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Query: UMLS:C0034065 (pulmonary embolism)
 14,979 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A study of partial CO2 ductance has been performed in patients under assisted ventilation. The authors propose methods for simultaneous measurement of paCO2, PAECO2, PECO2 and PICO2. This methodology is used in patients presenting different conditions accounting for respiratory resuscitation: barbiturate poisoning with healthy lungs, bronchial stasis, acute lung involvement, obstructive bronchopneumopathy and pulmonary embolism.
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PMID:[Determination of global diffusion of CO2 and its partial components under assisted respiration. Technical problems and practical value in respiratory resuscitation]. 2 53

The measurement of arterio-alveolar difference in CO2, easily performed, gives the percentage of non perfused ventilated pulmonary zones. The clinical value of this examination is illustrated by two observations. Its situation, among other tests of the respiratory function, is questioned particularly when the diagnosis of pulmonary embolism is concerned.
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PMID:[Arterio-alveolar difference in CO2 (AaDCO2) : measurement, interpretation, clinical value]. 67 97

Platelet survival time (autologous labeling with 51chromium) was measured in 63 patients in order to evaluate the role of platelets in the thromboembolic complications of patients with hypoxemia and pulmonary hypertension. Thirty-eight of these patients had chronic obstructive airways disease; 13, primary pulmonary hypertension; seven, recurrent pulmonary embolism; four, the Eisenmenger syndrome; and one, multiple pulmonary arteriovenous fistula. Forty-three patients were hypeakly associated with arterial oxygen tension ( r = 0.50), but not with the arterial carbon dioxide tension or the level of pulmonary artery pressure. Sulfinpyrazone lengthened platelet survival in 12 of 24 (50%) treated patients but this drug did not alter either arterial oxygen tension arterial carbon dioxide tension, or pulmonary artery pressure. Our results suggest that hypoxemia is associated with shortened platelet survival time and that platelets may, therefore, be involved in the thromboembolic complications that develop in patients with hypoxemia.
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PMID:Platelet survival time in patients with hypoxemia and pulmonary hypertension. 83 12

A 60-year-old patient suffered a pulmonary embolism following the application of an Esmarch and pneumatic tourniquet before arthroscopy of the knee. The diagnosis was suspected because of sudden hypotension, ECG changes, a decrease in end-expiratory carbon dioxide concentration and oxygen desaturation as indicated by pulse oximetry. Before performing a sternotomy and cardiopulmonary bypass for removal of pulmonary artery clots, the diagnosis was confirmed by the demonstration of severe right ventricular strain using transoesophageal echocardiography.
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PMID:Pulmonary embolism confirmed by transoesophageal echocardiography. 153 98

Acute pulmonary thromboembolism produces a number of pathophysiologic derangements of pulmonary function. Foremost among these alterations is increased pulmonary vascular resistance. For patients without preexistent cardiopulmonary disease, increased pulmonary vascular resistance is directly related to the degree of vascular obstruction demonstrated on the pulmonary arteriogram. Vasoconstriction, either reflexly or biochemically mediated, may contribute to increased pulmonary vascular resistance. Acute pulmonary thromboembolism also disturbs matching of ventilation and blood flow. Consequently, some lung units are overventilated relative to perfusion (increased dead space), while other lung units are underventilated relative to perfusion (venous admixture). True right-to-left shunting of mixed venous blood can occur through the lungs (intrapulmonary shunt) or across the atrial septum (intracardiac shunt). In addition, abnormalities of pulmonary gas exchange (carbon monoxide transfer), pulmonary compliance and airway resistance, and ventilatory control may accompany pulmonary embolism. Thrombolytic therapy can reverse the hemodynamic derangements of acute pulmonary thromboembolism more rapidly than anticoagulant therapy. Limited data suggest a sustained benefit of thrombolytic treatment on the pathophysiologic alterations of pulmonary vascular resistance and pulmonary gas exchange produced by acute pulmonary emboli.
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PMID:Pulmonary physiology during pulmonary embolism. 155 81

The end-tidal carbon dioxide concentration (ETCO2) of 47 patients undergoing prosthetic knee operations was monitored to detect pulmonary embolism during the anthroplasties. The ETCO2 of one patient dropped suddenly following the release of the tourniquet and insertion of the bone cement. Intracardiac aspiration did not reveal any air. At autopsy there was massive pulmonary thromboembolism and the deep veins of the right leg contained old formed thrombi. Patients undergoing such procedures should be investigated to exclude the presence of deep vein thrombosis so that measures to prevent pulmonary thromboembolism must be taken well in advance. As regards the occurrence of air embolism it is believed that insertion of the bone cement is the most important single factor in the prevention of air embolism during knee arthroplasty.
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PMID:Incidence of pulmonary embolism in total knee arthroplasty. 174 10

We report a series of seven patients (age: 43-77 years, preoperative American Society of Anesthesiologists (ASA) physical status II-III) with perioperative, life-threatening pulmonary embolism and severe cardiogenic shock treated with recombinant tissue type plasminogen activator (rt-PA). Diagnosis was established by ECG (n = 7), arterial blood gas analysis (n = 7), massive elevation of mean pulmonary arterial pressure (MPAP: 40 +/- 6 mmHg SD, n = 7), echocardiography (n = 3), increased arterial/end-tidal CO2 difference (30 +/- 16 mmHg, n = 3), and pulmonary angiography (n = 4). All patients had to be ventilated, six with an FIO2 of 1.0. To achieve a mean arterial pressure of above 60 mmHg all patients received norepinephrine 0.4 +/- 0.2 microgram.kg-1.min-1 in combination with dopamine 11 +/- 5 micrograms.kg-1.min-1 (n = 6), epinephrine 0.13 +/- 0.04 microgram.kg-1.min-1 (n = 5) or dobutamine 14 +/- 6 micrograms.kg-1.min-1 (n = 3). In addition, six of seven patients had to be resuscitated by external chest compression (duration of resuscitation: 5 to 40 min) prior to or during the thrombolytic therapy. The dosages of rt-PA ranged from 10 to 150 mg, and the duration of administration up to 31 h. Six patients survived neurologically intact. In these six patients MPAP had decreased from 41 +/- 6 mmHg to 33 +/- 6 mmHg (P less than 0.05, Wilcoxon rank test) 2 h after the start of thrombolytic therapy, with concomitant reduction of vasopressor and inotropic support.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Recombinant tissue-type plasminogen activator for the emergency treatment of perioperative life-threatening pulmonary embolism (stage IV). Results in 7 patients]. 190 1

By capnometry is understood measurement of carbon dioxide in the expiratory air. The concentration can be determined by various forms of spectometry. A new acoustic principle of measurement is more sensitive than the methods hitherto employed. Capnometry registers rapid intubation of the oesophagus. Sudden changes in expired carbon dioxide may be signs of malignant hyperthermia or pulmonary embolism. In addition, capnometry is a valuable aid in the regulation of mechanical ventilation. Recent investigations suggest that capnometry can be employed to confirm or refute clinical suspicion of pulmonary embolism and that measurement of expired carbon dioxide may be of prognostic value in resuscitation. It has not yet be elucidated whether nasal measurements in patients who are not intubated can provide reliable values.
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PMID:[Capnometry. Technique and clinical use in anesthesia and emergency medicine]. 194 18

In contrast to pulmonary parenchyma metastases or lymphangitic carcinomatosis, neoplastic emboli of small pulmonary arteries and capillaries frequently go unrecognized and are only discovered at autopsy. Five patients (48 +/- 12 years old) were admitted to 3 intensive care units for severe acute respiratory failure and died between the first and the tenth day following hospitalization. Each patient had a history of rapidly progressive dyspnea, and physical examination showed clinical evidence of right ventricular failure. The lungs were clear on chest X-rays and the ECG revealed sinus tachycardia with a right QRS axis. The mean partial pressures of oxygen (PaO2) and carbon dioxide (PaCO2) were, respectively, 50.8 +/- 9.1 mm Hg and 22.2 +/- 2.4 mm Hg. A swan-Ganz catheter, inserted into 4 patients, revealed pulmonary arterial hypertension (55, 43, 37, 28) with capillary wedge pressure within the normal limits and cardiac output normal or low (3.0, 3.8, 4.4, 5.0 l/min). Pulmonary angiograms from each patient showed decreased distal lung perfusion without any proximal defects suggestive of pulmonary embolism. The inferior vena cava always appeared clear. Malignant cells were found upon autopsy (4 cases) in the lumina of the pulmonary arterioles and the primary site of the cancer was determined in 3 patients (2 hepatomas and 1 pancreatic carcinoma). The last patient had a known breast cancer with bone marrow metastases and clinical, hemodynamic and angiographic evidence of neoplastic emboli. The clinical course of neoplastic emboli can suggest acute pulmonary embolism, but the diagnosis can only be advanced after pulmonary angiography, especially if the patient is to have a cancer.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Acute respiratory distress caused by distal neoplastic pulmonary emboli]. 209 8

Perfusion lung scintigrams, pulmonary gas exchange data, and chest roentgenograms were obtained in 33 patients during acute embolism and over the following six months in order to assess their clinical usefulness in monitoring the effect of therapy. To this purpose, the measurement of pulmonary gas exchange and the presence of chest x-ray findings were compared with perfusion lung scintigraphic abnormalities both at diagnosis and after 7, 30, and 180 days during treatment. More than 50 percent of the pulmonary arterial tree was obstructed at diagnosis, and a large part of perfusion recovery was complete within the first month. All of the gas exchange parameters were abnormal at diagnosis, and the rate of their improvement was related to that of perfusion recovery. Interestingly, PaO2st (ie, PaO2 corrected for hyperventilation) and VE tended to return to normal during the first month as a consequence of the progressive recovery of perfusion, whereas oxygen and carbon dioxide gradients and physiologic dead space showed the persistence of some abnormalities six months after diagnosis. Significant correlations were observed between the number of ULSs evaluated on the perfusion lung scintigram (and considered an index of the severity of pulmonary embolization) and all of the gas exchange parameters at diagnosis (correlation coefficients averaged from 0.41 to 0.73) and after 7 and 30 days. The enlargement of the right descending pulmonary artery and particularly the "sausage" sign and the Westermark sign were significantly associated with a higher degree of gas exchange impairment and with a more severe embolization. In conclusion, this study demonstrates that perfusion lung scintigraphy has a primary role in monitoring the recovery of patients with pulmonary embolism under treatment. Moreover, the chest roentgenogram may help in this purpose. A second major result is that the simple measurement of some gas exchange parameters may allow the assessment of functional recovery of these patients, thus giving additional information about the effect of therapy.
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PMID:Natural course of treated pulmonary embolism. Evaluation by perfusion lung scintigraphy, gas exchange, and chest roentgenogram. 210 9


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