Over a period of four years, 23 patients had the diagnosis of chronic pulmonary hypertension made on the basis of elevated resting pulmonary arterial pressures above 30 mmHg mean. Clinical features included dyspnea (100%), previous thromboembolism (43%), congestive failure (39%), venous thrombosis (35%), syncope (30%), lung disease (22%), recent trauma (22%), hemoptysis (17%) and precordial pain (17%). Pulmonary angiograms showed embolic occlusion in all but four patients, who were considered to have primary pulmonary hypertension. KimRay-Greenfield?vena caval filters were inserted in 18 patients. Three of them were in refractory shock at the time, and only the one who had successful intraluminal catheter embolectomy survived. These patients have been followed an average of 23 months with two embolic deaths, one from the right atrium and one bypassing a filter misplaced in the right iliac vein (overall mortality 22%). There has been no other known recurrent embolism, but one patient developed hematuria from the filter. The five patients who did not receive a filter have all died after intervals up to 18 months. Recurrent thromboembolism was documented in three and suspected in one patient with known embolic disease who died suddenly. Regardless of etiologic factors, pulmonary hypertension with cor pulmonale is associated with a high incidence of fatal thromboembolism. In our experience, maximal protection is afforded by long-term anticoagulation therapy and the placement of a venacaval filter.
In animals pulmonary hypertension, a decrease in total body O2 consumption and metabolic acidosis occur after transfusion of blood with an elevated screen filtration pressure (SFP) through standard blood transfusion filters. The purpose of this study was to define in detail the pulmonary abnormalities that develop following transfusion of blood with an elevated SFP through standard blood transfusion filters. Exchange transfusions of approximately twice blood volume were administered through standard commercially available blood transfusion filters (measured pore size--200 microns) to 6 animals. SFP measurements verified the presence of large numbers of aggregates in the transfusions. Although filters reduced SFP of the stored blood somewhat, numerous microaggregates passed the filters, and post-filtration SFP remained high. After transfusion average O2 consumption decreased to 77% of normal and metabolic acidosis developed. Pulmonary arterial hypertension was associated with an increase in pulmonary shunting of blood and a decrease in pulmonary diffusing capacity. The presence of extensive numbers of microemboli in the pulmonary arteriolar and capillary bed was confirmed by microscopic examination of lung tissue.
The relationship between elevated pulmonary extravascular water volume(PEWV)and small airway closure was examined. The slow accumulation of lung water was achieved by a combination of pulmonary venous hypertension and mild hemodilution. PEWV was measured using a double indicator method based on the differential right to left transit time for simultaneously injected Evans blue dye and tritiated water. Trapped gas volume (VTG) was measured by the helium equilibration technique. Clinically undetectable levels of pulmonary engorgement and edema were reproducibly associated with an increase in gas trapping. Positive end expiratory pressure reduced, but did not abolish, edema formation. Evaluation of airway closure, with consequent gas trapping and pulmonary shunting, is currently non-invasive, simple and safe. Determination of gas trapping or closing volume should be incorporated into the rountine pre-operative evaluation of patients prior to major surgery.
It was the purpose of this research to define the progression over several days of changes in pulmonary function and structure and to document the phases of recovery following transfusions to dogs of sublethal quantities of stored blood containing microaggregates. Ten dogs underwent partial exchange transfusions averaging 60% of blood volume through standard blood transfusion filters. Average screen filtration pressure (SFP) of the blood was 85 mm Hg. Pulmonary hypertension did not develop, but there were striking decreases in O2 consumption, increases in Qs/Qt and decreases in Do2. Changes became progressively more marked over the first 48 to 72 hours after the transfusions. Pulmonary function of surviving animals returned nearly to normal by the sixth day after transfusions. Pathologic examinations of the lungs of animals sequentially sacrificed over 6 days showed intravascular microemboli, alveolar cell hyperplasia and interstitial and alveolar pulmonary edema. Progressive recovery was associated with progressive resolution of all detrimental changes. In 6 animals exchange transfused 100% of their blood volumes through dacron wool (Swank) filters and in three control animals that were not transfused, there were no significant changes in pulmonary function or structure. These experiments define the progression of deterioration and recovery over 6 days of pulmonary function in dogs after sublethal pulmonary microembolism occurring during blood transfusion.
The clinical course of most patients with pulmonary embolism is one of gradual resolution with re-establishment of flow in the pulmonary arteries. In a small but definite group of patients, the emboli do not resolve and a state of chronic pulmonary embolism ensues. The primary thrombotic process in the systemic venous system may persist, and in some instances may be unrecognized. Such patients experience recurrent showers of emboli which may ultimately occlude a large part of the pulmonary arterial circulation with development of severe respiratory insufficiency. Six patients with this syndrome are described, and in each there was a history of dyspnea, cyanoiss, and exercise intolerance associated with a low arterial PO2, right ventricular hypertrophy, and pulmonary hypertension. Pulmonary scans and arteriograms demonstrated that more than half of the major pulmonary arteries were occluded and, in addition, smaller vessels were also obstructed. Pulmonary embolectomy was performed in each patient. Five of the 6 obtained a highly gratifying response, including relief of the dyspnea and cyanosis, an increase in arterial PO2, and a decrease in pulmonary arterial pressure. In each of the five in whom improvement occurred, the back-bleeding from the pulmonary artery at the time of embolectomy was quite good. In the sixth patient, the back-bleeding was very poor, and despite embolectomy, the vessel thrombosed postoperatively with no improvement in the patient's clinical course. Follow-up studies in these patients range up to 8 years with demonstration of continued patency of the pulmonary arteries as well as continued improvement in clinical symptoms and in the arterial PO2.
Recent studies demonstrated that epinephrine causes significant pulmonary A-V shunting. This study reports the effect of alpha and beta adrenergic blockade on this shunting. Sixty-three anesthetized mongrel dogs were ventilated with a mechanical respirator. Measurements of (1) the pulmonary shunt, (2) cardiac output, (3) mean pulmonary artery, pulmonary capillary wedge and systemic pressures, and (4) pulmonary and systemic vascular resistances were obtained at 5, 15 and 30 minute intervals during the first hour and hourly for 5 hours. Fifteen dogs received no treatment. All others received epinephrine hydrochloride, 2 mug/kg/min for 5 hours. Ten received epinephrine only. Ten were pretreated with propranolol hydrochloride, 250 mug/kg, 12 with phenoxybenzamine, 1 mg/kg, and 16 with phenoxybenzamine and propranolol. Propranolol significantly decreased the epinephrine induced pulmonary shunt at all times and was the most effective drug. Phenoxybenzamine decreased the early shunting, but less than propranolol, and did not decrease the late shunting. Blockade with propranolol and phenoxybenzamine was less effective than propranolol alone. Based on the observed hemodynamic changes it was suggested that beta blockade is effective in reducing epinephrine induced pulmonary insufficiency by favorably altering the flow and distribution of pulmonary blood flow which in turn decreases epinephrine induced ventilation-perfusion inequalities and capillary hypertension both of which result in shunting. Conversely phenoxybenzamine has an unfavorable effect on the pulmonary flow. These studies support previous work in animals and man which showed that beta adrenergic stimulation is important in the pathogenesis of pulmonary insufficiency. Because the amounts of epinephrine used produce blood levels observed in critical illness, these studies add support to a relationship between the increased catecholamine stimulation of critical illness and the associated and often unexplained pulmonary insufficiency.
Recurrent pulmonary emboli ultimately may produce respiratory insufficiency, severe hypoxemia, and progressive pulmonary hypertension. In many patients this syndrome is silent in its initial phases, and when thrombophlebitis is present it is often unresponsive to anticoagulant therapy. Unless pulmonary embolectomy is undertaken, most of these patients characteristically succumb with severe respiratory insufficiency. Twenty-five patients with this syndrome have been evaluated at the Duke University Medical Center, and 14 were selected for elective pulmonary embolectomy for relief of severe and incapacitating pulmonary insufficiency. In each patient preoperative pulmonary scans and arteriography demonstrated a high degree of vascular occlusion. The obstructing lesions affected both lungs in the majority of patients. Bronchial arteriography was found to be a very valuable method for demonstrating patency of the pulmonary arteries distal to occluding lesions by retrograde filling through collateral vessels joining the bronchial and pulmonary circulations. Preoperatively radionuclide angiocardiography revealed severe right ventricular dysfunction with significantly depressed ejection fractions at rest and during exercise. Retrograde pulmonary arterial flow as shown by selective bronchial arteriography was excellent in ten patients, fair in three, and absent in one. Long term follow-up indicated a clear relationship between the magnitude of arterial backflow at the time of embolectomy and the degree of clinical improvement. There were two perioperative deaths, one from massive reperfusion pulmonary hemorrhage and another from intractable right ventricular failure. Eleven patients with this syndrome were unsuitable candidates for embolectomy and of these, nine had severe distal emboli diffusely spread in the small pulmonary arteries and not amenable to direct removal. One patient had severe right ventricular failure with extreme pulmonary hypertension (145/45 mmHg) and another was massively obese with severe congestive heart failure and expired in the hospital a week later. In this group of 11 patients, three succumbed and most of the others are currently totally debilitated at rest (NYHA Class IV). Long-term follow-up of the surgically managed patients (1 to 15 years) shows that ten patients improved from NYHA functional Class IV to either I or II, another patient from Class III to Class I, and a final patient was only minimally improved.(ABSTRACT TRUNCATED AT 400 WORDS)