Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The importance of recognizing symptomatic heart failure with preserved left ventricular (LV) systolic function has only recently been appreciated. To determine its frequency and identify clinical features that make the bedside diagnosis likely, 82 patients admitted for decompensated heart failure were classified into 2 groups based on their LV systolic performance, as defined by fractional shortening (FS): group I (n = 59), with impaired systolic function (fractional shortening less than 24%), and group II (n = 23) with preserved systolic function (fractional shortening greater than or equal to 24%). Mean fractional shortening was 15 +/- 5% and 39 +/- 1% for groups I and II, respectively. Female gender (p less than 0.05), obesity (p less than 0.01) and diastolic blood pressure greater than or equal to 105 mm Hg (p less than 0.05) predominated in group II. Jugular venous distention was identified more frequently in group I (p less than 0.05). No statistically significant difference between the 2 groups was noted among various demographic variables (age, duration of symptoms, history of hypertension, ischemic heart disease and heavy alcohol drinking) or physical findings (S3 gallop, edema, cardiomegaly, pulmonary congestion and pulmonary edema). Echocardiographic mean left ventricular dimension measured 6.6 +/- 1 versus 5.0 +/- 1 cm (p less than 0.01) and mean posterior wall thickness 1.1 +/- 0.3 versus 1.4 +/- 0.4 cm (p less than 0.01) in group I and II, respectively. The combination of diastolic blood pressure greater than or equal to 105 mm Hg and an absence of jugular venous distention had a high specificity and positive predictive value (100%) for identifying group II patients.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Bedside diagnosis of preserved versus impaired left ventricular systolic function in heart failure. 173 66

When patients present with suspected prosthetic valve dysfunction, investigation is usually instituted to delineate the site and cause thereof. Precordial cross-sectional echocardiography is often helpful in this respect, but in the patient with acute pulmonary edema, imaging may be impaired because of discomfort and respiratory distress. The information obtained may also be suboptimal as a result of concomitant obesity, chest wall deformity, and pulmonary disease. In addition, further difficulties may relate to the acoustic shadowing produced by the metallic portion of the valve and its sewing ring, especially with valves in the mitral position. In such patients, cardiac catheterization may cause further decompensation and is associated with a recognized increase in morbidity and mortality. Angiography does not accurately site regurgitant jets in relation to the prosthetic valve concerned and will not detect the presence of vegetations. Transesophageal echocardiography circumvents many of these imaging difficulties and we evaluated its use in five patients with prosthetic heart valves who presented acutely ill, in severe pulmonary edema and suspected prosthetic heart valve failure. In each case, the diagnosis of valve dysfunction was established, and precise information regarding the site and cause of the failure was obtained. No complications or deterioration in patient condition resulted from the procedure and the findings were confirmed at surgery performed within 24 hours in all five patients. Transesophageal echocardiography should be included in the assessment of acute prosthetic heart valve failure.
 ...
PMID:The value of transesophageal echocardiography in the investigation of acute prosthetic valve dysfunction. 239 17

Methods of clinico-instrumental investigation and biochemical monitoring (CPK and its membranous fraction) were employed for examination of 432 patients with acute myocardial infarction (AMI). Among them there were patients with an uncomplicated course of disease (19.4%), recurrences (13.7%) and AMI spreading (9%). Lung edema, a cardiogenic shock, ventricular fibrillation and complicated cardiac rhythm disorders were not detected on the 1st day of disease. Clinico-anamnestic data provided no opportunity for defining factors promoting AMI recurrences whereas AMI spreading frequently developed in patients with repeated AMI, suffering from essential hypertension, obesity and heart failure. Higher diastolic pressure in the pulmonary artery, an increase in the cardiac volume, a decrease in the ejection fraction and left ventricular stroke work--changes which were most pronounced in AMI spreading, were noted in patients with AMI lingering forms. Signs of disseminated intravascular blood coagulation were noted in the venous and arterial blood of patients with lingering AMI forms. A high blood enzyme level was shown to be accompanied by a low level of antibodies to LDH and CPK.
 ...
PMID:[Clinico-pathogenetic variants of protracted forms of acute myocardial infarct]. 361 39

Respiratory insufficiency is one of the most common and most serious complications of the postoperative period. Preexisting risk factors include cardiopulmonary disease, significant smoking history, obesity and advanced age. The risk of postoperative respiratory insufficiency is increased in emergency surgical procedures (particularly those related to trauma), procedures involving the chest or upper abdomen and procedures requiring prolonged anesthesia. Postoperatively, prolonged sedation or neuromuscular blockade, cardiovascular instability, respiratory problems and immobilization are important risk factors. Common clinical causes of respiratory insufficiency are atelectasis, aspiration, pulmonary edema and pulmonary embolism. Management strategies are directed at treatment of the cause of the insufficiency and restoration of pulmonary function. All surgical patients should be carefully assessed before surgery, monitored closely during and after the procedure, and aggressively treated to prevent or correct respiratory insufficiency.
 ...
PMID:Postoperative respiratory insufficiency. 773 49

The central autonomic network (CAN) is an integral component of an internal regulation system through which the brain controls visceromotor, neuroendocrine, pain, and behavioral responses essential for survival. It includes the insular cortex, amygdala, hypothalamus, periaqueductal gray matter, parabrachial complex, nucleus of the tractus solitarius, and ventrolateral medulla. Inputs to the CAN are multiple, including viscerosensory inputs relayed on the nucleus of the tractus solitarius and humoral inputs relayed through the circumventricular organs. The CAN controls preganglionic sympathetic and parasympathetic, neuroendocrine, respiratory, and sphincter motoneurons. The CAN is characterized by reciprocal interconnections, parallel organization, state-dependent activity, and neurochemical complexity. The insular cortex and amygdala mediate high-order autonomic control, and their involvement in seizures or stroke may produce severe cardiac arrhythmias and other autonomic manifestations. The paraventricular and other hypothalamic nuclei contain mixed neuronal populations that control specific subsets of preganglionic sympathetic and parasympathetic neurons. Hypothalamic autonomic disorders commonly produce hypothermia or hyperthermia. Hyperthermia and autonomic hyperactivity occur in patients with head trauma, hydrocephalus, neuroleptic malignant syndrome, and fatal familial insomnia. In the medulla, the nucleus of the tractus solitarius and ventrolateral medulla contain a network of respiratory, cardiovagal, and vasomotor neurons. Medullary autonomic disorders may cause orthostatic hypotension, paroxysmal hypertension, and sleep apnea. Neurologic catastrophes, such as subarachnoid hemorrhage, may produce cardiac arrhythmias, myocardial injury, hypertension, and pulmonary edema. Multiple system atrophy affects preganglionic autonomic, respiratory, and neuroendocrine outputs. The CAN may be critically involved in panic disorders, essential hypertension, obesity, and other medical conditions.
 ...
PMID:The central autonomic network: functional organization, dysfunction, and perspective. 841 66

A 44-year-old morbidly obese and hypertensive woman had been diagnosed with idiopathic cardiomyopathy seven years previously. She was referred for consideration for heart transplantation because of progression of symptoms to class IV. Massive obesity and pulmonary hypertension were strong relative contraindications to transplantation. During outpatient evaluation, the patient developed pulmonary edema, was hospitalized, and became intensive care unit-bound and immobile. Exercise radionuclide angiocardiography revealed left ventricular ejection fraction of 17%, and left ventricular end-diastolic volume of 408 mL. A reduction ventriculoplasty procedure was performed by resection of the lateral wall of the left ventricle. The patient did very well, and was discharged on postoperative day nine. Two weeks after the procedure, exercise radionuclide angiocardiography demonstrated left ventricular ejection fraction of 30% (76% increase) and left ventricular end-diastolic volume of 293 mL (28% decrease). The patient remains in stable New York Heart Association class II, now three months postprocedure. This initial positive experience in New England encourages-continued investigation of the reduction ventriculoplasty procedure, either as a bridge or as an alternative to heart transplantation in patients with dilated cardiomyopathy.
 ...
PMID:Reduction ventriculoplasty for the cardiomyopathic heart: a case report. 909 83

Sleep-related breathing disorders (SRBD) include several disorders gradually developing from simple and loud snoring through upper airway resistance syndrome and sleep apnoea up to the Pickwickian syndrome. They are manifestant as a respiratory distress and apnoeic episodes, desaturation of oxygen in the blood and interruption of sleep. These symptoms are demonstrated in a case of a patient with the Pickwickian syndrome. SRBD may result in severe secondary life-threatening cardiovascular complications (nocturnal arrhythmias, sudden cardiac death, stroke and pulmonary oedema). They may contribute also to the development of important disorders of public health such as hypertension, obesity, and traffic accidents resulting from hypersomnolence and fatigue. (Tab. 1, Fig. 3, Ref. 46.)
 ...
PMID:[Sleep-related breathing disorders--an interdisciplinary topic in undergraduate and postgraduate medical education]. 926 12

Pulmonary edema that follows upper airway obstruction may occur in a variety of clinical situations. The predominant mechanism is forced inspiration against a closed or occluded glottis, inducing large intrapleural and transpulmonary pressure gradients favoring the transudation of fluid from the pulmonary capillaries into the interstitium. Postanesthetic laryngospasm has been implicated as the most frequent cause of this syndrome in adults. Risk factors for development of postlaryngospasm pulmonary edema include difficult intubation; nasal, oral, or pharyngeal surgical site; and obesity with obstructive apnea. The syndrome is recognized by development of hypoxia shortly (1-90 min) after a laryngospasm. A chest radiograph will reveal a symmetric bilateral infiltrate with normal heart size. Cardiogenic pulmonary edema and aspiration must be ruled out. Treatment is directed at correction of hypoxia with supplemental oxygen and use of diuretics (furosemide). Occasionally patients may require intubation.
 ...
PMID:Pulmonary edema following postoperative laryngospasm: case reports and review of the literature. 948 72

The lungs are a delicate interface between the atmosphere and our bodies across which oxygen diffuses from the air we breathe to the blood which carries oxygen to the cells and mitochondria. In healthy lungs at sea level where there is a surfeit of oxygen, this process occurs easily, whereas, in lungs with disease it becomes a task which may not be fully successful and hypoxemia may ensue or worsen. At high altitude where the barometric pressure (Pb) and thus the supply of oxygen is lower, the job of getting oxygen to the blood, even in the healthy lung is more difficult, and in the diseased lung it may be impossible. This presentation will review the lungs' responses to high altitude, with emphasis on the abnormal. Both acute and chronic responses of patients with pre-existing lung disease will be reviewed. Pulmonary diseases encountered at high altitude in previously healthy people, such as high altitude pulmonary edema and chronic mountain sickness will be touched on only as they pertain to other patients. Pre-existing lung disease (with and without hypoxemia at sea level) such as obstructive lung diseases (asthma, COPD, emphysema), and restrictive lung diseases (sarcoid, asbestosis, interstitial pulmonary fibrosis) will be discussed in terms of gas exchange, lung mechanics, and treatment at high altitude. Disorders of ventilatory control; e.g., obesity-hypoventilation syndrome and sleep apnea, may present formidable problems, and guidelines for their treatment will be discussed. Infectious lung diseases; e.g., pneumonia, cystic fibrosis, and pulmonary vascular disorders such as chronic mountain sickness, primary pulmonary hypertension, and congenital absence of the pulmonary artery are important disorders that require special attention because of the accentuated hypoxic pulmonary vascular response encountered at high altitude. The purpose therefore, is to provide the medical practitioner with the insight into prevention, recognition, and treatment of pulmonary problems encountered specifically at high altitude, as well as guidance on how best to advise patients with lung disease who want to fly in airplanes and/or ascend to high altitude for work or pleasure.
 ...
PMID:Lung disease at high altitude. 1063 92

Recent qualms about the safety of aesthetic lipoplasty may be attributable more to support system flaws than to technical process deficiencies. The authors here focus on perfunctory patient monitoring when sedative or analgesic drugs are given, cavalier infiltration of mega-dose lidocaine, cursory intraoperative patient observation by team members with conflicting responsibilities, anesthesia providers unfamiliar with the unique surgical physiology of liposuction, hurried-discharge policies that virtually ignore the residual depressant effects of sedatives and analgesics, and compressive dressings that impair postoperative chest-wall expansion and venous return. Whereas pulmonary embolism remains the leading process cause of morbidity from liposuction, complications from austere resource allocation to dedicated patient monitoring should be largely preventable. Not all lipoplasties require an anesthesia provider but-when heavy sedation, mega-dose lidocaine, or both, are projected-a trained team member dedicated exclusively to patient safety and comfort should be a minimum patient care standard. The potential role of lidocaine cardiotoxicity in tumescent anesthesia is widely underappreciated and that of hypothermia goes mostly unrecognized. These, plus largely preventable or potentially correctable perioperative events such as pulmonary edema, fluid imbalance, or improperly administered sedative and analgesic drugs, demand upgrading and expansion of monitoring, resuscitative, and recuperative facilities in physician offices. In fact, ASPS guidelines urge that anesthesia services be engaged for dedicated patient care whenever "major" liposuction or conscious sedation is projected, because liposuction is neither as benign nor as simple a procedure as heretofore reputed. To assess objectively the operative and anesthetic risk of obesity, document body mass index for the preoperative record; morbid obesity (body mass index >/= 35.0), for instance, is a known risk multiplier for sedatives and analgesics. Other system issues such as the dynamic profile of high-dose lidocaine pharmacokinetics, the deportation of fat globules in the bloodstream, and the incidence of intraoperative hypothermia remain as unresolved topics for interdisciplinary, multi-institutional clinical research.
 ...
PMID:Perioperative management of cosmetic liposuction. 1125 1


1 2 3 4 Next >>