Improvement In Pulmonary Hemodynamics Research Articles

Resolution of severe pulmonary hypertension after heterotopic cardiac transplantation

In patients with severe congestive heart failure, a marked elevation in pulmonary vascular resistance limits the success of orthotopic cardiac transplantation, thus providing the rationale for heterotopic transplantation. To determine the changes in pulmonary hemodynamics after heterotopic cardiac transplantation, postoperative right heart pressures were serially measured in five patients who underwent this operation for end-stage congestive heart failure accompanied by severe secondary pulmonary hypertension and elevation in calculated pulmonary vascular resistance. Hemodynamics were compared with those of a matched group of 10 orthotopic cardiac transplant recipients.Preoperatively, pulmonary artery mean and wedge pressures, pulmonary vascular resistance and transpulmonary pressure gradient (pulmonary artery mean minus wedge pressure) were significantly higher in the heterotopic group. Postoperatively, significant improvement in pulmonary hemodynamics occurred in both groups and, by 12 months, the pulmonary artery mean pressure, wedge pressure, pulmonary vascular resistance and transpulmonary pressure gradient were similar in the two groups. These findings suggest that pulmonary hypertension secondary to congestive heart failure, even when severe and associated with a high pulmonary vascular resistance, is to a great extent reversible.

Recombinant tissue-type plasminogen activator in canine embolic pulmonary hypertension. Effects of bolus versus short-term administration on dynamics of thrombolysis and on pulmonary vascular pressure-flow characteristics.

We used a canine model of embolic pulmonary hypertension, induced by injection of autologous radioactive blood clots, to investigate effects of recombinant tissue-type plasminogen activator (rt-PA) on dynamics of thrombolysis and on pulmonary pressure-flow (PQ) characteristics. Over 5 (rt-PA5) or 15 (rt-PA15) minutes, 1 mg/kg rt-PA was infused. Rate and extent of thrombolysis were assessed by counting over both lung fields with a gamma camera. Emboli increased mean pulmonary artery pressure from 14 to 36 mm Hg (p less than 0.005). This change was predominantly due to an increase in the effective outflow pressure (PI) (from 9 to 29 mm Hg, p less than 0.001), obtained by extrapolation from the linear PQ relation. While pulmonary hemodynamics improved with rt-PA5 and rt-PA15, the change was greatest with rt-PA15. For example, the increase in PI that occurred with embolization was abolished with rt-PA15. Also, the decrease in pulmonary artery pressure was greatest with rt-PA15. While not significantly different, extent of total clot lysis tended to be greatest with rt-PA15 (p less than 0.07). Also, while during infusion, the concentration of rt-PA5 was threefold that of rt-PA15, the corresponding rate of thrombolysis was similar with rt-PA5 and rt-PA15. These results indicate that the improvement in pulmonary hemodynamics with rt-PA is primarily explained by a decrease in PI. Furthermore, they suggest an upper limit to the dose-thrombolytic rate relation with rt-PA.

Oxygen Therapy Titrated to Raise Mixed Venous Oxygen Content in COPD

Supplemental oxygen therapy delivered at concentrations which increase PaO2 greater than 60 mm Hg often has minimal effects on either pulmonary hemodynamics or the oxygen tension of mixed venous blood (PvO2). Since mixed venous hypoxemia has been shown to contribute to pulmonary vasoconstriction in experimental conditions and is a determinant of survival in chronic obstructive pulmonary disease (COPD), we evaluated the hemodynamic effects of oxygen therapy titrated to raise PvO2 in 12 COPD patients who underwent right heart catheterization. After room air measurements of mean pulmonary artery pressure, cardia output, and pulmonary vascular resistance, they were randomized to either supplemental oxygen therapy given to raise PaO2 greater than or equal to 60 mm Hg (group 1, n = 6) or to raise PvO2 greater than or equal to 36 mm Hg (group 2, n = 6). An oxygen-conserving nasal cannula and oxygen concentrator were used. Baseline PaO2, PvO2, and hemodynamics were identical in each group and hemodynamics after four hours and 48 hours of continuous oxygen therapy were unchanged. Ten patients were catheterized after four months of continuous oxygen therapy (group 1, n = 4; group 2, n = 6). Although PvO2 in group 2 had been raised to normal levels (39.2 +/- 1.2 mm Hg), there was no significant improvement in pulmonary hemodynamics. Our preliminary study suggests that oxygen titrated to raise PvO2 to the normal range has no greater hemodynamic effect than oxygen therapy as it is currently prescribed.

Sustained improvement of pulmonary hemodynamics in patients at rest and during exercise after thrombolytic treatment of massive pulmonary embolism.

This study assessed the long-term effects of thrombolytic treatment in patients with acute massive pulmonary embolism (PE). Seven patients with PE that followed deep-vein thrombosis underwent pulmonary angiography and pressure measurements before and 6 +/- 3 days (mean +/- SD) and 15 +/- 4 months after treatment with intrapulmonary infusions of urokinase (average dose 1724 U/kg X hr) and heparin (average dose 17 U/kg X hr). Treatment was guided by daily measurements of pulmonary arterial (PA) pressure and was continued until PA pressure had normalized (average of 6 days). Late after treatment patients returned for pulmonary angiographic examination, right heart catheterization at rest and during bicycle exercise, and phlebography of the deep veins of both legs. Pulmonary angiograms showed massive obstruction before therapy (Walsh index 15 +/- 2 points of a maximum of 18 points), which was improved 6 days (3 +/- 3 points) and 15 months (1 +/- 2 points) after therapy. Mean PA pressure declined from 37 +/- 9 to 13 +/- 3 mm Hg after 6 days and to 15 +/- 3 mm Hg after 15 months. No recurrence of PE was observed. In six of seven patients at rest and during bicycle exercise (up to 100 W) in the supine position mean PA pressure and total pulmonary resistance remained within normal limits. Over the short term all patients showed clinical signs of deep-vein thrombosis; 15 months later four patients had normal deep veins, but three patients had still phlebographic signs of old thrombosis.(ABSTRACT TRUNCATED AT 250 WORDS)

The clinical use of fibrinolytic agents

Both streptokinase and urokinase have undergone extensive evaluation in recent years. A review of the available clinical reports suggests the following: (1) In acute peripheral venous thrombosis of less than five days' duration SK appears to produce total clot lysis with restoration of normal venous valve function in 30 to 50 per cent of patients. The results are less impressive when the patient has had symptoms for more than five days or has experienced recurrent episodes of venous thrombosis. (2) Both SK and UK produce rapid angiographically documented resolution of pulmonary emboli associated with improvement of pulmonary hemodynamics, especially in patients without a history of recurrent pulmonary embolism or associated cardiorespiratory disease. (3) SK produces lysis of arterial thrombi in 10 to 50 per cent of patients. However, the duration of improvement and the long-term usefulness of this therapeutic modality has not been determined. (4) Thrombolytic agents have been used in patients with myocardial infarction, stroke, and retinal vascular thrombosis. No conclusions are currently possible concerning the potential role of thrombolytic therapy in these conditions.