Alveolar Dead-Space Fraction and Arterial Saturation Predict Postoperative Course in Fontan Patients*

2020 ◽  
Vol 21 (4) ◽  
pp. e200-e206
Author(s):  
Eran Shostak ◽  
Ofer Schiller ◽  
Aviad Merzbach ◽  
Tzippy Shochat ◽  
Gabriel Amir ◽  
...  
Author(s):  
Imran A. Sayed ◽  
Scott Hagen ◽  
Victoria Rajamanickam ◽  
Petros V. Anagnostopoulos ◽  
Marlowe Eldridge ◽  
...  

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

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.


1962 ◽  
Vol 17 (3) ◽  
pp. 417-420 ◽  
Author(s):  
C. P. Larson ◽  
J. W. Severinghaus

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


1979 ◽  
Vol 47 (4) ◽  
pp. 745-753 ◽  
Author(s):  
K. Rehder ◽  
T. J. Knopp ◽  
A. D. Sessler ◽  
E. P. Didier

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.


1998 ◽  
Vol 5 (3) ◽  
pp. 215-218 ◽  
Author(s):  
Marc A Rodger ◽  
Gwynne Jones ◽  
Francois Raymond ◽  
Daniel Lalonde ◽  
Mike Proulx ◽  
...  

Physiological and alveolar dead space ventilation both increase in pulmonary embolism (PE) in proportion to the severity of vascular obstruction. The case of a patient with recurrent PE while on heparin therapy is presented. The recurrence was characterized clinically by severe pulmonary vascular obstruction and right heart dysfunction. The patient was treated with thrombolytic therapy, with excellent clinical and scintigraphic resolution. Dead space ventilation measurements at baseline, at the time of recurrence and after thrombolytic therapy are presented. The potential utility of dead space ventilation measurements for PE diagnosis and management are discussed.


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