Biomedical subjects

G F Dolan

Publications and source records attributed to G F Dolan.

At least 19 recordsLinked to original sources

PubMed1989

Oxygen transport and oxygen consumption during supplemental oxygen administration in patients with chronic obstructive pulmonary disease.

PURPOSE: Oxygen consumption (VO2) is independent of oxygen delivery (DO2) above a critical level of DO2. VO2 may become dependent on DO2 when oxygen demand exceeds oxygen supply. We studied DO2 VO2, and exercise capacity in 12 stable, ambulatory patients with chronic obstructive pulmonary disease (COPD) receiving ambient air and 26% oxygen to ascertain whether VO2 is dependent on DO2 in this patient sample. PATIENTS AND METHODS: An exercise protocol consisting of a symptom-limited, low-level treadmill test with progressive increments in workload was performed twice, once with patients breathing ambient air and once with patients breathing 26% oxygen. Expired gas, arterial and mixed venous blood values, and recordings of systemic and pulmonary artery pressures were obtained after a 10-minute period of rest (while standing) and during the last minute of each three-minute exercise level. RESULTS: Five patients had an increase in exercise capacity, defined as an increase in the maximal VO2 greater than 25%, using supplemental oxygen. In these patients, oxygen delivery increased from 10.9 +/- 3.4 to 13.8 +/- 4.7 mL/minute/kg (p = 0.008) at rest and from 16.2 +/- 5.0 to 24.7 +/- 2.7 mL/minute/kg (p = 0.046) during exercise with supplemental oxygen administration. VO2 increased from 0.329 +/- 0.065 to 0.436 +/- 0.109 L/minute (p = 0.029) at rest and from 0.776 +/- 0.275 to 1.119 +/- 0.482 L/minute (p = 0.048) during exercise. Three of these five patients had an arterial oxygen pressure greater than 55 mm Hg at rest. Seven patients had little or no increase in exercise capacity with supplemental oxygen. This patient group had no increase in VO2 at rest. The DO2 failed to increase at rest despite an increase in arterial oxygen content because of a reduction in cardiac output. CONCLUSION: These data demonstrate that DO2 may fail to increase in some patients with COPD and resting or exertional hypoxemia when supplemental oxygen is administered because of a reduction in cardiac output; that patients who fail to increase their DO2 are less likely to increase exercise capacity; and that some stable, ambulatory patients with COPD who do not qualify for supplemental oxygen at rest by current standards may have inadequate DO2 to meet physiologic needs.

Aged↗

PubMed1989

Exercise capacity following pulmonary rehabilitation in the elderly.

Pulmonary rehabilitation has proven beneficial for patients with chronic airway obstruction. In this study, the authors evaluate the effect of rehabilitation in elderly patients. Results show that the change in exercise capacity was not related to the patients' age, and suggest that age alone should not be an exclusionary criterion.

Adult↗

PubMed1988

Effect of posture, hydralazine, and nifedipine on hemodynamics, ventilation, and gas exchange in patients with chronic obstructive pulmonary disease.

A transient relationship between change in cardiac output (CO) and ventilation and a steady-state relationship between VCO2 and ventilation has been documented. We sought to evaluate the steady-state relationship between CO, and minute ventilation (VE) after positional change and after vasodilator administration in 24 patients with chronic obstructive pulmonary disease (COPD) and mild pulmonary hypertension. Cardiac output was 25% higher (p = 0.003) and VE was 25% lower (p = 0.0001) in the supine position. The change in VE showed a strong correlation with the change in VCO2 (r = 0.693; p = 0.0004), but not with the change in CO. Twelve patients received hydralazine 200 mg orally over 24 h, and 12 patients received nifedipine as a single 10-mg oral dose. Cardiac output increased from 5.05 +/- 1.25 L/min to 6.91 +/- 2.07 L/min (p = 0.008) after hydralazine and increased from 4.34 +/- 1.47 L/min to 5.85 +/- 2.15 L/min (p = 0.001) after nifedipine. Minute ventilation increased from 14.8 +/- 3.0 L/min to 17.3 +/- 4.4 L/min (p = 0.008) after hydralazine, but did not change after nifedipine. The change in VE showed a strong correlation with the change in VCO2 after hydralazine (r = 0.889; p = 0.0004) and after nifedipine (r = 0.756; p = 0.005), but did not correlate with the change in CO. These data demonstrate that the change in VE that accompanies positional change or vasodilator administration in patients with COPD is strongly correlated with the change in VCO2 but not with the change in CO when measured under steady-state conditions.

Carbon Dioxide↗

PubMed1987

Long-term effects of hydralazine on ventilation and blood gas values in patients with chronic obstructive pulmonary disease and pulmonary hypertension.

Hydralazine has been shown to increase minute ventilation, alveolar ventilation, and arterial partial pressure of oxygen (PaO2) after short-term administration in patients with chronic obstructive pulmonary disease and pulmonary hypertension. The effects of orally administered hydralazine on ventilation and blood gas values were evaluated after six to 18 months of treatment in 10 male patients who had demonstrated an increase in minute ventilation after 24 hours of treatment. Hydralazine was administered at a dose of 200 mg per day during the initial 24 hours and in doses ranging from 40 mg per day to 200 mg per day during long-term therapy. Following 24 hours of treatment, a statistically significant increase in minute ventilation, alveolar ventilation, and PaO2, and reduction in arterial partial pressure of carbon dioxide (PaCO2) were seen both at rest and during exercise. After six to 18 months of hydralazine therapy, the increase in minute ventilation at rest persisted when compared with the pre-hydralazine value (15.3 +/- 1.3 liters/minute versus 13.1 +/- 1.1 liters/minute; p less than 0.05). The improvement in PaO2 at rest continued relative to the pre-hydralazine value (70.9 +/- 3.2 mm Hg versus 65.1 +/- 3.0 mm Hg, p less than 0.05) as did the PaO2 during exercise (60.3 +/- 3.5 mm Hg versus 53.3 +/- 2.0 mm Hg; p less than 0.05). The reduction in PaCO2 at rest persisted compared with the pre-hydralazine value (41.2 +/- 2.4 mm Hg versus 47.0 +/- 3.0 mm Hg; p less than 0.05) as did the PaCO2 during exercise (44.0 +/- 2.8 mm Hg versus 48.0 +/- 2.8 mm Hg; p less than 0.05). No significant changes in minute ventilation, PaO2, or PaCO2 were seen at rest or during exercise, when re-measured after six to 18 months in an age- and sex-matched control group of 10 patients who did not receive hydralazine. These results demonstrate that the short-term effects of hydralazine on ventilation and blood gas values persisted after six to 18 months of treatment in this sample of patients, some of whom received doses less than 200 mg per day.

Blood Gas Analysis↗

PubMed1987

Effects of hydralazine on mouth occlusion pressure and ventilatory response to hypercapnia in patients with chronic obstructive pulmonary disease and pulmonary hypertension.

Hydralazine has been shown to increase minute ventilation (VE) in patients with chronic obstructive pulmonary disease and pulmonary hypertension. The mechanism by which hydralazine produces this effect has not been defined. We investigated the effects of orally administered hydralazine on hypercapnic ventilatory response (delta VE/delta PaCO2) and central respiratory drive (delta P0.1/delta PaCO2) as well as the effects on hemodynamics, ventilation, and gas exchange in 10 male patients (mean age, 59 +/- 2 yr). The patients had a severe degree of chronic air-flow obstruction (FEV1, 1.07 +/- 0.08 L) and mild pulmonary hypertension (mean pulmonary artery pressure, 25 +/- 4 mm Hg). After hydralazine, the slope of delta VE/delta PaCO2 increased by 177% (p less than 0.005), and the slope of delta P0.1/delta PaCO2 increased by 145% (p less than 0.05). Resting ventilation increased from 14.8 +/- 1.0 to 17.1 +/- 1.4 L/min (p less than 0.02), primarily as a result of increased respiratory frequency. After hydralazine, PaO2 increased from 66 +/- 4 to 70 +/- 3 mm Hg (p less than 0.05) at rest and from 54 +/- 3 to 59 +/- 3 mm Hg (p less than 0.02) during exercise. PaCO2 decreased from 46 +/- 3 to 42 +/- 3 mm Hg (p less than 0.001) at rest and from 50 +/- 3 to 45 +/- 3 mm Hg (p less than 0.001) during exercise. No change was seen in the dead space to tidal volume ratio or the degree of venous admixture. Mean pulmonary artery pressure and total pulmonary resistance both at rest and during exercise were unchanged after hydralazine.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗

PubMed1986

Pulmonary hypertension in chronic obstructive pulmonary disease. Multivariate analysis.

The severity of pulmonary hypertension was evaluated by right cardiac catheterization in 89 patients with stable chronic obstructive pulmonary disease, both at rest and during maximum treadmill exercise. Thirty-one patients were found to have pulmonary hypertension at rest, defined as a mean pulmonary arterial pressure of 20 mm Hg or more. Although the remaining 58 patients had normal mean pulmonary arterial pressure at rest, three developed pulmonary hypertension during exercise (mean pulmonary arterial pressure greater than or equal to 35 mm Hg). Multiple anthropometric, spirometric, radiographic, and gas-exchange variables were analyzed and correlated with the hemodynamic data to define their value in predicting mean pulmonary arterial pressure. While arterial oxygen pressure (PaO2) at maximum exercise was the variable most highly correlated with resting mean pulmonary arterial pressure (r = -0.67), stepwise multiple linear regression analysis indicated that measurement of the diameter of the right descending pulmonary artery and arterial carbon dioxide tension (PaCO2) also contributed to the prediction of mean pulmonary arterial pressure. Spirometric indices of airflow obstruction, hyperinflation, and the diffusing capacity of the lung for carbon monoxide correlated poorly with the severity of pulmonary hypertension and consequently were not useful predictors of mean pulmonary arterial pressure. The threshold criteria of a PaO2 less than 60 mm Hg or a PaCO2 more than 40 mm Hg were reasonably accurate for a diagnosis of pulmonary hypertension. These arterial blood gas criteria were superior to the spirometric and radiographic variables examined in predicting pulmonary hypertension prior to the development of clinically overt cor pulmonale.

Aged↗

PubMed1986

Supine change in arterial oxygenation in patients with chronic obstructive pulmonary disease.

In normal subjects, recumbent PaO2 differs from upright PaO2 as a function of the relationship between FRC and closing volume. However, in patients with lung disease, the factors controlling PaO2 change. Furthermore, the distribution of airway closure does not strictly reflect gravitational gradients in pleural pressure. Hence, we evaluated the effects of recumbency on PaO2 in patients with advanced COPD. We conducted pulmonary function tests and measured PaO2, AaPO2, change from upright to supine FRC, VE, cardiac output (QT), and mixed venous oxygen saturation (SvO2). Eight patients with COPD in whom PaO2 decreased in the supine position (Group I) were compared with 8 patients with COPD in whom PaO2 improved in the recumbent position (Group II); the only anthropometric difference between the groups was greater body weight in Group II (p less than 0.05). Pulmonary function was comparable in the 2 groups. In both groups, FRC decreased with recumbency, but supine FRC and delta FRC did not differ between groups nor correlate significantly with PaO2, AaPO2, or venous admixture (QVA/QT). Supine SVO2 increased in both groups, but supine QT increased significantly only in Group I. In Group II, recumbent QVA/QT did not change significantly, whereas recumbent QVA/QT increased (p less than 0.02) in Group I. The cause for increased QVA/QT in Group I was reduced VE plus increased QT while supine; in contrast, by maintaining a higher supine VE and by not increasing QT significantly, an increase in QVA/QT was prevented in Group II subjects, an increase that would otherwise have overwhelmed the benefits of increased recumbent SVO2 on PaO2.(ABSTRACT TRUNCATED AT 250 WORDS)

Arteries↗

PubMed1985

Relationship of ventricular ectopy to oxyhemoglobin desaturation in patients with obstructive sleep apnea.

Patients with obstructive sleep apnea are considered to be at increased risk of sudden, presumably arrhythmia-related death during sleep. The present study was undertaken to determine the relationship between ventricular ectopy and the severity of oxyhemoglobin desaturation in these patients. Thirty-one male patients with obstructive sleep apnea (mean age, 55 +/- 11 years) underwent overnight polysomnography. Arterial oxyhemoglobin saturation (SaO2) was monitored by ear oximetry, and premature ventricular complexes (PVC) were detected using electrocardiographic leads CC5 and CM5. The data were recorded on electromagnetic tape for subsequent computer-assisted analysis to obtain PVC frequency as a function of decile levels of SaO2. Total sleep time averaged 333 +/- 75 minutes, the apnea index was 44 +/- 26 per hour, and the hypopnea index was 18 +/- 24 per hour. Premature ventricular complexes were observed in 23 (74 percent) of the subjects. By analysis of variance, no significant relationship was found between PVC frequency and decile levels of SaO2 for saturations greater than 60 percent; however, in the 16 subjects with SaO2 below 60 percent, a significant increase in PVC frequency was detected with decreasing SaO2 (p less than 0.01). Ventricular bigeminy was observed with SaO2 below 60 percent in three of these 16 subjects. From these results, we conclude that patients with obstructive sleep apnea are at relatively low risk of developing ventricular arrhythmias provided SaO2 remains greater than 60 percent, while those with SaO2 below 60 percent are at increased risk and should be managed accordingly.

Adult↗

PubMed1984

Effects of hydralazine on hemodynamics, ventilation, and gas exchange in patients with chronic obstructive pulmonary disease and pulmonary hypertension.

Reports on hemodynamic effects of hydralazine on pulmonary hypertension (primary or secondary) usually include cases with severe disease or with mixed varieties of pulmonary vascular disease. Serious side effects and death have been reported. Effects of this drug on ventilation and gas exchange are unknown. We investigated the short-term effects of hydralazine treatment on hemodynamics, ventilation, and gas exchange in a relatively homogeneous group of patients with severe chronic obstructive pulmonary disease and moderate exertional pulmonary hypertension (mean pulmonary artery pressure, 43 +/- 3 mmHg). Hydralazine produced significant improvement in cardiac index, total pulmonary resistance, and oxygen transport. We also observed significant improvement in alveolar ventilation (mean PaCO2, decreased from 47 +/- 2 to 40 +/- 3 mmHg at rest and from 51 +/- 3 to 43 +/- 3 mmHg during exercise). The severe exertional hypoxemia of the group (mean PaO2, 48 +/- 2 mmHg) improved significantly (mean PaO2, 57 +/- 3 mmHg). Four of 11 patients showed increased exercise tolerance after hydralazine. This change is probably related to a combined improvement in hemodynamics plus a newly observed improvement in gas exchange and ventilation. Three of 14 patients could not tolerate hydralazine because of marked tachycardia. Serious side effects were not observed in the remaining group.

Drug Tolerance↗

PubMed1984

Myocardial stress. Exercise versus sleep in patients with COPD.

Epidemiologic investigation has revealed that patients with pulmonary disease are at increased risk of dying during the early morning hours. To provide a pathophysiologic explanation for these excessive nocturnal mortality statistics, we tested the hypothesis that episodes of arterial O2 desaturation during sleep can produce as severe a stress on the maintenance of myocardial O2 balance as maximal exercise in patients with chronic obstructive pulmonary disease (COPD). Thirty-one subjects with COPD underwent both overnight sleep and treadmill exercise study to their dyspnea-limited maximum. During both activities, systemic blood pressure was directly recorded and myocardial oxygen consumption (MVO2) estimated from the pulse rate (HR) - systolic blood pressure (SBP) product. Arterial O2 content (CaO2) was calculated from hemoglobin concentration and arterial O2 saturation (SaO2) measured by ear oximetry. Using these data and the Fick principle, myocardial blood flow (MBF) was continuously estimated during both exercise and sleep. During sleep, mean SaO2 was 88 +/- 7 percent while the average of the lowest SaO2 recorded for each subject was 71 +/- 14 percent. Episodes of nocturnal oxyhemoglobin desaturation produced consistent elevations in SBP frequently accompanied by an increase in HR. Because this hemodynamic response resulted in increased MVO2 at precisely the times when arterial O2 contents were low, high demands for MBF were generated. The average of the highest individual values for MBF during sleep was 244 +/- 144 (ml/100 g LV/min). This value was not significantly different from the value of MBF = 281 +/- 91 (ml/100 g LV/min) determined for maximal exercise. This finding suggests that the demand for coronary blood flow during episodes of nocturnal hypoxemia can be transiently as great as during maximal exercise in patients with COPD.

Adult↗

PubMed1983

Transpleural CO2 diffusion in excised dog lungs.

Previous studies of transpleural gas diffusion have reported both linear and nonlinear relationships between total gas transfer and the transpleural driving gradient estimated as the difference between pleural and end-tidal gas tensions. The present studies were undertaken to explain these conflicting results by examining the role of convective mixing as well as the validity of using measurements of end-tidal gas to estimate subpleural gas tensions and calculate the transpleural partial pressure gradient. Nine excised nonperfused dog lungs were ventilated with room air under varying conditions of frequency (f), tidal volume (VT) and pleural CO2 concentration (FplCO2). The relationship between CO2 elimination (VCO2) and the transpleural CO2 concentration gradient estimated by (FplCO2-FETCO2) was found to be linear for every level of ventilation (constant convective mixing) studied. The slope of this relationship, equal to the pleural CO2 diffusing capacity (DplCO2) was found to decrease as ventilation was decreased whether achieved by reductions in f or VT. Because changes in membrane geometry were insufficient to explain the differences in DplCO2, seven additional excised dog lungs were studied ultrastructurally following 4 h of ventilation with room air at a pleural CO2 concentration of 6%. Previous studies under similar conditions have shown that changes in type II pneumocyte lamellar body volume density Vv(LB/cyto) are related to the alveolar concentration of CO2. The results indicated that the concentration of CO2 in alveoli located within 1 mm of the pleural surface was substantially greater than the value estimated by FETCO2. Consequently, (FplCO2-FETCO2) over-estimates the transpleural concentration gradient and produces erroneously low estimates of the diffusing capacity of the pleural membrane.

Animals↗

PubMed1982

Factors regulating lamellar body volume density of type II pneumocytes in excised dog lungs.

Pulmonary arterial occlusion (PAO) produces multiple alterations in the physiological/biochemical environment of lung cells as well as dysfunction of the lung's surfactant system, which is considered to play a significant role in mediating lung injury. The present studies were performed using 66 excised dog lungs to evaluate the impact of alterations in ventilation, substrate availability, alveolar CO2 tension, hydrogen ion and bicarbonate concentrations, and temperature and neural denervation on the lamellar body (LB) volume density of type II pneumocytes. Ventilating excised nonperfused dog lungs with room air (0% CO2) for 4 h at 38 degrees C resulted in severe reductions (68-77%) in LB volume density. Supplementing inspired gas with 5% CO2 prevented LB depletion, while ventilation with 2.5% CO2 moderated the severity of depletion to 17-27% of control. Ventilation with 10% CO2 tended to increase LB volume density by increasing the number of LBs per cell, whereas reductions in LB volume density predominantly resulted from a decrease in LB size. The level of ventilation had no significant effect on LB volume density independent of inspired CO2 concentration. Reducing temperature to 5 degrees C prevented LB depletion. Lung perfusion with autologous whole blood failed to moderate the severity of LB depletion during room air ventilation despite the increased availability of metabolic substrates for cellular metabolism. Adding hydrochloric acid to maintain physiologically normal hydrogen ion concentrations in the perfusing blood had a small effect in ameliorating the severity of LB depletion. These results indicate that alveolar CO2 tension and bicarbonate concentration are major factors regulating the LB content of type II pneumocytes and suggest an important link between the gas exchange and phospholipid metabolic functions of the lung.

Animals↗

PubMed1981

Gas exchange in nonperfused dog lungs.

Gas exchange was studied under conditions of zero perfusion both in situ and in vitro. Six dogs, anesthetized with pentobarbital sodium, underwent surgical interruption of both pulmonary and bronchial circulations to the left lung. Despite the absence of perfusion, O2 uptake for the left lung ranged from 0.76 to 0.98 ml/min, whereas CO2 elimination greatly exceeded O2 uptake ranging from 1.68 to 4.34 ml/min. In addition, CO2 output was observed to vary directly with the level of minute ventilation (VE) and inversely with end-tidal CO2 concentration. To investigate the mechanisms responsible for these findings we studied 20 excised, ventilated, but nonperfused dog lungs to evaluate the relative roles of tissue metabolism and transpleural diffusion to gas exchange. The results obtained with these excised lungs under conditions of varying VE and extrapleural gas concentrations indicate that the high respiratory exchange ratios observed in situ can be explained by the greater rate with which CO2 diffuses through the pleura, and that reduced ventilation decreases total gas transfer by decreasing the transpleural partial pressure driving gradient. Our data further document that the concentration of CO2 in alveolar gas may differ significantly from that present in inspired gas under conditions of ventilation-perfusion ratio equal to infinity, and that tissue metabolism as well as transpleural diffusion contribute to gas exchange in nonperfused lung.

Animals↗

PubMed1981

Mixed venous oxygenation, exercise, body posture, and v/q ratio in chronic obstructive pulmonary disease.

Mixed venous oxygenation (partial pressure, PVO2; saturation, SVO2) and its impact on pulmonary function at rest in the supine position (SUP), at rest in the standing position (STAND), and during maximal treadmill exercise (Emax), were studied in 41 stable patients with chronic obstructive pulmonary disease, using arterial and right heart (Swan-Ganz) catheterization. The patients represented a broad spectrum of disease severity (VC, 3.1 +/- 0.9 L; FEF 25-75, 1.0 +/- 0.7 L). It was found that: (a) venous oxygenation was uniform among different patients in the supine position at rest (PVO2, 33.8 +/- 2.4 mmHg' SVO2, 76.2 +/- 3.6%), regardless of the heterogeneity in airway obstruction, as previously reported by others; (b) venous oxygenation was also uniform in STAND (PVO2, 29.5 +/- 2.5 mmHg; SVO2, 58 +/- 3.9%) and treadmill Emax (PVO2, 22.4 +/- 3.3 mmHg; SVO2, 34.4 +/- 6%), an observation not previously reported; (c) the orthostatic mixed venous desaturation at rest was pronounced, and was nearly as great as that from STAND to Emax; (d) the potential effect of mixed venous desaturation on alveolar O2 partial pressure (PAO2) and end-capillary O2 saturation (SCO2) was not obvious from SUP to STAND, and from STAND to Emax conditions, being masked by an appropriate increase in overall V/Q ratio; (e) because of constant SCO2 and low interindividual variations of SVO2, there was a high correlation of arterial saturation (SaO2) to venous admixture (Qva/Qt, sum of true shunt and shuntlike components) for each of the conditions studied. Hence, because of high correlation of the equations relating SaO2 to Qva/Qt (r greater than 0.9), these relationships might be used for noninvasive prediction of Qva/Qt from SaO2 in patients with COPD.

Carbon Dioxide↗

PubMed1979

Immersion vs pressure-breathing and diaphragmatic function in the upright position.

In seven anesthetized dogs, immersion in the upright position to mid-neck level (IM) was compared to pressure breathing (PB) under dry conditions during constant-stimulus diaphragmatic contraction (EPS). The comparison was in terms of EPS-induced changes in alveolar pressure under static condition (Pmus); EPS-induced tidal volume (VT); and the VT/Pmus ratio (C'). It was found that at iso-lung volume (V): (a) Pmus was greater in IM than in PB, the difference increased at higher V; (b) VT was greater in IM than in PB, but the VT difference (deltaVT) did not parallel that in Pmus; VT was maximum at a V equal to approximately 90% of FRC in air (FRCd) and decreased below and above this volume; (c) during both IM and PB, the VT-V relationship reflected a biphasic relationship of C' to V and appeared to be inherent to the upright position.

Animals↗

PubMed1979

Hypoxemia during exercise in patients with chronic obstructive pulmonary disease.

Arterial oxygenation at rest and during maximal treadmill exercise was studied in a group of 17 patients with chronic obstructive pulmonary disease. Patients who developed exertional hypoxemia (subgroup 1) were compared to others who did not (subgroup 2). There was no significant difference between the 2 subgroups at rest in terms of mixed venous PO2, cardiac output, or venous admixture. Subgroup 1 had more severe respiratory impairment than subgroup 2, but there was marked overlap of their respective lung volumes and flows. Both subgroups showed the same extent of desaturation of mixed venous blood during maximal treadmill exercise, so that exertional hypoxemia cannot be explained on the basis of low mixed venous O2. The marked difference between subgroup 1 and subgroup 2 was that the latter showed decreased venous admixture on exercise. Because of the relative constancy of mixed venous blood desaturation, arterial saturation was closely correlated with venous admixture both at rest (r = 0.931) and during exercise (r = 0.985).

Arteries↗

PubMed1978

Functional residual capacity and body position in the dog.

Resting lung volumes in the supine position (FRCs) were determined by N2 washout method in 67 dogs under pentobarbital anesthesia and computed in ml/kg body weight (BW). In 21 other dogs, FRCs and the change in FRC from the supine to upright positions (deltaFRC) were determined; these lung volumes were expressed in ml/kg BW and in percentage of TLC40 (lung volume at 40 cmH2O positive-pressure inflation). It was found that a) FRCs averaged 38.6 plus or minus 8.2 and 42 plus or minus 5.9 ml/kg BW in the two groups of dogs; b) deltaFRC averaged 23 plus or minus 4 ml/kg BW resulted in large data dispersion, a large coefficient of variation (CV) and a poor correlation (r) of lung volume to BW; D) on the contrary, marked uniformity of FRCs and FRCu (upright FRC) was obtained by expressing the resting lung volumes in %TLC40, allowing an accurate prediction of FRC from the inspiratory capacity (IC). Relationship of FRCu to TLC was comparable to human data reported in the literature. FRCs (%TLC40) was smaller than values previously reported for awake human subjects, probably due to the FRCs reduction in our dogs by anesthesia.

Animals↗

PubMed1977

Clinically suspected deep venous thrombosis of the lower extremities. A comparison of venography, impedance plethysmography, and radiolabeled fibrinogen.

To define the utility of new diagnostic approaches in patients with clinically suspected deep venous thrombosis of the lower extremities, 42 legs of 33 patients were studied by fibrinogen labeled with radioactivie iodine (125I) impedance plethysmography (IPG), and contrast venography. The clinical diagnosis was confirmed in approximately two thirds of the legs and patients. In venogram-positive legs, fibrinogen 125I was positive in 70%, IPG in 61%, and one of the two in 78%. In venogram-negative legs, fibrinogen 125I was positive in four (21%) and IPG was negative in all. It was found that the size, age, and location of the thrombus, collateral vein development, heparin sodium therapy, and technical-interpretive choices can influence both IPG and fibrinogen 125I results. The data demonstrate that the fibrinogen 125I and IPG procedures can assist physicians in the diagnosis of clinically suspected deep venous thrombosis of the lower extremities.

False Negative Reactions↗