Mixed Venous Oxygen Tension Research Articles

Pulmonary gas exchange response to weaning with pressure-support ventilation in exacerbated chronic obstructive pulmonary disease patients.

To assess if pressure-support ventilation (PSV) can improve ventilation-perfusion (V(A)/Q) imbalance observed during the transition from positive-pressure ventilation to spontaneous breathing in intubated chronic obstructive pulmonary disease (COPD) patients during weaning. Prospective study. Respiratory intensive care unit of a tertiary university hospital. Seven mechanically ventilated COPD male patients (age 68+/-6 (SD) years; FEV(1) 26+/-6% predicted) during weaning. Patients were studied during three ventilatory modalities: (1) assist-control ventilation (ACV), tidal volume (V(T)), 8-10 ml. kg(-1); (2) PSV aimed to match V(T)in ACV, 15+/-1 cmH(2)O and (3) spontaneous breathing. Arterial and mixed venous respiratory blood gases, V(A)/Q distributions, hemodynamics and breathing pattern were measured. Compared with both ACV and PSV, during spontaneous breathing patients exhibited decreases in V(T) (of 43%, p<0.001) and increases in respiratory rate (of 79%, p<0.001), PaCO(2) (of 8.5 mmHg, p=0.001), cardiac output (of 27%, p<0.001) and mixed venous oxygen tension (of 3.4 mmHg, p=0.003), while PaO(2) remained unchanged throughout the study. Except for a shift of the pulmonary blood flow distribution to areas with lower V(A)/Q ratios (p=0.044) and an increase of dead space (of 25%, p=0.004) during spontaneous breathing, no other changes in V(A)/Q distributions occurred. No differences were shown between ACV and PSV modalities. In COPD patients during weaning, PSV avoided V(A)/Q worsening during the transition from positive-pressure ventilation to spontaneous breathing. Hemodynamics, blood gases or V(A)/Q mismatch were no different between ACV and PSV when both modalities provided similar levels of ventilatory assistance.

Association Between the Angiotensin-Converting Enzyme Gene Polymorphisms and Tissue Oxygenation During Exercise in Patients With COPD

We have recently determined that the angiotensin-converting enzyme (ACE) DD genotype might be associated with pulmonary hypertension during exercise in patients with COPD. Therefore, this study was designed to determine whether ACE gene polymorphisms adversely affect tissue oxygenation during exercise in patients with COPD. Cross-sectional analysis. University hospital. Thirty-nine patients (14 patients with II genotype, 12 patients with ID genotype, and 13 patients with DD genotype). All patients underwent right-heart catheterization and constant-load exercise testing for 5 min on an ergometer. The ratio of the change in oxygen delivery (DO(2)) to the increase in oxygen consumption (O(2)) during exercise (DeltaDO(2)/DeltaO(2)) was significantly lower in patients with the DD genotype (1.5 +/- 0.2) than in those with the II genotype (1.9 +/- 0.3, p = 0.0006) and the ID genotype (1.7 +/- 0.2, p = 0.037). Mixed venous oxygen tension (PO(2)) after exercise in patients with the DD genotype (23.5 +/- 1.5 mm Hg) was also significantly lower than in patients with the II genotype (26.7 +/- 1.6 mm Hg, p = 0.0002) and the ID genotype (25.0 plus minus 2.0 mm Hg, p = 0.045). In addition, the change in plasma concentration of lactate during exercise (DeltaLactate) was significantly higher in patients with DD genotype (33.3 +/- 4.3 mmol/L) than in those with the II genotype (25.5 +/- 3.6 mmol/L, p = 0.0002) and the ID genotype (28.8 +/- 4.0 mmol/L, p = 0.029). The mean pulmonary arterial pressure after exercise was significantly correlated with DeltaDO(2)/DeltaO(2) (r = - 0.423, p = 0.0076) but not with PvO(2) after exercise and with DeltaLactate. The ACE DD genotype may be associated with an impairment in peripheral tissue oxygenation during exercise in patients with COPD.

Polymerized Hemoglobin Therapy in a Foal with Neonatal Isoerythrolysis

Abstract Objective: To present the successful management of a foal with severe neonatal isoerythrolysis (NI) given polymerized (bovine) hemoglobin while awaiting appropriate red blood cells for transfusion. Case Summary: A foal with peracute neonatal isoerythrolysis, anemia and low venous oxygen tension was stabilized with intravenous polymerized hemoglobin. Polymerized hemoglobin treatment maintained the foal's oxygen requirement for up to 18 hours permitting adequate time for preparation of the donor's washed red blood cells for transfusion. The clinical findings and venous oxygen tension improved following the hemoglobin administration. No adverse effects were noted from the polymerized hemoglobin administration. Unique information provided: This paper presents a foal with an uncommon cause of NI due to anti‐Pa antibodies and the short term management of NI using polymerized hemoglobin while awaiting a washed and packed RBC transfusion. Clinical and laboratory findings (trigger factors), which can be used to determine the need for a blood transfusion, are discussed. These “trigger factors” include weakness, tachypnea and tachycardia, increased anion gap and decrease in hematocrit, hemoglobin concentration and mixed venous (pulmonary artery) oxygen tension (approximated using jugular venous samples). (J Vet Emerg Crit Care 2001; 11(2): 141–146)

Cardiopulmonary effects of a two hour medetomidine infusion and its antagonism by atipamezole in horses and ponies

The cardiopulmonary effects of an intravenous (iv) medetomidine injection (5 μg/kg) followed 5 min later by its infusion at 3.5 μg/kg/h for 115 rnin were studied in 9 horses and ponies. Five minutes after the end of infusion 60 μg/kg atipamezole were given. Physiological data during infusion were compared with pre-sedation values. Stroke volume was reduced significantly 5 min after initial medetomidine injection. Cardiac index was reduced significantly and systemic vascular resistance increased significantly for the first 20 min, but returned towards pre-sedation values after this time. Arterial blood pressures were reduced significantly from 30 min until the end of the procedure (minimum MAP was 102.4 ± 9.61 mmHg). Mixed venous oxygen tension was reduced significantly during the infusion. Respiratory rate fell and PaCO 2 - rose significantly from 40 min onward. Other variables showed no significant changes. The horses recovered rapidly after atipamezole was injected. Arterial blood pressures remained significantly lowered, but other cardiovascular variables returned towards pre-sedation values. It is concluded that the infusion of medetomidine at 3.5 μg/kg/h causes minimum cardiopulmonary depression once the effects of an initial 5 μg/kg injection have waned, and so could prove suitable as part of an anaesthetic technique in equidae.

Effects of isosorbide dinitrate on electrocardiography, hemodynamics, and ventilation in patients with exercise-induced elevation of pulmonary artery wedge pressure.

The mechanisms underlying exertional hyperpnea in patients with coronary artery disease and transient left ventricular dysfunction are still not fully understood. The study was undertaken to investigate whether the ventilatory response to exercise reflects the effects of acute medical treatment of exercise-induced left ventricular dysfunction, and to evaluate mechanisms relevant to excessive exertional ventilation. In 11 male patients, aged 65.2 +/- 6.0 years, all with pulmonary artery wedge pressure (PAWP) > 25 mmHg and ST depression > 2 mm during moderate supine exercise, ventilation (V), oxygen uptake (VO2), hemodynamics, electrocardiogram (ECG), and arterial and mixed venous blood gases were examined during supine rest and exercise, before and at hourly intervals after peroral intake of 30 mg isosorbide dinitrate (ISDN). Six similar patients were examined with the same protocol without ISDN administration and comprised a control group. Before administration of ISDN, exercise PAWP was 35.3 +/- 5.9 mmHg, ECG showed 2.77 +/- 1.06 mm ST depression, and V/VO2 was 31.8 +/- 4.8 l/l. One h after ISDN administration, exercise mean PAWP was 11.0 +/- 2.5 mmHg (p < 0.001), ST depression 0.59 +/- 0.8 mm (p < 0.001), whereas V/VO2 was unchanged, 30.1 +/- 5.3 l/l. Two h later, PAWP remained reduced and there were only minor ST depressions, while V/VO2 remained high. Exercise cardiac index (CI) and mixed venous oxygen tension (PvO2), initially 4.7 +/- 0.67 l/min/m2 and 3.54 +/- 0.35 kPa, respectively, remained at the same low level throughout the study. In the six nontreated patients, there were no significant changes in ST depression, exercise PAWP, or exertional ventilation. Isosorbide dinitrate treatment markedly improved exercise-induced left heart dysfunction, whereas excessive ventilatory response was unaffected, even after 3 h. Thus, measurements of the exercise hyperpnea did not properly reflect effective reduction of myocardial ischemia.

Effect of Hyperoxia and Hypoxia on Subcutaneous Tissue Gases and pH

The effect of different fractions of inspired oxygen on subcutaneous oxygen tension, carbon dioxide tension and pH in relation to arterial and mixed venous blood gases and pH and hemodynamic variables was evaluated in 13 domestic pigs. Subcutaneous, arterial and mixed venous oxygen tensions were closely correlated (r = 0.94). A minor significant increase in subcutaneous carbon dioxide tension was noted during hyperoxia (p < 0.05). A major increase (33%) was noted during the last step of hypoxia, when arterial and mixed venous carbon dioxide tensions increased only 12 and 17%, respectively. A minor decrease in subcutaneous pH was noted during hyperoxia (p < 0.05) and a major decrease during hypoxia (p < 0.05). Measurements of subcutaneous tissue gases and pH are indicators of oxygen utilization during hyper- and hypoxia.

Effects of inhaled nitric oxide 10 ppm in spontaneously breathing horses anaesthetized with halothane

Inhaled nitric oxide, a selective pulmonary vasodilator, is known to improve arterial oxygenation after cardiopulmonary bypass and during acute respiratory distress syndrome in humans. During general anaesthesia with spontaneous ventilation, healthy adult horses develop large alveolar-arterial oxygen tension differences. In this study, we have determined the effects of inhaled nitric oxide (10 parts per million (ppm)) on venous admixture and pulmonary haemodynamics in horses anaesthetized with halothane. Seven adult horses were studied twice in random sequence. After premedication with romifidine 100 micrograms kg-1, anaesthesia was induced with ketamine 2.2 mg kg-1 and maintained with 1.1 MAC (0.95%) of halothane in oxygen. Horses breathed spontaneously. After 65 min, each horse had nitric oxide 10 ppm added to the inspired gas for 20 min (procedure HA + NO) or anaesthesia was continued with halothane in oxygen (procedure HA). Cardiac output, minute ventilation, arterial and mixed venous oxygen and carbon dioxide tensions, and mean pulmonary and carotid arterial pressures were measured for 100 min. Shunt fraction and pulmonary and systemic vascular resistances were calculated. Shunt fraction (SF) and mean pulmonary artery pressure (PPA mean) were not different between the two groups after 65 min of general anaesthesia (HA: SF 0.20 (SD 0.06), PPA mean 45 (8) mm Hg; HA + NO: SF 0.21 (0.04), PPA mean 44 (7) mm Hg) or after 85 min (HA: SF 0.22 (0.07), PPA mean 45 (8) mm Hg; HA + NO: SF 0.20 (0.03), PPA mean 43 (7) mm Hg). There were no significant effects of time or nitric oxide inhalation on any other variable. There was a significant correlation (r = 0.80, P < 0.05) between calculated shunt fraction 65 min after induction of anaesthesia and body weight.

Plasma Endothelin-1 Level in Chronic Obstructive Pulmonary Disease: Relationship with Natriuretic Peptide

Background and Objective: Endothelin-1 (ET-1) is a potent vasoconstrictor peptide produced by the vascular endothelium. The purpose of this study was to elucidate the pathophysiological role of ET-1 in patients with pulmonary hypertension secondary to chronic obstructive pulmonary disease (COPD). Method: We measured plasma ET-1 levels during right heart catheterization both at rest and during exercise on room air and while breathing oxygen in patients with COPD. In addition, we simultaneously measured plasma levels of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP). Results: Plasma ET-1 levels at rest were significantly higher in 21 patients with COPD than in 16 control subjects (p < 0.001). For COPD patients, there was no correlation between the plasma ET-1 level and pulmonary arterial pressure or pulmonary vascular resistance at rest. On the other hand, there was a significant negative correlation between plasma ET-1 level and mixed venous oxygen tension (r = –0.503, p < 0.05). Also, the plasma ET-1 level was positively correlated with those of ANP (r = 0.540, p < 0.05) and BNP (r = 0.533, p < 0.05) at baseline. Oxygen administration significantly decreased plasma ET-1 levels at rest (p < 0.05). Plasma ET-1 levels did not change significantly with exercise despite the progression of pulmonary hypertension and hypoxemia. In contrast, plasma ANP and BNP levels both increased markedly with exercise (p < 0.01). Conclusion: We conclude that in patients with COPD, the plasma ET-1 level is not affected by acute progression of pulmonary hypertension and hypoxemia during exercise, and persistent hypoxemia may be associated with an increase in the plasma ET-1 level. In addition, our findings suggest that ANP and BNP may modulate the pulmonary vascular tone by interacting with ET-1 in these patients.

A physiology simulator: validation of its respiratory components and its ability to predict the patient's response to changes in mechanical ventilation

We aimed to validate the mathematical validity and accuracy of the respiratory components of the Nottingham Physiology Simulator (NPS), a computer simulation of physiological models. Subsequently, we aimed to assess the accuracy of the NPS in predicting the effects of a change in mechanical ventilation on patient arterial blood-gas tensions. The NPS was supplied with the following measured or calculated values from patients receiving intensive therapy: pulmonary shunt and physiological deadspace fractions, oxygen consumption, respiratory quotient, cardiac output, inspired oxygen fraction, expired minute volume, haemoglobin concentration, temperature and arterial base excess. Values calculated by the NPS for arterial oxygen tension and saturation (PaO2 and SaO2), mixed venous oxygen tension and saturation (PvO2 and SvO2), arterial and mixed venous carbon dioxide tension (PaCO2 and PvCO2) and arterial pH were accurate compared with measured values. Subsequently, arterial gas responses to changes in minute volume of FiO2 were measured in 31 patients and were compared with the NPS prediction for each response. The 95% limits of agreement in predicting the magnitude of change were: arterial oxygen tension -2.07 to 2.47 kPa; PaCO2 -0.33 to 0.67 kPa; and pH -0.023 to 0.033. This investigation has validated respiratory components of the NPS. We recommend the NPS as a clinical tool for predicting the effects of alterations in mechanical ventilation in stable patients in the intensive care unit.

Protective Effects of Ischemic Preconditioning on Donor Lung in Canine Lung Transplantation

Myocardial ischemic preconditioning has been found to protect the myocardium. We hypothesized that lung ischemic preconditioning might enhance canine lung preservation and reduce allograft lung dysfunction after transplantation. Ten pairs of adult canines underwent left lung allotransplantation. Five donors were treated with ischemic preconditioning (their left hilus clamped for 10 min and released for 15 min [group IP]), and five donors were not treated with ischemic preconditioning (group C). The donor lungs were flushed with 4 degrees C Euro-Collins solution (ECS) and stored in the same solution for 2 1/2 h, then transplanted to the recipient canines. The animals were observed for 1 to 2 h after transplantation. The lung venous blood of the recipient and donor lung tissue was collected just after thoracotomy and 1 h after reperfusion of the transplanted lung in both groups. The numbers of polymorphonuclear leukocytes (PMNs) in the pulmonary venous blood after reperfusion were significantly higher in group IP than in group C (p<0.05). However, the numbers of PMNs in lung interstitium under microscopy were less in group IP than in group C. The thromboxane B2, malondialdehyde, and mean pulmonary artery pressure contents were significantly lower in group IP than in group C (p<0.05), and the superoxide dismutase and mixed venous oxygen tension values were significantly higher in group IP than in group C (p<0.05). Histologic findings show less damage in group IP than in group C. The protective effects of ischemic preconditioning in conjunction with ECS flush and storage were superior to using ECS alone. The possible mechanisms were that ischemic preconditioning inhibited the accumulation and activation of PMNs in lung tissue and reduced the production of oxygen-free radicals.

Central and mixed venous blood oxygen correlate well during acute normovolemic hemodilution in anesthetized pigs

Central venous oxygen saturation (ScvO2) and oxygen tension (PcvO2), obtained from the superior vena cava, correlate well with mixed venous (pulmonary arterial) oxygen saturation (SvO2) and tension (pvO2) when the hematocrit is normal. The present study was undertaken to assess whether extreme hemodilution affects this relation. We compared mixed and central venous blood during graded arterial desaturation (inspired fraction of oxygen (FIO2) between 1.0 and 0.10) in 10 hemodiluted pigs, and in 10 pigs with normal hematocrit (control), during fentanyl-ketamine-pancuronium anesthesia and mechanical ventilation. Arterial oxygen saturation decreased from 100% at FIO2 = 1.0 to 44 +/- 12% at FIO2 = 0.10 (mean +/- SD). Venous oxygen saturation ranged from 3.5% to 97.3%. The regression coefficient between SvO2 and ScvO2 was 0.97 (R2 = 0.93, bias -2.4 +/- 5.8%) in the hemodiluted and 0.99 (R2 = 0.97, bias -3.0 +/- 5.0%) in the control group. Venous oxygen tension values ranged from 0.5 kPa to 9.5 kPa, and the regression coefficient for oxygen tension was 0.94 (R2 = 0.89, bias -0.20 +/- 0.47 kPa) in the hemodiluted and 0.99 (R2 = 0.97, bias -0.43 +/- 0.48 kPa) in the control group. The regression coefficient for pH was 0.95 in the hemodiluted and 0.98 in the control animals. The findings indicate that also during hemodilution monitoring of central venous blood oxygen may be as useful as monitoring of mixed venous blood oxygen.

The Effects of Prostaglandin I2, Prostaglandin E1, and Nitroglycerin on Hemodynamics and Blood Gas Exchanges in Pulmonary Hypertension in Dogs

Background : The ideal drug for treatment of pulmonary hypertension would be a vasodilator which acts preferentially on the pulmonary vascular bed. The aim of this study was to compare the effects of prostaglandin I2 (PGI2) on central hemodynamics and right ventricular function with the more widely used vasodilators, prostaglandin E1 (PGE1) and nitroglycerin (NTG) and to investigate whether PGI2 is more selective to the pulmonary vascular bed compared with PGE1 and NTG in dogs. Methods : We have used a method for producing sustained pulmonary hypertension in vivo by continuous infusion of U46619 adjusting the infusion rate until a mean pulmonary artery pressure (PAP) exceeded 25 mmHg. And the pulmonary and systemic effects of the three pulmonary vasodilators were compared at doses producing equivalent, lowered approximately 20% of mean arterial pressures (MAP) or mean PAP returned to baseline. Results : After infusion of the three vasodilators, heart rate, cardiac output, and mean PAP/MAP ratio were significantly increased, but there was no statistical significant differences among the three vasodilators. PGI2 and PGE1 significantly increased (worsened) the PVR/SVR ratio, but NTG decreased. However there was no significant difference among the three vasodilators. After infusion of the three vasodilators, the arterial oxygen tension (PaO2), mixed venous oxygen tension (PO2), O2 deliver, and O2 uptake were increased, and shunt ratio (s/t(%)) were significantly decreased, but there were no significant differences among three vasodilators. Conclusions : PGI2, PGE1, and NTG all decreased both PVR and SVR. None of these vasodilators were more selective to the pulmonary vascular bed, myocardial performance, and improved gas exchange. (Korean J Anesthesiol 1998; 35: 633∼641)

Changes of Blood Gases, Plasma Catecholamine Concentrations and Hemodynamic Data in Anesthetized Dogs during Graded Hypoxia Induced by Nitrous Oxide

The sympathoadrenal system plays an important role in homeostasis in widely varing external environments. Conflicting findings, however, have been reported on its response to hypoxia. We investigated the effect of hypoxia on the sympathoadrenal system in dogs under halothane anesthesia by measuring levels of circulating catecholamines in response to graded hypoxia. Ten healthy mongreal dogs were mechanically ventilated with different hypoxic gas mixtures. Graded hypoxia and reoxygenation were induced by progressively decreasing the oxygen fraction in the inhalation gas mixture from 21%(control) to 15%, 10% and 5% at every 5 minutes, and then reoxygenated with 60% oxygen. Mean arterial pressure, central venous pressure and mean pulmonary arterial pressure were measured directly using pressure transducers. Cardiac output was measured by the thermodilutional method. For analysis of blood gas, saturation and content, arterial and mixed venous blood were sampled via the femoral and pulmonary artery at the end of each hypoxic condition. The concentration of plasma catecholamines was determined by radioenzymatic assay. According to the exposure of graded hypoxia, not only did arterial and mixed venous oxygen tension decreased markedly at 10% and 5% oxygen, but also arterial and mixed venous oxygen saturation decreased significantly. An increased trend of the oxygen extraction ratio was seen during graded hypoxia. Cardiac output, mean arterial pressure and systemic vascular resistance were unchanged or increased slightly. Pulmonary arterial pressure(PAP) and pulmonary vascular resistance(PVR) were increased by 55%, 76% in 10% oxygen and by 82%, 95% in 5% oxygen, respectively(p

Evaluation of the Capabilities of a Hemoglobin Vesicle as an Artificial Oxygen Carrier in a Rat Exchange Transfusion Model

Encapsulation of hemoglobin within a liposome is one of the strategies in the development of artificial oxygen carriers. It maintains the oxygen transporting properties of hemoglobin and, at the same time, eliminates the side effects of cell free hemoglobin. Hemoglobin vesicles (HbV) are a type of liposome encapsulated hemoglobin. They have a particle size of approximately 250 nm, a hemoglobin concentration of 10 g/dl, and the oxygen affinity, P50, is regulated to 32 Torr. In this study the authors examined the oxygen transporting capability of HbV in vivo, by performing exchange transfusions in rats. Exchange transfusion (90% of the estimated circulatory volume) with HbV suspended in 5% albumin (containing 160 mEq/L, sodium and 107 mEq/L, chloride) was carried out in male Wistar rats. Mean arterial pressure and heart rate were monitored through the arterial catheter. Arterial blood samples for gas analyses were also obtained from the arterial catheter. Abdominal aortic blood flow was measured by an ultrasonic pulsed Doppler flowmeter as an indicator of cardiac output. The oxygen tension of blood withdrawn from the right atrium was measured as an indicator of mixed venous oxygen tension. These values were employed to calculate oxygen delivery and consumption. Renal cortical and skeletal muscle tissue oxygen tensions were monitored as indicators of tissue perfusion. Five percent albumin and washed rat red blood cells suspended in 5% albumin containing 10 g/dl of hemoglobin; were employed as controls. At the completion of a 90% exchange transfusion, renal cortical and skeletal muscle tissue oxygen tensions, along with oxygen delivery and consumption, were sustained almost equally well with the HbV suspension compared to the washed rat red blood cell suspension, but declined significantly with the albumin suspension. The results indicate that the oxygen transporting capability of HbV was almost equivalent to that of rat red blood cells.

Mechanisms of worsening gas exchange during acute exacerbations of chronic obstructive pulmonary disease.

This study was undertaken to investigate the mechanisms that determine abnormal gas exchange during acute exacerbations of chronic obstructive pulmonary disease (COPD). Thirteen COPD patients, hospitalized because of an exacerbation, were studied after admission and 38+/-10 (+/-SD) days after discharge, once they were clinically stable. Measurements included forced spirometry, arterial blood gas values, minute ventilation (V'E), cardiac output (Q'), oxygen consumption (V'O2), and ventilation/perfusion (V'A/Q') relationships, assessed by the inert gas technique. Exacerbations were characterized by very severe airflow obstruction (forced expiratory volume in one second (FEV1) 0.74+/-0.17 vs 0.91+/-0.19 L, during exacerbation and stable conditions, respectively; p=0.01), severe hypoxaemia (ratio between arterial oxygen tension and inspired oxygen fraction (Pa,O2/FI,O2) 32.7+/-7.7 vs 37.6+/-6.9 kPa (245+/-58 vs 282+/-52 mmHg); p=0.01) and hypercapnia (arterial carbon dioxide tension (Pa,CO2) 6.8+/-1.6 vs 5.9+/-0.8 kPa (51+/-12 vs 44+/-6 mmHg); p=0.04). V'A/Q' inequality increased during exacerbation (log SD Q', 1.10+/-0.29 vs 0.96+/-0.27; normal < or = 0.6; p=0.04) as a result of greater perfusion in poorly-ventilated alveoli. Shunt was almost negligible on both measurements. V'E remained essentially unchanged during exacerbation (10.5+/-2.2 vs 9.2+/-1.8 L x min(-1); p=0.1), whereas both Q' (6.1+/-2.4 vs 5.1+/-1.7 L x min(-1); p=0.05) and V'O2 (300+/-49 vs 248+/-59 mL x min(-1); p=0.03) increased significantly. Worsening of hypoxaemia was explained mainly by the increase both in V'A/Q' inequality and V'O2, whereas the increase in Q' partially counterbalanced the effect of greater V'O2 on mixed venous oxygen tension (PV,O2). We conclude that worsening of gas exchange during exacerbations of chronic obstructive pulmonary disease is primarily produced by increased ventilation/perfusion inequality, and that this effect is amplified by the decrease of mixed venous oxygen tension that results from greater oxygen consumption, presumably because of increased work of the respiratory muscles.

Cardiopulmonary and gastrointestinal motility effects of xylazine/ketamine-induced anesthesia in horses previously treated with glycopyrrolate

Abstract Objective To assess the usefulness of glycopyrrolate (GLY) in preventing the decrease in cardiac index (Cl) usually caused by xylazine (XYL)/ketamine (KET)-induced anesthesia in horses. Animals 6 healthy horses. Procedure Horses were treated with saline solution or 2.5 μg of GLY/kg of body weight, administered IV. 15 minutes later, XYL (1 mg/kg) was administered IV followed 5 minutes later by KET (2 mg/kg) administration. The horses were positioned in left lateral recumbency, insufflated with 15 L of oxygen/min, and maintained for 30 minutes on the infusion of 0.05 mg of XYL and 0.1 mg of KET/kg/min. Mean, systolic, and diastolic arterial blood pressures, mean pulmonary arterial and central venous pressures, heart rate, Cl, and arterial and mixed venous blood gas tensions were recorded up to 40 minutes after anesthesia induction. Intestinal motility was assessed by auscultation of 4 abdominal quadrants for 24 hours after induction. Data were analyzed by Wilcoxon's rank-sum test for nonparametric observations, and by ANOVA for repeated measures and Scheffe's test for continuous parametric variables. Results Horses given GLY had significantly higher heart rate; mean, systolic, and diastolic arterial blood pressures; Cl; oxygen delivery; and mixed venous oxygen tensions, with significantly less tissue oxygen extraction, compared with saline-treated horses. Both groups had complete loss of intestinal motility associated with general anesthesia. Conclusions GLY significantly reduced the cardiovascular dysfunction attributable to general anesthesia with XYL and KET. The return of intestinal motility was delayed by 3 to 6 hours without causing any serious side effects. (Am J Vet Res 1996;57:1762–1770)

Role of pulmonary vascular disorder in determining exercise capacity in patients with severe chronic obstructive pulmonary disease.

In patients with chronic obstructive pulmonary disease (COPD), the primary cardiovascular complication is the development of pulmonary hypertension, especially during exercise. The purpose of this study was to determine whether pulmonary vascular disorder plays an important role in determining exercise capacity in patients with severe COPD. Twenty-one male patients with severe COPD (mean FEV1 = 0.91 +/- 0.26 1) performed a progressive incremental exercise test, until symptom-limited maximum, to determine maximal exercise capacity, and then a constant-load exercise test for 5 min at a workload (20-60 W) corresponding to 60% of maximal workload during right heart catheterization to characterize the haemodynamic behavior of pulmonary circulation during exercise. The severity of the pulmonary vascular disorder was assessed using the slope of the mean pulmonary arterial pressure (PAP) - cardiac index (CI) relationship during constant-load exercise (P-Q slope). A significant inverse correlation was found between the maximal oxygen consumption (VO2max) and P-Q slope (r = -0.669), but not between VO2max and indices of expiratory airflow obstruction. In addition, the P-Q slope was inversely correlated with mixed venous oxygen tension (PvO2) at the end of constant-load exercise (r = -0.679) and with the change in oxygen delivery relative to oxygen consumption (delta DO2/delta VO2) during constant-load exercise (r = -0.671). These findings suggest that in patients with COPD, the functional impairment of the pulmonary vasculature is associated with disturbance in oxygen transport to the peripheral muscle during exercise, resulting in reduction of exercise capacity. We conclude that pulmonary vascular disorder may be an important factor in determining the exercise capacity of patients with severe COPD.

Cardiopulmonary effects of desflurane in ponies, after induction of anaesthesia with xylazine and ketamine.

Cardiopulmonary parameters were measured in 12 ponies (small horses) before anaesthesia and, following induction with xylazine and ketamine, during maintenance of anaesthesia with desflurane. In six of the ponies (group A) anaesthesia was maintained for three hours with desflurane at an end-tidal concentration of 7.4 per cent. In the other six ponies (group B), anaesthesia was maintained in the same way for one hour and then the effects of end-tidal desflurane concentrations of 7.4 per cent and 9.6 per cent with and without artificial ventilation were investigated. In group A ponies the arterial blood pressure and the systemic vascular resistance index (SVRI) decreased significantly during the first 45 minutes of anaesthesia but recovered with time. The cardiac index and heart rates were unchanged throughout the measurement period but arterial carbon dioxide tensions increased significantly. In group B ponies, with either mode of ventilation, increasing desflurane concentration resulted in decreases in arterial blood pressure, cardiac index and mixed venous oxygen tension, although the changes were not always statistically significant. There were marked individual differences in the cardiovascular responses to the high desflurane concentrations, the minimum mean arterial blood pressure ranging from 35 to 62 mm Hg, and the cardiac index from 23 to 50 ml/kg/min. The study concludes that during maintenance of anaesthesia with end tidal concentrations of desflurane of 7.4 per cent, cardiac index is well maintained and the initial fall in arterial blood pressures results from a fall in SVRI. However, increasing the concentration of desflurane causes a fall in blood pressure due to cardiac depression.

Analysis of P 50 and oxygen transport in patients after cardiac surgery

ObjectiveTo determine whether standard P50 after cardiac surgery decreases and whether decreased P50 is related to the transfusion of red blood cells (RBCs), acid-base changes, body temperature, oxygen parameters and/or duration of cardiopulmonary bypass (CPB).DesignPilot study in cardiac surgery patients.SettingUniversity hospital.Patients12 consecutive elective cardiac surgery patients.InterventionsBlood was taken before surgery, after CPB and in the intensive care unit until 18 h post-operatively. Cardiac output and oxygen consumption were measured. Buffy coat-poor RBCs were transfused, anticoagulated with citratephosphate-dextrose buffer and stored in saline-adenine-glucose-mannitol at 4°C, when haemoglobin was <5.6 mmol·l−1.Measurements and resultsStandard P50 was calculated from measured partial pressure of oxygen and of carbon dioxide, pH and oxygen saturation in mixed venous blood (SvO2) using the Severinghaus formula. Median length of RBC storage was 25 days. Standard P50 after surgery was significantly lower than baseline value (p=0.0001). The number of RBC units transfused and duration of CPB were conjointly associated with P50 (R 2=0.72). Patients who received more RBCs consumed more oxygen.ConclusionCardiac surgery patients receiving more RBC units have lower standard P50 and consume more oxygen. P50 decreased more when the CPB took longer. Because a decrease in P50 implies a low ratio of mixed venous oxygen tension (PvO2) to SvO2, a shift in P50 should be taken into account when using SvO2 as a measure of global oxygen availability. When a direct measurement of SvO2 is not available, PvO2 should be used instead of calculated SvO2.

Analysis of P50 and oxygen transport in patients after cardiac surgery.

To determine whether standard P50 after cardiac surgery decreases and whether decreased P50 is related to the transfusion of red blood cells (RBCs), acid-base changes, body temperature, oxygen parameters and/or duration of cardiopulmonary bypass (CPB). Pilot study in cardiac surgery patients. University hospital. 12 Consecutive elective cardiac surgery patients. Blood was taken before surgery, after CPB and in the intensive care unit until 18 h post-operatively. Cardiac output and oxygen consumption were measured. Buffy coat-poor RBCs were transfused, anticoagulated with citrate-phosphate-dextrose buffer and stored in saline-adenine-glucose-mannitol at 4 degrees C, when haemoglobin was < 5.6 mmol.l-1. Standard P50 was calculated from measured partial pressure of oxygen and of carbon dioxide, pH and oxygen saturation in mixed venous blood (SvO2) using the Severinghaus formula. Median length of RBC storage was 25 days. Standard P50 after surgery was significantly lower than baseline value (p = 0.0001). The number of RBC units transfused and duration of CPB were conjointly associated with P50 (R2 = 0.72). Patients who received more RBCs consumed more oxygen. Cardiac surgery patients receiving more RBC units have lower standard P50 and consume more oxygen. P50 decreased more when the CPB took longer. Because a decrease in P50 implies a low ratio of mixed venous oxygen tension (PvO2) to SvO2, a shift in P50 should be taken into account when using SvO2 as a measure of global oxygen availability. When a direct measurement of SvO2 is not available, PvO2 should be used instead of calculated SvO2.