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Biomedical subjects

M A Matthay

Publications and source records attributed to M A Matthay.

At least 199 records · Page 11Linked to original sources
PubMed1988

Relationship of pleural effusions to increased permeability pulmonary edema in anesthetized sheep.

We studied anesthetized sheep to determine the relationship between increased permeability pulmonary edema and the development and mechanism of pleural effusion formation. In 12 sheep with intact, closed thoraces, we studied the time course of pleural liquid formation after 0.12 ml/kg i.v. oleic acid. After 1 h, there were no pleural effusions, even though extravascular lung water increased 50% to 6.0 +/- 0.7 g/g dry lung. By 3 h pleural effusions had formed, they reached a maximum at 5 h (48.5 +/- 16.9 ml/thorax), and at 8 h there was no additional accumulation of pleural liquid (45.5 +/- 16.9 ml). Morphologic studies by light and electron microscopy demonstrated subpleural edema but no detectable injury to the visceral pleura, suggesting that the pleural liquid originated from the lung and not the pleura. In nine sheep, we quantified the rate of formation of pleural liquid by enclosing one lung in a plastic bag. By comparing in the same sheep the volume of pleural liquid collected from the enclosed lung to the volume found in the opposite intact chest, we estimated the rate of liquid absorption from the intact chest to be 0.32 ml/(kg.h); we had previously reported a liquid absorption rate of 0.28 ml/(kg.h) in normal sheep. These studies also supported the conclusion that the majority of the pleural liquid originated from the lung because we could account for all of the pleural liquid that was formed and cleared. The volume of pleural liquid collected from the enclosed lungs was equal to 21% of the excess lung liquid that formed after oleic acid-induced lung injury. Thus, the pleural space and parietal pleural lymphatic pathways are important pathways for the clearance of pulmonary edema liquid after experimentally induced increased permeability pulmonary edema.

Animals↗
PubMed1987

Beta-adrenergic agonists increase lung liquid clearance in anesthetized sheep.

We did experiments to determine whether beta-adrenergic agonists increase lung liquid clearance in anesthetized ventilated adult sheep and, if so, whether the increase is mediated by beta receptors and what mechanism is involved. We instilled 100 ml of autologous serum either alone or with a beta-adrenergic agonist (terbutaline, 10(-5) M, or epinephrine, 5.5 X 10(-6) M) into one lower lobe. After 4 h both terbutaline and epinephrine increased lung liquid clearance. The increase in lung liquid clearance was inhibited when propranolol (a beta blocker) or amiloride (a sodium channel blocker) was added to the terbutaline. Increased clearance was not explained by changes in pulmonary hemodynamics, pulmonary blood flow, or lung lymph flow. We conclude that beta-adrenergic agonists increase lung liquid clearance in anesthetized intact adult sheep. This increase is mediated through beta receptors and probably depends on increased active transport of sodium across the alveolar barrier.

Adrenergic beta-Agonists↗
PubMed1987

Adult respiratory distress syndrome related to antilymphocyte globulin therapy.

A 21-year-old man developed the adult respiratory distress syndrome (ARDS) within five hours of receiving antilymphocyte globulin. No other identifiable cause of ARDS was present. The mechanism for development of acute lung injury is unknown, but may be related either to direct lung cytotoxicity or to complement-mediated leukocyte and platelet destruction with secondary lung injury from inflammatory mediators.

Adult↗
PubMed1987

Lack of association of pleural effusion with chronic pulmonary arterial and right atrial hypertension.

Right atrial hypertension has been considered to have a major physiologic influence on the formation of transudative pleural effusions. Since pleural fluid is thought to be cleared primarily by the parietal pleural lymphatic vessels that empty into the systemic veins, systemic venous hypertension secondary to right atrial hypertension should decrease the lymphatic drainage of the pleural space. We retrospectively studied nine patients and prospectively studied 18 patients with long-term right atrial or pulmonary arterial hypertension (or both). All patients had stable respiratory symptoms, and none had a significantly elevated pulmonary arterial wedge pressure. Our purpose was to determine the relationship of right atrial and pulmonary arterial hypertension to the development of transudative pleural effusions. Posteroanterior and bilateral decubitus chest roentgenograms and ultrasound were used to detect pleural effusions. Pleural effusions were not identified in any of the 27 patients, even in four patients with right atrial pressures greater than 20 mm Hg. We conclude that chronic elevation of right atrial pressure or pulmonary arterial pressure (or both) alone is not a cause of pleural effusion. In contrast, elevation of left atrial and pulmonary arterial wedge pressures is associated with the formation of transudative pleural effusions in man. Thus, if pleural effusions are detected in patients who have cor pulmonale, a search should be made for coexisting left heart failure or a primary cause of pleural inflammation, such as pulmonary emboli or infection.

Blood Pressure↗
PubMed1986

Pulmonary embolism. Guide to diagnosis, treatment, and prevention.

While more remains to be learned about the natural history of deep vein thrombosis and pulmonary embolism, better information is now available on which to base decisions about diagnosis and treatment. Several retrospective and prospective studies have placed the value of lung scanning, venography, and pulmonary angiography in better perspective. Newer diagnostic techniques for deep vein thrombosis, such as 125I-labeled fibrinogen scanning and impedance plethysmography, are valuable and should be more widely used. Other diagnostic techniques for pulmonary embolism, such as computed tomography and nuclear magnetic resonance imaging, may be of value but are still untested. More effective therapies are now available. Moderate-dose subcutaneous heparin and lower-dose warfarin for long-term therapy of deep vein thrombosis are attractive alternatives to standard warfarin therapy. Thrombolytic therapy has not replaced standard intravenous heparin therapy, although it should be considered in treatment of a massive pulmonary embolus. Perhaps most important, prevention of deep vein thrombosis in most patients at high risk is possible with minidose heparin therapy or intermittent pneumatic compression. One of these methods of prophylaxis should be used in all high-risk patients as the only current effective way to decrease the mortality of pulmonary embolism.

Angiography↗
PubMed1986

Poor correlation between pulmonary arterial wedge pressure and left ventricular end-diastolic volume after coronary artery bypass graft surgery.

The authors studied 12 surgical patients in the intensive care unit post coronary artery bypass graft surgery and ten nonsurgical patients in the coronary care unit with chronic heart failure to determine the usefulness of the pulmonary arterial wedge pressure as an indicator of left ventricular preload. Left ventricular end diastolic volume was derived from concomitant determination of ejection fraction (gated blood pool scintigraphy) and stroke volume (determined from thermodilution cardiac output). In the nonsurgical patients, there was a significant correlation between changes in pulmonary arterial wedge pressure and left ventricular end-diastolic volume (P less than 0.05, r = 0.57). In the 12 patients studied during the first few hours after surgery, there was a poor correlation between changes in pulmonary wedge pressure (range = 4-32 mmHg) and left ventricular end-diastolic volume (range = 25-119 ml/m2), and a poor correlation between pulmonary arterial wedge pressures and stroke work index. In contrast, there was a good correlation between left ventricular end-diastolic volume and stroke work index. The poor correlation between the pulmonary arterial wedge pressure and left ventricular end-diastolic volume was not explained by changes in systemic or pulmonary vascular resistance. The altered ventricular pressure-volume relationship may reflect acute changes in ventricular compliance in the first few hours following coronary artery bypass graft surgery. While measurement of pulmonary arterial wedge pressure remains valuable in clinical management to avoid pulmonary edema, it cannot reliably be used as an index of left ventricular preload while attempting to optimize stroke volume in patients immediately following coronary artery bypass graft surgery.

Aged↗
PubMed1986

Central intravascular pressure measurements: when should we believe them?

With the widespread use of invasive hemodynamic monitoring of the pulmonary circulation to aid in diagnosis and therapy of cardiac and respiratory failure, shock, and pulmonary hypertension, diagnostic radiologists have become accustomed to interpreting chest radiographs in the context of measured intrathoracic intravascular pressures. Unfortunately, errors in measurement and interpretation of these pressures are common. Perhaps the most difficult aspect of invasive hemodynamic monitoring is the interpretation of measured pressures in the context of a variety of clinical circumstances and disease states, some of which may dramatically alter the usual relationship between the pulmonary artery wedge pressure and left ventricular preload. Without detailed information about the techniques used to obtain these measurements and the clinical status of the patient at the time that they are made, the measurements should not be used as a standard against which clinical and radiographic findings are judged.

Blood Pressure Determination↗
PubMed1986

Clinical spectrum of pulmonary mucormycosis.

Pulmonary mucormycosis is an uncommon, but important, opportunistic fungal pneumonia which is often diagnosed post-mortem. This review emphasizes clinical and pathologic characteristics of pulmonary mucormycosis that differentiate this infection from other fungal pneumonias. The most common clinical presentation of pulmonary mucormycosis is a rapidly progressive pneumonia with diffuse infiltrates on chest radiographic examination of a patient with an underlying hematologic malignancy treated with immunosuppressive drugs. Other immunocompromised hosts at risk for pulmonary mucormycosis include patients with diabetes mellitus who may develop a distinctive endobronchial form of this disease. Early consideration of this diagnosis, along with aggressive diagnostic evaluation, are critical to effective therapy and patient survival. While treatment with amphotericin B is the mainstay of therapy for pulmonary mucormycosis, diabetics with endobronchial disease may benefit from early, aggressive surgical resection of the involved lung tissue.

Adult↗
PubMed1986

Helium-oxygen gas therapy. Use and availability for the emergency treatment of inoperable airway obstruction.

Inoperable obstruction of the upper airway due to extrinsic malignancy may present as respiratory failure. We treated such a patient for 48 hours with 80 percent: 20 percent helium-oxygen delivered by a nonrebreathing mask while chemotherapy and radiation therapy reduced the tumor size. The need for intubation, mechanical ventilation, and high risk surgical intervention was avoided through the use of this gas therapy. We then surveyed San Francisco Bay area hospitals and found that fewer than one half could provide this potentially lifesaving gas therapy in an emergency situation. Physiologic basis of helium-oxygen gas therapy is reviewed and recommendations made for its use and availability.

Adolescent↗
PubMed1986

Pathophysiology of the adult respiratory distress syndrome. What have we learned from human studies?

Clinical studies of ARDS have been successful in determining the most common predisposing clinical disorders and the natural history of this syndrome. Sepsis, gastric aspiration, and major trauma are the most frequently associated high-risk factors. Overall mortality is in the range of 60% to 70%, but is even higher if ARDS is associated with sepsis, severe acidemia, or decreased renal function. It is evident that multisystem failure is responsible for death in many patients, as well as secondary pulmonary and extrapulmonary infections. Pathologic studies have provided descriptive information regarding the acute, subacute, and chronic phases of the syndrome, but little insight into the precise pathogenesis of the initial lung injury or the progressive fibrosing alveolitis and lung destruction that develops in some patients. There has been considerable circumstantial evidence from clinical studies implicating the neutrophil as a potentially important mediator of the early changes in lung endothelial and epithelial permeability. However, not all investigators have found the same alterations in neutrophil function in the circulation or in the lavage from the lungs of patients with ARDS. Also, the heterogeneous etiologies of ARDS make it difficult to be sure that there is a final common pathway for acute lung injury in all ARDS patients. In addition, there are a host of mediators, including products of complement activation and arachidonic acid metabolism, that may be important in amplifying the inflammatory response. Also, abnormalities of surfactant production and collagen turnover, as well as impaired host defenses in the lung, may contribute to the progressive respiratory failure that occurs in some ARDS patients, even though the acute, exudative phase of lung injury has resolved. Future human studies may provide useful information about the mechanisms of the acute lung injury through studies of circulating plasma markers, blood elements, and lavage fluids from high-risk patients. On the other hand, samples of cells and mediators from the airspaces with lavage still may not reflect the critical interactions of mediators and cells with the lung endothelium that lead to the protein-rich pulmonary edema that characterizes the first phase of ARDS. Thus, experimental studies must continue to study the details of the early phases of acute lung injury (see article by Flick, page 455). Finally, it is clear that treatment designed to reduce the severity and the incidence of ARDS must be started early, since the syndrome develops so rapidly in high-risk patients.(ABSTRACT TRUNCATED AT 400 WORDS)

Blood Platelets↗
PubMed1985

Undrained bloody pericardial effusion in the early postoperative period after coronary bypass surgery: a prospective blood pool study.

To assess the clinical importance of hemopericardium after cardiac surgery, serial blood pool scintigrams were performed in 13 random patients throughout the initial hours after coronary artery bypass graft surgery. Scintigraphic measurements of pericardial fluid accumulation and left ventricular ejection fraction were made. Hemodynamics, cardiac, output, and chest tube drainage were monitored; and symptoms of postpericardiotomy syndrome were recorded for a mean of 7.4 months after surgery. Seven of the 13 patients had no scintigraphic evidence of bloody pericardial effusion. Six patients had scintigraphic evidence of bloody pericardial effusion; three of these effusions were small, localized posteriorly, and evident throughout the study. In two other patients large collections of fluid (over 100 ml) developed. In one of these patients increased mediastinal drainage required reoperation. The other patient remained stable although mediastinal drainage decreased. The sixth patient showed a moderate effusion (95 ml) that decreased without evident effusion or drainage when the last image was taken. Two patients (one with evidence of a postoperative bloody effusion), had symptoms of postpericardiotomy syndrome in the follow-up period. This study reports the generally benign occurrence of bloody postoperative mediastinal effusions, the frequent accumulation of substantial amounts of undrained sanguineous fluid, and the lack of connection between the presence and or amount of pericardial blood and the postpericardiotomy syndrome. The importance of these scintigraphic findings can be interpreted only with knowledge of associated mediastinal drainage.

Aged↗
PubMed1985

Long-term clearance of liquid and protein from the lungs of unanesthetized sheep.

We measured the removal of 100 ml of autologous serum from the air spaces and lungs of unanesthetized, spontaneously breathing sheep at 4, 12, and 24 h. In the first 4 h, there was a rapid clearance of the liquid volume (8.3%/h), similar to our results in anesthetized ventilated sheep (Matthay et al., J. Appl. Physiol. 53: 96-104, 1982). However, liquid removal progressively slowed to 3.3 and 1.4%/h at 12 and 24 h, respectively. In contrast, protein clearance (as measured by 125I-albumin instilled with the serum) was monoexponential and slow (1%/h). The slowing of liquid clearance appears to be a function of the rising protein osmotic pressure of the residual protein in the air spaces (protein concentration doubled in 24 h). Because protein solutions are chemotactic for neutrophils, we quantified the movement of liquid from the extracellular space into the alveolar compartment with a plasma protein tracer (131I-albumin), so that our final calculation of alveolar liquid clearance would take into account bidirectional movement of liquid across the alveolar barrier. The corrected values for net liquid clearance are slightly faster (less than 10% of the instilled volume).

Animals↗
PubMed1985

Relationship of pleural effusions to pulmonary hemodynamics in patients with congestive heart failure.

On the basis of both experimental and clinical studies it is not clear whether left, right, or biventricular heart failure are necessary for the formation of pleural effusions. In order to study the relationship of pulmonary hemodynamics and the presence of pleural effusions in patients with congestive heart failure, we prospectively evaluated 37 patients admitted to the coronary care unit with congestive heart failure secondary to ischemic heart disease or a cardiomyopathy. We used real-time ultrasonography to document the presence of pleural effusions. We found that 19 of the 37 patients with heart failure had pleural effusions. Mean pulmonary artery wedge pressure was 24.1 +/- 1.3 mmHg (SE) in the 19 patients with pleural effusions versus 17.2 +/- 1.5 mmHg (SE) (p less than 0.001) in the 18 patients without pleural effusions. Pulmonary artery pressure was also higher in patients with pleural effusions with a mean value of 38.0 +/- 1.5 mmHg (SE) versus 30.7 +/- 2.1 mmHg (SE) (p less than 0.05) in the patients without pleural effusions. In contrast, mean right atrial pressure was not different between patients with pleural effusions (12.6 +/- 1.5 mmHg) (SE) versus those without pleural effusions (9.8 +/- 1.0 mmHg) (SE) (p = NS). In addition, there was no difference in cardiac output, pulmonary vascular resistance, or total protein concentrations between patients with and without pleural effusions. We conclude that, in patients with congestive heart failure, an elevated left atrial pressure is closely correlated with the presence of pleural effusions, while concurrent elevation of right atrial pressure is not associated with the presence of pleural effusions.

Blood Pressure↗