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

A prospective study of congestive cardiac failure in 221 elderly Nigerians seen at Ahmadu Bello University Hospital, Zaria, and Ife University Teaching Hospitals Complex, Ile-Ife from 1974 to 1979 is reported. Hypertension, iodopathic cardiomegaly and pulmonary heart disease were major causes of cardiac failure. No case of coronary atherosclerotic heart disease was seen. Ventricular conduction defect was the commonest E.C.G. abnormality recorded. In over half of the patients, there was coexisting disease, mild to moderate anaemia being the most common.
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PMID:Congestive cardiac failure in elderly Nigerians: a prospective clinical study. 645 36

The haemodynamic definition of chronic cor pulmonale is precapillary pulmonary artery hypertension (P.A.H.T.), which determines the long term prognosis of chronic respiratory failure (C.R.F.) due to chronic obstructive airways disease (C.O.A.D.). The essential element of the various causes for an increase in pulmonary arterial pressure (PAP) is an increase in pulmonary arterial resistance secondary to alveolar hypoxia. At the present time, only long term oxygen therapy at home seems capable of limiting the progression of P.A.H.T., with a favourable influence on survival as demonstrated by two recent Anglo-Saxon multicenter surveys. The value of new drugs which have been proposed as a complement to or even a replacement for oxygen therapy, such as Almitrine dimesylate and Nifedipine, is currently being evaluated.
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PMID:[Effect of oxygen therapy on chronic pulmonary artery hypertension]. 646 2

The authors report a cause of acute cor pulmonale caused by Schistosoma mansoni bilharziosis. The clinical feature was a collapse with right ventricular failure following a delivery. The hemodynamic exploration showed a pre-capillary and supra-systemic pulmonary hypertension. The histopathologic study in post-mortem showed pulmonary lesions of fibrosis endarteritis with granulomatosis reaction round many eggs of Schistosoma mansoni. The authors discuss the frequency of various anatomic lesions (20, 30%), hemodynamic (20%) and clinical (2,5%) of the pulmonary bilharziosis. They recall the anatomical and histological mechanisms of the pulmonary artery hypertension in this disease. They emphasize the originality of this observation which is due to its super acute character and its Schistosoma mansoni bilharziosis etiology whereas pulmonary demonstrations are usually due to Schistosoma haematobium.
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PMID:[Acute bilharzial cor pulmonale due to Schistosoma mansoni]. 652 24

In surgical procedures intra- and postoperative cardiopulmonary complications rank first in the elderly patient. Cardiovascular risk factors in the preoperative judgement include chronic cor pulmonale, coronary heart disease and cardiac rhythm disturbances. Moreover pulmonary-respiratory risks and arterial hypertension play a very important role. In order to lower the intra- and postoperative risks, it is necessary to establish a thorough preoperative diagnosis and to establish a differential therapeutic work-up considering the underlying heart disease. Here balanced electrolytes seem to be particularly important. Only under these circumstances it will be possible to perform major surgical procedures in the elderly patient with an acceptable risk.
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PMID:[Cardiopulmonary risk factors. Recognition, evaluation and treatment in surgical interventions in advanced age]. 662 72

Hydralazine was administered to eight patients (mean age, 69 +/- 2 years) who had stable, advanced chronic obstructive pulmonary disease (COPD), pulmonary arterial hypertension (mean pulmonary arterial pressure, 31 +/- 3 mm Hg), and cor pulmonale. All of the patients were studied at rest and during exercise. After intravenous administration of hydralazine at rest, there were statistically significant increases in pulmonary arterial pressure (p less than 0.05), cardiac index (p less than 0.005), arterial oxygen saturation (p less than 0.01), and mixed venous saturation (SvO2) (p less than 0.005). Pulmonary vascular resistance did not change, and systemic resistance decreased (p less than 0.005). During exercise, pulmonary arterial pressure increased in all patients, and this increase was not blunted by hydralazine; however, cardiac index (p less than 0.005), arterial oxygen pressure (p less than 0.005), and SvO2 (p less than 0.001) increased further during exercise. The increase in pulmonary vascular resistance was significantly blunted by hydralazine (p less than 0.005). Therapy with the drug was continued orally in seven patients because one patient showed a deleterious response in pulmonary hemodynamics. After seven days of oral hydralazine, pulmonary arterial pressure and pulmonary vascular resistance were not statistically different from control. There were statistically significant increases in cardiac index (p less than 0.005) and SvO2 (p less than 0.05), systemic resistance decreased (p less than 0.01). The same condition was found during exercise; however, only two patients showed pulmonary gas exchange and pulmonary hemodynamic benefit at rest and during exercise with hydralazine therapy. Our results suggest that it is unlikely that vasodilator therapy with hydralazine will be useful in patients with advanced stable COPD and cor pulmonale who seem to have fixed pulmonary vascular disease.
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PMID:Hemodynamic effect of hydralazine in advanced, stable chronic obstructive pulmonary disease with cor pulmonale. Immediate and short-term evaluation at rest and during exercise. 669 95

This study was to determine if the diameters of pulmonary arteries measured from computed tomographic (CT) scans could be used 1) as indicators of pulmonary artery hypertension and 2) as a reliable base for calculating mean pulmonary artery pressure. The diameters of the main, left, proximal right, distal right, interlobar, and left descending pulmonary arteries were measured from CT scans in 32 patients with cardiopulmonary disease and in 26 age- and sex-matched control subjects. Diameters were measured using a special computer program that could display a CT density profile of the artery and its adjacent tissues. The upper limit of normal diameter for the main pulmonary artery was found to be 28.6 mm (mean + 2 SD). In the patient group, the diameters were correlated with data from cardiac catheterization. In these patients, a diameter of the main pulmonary artery above 28.6 mm readily predicted the presence of pulmonary hypertension. The calculated cross-sectional areas of the main and interlobar pulmonary arteries (normalized for body surface area [BAS]) were found to give the best estimates of mean pulmonary artery pressure (r = 0.89, P less than 0.001 and r = 0.66, P less than 0.001). Multiple regression analysis gave the useful equation: mean pulmonary artery pressure = -10.92 + 0.07646 X area of main pulmonary artery/BSA + 0.08084 X area of the right interlobar pulmonary artery/BSA (r = 0.93, P less than 0.0001). Because CT allows precise, noninvasive measurement of the diameter of pulmonary arteries, it can be of value in detecting pulmonary hypertension and estimating mean pulmonary artery pressure.
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PMID:CT-determined pulmonary artery diameters in predicting pulmonary hypertension. 670 16

The cardiopulmonary effects and tendencies to produce ventricular arrhythmias were evaluated in 13 dogs given a surgical plane of anesthesia by thiopental (IV) or a combination of thiopental and lidocaine (IV). Thiopental (22 mg/kg of body weight) was compared with a combination of thiopental (11 mg/kg) and lidocaine (8.8 mg/kg). Preanesthetic agents were not given. Both methods for IV anesthesia provided a smooth induction suitable for easy intubation. The thiopental/lidocaine combination had a shorter duration, produced no arrhythmias, and resulted in less cardiopulmonary depression than did thiopental alone. Bigeminy developed after intubation during 19 of 20 thiopental inductions as compared with that in 0 of 22 thiopental/lidocaine inductions. The bigeminies were preceded by systemic hypertension and tachycardia which developed as the trachea was being intubated. The increase in aortic pressure and heart rate was minimal after intubation during the thiopental/lidocaine inductions. Five minutes after administration of thiopental alone, increases in heart rate, aortic pressure, total peripheral vascular resistance, and left ventricular systolic and end-diastolic pressures were observed. When these increases in rate, preload, and afterload were considered in relation to a stabile maximum positive first derivative of left ventricular pressure, left ventricular contractility was considered to be decreased. Mild respiratory acidosis and hypoxemia were present at 5 and 10 minutes after thiopental induction. Because the combination of thiopental/lidocaine had less cardiopulmonary depressive effects and protected against arrhythmias, it would appear to be a good method for anesthetic induction of the patient with cardiopulmonary disease. In the patient with normal cardiopulmonary function, thiopental produces only a moderate and reversible depression.
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PMID:Cardiopulmonary effects of thiopental/lidocaine combination during anesthetic induction in the dog. 682 18

Echocardiography was used to evaluate left ventricular function in 43 consecutive patients with suspected cor pulmonale who clinically had no other heart disease or hypertension. Adequate echocardiographic evidence was obtained by either standard left parasternal position or subxiphoid position in 40 patients (93%). Echocardiographic evidence of either dilatation of the left ventricular cavity or thickening of the right ventricular free wall was present in 37 patients (93%). Small left ventricular end-diastolic cavities suggested that many of these patients had functional left ventricle volume depletion. Echocardiographic evidence of left ventricular dysfunction was present in only three patients (8%).
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PMID:Echocardiography in patients with suspected cor pulmonale. 707 31

The presenting symptom complex, diagnostic features, and therapeutic alternatives for obstructive and central sleep apnea are discussed in relation to two illustrative patients. Heavy snoring and restlessness during sleep in an obese individual, usually a male, may indicate obstructive apnea. Daytime hypersomnolence, intellectual deterioration, mental depression, impotence, cardiac arrhythmias, cor pulmonale, systemic hypertension, and erythrocytosis are the most common complications. Tracheostomy, the classic form of therapy, can be replaced by pharmacologic intervention in most patients. The clinical presentation of central apnea is less dramatic, but neurological and cardiac complications can occur. Therapy is less well established for this entity. Knowledge of the increased incidence of these disorders and awareness of more subtle complications indicate that sleep apnea should be placed in the differential diagnosis of pulmonary and systemic hypertension, hypersomnolence states, mental deterioration, psychiatric illness, and even insomnia.
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PMID:Diagnosis and therapy of sleep apnea. 722 83

A case of severe head injury associated with fulminant pulmonary edema considered as neurogenic which developed within short time after the injury was presented. A five-year-old boy who had no previous history of cardiopulmonary disease was struck on his right frontal region by car accident at 15.30 PM on July 5 of 1979. Immediately after the impact he lost his consciousness and subsequently transferred to a local hospital where bilateral dilated pupil and flaccid paralysis of the limbs were noted. On transmission of the patient to Omuta City Hospital 30 minutes after the injury, massive foamy fluid was discharged from the tracheal tube. On admission, he was comatous, with bilateral dilated and fixed pupils and flaccid paralysis of the limbs. There was no retinal bleeding. He showed ataxic respiration with severe stridor and massive discharge of foamy fluid pinkish in colour from the trachea characteristic in pulmonary edema was significant. Chest x-ray film demonstrated perihilar densities suggesting pulmonary edema. CT scan showed extremely small ventricle on both sides without manifestations of intracranial hematomas or cerebral contusion. With an intensive medical treatments including corticosteroids, alkalizing agents and alpha-blocker were administered under controlled respiration, the discharge of edema fluid was gradually decreased and the findings on blood gases were also improved. However neurological signs were aggravated and he died 8 hours after the injury. Central venous pressure was maintained at the level between 8 to 10 cm. From these clinical findings the pulmonary edema was concluded as neurogenic. Direct or indirect injury to the hypothalamic efferent pathway at the level of lower brain stem seemed to be important as the cause of neurogenic pulmonary edema in this case. The possible pathophysiology of neurogenic pulmonary edema associated with brain stem injury and intracranial hypertension was discussed with other related literature.
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PMID:[Neurogenic pulmonary edema following severe head injury--case report (author's transl)]. 724 16


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