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 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent studies in patients with either obstructive or nonobstructive hypertrophic cardiomyopathy have suggested that increased resistance to diastolic filling of the stiff left ventricle may be an important mechanism contributing to symptoms. These observations have led to exploration of the effects of calcium channel blockers on systolic and diastolic function in patients with hypertrophic cardiomyopathy. Acute hemodynamic studies using verapamil and nifedipine have shown that these agents tend to cause: (1) a slight fall in systemic arterial pressure and reflex increase in heart rate; (2) a reduction in left ventricular outflow gradient in most but not all patients; and (3) variable effect on left-side heart filling pressures. In contrast to beta-adrenergic blockers, these hemodynamic effects are not associated with depression of systolic function, but appear to be related to improved left ventricular distensibility. Clinical trials have suggested that long-term administration of verapamil in patients with hypertrophic cardiomyopathy promotes improvement in symptomatic status and exercise tolerance in many but not all patients; similar results have been reported in preliminary studies using nifedipine. Potential major adverse effects include depression of sinoatrial activity and atrioventricular conduction with verapamil, and marked hypotension and, rarely, pulmonary edema with both verapamil and nifedipine.
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PMID:Use of calcium channel blockers in hypertrophic cardiomyopathy. 403 50

A review of the prelegal abortion scene in the US precedes discussion of the effect of injected soap, phenol, cresol, and their compounds. The latter is based on a review of 4 toxicology books. There is little difference in the symptoms after the instillation of phenols, cresols, or soaps. Any one of those agents can cause vaginal bleeding, abdominal pain and distension, nausea, vomiting, and cramps. The damage produced by the use of Lysol thus is due to both the phenol and soap components of the compound. Following instillation into the uterus, there is coagulation necrosis of the decidua and placental site. The toxin will invariable cause thrombosis of the intrauterine and parametrial veins. The thrombosis may spread to the entire pelvic vein plexus and paravaginal, paracervical, and ovarian veins. The liver and kidney are affected by the toxin. Icterus and bile pigments in the urine and clinical evidence of liver damage are seen often. Pulmonary edema has been described as have microscopic to massive pulmonary oil emboli and thrombosis. Depression of all bone marrow elements due to toxin has been reported. The red blood cells are further depressed in number because of hemolysis. Cerebral changes include oil emboli, cerebral coagulation, necrosis, and petechial hemorrhages. Until Studdiford and Douglas described gram-negative sepsis causing shock, patients admitted with hypotension accompanying septic abortion were thought to have concealed blood loss. Studdiford and Douglas showed that gram-negative septicemia could produce hypotension. With the advent of massive antibiotic therapy for septic abortion and septic shock, most of these patients could be saved. The kidneys, after exposure to phenolic-soap comounds, show mainly lower nephron changes. As long as the toxin is in the system those changes continue until irreversible renal damage occurs. It is essential to remove the source of the poison (the affected uterus) and then remove the circulating toxins. the main problem is removal of the circulating toxin. In addition to the problems produced by fixed and circulating toxin, it has been shown that most phenol-soap induced abortions are infected. Thus it is necessary to employ the optimal antibiotic therapy for septic incomplete abortion. The initial management phase moves along classic lines. First is monitoring the vital state and supporting the systems. This includes maintaining an intravenous solution with a large-bore needle, monitoring central venous pressure, measuring urinary output, monitoring the vital signs, maintaining adequate oxygenation, and supporting the blood pressure with blood vasopressors or other agents, as needed. Second is diagnosing the extent of the illness. Third is the initial treatment, which includes reestablishment of the blood volume with blood transfusions; aggressive coverage with double or triple antibiotic therapy; correction of hypofibrinogenemia with cryoprecipitate, fresh whole blood or fresh frozen plasma, as indicated; and avoidance of overhydration in the presence of actual or suspected renal failure. After antibiotic coverage has been established, removal of retained products of conception is indicated.
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PMID:Treatment of women who have undergone chemically induced abortions. 404 35

Fat embolism following major trauma may be associated with a clinical syndrome with widespread pulmonary and systemic manifestations, the most serious being profound hypoxia with secondary atelectasis, pulmonary edema and pulmonary hypertension, and cerebral depression. Though the origin of the embolic fat is debated, there is evidence to support its origin from both the bone marrow and intravascular chylomicron coalescence.The clinical manifestations are largely explained by a prime assault upon the lung parenchyma and alteration in platelet characteristics.Early recognition and treatment of the condition is essential, adequate oxygenation being of prime importance. Steroids and heparin have been found to be of benefit.
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PMID:Fat embolism: a rational approach to treatment. 475 Mar

In order to evaluate the incidence of myocardial ischaemia in patients who developed acute pulmonary oedema during the immediate post-operative period, continuous monitoring of the electrocardiogram by the Holter method was used in 200 consecutive patients with coronary artery disease. Fourteen of these patients exhibited ST segment depression during the post-operative period and 13 during surgery. Nine patients developed acute pulmonary oedema immediately after the operation and in 7 cases the oedema was preceded by myocardial ischaemia. A continuous nitroglycerin infusion brought about regression of the pulmonary oedema in 8 cases. One patient died despite treatment. These findings underline the part played by myocardial ischaemia in the pathogenesis of acute post-operative pulmonary oedema in patients with coronary artery disease.
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PMID:[Acute postoperative pulmonary edema in the coronary patient: effects of myocardial ischemia]. 622 2

In 200 young patients with apparently idiopathic spontaneous pneumothorax, the following radiologic features were analyzed: degree of collapse on the initial chest film, areas of atelectasis, and presence of blebs, apical opacities, fibrous adhesions, pleural effusions, and controlateral shift of mediastinal structures. Confrontation of apical changes with pathologic findings in operative specimens suggests that mesothelial rupture with reactive hyperplasia results in a "pneumatization chamber" visible as a bullous image. Following drainage, homolateral shifts of mediastinum and four cases of pulmonary edema were recorded. Risk factors for pulmonary edema include severe pulmonary collapse with areas of atelectasis, persisting for more than 48 hours and an aspiration which either exceeded 1.5 l. of air or was performed with a depression of more than 30 cm of water.
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PMID:[Radiology of spontaneous pneumothorax in young patients. Apropos of 200 cases]. 632 55

A case of babesiosis in an asplenic individual is reported. A course characterized by fever, haemolysis, hepatitis, depressed mental status and non-cardiac pulmonary oedema was observed. Studies performed on the patient's lymphocytes revealed profound depression in mitogenic responses during her acute disease which returned to normal with recovery. Serum factor(s) were implicated in causing these changes. Review of the literature on babesiosis in asplenic hosts revealed European patients with disease caused by bovine species of Babesia are at significantly higher risk of a fatal outcome than North Americans with disease caused by murine species.
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PMID:Babesiosis in asplenic hosts. 633 94

The choice of the initial asanguinous fluid--either crystalloid or colloid--used for the resuscitation of the hypovolemic patient remains controversial. Colloid supporters argue for the careful preservation of the plasma colloid osmotic pressure (PCOP) to protect the lung from pulmonary edema. A careful analysis of the Starling microvascular forces operative at the pulmonary capillary makes such an effect unlikely. In fact, the lung is relatively immune to hemodilution and any decrease in PCOP is roughly one fourth as important as increases in hydrostatic pressure in causing increased fluid exchange. A critical review of the experimental and clinical studies comparing crystalloid versus colloid resuscitation essentially shows no physiologic difference in the two solutions. Using the thermal-green dye technique of extra-vascular lung water (EVLW) measurement in twenty crystalloid resuscitated trauma (n = 10) and burn (n = 10) patients, we have specifically evaluated the pulmonary effects of profound depression of PCOP and a negative PCOP - PAWP gradient (a shorthand form of the Starling equation argued to predict the presence of pulmonary edema if + 4 mm Hg or less). Average resuscitative fluid volumes during the first two hospital days were: 31.8 litres of crystalloid and no colloid for each burn patient; and 18.5 liters of crystalloid, 21 units of blood and 1 liter of colloid (as fresh frozen plasma) for each trauma patient. EVLW remained in the normal range of 7.0 +/- 1.0 ml/kg during the first five hospital days for all patients despite profound decrease in PCOP (less than 15 mm Hg) and a low or negative PCOP - PAWP gradient. Crystalloid resuscitation clearly is not harmful to the lung and it is equally as effective as colloid resuscitation. Crystalloid is markedly less expensive than colloid and, given the greater cost of colloid without evident benefit, one wonders how their further use can be justified.
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PMID:Crystalloid versus colloid for fluid resuscitation of hypovolemic patients. 634 5

William Osler described the first reported case of narcotic-induced pulmonary edema in 1880. The description is that of autopsy findings of a patient who died of narcotic poisoning. Since that time, noncardiogenic pulmonary edema has come to be known to accompany overdose with a number of drugs, most notably heroin. Clinical manifestations and radiographic findings vary. The exact pathogenesis is unclear, although the mechanism is known to involve increased alveolar capillary permeability. Treatment consists of reversal of respiratory depression, oxygenation, and respiratory support. Rapid improvement with treatment is the rule.
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PMID:William Osler: narcotic-induced pulmonary edema. 638 71

In acute myocardial infarction depression of the ST segment in leads distant from those showing ST elevation has been considered to be "reciprocal" but might reflect local ischaemia. To examine this possibility 103 consecutive patients who underwent exercise testing early after myocardial infarction were reviewed. Treadmill exercise testing was performed a mean of 12 (range 5-30) days after infarction using a limited Naughton protocol. Thirty five (34%) of the patients had had reciprocal change, defined as greater than or equal to 1 mm ST depression in leads remote from the site of the infarct, within 48 hours of infarction. Twenty two (63%) of the 35 patients developed exercise induced ST depression in the leads previously showing reciprocal change. Coronary artery disease was assessed in 10 of these patients by arteriography and in four at necropsy: all but one had stenosis of greater than or equal to 50% in a coronary artery supplying the reciprocal territory in addition to the disease in the vessel to the infarct site. Of patients with reciprocal ST depression, 23.5% experienced nonfatal reinfarction, pulmonary oedema after discharge, or death compared with only 9.5% of patients without reciprocal ST depression. Eight (23.5%) patients with reciprocal depression had ventricular fibrillation while in hospital compared with only two (3%) patients without. Reciprocal ST depression in acute myocardial infarction may reflect ischaemia in territory distant from the site of infarction and is associated with a high risk of fatal arrhythmias and late morbidity.
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PMID:"Reciprocal" depression of the ST segment in acute myocardial infarction. 641 Dec 61

A retrospective study was conducted on 488 patients admitted in our rehabilitation center after a recent acute myocardial infarction. Purpose of the study was to assess the incidence and prognostic value of exertional hypotension in these patients. Of 488 patients admitted to the study 33 (6%) were found to have exertional hypotension; 14 patients had an inferior myocardial infarction, 18 patients had an anterior myocardial infarction, 3 patients had a history of previous myocardial infarction. In the follow-up period (28.3 +/- 13.2 months) the worse prognosis (death or pulmonary oedema) was associated with the presence during exercise of hypotension, ST segment elevation in leads were Q waves were present and no ST depression in other leads. In conclusion, recent anterior myocardial infarctions associated with hypotension and ST segment elevation during exercise appear to be at risk for future cardiac events.
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PMID:Exertional hypotension after myocardial infarction. 650 Feb 24


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