Inflation of the PAC balloon caused a slight but statistically significant reduction in PetC02 (0 to 15 mm Hg, Table 1), but no significant differences in any variable of pulmonary and systemic hemodynamics (Table 2). However, there was a significant decrease (more than 50 mm Hg) in PaOa/FIOg in 15 patients (14.9 percent); seven of these patients (6.9 percent) showed a more remarkable decrease (more than 100 mm Hg) in PaOj/FIOg during PAOP measurement (Fig 1). On the other hand, 11 out of 101 patients (10.9 percent) showed a significant increase (more than 50 mm Hg) in PaCVFIo2. There was no significant correlation between changes in PaO/FIOg and those in PetC02 (r = 0.26), nor between changes in PkCV FIo2 and control PAP (r = 0.09, Fig 2).
Although patients’ ages or sizes (body surface area, body mass index and height) did not correlate with the changes in Pa(VFIo2, there was a significant difference in the changes in PaOa/FIo2 between male and female patients (Fig 1); 11 of 15 patients who showed remarkable decreases in PaOj/FIOjj (more than 50 mm Hg) were female. The patients with coronary artery disease tended to have decreases in Pa(VFIo2 (Table 3) and in those with either coronary artery disease or valvular heart disease, there were significant correlations between changes in PaOa/FIOj and control AP (Fig 3). Twenty-nine patients (28.7 percent) were cigarette smokers and they were all male patients. No significant change in FsO/Flo2 was found in both smoking and nonsmoking male patients.
Examinations of the chest radiographs of 60 patients revealed that the tip of the PAC was located either in the right main pulmonary artery (33 patients), the right side of lobar arteries (23 patients), or the left main pulmonary artery (four patients). In the patients with the PAC located in the right main pulmonary artery, Pa(VFIo2 decreased significantly during the balloon inflation (p<0.05). Among five different anesthesia techniques used, the patients with high-dose Fentanyl anesthesia only had a statistically significant decrease in PaC>2/FIo2 during the PAC balloon inflation (Fig 4). other
Table 1—Values of Arterial Blood Gases and End-Tidal CO* before and during Inflation of the Balloon
|Inflation of the Balloon*||A(Range)|
|PaOg/FIo2 (mm Hg)||449 ±87||439 ±94||-9± 58 (-186-153)|
|Male (n = 61)||433 ±89||437 ±95||3 ±41 (-126-112)|
|Female (n = 40)||468 ±83||440 ±96t||-28± 73 (-186—153)|
|PaC02 (mm Hg)||35±5||35±6||0±3 (-20-9)|
|pHa||7.44±0.05||7.44±0.05||-0± 0.02 (-0.12-0.05)|
|Base excess (mEq/L)||0.8±2.4||1.0±2.6||0.2± 1.4 (-8.1—4.0)|
|PetCOj (mm Hg)||31 ±5||28±5t||— 2±4 (-15-0)|
Table 2—Hemodynamic Variables before and during Inflation of the Balloon
|Inflation of the Balloon*|
|SAP (mm Hg)||121 ±23||120 ±23|
|DAP (mm Hg)||67 ± 17||66± 15|
|HR (breaths per minute)||70 ± 16||70 ±17|
|SPAP (mm Hg)||24± 17|
|DPAP (mm Hg)||9±4|
|PAOP (mm Hg)||7±4|
|RAP (mm Hg)||6±3||6±3|
|CO (L/min)||4.4± 1.4|
Table 3—Changes in FaOJFlot following the Inflation of the Balloon in Rtiients with Cardiac Disease, Pulmonary Carcinoma and Other Disorders
|Primary Disorders||n||Inflation of the Balloon*|
|Valvular heart disease||19||468 ±68||456 ±99||(mm||Hg)|
|Coronary artery disease||15||460 ±95||418±112f||(mm||Hg)|
|Other cardiac disease||7||483 ±87||450 ±71||(mm||Hg)|
|Pulmonary carcinoma||21||435 ±104||427 ±105||(mm||Hg)|
|Others||39||431 ±81||440 ±83||(mm||Hg)|
Figure 1. Changes of PaOa/FIo2 during PAOP measurements with respect to gender difference.
Figure 2. No correlation between changes in FaOj/FIo, during PAOP measurements and baseline values of SPAP
Figure 3. Correlation between changes in PaO/FIOj during PAOP measurements and baseline values of SPAP in patients with coronary artery disease (left) and in those with valvular heart disease (right).
Figure 4. Influence of anesthetic agents used on PaOa/FIo2 during the balloon inflation.