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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied the hemodynamic events that followed abrupt withdrawal of nitroprusside in 20 patients with severe chronic heart failure. With nitroprusside, cardiac index increased from 1.96 to 2.87 liters per minute per square meter of body-surface area, but it decreased to 1.66 (P less than 0.001) after withdrawal of nitroprusside. Left ventricular filling pressure and systemic vascular resistance decreased from 23.9 to 15.3 mm Hg and from 1642 to 921 dyn.sec.cm-5, respectively, with nitroprusside, but increased to 30.4 mm Hg and 2109 dyn.sec.cm-5 (both P less than 0.001) upon its discontinuation. These rebound changes were maximal 10 to 30 minutes after nitroprusside withdrawal and returned to control levels one to three hours later. Although in 17 of 20 patients, these rebound changes caused no or minimal exacerbation of symptoms, pulmonary edema, which resolved in three patients. Activation of reflex vasoconstrictive forces during vasodilator therapy may explain these effects of withdrawal.
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PMID:Rebound hemodynamic events after the abrupt withdrawal of nitroprusside in patients with severe chronic heart failure. 50 11

After the acute onset of heart failure and in the absence of acute myocardial infarction, plasma volume may occasionally be depleted to the extent that the patient presents with clinical signs of circulatory shock. In five patients, the acute onset of clinical and radiographic signs of cardiogenic pulmonary edema were associated with reduction in arterial blood pressure and cardiac output. The pulmonary arterial wedge pressure was within normal limits but a reduction in plasma volume was demonstrated, which is best explained by the rapid translocation of plasma water that represented pulmonary (and most likely also peripheral) edema fluid. The infusion of 5 percent albumin solution significantly increased cardiac output, mean arterial pressure and cardiac work, reversed lactic acidosis, enhanced furosemide-induced diuresis and was followed by a decrease in both clinical and radiographic signs of pulmonary edema. These observations confirm that volume expansion may constitute appropriate treatment for some patients with cardiogenic pulmonary edema who may present with hypotension and who are unresponsive to conventional therapy.
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PMID:Hypovolemia and hypotension complicating management of acute cardiogenic pulmonary edema. 50 39

Electron microscopic studies on the alveolar-capillary barrier were carried out in 13 patients of chronic pulmonary edema and/or congestion resulting from heart disease of various etiologies. The characteristic findings are tremendous proliferation of type II granular pneumocyte and irregular thickening of alveolar epithelial and capillary basement membrane. These ultrastructural changes correlated to the duration of heart failure and mean pulmonary arterial wedge pressure despite of disease groups and the age of the patients. In particular, lamination of capillary basement membrane with fragmentation was more specific finding which was observed only in patients with mean pulmonary arterial wedge pressure above 35 mmHg and duration of heart failure over 6 hears. There was no apparent relationship existed between the ultrastructural changes and pulmonary arterial pressure. In addition to these characteristic changes the remaining ultrastructural changes of the alveolar-capillary barrier were difficult to make a correlation to clinical course and cardio-pulmonary hemodynamics.
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PMID:Electron microscopic studies on the alveolar-capillary barrier in the patients of chronic pulmonary edema. 51 67

The use of vasodilators represents a new approach to the treatment of cardiac insufficiency, either chronic or acute. Their field of action is venous, arterial or mixed. Decreasing the pre-load, the "venous" vasodilators lighten the congestive symptoms of cardiac insufficiency. By decreasing the post-load, the "arterial" vasodilation increases the cardiac output. Some vasodilators, venously administered, imply a continuous hemodynamic checking (Sodium Nitroprussiate, Phentolamine, injectable Trinitrine). Others are active orally (Trinitrine, Isosorbide Dinitrate, Hydralazine, etc.). Vasodilating treatment is recommended for acute cardiac insufficiency, particularly during myocardium infarct and some acute valvular insufficiencies. It is also successfully used in acute lung edema. Finally it takes an increasing importance in the treatment of chronic cardiac insufficiency.
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PMID:[Vasodilators in the treatment of cardiac insufficiency (author's transl)]. 53 77

Following a case of mannitol-induced respiratory and circulatory collapse, the effects of hyperosmolar injections on pulmonary arterial pressure, systemic blood pressure, and cardiac output were studied in dogs. The injection of 20 ml of 10% NaCl into the pulmonary artery increased pulmonary arterial pressure and decreased systemic blood pressure by approximately 50% of control values. Injections of solutions of equal hyperosmolar strength, 50 ml of 25% mannitol or 50 ml of 4% NaCl into the pulmonary artery produced no significant elevation of pulmonary arterial pressure, but were associated with comparable decreases in systemic blood pressure. When allowed to vary, cardiac output increased with injections of all three hyperosmolar solutions, yet was still accompanied by falls in systemic blood pressure as large as when cardiac output was held constant. Vagotomy did not prevent these changes in systemic and pulmonary arterial pressure, nor the increase in cardiac output. After five to 10 injections, the decreases in system blood pressure with any of the solutions and the increases in pulmonary arterial pressure with 10% NaCl disappeared and further injections were without effect. It is concluded that adminstration of mannitol probably does not cause pulmonary edema due to fluid overload, nor does it cause heart failure as evidenced by increases in pulmonary arterial pressure. However, rapid injection may cause a fall in blood pressure and may on occasion be accompanied by bronchospasm, especially in sensitive subjects.
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PMID:Hypotension and respiratory distress caused by rapid infusion of mannitol or hypertonic saline. 57 Dec 22

Multiple muscular ventricular septal defects were closed through an apical left ventriculotomy in 11 patients. The patients were divided into two groups: Group 1, 8 patients who had transposition of the great arteries, and group 2, 3 patients without transposition. There were 4 deaths in Group 1 and non in Group 2. Two of the deaths were caused by a hypoplastic right ventricle, 1 by airway obstruction, and 1 by heart failure and pulmonary edema in a patient who had additional unrecognized muscular defects. An apical left ventriculotomy provides excellent exposure of the septum. The field is not obscured by trabecular bands or papillary muscles. Although 1 patient died because of residual VSDs, this approach, compared with previously described methods, minimizes the risk of unrecognized defects.
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PMID:Left ventricular approach to multiple ventricular septal defects. 59 66

The hospital mortality in 1,246 consecutive acute myocardial infarction patients treated in a large community hospital coronary care unit was 14.4%. Of the total, 52.3% showed no evidence of heart failure, 25.8% had mild to moderate failure, 9.9% had pulmonary edema, and 12% developed cardiogenic shock; the mortality in these groups was 2.2%, 7.4%, 8.9%, and 87.2%, respectively. The mortalitiy in the 1,097 patints who did not have cardiogenic shock was 4.5%. Only one patient died as a result of primary ventricular fibrillation (0.08%). The mortality of complete heart block in the absence of cardiogenic shock (8.3%) was not significantly different from that of comparable patients who did not have complete heart block (4.3%). These results are lower than those generally reported.
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PMID:Treatment of myocardial infarction in a community hospital coronary care unit. Experience with 1,246 patients. 62 50

Acute pancreatitis and cardiac disease were diagnosed in a dog with pulmonary edema. The early clinical course and initial thoracic radiographs suggested that the pulmonary edema was noncardiogenic. The late clinical course was complicated by heart failure. The dog died, and a necropsy was performed. Histologically, an acute, severe capillary-alveolar membrane lesion was found in the lungs. Review of the human medical literature indicated that respiratory complications, including pulmonary edema, are commonly recognized in people with acute pancreatitis. Furthermore, in acute pancreatitis of human beings, the existence of specific mechanisms of pulmonary injury is suspected. Retrospective consideration of this case suggested that the initial pulmonary edema was induced by acute pancreatitis.
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PMID:Pulmonary edema in a dog with acute pancreatitis and cardiac disease. 64 Sep 32

In an attempt to assess cardiac risk in non-cardiac surgery, 1001 patients over 40 years of age who underwent major operative procedures were examined preoperatively, observed through surgery, studied with at least one postoperative electrocardiogram, and followed until hospital discharge or death. Documented postoperative myocardial infarction occurred in only 18 patients; though most of these patients had some pre-existing heart disease, there were few preoperative factors which were statistically correlated with postoperative infarction. Postoperative pulmonary edema was strongly correlated with preoperative heart failure, but 21 of the 36 patients who developed pulmonary edema did not have any prior history of heart failure. Nearly all of these 21 patients were elderly, had abnormal preoperative electrocardiograms, and had intraabdominal or intrathoracic surgery. In the absence of an acute infarction, bifascicular conduction defects, with or without PR interval prolongation, never progressed to complete heart block. Spinal anesthesia protected against postoperative heart failure but not against other cardiac complication. By multivariate regression analysis, postoperative cardiac death was significantly correlated with (a) myocardial infarction in the previous 6 months; (b) third heart sound or jugular venous distention immediately preoperatively; (c) more than five premature ventricular contractions per minute documented at any time preoperatively; (d) rhythm other than sinus, or premature atrial contractions on preoperative electrocardiogram; (e) age over 70 years; (f) significant valvular aortic stenosis; (g) emergency operation; (h) a 33% or greater fall in systolic blood pressure for more than 10 minutes intraoperatively. Notably unimportant factors included smoking, glucose intolerance, hyperlipidemia, hypertension, peripheral atherosclerotic vascular disease, angina, and distant myocardial infarction.
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PMID:Cardiac risk factors and complications in non-cardiac surgery. 66 58

To provide an understanding of the clinical characteristics of patients with acute myocardial infarction (MI) and bundle branch block, experience from five centers was accumulated. Patients in whom bundle branch block first appeared after the onset of cardiogenic shock were excluded. In 432 patients, the most common types of block were left (38%) and right with left anterior fascicular block (34%). In 42% of the patients, bundle branch block was new. Progression to high degree (second or third degree) atrioventricular (AV) block via a Type II pattern occurred in 22% of the patients. Hospital and first year follow-up mortality rates were 28% and 28%, respectively. Only 46% of the patients developed pulmonary edema or shock (Killip Class III or IV), and hospital mortality was related to the amount of heart failure (8%, 7%, 27%, 83% for Killip Classes I-IV, respectively). Patients with progression to second degree or third degree AV block via a Type II pattern had increased hospital mortality compared with patients without this complication (47% vs 23%, P less than 0.001). In the absence of pulmonary edema or shock, patients with Type II second degree or third degree AV block still had a higher mortality rate than patients without advanced AV block (31% vs 2%, P less than 0.005), with nearly all the deaths due to abrupt development of AV block. Thus, in many patients MI with bundle branch block is associated with severe heart failure. However, this was not true for a majority of the patients, in whom therapy aimed at preventing morbidity and mortality due to the bradyarrhythmia of advanced AV block might be beneficial.
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PMID:The clinical significance of bundle branch block complicating acute myocardial infarction. 1. Clinical characteristics, hospital mortality, and one-year follow-up. 68 79


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