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

The effect of the new positive inotropic and vasodilatator bipyridine-derivate Amrinon on catecholamine-refractive heart insufficiency in septic shock is described. A bolus dose of 1 mg/kg b.w., followed by continuous infusion of Amrinon 10 micrograms/kg b.w./min improved the haemodynamic parameters of all seven patients. The severe tachycardia before therapy was diminished more than 30%, the blood-pressure increased about 25-30%. RAP, PAP and PCWP showed a diminution of 35-45%. The cardiac output increased nearly 100% under therapy. All patients had IPPV with high inspiratory oxygen concentration, with inversed-ratio-ventilation and high positive end-expiratory pressure. Under Amrinon-therapy the initial pulmonary insufficiency diminished. The oliguria/anuria existing before Amrinon-therapy was improved also. Amrinon was given over 24-36 hours, the total dose was between 800 and 1440 mg. Six of the seven patients survived their severe illness; one patient died of pulmonary embolism, confirmed by autopsy, four weeks after Amrinon-therapy.
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PMID:[Amrinone in catecholamine refractory heart failure in septic shock]. 409 58

Twenty-three patients are reported in whom a diagnosis of acute massive pulmonary embolism was confirmed by pulmonary arteriography. All patients had a history of less than 48 hours' duration and only two had previous cardiorespiratory disease. In such patients the haemodynamic abnormalities determined at catheterization are due to pulmonary embolism as an isolated disturbance. These abnormalities include an only moderate degree of pulmonary hypertension (PA systolic pressure 38.4+/-6.8 mm. Hg), right ventricular ;failure' (RVED 11.5+/-4.9 mm. Hg), arterial oxygen desaturation (86.4+/-11.2%) and a wide arteriovenous oxygen difference (8.1+/-1.8 ml./100 ml.), and low cardiac output. These haemodynamic abnormalities find their expression in the presentation and the clinical, electrocardiographic, and radiological findings which are described.
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PMID:Acute massive pulmonary embolism. Clinical and haemodynamic findings in 23 patients studied by cardiac catheterization and pulmonary arteriography. 543 13

The alveolar to arterial difference of oxygen [(A-a)DO2] depends on variables such as ventilation, cardiac output, respiratory exchange ratio and arterial PO2. The arterial PO2 itself depends on the ventilation to perfusion ratio (V/Q) pulmonary shunt, (a-v) O2 difference, and the metabolic status of the patient. When the alveolar-ventilation is normal, the (A-a)DO2 reflects gas exchange abnormalities and when the alveolar-ventilation is increased, the (A-a)DO2 can increase because of a decrease in PaCO2. The factors capable of altering the alveolar to arterial oxygen difference were investigated in ninety patients with pulmonary disease: (pulmonary embolism, lung fibrosis and chronic obstructive lung disease), both at rest and during exercise. At rest when alveolar ventilation was increased, the (A-a)DO2 broadened due to the decrease in PaCO2. During exercise the (A-a)DO2 also increased and the PaCO2 was not significantly modified, therefore admixture it is the result of an increase in the proportion of venous. The difference between the mixed venous and arterial PO2 decreased due to alveolar hypoventilation reducing in consequence the (A-a)DO2. We conclude that in the group studied the increase in the (A-a)DO2 is mainly due to V/Q imbalance at rest and during exercise.
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PMID:[Alveolar-arterial oxygen gradient in cardiopulmonary patients breathing ambient air at rest and during exercise]. 641 98

It is estimated that 600,000 or more symptomatic episodes of pulmonary embolism occur each year in the United States, and this diagnosis is one that may often be missed. This article provides an appraisal of currently used diagnostic procedures, including laboratory tests, arterial oxygen tension, chest radiography, electrocardiography, lung scanning, and selective pulmonary angiography, and examines the available therapeutic options and their indications.
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PMID:Pulmonary embolism. 654 48

Two quadriplegic patients suddenly lost consciousness and were found to have an elevated alveolar-arteriolar oxygen gradient. Their chest x-ray films were normal. Perfusion scintiscans of their lungs showed large areas with markedly reduced or absent perfusion. Ventilation scintiscans demonstrated absent or decreased ventilation to the hypoperfused areas, suggesting mucous plugging. In quadriplegic subjects who have an ineffective cough, acute mucous plugging can produce the sudden onset of hypoxia with essentially normal chest x-ray films, thus mimicking acute pulmonary embolism.
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PMID:Mucous plugging simulating pulmonary embolism in patients with quadriplegia. 669 93

A cardiorespiratory monitoring system allows the measurement of FAECO2 and FECO2 in the expired air of the patient at the mouth (endtidal CO2) and in a mixing box. From these parameters, combined with the measured PACO2, the alveolo-expired (DuA = PECO2/PAECO2) and alveolar-arterial (Dua = PAECO2/PACO2) ductances which assimilate the respiratory system to a two-stage exchanger have brought about a lot of valuable information 1. DuA improves by 20% in 20 patients after removal of bronchial obstruction (p < 0.001) and by 9% in 7 intubated patients after tracheotomy (p < 0.02). DuA falls by 15% (p < 0.001) in 10 patients with hypocapnia (PaCO2 = 28 mmHg) after a dead space adjunction with the aim of normalizing PaCO2 (paCO2 = 35 mmHg). 2. Dua falls by 33% in six patients after pulmonary embolism, proved by angiography (p 0.001) by 9% in 34 patients after 30 min of pure oxygen breathing (p 0.001). On the other hand, inthe absence of clinical or radiological pulmonary edema, in increases by 19% in 38 patients with hypervolemia after diuresis (furosemide) (p < 0.001). Thus since DuACO2 varies with anatomical dead space and the air distribution disorder, DuaCO2 evolves according to the disorders of the blood distribution and arterial-alveolar diffusion. The determination of these coefficients, in the absence of significant changes in the arterial blood gases, helps the diagnosis, guides the early treatment and allows for the monitoring of its efficiency.
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PMID:The continuous monitoring of CO2 ductances in pulmonary intensive care. 677 20

The role of active and passive factors involved in the genesis of Pulmonary Arterial Hypertension (PAH) is analyzed in a group of eighty patients with several cardiopathies and pneumopathies. The group include: 20 patients with Chronic Obstructive Lung Disease (NODC), 20 with Diffuse intersticial pneumopathy (NI), 12 with Cardiorespiratory Syndrome of the grossly obese (OB), 6 with Pulmonary Embolism (TEP), 6 with Mitral Stenosis (CRI), 5 with Hypertensive Ventricular Septal Defect (CIV + HAP) and 11 patients with Pulmonary Arterial Hypertension of Unknown etiology (HAP-ED). For the analysis, the Harvey and Enson's formulas were used. The conclusions of the study are: 1) The compliance of the elastic arteries of the lung in the groups of NOC, NI and OB is normal but in the other groups seems to be modified. 2) In the groups of NI and OB the interrelationship of factors such as alveolar hypoxia and pulmonary wedge pressure (PWP) play the major role in the genesis of PAH, although the role of the PaCO2 in the OB group remains to be established. 3) In the groups of NOC, CRI and TEP the PWP is not determinant. The absence of a significant correlation between arterial oxygen unsaturation and pulmonary diastolic pressure in the NOC group suggests other factors. 4) The vascular structural damage seems to be the most important factor in the genesis of PAH in the HAP-ED and CIV + HAP groups.
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PMID:[Active and passive factors in the genesis of pulmonary arterial hypertension in various cardiopathies and pneumopathies]. 678 61

Vasodilators including isoproterenol, nitroprusside, nitroglycerin, and oxygen were administered to 5 patients with chronic pulmonary hypertension secondary to pulmonary embolism. The patients' mean pulmonary artery pressure was 54 +/- 8 mmHg, and their average total pulmonary resistance (TRP) was 17 +/- 11 mmHg/L/min. Each patient experienced a decrease in TRP in response to at least 1 of the vasodilators, and the mean maximal decrease was to 57 +/- 10% of the baseline value. Although these decrements in TRP were accompanied by an increase in cardiac output in all but 1 patient, changes in PAP were variable. Treatment with nitroglycerin was continued in 3 of the 5 patients and all 3 have reported improvement in their exercise tolerance. We conclude that the elevated TPR seen in patients with chronic embolic pulmonary hypertension is due to increased vascular tone in addition to fixed vascular obstruction.
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PMID:Partial reversibility of chronic pulmonary hypertension caused by pulmonary thromboembolic disease. 678 32

Hypoxemia usually accompanies acute pulmonary embolism in humans, but its mechanism remains poorly understood. We studied 2 patients with acute, massive pulmonary embolism (APE) documented by pulmonary angiography. Both patients had a markedly increased alveolar-arterial oxygen difference (AaPO2). The technique of multiple inert gas elimination was used to determine the distribution of ventilation-perfusion ratios (VA/Q). An increase in VA/Q inequality was found in both patients, but this increased inequality was caused entirely by an increase in the ventilation of lung units with high VA/Q ratio. No blood flow was found perfusing lung units with a VA/Q ratio of less than 1.0. Both patients, however, had a large amount of blood flow (20 and 39% of the cardiac output) perfusing unventilated lung units (shunt), and the percent of minute ventilation to unperfused lung units as well as the VD/VT determined from the Bohr equation were increased. We conclude that in these 2 patients with APE, VA/Q inequality did not play a major role in their hypoxemia and that the widened AaPO2 is explained by the large shunts that were found.
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PMID:The mechanisms of abnormal gas exchange in acute massive pulmonary embolism. 687 59

Quantitative deficiency of surfactant in neonates results in hyaline membrane disease. Although surfactant is also required for normal gas exchange in adults, no disorders have been clearly attributable to a deficient amount of surfactant. Based on studies in our laboratories as well as on information and ideas in the literature, we suggest that a physical alteration in surfactant may lead to, or contribute to, the development of some forms of "adult" respiratory distress syndrome." In particular, we suggest that an altered breathing pattern contributes to the alveolar collapse and liver-like appearance of the lung found in certain clinical entities, i.e., pulmonary embolism and oxygen toxicity. We hypothesize that in these conditions shallow breathing leads to the aggregation of surfactant into a less functional form resulting in increased alveolar surface tension and atelectasis. The increase in surface tension would also contribute to the edema found in these conditions.
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PMID:A hypothesis relating breathing pattern to some forms of the "adult respiratory distress syndrome". 689 77


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