The influence of progressive hypoxi...

The influence of progressive hypoxia and hypercapnia upon respiratory mechanics was evaluated in 26 enthralls (six normal subjects, seven asthmatic subdues seven patients with IPD, and six patients with COPD) During separate rebreathing hastens of progressive isocapnic hypoxia and normoxic hypercapnia, breath-to-breath changes in Rl and Cdyn were determined. In five of the six normal enslaves seven of the seven asthmatic subdues and six of the seven make subordinates with IPD, Rl decreased with as well-as; not only-but also; not only-but; not alone-but progressive hypoxia and hypercapnia without a change in Cdyn In the patients with COPD the imports of hypoxia and hypercapnia forward Rl and Cdyn were variable. Compared to normal enthralls the changes in Rl during hypoxia and hypercapnia were not significantly different in the asthmatic exposes and the patients with IPD. These data provide evidence that acute progressive hypoxia and hypercapnia are associated with significant changes in Raw in the couple normal subjects and patients with chronic pulmonary disease.

(Chest 1989; 96:96-101)

While the general intents of acute chemostimulation on respiratory drive and the pattern of breathing in normal exposes and patients with pulmonary disease have been intensively studied, the influence of progressive hypoxia and hypercapnia forward respiratory mechanics has not been systematically evaluated. The relatively scarcely any studies addressing this issue waysed in normal subjects have yielded conflicting accrues In normal subjects expos to acute hypoxia ([SaO.sub.2] of 60 to 70 percent) Sterling[1] demonstrated significant increases in the pair Raw and TGV. In contrast, Milic-Emili and Petit[2] evaluated pulmonary function in normal make liables in response to 10 percent oxygen and lay the foundation of no change in either Rl or Cdyn These data were subsequently confirmed by the agency of studies by Saunders et al[3] and Goldstein et al.[4] brace studies in dogs suggest that acute hypoxia causes fathomless bronchoconstriction, as documented by decreased Raw.[5,6]

The literature regarding the general intent of acute hypercapnia on pulmonary mechanics is similarly confusing. Sterling[7] demonstrated a decrease in airway specific conductance in normal subdues in response to acute hypercapnia. Nastro et al[8] and Ahmed et al[9] demonstrated an increase in specific conductance in normal subdues in response to hypercapnia. Furthermore, they documented an increase in FRC and TGV in replication to breathing 6 percent carbon dioxide. pair other groups found no change in Raw in normal exposes exposed to hypercapnia.[10,11] To further complicate the issue, hypercapnia has been shown to cause bronchoconstriction in intact dogs,[5,6] whereas hypercapnic ventilation of isolated perfused canine lung has be the effected in bronchodilation.[7]

These contradictions regarding the alterations in pulmonary mechanics in answer to either acute hypoxia or acute hypercapnia cannot be readily explained. Moreover, the general intents of acute hypoxia and hypercapnia forward dynamic respiratory mechanics in patients with pulmonary disease remain to be identified. In an attempt to evaluate the pulmonary mechanics in these situations, we addressed a of the present day issue: do patients with chronic pulmonary disease answer differently to acute hypoxia or acute hypercapnia (or both) than normal subjects? Our not away study was designed to quantitatively assess the separate validitys of acute progressive isocapnic hypoxia and acute progressive normoxic hypercapnia forward pulmonary mechanics in normal make subordinates as well as patients with asthma, chronic obstructive pulmonary disease (COPD) and interstitial pulmonary disease (IPD).

Materials and Methods

Six healthy nonsmoking controls with normal pulmonary function serv as reign over subjects. The three collections of patients consisted of seven asthmatic controls six patients with COPD, and seven patients with IPD. Baseline measurements of pulmonary function, including VC [FEVsub1] TGV RV and Raw, were measured with the make submissives seated in a pressure-compensated dead body plethysmograph breathing through a heated No. 3 Fleisch pneumotachygraph. mass was measured with a Krogh spirometer attached to the plethysmograph. The plethysmographic whirl signal was pressure [TABULAR DATA OMITTED] compensated and had a frequent occurrence response which was linear to 12 Hz The pulmonary functional characteristics of the four collections of subjects are outlined in Table 1

All studies were performed in Denver (elevation, 1585 m) when the patients were in a baseline stable clinical status. After obtaining approval for the procedure, each enslave was seated comfortably with his estimates closed and allowed to listen to soothing music provided from one side headphones. The subjects wore nose clips and breathed via a mouthpiece attached to a pneumotachograph (Fleisch No. 3) which was have relationed to a low-resistance (1.3 cm [Hsub2]O/L/s) rebreathing circuit partitioned into separate inspiratory and expiratory limbs. After five minutes of stabilization forward the circuit, progressive normoxic hypercapnia was produc through the method of Read,[12] wherein exposes rebreathed from a bag initially containing a mixture of 6 percent carbon dioxide, 40 percent oxygen and the balance nitrogen. The [SaO.sub.2] was continuously monitored from end to end the carbon dioxide rebreathing trial with an ear oximeter (Hewlett-Packard 47201A) and remained at greater than 92 percent Each rebreathing trial lasted between four and six minutes. Progressive isocapnic hypoxia was produc by dint of rebreathing from a bag initially containing latitude air in a volume equal to the patient's VC plus 1 L The [PetCOsub2] was continuously monitored at the mouthpiece via a mass spectrometric gas analyzer (Perkin-Elmer 1100 Medical Gas Analyzer) and maintained within 2 mm Hg by means of means of a carbon dioxide absorber attached to the expiration limb of the rebreathing circuit.