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

Recognition of heart failure (HF) may be difficult in patients presenting with acute dyspnoea, particularly in the presence of chronic airways obstruction. Since increased secretion of the cardiac hormones atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) occurs early in the course of HF, we have assessed the value of measuring these hormones in plasma in the diagnosis of suspected HF in 52 elderly patients presenting with acute dyspnoea, and compared values with left-ventricular ejection fraction (LVEF), a standard measure of left-ventricular function, by radionuclide angiography. Patients were enrolled prospectively. On the basis of clinical findings, conventional tests, and response to specific treatment, 20 of the 52 patients were classified as having primary lung disorder (PLD), 12 as HF alone, and 20 as HF with underlying PLD (HF/PLD). Compared with findings in PLD patients, LVEF was significantly depressed in HF and HF/PLD patients (p < 0.001), whereas both plasma ANP and BNP were significantly increased (p < 0.001). Admission plasma BNP concentration more accurately reflected the final diagnosis of HF (93% sensitivity and 90% specificity when BNP > or = 22 pmol/L) than LVEF or plasma ANP concentration. When all patients were considered together, there were strong negative correlations between LVEF and log BNP (r = -0.7, p < 0.001) and log ANP (r = -0.59, p < 0.001). Our finding that plasma BNP is raised in dyspnoeic patients with HF but not in acutely breathless patients with PLD, suggests that rapid BNP assays may assist in the diagnosis of patients with acute dyspnoea.
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PMID:Plasma brain natriuretic peptide in assessment of acute dyspnoea. 790 5

This article describes the use of nebulized morphine in the management of dyspnea in two patients with end-stage chronic lung disease, and two patients with end-stage heart failure. All four patients had relief of breathlessness. Arterial blood gas results and vital signs were monitored pre- and postnebulized morphine in two of the patients and demonstrated little change. Nebulized morphine appears to be well tolerated in this patient population.
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PMID:Case studies outlining use of nebulized morphine for patients with end-stage chronic lung and cardiac disease. 796 63

The metabolism of the skeletal muscles during exercise and recovery was investigated using phosphocreatinine (PCr) and inorganic phosphate (Pi) in patients with chronic heart failure. PCr/Pi ratio, which is closely related to the ATP/ADP ratio, and the pH were measured by 31P-magnetic resonance spectroscopy (31P-MRS) during and after forearm exercise in 9 patients with chronic heart failure, 11 patients with chronic lung disease, and 8 normal subjects. Exercise and recovery scans were recorded every minute for 4 min. The PCr/Pi ratio in patients was lower during the recovery period and significantly lower 3 and 4 min after exercise than in normal subjects. The pH values after exercise were lower in patients, although not significantly. The PCr/Pi ratio 4 min after exercise in patients was not correlated with parameters of cardiac function or arterial and mixed venous oxygen tension. Nutritional parameters did not vary statistically among the groups. Metabolic abnormalities may be present in the skeletal muscles of patients' group, which are not due to undernutrition, possibly as a result of exercise deconditioning and probably a shift in fiber distribution (type I decreases, type IIb increases) and a decrease in oxidative capacity.
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PMID:[Alterations of skeletal muscle metabolism in patients with congestive heart failure]. 804 95

Spirometry was performed by 5,201 elderly participants of the Cardiovascular Health Study during their baseline examination and a subset of the ATS/DLD-78 respiratory questionnaire was administered by trained interviewers. In never smokers (46 percent of the cohort), the overall prevalence of chronic cough was 9 percent, chronic phlegm was 13 percent, attacks of wheezing with dyspnea were 8 percent, and grade 3 dyspnea on exertion was 10 percent. The prevalence of lung disease in current smokers (12 percent of the cohort) was 8/7 percent (men/women) with chronic bronchitis and 14/5 percent with emphysema. Overall, 6 percent reported asthma (a physician-confirmed history) and 12 percent reported hay fever. Using a logistic regression model, attacks of wheezing with dyspnea were strongly associated with a lower FEV1, coronary heart disease, heart failure, and a large waist size (in participants without a diagnosis of asthma, chronic bronchitis, or emphysema). Undiagnosed airways obstruction was twice as likely in women and those with lower income, and was associated with current and former smoking, pack-years of smoking, and chronic cough. Dyspnea on exertion (DOE) was three times or more likely if a participant reported heart failure, coronary heart disease, or emphysema; and much more likely if their FEV1 or FVC was substantially reduced. Dyspnea on exertion was also positively associated with older age, chronic bronchitis or asthma, a larger waist or hip size, pack-years of smoking, and less education. We conclude that DOE and attacks of wheezing with dyspnea are commonly associated with cardiovascular disease and a low FEV1 in those over 65 years and that airways obstruction frequently remains undiagnosed in the elderly.
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PMID:Prevalence and correlates of respiratory symptoms and disease in the elderly. Cardiovascular Health Study. 808 66

Unilateral pulmonary edema is a distinctly unusual clinical entity, often misdiagnosed initially as one of the more common causes of focal lung disease. Predominantly lobar pulmonary edema is rarer still. We report a case of right upper lobe pulmonary edema caused by the acute onset of severe mitral regurgitation. In addition, we briefly review the other causes of unilateral pulmonary edema, focusing on the cases that have been reported in association with heart failure and valvular heart disease. The majority of cases of right upper lobe pulmonary edema have been associated with mitral regurgitation. In addition to confirming the presence of mitral regurgitation, transesophageal echocardiography proved useful in delineating the mechanism for edema formation. It detected differential gradients between the right and left pulmonary venous systems and documented the direction of the regurgitant flow.
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PMID:Right upper lobe pulmonary edema caused by acute mitral regurgitation. Diagnosis by transesophageal echocardiography. 813 90

The ventriculoatrial shunt (VAS) was developed to control hydrocephalic syndromes effectively. Several complications, however, have been described after the procedure. One of the most serious consequences is the development of severe pulmonary hypertension attributed to multiple and recurrent pulmonary embolization caused by the catheter of the VAS; however, the frequency is exceedingly low. Herein we describe the experience with three patients in whom severe pulmonary hypertension developed after a VAS procedure. In two patients, refractory heart failure developed, an outcome that caused death within a brief period. The third patient underwent atrial thrombectomy and then pulmonary thromboendarterectomy; recovery was complete. Scientific evidence shows that initial embolization predisposes pulmonary vessels to develop further in situ thrombosis; thus, the vascular lung disease progresses despite removal of the embolic source. A review of the literature revealed that in patients with a VAS, pulmonary embolism and pulmonary hypertension were clinically diagnosed in only 0.4% and 0.3% of the cases, respectively, whereas postmortem diagnoses of pulmonary embolism and pulmonary hypertension were established in 59.7% and 6.3%, respectively. These discrepancies point out the difficulty of establishing the diagnosis of these serious pulmonary vascular complications while the patient is alive.
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PMID:Development of pulmonary hypertension after placement of a ventriculoatrial shunt. 824 20

We evaluated the following spirometric values: forced vital capacity (FVC), first second expiratory volume (FEV1), FEV1/FVC, the lung volumes, total lung capacity (TLC), residual volume (RV), and single breath diffusing capacity for CO in 22 patients, before and after heart transplant. We found abnormal pulmonary function in 21 patients before heart transplantation. Despite postoperative increases in lung volumes in 10 patients, abnormal pulmonary function persisted in 20 patients after heart transplant. Mean values for lung volumes and flow rates did not change but diffusion for CO decreased significantly after heart transplantation. Diffusion failed to correlate with ejection fraction, pulmonary arterial pressure, pulmonary capillary wedge pressure (PCWP), and pulmonary vascular resistance; however, in a subset of patients with improved postoperative lung volumes, preoperative diffusion for CO correlated with preoperative PCWP. We conclude that pulmonary function abnormalities are common among heart transplant recipients. Diffusion abnormalities are not linearly related to indices of cardiac function measured before transplantation and diffusion abnormalities appear to be multifactorial in cause. The posttransplant decrease in diffusion appears to result from the combined effects of decreased postoperative lung volumes in some patients and relief of heart failure induced pulmonary vascular engorgement in others. Improvement in lung volumes and flow rates may occur but cannot be expected after heart transplantation, and diffusion decreases after heart transplantation. The fact that pulmonary function and lung volumes do not improve following heart transplantation implies to underlying lung disease or permanent lung alterations result from chronic heart failure.
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PMID:Diffusing capacity decreases after heart transplantation. 844 81

Five men were investigated after having pulmonary aluminosis due to exposure to aluminium pyrotechnic flake powder during the late 1940s. Two of the men had died 6 years and 20 years after exposure respectively, due to their lung disease. One man had died from heart failure 34 years after the end of exposure. Today, more than 40 years after exposure, two men were available for investigation. They had no respiratory symptoms and their vital lung capacities had not deteriorated during these years. One of the two survivors had developed a dementia with motor disturbances, which is not consistent with Alzheimer's dementia. This man had a very high concentration of aluminium in his cerebrospinal fluid. The other survivor had a normal concentration and was not demented.
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PMID:A follow-up study of five cases of aluminosis. 891 43

The investigation of left ventricular contractile reserve usually requires the determination of left ventricular volume, but its measurement with radionuclide angiography is difficult. The aim of this study was to determine left ventricular volume directly during exercise by the simultaneous measurement of peak exercise left ventricular ejection fraction (LVEF) and oxygen consumption (VO2max) and to compare the results with another geometric method. In the absence of lung disease, the systemic arteriovenous oxygen difference (DAVmax) during maximal exercise converges to 0.13-0.14 ml O2 per ml blood. The measurement of VO2max allows maximal cardiac output (COmax) to be calculated as VO2max = COmax. DAVmax. By simultaneously determining LVEFex, exercise end-diastolic volume (EDVex) can then be expressed as a linear function of VO2max, maximal heart rate (HRmax), DAVmax and LVEFex. Then, the relationship between end-diastolic counts and true volume can be derived at rest. The two methods were closely correlated (r = 0.91, P < 0.001), despite the geometric method being less accurate when applied to low counting statistic acquisitions. We conclude that rest and exercise left ventricular volume can be determined non-invasively by the simultaneous measurement of VO2max and LVEFex. Furthermore, this method provides additional prognostic information which is clinically relevant in the staging of patients with heart failure.
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PMID:Determination of left ventricular cardiac volume by simultaneous radionuclide angiography and measurement of oxygen consumption at rest and during maximal exercise: a comparison of two non-invasive isotopic procedures. 900

Right-to-left intracardiac shunting across a patent foramen ovale (PFO) has been reported in patients with pulmonary embolism, right ventricular (RV) infarction, positive pressure ventilation with positive end-expiratory pressure, heart failure with left ventricular assist devices, cardiac tamponade, and unilateral diaphragmatic paralysis. The primary driving force for these shunts is a reduction in the compliance of the pulmonary bed or right ventricle; right atrial pressure is usually elevated and pulmonary hypertension is frequently present. Significant shunting and hypoxemia are unusual in the absence of these diseases. We encountered a patient with normal pulmonary pressures, severe hypoxemia, pulmonary disease, and intracardiac shunting across a PFO in whom it was difficult to determine how great a role intracardiac shunting was playing in his hypoxemia. To assess this, we performed percutaneous balloon catheter occlusion of the PFO, using transthoracic echocardiography with contrast to confirm closure of the PFO. Therapeutic balloon occlusion has been reported in severe hypoxemia due to shunting across a PFO in a patient with RV infarction. Our case is unique, however, in two respects. First, this patient had normal right-sided cardiac pressures and normal RV function and, thus, no obvious driving force for a significant right-to-left shunt. Second, transthoracic echocardiography with contrast was used before and after balloon inflation to confirm closure of the PFO. This technique helped to answer the important clinical question of whether surgical closure of the PFO in this patient with both lung disease and intracardiac shunting would significantly improve his oxygenation.
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PMID:Percutaneous balloon catheter closure of a patent foramen ovale in a patient with pulmonary disease, profound hypoxemia, and normal right heart pressures. 906 23


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