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

Atrial septal defect (ASD) is the most common congenital cardiac anomaly manifested in adulthood. Clinical and radiographic features are well defined in patients less than 30 years of age. In older patients, however, the clinical symptoms are often atypical, and the auscultatory findings may be misleading. The radiographic manifestations in older patients have not been well described. In the current study, of 70 patients over the age of 50 years with proved ASD, 21 (30%) had atypical radiographic features, including apparently normal vascularity, left atrial enlargement, pulmonary venous hypertension, and pulmonary edema. In a control group of 70 younger patients with ASD, only 5.7% had atypical findings. The development of pulmonary venous hypertension and pulmonary edema in older patients was associated with smaller defects and a higher prevalence of mitral valve disease, left ventricular dysfunction, and pulmonary arterial hypertension than seen in older patients with typical radiographic findings.
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PMID:Atrial septal defect in older adults: atypical radiographic appearances. 296 75

Phentolamine (Phe) prevents the induction by epinephrine (E: 1800 nmol/kg, i.v.) of lung edema (LE) in urethane-anesthetized and bivagotomized rats in a dose-related manner (from 246 to 3933 nmol/kg, i.v.). Since Phe blocks and E activates both alpha 1- and alpha 2-adrenoceptors, the evidence does not allow us to link LE to selective (alpha 1 or alpha 2) or non-selective (alpha 1 + alpha 2) alpha-adrenoceptor activation. Accordingly, we tried to find out whether: phenylephrine (PE), a selective alpha 1-adrenoceptor agonist, and B-HT 920, a selective alpha 2-adrenoceptor agonist, would cause LE; prazosin (Praz), a selective alpha 1-adrenoceptor antagonist, and yohimbine (Yoh), a selective alpha 2-adrenoceptor antagonist, would protect rats against LE caused by E or PE. We found that: 1) PE (from 736 to 5892 nmol/kg, i.v.), but not B-HT 920 (from 190 to 12200 nmol/kg, i.v.), caused LE, while both drugs increased arterial blood pressure; 2) Praz prevented induction of LE, whether by E (1800 nmol/kg, i.v.) or by PE (5892 nmol/kg, i.v.), in a dose-related manner (from 15 to 119 nmol/kg, i.v.). In contrast, Yoh was ineffective at doses up to 7675 nmol/kg, i.v. We conclude, therefore, that E-induced LE in urethane-anesthetized and bivagotomized rats strictly depends on alpha 1-adrenoceptor activation. The outcome of E-induced LE is usually rat death, the incidence of which depends on the dose. Since alpha 1-adrenoceptor agonists rank in the same order of potency for the induction of death as for that of LE, and since Phe and Praz protect from death at LE-preventing doses, there seems to be some link between LE and death, even though protection against death is obtained with doses of antagonists lower than those abolishing induction of LE. Finally, alpha 1-agonists cause maximum arterial hypertension at all doses used, irrespective of induction of LE and of protective pretreatment against LE.
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PMID:Studies on epinephrine-induced lung edema in the rat. I. Selective alpha 1-adrenoceptor involvement. 301 61

This paper summarizes the role of the renal pressure natriuresis and diuresis mechanisms in maintaining sodium and water balance in hypertension. In all forms of chronic hypertension studied to date, the renal pressure natriuresis and diuresis mechanisms are abnormal, since increased arterial pressure is required to maintain normal excretion of sodium and water, and therefore fluid balance. When renal perfusion pressure is prevented from increasing in various forms of experimental hypertension, caused by infusion of mineralocorticoids, angiotensin II, vasopressin, or norepinephrine and adrenocorticotrophic hormone (ACTH), sodium and water retention continues until ascites, pulmonary oedema and circulatory collapse occur within a few days. Thus, chronic hypertension appears to be an essential homeostatic response that permits sodium and water balance to be maintained despite various abnormalities which tend to decrease renal excretory capability. The intrarenal mechanisms by which increased renal perfusion pressure maintains sodium and water balance in hypertension have not been fully elucidated, but appear to involve small changes in glomerular filtration rate (GFR) and reductions in fractional sodium reabsorption, due either to the direct hydraulic effects of pressure or to various indirect effects, such as changes in angiotensin II formation.
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PMID:Mechanisms of sodium balance in hypertension: role of pressure natriuresis. 302 42

The pathogenesis, diagnosis, and management of six clinical syndromes associated with acute myocardial infarction and hemodynamic instability are discussed: (1) autonomic disturbances with hypertension-tachycardia or hypotension-bradycardia; (2) pulmonary edema; (3) cardiogenic shock; (4) right ventricular infarction; (5) rupture of ventricular free wall or septum; and (6) papillary muscle rupture.
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PMID:Treatment of the hemodynamically unstable patient. 304 75

Intravenous nitroglycerin would appear to be an ideal agent for the treatment of severe pregnancy-induced hypertension complicated by cardiogenic pulmonary edema. Nitroglycerin infusion effectively reduces preload by venous dilatation and, at higher doses, results in arterial vasodilatation. Because of these pharmacologic properties, the effects of intravenous nitroglycerin were studied in three patients with severe pregnancy-induced hypertension complicated by pulmonary edema. The major cardiovascular effects of nitroglycerin were to reduce the mean pulmonary capillary wedge pressure from 27 +/- 4 to 14 +/- 6 mm Hg, which result in a change in the colloid osmotic pressure to pulmonary capillary wedge pressure gradient from -10 to 2 mm Hg. No significant changes occurred in heart rate, central venous pressure, or cardiac index. Analysis of oxygen-related parameters revealed a significant (p less than 0.05) increase in oxygen delivery and extraction accompanied by a 53% increase in oxygen consumption. The changes in oxygen-related variables appeared to be secondary to a fall in mixed venous oxygen tension from 39 +/- 4 to 33 +/- 1 torr. These changes occurred without any significant improvement in arterial oxygen tension. We conclude that while intravenous nitroglycerin expeditiously corrects the hydrostatic derangements of pulmonary edema seen in pregnancy-induced hypertension, a rapid improvement in arterial oxygenation does not occur.
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PMID:Role of intravenous nitroglycerin in the treatment of severe pregnancy-induced hypertension complicated by pulmonary edema. 308 Aug 87

The combined transplantation of heart and lungs, first done successfully by the Stanford Team (USA) in 1982, at present seems to be superseding lung transplantation alone, and has broadened the indications of heart transplantation to include terminal heart failure with fixed pulmonary arterial hypertension. After reviewing the causes for failure in lung transplants, the authors stress the superiority of heart-lung transplants compared to isolated lung transplantations: healing of the tracheal anastomosis, ease of detection of rejects by endomyocardial biopsy and the lack of inhomogeneity of the ventilation/perfusion ratios. This operation still poses problems of surgical technique as the mediastinal nerves need to be preserved and the risk of haemorrhage linked to the mediastinal dissection or to the eventual pulmonary separation under cardiopulmonary bypass is important. Donor subjects for cardiopulmonary transplantation are rare as they ought to have a thoracic cage of matching size to the recipient and to be free of pulmonary infection and trauma. The post-operative complications are essentially those of immediate haemorrhage, graft rejection, pulmonary oedema and infection. The late complications are coronary atherosclerosis and bronchiolitis obliterans. The indications of such a transplant are currently reserved for primary or secondary pulmonary hypertension and to respiratory failure with a normal thoracic cage and ventilatory mechanics.
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PMID:[Heart-lung transplantation]. 310 71

Eight patients with pulmonary oedema and 6 patients with cardiac asthma (primary disease: in 7 patients acute myocardial infarction, in 6--hypertension, in 1--mitral defect) were given sublingually a combination of 0.5 mg nitroglycerin, 10 mg Isodinit (isosorbid dinitrate) and 4 mg Sidnofarm (molsidomine) in powder form. This resulted in a rapid, pronounced and protracted reduction of dyspnoea, pulmonary congestion, respiration rate, and heart rate in the course of a four-hour observation rate, in more than 80% of cases. In patients with high blood pressure it dropped by 27% vs. the initial level; in patients with hypotension the change was only minimal. Pulmonary diastolic pressure began to drop from the 3rd minute after administration of the agents and the maximal decrease was attained after 30 min (34% of the initial value); even 4 hours after administration the values were below the initial level. The mentioned drug combination appears to be valuable especially in the first stage of treatment of cardiac asthma and pulmonary oedema.
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PMID:Application of a combination of sublingually administered vasodilating drugs for rapid action on pulmonary hypertension in patients with cardiac asthma and with pulmonary oedema. 311 25

The objectives of the present study were to determine whether an intracisternal injection of fibrinogen-sodium citrate, a model of neurogenic pulmonary edema (NPE), produces protein-rich or protein-poor pulmonary edema, and to determine whether the edema is associated with pulmonary vascular hypertension and pulmonary congestion. Fibrinogen (6-10 mg/ml) dissolved in 0.055 M sodium citrate was injected into the cisterna magna of six New Zealand White rabbits. Six additional rabbits were injected with saline to control for the effects of intracranial hypertension and pulmonary vascular hypertension. The fibrinogen-sodium citrate solution or sodium citrate alone, as opposed to saline, produced systemic and pulmonary vascular hypertension, pulmonary edema, hypoxemia, hypercapnia, and acidosis. The lungs from fibrinogen-injected rabbits were edematous, congested, and liverlike in appearance. Tracheal froth that was blood tinged and protein rich was present in five of the six rabbits. Microscopic examination of lung biopsies revealed erythrocytes and plasma in the alveoli and focal injury to the pulmonary microvascular endothelium. Fibrinogen-sodium citrate increased (P less than 0.05) the extravascular lung water (EVLW) (10.3 +/- 2.0 vs. 5.5 +/- 0.6 g, means +/- SE), lung blood weight (9.7 +/- 1.3 vs. 3.8 +/- 0.6 g), total dry lung weight (3.2 +/- 0.4 vs. 2.0 +/- 0.1 g), and the EVLW-to-blood-free dry lung weight ratio (7.0 +/- 0.8 vs. 4.0 +/- 0.3 g) from saline-control values. There was no difference in the blood-fre dry lung weight (1.4 +/- 0.1 vs. 1.3 +/- 0.1 g) between the two groups. These findings demonstrate that pulmonary congestion, pulmonary vascular hypertension, and focal endothelial injury contribute to the development of NPE.
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PMID:Endothelial injury and pulmonary congestion characterize neurogenic pulmonary edema in rabbits. 311 22

Chest X-rays were used to evaluate the hemodynamic status of 86 patients with acute myocardial infarction. The chest films, divided into three groups depending on the degree of pulmonary venous hypertension revealed: grade 1, pulmonary-venous congestion; grade 2, interstitial pulmonary edema; grade 3, diffuse alveolar edema. On clinical examination, four grades of congestive heart failure were distinguished in acute myocardial infarction. In 69% of our patients radiological and clinical grading of left ventricular failure led to precisely the same conclusions. Pulmonary capillary wedge pressure was measured in 31 patients with acute infarction. Radiological criteria of the degree of pulmonary vascular congestion, when related to pulmonary capillary wedge measurements, provide a basis for consistent therapy of left ventricular failure secondary to acute myocardial infarction.
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PMID:[X-ray changes in the thoracic organs in acute heart infarct]. 318 76

Nine children, hospitalized for severe respiratory failure following scorpion envenomation, were a part of a group of 61 youngsters and infants admitted to the Pediatric Intensive Care Unit of the Soroka Medical Center, Beer-Sheva during the years 1983-87 because of scorpion venom intoxication. Four out of the nine had cardiogenic shock, three had severe systemic hypertension and one had severe airway obstruction. All nine patients had central nervous system manifestations, including lethargy, confusion and agitation (three cases), and markedly reduced level of consciousness (six cases). Hemodynamic studies performed in two patients showed 'high pressure' (cardiogenic) pulmonary edema. Seven patients recovered completely, one died and another one was left severely handicapped. Hydralazine i.v. showed a remarkable effect on the systemic blood pressure and central nervous system disturbances in addition to mechanical ventilation. Based on our own experience and previous clinical and experimental studies, the possible pathogenetic mechanisms underlying the respiratory and central nervous system dysfunction following scorpion sting are discussed.
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PMID:Respiratory failure in children following envenomation by the scorpion Leiurus quinquestriatus: hemodynamic and neurological aspects. 320 82


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