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

Neoplastic thrombosis of the pulmonary artery is a rare and little known cause of pulmonary arterial hypertension. The clinical picture is one of acute respiratory failure and progressive right ventricular failure caused by pre-capillary pulmonary hypertension. In the living patient there is no way of distinguishing this condition from that of subacute cor pulmonale due to embolism, especially as the primary tumour is not always found either because it is too small or because it has already regressed by the time it has metastasised. The diagnosis usually rests on histological examination of the lungs, and two pathological types can be distinguished: carcinomatous lymphangitis with secondary invasion and thrombosis of the pulmonary arterioles on the one hand, and the neoplastic arterial emboli of a chorio-epithelioma on the other.
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PMID:[Pulmonary arterial hypertension caused by neoplastic thrombosis of the pulmonary artery]. 10 82

We repeatedly assessed pulmonary and systemic hemodynamics in 30 patients undergoing therapy for severe acute respiratory failure of diverse causes. Pulmonary-artery hypertension and elevated pulmonar vascular resistance were observed in all patients after correction of systemic hypoxemia. Increasing pulmonary blood flow by isoproterenol infusion or decreasing pulmonary blood flow by partial bypass of the right side of the heart minimally altered pulmonary-artery pressure. Although neither elevated pulmonary vascular resistance nor low cardiac index reliably predicted death, survivors had preogressive decreases of pulmonary vascular resistance with time, whereas nonsurvivors tended to maintain or increase pulmonary vascular resistance. Right ventricular stroke-work index was markedly elevated in all patients. The work load imposed upon the right ventricle by elevation of pulmonary vascular resistance may be a factor limiting survival in severe acute respiratory failure.
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PMID:Pulmonary hypertension in severe acute respiratory failure. 83 25

Oliguric ARF occurred in 0.5% of battle casualties who reached the field medical care system and raised their mortality expectancy from less than 5% to nearly 90%, due primarily to fluid volume overload and/or myocardial potassium intoxication. For their effective treatment the Renal Insufficiency Center with laboratory and a Brigham-Kolff rotating drum dialyzer began operations in 1952, as depicted in a videotape prepared for this presentation from motion picture footage filmed in early 1953. Our Surgical Research Team's major findings relevant to ARF were: (1) Renal function was depressed in most battle casualties in proportion to the severity of their wounds and blood loss. (2) Among the more severely wounded some developed nonoliguric; others, oliguric ARF. (3) Oliguria lasted from 3 days to 3 weeks without a discernible peak frequency of beginning diuresis at 10 days. (4) During oliguria, posttraumatic catabolism greatly accelerated extracellular accumulations of nitrogen, potassium, phosphate, and hydrogen ion with rapid, concurrent clinical deterioration. (5) Dialysis "on indication" produced an oscillating clinical and chemical course. (6) ARF was then revealed as a wasting disease complicated by infections, poor wound healing until diuresis occurred, anemia and bleeding, and hypertension during dialyses and in early diuresis. (7) The overall mortality rate was reduced.
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PMID:Acute renal failure during the Korean War. 150 54

Pulmonary arterial hypertension develops in acute respiratory failure and mostly an enhanced PADd-PCWP gradient has an important effect on the outcome of that complication. Considering that this critical state of septic burned patients may last for weeks, the long-term direct monitoring of pulmonary arterial blood pressure with indwelling Swan-Ganz catheter is impossible because of the high risk of endocarditis. Therefore, the aim of this study was to elaborate a noninvasive method to estimate the pulmonary arterial hypertension. Determination of cardiac index and pulmonary arterial blood pressure was carried out with Swan-Ganz catheter, P32 Statham transducer, cardiac output computers (Gould IM 1000, Marquette 7010). Extended systolic time interval measurements (with Medicor 661 polygraph completed by PC program package) were performed simultaneously in 7 burned patients (av. age 38.7 ys, means of TBS 38%) with acute respiratory failure at 38 occasions. The values of cardiac indices with the two methods were practically the same CI t = 3.4 +/- 1.21 1/min/m2 CI s = 3.1 +/- 1.10 1/min/m2; regression equation: CI s = 0.874 CIt + 0.135, r = 0.98, n = 38. Close correlations have been found between PAPm and PO2/FiO2 (r = 0.75), as well as between PAP values and some noninvasively measured hemodynamic data. Using these interrelations: 1) regression equations for PAPs., PAPm, PAPd, PCWP, PVRI were elaborated (r values: 0.855, 0.869, 0.681, 0.644, 0.817 respectively); 2) discriminant analysis with noninvasive parameters correctly classified the cases at critical PAPd-PCWP gradient (greater than 4 mm/Hg) in 84%. These results suggest that a continuous noninvasive hemodynamic and blood gas monitoring completed with a periodic bedside computer analysis of the PC-processed data for calculation of the pulmonary arterial pressure may be enough for the therapy during the long-term critical periods.
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PMID:Noninvasive estimation of pulmonary arterial blood pressure in burned patients with acute respiratory failure. 176 49

In contrast to pulmonary parenchyma metastases or lymphangitic carcinomatosis, neoplastic emboli of small pulmonary arteries and capillaries frequently go unrecognized and are only discovered at autopsy. Five patients (48 +/- 12 years old) were admitted to 3 intensive care units for severe acute respiratory failure and died between the first and the tenth day following hospitalization. Each patient had a history of rapidly progressive dyspnea, and physical examination showed clinical evidence of right ventricular failure. The lungs were clear on chest X-rays and the ECG revealed sinus tachycardia with a right QRS axis. The mean partial pressures of oxygen (PaO2) and carbon dioxide (PaCO2) were, respectively, 50.8 +/- 9.1 mm Hg and 22.2 +/- 2.4 mm Hg. A swan-Ganz catheter, inserted into 4 patients, revealed pulmonary arterial hypertension (55, 43, 37, 28) with capillary wedge pressure within the normal limits and cardiac output normal or low (3.0, 3.8, 4.4, 5.0 l/min). Pulmonary angiograms from each patient showed decreased distal lung perfusion without any proximal defects suggestive of pulmonary embolism. The inferior vena cava always appeared clear. Malignant cells were found upon autopsy (4 cases) in the lumina of the pulmonary arterioles and the primary site of the cancer was determined in 3 patients (2 hepatomas and 1 pancreatic carcinoma). The last patient had a known breast cancer with bone marrow metastases and clinical, hemodynamic and angiographic evidence of neoplastic emboli. The clinical course of neoplastic emboli can suggest acute pulmonary embolism, but the diagnosis can only be advanced after pulmonary angiography, especially if the patient is to have a cancer.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Acute respiratory distress caused by distal neoplastic pulmonary emboli]. 209 8

alpha-Toxin, the major, pore-forming exotoxin of Staphylococcus aureus, caused acute hypertension when perfused through blood-free rabbit lungs (21). This reaction is mediated by pulmonary thromboxane generation, for which toxin-induced calcium flux into target cells with subsequent stimulation of arachidonic acid metabolism is predominantly responsible. In the present study, we investigated the effects of alpha-toxin on the integrity of the lung microvasculature. Thromboxane generation was inhibited in all experiments to suppress the development of pulmonary hypertension. Application of low alpha-toxin concentrations (5 to 40 ng/ml) induced protracted, severe vascular leakage in a dose-dependent manner. After a lag period of 40 to 120 minutes, gravimetrically determined capillary filtration coefficients progressively increased to greater than 10-fold values, and this was followed by pronounced weight gain of the isolated organs. These physiologic alterations were paralleled by dose- and time-dependent structural changes documented by electron microscopic examination of perfusion-fixed lungs. Increasing electron density of microvascular endothelial cell nuclei and subsequently of their cytoplasma was noted, followed by detachment of these cells from the mutual endoepithelial basal lamina. Edema was localized in the blood-gas exchange area, in contrast to hydrostatically induced lung fluid accumulation. These results identify pulmonary microvascular endothelium cells as highly susceptible targets for attack by alpha-toxin. Given a similar sensitivity of human endothelial cells, alpha-toxin might directly contribute to the pathogenesis of acute respiratory failure under conditions of severe infection with Staphylococcus aureus.
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PMID:Staphylococcal alpha-toxin-induced vascular leakage in isolated perfused rabbit lungs. 239 29

In chronic obstructive bronchopneumopathies (COBP), pulmonary artery hypertension (PAH) is usually mild but may markedly intensify during episodes of acute respiratory failure, muscular exercise, and sleep, PAH may, even if of low level, lead to right heart failure. The prognostic value of PAH and its degree in COBP patients has been well established by a number of recent studies. Chronologic changes in pulmonary artery pressure (PAP) tend to be minimal in the majority of COBP patients (of the order of +0.5-0.6 mm Hg/year in most studies). However, in a minority of patients (about 30%) pulmonary hypertension worsens seriously due to progressive deterioration of arterial blood gases. Longterm oxygen therapy (LOT) for 16 h/day rarely serves to normalize PAP but may reverse the progress of pulmonary hypertension, particularly in patients with progressive aggravation thereof. Recent studies have made it clear that LOT has beneficial hemodynamic effects in a relatively large percentage of COBP patients with PAH.
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PMID:[Development of pulmonary arterial hypertension in chronic obstructive bronchopneumopathies]. 269 44

The authors reviewed the actions of nifedipine, a blocker of calcium channels, on the systemic and pulmonary circulation. The mechanism of action of the drug on the systemic and pulmonary circulation and on the gas exchange is discussed. The main effects of nifedipine on the coronary circulation and indications for therapeutic use of the drug are discussed on the topics of coronary insufficiency, systemic and pulmonary blood hypertension, acute respiratory failure, and Raynaud's phenomenon.
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PMID:[Hemodynamic and pulmonary effects of nifedipine]. 269 29

In order to examine the prognostic value of pulmonary arterial hypertension (PAH) in patients with moderate and severe acute respiratory failure (ARF), 225 patients with ARF who had been treated with mechanical ventilation and admitted to our ICU during a 3-yr period (January, 1983 to January, 1986) were prospectively studied. All 70 (31%) patients with moderate and severe ARF also had some form of hemodynamic or pulmonary instability, and were monitored with a pulmonary artery catheter. Of these 70 patients, 38 (54%) had PAH (mean BP 29 +/- 6 mm Hg); their mortality was 79% (30/38). The rest of the patients (n = 32) did not have PAH (mean BP was 15 +/- 3 mm Hg) and their mortality was 44% (14/32) (p less than .01). Thirty patients met all the criteria for adult respiratory distress syndrome (ARDS), and their mortality was 70% (21/30); all of them were included among the 38 PAH patients. ARDS patients who died had a significantly higher pulmonary vascular resistance and a significantly lower cardiac index than patients who survived (p less than .001). We conclude that PAH (present in all our ARDS patients) is a good predictor of mortality in ARF of diverse causes.
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PMID:Pulmonary hypertension in acute respiratory failure. 272 Dec 10

In 106 patients suffering from acute respiratory failure of different severity 157 bedside balloon occlusion pulmonary angiographic studies have been performed through a pulmonary artery catheter to assess the frequency and extent of intravascular occlusive disease. The vascular alterations in acute respiratory failure impair the prognosis essentially. The decreasing pulmonary vascular cross-section causes a greater pulmonary vascular resistance and consecutive pulmonary artery hypertension and finally right heart failure. In 33% of patients multiple thrombosis and in 15.1% singularly pulmonary artery filling defects could be shown. In 21.7% a decreased background opacification caused by extensive microthrombosis was present. Only in 30.2% the angiography was interpreted as normal. The mortality rate was significant higher in patients with multiple macro- and microthrombosis (82.9% respectively 52.2%) compared to patients with singular pulmonary artery filling defects and normal angiography (37.5% respectively 28.1%). The angiographic result was further correlated with the severity of the acute respiratory failure, the haemodynamic and haemostasiologic data, the degree of consolidation in the chest-X-ray and the post mortem angiographic studies.
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PMID:[Incidence and prognostic significance of pulmonary artery thromboses in patients with acute respiratory failure: a study of 106 patients using bilateral pulmonary balloon occlusion angiography]. 280 May 53


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