Mixed Venous Oxygen Tension Research Articles

Oxygen Delivery and Consumption during Hypothermia and Rewarming in the Dog

Changes in oxygen consumption (VO2) and oxygen delivery (DO2) were compared in three groups of paralyzed, sedated dogs: 1) a group (n = 5) cooled to 29 degrees C and immediately rewarmed to 37 degrees C; 2) a group (n = 5) cooled to and maintained at 29 degrees C for 24 h, and then rewarmed; and 3) a group (n = 5) maintained at 37 degrees C for 24 h. During the cooling phase, in both the acute and prolonged hypothermia animals, VO2 and DO2 decreased significantly from control values (P less than 0.05). The decrease in DO2 occurred as a result of a similar decrease in cardiac index (CI; P less than 0.05) that was associated with a significant increase in systemic vascular resistance index (SVRI; P less than 0.05). Arteriovenous oxygen content difference (C(a-v)O2), O2 extraction ratio, mixed venous oxygen tension (PVO2), pH, and base deficit (BD) were not different from control values even during prolonged hypothermia. Normothermic control dogs also demonstrated a significant decrease in CI (P less than 0.05) at 24 h. Surface rewarming increased VO2 back to control values in the acute hypothermia group and to values above control (P less than 0.05) in the prolonged hypothermia group. DO2 remained below control in both groups, resulting in a significant increase in O2 extraction (P less than 0.05) and a decrease in PVO2 (P less than 0.05) in the prolonged hypothermia animals. Following rewarming administration of sodium nitroprusside returned DO2, CI, and SVRI to control values but did not increase VO2. All animals survived the study without need for inotropic support.(ABSTRACT TRUNCATED AT 250 WORDS)

Prostaglandin E 1 and intrapulmonary shunt in cardiac surgical patients with pulmonary hypertension

Unlike many other vasodilators, prostaglandin E 1 may reduce pulmonary vascular resistance without changing intrapulmonary shunt in patients with adult respiratory distress syndrome. Whether the same is true for surgical patients with cardiogenic pulmonary hypertension but normal gas exchange remains unclear. Data from the intraoperative records of 8 patients with pulmonary hypertension and elevated pulmonary vascular resistance were used for the study. Hemodynamic variables had been monitored through radial arterial cannulas and pulmonary arterial catheters. Arterial and mixed venous oxygen tension, carbon dioxide tension, oxygen saturation, and hemoglobin level, as well as cardiac output and pulmonary capillary wedge pressure, had been determined in each patient before prostaglandin E 1 infusion was started and again when the desired pulmonary vascular response had been achieved. Pulmonary and systemic vascular resistances and intrapulmonary shunt were calculated from standard formulas. Infusion rates of prostaglandin E 1 ranged from 7 to 135 ng/kg/min. Prostaglandin E 1 reduced mean pulmonary arterial pressure, pulmonary vascular resistance, and pulmonary capillary wedge pressure but did not change intrapulmonary shunt. Heart rate and mean arterial and right atrial pressures were not changed, whereas systemic vascular resistance decreased and cardiac output increased. The present study shows that prostaglandin E 1 reduces pulmonary arterial pressure and pulmonary vascular resistance without dramatic changes in intrapulmonary shunt in patients with pulmonary hypertension secondary to cardiac disease.

Effect of Increased Intracranial Pressure on Regional Hypoxic Pulmonary Vasoconstriction

The effects of increased intracranial pressure (ICP) and increased cardiac output (QT) on the pulmonary vascular response to regional alveolar hypoxia were compared in pentobarbital-anesthetized, closed-chested dogs. A bronchial divider was inserted, the right lung (RL) was continuously ventilated with 100% O2, and the left lung (LL) was ventilated with either 100% O2 (hyperoxia) or a hypoxic gas mixture (hypoxia). Sulfur hexafluoride (SF6) was used to measure differential lung blood flow and the multiple inert gas technique assessed gas exchange. The response to LL alveolar hypoxia (hypoxic pulmonary vasoconstriction, HPV) was studied in each animal prior to, during, and after the ICP was increased by infusing mock cerebrospinal fluid (CSF) into a lateral ventricle so that cerebral perfusion pressure was 25 mmHg. During both control periods, QT was randomly altered by opening (high QT) or closing (normal QT) two arteriovenous fistulas. Increasing ICP significantly increased QT (P less than 0.01), pulmonary artery pressure (PAP) (P less than 0.05), and mixed venous oxygen tension (PVO2) (P less than 0.05), compared with normal QT controls. Opening the arteriovenous fistulas achieved similar increases in QT (P less than 0.01), PAP (P less than 0.05), and PVO2 (P less than 0.05). The percentage of blood flow to the LL (QL/QT%) during hyperoxia was 43.9 +/- 0.8% (mean +/- SE) and did not vary with manipulation of QT or ICP. QL/QT% during LL hypoxia was significantly increased by both increased ICP (24.6 +/- 3.5%) and high QT (23.1 +/- 1.0%) compared with normal QT (16.8 +/- 2.1) controls (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

The role of oxygen extraction in peripheral tissues in exercise capacity in chronic heart failure.

To elucidate the role of oxygen extraction during exercise in chronic heart failure (CHF), 26 patients underwent the symptom-limited maximal exercise. Hemodynamics, oxygen uptake (VO2) and blood gas were examined during exercise. Group I (n = 16, VO2max less than 20 ml/min/kg) showed severe cardiac dysfunction during exercise compared with group II (n = 10, VO2max greater than or equal to 20 ml/min/kg). Though VO2 was similar in both groups at rest and with a 25-watt load, oxygen extraction was significantly higher in group I than in group II. At the maximal work load, VO2max was significantly lower in group I, whereas there was no significant difference in oxygen extraction between the two groups. With a 25-watt load, mixed venous partial oxygen tension was similar, however, oxygen saturation was significantly lower in group I. It was concluded that oxygen extraction during exercise rapidly increased in group I, and this may play an important role in the maintenance of exercise capacity during mild physical activity in CHF.

New indices of arterial oxygen status: An experience on 168 subjects

We investigated the repeatability and the clinical usefulness of assessing several parameters related to oxygen status in arterial blood. pH, PaCO2, PaO2, oxygen saturation, total hemoglobin concentration, and fractions of carboxy- and methemoglobin were measured in arterial blood. Applying a new algorithm, other parameters were calculated from the above mentioned, among which total oxygen concentration, half saturation tension, 2,3-DPG concentration, uncompensated mixed venous oxygen tension, and cardiac oxygen compensation factor. In 12 subjects we performed three simultaneous determinations of these indices with a good repeatability of the measures. Then, we examined the same parameters in 92 subjects with normal PaO2, 52 patients with respiratory failure (38 normocapnic and 14 hypercapnic), 9 of which were monitored to follow the behaviour of the measures with time according to variations of the clinical status, and in 12 subjects before and after exercise. We found that important alterations in oxygen transport and delivery may be present even when oxygen tension in arterial blood is normal. Furthermore, oxygen status of arterial blood in respiratory failure may be affected by several factors, whose knowledge is essential for a proper treatment. Our data suggest that such an approach to the evaluation of oxygen status offers interesting clinical perspectives.

Transcutaneous oxygen tension measurements during hemorrhagic hypoperfusion using trendelenburg and the pneumatic antishock garment

Transcutaneous oxygen tension (PtCO2) was observed during hemorrhagic hypoperfusion using four therapeutic modalities: pneumatic antishock garment (PASG), 20 degrees Trendelenburg positioning, combined PASG-Trendelenburg, and whole blood infusion. Anesthetized mongrel dogs were mechanically ventilated. A heated transcutaneous oxygen sensor was applied to the skin overlying the sternum. Animals were bled over 10 min of 25% of their calculated blood volume. A therapeutic intervention was applied at the onset of hemorrhage (PASG, Trendelenburg, PASG-Trendelenburg or control). All animals were observed for 20 min, then during a 10-min shed blood reinfusion period, and for 20 min thereafter. PtCO2 was measured continuously and the following were measured serially: cardiac output, mean arterial pressure (MAP), mixed venous oxygen tension (MvO2), and arterial oxygen tension (PaO2). Cardiac index (CI) and the oxygen extraction ratio were calculated. PtCO2 decreased immediately after hemorrhage in all animals. Control values remained consistently below values for active interventions during this time. All groups regained baseline levels of PtCO2 after reinfusion of shed blood volume. PaO2 remained nearly constant during all experiments. MAP and CI fell in all groups following hemorrhage but did so less precipitously in the PASG group. The PASG and PASG-Trendelenburg groups showed the greatest increase in CI during reinfusion. These results suggest that when PtCO2 is relied upon as an indicator of adequacy of resuscitation during moderate hemorrhagic shock, that cutaneous perfusion may be improved by the PASG or Trendelenburg position, and that perfusion is most effectively restored by blood infusion.

Lung angiotensin converting enzyme activity in rats with differing susceptibilities to chronic hypoxia.

The decrease in lung angiotensin converting enzyme (ACE) activity occurring in rats during chronic hypoxia might be related to the pulmonary haemodynamic response or to the hypoxia. A study in rats was carried out to investigate this question. Rats from the Hilltop (H) strain are known to develop more severe pulmonary hypertension as a result of chronic hypoxia than rats from the Madison (M) strain despite having virtually identical arterial and mixed venous oxygen tensions. Rats from H and M strains were exposed to hypoxia (0.5 atm) for 3-21 days and lung and serum ACE activities were determined. After three days' hypobaria lung ACE activity was significantly lower and serum ACE significantly higher in H than in M rats. Linear regressions for lung ACE activity and right ventricular:body weight ratios showed significant inverse correlations and were similar in the two strains. The results suggest that pulmonary hypertension and not hypoxia determines the reduction in lung ACE activity, possibly by releasing ACE into the blood stream.

Ventilation‐perfusion inequality during endotoxin‐induced pulmonary vasoconstriction in conscious sheep: mechanisms of hypoxia

In sheep low-dose endotoxin infusion causes transient thromboxane-mediated pulmonary vaso- and bronchoconstriction. These changes are paralleled by a decrease of arterial PO2. To elucidate the mechanisms of hypoxia we analysed ventilation-perfusion (VA/Q) distributions by the multiple inert gas elimination technique before and after endotoxin infusion in six conscious sheep. We found that hypoxia after endotoxin could be explained by both a VA/Q inequality and a simultaneous decrease in the mixed venous oxygen tension. The latter was due to a decrease of cardiac output. True shunt did not contribute to hypoxia as it was unchanged.

The role of physiological deadspace and shunt in the gas exchange of patients with pulmonary hypertension: a study of exercise and prostacyclin infusion

Haemodynamic and gas exchange measurements were made at rest, on supine exercise and on acute vasodilatation with intravenous prostacyclin in eight patients with pulmonary hypertension. This enabled an assessment of the contribution of V/Q imbalance to the abnormal gas exchange on the condition. At rest arterial oxygen tension, PaO2 (mean 8.1 +/- 1.7 kPa) and mixed venous oxygen tension, PVO2 (3.6 +/- 0.4) were reduced. The physiological shunt, Qs/Qt (15 +/- 17%) and the dead space, Vd/Vt (0.47 +/- 0.11) were elevated above normal. Exercise produced an increase in cardiac index, a fall in PVO2, no significant change in PaO2 and also no appreciable changes in the Vd/Vt and Qs/Qt. Intravenous prostacyclin increased the cardiac index and raised the PVO2 and the PaO2 but again with no significant changes in Vd/Vt and Qs/Qt. We conclude that ventilation-perfusion imbalance as shown by increased Vd/Vt and Qs/Qt, contributes significantly to the abnormal gas exchange in pulmonary hypertension. But neither index was altered by exercise or vasodilation; the latter improves the hypoxemia by increasing the PVO2 from an increase in the cardiac output.

Relationship between oxygen uptake and oxygen delivery in patients with pulmonary hypertension.

Dependency of oxygen consumption (VO2) on oxygen delivery (DO2) in patients with adult respiratory distress syndrome and with congestive heart failure has been reported previously. We evaluated this relationship in 11 patients with pulmonary hypertension, 8 with primary pulmonary hypertension (PPH), and 3 with pulmonary hypertension secondary to chronic obstructive lung disease (SPH) at baseline and during treatment with vasodilating calcium channel antagonists. The mean baseline DO2 and VO2 were 11.0 +/- 4.2 and 3.9 +/- 1.1 ml/min/kg, respectively. After increasing cardiac output via vasodilators, we obtained an average of 3 additional data points per patient. We found a significant relationship between changes in VO2 and changes in DO2 (delta VO2 = -0.19 +/- 0.27 x delta DO2; r = 0.88, n = 37). In 4 patients, VO2 was determined both by respired gas analysis and by calculation from thermodilution cardiac output and measured arteriovenous oxygen gradient; results by the 2 methods were virtually identical. There was no significant relationship between cardiac output and mixed venous oxygen content or mixed venous oxygen tension (r = 0.20 and 0.47, respectively). Mean baseline oxygen extraction ratio was 36.7 +/- 6.4% and did not increase significantly after vasodilator therapy. We conclude that in patients with pulmonary hypertension, changes in oxygen consumption appear to be dependent on changes in oxygen delivery. This may represent evidence of tissue hypoxemia, which is otherwise not apparent. This dependency may support the use of vasodilators in these patients.

Evaluation of whole body autoregulation in conscious dogs.

The ability of the systemic circulation to maintain cardiac output during decreases in arterial pressure was evaluated in conscious dogs with intact reflexes (n = 8) and during pharmacological blockade of the autonomic nervous system, angiotensin II formation, and arginine vasopressin (n = 6). Cardiac output was measured electromagnetically, and aortic pressure was controlled via a gravity reservoir connected to a carotid artery. When aortic pressure was decreased in either small steps to approximately 60% of control, or decreased in a single square-wave step to 75% of control and maintained for 2 h, cardiac output decreased to the same or a greater extent in both control and areflexic dogs. Thus total peripheral resistance did not decrease, and autoregulation of the cardiac output did not occur in response to short-term (less than or equal to 2 h) decreases in arterial pressure, even in the absence of the major pressor systems. After long-term (greater than 8 h) decreases in arterial pressure to 75% of control in five dogs with all reflexes intact, significant autoregulation of the cardiac output occurred. The relationship between the gain of blood flow autoregulation and the corresponding values of mixed venous oxygen tension suggests that whole body autoregulation results when oxygen extraction reserve becomes limited.

Effects of Removing Oxygen from Patients with Chronic Obstructive Pulmonary Disease

To determine the acute physiologic effects of removing oxygen from patients with chronic obstructive pulmonary disease (COPD) who are receiving long-term oxygen therapy, we made serial measurements in 20 patients during and after stopping low-flow oxygen therapy. Removing oxygen caused an increase in pulmonary vascular resistance, requiring 2 to 3 h to reach a new steady state. Removing oxygen therapy increased pulmonary vascular resistance index (PVRI) by 31% during rest (8.14 +/- 0.61 versus 6.23 +/- 0.51 units, p less than 0.001) and by 29% during exercise (8.11 +/- 0.9 versus 6.31 +/- 0.7, p less than 0.001). The increase in PVRI occurred because of an increase in pulmonary arterial pressure without a change in pulmonary capillary wedge pressure or cardiac index. At rest the increase in pulmonary arterial pressure caused by stopping oxygen correlated with the decrease in arterial oxygen saturation (r = 0.70, p less than 0.01). Removing oxygen decreased stroke volume index during rest and exercise. Although removing oxygen increased pulmonary vascular resistance, it did not affect systemic arterial pressure or vascular resistance. Stopping oxygen reduced arterial and mixed venous oxygen tension and oxygen delivery during rest and exercise. In patients who had a normal PaCO2 while breathing room air, removing oxygen therapy increased their oxygen consumption; conversely, in those patients who had an elevated PaCO2 while breathing room air, stopping oxygen therapy reduced oxygen delivery and oxygen consumption.(ABSTRACT TRUNCATED AT 250 WORDS)

The Effects of Vasodilation with Prostacyclin on Oxygen Delivery and Uptake in Critically Ill Patients

We hypothesized that inadequate oxygenation of peripheral tissues may be unrecognized in critically ill patients and may worsen their prognosis. To test this hypothesis, we measured oxygen delivery to tissues, oxygen uptake, and the extraction ratio (uptake/delivery) before and during a 30-minute infusion of a vasodilator, prostacyclin (5 ng per kilogram of body weight per minute), in 27 critically ill patients with acute respiratory failure. Prostacyclin produced an increase in oxygen delivery (median value before vs. during infusion, 375 vs. 492 ml of oxygen per minute per square meter of body-surface area, P less than 0.001) that was similar in the 14 patients who survived and the 13 who died. This increase in oxygen delivery was associated with a significantly greater increase in oxygen uptake in the patients who died as compared with the survivors (median increase, 19 vs. 5 percent, P less than 0.001). In the survivors, the oxygen extraction ratio fell (median change, -17 percent; range, -27 to -6 percent) and the mixed venous oxygen tension increased. In the patients who died, the extraction ratio rose (median change, 11 percent; range -24 to +40 percent) and the mixed venous oxygen tension did not change. These data suggest the presence of a substantial oxygen debt in patients who subsequently die. Inadequate tissue oxygenation, which may be difficult to recognize, appears to be an important mechanism contributing to the development of irreversible multiple organ failure and subsequent death in some patients with acute respiratory failure.

Effects of ritodrine hydrochloride on arteriovenous blood gas and shunt in healthy pregnant yellow baboons

Although the cardiovascular, renal, and metabolic effects of ritodrine hydrochloride have been extensively investigated, its effect on shunt and oxygen dynamics have not. To define the effects of ritodrine hydrochloride on these parameters, six pregnant baboons were exposed to both low (1.5 μg/kg/min) and high (5 μg/kg/min) concentrations of the drug and compared with six control animals not exposed. Ritodrine had no effect on arterial or mixed venous oxygen tension, the arteriovenous oxygen content difference, or the venous-arterial shunt fractiin. The treated animals did manifest a significant decline in both arterial (p < 0.05) and mixed venous carbon dioxide (p < 0.01) pressures, with associated increases in the respective pH values (p < 0.001 and p <0.01). Total pulmonary resistance also showed a significant fall during ritodrine treatment (p < 0.05). These data support a minimal, if any, impact of ritodrine hydrochloride on the blunting of normal hypoxic pulmonary vasoconstriction. Furthermore, these data are of potential use as a reference in the treatment of pregnant women who have sustained life-threatening insults from exposure to these agents.

Kinetics of mixed venous oxygen tension during rhythmic contraction of the hindlimb of dogs.

Change in mixed venous oxygen tension (PVO2) during transition from rest to exercise induced by rhythmic contractions of the hindlimb of dogs was continuously monitored using intravascular oxygen electrodes. The rapid fall in PVO2, on the average 9.5 sec after the onset of rhythmic contraction, was found. The time course of change in PVO2 was not altered by ligation of the splenic artery and vein. Oxygen tension of venous blood in the superior vena cava and the inferior vena cava was monitored in order to elucidate the mechanism of rapid fall in PVO2 following induced exercise. Oxygen tension of venous blood in the superior vena cava did not fall at the onset of contraction. Oxygen tension of venous blood in the distal and proximal end of the inferior vena cava began to fall at 4.4 sec and at 6.9 sec after the onset of contraction on the average, respectively. There was no significant difference between the hematocrit of mixed venous blood at rest and after 15 sec of exercise. These findings suggest that the rapid fall of PVO2 results from a surge of low oxygenated blood from the exercising hindlimb and that this change in blood gas tensions possibly reaches the lung within 10 sec after the onset of exercise.

Dependence of Oxygen Consumption on Oxygen Delivery in Patients with Chronic Congestive Heart Failure

We previously have shown that in patients with adult respiratory distress syndrome (ARDS) oxygen consumption (VO2) is linearly related to oxygen delivery (DO2) below a threshold DO2 of 21 ml/min/kg. To evaluate this relationship in chronic congestive heart failure (CHF), we studied eight patients with chronic CHF at baseline and during treatment with nitroglycerin. The resting DO2 and VO2 were 10.7 +/- 2.3 ml/min/kg and 3.8 +/- 0.87 ml/min/kg, respectively. In our eight patients, we found a significant relationship between changes in VO2 and in DO2 (delta VO2 = 0.16 + 0.34 X delta DO2, r = 0.84, n = 29). There was no significant relationship between DO2 and mixed venous oxygen tension (PvO2, r = 0.16), nor was there a significant relationship between cardiac output (Qt) and PvO2 (r = 0.21). We conclude that in patients with chronic CHF, changes in VO2 appear to be dependent on changes in DO2. This may represent an adaptive tissue response to chronically reduced systemic oxygen transport.

ADDITIONAL BLOOD-GAS VARIABLES FOR THE RATIONAL CONTROL OF OXYGEN THERAPY : With Allowance for Shifts of the Oxygen Dissociation Curve

When a sample of arterial blood is analysed for oxygen tension and, using a modern oximeter, for haemoglobin concentration and saturation, it is possible to calculate the position of the oxygen dissociation curve and two new variables: "P95" and "C(a-x)O2". P95 is the tension at which the haemoglobin would be 95% saturated and can, therefore, constitute a target tension for near-maximum arterial content of oxygen. C(a-x)O2 (the "conditional extraction" of oxygen) is the amount of oxygen, in ml/dl blood, which can be extracted from the arterial blood for a hypothetical mixed-venous oxygen tension PxO2. It is explained how it is possible to estimate the adequacy of tissue oxygenation by comparing any available estimate of the required extraction (normally about 5 ml dl-1) with conditional extractions calculated for three hypothetical values of PxO2 covering the clinical range. Methods of calculation are given. For accurate results at high arterial saturations, a peripheral venous sample may be required in addition to the arterial sample.

The effects of vasodilation with prostacyclin on oxygen delivery and uptake in critically ill patients.

We hypothesized that inadequate oxygenation of peripheral tissues may be unrecognized in critically ill patients and may worsen their prognosis. To test this hypothesis, we measured oxygen delivery to tissues, oxygen uptake, and the extraction ratio (uptake/delivery) before and during a 30-minute infusion of a vasodilator, prostacyclin (5 ng per kilogram of body weight per minute), in 27 critically ill patients with acute respiratory failure. Prostacyclin produced an increase in oxygen delivery (median value before vs. during infusion, 375 vs. 492 ml of oxygen per minute per square meter of body-surface area, P less than 0.001) that was similar in the 14 patients who survived and the 13 who died. This increase in oxygen delivery was associated with a significantly greater increase in oxygen uptake in the patients who died as compared with the survivors (median increase, 19 vs. 5 percent, P less than 0.001). In the survivors, the oxygen extraction ratio fell (median change, -17 percent; range, -27 to -6 percent) and the mixed venous oxygen tension increased. In the patients who died, the extraction ratio rose (median change, 11 percent; range -24 to +40 percent) and the mixed venous oxygen tension did not change. These data suggest the presence of a substantial oxygen debt in patients who subsequently die. Inadequate tissue oxygenation, which may be difficult to recognize, appears to be an important mechanism contributing to the development of irreversible multiple organ failure and subsequent death in some patients with acute respiratory failure.

Pulmonary Vasodilator Therapy for Chronic Obstructive Pulmonary Disease and Cor Pulmonale: Treatment with Nifedipine, Nitroglycerin, and Oxygen

The present study was undertaken to evaluate the short-term effects of nitroglycerin, nifedipine, and supplemental oxygen on hemodynamics and gas exchange in 11 patients in stable condition with chronic obstructive pulmonary disease and cor pulmonale. In general, both intravenous nitroglycerin and sublingual nifedipine significantly reduced the pulmonary vascular resistance index. For the group as a whole, nifedipine decreased the pulmonary vascular resistance index by significantly increasing the cardiac index, with minimal reductions in mean pulmonary arterial pressure. Conversely, nitroglycerin decreased the pulmonary vascular resistance index by markedly reducing the mean pulmonary arterial pressure but also decreased the cardiac index in some patients. Nitroglycerin also caused a significant decrease in mixed venous oxygen tension. Administration of oxygen did not cause any clinically significant improvement in resting hemodynamics following short-term administration. During the follow-up period, eight of 11 patients who were treated with pulmonary vasodilators in addition to long-term therapy with low-flow oxygen died within a mean of six months. This rate of survival was not significantly different than an age-matched and sexmatched control group with similar severity of disease who received only long-term therapy with low-flow oxygen. Based on these data, it seems unlikely that a substantial increase in survival will be obtained by combining pulmonary vasodilators with long-term oxygen therapy in patients with stable emphysema who have cor pulmonale and carbon dioxide retention. The present study was undertaken to evaluate the short-term effects of nitroglycerin, nifedipine, and supplemental oxygen on hemodynamics and gas exchange in 11 patients in stable condition with chronic obstructive pulmonary disease and cor pulmonale. In general, both intravenous nitroglycerin and sublingual nifedipine significantly reduced the pulmonary vascular resistance index. For the group as a whole, nifedipine decreased the pulmonary vascular resistance index by significantly increasing the cardiac index, with minimal reductions in mean pulmonary arterial pressure. Conversely, nitroglycerin decreased the pulmonary vascular resistance index by markedly reducing the mean pulmonary arterial pressure but also decreased the cardiac index in some patients. Nitroglycerin also caused a significant decrease in mixed venous oxygen tension. Administration of oxygen did not cause any clinically significant improvement in resting hemodynamics following short-term administration. During the follow-up period, eight of 11 patients who were treated with pulmonary vasodilators in addition to long-term therapy with low-flow oxygen died within a mean of six months. This rate of survival was not significantly different than an age-matched and sexmatched control group with similar severity of disease who received only long-term therapy with low-flow oxygen. Based on these data, it seems unlikely that a substantial increase in survival will be obtained by combining pulmonary vasodilators with long-term oxygen therapy in patients with stable emphysema who have cor pulmonale and carbon dioxide retention.

Pulmonary marrow embolism: a dog model simulating dual component cemented arthroplasty.

The cardiopulmonary changes resulting from cemented arthroplasty procedures were monitored in 11 dogs with a single prosthesis implanted and nine dogs with a dual arthroplasty procedure. These changes were characterized by decreased BP, elevated PPA, and elevated PVR, associated with decreases in PaO2, cardiac output and mixed venous oxygen tension. All changes were more pronounced and prolonged in the dual component arthroplasty group. Histologic lung examination and morphometry demonstrated significant degrees of marrow (fat) microembolism in the dual arthroplasty model. Cardiopulmonary collapse has been associated with Guepar dual component arthroplasties clinically and these patients are at increased risk and should be monitored continuously. Prophylactic measures include meticulous lavage of the intramedullary cavity, increased FIO2, and maintenance of intravascular volume and cardiac output. The bilateral arthroplasty model is useful in investigating therapeutic interventions which may detect and prevent the marrow microembolism syndrome intraoperatively.