 ◽  
Author(s):  
J. A. Romand ◽  
M. R. Pinsky ◽  
L. Firestone ◽  
H. A. Zar ◽  
J. R. Lancaster
Keyword(s):  
Nitric Oxide ◽  
Acute Lung Injury ◽  
Gas Exchange ◽  
Lung Injury ◽  
Dead Space ◽  
Left Ventricular ◽  
Right Atrial ◽  
Adrenergic Blockade ◽  
Pulmonary Hemodynamics ◽  
Beta Adrenergic

Increased pulmonary vascular resistance (PVR) and mismatch in ventilation-to-perfusion ratio characterize acute lung injury (ALI). Pulmonary arterial pressure (Ppa) decreases when nitric oxide (NO) is inhaled during hypoxic pulmonary vasoconstriction (HPV); thus NO inhalation may reduce PVR and improve gas exchange in ALI. We studied the hemodynamic and gas exchange effects of NO inhalation during HPV and then ALI in eight anesthetized open-chest mechanically ventilated dogs. Right atrial pressure, Ppa, and left ventricular and arterial pressures were measured, and cardiac output was estimated by an aortic flow probe. Shunt and dead space were also estimated. The effect of 5-min exposures to 0, 17, 28, 47, and 0 ppm inhaled NO was recorded during hyperoxia, hypoxia, and oleic acid-induced ALI. During ALI, partial beta-adrenergic blockade (propranolol, 0.15 mg/kg i.v.) was induced and 74 ppm NO was inhaled. Nitrosylhemoglobin (NO-Hb) and methemoglobin (MetHb) levels were measured. During hyperoxia, NO inhalation had no measurable effects. Hypoxia increased Ppa (from 19.8 +/- 6.1 to 28.3 +/- 8.7 mmHg, P < 0.01) and calculated PVR (from 437 +/- 139 to 720 +/- 264 dyn.s.cm-5, P < 0.01), both of which decreased with 17 ppm NO. ALI decreased arterial PO2 and increased airway pressure, shunt, and dead space ventilation. Ppa (19.8 +/- 6.1 vs. 23.4 +/- 7.7 mmHg) and PVR (437 +/- 139 vs. 695 +/- 359 dyn.s.cm-5, P < 0.05) were greater during ALI than during hyperoxia. No inhalation had no measureable effect during ALI before or after beta-adrenergic blockade. MetHb remained low, and NO-Hb was unmeasurable. Bolus infusion of nitroglycerin (15 micrograms) induced an immediate decrease in Ppa and PVR during ALI.(ABSTRACT TRUNCATED AT 250 WORDS)

Sign in / Sign up

Export Citation Format

Share Document