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

Congenital aortic stenosis accounts for about 5% of cardiac malformations recognized in childhood. It belongs to the category of acyanotic congenital heart disease. These lesions produce a load on the heart because of left ventricular outflow tract obstruction. Severe aortic stenosis in the newborn period (critical aortic stenosis) presents with signs of left sided heart failure (pulmonary edema, poor perfusion), right sided heart failure (hepatomegaly, peripheral edema) and may progress rapidly to total circulatory collapse. We present a case of an infant with critical aortic stenosis presenting with cyanosis, who was entirely dependent on ductal patency for systemic output. When oxygen was given, the ductus started to close, with a worsening of the left sided output and subsequent acidosis. With the right to left shunt across the ductus, the baby was cyanotic and dependent on prostaglandin to keep the ductus open. There was minimal flow across the aortic valve because of the stenosis and extremely poor left ventricular function prior to surgery. After relief of the aortic valvular obstruction, there was finally good antegrade flow across the aortic valve, terminating cyanosis.
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PMID:One day old infant with acyanotic congenital heart disease: critical aortic stenosis. 1056 81

It is sometimes necessary for the practitioner to transfuse the ruminant with whole blood or plasma. These techniques are often difficult to perform in practice, are time-consuming, expensive, and stressful to the animal. Acute loss of 20% to 25% of the blood volume will result in marked clinical signs of anemia, including tachycardia and maniacal behavior. The PCV is only a useful tool with which to monitor acute blood loss after intravascular equilibration with other fluid compartments has occurred. An acutely developing PCV of 15% or less may require transfusion. Chronic anemia with PCV of 7% to 12% can be tolerated without transfusion if the animal is not stressed and no further decline in erythrocyte mass occurs. Seventy-five percent of transfused bovine erythrocytes are destroyed within 48 hours of transfusion. A transfusion rate of 10 to 20 mL/kg recipient weight is necessary to result in any appreciable increase in PCV. A nonpregnant donor can contribute 10 to 15 mL of blood/kg body weight at 2- to 4-week intervals. Sodium citrate is an effective anticoagulant, but acid citrate dextrose should be used if blood is to be stored for more than a few hours. Blood should not be stored more than 2 weeks prior to administration. Heparin is an unsuitable anticoagulant because the quantity of heparin required for clot-free blood collection will lead to coagulation defects in the recipient. Blood cross-matching is only rarely performed in the ruminant. In field situations, it is advisable to inject 200 mL of donor blood into the adult recipient and wait 10 minutes. If no reaction occurs, the rest of the blood can probably be safely administered as long as volume overload problems do not develop. Adverse reactions are most commonly seen in very young animals or pregnant cattle. Signs of blood or plasma transfusion reaction include hiccoughing, tachycardia, tachypnea, sweating, muscle tremors, pruritus, salivation, cough, dyspnea, fever, lacrimation, hematuria, hemoglobinuria, collapse, apnea, and opisthotonos. Intravenous epinephrine HCl 1:1000 can be administered (0.2 to 0.5 mL) intravenously or (4 to 5 mL) intramuscularly (preferable) if clinical signs are severe. Pretreatment with antipyretics and slowing the administration rate may decrease the febrile response. Blood or plasma administered too rapidly will also result in signs of cardiovascular overload, acute heart failure, and pulmonary hypertension and edema. Furosemide and slower administration of blood or plasma should alleviate this problem. Administration rates have been suggested starting from 10 mL/kg/hr; faster rates may be necessary in peracute hemorrhage. Plasma should be administered when failure of absorption of passive maternal antibody has occurred or when protein-loosing enteropathy or nephropathy results in a total protein of less than 3 g/dL or less than 1.5 g albumin/dL. Plasma can be stored at household freezer temperatures (-15 to -20 degrees C) for a year; coagulation factors will be destroyed after 2 to 4 months when stored in this manner. To maintain viability of coagulation factors, plasma must be stored at -80 degrees C for less than 12 months. When administering plasma, a blood donor set with a built-in filter should always be used. When bovine plasma is thawed, precipitants form in the plasma and infusion of these microaggregates may result in fatal reactions in the recipient.
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PMID:Use of blood and blood products. 1057 16

A 75-year-old man with a recent history of pulmonary embolism, presented with collapse followed by a gran mal seizure and right-sided non-pulsatile proptosis. On recovery, he had diplopia on lateral and upward gaze and signs of congestive cardiac failure. Further pulmonary embolism was proven by lung scintigraphy. Computed tomography of his orbits confirmed a contrast-enhancing space-occupying lesion of the medial wall of the right orbit, with no intracranial abnormality. The patient was investigated for metastatic tumour as a possible cause of the space-occupying lesion and the unprovoked thromboembolic event, but no evidence of malignancy was found. The orbital lesion was not biopsied because of the risk of bleeding from anticoagulation. Three weeks later, the patient represented with recurrent cardiac failure, proptosis, and diplopia. A transorbital ultrasound confirmed an encapsulated, well-defined vascular lesion, with typical appearances and Doppler flow characteristics of a cavernous haemangioma. Diuretic therapy abolished the proptosis and diplopia in tandem with relief of the cardiac failure. This is the first description of recurrent proptosis with diplopia due to recurrent congestive expansion of an orbital cavernous haemangioma.
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PMID:Recurrent proptotic diplopia due to congestive expansion of cavernous haemangioma with relapsing right-sided cardiac failure. 1062 2

The study of sleep, which initially focused on the neurophysiological mechanisms and cardiorespiratory function during the night, has shown the presence of sleep-related breathing disorders that epidemiological, pathophysiological and clinical data have indicated to be associated with increased cardiovascular morbidity and mortality: the obstructive sleep apnea syndrome (OSAS) and the central sleep apnea syndrome (CSAS). OSAS is a condition characterized by repetitive respiratory pauses due to the pharynx wall collapse, with a subsequent obstruction to the airflow. The hemodynamic consequences due to the markedly increased negative intrathoracic pressure (induced by the respiratory muscle effort towards the closed upper airways), the progressive hypercapnic hypoxemia and the arousal terminating the apneas, are the pathophysiological keys of the cardiovascular effects of OSAS and may explain the association between OSAS and the documented increase of cardiovascular morbidity and mortality. CSAS is a breathing disorder characterized by recurrent episodes of central hypopneas or apneas and hyperventilation which, is the classical form described by Cheyne and Stokes, show a crescendo-decrescendo pattern of respiration. Pathophysiological and epidemiological data clearly indicate the link between CSAS and heart failure, also showing a correlation between respiratory disorders and the severity of hemodynamic impairment. However, other mechanisms are involved in the genesis of CSAS in explaining the variable presence of CSAS independent of cardiac function and, more importantly, the impact of CSAS on poor prognosis in heart failure. In conclusion, the data available indicate the need to include screening for sleep-related breathing disorders in the evaluation of cardiac patients who are at risk for OSAS and, particularly, in patients with heart failure, who could really benefit from treatment of the respiratory disorder.
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PMID:[The assessment of breathing during sleep: a curiosity or clinical necessity?]. 1083 29

Two patients had percutaneous cardiopulmonary support (PCPS) used as a bridge to emergency surgery. A 66-year-old man admitted with profound cardiogenic shock underwent direct stenting under PCPS with the diagnosis of acute myocardial infarction of the left main trunk, with the intention of performing revascularization as soon as possible. Subsequently, double coronary artery bypass grafting was successfully accomplished. A 69-year-old woman, admitted with acute heart failure due to critical aortic stenosis, manifested cardiogenic shock while undergoing catheterization. PCPS was immediately instituted until the acute deterioration of her hemodynamic state could be reversed, and was continued uneventfully till aortic valve replacement was performed. These results suggest that the current PCPS system is an effective response to acute circulatory collapse and will contributed to the improved survival of patients.
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PMID:Percutaneous cardiopulmonary support as a bridge to emergency operation--two surviving cases. 1092 83

This overview discusses pathogenesis, clinical presentation, prognostic implications and therapy of central sleep apnea with special reference to Cheyne-Stokes-Respiration or periodic breathing. In contrast to obstructive sleep apnea due to upper airway collapse during sleep, central sleep apnea (CSA) is mainly due to an instability of the breathing control system. Causes of central sleep apnea include alveolar hypoventilation disorders, heart failure, neurologic and autonomic disorders and idiopathic forms of CSA. Patients with idiopathic CSA often complain of insomnia and awakening during sleep but may also suffer from daytime sleepiness. Cheyne-Stokes-Respiration or peridic breathing is often associated with heart failure and neurological disorders especially those involving the brainstem. In heart failure periodic breathing has enormous prognostic implications. Treatment options for central sleep apnea are oxygen supplementation, medical therapy (i.e. acetazolamide) and CPAP. For patients with central sleep apnoea associated with alveolar hypoventilation nasal ventilation is treatment of choice. Newer nasal ventilation techniques (BiPAP, AutoSetCS) are under investigation for heart failure patients with Cheyne-Stokes-Respiration.
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PMID:[Central sleep apnea syndrome and Cheyne-Stokes respiration]. 1095 54

A left ventricular assist device (LVAD) is an effective method to rescue severe heart failure. Although some require a biventricular assist, the control method for the biventricular assist device (BVAD) with a rotary pump is rarely shown. The objective of this study was to investigate the strategy for controlling BVAD with rotary pumps by in vivo studies. Using 5 piglets, we set a BVAD through a left thoracotomy and made global ischemia for 30 min by clamping the base of the ascending aorta. After unclamping, the analysis of pumping performance acted for 6 h reperfusion. We set the target flow of the LVAD and set the right ventricular assist device (RVAD) speed limit as less than when the atrial collapse occurs. To detect the ventricular collapse without any specific sensor, we calculated the index of current amplitude from motor current waveform and simultaneous mean current value. In all cases, over 6 h of observation was performed, and the RVAD was weaned almost automatically.
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PMID:Control strategy for biventricular assistance with mixed-flow pumps. 1097 Dec 43

The estimation of right atrial pressure is often needed for the diagnosis, management and monitoring of various pathologic hemodynamic conditions and plays a significant role in patients with chronic heart failure. In the past decade several attempts have been made to non-invasively estimate right atrial pressure, and echocardiography has always been considered the most reliable tool. Morphologic parameters such as respiratory motion of the inferior vena cava, its respiratory diameters and percent collapse (caval index), left hepatic vein diameter or right atrial dimension (areas, volumes) were initially studied. More recently, functional data such as left hepatic or tricuspid flow variables have been considered. Some of these indexes, however, offer only semiquantitative measures of right atrial pressure, and have failed to demonstrate any prognostic value. Others, although highly sensitive and specific, are useful only in selected groups of patients because of technical or clinical limitations. In recent years, attention has focused on Doppler diastolic tricuspid flow as a means of predicting mean right atrial pressure. Analyzing the Doppler tricuspid velocity profile and mean right atrial pressure (Swan-Ganz catheter) simultaneously recorded in patients with severe left ventricular systolic dysfunction and chronic heart failure, acceleration rate of early filling emerged as the strongest independent predictor of right atrial pressure both in patients in sinus rhythm and in those with atrial fibrillation (r = 0.98), irrespective of whether the recordings are at baseline or after acute loading manipulations.
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PMID:[Non-invasive evaluation of the hemodynamic profile in patients with heart failure: estimation of right atrial pressure]. 1106 14

The fatal circulatory derangements often observed when resuscitating victims of accidental hypothermia by rewarming are recognized as a falling cardiac output and a sudden drop in blood pressure, termed "rewarming shock". The real cause of this rewarming shock, or rewarming collapse, is, so far, unknown. This review presents current information exploring different aspects of the compromised circulatory function during hypothermia and especially after rewarming and supports the hypothesis that posthypothermic circulatory instability may be caused by cardiac insufficiency and alteration of the peripheral vascular bed. Cellular calcium overload, disturbed calcium homeostasis, changes in myocardial myofilament responsiveness to intracellular calcium as well as impaired high energy phosphate homeostasis could all be proposed as important factors leading to the changes observed in the hypothermic heart. Together with alteration of capillary function, increased capillary leakage of plasma protein, changes in intra- and extravascular volume-homeostasis and alteration of autonomous vascular control they all contribute to a maintained low cardiac output during and after rewarming which is associated with a fatal outcome.
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PMID:Rewarming from hypothermia. Newer aspects on the pathophysiology of rewarming shock. 1120 78

The protective effects of a new, selective, plant-derived platelet-activating factor (PAF) antagonist, yangambin, on the cardiovascular alterations and mortality due to endotoxic shock were investigated in anaesthetized rats. We also studied the involvement of PAF in the induction of the vascular and cardiac hyporesponsiveness to adrenergic stimulation observed during endotoxaemia. The animals were sensitized to the lethal effects of Escherichia coli lipopolysaccharide (LPS) with D(+)-galactosamine (50 mg/kg, i.v.) 15 min before LPS injection. LPS (3 mg/kg, i.v.) induced a progressive and marked decrease in mean arterial blood pressure from 85+/-4 to 30+/-3 mmHg and a reduction of cardiac output (CO) from 180+/-7 to 37+/-3 ml/min (120 min) accompanied by a maintenance of systemic vascular resistance, suggesting that cardiovascular collapse resulted mainly from myocardial depression. The maximum pressor responses to noradrenaline (0.3-3.0 microg/kg, i.v.) fell from 72+/-9 (control) to 5+/-1 mmHg (LPS) while the CO responses decreased from 81+/-5 to 8+/-3 ml/min. Pre-treatment with yangambin (30 mg/kg, i.v.) or with WEB 2086 (5 mg/kg, i.v.), a reference PAF receptor antagonist, completely prevented the LPS-induced cardiovascular collapse and abolished the sharp reductions of the arterial blood pressure and CO responses to noradrenaline observed during endotoxaemia. Post-treatment with yangambin 90 min after LPS administration did not reverse the arterial hypotension, cardiac failure or cardiovascular hyporesponsiveness to catecholamines. Finally, the acute (150 min) survival rates of endotoxic shock increased from 0% (LPS group) to 100% in the groups pretreated with either yangambin or WEB 2086. The long-term (7-day) survival also increased from 0% (LPS group) to 85% (yangambin pre-treatment group). In conclusion, these data suggest a role for PAF in the pathogenesis of endotoxin-induced vascular and cardiac hyporesponsiveness to catecholamines and confirm its involvement in the complex cascade of multiple mediators released during endotoxic/septic shock. Yangambin proved to be an effective pharmacological agent against cardiovascular collapse and mortality in endotoxin shock.
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PMID:Protective effects of yangambin on cardiovascular hyporeactivity to catecholamines in rats with endotoxin-induced shock. 1128 40


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