We have observed patients who clinically have the obstructive sleep apnea syndrome but have no apneas, instead having recurrent nocturnal hypoventilation. There is disagreement about the definition and significance of such sleep-related hypopneas. We have thus analyzed breathing patterns, oxygenation and sleep records of 50 consecutive patients referred with the clinical features of the sleep apnea syndrome and found to have abnormal breathing during sleep to determine: (1) the best definition of hypopnea, and (2) how frequently patients have the clinical features of the sleep apnea syndrome without recurrent apneas. Hypopnea definitions based on decreases in thoracoabdominal movement yielded hypopnea frequencies that were significantly closer to desaturation and arousal frequencies than hypopnea definitions based on flow reduction. The best hypopnea definition was that of a 50% reduction in thoracoabdominal movement lasting for 10 s. This was validated in 33 normal subjects, all of whom had fewer than 11 hypopneas/h, and fewer than 14 apneas plus hypopneas/h of sleep. Thirty-two of the 50 patients had 10 or more apneas/h, the remaining 18 having 9 to 98 hypopneas/h such that all patients had more than 16 apneas plus hypopneas/h. Patients with recurrent hypopneas were clinically indistinguishable from and had a similar frequency of 4% desaturations (zero to 104/h) and arousals (7 to 98/h) to the patients with frequent apneas. This study confirms that hypopneas are clinically important and that the "sleep apnea syndrome" may occur in the absence of recurrent apneas.

We used a computerized microscopic image analysis system to directly measure the surface area of distal air spaces in methacrylate-embedded blocks randomly selected from inflation-fixed lobes that were resected from 45 patients as treatment of their peripheral lung tumors. In 28 of these patients, a preoperative computer tomography (CT) scan, at 6 and 10 cm below the sternal notch, was used to generate frequency histograms of CT numbers (measured as EMI units), a measure of lung density, in pixels from the lung or lobe that was subsequently resected. A similar CT number histogram was also derived from the lateral two fifths of the area of lobe/lung that was to be resected. The EMI unit that defined the lowest fifth percentile of this latter histogram correlated (n = 28, r = -0.77, p less than 0.001) with the mean value of the surface area of the walls of distal airspaces per unit lung volume (AWUV) in the five 1 mm x 1 mm microscopic fields with the lowest AWUV values, out of the 20 to 35 such fields examined in each patient. In the 34 of the 45 patients in whom we also measured volume-corrected diffusing capacity (DLCO/VA), this also correlated (n = 34, r = 0.84, p less than 0.001) with this value of AWUV, which measures the surface area of airspaces distal to the terminal bronchioles--reflecting an increase in airspace size, a defining characteristic of emphysema. However, a low DLCO/VA is nonspecific, whereas an abnormally low regional lung density is more likely to be specific for emphysema. In addition, highlighting those pixels of the CT display with low CT numbers (i.e., EMI units -500 [air] to -450, where zero = water) can locate areas of macroscopic emphysema, as shown by subsequent pathologic examination. Thus the quantitative CT scan can diagnose, quantitate, and locate mild to moderate emphysema, in humans, in life, noninvasively.

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We have used the CT transthoracic scan to measure regional lung density in vivo, as our previous studies have shown that this correlates with the increase in size of distal air spaces, which is a defining characteristic of emphysema. We have studied 32 patients with chronic airflow limitation (FEV1, 15 to 68% predicted) caused by chronic bronchitis and emphysema (synonym, COPD), with a wide range of arterial PO2 (38 to 90 mm Hg) and PCO2 (32 to 63 mm Hg) while breathing air at rest. We could find no significant relationships between the extent of emphysema (as assessed in vivo by the EMI number defining the lowest fifth percentile of the CT density histogram of the lung fields) and either arterial blood gas tensions, mean pulmonary arterial pressure, cardiac output, or calculated total pulmonary vascular resistance while at rest (n = 32) or during supine leg exercise (n = 29). We conclude that the extent of emphysema does not correlate with the clinical or pathologic features of the "pink and puffing" (i.e., mild hypoxemia, no CO2 retention, no pulmonary hypertension, etc.) or "blue and bloated" (i.e., hypoxemia, CO2 retention, pulmonary hypertension) pattern of patients with COPD nor to the spectrum of hemodynamic and gas exchange abnormalities that commonly occur in patients between these two extreme examples. Thus, "pink puffers" should not be equated with "the emphysematous" pattern of this disease. Although these clinicophysiologic patterns remain valid as descriptions, they do not relate to the extent of underlying emphysema in COPD.