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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Large volumes of normal saline were infused intravenously in 6 dogs until obvious pulmonary edema was observed radiographically. Following volume overload, statistically significant increases occurred in the size of the heart, left atrium, pulmonary arteries and veins, and systemic veins, without the development of congestive heart failure (CHF). The left ventricular end-diastolic pressure remained normal, and cardiac output and stroke volume increased. The results suggest that, in the absence of left ventricular failure, acute volume overload may simulate the radiographic changes produced by CHF. Pulmonary edema may have occurred at least partly from a marked decrease in serum colloid osmotic pressure.
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PMID:Cardiopulmonary effects of intravenous fluid overload: radiologic manifestations. 15 36

Afterload reduction with sodium nitroprusside was performed in a patient with idiopathic lactic acidosis in whom sodium bicarbonate therapy had precipitated pulmonary edema. The drug reduced mean pulmonary-artery wedge pressure from 28 to 12 mm Hg, accompanied by a modest rise in left ventricular stroke work index from 33 to 43 g-m per square meter. Concomitantly, there was dramatic resolution of the metabolic acidemia, the arterial pH rising from 7.19 to 7.61, arterial carbon dioxide tension from 13 to 26 mm Hg, and bicarbonate content from 6 to 28 mEq per liter, and the anion gap falling from 32 to 11 mEq per liter. Metabolic improvement occurred despite a fall in cardiac output from 5.5 to 4.8 liters per minute. These findings support the concept that regional vasoconstriction plays a part in idiopathic lactic acidosis, and suggests that vasodilators may be an effective form of therapy for this almost uniformly fatal disorder.
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PMID:Vasodilator therapy of idiopathic lactic acidosis. 23 36

Artificial ventilation with positive end-expiratory pressure (PEEP) reduces venous return by raising intrathoracic pressure. To determine whether PEEP decreases cardiac output further by depressing myocardial function, we constructed Starling curves, using rapid dextran infusion in 7 anesthetized dogs ventilated with zero (ZEEP) and 20 cm PEEP. The changes in stroke volume and in left ventricular stroke work (LVSW) when PEEP was added or removed were significantly greater than could be attributed to the corresponding change in transmural left ventricular end-diastolic pressure (LVEDPTM) on these Starling curves. To the extent that PEEP did not alter left ventricular diastolic volume-pressure characteristics, these data indicated PEEP depressed ventricular function. Identical changes with PEEP in cardiac output (-30%), esophageal pressure (+10 cmH2O), and left ventricular function were observed after pulmonary edema was induced with oleic acid. These results confirm and extend recent suggestions that high levels of PEEP depress left ventricular function in dogs, accounting for about half of the reduction in cardiac output before and during acute pulmonary edema.
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PMID:Effect of positive end-expiratory pressure on ventricular function in dogs. 37 68

The effects of induced hypocapnia, hypothermia, and hypertension were surveyed in a primate model of acute stroke during and following a 48-hour period of intensive care. The results were compared to a group of nine control animals previously studied. Hypocapnia (PaCO2=25 torr) was examined in five animals and did not appear to alter the expected mortality, degree of neurological deficit, or frequency of infarction. There was, however, a suggestion that the size of infarction may be reduced. Hypothermia (29 degrees C) in five animals had a detrimental effect in that no animals survived following the intensive care period and all had infarction with massive edema. We speculate that hypothermia caused a sufficient increase in blood viscosity as to compromise collateral flow, thereby accounting for this detrimental effect. Induced hypertension (to 20% above control levels) was abandoned after three animals because of severe systemic effects (cardiac failure and pulmonary edema) resulting in death during the period of intensive care.
Stroke
PMID:Failure of prolonged hypocapnia, hypothermia, or hypertension to favorably alter acute stroke in primates. 40 43

A 14-year-old boy had a protracted illness characterized by bilateral tenderness and weakness of the extremities; the illness was considered to be a connective tissue disease similar to polymyositis. Not until nine months later, when the patient had new cardiac murmurs, pulmonary edema, and then a cerebrovascular accident, was the true nature of his illness suspected. The diagnosis of left atrial myxoma with the triad of constitutional, obstructive, and embolic effects was confirmed by echocardiographic studies and cardiac catheterization. The tumor was successfully removed.
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PMID:Atrial myxoma mimicking a collagen disorder. 42 37

Death may follow anesthetic incident in unsuspected pheochromocytoma. They may lead to hypertensive crisis with cerebrovascular accident and severe arythmias or acute left heart failure with pulmonary edema. We report a case illustrating these problems and in which death has followed. Analysis of the 18 cases recorded in world litterature demonstrates a mortality rate of 85 p. cent. The accident can occur in association with surgery, anesthesia and certain, even minor, investigatory procedures. However if the crisis is recognized and appropriatly treated, the patient may recover before irreversible shock occurs.
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PMID:[Hypertensive accident in a surgical patient with unsuspected pheochromocytoma (author's transl)]. 48 83

Intraruminal administration of 0.25 g of 3-methylindole (3MI; skatole/kg of body weight) to seven young calves generally caused mild respiratory signs and lesions, accompanied by only slight changes in cardiopulmonary function. Moderate depression, trembling, and irregular respiratory rate were observed between postadministration hours (PAH) 6 and 12. By PAH 24 at this dosage, abnormal clinical signs were not present. Statistically significant (P less than or equal to 0.05) changes observed in blood gas data from the seven calves were a decrease in aortic oxygen tension at PAH 12, increases in free-flowing venous oxygen tension in the intervals between PAH 6 and 12 and between PAH 6 and 24, and an increase in occluded venous oxygen tension at PAH 24. All calves had increases (although generally not statistically significant) in heart rate, cardiac output, cardiac index, stroke volume, and stroke index after 3MI administration. Mean aortic and pulmonary arterial pressure changes were generally small and variable. At necropsy, the lungs of the calves did not collapse when the thorax was opened. Patchy areas of consolidation (0.5 cm in diameter) were scattered throughout the parenchyma. Pulmonary edema or emphysema was not observed grossly. Microscopically, the alveolar septae were irregularly thickened because of edema, infiltration by polymorphonuclear and mononuclear cells, and vascular congestion. Interstitial lesions were patchy in distribution and severity and corresponded to the areas of consolidation observed grossly. Alveolar epithelial hypertrophy and hyperplasia were present, and an occasional focus of alevoli contained fluid of edema. Degeneration of individual hepatocytes was observed in scattered areas of the liver, especially in the periportal areas. It was concluded that differences in 3MI dosage response may exist between young calves and adult cattle in which calves are more resistant to the pulmonary cytotoxicity of 3MI.
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PMID:Pathophysiologic studies of calves given 3-methylindole intraruminally. 51 32

Fifteen postoperative surgical patients, in whom noncardiac pulmonary edema developed were studied. A presumptive diagnosis of left ventricle failure would have been based on historical evidence of heart disease (80%), electrocardiographic changes of ischemia or arrythmia (87%), or cardiogenic shock (20%). (see article) Fig. 6. PAEDP-PCW gradient. Note that arterial oxygen tension had an inverse relationship to this pressure differential. Roentgenographic findings included pulmonary edema (73%), pulmonary vascular congestion (60%), cardiomegaly or congestive heart failure (40%). Mean increase in A-aDO2 was 290 torr. Further cardiovascular investigation seemed to exclude left ventricular failure. Mean cardiac index was 4.1 plus or minus 1.3 L/min/m2; pulmonary capillary wedge pressure 4 plus or minus 2.7 torr, and stroke work was 87 plus or minus 8.7 gm-meters. Possible etiologic agents included elevated pulmonary artery pressure (67%), allergic reactions (27%), peritonitis or multiple system trauma (54%), or multiple transfusions (33%). Forty-seven per cent of the entire group survived. Therapy was directed toward the underlying noncardiogenic suspected etiology. Direct cardiovascular measurements were necessary to correct the erroneous though seemingly well founded suspected diagnosis of left ventricular failure in these patients.
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PMID:"Pseudocardiogenic" pulmonary edema. 111 52

Hemodynamics were studied in seven conscious dogs during acute hypobaric stress at 14,000 ft simulated altitude. Silastic catheters were chronically implanted in the pulmonary artery, left atrium, and aorta. Pulmonary and central aortic pressures, cardiac output, and pulmonary blood volume were determined under conditions of normoxia and acute hypoxia in a hypobaric chamber maintained at 446 mm Hg pressure (14,000 ft). Altitude resulted in significant increases in heart rate, cardiac output, pulmonary blood volume, and pulmonary artery pressure. Left atrial pressure and calculated systemic vascular resistance decreased during hypobaric hypoxia while stroke volume, stroke work index, arterial pressure and pulmonary vascular resistance remained unchanged. Arterial blood PO2 decreased markedly at altitude, and all animals hyperventilated with resultant systemic hypocarbic alkalosis. The combination of elevated pulmonary arterial pressure and increased pulmonary blood volume may by an etiologic factor in the development of high-altitude pulmonary edema.
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PMID:Circulatory response to acute hypobaric hypoxia in conscious dogs. 125 2

In the initial evaluation of cardiac patients, valuable information can be derived from the chest radiograph. In general, acute left-sided heart failure is shown by an erate cardiomegaly, cephalization of the pulmonary vascularity, and a mixed type of pulmonary edema. Gross alveolar pulmonary edema with a normal or minimally enlarged heart. Subacute failure is associated with modcardiomegaly, striking cephalization, and interstitial pulmonary edema are hallmarks of chronic left-sided heart failure. Right-sided heart failure is shown by enlarged systemic veins and right-sided chambers as well as pulmonary oligemia. Pleural effusions in heart failure tend to be bilateral or unilateral on the right side.
Heart Dis Stroke
PMID:Radiographic diagnosis of heart failure. 134 88


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