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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Evidence suggests that the initial phase of neurogenic pulmonary oedema results from a centrally mediated, massive, sympathetic discharge. It is postulated that this produces intense, generlised, but transient, vasoconstriction with a resultant shift of blood from the high-resistance systemic circulation to the low-resistance pulmonary circulation. Pronounced increases in pulmonary vascular pressures and blood-volume then produce pulmonary oedema because of the hydrostatic effect of increased pulmonary capillary pressure. In addition, pulmonary hypertension and hypervolaemia injure pulmonary blood-vessels, altering pulmonary capillary permeability and producing lung haemorrhage. After the transient systemic and pulmonary vascular hypertension subside, the patient is left with abnormal pulmonary capillary permeability, so that pulmonary oedema persists in the face of normal haemodynamic and cardiac function.
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PMID:Pathogenesis of neurogenic pulmonary oedema. 5 77

Cerebral ischemia of 15 min was produced in rats by increasing intracranial pressure above the systolic blood pressure level by infusing artificial cerebrospinal fluid into the cisterna magna. Pulmonary edema was prevented by blocking the vasomotor response with a ganglioplegic agent, and reducing the fluid load by peritoneal dialysis. The EEG flattened after 10.1 +/- 1.5 sec. followed by a dilatation of the pupils after 1--2 min. The EEG began to recover in 21 of 32 rats after 8 to 35 min of recirculation. Spectral analysis revealed an initial return of slow waves and spindles followed by continuous fast frequency activity. The EEG did not recover or was secondarily suppressed in 12 animals after a few hours. Electrophysiological recovery depended on the cardiocirculatory and respiratory state, the recovery being optimal in animals with mild hypertension and a normal acid-base status of the blood.
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PMID:Electrophysiological recovery after compression ischemia of the rat brain. 7 50

5 patients developed pulmonary oedema after retrograde femoral arteriography under general anesthesia. Because of the haemodynamic changes associated with radiographic contrast media, a good preoperative cardiological assessment is essential. The volume and nature of the contrast media injected and any other fluid administered should be carefully monitored. There is no apparent safe maximum dose of radiographic contrast media, but this work suggests that for 'Conray 420' (sodium iothalamate 70% w/v) a total dose should be less than 200 ml in a fit patient. The dose should be substantially smaller in patients with a history of evidence of myocardial infarction, myocardial insufficiency, myocardial ischaemia, or hypertension.
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PMID:Pulmonary oedema after radiological investigation of peripheral occlusive vascular disease. Adverse reaction to contrast media. 7 42

Left ventricular wall motion abnormalities, the extent and location of coronary artery stenoses, and the radiographic evidence of pulmonary venous hypertension were analyzed in a retrospective study of 40 patients who had surgically proven rupture of the interventricular septum after myocardial infarction. In 33 patients in whom chest films were available, interstitial or alveolar pulmonary edema was present in 78%, while left ventricular enlargement was present in 82%. Of 26 patients who had coronary angiography, complete occlusion of the right coronary artery, left anterior descending artery, or left circumflex artery was present in 92%, with few, if any, collateral vessels around the occlusion. The location of the rupture in the muscular septum was always in the region of akinesis or dyskinesis. Posterior defects were associated with posterobasal and diaphragmatic akinesis, and anterior defects with apical akinesis. Left ventricular aneurysms were adjacent to the septal rupture in 68%, and 74% had mitral regurgitation. The right ventricular diaphragmatic wall in posterior rupture was always akinetic, indicating right ventricular infarction. Thus ventricular septal defect after myocardial infarction (1) tends to occur with multiple coronary occlusions about which little collateral flow develops; (2) can accurately be localized anteriorly or posteriorly in the muscular septum by the location of the akinetic left ventricular wall segment; and (3) has an associated right ventricular infarct when rupture is posterior.
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PMID:Coronary, ventricular, and pulmonary abnormalities associated with rupture of the interventricular septum complicating myocardial infarction. 10 43

Clinical studies have long suggested the presence of a specific cardiomyopathy in sickle cell anemia secondary to intracoronary thrombosis and subsequent infarction. Fifty-two autopsy patients were studied (48 with SS hemoglobin, 4 with S-C or S-Thal hemoglobin) to ascertain the range of cardiac pathologic abnormalities associated with this disease. The average age was 17 years (range 1 month to 48 years). Renal failure and infection were the most common causes of death; the former was a more common cause in adults than in children. Right and left ventricular hypertrophy and dilatation were the most common abnormal pathologic findings. No evidence of recent or remote myocardial infarction, coronary thrombosis or arteritis was noted in any patient. Eight patients who were studied with postmortem coronary arteriograms exhibited markedly increased coronary arterial caliber with no evidence of atherosclerosis. Seventeen of the 52 patients studied had clinical evidence of congestive heart failure before death. Of these 17 patients, 7 had moderate to severe left ventricular hypertrophy associated with chronic renal failure and hypertension, 2 had right ventricular hypertrophy with organized pulmonary thrombosis, 2 had rheumatic mitral valve disease and 2 died during the second trimester of pregnancy. Two of the 17 patients thought to have pulmonary edema before death in fact had aspiration pneumonia and hemorrhagic pneumonitis, respectively. The data suggest that cardiac dysfunction in sickle cell anemia can usually be explained by the adverse effect of coexisting disease on the diminished cardiac reserve of chronic anemia. The data do not support the concept of a specific "sickle cell cardiomyopathy".
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PMID:Clinicopathologic analysis of cardiac dysfunction in 52 patients with sickle cell anemia. 15 Jul 86

Evidence suggests the following pathogenesis for neurogenic pulmonary edema. The initial phase results from a centrally mediated, massive, sympathetic discharge. This produces intense, generalized, but transient, vasoconstriction with a resultant shift of blood from the high-resistance systemic circulation to the lowresistance pulmonary circulation. Marked increases in pulmonary vascular pressures and marked increases in pulmonary blood volume then produce pulmonary edema because of the hydrostatic effect of increased pulmonary capillary pressure. In addition, pulmonary hypertension and hypervolemia injure pulmonary blood vessels, altering pulmonary capillary permeability and producing lung hemorrhage. After the transient systemic and pulmonary vascular hypertension subside, the patient is left with abnormal pulmonary capillary permeability, so that pulmonary edema persists in the face of normal hemodynamics and normal cardia function.
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PMID:Speculations on neurogenic pulmonary edema (NPE). 17 54

1. In 27 severe primary hypertensive patients nifedipine (10 mg), administered orally, induced prompt (-21% of control at 30 min) and persistent (-17% at 120 min) fall of mean arterial pressure mediated through reduction of peripheral vascular resistance with rise of cardiac output. 2. The sublingual route (nine cases) showed more rapid onset of action and equal antihypertensive effectiveness. 3. In five patients with hypertensive crisis and acute left ventricular failure, the drug strikingly reduced systemic and pulmonary arterial pressures and relieved pulmonary oedema. 4. Prompt efficacy, ease of administration, absence of important side effects indicate that nifedipine may be a useful therapeutic agent in severe hypertension and in critical conditions that require rapid lowering of blood pressure.
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PMID:Haemodynamic effects of a calcium antagonistic agent (nifedipine) in hypertension: therapeutic implications. 28 70

Three patients presenting with pulmonary edema associated with head trauma and increased intracranial pressure are described. Pulmonary edema is a clearly recognized complication of head trauma; the pathogenic mechanisms appear to be regulated by increased intracerebral pressure, sympathetically induced vascular hypertension, and increased pulmonary capillary permeability. If there is evidence that neurogenic pulmonary edema is the underlying etiology, therapeutic modalities should be directed at reducing intracranial pressure and strict attention paid to the interaction between intrathoracic and intracranial pressures in order to avoid the high mortality rate associated with this condition.
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PMID:Neurogenic pulmonary edema in childhood. 37 99

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.
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PMID:Failure of prolonged hypocapnia, hypothermia, or hypertension to favorably alter acute stroke in primates. 40 43

Hemodynamic changes and samples of fluid from pulmonary edema were studied in a 50-year-old woman who developed florid pulmonary edema following intracranial hemorrhage. Marked systemic and pulmonary arterial hypertension were associated with the rapid production of edema fluid that contained red blood cells, but had a lower protein content than plasma. After restoration of pulmonary vascular pressures to a normal range, the production of fluid ceased, and clinical signs of edema resolved. These findings point to the sudden increase in pulmonary microvascular pressure as the cause of pulmonary edema in this patient. Our findings contrast with those of previous reports and with speculations on the extent of a defect in permeability accounting for pulmonary edema following injury to the brain.
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PMID:Pulmonary edema following intracranial hemorrhage. 43 31


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