Mean Pulmonary Artery Pressure Values Research Articles

Effectiveness of prophylactic levosimendan in high-risk valve surgery patients : cardiovascular topics

Levosimendan has anti-ischaemic effects, improves myocardial contractility and increases systemic, pulmonary and coronary vasodilatation. These properties suggest potential advantages in high-risk cardiac valve surgery patients where cardioprotection would be valuable. The present study investigated the peri-operative haemodynamic effects of prophylactic levosimendan infusion in cardiac valve surgery patients with low ejection fraction and/or severe pulmonary arterial hypertension. Between May 2006 and July 2007, 20 consecutive patients with severe pulmonary arterial hypertension (systolic pulmonary artery pressure ≥ 60 mmHg) and/or low ejection fraction (< 50%) who underwent valve surgery in our clinic were included in the study and randomised into two groups. Levosimendan was administered to 10 patients in group I and not to the 10 patients in the control group. Cardiac output (CO), cardiac index (CI), systemic vascular resistance (SVR), pulmonary vascular resistance (PVR) and mean pulmonary artery pressure (MPAP) were recorded for each patient preoperatively and for 24 hours following the operation. CO and CI values were higher in the levosimendan group during the study period (p < 0.05). MPAP and PVR values were significantly lower in the levosimendan group for the 24-hour period (p < 0.05) and SVR values were significantly lower after 24 hours in both groups. When clinical results were considered, no difference in favour of levosimendan was detected regarding the mortality and morbidity rates between the groups. Levosimendan improved the haemodynamics in cardiac valve surgery patients with low ejection fraction and/or severe pulmonary arterial hypertension, and facilitated weaning from cardiopulmonary bypass in such high-risk patients when started as a prophylactic agent.

Derivation of Mean Pulmonary Artery Pressure from Noninvasive Parameters

The assessment of pulmonary pressure is important for the diagnosis and management of patients with pulmonary hypertension. Mean pulmonary artery pressure (MPAP) has been used in the current definition of pulmonary hypertension. However, invasive derivation by Doppler echocardiography provides the peak pulmonary artery systolic pressure (PASP). The aim of this study was to derive a method to predict MPAP from PASP. Invasive hemodynamic pressures in 307 patients who underwent right heart catheterization were examined. Simple regression techniques were used to determine the relationship between MPAP and PASP in a derivation cohort (n= 198) and a validation sample (n= 109). Bland-Altman analysis was performed to examine predicted versus observed values of MPAP. MPAP and PASP at catheterization were strongly related over a range of pressures (R(2)= 0.89, n= 198; SE, 4.04; P < .0001). The relation of MPAP to PASP in the derivation cohort (MPAP= 0.61 × PASP+ 1.95 mm Hg) was validated in the test sample, with an R(2) value of 0.94 for predicted versus observed MPAP (SE, 2.87; P< .0001). The relationship of predicted versus observed MPAP was constant across different degrees of pressure elevation, as well as different etiologies of pulmonary hypertension. Applying the equation to Doppler-derived pulmonary pressures, there was excellent correlation of predicted MPAP from echocardiography and invasively measured MPAP (R(2)= 0.78, P < .0001). MPAP can be accurately predicted from PASP over a wide pressure range for different etiologies of pulmonary hypertension. This finding may help define MPAP noninvasively.

Changes in pulmonary artery pressures during ethanol sclerotherapy for arteriovenous malformations: identifying the most vulnerable period

To evaluate the changes in pulmonary artery pressure (PAP) during ethanol embolization and to identify the most vulnerable period associated with cardiovascular collapse in patients with arteriovenous malformations (AVMs). Twenty-three patients (30 sessions) with AVMs were enrolled. PAP was measured at the following times: baseline (T(baseline)); immediately before (T(pre)), and after (T(post)) bolus injection of absolute ethanol; at the time of maximum mean PAP value during a session (T(highest-ethanol)); 10 min after final injection (T(final)); after restoration of spontaneous breathing (T(resp)); at extubation (T(extubation)); 30 min after extubation (T(extubation-30)(min)); and at the time of maximum mean PAP after patient resumed spontaneous respiration (T(highest-resp)). Nitroglycerin was infused (range 0.5-3 μg/kg/min) in all patients to attenuate the effect of ethanol on pulmonary vasoconstriction. The PAPs of T(highest-ethanol), T(resp), T(extubation), and T(highest-resp) were significantly higher than the corresponding values for T(baseline) and T(final) (all p<0.05). The systolic and mean PAPs of T(highest-resp) were significantly higher than those at T(highest-ethanol) (both p<0.05). In 24 sessions (80%), the highest mean PAP was detected during the recovery period. The greatest rise in PAP was noted during the recovery period in patients undergoing ethanol embolotherapy. Therefore, PAP monitoring and nitroglycerin infusions are recommended during the recovery period because early detection of an increase in PAP and prompt management may prevent detrimental complications.

Bispectral Index Monitoring to Guide End-Tidal Isoflurane Concentration at Three Phases of Operation in Patients With End-Stage Liver Disease Undergoing Orthotopic Liver Transplantation

It has been shown that anesthetic requirements during liver transplantation are inversely proportional to the degree of hepatic dysfunction. We investigate alterations during the three phases of requirements for intraoperative isoflurane within the target of 40 to 55 Bispectral Index (BIS) values concerning patients with end-stage liver disease who are undergoing liver transplantation. After faculty ethics committee approval, we studied 50 patients of (age range, 18 to 65 years) who were undergoing liver transplantation. After induction, we used isoflurane with air/oxygen (FiO 2 = 0.5%) for anesthestic maintenance. The isoflurane concentration was set within the range of 40 to 55 BIS values. Remifentanil (0.15 μg/kg/min) was infused for analgesia and cisatracurium was administered via continuous infusion. After anesthetic induction, we inserted arterial, pulmonary artery, and central venous catheters. The heart rate, mean arterial pressure (MAP), mean pulmonary arterial pressure (MPAP), body temperature, BIS values, end-tidal isoflurane concentration (ETiso) and end-tidal carbon dioxide concentration (ETCO 2) were recorded at 30-minute intervals during the dissection and neohepatic phases, at 15-minute intervals during the anhepatic phase. In addition, we calculated the cardiac index during the three phases. There was no difference in heart rates among the operative phases. In contrast, there were significant changes in MAP, MPAP, BIS, ETCO 2 and body temperature values. However, all of these parameters were in physiological ranges and clinically acceptable. The ETiso values were lowest in the anhepatic phase compared to other phases, but the differences were not clinically important. The ETiso values in the dissection and neohepatic phases were compared with the anhepatic phase higher 5% and 8.6% respectively. During liver transplantation, ETiso requirement for the anhepatic phase was lower compared with the other two phases within the range of 40 to 55 BIS values.

Effects of head and body cooling on hemodynamics during immersed prone exercise at 1 ATA

Immersion pulmonary edema (IPE) is a condition with sudden onset in divers and swimmers suspected to be due to pulmonary arterial or venous hypertension induced by exercise in cold water, although it does occur even with adequate thermal protection. We tested the hypothesis that cold head immersion could facilitate IPE via a reflex rise in pulmonary vascular pressure due solely to cooling of the head. Ten volunteers were instrumented with ECG and radial and pulmonary artery catheters and studied at 1 atm absolute (ATA) during dry and immersed rest and exercise in thermoneutral (29-31 degrees C) and cold (18-20 degrees C) water. A head tent varied the temperature of the water surrounding the head independently of the trunk and limbs. Heart rate, Fick cardiac output (CO), mean arterial pressure (MAP), mean pulmonary artery pressure (MPAP), pulmonary artery wedge pressure (PAWP), and central venous pressure (CVP) were measured. MPAP, PAWP, and CO were significantly higher in cold pool water (P < or = 0.004). Resting MPAP and PAWP values (means +/- SD) were 20 +/- 2.9/13 +/- 3.9 (cold body/cold head), 21 +/- 3.1/14 +/- 5.2 (cold/warm), 14 +/- 1.5/10 +/- 2.2 (warm/warm), and 15 +/- 1.6/10 +/- 2.6 mmHg (warm/cold). Exercise values were higher; cold body immersion augmented the rise in MPAP during exercise. MAP increased during immersion, especially in cold water (P < 0.0001). Except for a transient additive effect on MAP and MPAP during rapid head cooling, cold water on the head had no effect on vascular pressures. The results support a hemodynamic cause for IPE mediated in part by cooling of the trunk and extremities. This does not support the use of increased head insulation to prevent IPE.

Magnetic Resonance–Derived 3-Dimensional Blood Flow Patterns in the Main Pulmonary Artery as a Marker of Pulmonary Hypertension and a Measure of Elevated Mean Pulmonary Arterial Pressure

Pulmonary hypertension is a disease characterized by an elevation in pulmonary arterial pressure that is diagnosed invasively via right heart catheterization. Such pathological altered pressures in the pulmonary vascular system should lead to changes in blood flow patterns in the main pulmonary artery. Forty-eight subjects (22 with manifest pulmonary hypertension, 13 with latent pulmonary hypertension, and 13 normal control subjects) underwent time-resolved 3D magnetic resonance phase-contrast imaging of the main pulmonary artery. Velocity fields that resulted from measurements were calculated, visualized, and analyzed with dedicated software. Main findings were as follows: (1) Manifest pulmonary hypertension coincides with the appearance of a vortex of blood flow in the main pulmonary artery (sensitivity and specificity of 1.00, 95% confidence intervals of 0.84 to 1.00 and 0.87 to 1.00, respectively), and (2) the relative period of existence of the vortex correlates significantly with mean pulmonary arterial pressure at rest (correlation coefficient of 0.94). To test the diagnostic performance of the vortex criterion, we furthermore investigated 55 patients in a blinded prospective study (22 with manifest pulmonary hypertension, 32 with latent pulmonary hypertension, and 1 healthy subject), which resulted in a sensitivity of 1.00 and specificity of 0.91 (95% confidence intervals of 0.84 to 1.00 and 0.76 to 0.98, respectively). Comparison of catheter-derived mean pulmonary artery pressure measurements and calculated mean pulmonary artery pressure values resulted in a standard deviation of differences of 3.6 mm Hg. Vortices of blood flow in the main pulmonary artery enable the identification of manifest pulmonary hypertension. Elevated mean pulmonary arterial pressures can be measured from the period of vortex existence.

Does carbon monoxide treatment alter cytokine levels after endotoxin infusion in pigs? A randomized controlled study

BackgroundCarbon monoxide (CO) has recently been suggested to have anti-inflammatory properties, but data seem to be contradictory and species-specific. Thus, in studies on macrophages and mice, pretreatment with CO attenuated the inflammatory response after endotoxin exposure. On the other hand, human studies showed no effect of CO on the inflammatory response. Anti-inflammatory efficacy of CO has been shown at concentrations above 10% carboxyhaemoglobin. This study was undertaken to elucidate the possible anti-inflammatory effects of CO at lower CO concentrations.MethodsEffects of CO administration on cytokine (TNF-alpha, IL-6, IL-1beta and IL-10) release were investigated in a porcine model in which a systemic inflammatory response syndrome was induced by endotoxin infusion. Endotoxin was infused in 20 anaesthetized and normoventilated pigs. Ten animals were targeted with inhaled CO to maintain 5% COHb, and 10 animals were controls.ResultsIn the control group, mean pulmonary artery pressure increased from a baseline value of 17 mmHg (mean, n = 10) to 42 mmHg (mean, n = 10) following 1 hour of endotoxin infusion. Similar mean pulmonary artery pressure values were found in animals exposed to carbon monoxide. Plasma levels of all of the measured cytokines increased in response to the endotoxin infusion. The largest increase was observed in TNF-alpha, which peaked after 1.5 hours at 9398 pg/ml in the control group and at 13395 pg/ml in the carbon monoxide-exposed group. A similar peak was found for IL-10 while the IL-6 concentration was maximal after 2.5 hours. IL-1beta concentrations increased continuously during the experiment. There were no significant differences between carbon monoxide-exposed animals and controls in any of the measured cytokines.ConclusionOur conclusion is that 5% COHb does not modify the cytokine response following endotoxin infusion in pigs.

Noninvasive, Indirect Measurement of Pulmonary Artery Pressure

The gold standard for measuring pulmonary artery pressure (PAP) is right heart catheterization. However, the usefulness of this technique is limited in patients with lung disease because of a poor acoustic window. The aim of this study was to assess PAP in a group of healthy persons using a noninvasive, indirect measurement procedure derived from the venous return flow velocity wave.Twenty-three healthy volunteers with a mean (SD) age of 34 (9) years were evaluated. Measurements were made with a Hitachi EUB 5000 ultrasound device (3.5 MHz wave). The subject was placed in supine decubitus with neck hyperextended and head turned to one side. B-mode images were used to locate the point in the internal jugular vein 1 cm higher than its union with the subclavian vein. A color flow image was obtained of the vessel and a pulsed wave was then used to measure velocities. After 5 identical cycles, an estimate of PAP was derived from the ratio of maximum diastolic and systolic flow rates.On the right side, the mean (SD) ratio between flow rates was 0.50 (0.08), corresponding to a mean PAP of 15 (2.4) mm Hg. On the left side, the ratio was 0.55 (0.09), corresponding to a mean PAP of 16 (2.8) mm Hg. The nonsignificant difference between mean PAP values on the right and left was 1.3 (3.1) mm Hg, and higher values were on the left.Mean PAP values obtained with the described procedure are within the normal range for a healthy population. Transcutaneous venous Doppler ultrasound is useful for estimating PAP in healthy individuals.

Pattern of Variables Describing Desaturator COPD Patients, as Revealed by Cluster Analysis

The aims of this study were to define, by cluster analysis, a pattern of clinical variables that differentiate desaturator (D) from nondesaturator (ND) patients affected by COPD, and to identify daytime variables that are predictive of nocturnal desaturation. Fifty-one random, consecutive COPD outpatients (20 women; mean [+/- SD] age, 69.6 +/- 4.0 years) with mild daytime hypoxemia (Pao(2), 60 to 70 mm Hg) were enrolled into the study. Obstructive sleep apnea syndrome patients were excluded. Lung volumes, arterial blood gas levels, and mean pulmonary artery pressure (MPAP) were measured, and nocturnal desaturation was evaluated with nighttime polygraphy. With least squares simple linear regression, the percentage of total recording time was highly correlated with a total nocturnal recording time of arterial oxygen saturation of < 90 mm Hg (T90) and MPAP (R = 0.84; R2= 71.20%); T90 was also highly correlated with daytime Paco2 (R = 0.70; R2= 48.96%). Multiple regression showed that T90 was highly correlated with both MPAP and Paco2 (R2= 97.75%). Hierarchical cluster analysis conducted with these three variables showed that D and ND patients differed in both nocturnal and daytime variables. The mean T90 was 30 +/- 3.5% in 19.2% and 8%, respectively, of the D and ND groups. Moreover, two D subgroups differing in MPAP and two ND subgroups differing in Paco2 were identified. D patients may be identified by a pattern of T90, MPAP, and Paco2 values, rather than by T90 alone, with the latter two variables being predictors of nocturnal desaturation severity.

The effects of tonsillectomy and adenoidectomy on pulmonary arterial pressure in children

Purpose It is well known that hypertrophic tonsils and adenoids may cause upper-airway obstruction. The aim of this study is to determine the mean pulmonary arterial pressure (mPAP) in children with hypertrophic tonsils and adenoids and to clarify whether tonsillectomy and adenoidectomy (T&A) has any effect on mean pulmonary arterial pressure of these children. Materials and methods Fifty-two randomly selected children (36 male, 16 female) aged between 4 and 11 (mean 7.7 ± 2.5) a with a diagnosis of upper-airway obstruction resulting from hypertrophied tonsils and adenoids were included in our study. Thirty-three children were assigned as controls with similar age and sex distrubution with the study groups. Mean pulmonary arterial pressure was measured by using Doppler echocardiography preoperatively and mean 5.4 ± 2.9 months postoperatively in all subjects. Results When the mean pulmonary arterial pressure values of study and control group compared preoperatively, the mean pulmonary arterial pressure levels of the children in the study group were significantly higher than the mean pulmonary arterial pressure levels of the children in the control group ( P < .05) (study group mean PAP = 23.13 ± 7.68, control group mean PAP = 16.11 ± 7.24) (Levene’s test, P < .05). When the preoperative and postoperative results were compared, it was found that there was a statistically significant decrease in mean pulmonary arterial pressures in these 52 children (preoperative mean PAP = 23.13 ± 7.68, postoperative mean PAP = 17.00 ± 6.99) (paired sample t test, P < .05). Twenty-seven of the 52 subjects in the study group were pulmonary hypertensive preoperatively. mPAPs of 18 of these children decreased to normal range yielding 9 subjects, and this was also found ststistically significant (McNemar test, P < .001). Conclusion This study showed that obstructive adenoid and tonsillar hypertrophy causes higher mPAP values in children and revealed that T&A is an effective therapeutic measure in such patients.

Anesthetic Management of Pulmonary Arterial Pressure Change during the Ethanol Sclerotherapy of Peripheral Arteriovenous Malformations

Background: We frequently experience the elevation of pulmonary arterial pressure (PAP) during ethanol sclerotherapy of arteriovenous malformations. But, the study on the degree of PAP elevation during ethanol sclerotherapy has not yet been made. Therefore, we evaluated the PAP elevation during ethanol sclerotherapy. Methods: We retrospectively reviewed PAP changes in 124 procedures conducted on 41 arteriovenous malformation patients during ethanol sclerotherapy. We investigated the degree of elevation of PAP and the incidences of pulmonary arterial hypertension during ethanol sclerotherapy. Results: High incidences of pulmonary arterial hypertension were observed during ethanol sclerotherapy (53/124 procedures, 42.7%). The mean highest PAP values were 33.8 10.9 mmHg (systolic), 25.2 7.9 mmHg (mean), and 18.3 7.4 mmHg(diastolic). Incidence of nitroglycerine administration was 47.5% (59/124 procedures). Mean PAP values at the end of procedure was 29.1 9.1 mmHg (systolic), 22.0 7.0 mmHg (mean), and 16.1 6.4 mmHg (diastolic). Conclusion: The incidences of pulmonary hypertension during ethanol sclerotherapy were high. Therefore, cautious management and close cooperation between anesthesiologist and interventional radiologist are essential to prevent dreadful outcome.

Polymorphism of the serotonin transporter gene and pulmonary hypertension in chronic obstructive pulmonary disease.

The serotonin transporter (5-HTT) is involved in the pulmonary artery smooth muscle hyperplasia that leads to pulmonary hypertension (PH). Because hypoxia and 5-HTT gene polymorphism control 5-HTT expression, we examined 5-HTT gene polymorphism and PH in hypoxemic patients with advanced chronic obstructive pulmonary disease (COPD). In 103 patients with COPD recruited in France (n=67) and the UK (n=36), we determined 5-HTT gene polymorphism and pulmonary artery pressure (PAP) measured during right heart catheterization (France) or Doppler echocardiography (UK). Ninety-eight subjects from the 2 countries served as control subjects. The distribution of 5-HTT gene polymorphism did not differ between patients and control subjects. In patients carrying the LL genotype, which is associated with higher levels of 5-HTT expression in pulmonary artery smooth muscle cells than the LS and SS genotypes, PH was more severe than in LS or SS patients. Mean PAP values in patients from France with the LL, LS, and SS genotypes were 34+/-3, 23+/-1, and 22+/-2 mm Hg (mean+/-SEM), respectively (P<0.01). Corresponding systolic PAP values in the UK were 40+/-3, 28+/-3, and 24+/-3 mm Hg, respectively (P<0.01). Compared with control subjects, platelet 5-HTT protein was increased in COPD patients in proportion to the hypoxemia level, and strong 5-HTT immunostaining was observed in remodeled pulmonary arteries from COPD patients. 5-HTT gene polymorphism appears to determine the severity of PH in hypoxemic patients with COPD. Because PH is an important prognostic factor in this disease, recognition of patients at risk for PH should be helpful in managing COPD.

Hemodynamic Responses to Electroconvulsive Therapy in a Hypertensive Patient with End-Stage Pulmonary Fibrosis

Hemodynamic Responses to Electroconvulsive Therapy in a Hypertensive Patient with End-Stage Pulmonary Fibrosis

Hemodynamic effects of partial liquid ventilation with perfluorocarbon in acute lung injury.

To assess the effect of partial liquid ventilation with perfluorocarbons on hemodynamics and gas exchange in large pigs with induced acute lung injury (ALI). Randomized, prospective, double-control, experimental study. Experimental intensive care unit of a university. Eighteen large pigs (50 +/- 5 kg body weight) with an average anterior posterior thoracic diameter of 24 cm and induced acute lung injury. All animals were surfactant depleted by lung lavage to a PaO2 below 100 mmHg and randomized to receive either perflubron (n = 6) or saline (n = 6) in five intratracheal doses of 5 ml/kg at 20-min intervals, or no instillation (n = 6). In all animals heart rate, arterial pressures, pulmonary pressures, cardiac output and blood gases were recorded at 20-min intervals. There was no deleterious effect on any hemodynamic parameter in the perflubron group, whereas systolic and mean pulmonary arterial pressure values showed a persistent decrease after the first 5 ml/kg of perflubron, from 48.7 +/- 14.1 to 40.8 +/- 11.7 mmHg and from 39.7 +/- 13.2 to 35.2 +/- 12.0 mmHg, respectively. Perflubron resulted in a significant (ANOVA P < 0.01), dose-dependent increase in PaO2 values from 86.3 +/- 22.4 to a maximum of 342.4 +/- 59.4 mmHg at a dose of 25 ml/kg; the other groups showed no significant increase in PaO2. Tracheal instillation of perflubron in induced ALI results in a dose-dependent increase in PaO2 and has no deleterious effect on hemodynamic parameters.

PHYSIOLOGICAL ANALYSIS OF PULMONARY HEMODYNAMICS IN INFANTS WITH PULMONARY HYPERTENSION ASSOCIATED

Pulmonary hypertension is a serious complication in patients with bronchopulmonary dysplasia. The author studied the effect of tolazoline and 100% oxygen on pulmonary hemodynamics in 12 infants including 11 who were oxygen-dependent with bronchopulmonary dysplasia and pulmonary hypertension. Cardiac catheterizations were performed on all cases, at 4 months to 4 years of age. Mean pulmonary arterial pressure and pulmonary vascular resistance were measured (1) before and after tolazoline injection (1 mg/kg, into the main pulmonary artery), then after a 30-minute stabilization period, (2) before and after a 5-minute 100% oxygen inhalation period. In room air, the arterial O2 saturation values were 87 ± 6 %, the mean pulmonary artery pressure values were 39 ± 4 mmHg, the pulmonary vascular resistance values were 7.7 ± 1.2 Wood units·m2. After tolazoline injection and the 5-minute 100% oxygen inhalation, the mean pulmonary artery pressure decreased significantly (p<0.01). The percent decrease in mean pulmonary artery pressure after inhaling 100% oxygen for 5 minutes was greater than that after tolazoline injection (p<0.05). There were no correlations between the percent decrease in mean pulmonary artery pressure after the 100% oxygen inhalation and that following tolazoline injection. The percent decrease in mean pulmonary artery pressure after 100% oxygen inhalation was inversely related to the arterial oxygen saturation in room air (r=0.68, p<0.05), while that after tolazoline injection was not.

Clinical Pathophysiological Studies on the Effect of Induced Hypoxemia on the pulmonary Circulation : A Consideration on the Pathogenetic Mechanism of Shock Induced by Hypoxemia.

While there are many reports as to the elevation of the pulmonary artery blood pressure during an induced hypoxemia, quantitative relationships between the change in respiration and that in the pulmonary circulation is not yet fully clarified in cases with different diseases. Many studies have been done in this department since 1954 by using the method of induced hypoxemia combined with the cardiac and venous catheterization on the blood circulation through various organs, such as the heart, brain, liver and kidneys, and the response to the induced hypoxemia has been studied in a variety of conditions. This paper aims to describe the author's study on the effect of induced hypoxemia on the pulmonary circulation and also his consideration on the relation between the pulmonary and the systemic circulation in normal subjects, patients with pulmonary tuberculosis and cardiac patients.Methods and Subjects Each subject was examined by the cardiac and venous catheterization method under the resting and fasting condition; with the catheter tip in a main pulmonary artery, the subject was made to breathe from a sourve of 10% O2 gas with half mask and Douglas bag for a period of 20 minutes.The pulmonary artery pressure was recorded by an electro-manometer at intervals of 5 minutes; the blood gas was measured on the mixed venous blood and arterial blood at the same time. The subjects examined 23 cases in total, including 5 normal subjects (Group A), 12 patients with pulmonary tuberculosis (Group B), 6 cases with cardiac diseases (Group C) consisting of 5 cases with mitral stenosis and one case of ventricular septal defect.Results(1) Respiration and O2 consumption : The rate of respiration and minute ventilation volume were increased in all groups, i.e., hyperventilation, and there was no significant difference among the groups. The rate of O2 consumption (per minute) was decreased in all groups; it was decreased more markedly in pulmonary and cardiac patients than in normal subjects, the difference being statistically significant.(2) Blood gas : The O2 contents were markedly reduced in the arterial blood and mixed venous blood. The recorded arterial blood O2 saturations were; normal subjects (62.8%), pulmonary tuberculosis (63.0%) and cardiac disease (59.8%). The mixed venous blood O2 saturations were : normal sebjects (42.6%), pulmonary tuberculosis (43.5%) and cardiac disease (42.5%). There was no significant difference among the groups. The CO2 contents of the arterial blood and mixed venous blood were slightly reduced in all groups, the decrease being more marked in the group of pulmonary tuberculosis than in other groups.(3) Systemic circulation : The mean brachial artery blood pressure was lowered in all cases, but relatively more markedly in pulmonary (10%) and cardiac patients (18.7%) than in normal subjects (4.4%).(4) Pulmonary Circulation : The mean pulmonary artery pressure was elevated in all groups; the degree of such elevation was obviously different from group to group and in ascending order as follows : normal subjects, pulmonary patients, cardiac patients. The elevation of the mean pulmonary artery pressure value per 10% decrease in oxygen saturation of the systemic arterial blood amounted to 1.3, 1.9, 3.3 mmHg respectively. The pulmonary "capillary" pressure was not altered in all groups.While the pulmonary blood flow was reduced in all groups, and it was then reduced more markedly in pulmonary (30.1%) and cardiac patients (29.8%) than in normal subjects (10%). The pulmonary vascular resistance was therefore increased in all groups and it was increased more markedly in pulmonary and cardiac cases than in normal subjects.The pressure work of the right ventricle was increased markedly (22 %) in normal subjects, but slightly (13%) in cardiac patients. [the rest omitted]