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

Sixty-three patients undergoing isotope ventilation/perfusion scintigraphy for suspected pulmonary embolism were monitored using pulse oximetry. Xenon inhalation had no adverse effect on arterial oxygen saturation. Fifty-seven per cent of patients demonstrated a drop in oxygen saturation of 2-10% within 5 min of injection of macroaggregates. Small changes in arterial oxygen saturation reflect larger changes in the arteriole partial pressure of oxygen. In 10 patients, oxygen saturation dropped to 91% and below, corresponding to an arterial pO2 of less than 60 mm Hg. The effect lasted up to 30 min and is thought unlikely to be simply due to arteriolar blockade. Falls in arterial oxygen saturation cannot be correlated with any specific pulmonary pathology and appear unlikely to be of any clinical significance in most patients.
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PMID:Changes in arterial oxygen saturation during isotope perfusion scans using human macroaggregates of albumin. 175 56

In a rehabilitation setting, pulmonary embolism is a relatively frequent and life-threatening complication. Deciding when a patient may be experiencing this condition is difficult, however, because of frequent deficits in patient communication skills (eg, aphasia and cognitive deficits) and the multisystem illnesses affecting many rehabilitation patients. We reviewed the charts of 30 rehabilitation patients transferred emergently during the years 1986 to 1988 with a diagnosis of pulmonary embolism, which was subsequently documented by ventilation-perfusion scanning. The average age of the 30 patients was 65; 63% were women and 20 (67%) had an admitting diagnosis of stroke. The most common new-onset clinical findings in the 24 hours before discharge were unusual facial skin color changes (pale, flushed, or cyanotic) (57%), chest or upper back pain (47%), tachycardia (heart rate more than 100 bpm) (40%), hypoxemia (arterial oxygen saturation less than or equal to 90%) (40%), and fever less than 101F (37%). In 63% of the patients, either anxiety, restlessness, diaphoresis, or dyspnea was also noted in the 24 hours before discharge. The data suggest that careful physician and nursing scrutiny may identify clinical signs characteristic of pulmonary embolism, and that the de novo appearance of these constellations of findings may help to select candidates for ventilation-perfusion scanning.
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PMID:Clinical findings associated with pulmonary embolism in a rehabilitation setting. 185 63

In a canine model of pulmonary embolism (PE) produced by infusion of autologous blood clots, mean arterial blood pressure (MAP) decreased to 73 +/- 4 mm Hg while cardiac output (CO) decreased to less than 50 percent of baseline. Intravenous infusion of phenylephrine (PHEN) and norepinephrine (NE) restored MAP to somewhat above baseline values. However, only NE restored CO to control levels. The right ventricular myocardial blood flow increased 15 percent in the PE group with PHEN and 229 percent with NE at equipressor concentrations. The right ventricular myocardial oxygen consumption (RVMVo2) was not significantly different between PE and PE + PHEN while PE + NE increased RVMVO2 by 144 percent to 20.2 +/- 1.8 ml/min/100 g. The RV output was not adequately restored with PE, but when RV contractility was augmented with NE, RV output was restored to baseline. Right ventricular minute work increased 100 percent with NE and was maintained with a 100 percent increase in oxygen consumption. Calculated pulmonary vascular resistance (PVR) was decreased during PE by 36 percent with PE + PHEN while PVR in NE-treated dogs decreased by 59 percent. In NE-treated animals, systemic vascular resistance (SVR) was restored to control levels while in PHEN-treated animals SVR increased about 75 percent from baseline. We conclude that the salutary effects of NE on RV output are due to both alpha and beta receptor stimulation, which increased contractility, RVMBF, and RVMVo2, and decreased both PVR and SVR. In the PHEN-treated dogs, our indices of minute-work, RVMBF, and RVMVo2 suggest that coronary autoregulation was intact; however, there was no apparent benefit to RV output. This study suggests that in the clinical setting of acute PE, the judicious use of NE, rather than PHEN, may be more beneficial in restoring RV function and systemic hemodynamics.
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PMID:Norepinephrine and phenylephrine effects on right ventricular function in experimental canine pulmonary embolism. 188 75

The authors examined in 60 patients with acute pulmonary embolism values of blood gases and acid-base equilibrium, incl. 30 from arterialized capillary blood, in another 30 subjects from arterial blood. On analysis of capillary blood hypoxaemia was present in all subjects, on analysis of arterial blood only in 63%. Respiratory alkalosis was found on capillary examination in 37%, on arterial examination in 23% of the patients. Hypoxaemia and hypocapnia thus are not specific phenomena in acute pulmonary embolism, in particular when accurate blood collection for analysis is respected, and normal values of paO2 and paCO2 do not rule out the presence of pulmonary embolism. In the development of hypoxaemia in patients with pulmonary embolism participates above all an incomplete right-to-left pulmonary shunt, as revealed during calculation of the magnitude of the shunt by means of the so-called oxygen method in 30 patients with embolism, as compared with a group of 10 healthy subjects.
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PMID:[The importance of blood gas analysis and acid-base equilibrium in pulmonary embolism]. 190 44

A 65-year-old man was admitted to our hospital because of shortness of breath on exertion. As the results of examinations including pulmonary angiography, pulmonary perfusion scan and pulmonary ventilation scan, we diagnosed the case as chronic recurrent pulmonary embolism. Although the patient received thrombolytic therapy by a tissue plasminogen activator (t-PA), there was no noticeable improvement. However, oxygen and vasodilator therapy had marked effective on the hemodynamics. In chronic pulmonary embolism, vasodilators are generally not considered to be effective for improvement of hemodynamics. However, if the acute effects of vasodilators were confirmed, we should try to administer them while paying attention to possible adverse effects.
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PMID:[Acute and chronic effects of vasodilators in a case of chronic recurrent pulmonary embolism]. 190 16

The history, physical examination, chest radiograph, electrocardiogram and blood gases were evaluated in patients with suspected acute pulmonary embolism (PE) and no history or evidence of pre-existing cardiac or pulmonary disease. The investigation focused upon patients with no previous cardiac or pulmonary disease in order to evaluate the clinical characteristics that were due only to PE. Acute PE was present in 117 patients and PE was excluded in 248 patients. Among the patients with PE, dyspnea or tachypnea (greater than or equal to 20/min) was present in 105 of 117 (90 percent). Dyspnea, hemoptysis, or pleuritic pain was present in 107 of 117 (91 percent). The partial pressure of oxygen in arterial blood on room air was less than 80 mm Hg in 65 of 88 (74 percent). The alveolar-arterial oxygen gradient was greater than 20 mm Hg in 76 of 88 (86 percent). The chest radiograph was abnormal in 98 of 117 (84 percent). Atelectasis and/or pulmonary parenchymal abnormalities were most common, 79 of 117 (68 percent). Nonspecific ST segment or T wave change was the most common electrocardiographic abnormality, in 44 of 89 (49 percent). Dyspnea, tachypnea, or signs of deep venous thrombosis was present in 107 of 117 (91 percent). Dyspnea or tachypnea or pleuritic pain was present in 113 of 117 (97 percent). Dyspnea or tachypnea or pleuritic pain was present in 113 of 117 (97 percent). Dyspnea or tachypnea or pleuritic pain or atelectasis or a parenchymal abnormality on the chest radiograph was present in 115 of 117 (98 percent). In conclusion, among the patients with pulmonary embolism that were identified, only a small percentage did not have these important manifestations or combinations of manifestations. Clinical evaluation, though nonspecific, is of considerable value in the selection of patients in whom there is a need for further diagnostic studies.
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PMID:Clinical, laboratory, roentgenographic, and electrocardiographic findings in patients with acute pulmonary embolism and no pre-existing cardiac or pulmonary disease. 841 19

The authors examined the records of all patients referred for right heart catheterization between 1963-84 because of persistent dyspnoea after one or more episodes of pulmonary emboli. Patients with a history of congestive heart failure, angina, restrictive or obstructive pulmonary disease that could explain their symptoms were excluded. Catheterization was performed 15.8 +/- 24 months after the first suspected episode of pulmonary embolism. Seven of the 29 patients included had resting pulmonary hypertension (PH). All of these had an alveolo-arterial oxygen difference (AaDO2) greater than 25 mmHg. Twenty patients of the group, taken as a whole, had an AaDO2 greater than 25 mmHg. Information was available from 1 month to 5 years later in 6/9 patients with an AaDO2 less than 25 mmHg. In all of them dyspnoea improved or resolved. Information was available in 15/20 patients with AaDO2 greater than 25 mmHg. Three of 8 patients without PH but with an increased AaDO2 on the initial catheterization developed PH within 2 years. Dyspnoea increased in 1 of the remaining five. Four patients who initially had PH developed right heart failure 6 months-3 years later. In the remaining 3, dyspnoea was stable in 1, increased in 1 and one patient died with autopsy evidence of multiple pulmonary emboli. Abnormal oxygenation predicts the presence or subsequent development of PH in patients who are chronically dyspnoeic after pulmonary embolism.
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PMID:AaDO2 as a predictor of pulmonary hypertension resulting from pulmonary emboli. 191 74

Spinal cord injury increases the risk of many life-threatening medical problems, including respiratory failure, pulmonary embolism, and renal failure. Respiratory failure results from paralysis of muscles of inspiration (which impairs oxygen transport to alveoli) and of expiration (which impairs cough and predisposes to pneumonia and atelectasis). Respiratory failure in patients with spinal cord injury can be prevented by proper positioning of the patient, training of ventilatory muscles, pulmonary toilet, and aggressive use of antibiotics and bronchodilators. When respiratory failure occurs, it can be managed by administration of oxygen, intubation, and mechanical ventilation, and in instances of paralysis of the diaphragm, by diaphragmatic pacing. The risk of deep vein thrombosis and pulmonary embolism in acute spinal cord disease is increased by the immobilization of the patient and abnormalities in clotting factors. Thrombotic disease in spinal cord disease can be prevented by intermittent calf compression and heparinization. If pulmonary embolism develops, the patient should be started on a regimen of warfarin for at least 3 months. If anticoagulation is contraindicated, a Greenfield filter can be placed. However, concurrent use of quad cough places the patient at increased risk for complications from the Greenfield filter. Chronic pyelonephritis and systemic amyloidosis are the most common causes of renal failure in the patient with spinal cord disease. Renal failure can be prevented by maintaining a low postvoid residual volume, avoidance of indwelling catheters, use of medications that are not nephrotoxic, and rapid treatment of infection. Hemodialysis and peritoneal dialysis can extend the life of the patient with spinal cord disease in whom renal failure develops, and successful use of renal transplantation has recently been reported.
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PMID:Medical complications of spinal cord disease. 192 58

Radionuclide imaging of the lungs with 99Tcm-labelled macroaggregates of human serum albumin (99Tcm-MAA) is a safe, reliable and non-invasive method of diagnosing pulmonary embolism. It has been suggested that following intravenous injection of 99Tcm-MAA, arterial oxygen saturation falls significantly. Oxygen saturation was measured in 101 patients who had received an intravenous injection of 99Tcm-MAA prior to a perfusion lung scan. Readings were taken using a pulse oximeter at rest, immediately following injection, 10, 30 and 60 min post-injection. Twenty-five normal volunteers who were not injected acted as controls. Forty patients showed no change in oxygen saturation throughout the study. A fall of 1% was seen in 32 patients and 2-3% in 26 patients. Of the three patients who demonstrated a reduction in saturation of 6, 7 and 13%, two had chronic airways disease and one had left ventricular failure. Twenty out of 25 normal controls showed no change in saturation over the period of observation. Five showed a fluctuation of 1-2% between the measurements. All patients and controls remained asymptomatic with almost all readings returning to the initial values after 1 h. It was the patients with chest or heart disease who showed a fall in saturation. The study shows that the majority of patients undergoing a perfusion scan with 99Tcm-MAA show no significant fall in oxygen saturation. If a fall occurs, it may be related to the underlying disease process rather than to 99Tcm-MAA.
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PMID:Arterial oxygen saturation in patients undergoing perfusion lung scanning with 99Tcm-labelled macroaggregates of human serum albumin. 194 92

Pulmonary emboli can cause severe hemodynamic and respiratory disorders whose physiopathologic mechanisms need to be well understood to ensure appropriate treatment. In previously healthy subjects only massive obstructions (greater than 50%) have dangerous effects due to the very large functional reserve of the pulmonary vascular bed. The same is not always true where there are previous anomalies of pulmonary circulation. In man, vascular obstruction appears to be primarily mechanical, although the presence of emboli may also trigger the release of vasoconstrictor mediators. In the animal it is accepted that these mediators may play an important role, in particular by increasing the critical closing pressure in pulmonary microcirculation. Apart from resistance to continuous bloodflow, the vascular obstruction may accentuate a number of dynamic phenomena specifically obstructing the passage of a pulsatile flow. The aggregate obstacles to right ventricular ejection are known by the term pulmonary artery impedance. Gas exchanges can be disturbed by a wide variety of mechanisms. Arterial hypoxemia chiefly results from maldistribution of the ventilation/perfusion ratio and, in severe forms associated with a fall in cardiac output, from diminution of the partial oxygen pressure of mixed venous blood. The right auricular pressure increase may sometimes contribute to hypoxemia by causing reopening of a permeable ductus Botalli with onset of right-left shunt. This possibility should be considered if oxygen administration does not correct hypoxemia. The dead space effect is not always in relation to the size of the vascular obstruction due to hypocapnic bronchoconstriction in the hypoperfused areas.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Hemodynamics and gas exchange in pulmonary embolism: physiopathology and treatment]. 194 64


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