Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

We describe an 8-day-old baby girl presenting a fatal infantile form of hypertrophic obstructive cardiomyopathy, associated with an A8296G mutation in the mitochondrial tRNA(Lys) gene. She was born from a healthy unrelated couple, and was the first infant of dizygotic twins. Soon after birth, she was noted to have tachypnea and generalized hypotonia. She had high levels of lactate and pyruvate, and was diagnosed as having hypertrophic cardiomyopathy using echocardiography. She died by cardiac failure. Mitochondrial DNA analysis was performed by sequencing after PCR-subcloning methods, and the percentage of mutation was measured using PCR-RFLP methods. In various tissues obtained at autopsy, analysis showed a heteroplasmic population of A8296G mutation in the mitochondrial tRNA(Lys) gene in all the tissues examined. Maternal inheritance was demonstrated in the family members. Our data demonstrated that an A8296G mutation in the mitochondrial tRNA(Lys) gene showed clinical heterogeneity from a milder form previously reported as mitochondrial diabetes mellitus, to a more severe form as hypertrophic obstructive cardiomyopathy, according to the spatial distribution of this mutation. Hum Mutat 15:382, 2000.
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PMID:Fatal hypertrophic cardiomyopathy associated with an A8296G mutation in the mitochondrial tRNA(Lys) gene. 1073 88

This report describes a 14-year-old girl with fulminant myocarditis who was successfully treated with a percutaneous cardiopulmonary support (PCPS). She developed progressive cardiac failure after a 3-week history of progressive fatigue, fever, tachypnea, and dyspnea requiring inotropic support, mechanical ventilation, and intra-aortic balloon pumping. Her condition continued to deteriorate, and she was cannulated for PCPS using a right femoral artery/femoral vein approach, which resulted in rapid improvement and hemodynamic stabilization. This case documents that circulatory support with PCPS is effective for treating children with fulminant myocarditis.
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PMID:Rescue of a child with fulminant myocarditis using percutaneous cardiopulmonary support. 1075 88

Congestive heart failure describes a syndrome with complex and variable symptoms and signs, including dyspnea, increased fatigability, tachypnea, tachycardia, pulmonary rales, and peripheral edema. Although this syndrome usually is associated with low cardiac output, it may occur in a number of so-called high output states, when the cardiac output is normal or greater than normal. A high output state may occur in chronic severe anemia, large arteriovenous fistula or multiple small arteriovenous shunts as in Paget's bone disease, some forms of severe hepatic or renal disorders, and acutely in septic shock. The syndrome of systemic congestion in a high output state is traditionally referred to as high output heart failure. However, the term is a misnomer because the heart in these conditions is normal, capable of generating very high cardiac output. The underlying problem in high output failure is a decrease in the systemic vascular resistance that threatens the arterial blood pressure and causes activation of neurohormones, resulting in an increase in salt and water retention by the kidney. Many of the high output states are curable conditions, and because they are associated with decreased peripheral vascular resistance, the use of vasodilator therapy for treatment of congestion may aggravate the problem. There are other clinically important issues in high output failure that have received little attention in the current medical literature. This article reviews the available data on high output cardiac failure with particular emphasis on the underlying mechanisms and treatment.
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PMID:High Output Cardiac Failure. 1124 61

In its simplest and most succinct definition, heart failure can be defined as an inability of the heart to meet the metabolic demands of the body. Despite the diverse etiologies of heart failure in the pediatric population, the presentation of heart failure represents a common constellation of symptoms, signs, and physical findings. In infants, an inability to maintain growth either secondary to decreased nutritional intake or an increased catabolic state is a hallmark of heart failure. Infants exhibit increased sympathetic tone with excessive diaphoresis and increased heart rate. Physical findings in the infants with congestive heart failure (CHF) include increased work of breathing, tachypnea and hepatomegaly. In older children, in contrast, new onset heart failure may be less overtly symptomatic. Malaise, decrease in the level of daily activity, and weight loss may be present. Symptoms of abdominal pain and nausea and anorexia can be present and sometimes divert attention from the real etiology. Physical findings include rales and peripheral edema. If there is hepatomegaly, there will likely be hepatic tenderness as well. A gallop rhythm and tachycardia are commonly present. The long-term treatment of CHF in children includes digoxin, diuretics and afterload reduction with angiotensin-converting enzyme (ACE) inhibitors. Digoxin decreases sympathetic tone and improves growth in infants. Diuretics should be used to relieve symptoms but may not be necessary in all children. ACE inhibitors are increasingly valuable in maintaining cardiac function long term. New uses of medications include the addition of spironalactone (Aldactone, G. D. Searle & Co., Chicago, IL) which, in adults, has been shown to significantly decrease both the death rate from CHF and the need for hospitalization. Beta-Blockers have been used in children in limited studies and may have a role in the treatment of patients with idiopathic dilated cardiomyopathy. Surgical treatment, such as partial vectriculectomy, has shown short-term benefit and has been used sparingly in infants.
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PMID:Treatment of heart failure in infants and children. 1172 82

A 52-year-old female suspected of hypercoagulability underwent modified radical hysterectomy and left oophorectomy for uterus cancer and left giant ovarian tumor under general combined with epidural anesthesia. On the day after the operation, the patient complained of dyspnea and developed tachypnea, a low Spo2, and hypotension after the intermittent external pneumatic compression of the legs. Echocardiography showed acute right cardiac failure and pulmonary angiography revealed massive pulmonary thromboembolism. The patient fell into shock with severe hypotension and unconsciousness during the catheter fragmentation and aspiration therapy for pulmonary thrombi. Bolus intravenous injection of monteplase 1.6 million units, a mutant of tissue plasminogen activator with a longer half-life, rapidly improved the shock status and stabilized the hemodynamic condition. Monteplase would be useful for life-threatening pulmonary thromboembolism although the risk of hemorrhagic complication remains.
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PMID:[A case of successful thrombolysis by recombinant tissue plasminogen activator for postoperative pulmonary thromboembolism]. 1188 94

In this prospective study 37 children (ranging 2 months-15 years) with acute pneumonia were evaluated by Doppler echocardiography for the presence of pulmonary hypertension (PH). The goal of this study was to determine the frequency of PH in children with acute pneumonia because the diagnosis of PH influenced the treatment of pneumonia in these patients. The patients who had more than 35 mmHg of systolic pulmonary arterial pressure were considered to have PH. In our study PH was found in 15 (40.5%) of 37 patients. We did not find any significant difference for the parameters including the age, weight, height, clinical symptoms and signs (fever, cough, dyspnea, tachycardia and tachypnea etc.), and laboratory findings such as hemoglobin, PCO2, HCO3 and PO2 between the patients with and without PH (p>0.05). However, there was a significant difference in cyanosis, cardiac failure, blood pH level and O2 saturation measured by pulse oximetry between the patients with and without PH (p<0.05).
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PMID:Doppler echocardiographic evaluation of pulmonary artery pressure in children with acute pneumonia. 1189 Feb 20

The changes in breathing pattern and lung mechanics in response to incremental exercise were compared in 14 subjects with chronic heart failure and 15 normal subjects. In chronic heart failure subjects, exercise hyperpnea was achieved by increasing breathing frequency more than tidal volume. The rate of increase in breathing frequency with carbon dioxide output was inversely correlated (r = -0.61, P < 0.05) with dynamic lung compliance measured at rest, but not with static lung compliance either at rest or at maximum exercise. Although decrease in expiratory flow reserve near functional residual capacity in chronic heart failure occurred earlier with exercise than in the normal subjects (P < 0.01), it was not correlated with changes in breathing pattern or occurrence of tachypnea. Tachypnea was achieved in chronic heart failure subjects with an increase in duty cycle because of a greater than normal decrease in expiratory time with exercise. We conclude that in chronic heart failure preexisting increase in lung stiffness plays a significant role in causing tachypnea during exercise. The results of the present study do not support the hypothesis that dynamic compression of the airways downstream from the flow-limiting segment occurring during exercise contributes to hyperpnea.
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PMID:Exercise hyperpnea in chronic heart failure: relationships to lung stiffness and expiratory flow limitation. 1189 4

Peripartum cardiomyopathy (PPCM) is rare cardiac complication afflicting women during pregnancy or until 5 months post partum with the typical signs of acute cardiac failure. PPCM is similar to dilated cardiomyopathy (DCM) in terms of symptoms, histopathology and treatment but is characterized by a better outcome with a high rate of spontaneous normalization of left-ventricular size and function. The understanding of the etiology is limited. However, viral myocarditis and autoimmune factors might be involved in the development of PPCM. Clinically, PPCM shows pulmonary symptoms such as dyspnea, tachypnea and coughing. The diagnosis is finally established by echocardiography. It has to be assumed that PPCM is often undetected or misdiagnosed because of the low incidence, the unspecific symptoms and the fact that other pregnancy-related factors have similar clinical appearance. The treatment is also unspecific and similar to DCM and acute cardiac failure. The severity of the disease requires an interdisciplinary approach in a perinatal center with consequent follow-up of the patients for risk stratification including echocardiography.
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PMID:[Peripartum cardiomyopathy-the (un)known obstetricalcardiologic emergency situation]. 1457 44

Noncardiogenic pulmonary edema, and, to a lesser extent, acute respiratory distress syndrome (ARDS), are common clinical manifestations of drug-induced lung diseases. Clinical features and radiographic appearances are generally indistinguishable from other causes of pulmonary edema and ARDS. Typical manifestations include dyspnea, chest discomfort, tachypnea, and hypoxemia. Chest radiographs commonly reveal interstitial and alveolar filling infiltrates. Unlike pulmonary edema that is due to congestive heart failure, cardiomegaly and pulmonary vascular redistribution are generally absent in cases that are drug-related. Rare cases of drug-induced myocarditis with heart failure and pulmonary edema have been described. Results from laboratory evaluation and respiratory function tests are nonspecific.
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PMID:Drug-induced pulmonary edema and acute respiratory distress syndrome. 1506 1


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