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

A case is reported of bronchial stenosis due to a vascular cause in a patient with chronic obstructive lung disease, cor pulmonale and pulmonary arterial hypertension. This led to right lower lobe atelectasis and acute respiratory failure (pHa 7.24; PaCO2 85 mmHg; PaO2 44 mmHg) with important right-to-left shunting. This diagnosis was only suggested on day 7 by fibreoptic bronchoscopy and confirmed a week later by tomography and digital angiography. Nifedipine, used to reduce the pulmonary arterial hypertension, increased the cardiac index (31.min-1.m-2 to 3.3.1.min-1.m-2) and oxygen transport (488 ml.min-1.m-2 to 554 ml.min-1.m-2), despite increasing the shunt effect (Qs/QT: 26% to 31%). This and the antiinflammatory action of methylprednisolone were probably responsible for the favourable outcome.
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PMID:[Bronchial stenosis of vascular origin in pulmonary arterial hypertension]. 304 7

Pulmonary arterial rupture due to the use of a Swan-Ganz catheter is a rare accident, with an estimated 2% incidence rate. It is fatal in almost 50% of cases. Predisposing factors are age greater than 60 years, pulmonary arterial hypertension and anticoagulant treatment. In patients older than 60 years, changes in the arterial wall increase the risk of rupture; pulmonary hypertension leads to too distal a movement of the catheter, and a concomitant treatment with anticoagulant drugs increases the amount of blood lost. Handling errors when setting up the catheter are often the cause of these accidents, especially a balloon too blown up and a catheter pushed too far. A subsequent movement of the catheter can be a cause of rupture during cardiac surgery. Haemoptysis is the major symptom of this accident, being found in 90% of cases. It can however be of minor importance; if it is ignored, this can lead to a secondary overwhelming haemorrhage. The haemorrhage can be life-threatening because of the cardiovascular collapse and acute respiratory failure by asphyxia. The treatment can only be carried out in intensive care. It will depend on the severity of the accident. It can go from an expectant wait after partial or total removal of the catheter, to an emergency thoracotomy for vascular suture, segmentectomy or even lobectomy. Intermediate measures include turning the patient onto the healthy side, injecting adrenaline or a clot of the patient's blood by the distal end of the catheter, placing a Fogarty catheter in the affected bronchus, or tracheal intubation with a double-lumen catheter and using mechanical ventilation with PEEP.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Perforation of the pulmonary artery following Swan-Ganz catheterization]. 306 41

Extracorporeal circulation can cause lung damage, which would be especially counterproductive during extracorporeal gas exchange for the treatment of acute respiratory failure. To test the hypothesis that partial venovenous bypass with extracorporeal CO2-removal combined with low-frequency positive pressure ventilation (ECCO2R-LFPPV) can adversely affect lung fluid balance, extravascular thermal lung volume (ETV) and hemodynamics were assessed before, during and after ECCO2R-LFPPV in normal closed chest dogs. In series I dogs (n = 6) subjected to 10 h of ECCO2R-LFPPV, ETV did not change significantly from control (7.1 ml/kg +/- 0.99 SE) during or after bypass. Gravimetric extravascular lung water and lung histology after bypass were found to be normal. In series II dogs (n = 5), subjected to shorter periods of ECCO2R-LFPPV, ETV also remained unchanged. In contrast to previous reports using sheep, pulmonary arterial hypertension during bypass was not observed. Thus, ECCO2R-LFPPV was not associated with increased lung water, pulmonary hypertension or morphological lung changes under the conditions studied and does not seem to cause lung damage in normal lungs.
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PMID:Lung extravascular volume during venovenous bypass with extracorporeal CO2-removal in dogs. 312 77

This study describes the case of a 58 year old man who presented with an episode of acute respiratory failure and right heart decompensation. After recovery from the acute illness, hypoxaemia, hypercapnia and pulmonary arterial hypertension remained, the causes of which were not known. There was no airway obstruction, only a moderate restrictive ventilatory defect, a little weight increase and a unilateral diaphragmatic paralysis. Obstructive sleep apnoea was finally suspected and confirmed by sleep recording. The obstructive sleep apnoea probably explained the respiratory insufficiency and the pulmonary hypertension. Loss of weight was associated with the disappearance of hypercapnia and pulmonary hypertension. As a result of this study, the value of sleep recording is emphasized. When respiratory failure or pulmonary hypertension seem unexplained, think of obstructive sleep apnoea.
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PMID:[Value of sleep polygraph examination in the etiological diagnosis of apparently inexplicable respiratory insufficiency]. 404 63

Permanent pulmonary arterial hypertension is a standard part of the prognosis for patients with chronic respiratory insufficiency. As a decrease of pulmonary arterial hypoxic vasoconstriction may be obtained by calcium antagonists, we studied the effects of nifedipine (10 mg sublingually) in 10 patients with chronic respiratory insufficiency without acute respiratory failure. Our results show that maximal expiratory air flow was not altered. The pulmonary antihypertensive action of this drug, which is less effective than oxygen breathing at low concentration, was associated with a constant decrease of arterial oxygen partial pressure; the oxygen transport was not sustained for every patient. This result suggests that considerable caution should be exercised in using this drug for the treatment of pulmonary arterial hypertension in patients with chronic respiratory insufficiency without acute failure.
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PMID:Effects of nifedipine on pulmonary arterial hypertension in patients with respiratory insufficiency without acute failure. 643 15

We present two patients with acute respiratory failure secondary to cold and exercise-induced asthma. Neither patient had a prior history of asthma, and both had recently been placed on therapy with propranolol for treatment of hypertension. We discuss the postulated mechanism of bronchospasm in these patients. In addition, we urge aggressive searching for any change in respiratory symptoms in patients receiving propranolol.
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PMID:Life-threatening cold and exercise-induced asthma potentiated by administration of propranolol. 747 27

Nitric oxide was identified as the relaxing factor derived from the endothelium in 1987. Nitric oxide synthesis allows the vascular system to maintain a state of vasodilation, thereby regulating arterial pressure. Nitric oxide is also found in platelets, where it inhibits adhesion and aggregation; in the immune system, where it is responsible for the cytotoxic action of macrophages; and in the nervous system, where it acts as neurotransmitter. A deficit in endogenous synthesis of nitric oxide contributes to such conditions as essential arterial hypertension, pulmonary hypertension and heart disease. An excess of nitrous oxide induced by endotoxins and cytokinins, meanwhile, is believed to be responsible for hypotension in septic shock and for hyperdynamic circulatory state in cirrhosis of the liver. Nitric oxide has also been implicated in the rejection of transplanted organs and in cell damage after reperfusion. Inhaled nitrous oxide gas reduces pulmonary hypertension without triggering systemic hypotension in both experimental and clinical conditions. It also produces selective vasodilation when used to ventilate specific pulmonary areas, thereby improving the ventilation/perfusion ratio and, hence, oxygenation. Nitric oxide inhalation is effective in pulmonary hypertension-coincident with chronic obstructive lung disease, in persistent neonatal pulmonary hypertension and in pulmonary hypertension with congenital or acquired heart disease. Likewise, it reduces intrapulmonary shunt in acute respiratory failure and improves gas exchange. Under experimental conditions nitric oxide acts as a bronchodilator, although it seems to be less effective for this purpose in clinical use.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Nitric oxide]. 789 26

Acute glomerulonephritis (AGN) remains fairly common in the developing world although its frequency has declined in the industrial countries. The pattern of AGN was studied in one hundred hospitalised children. We recorded an increased prevalence in school age, i.e., 6-15 years (75%) and the occurrence of a streptococcal infection (90%), most often a pharyngeal infection (86%), one to three weeks preceding the illness. The problems that needed specific management during the acute phase were hypertension (39%), encephalopathy (5%) and ARF with hyperkalemia, 2% of the patients needing haemodialysis. Most of our patients (98%) recovered with 2% progressing to RPGN. The excellent prognosis of AGN with proper management emphasises the need for optimal care during the acute phase in the hospitalised children.
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PMID:Acute glomerulonephritis in children. 807 77

We studied 19 peripartum patients with acute respiratory failure associated with pregnancy. Although it is an uncommon event, noncardiogenic pulmonary edema is the most common cause of respiratory failure in the peripartum period. This acute lung injury syndrome was observed to be associated with a variety of complications of pregnancy including premature labor, the use of tocolytics, infection, hypertension, leukoagglutinin reactions, aspiration, abruptio placentae, and amniotic fluid embolism. From 1989 through 1992 there were 10,852 deliveries and 19 patients with noncardiogenic pulmonary edema at our institution. Analyzing these cases has led us to favor the hypothesis that the respiratory failure associated with the various complications of pregnancy primarily represents the fatal and nonfatal cases of amniotic fluid embolism that Steiner and Lushbaugh initially believed undoubtedly to exist. Moreover, we suggest, as have others, that the nonspecific symptom complex of inflammation, coagulopathy, and cardiopulmonary failure represents the release of soluble mediators into the maternal circulation. It is not clear what the predominant mediator is, but we have focused on platelet activating factor. It is also not established whether the mediator(s) is of amniotic fluid origin or a result of maternal anaphylactoid-type of response to a fetal or amnioplacental antigen. In conclusion, monitoring maternal oxygenation either directly or indirectly by oximetry should be considered routinely in the peripartum period, especially in complicated pregnancies, to detect at an early stage "asymptomatic" or preclinical cases of noncardiogenic pulmonary edema, in hopes of then modifying management to prevent their progression.
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PMID:Acute respiratory failure in pregnancy. An analysis of 19 cases. 946 62

Diffuse hypoxic pneumonia was found to be caused by angiotensin converting enzyme (ACE) inhibitors in two patients given enalapril and fosinopril for hypertension. Both patients developed sub-acute respiratory failure and lost weight. Imaging explorations showed multiple areas of alveolar consolidation, moderate pleural effusion and in one case linear opacities. In both cases, peripheral eosinophila was found and the bronchoalveolar lavage fluid contained lymphocytes. Progressive improvement was achieved after withdrawal of the ACE and corticosteroid therapy for three months. Subsequent x-rays and respiratory function tests returned to normal apart from persistently low CO diffusion in one patient. In view of other cases reported in the literature, ACE inhibitors should probably be included in the list of drugs capable of inducing pneumonia, notably eosinophilic pneumonia.
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PMID:[Hypoxic eosinophilic pneumonia in two patients treated with ACE inhibitors]. 992 37


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