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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We describe a patient who presented with acute massive pulmonary edema, clinically and on chest roentgenogram. Two hours later the patient became hypotensive and was found to have a low pulmonary capillary wedge pressure (PCWP). The blood pressure returned to normal after administration of fluids. Acute pulmonary edema develops if PCWP rises higher than 25 to 30 mm Hg. In our patient, the elevated PCWP fell to low normal within two hours, when chest roentgenogram and clinical examination still suggested severe pulmonary edema. A phase lag existed between lowering of the pulmonary capillary wedge pressure and clearing of fluid from the alveolar and interstitial spaces in the lungs. At least three different pathogenetic mechanisms in patients with coronary artery disease can produce this phase lag. Transient global ischemia of the left ventricle was thought to be the responsible mechanism in our patient.
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PMID:Cardiac-pulmonary edema and low pulmonary capillary wedge pressure. 50 73

Induction of anaesthesia with ketamine 1.5 mg/kg i.v. in a patient with coronary artery disease caused an increase in mean pulmonary artery pressure from 27 to 65 mmHg, a threefold rise in pulmonary vascular resistance and an increase of the left ventricular filling pressure from 18 to 48 mmHg which was associated with arterial hypoxaemia due to pulmonary edema. Fentanyl (0.01 mg/kg i.v.) promptly reversed the systemic and pulmonary vascular effects of ketamine.
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PMID:[Pulmonary hypertension and pulmonary edema caused by intravenous ketamine (author's transl)]. 71 52

Epidemiologic investigations have provided a portrait of the potential candidate for coronary heart disease. This is important because studies of the evolution of coronary disease in the general population reveal that it is a common disease that frequently attacks without warning, can be silent in its most dangerous form and can present with sudden death as the first symptom. Progress in identifyin- persons in jeopardy and the factors needing correction makes it theoretically possible to interrupt the chain of factors that eventuate in this disease. Coronary disease does not really begin with crushing chest pain, pulmonary edema, shock, angina or ventricular fibrillation, but rather with more subtle signs like a poor coronary risk profile. The risk factors can be treated quantitatively as ingredients of a cardiovascular risk profile and their joint effect estimated. An efficient practicable set of variables for this purpose is a casual blood test for cholesterol and sugar, a blood pressure determination, an electrocardiogram and a cigarette smoking history. With this set of variables the risk of coronary heart diseases can be estimated over a 30-fold range and 10 percent of the asymptomatic population identified in whom 25 percent of the coronary disease, 40 percent of the occlusive peripheral arterial disease and 50 percent of the strokes and congestive heart failure will evolve. The periodic use of the electrocardiogram at rest and after exercise in persons with a poor risk profile can demonstrate persons with asymptomatic ischemic cardiomyopathy due to advanced coronary artery disease. Most cases of angina pectoris or myocardial infarction represent medical failures; the conditions should have been detected years earlier for preventive management. About 30 percent of patients with infraction will shortly experience new angina, have an annual death rate of 4 percent and a fourfold increased risk of sudden death. Reinfarction will occur at an annual rate of 6 percent, and half the recurrences will be fatal. Congestive heart failure must be expected at 10 times and strokes at 5 times the rate found in the general population. Although no major innovations are required to identify candidates for coronary disease and to estimate their risk, we have much to learn about motivating changes in behavior to control risk factors. Approaches to prevention of coronary heart disease include public health measures to alter the ecology in favor of cardiovascular health, preventive medicine directed at highly vulnerable candidates and hygienic measures initiated by an informed public in its own behalf.
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PMID:Some lessons in cardiovascular epidemiology from Framingham. 124 56

Surgery has become an accepted method of treatment for coronary artery disease and its complications. Revascularization results in significant improvement in symptoms for patients with angina pectoris. Occasionally, patients requiring surgery for angina pectoris will sustain reversible ischemic damage during operation; such patients can be successfully weaned from cardiopulmonary bypass with full recovery when intra-aortic balloon counterpulsation is used. Arrhythmias associated with ischemic damage to the myocardium also can be controlled when IABCP is used for physiologic assistance. Patients in cardiogenicshock of pulmonary edema after acute myocardial infarction have an ominous prognosis. When decompensation occurs, IABCP may be used to stabilize the patient and to allow study and corrective surgery if possible. The prognosis is better for patients with ventricular septal defect, although selected patients without a mechanical defect of the myocardium can be salvaged if the response to IABCP is favorable. Counterpulsation has also been shown to be useful in achieving pulsatile cardiopulmonary bypass and in assisting high-risk patients through operation. External pressure circulatory assist (EPCA) is less effective than IABCP in assisting the failing myocardium; however, the external device is noninvasive and may be a useful adjunct in situations where IABCP is not feasible.
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PMID:Mechanical circulatory assistance for the treatment of complications of coronary artery disease. 125 7

Over the span of two or three days in August, 1972, in two separate communities in eastern Massachusetts two men, one aged 39, the other 66, each without previous overt heart disease, were stung by wasps. Each went into shock rapidly after an interval of over a half-hour developed chest pain and, later, sequential electrocardiographic changes diagnostic of acute myocardial infarction. Each survived; each had normal electrocardiograms before the sting. Though preexistent coronary artery disease can be excluded in neither, the view is favored that acute myocardial infarction in each was caused by deficient coronary perfusion secondary to anaphylactic shock induced by the wasp stings. An intriguing case was just recently reported58 of a 62-year-old man with previous angina who developed pulmonary edema but no chest pain following wasp sting and went on to show rapidly reversed electrocardiographic changes attributable to subendocardial ischemia or infarction. In a sense, this sequence fills the gap as an intermediate phase between the normal and the two individuals described here who developed pain after anaphylactic shock, then proceeded, perhaps through this phase, to develop transmural infarction.
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PMID:Acute myocardial infarction following wasp sting. Report of two cases and critical survey of the literature. 125 36

To elucidate the clinical characteristics of pulmonary edema in unstable angina, 120 patients with unstable angina who admitted to the hospital within 6 hours after the onset of chest pain were studied. The criteria for the diagnosis of pulmonary edema included interstitial pulmonary edema and diffuse alveolar edema. Pulmonary edema was present in 24 patients. In these patients, the duration of chest pain was relatively longer, and the incidences of diabetes mellitus, emergency coronary revascularization and multiple-vessel coronary artery disease were higher than in those without pulmonary edema. In addition, in-hospital mortality rate in patients with pulmonary edema was higher than in those without it (21 vs 1%, p < 0.001), which is probably due to a large area of myocardial ischemia. For these patients, therefore, early diagnosis and appropriate therapy to save viable segments of the myocardium are mandatory.
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PMID:[Clinical characteristics of pulmonary edema in patients with unstable angina]. 134 24

Congestive heart failure (CHF) is typically associated with impaired left ventricular (LV) systolic performance. Few reports exist describing the long-term outcome in patients with CHF and normal LV systolic function. Fifty-two patients initially hospitalized with CHF and intact LV function (ejection fraction greater than or equal to 45%) were followed for 7 years. Mean age when initially identified was 71 +/- 11 years (range 36 to 96), and average LV ejection fraction was 61 +/- 11%. CHF was graded by a clinicoradiographic index, with a mean of 7.0 +/- 2.3 (range 3 to 12, 13 indicates worst CHF). A third heart sound was present in 19 patients (37%), and 17 (33%) had presented with acute pulmonary edema. Principal cardiovascular diagnoses were coronary artery disease in 27 (52%), hypertensive heart disease in 16 (31%) and restrictive cardiomyopathy in 7 (13%). At 7 years, cardiovascular mortality was 46% (24 of 52), and noncardiovascular mortality was 10% (5 of 52). Survival was not correlated with age, principal diagnosis, third heart sound, pulmonary edema at presentation, LV ejection fraction, or presence or degree of LV diastolic dysfunction. Cardiovascular morbidity, consisting of nonfatal recurrent CHF, myocardial infarction, unstable angina or other cardiovascular events occurred in 29% (15 of 52). Combined cardiovascular mortality and morbidity was 75% (39 of 52). In patients with CHF, intact LV systolic function does not confer the same favorable prognosis it defines in other clinical situations. For such patients, the risk of future cardiovascular events is high, a finding that should be considered when designing therapeutic strategies in this group.
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PMID:Long-term outcome in patients with congestive heart failure and intact systolic left ventricular performance. 157 93

The frequency, clinical characteristics, and outcome of patients admitted with heart failure to a district general hospital in North-West London serving a population of approximately 155,000 was assessed over a six-month period. The number of patients with heart failure was determined by both a prospective ward survey and a retrospective study of all patient records with diagnostic codes for heart failure or pulmonary oedema. During those six months, 2,877 patients were admitted to the medical and geriatric services of whom 140 (4.9%) had heart failure. Only 29 patients in heart failure were under the age of 65 years. In 86 patients the mode of presentation was acute pulmonary oedema. Fifty-two (37%) patients had an arrhythmia at the time of admission of whom 48 had atrial fibrillation. An electrocardiogram, a chest X-ray, and an echocardiogram were performed in 137, 136, and 81 patients respectively. The aetiology of heart failure was considered to be coronary artery disease (41%), valve disease (9%), hypertension (6%), cor pulmonale (4%), a dilated cardiomyopathy (1%), congenital heart disease (1%), thyrotoxicosis (1%), and unknown (36%). During the period of hospital stay 42 patients (30%) died; a further 20 patients (14%) died in a one-year follow-up. In a district general hospital heart failure is a common reason for admission and patients remain in hospital for a considerable time. Arrhythmias are commonly associated with heart failure. The prognosis is poor and the hospital mortality high. The management of heart failure is an important consideration in allocating hospital resources in a district general hospital.
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PMID:Heart failure in a district general hospital. 842 54

Pulmonary edema is a serious complication of heart failure, but often patients with chronic heart failure resist pulmonary edema despite elevated pulmonary venous pressures. This protection might be a result of decreased pulmonary microvascular permeability. Double-isotope scintigraphy with 113mindium-labeled transferrin and 99mtechnetium-labeled erythrocytes allows noninvasive estimation of pulmonary microvascular permeability; an index of transferrin accumulation is calculated that reflects microvascular permeability. Fourteen patients with severe chronic left ventricular dysfunction were compared with a control group of 15 patients with mild coronary artery disease. In the control group the transferrin accumulation index was 0.35 (range -0.3 to 1.0) x 10(-3)/min, and in patients with heart failure the index was 0.0 (range -1.0 to 0.7) x 10(-3)/min, which was significantly lower (p less than 0.01). The reduction in the transferrin accumulation index correlated weakly with the duration of heart failure (R = -0.5, p less than 0.02). These data indicate reduced protein efflux consistent with a decrease in pulmonary microvascular permeability in patients with severe chronic heart failure. Similar changes have been observed in severe mitral stenosis and may reflect a generalized adaptation to chronic pulmonary venous hypertension.
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PMID:Reduced pulmonary microvascular permeability in severe chronic left heart failure. 161 97

Clinical data on 10,451 high-dose (up to 0.84 mg/kg over 10 minutes) dipyridamole-echocardiography tests (DET) performed in 9,122 patients were prospectively collected from 33 echocardiographic laboratories, each contributing greater than 100 tests. All patients were studied for documented or suspected coronary artery disease (1,117 early [less than 18 days] after acute myocardial infarction and 293 had unstable angina). Significant side effects including major adverse reactions and minor but limiting side effects occurred in 113 patients (1.2%). Major adverse reactions occurred in 7 cases (0.07%). In 6 of these cases, adverse reactions were associated with echocardiographically assessed ischemia and included 1 prolonged cardiac asystole (complicated by acute myocardial infarction and coma, with death after 23 days), 1 short-lasting cardiac asystole, 2 myocardial infarctions, 1 pulmonary edema and 1 sustained ventricular tachycardia. In all 6 cases, the cardiologist-echocardiographer performing the study had a limited experience (less than 100 tests) with DET, and at off-line reading in 5 cases, the obvious echo-positivity preceded the onset of complications by 1 to 5 minutes. The only ischemia-independent major side effect was a short-lasting cardiac asystole that was reversed by aminophylline and atropine. Significant side effects associated with echocardiographically assessed ischemia occurred in 89 additional cases (21 with and 68 without concomitant echocardiographically assessed myocardial ischemia). The most frequent of these side effects was hypotension or bradycardia, or both, which occurred in 40 patients with negative and 6 with positive DET. In all cases, side effects promptly subsided after aminophylline. In 1,857 cases, the high dose was not given for echo-positivity before the eighth minute.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Safety of intravenous high-dose dipyridamole echocardiography. The Echo-Persantine International Cooperative Study Group. 162 16


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