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)

Asthma bronchiale (a.b.) is defined as paroxysmal or permanent, partly or completely reversible dyspnoea due to a bronchospasm resulting from pathological hyperreactivity of the bronchial system. In the pathogenesis participate allergic, immuno-infiltrative and genetic factors, irritating substances (environment) and infectious. The allergic constituent acts via sensitization and allergization of the mast cell, to its degranulation with release of mediators (histamine, serotonin, leukotrienes, thromboxane, PAF) with subsequent bronchoconstriction and production of viscous mucus. As to adrenergic factors, a block of beta-adrenergic receptors and reduced adrenal function is involved. As to non-adrenergic factors an increased sensitivity of the parasympathetic--vagus is involved which conditions bronchoconstriction and hyperkrinia. From the clinical aspect extrinsic (atopic) and intrinsic (cryptogenic) asthma bronchiale can be differentiated. The former is encountered more frequently in childhood and adolescence, in subjects with a positive family-history, high IgE and positive skin tests and a known allergen. The latter type of a.b. is found in adolescence, in subjects with a negative family-history, with eosinophilia; it is conditioned by infection (e.g. chronic bronchitis), strain, cold and takes a dangerous course (aspirin). As to the course, attacks of a.b. are involved with a symptom-free interval (extrinsic a.) easily controlled by treatment. Then there is the chronic form with a variable course and the necessity of permanent treatment. Status asthmaticus is in recent years with increasing frequency the cause of death and thus calls for maximal treatment. It is the third most serious form of a.b. Assessment of arterial blood gases is very important as a check of treatment as well as from the prognostic aspect (cross-over intubation). From the differential diagnostic aspect we must consider the asthmoid component in chronic bronchitis, pulmonary embolism, left-sided cardiac failure, tracheal or bronchial compression by an aortal aneurysm, tumour. The differential diagnosis is not always easy.
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PMID:[Bronchial asthma. Pathogenesis and clinical aspects]. 145 62

So far propofol has only been used in clinical settings for sedation and induction of anaesthesia. This study describes several indications in preclinical and emergency events. All users were anaesthetists, so that experience of administration and dosage was extremely helpful. Since the drug met the expected criteria it is now regularly used for the sedation of ventilated patients during transport. The most important indications for preclinical induction of anesthesia with propofol are patients with isolated head injury and patients with respiratory insufficiency due to status asthmaticus resistant to therapy. After repeated unsuccessful attempts at therapeutic intervention with benzodiazepines and other antiepileptics we were able to interrupt status epilepticus in 11 patients by means of propofol, thereby preventing the patient from being intubated as a consequence of iatrogenic respiratory failure. However, emergency doctors must always be aware of the severe cardiocirculatory side effects of the drug, and must, hence, ensure that hypovolaemia or cardiac failure is excluded or corrected prior to propofol administration.
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PMID:[Propofol in emergency care--areas of application and initial experiences]. 781 Jan 46

We investigated the efficacy and the side effects of "high-dose isoproterenol continuous nebulization" for childhood status asthmaticus. Subjects were 34 children who were hospitalized and underwent the nebulization therapy. The 50 ml solution of 0.5% dl-isoproterenol was diluted in 500 ml of normal saline and nebulized through an ultrasound nebulizer. The period of continuous nebulization was 25.5 +/- 16.0 hours. The Wood's clinical score clearly decreased in 32 cases, the average score changing from 7.7 +/- 0.8 to 2.9 +/- 1.3. Heart rate was elevated significantly during the first 3 hours (156 +/- 25/min at the start of the nebulization, 180 +/- 20/min at 1 hour, 171 +/- 23 at 3 hours), and then it decreased gradually to 122 +/- 25/min at the cessation of the nebulization. Serum GOT, LDH, CPK, and potassium were elevated after the nebulization compared with the values before the treatment, though the changes were not statistically significant. CPK-MB fraction after the nebulization was higher than normal range in 12 of 13 subjects. Of 34 subjects, 11 (32%) complained nausea or vomited, 2 showed arrhythmia on ECG (ventricular premature conduction), 1 developed myocardiac infarction, and 1 developed possible heart failure, some of which might be attributable to the pharmacological side effects of isoproterenol nebulization. We conclude that "high-dose isoproterenol continuous nebulization" is an effective method for childhood status asthmaticus, but there is some risk of serious side effects. This method was originally developed as a method indicated for the case of respiratory failure or threatened respiratory failure following status asthmaticus, and we should not extend the indication of this method thoughness.
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PMID:[Isoproterenol continuous nebulization for childhood status asthmaticus. I. Efficacy and side effects of high-dose method]. 965 72

Conventional pharmacotherapy of severe asthma and status asthmaticus includes beta2-sympathomimetics, theophylline, corticosteroids and occasionally topical anticholinergics (ipratropium bromide). Since hypoxemia is the most severe phenomenon in status asthmaticus the administration of oxygen is mandatory. However, if the bronchodilating therapy fails and hypoxemia continues, usually respiratory failure develops due to progressive respiratory muscle failure. An increasing PaCO(2) and respiratory acidosis are indications for mechanical ventilatory support to unload the failing respiratory pump. Nowadays, there is increasing consensus that ventilatory support should be administered primarily as non-invasive ventilation (NIV) via a face mask1. However, in a significant number of patients with severe asthma NIV is either contraindicated or insufficient. In this case usually the patient must be endotracheally intubated and mechanically ventilated "invasively". Intubation and ventilation of patients with severe asthma or status asthmaticus is associated with a high incidence of complications compared to patients ventilated for other causes of respiratory failure2,3. Therefore the risks of invasive mechanical ventilation have to be weighted carefully to ongoing conservative therapy and NIV. Cardiopulmonary arrest and severe hypoxemia in spite of O2 supplement and NIV are absolute criteria for intubation and ventilation. Mostly deterioration in mental status and exhaustion are the clinical findings leading to mechanical ventilation. Decision is guided rather by the course of the deterioration (how fast the patient's condition is worsening) than by pathological values alone. An increased PaCO(2) with moderate respiratory acidosis alone is not per se an indication for mechanical ventilation. However, a continuously rising PaCO(2) or the development of a severe metabolic acidosis after 1 hour of NIV is a strong argument for invasive mechanical ventilation. Other criteria are evidence of cardiac failure with fall in pulse volume and dysrhythmias, pneumomediastinum or pneumothorax (which has to be drained before mechanical ventilation!).
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PMID:Ventilating the patient with severe asthma: nonconventional therapy. 1276 62

In critically ill patients, adequate sedation increases comfort, minimizes stress response and facilitates diagnostic and therapeutic procedures. Propofol (2-, 6-diisopropylphenol) is an intravenous sedative-hypnotic agent popular for sedation in the Intensive Care Unit. The favorable propofol pharmacokinetic, characterized by a three compartment linear model, allows rapid onset and short duration of action. The emergence time from sedation with propofol varies with the depth and the duration of sedation and the patient's bodyweight. Propofol causes hypotension, particularly in volume depleted patients, decreases cerebral oxygen consumption, reduces intracranial pressure and has potent anti-convulsant properties. It is a potent antioxidant, has anti-inflammatory properties and is a bronchodilator. As a consequence of these properties, propofol is being increasingly used in the management of traumatic head injury, status epilepticus, delirium tremens, status asthmaticus and in septic patients. Prolonged use (>48 h) of high doses of propofol (>66 mcg/Kg/min) has been associated with lactic acidosis, bradycardia, and lipidemia in pediatric patients. A rare complication firstly reported in pediatrics patients and also observed in adults is known as "propofol syndrome" characterized by myocardial failure, metabolic acidosis and rhabdomiolysis. Hyperkalemia and renal failure have also been associated with this syndrome. Hypertriglyceridemia and pancreatitis are uncommon complications. A large number of trials have compared the use of propofol with midazolam. Sedation with propofol is associated with adequate sedation in ICU patients, shorter weaning time and earlier tracheal extubation compared to midazolam, but not before ICU discharge.
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PMID:Sedation in PACU: the role of propofol. 1630 51

We encountered a 2-year-old child with life-threatening hypercapnia, with a PaCO(2) of 238 mm Hg and severe respiratory and metabolic acidosis, due to status asthmaticus that was refractory to steroid and bronchodilator therapy. Suspecting ventilatory failure and excessive ventilation-induced obstructive shock, we started respiratory physiotherapy in synchrony with her respiration, to facilitate exhalation from her over-inflated lungs. Isoflurane inhalation was commenced in preparation for extracorporeal circulation, to reduce the hypercapnia. The combination of respiratory physiotherapy and isoflurane inhalation resulted in a rapid decrease in ventilatory resistance and PaCO(2) levels within a few minutes, with recovery of consciousness within 60 min. Isoflurane inhalation was gradually discontinued and steroid and aminophylline therapy were commenced. The patient recovered completely without any recurrence of her bronchospasm and without any residual neurological deficits. In our patient with a severe asthmatic attack, decreased exhalation secondary to asthma and overventilation during artificial ventilation resulted in overinflation of the lungs, which in turn led to cerebral edema and obstructive cardiac failure. The favorable outcome in this case was due to the short duration of hypercapnia. Hence, we conclude that the duration of hypercapnia is an important determinant of the morbidity and mortality of status asthmaticus-induced severe hypercapnia.
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PMID:Treatment of life-threatening hypercapnia with isoflurane in an infant with status asthmaticus. 2431 Aug 52

We report the case of a patient with cardiovascular and respiratory failure due to severe anaphylaxis requiring multiple extracorporeal membrane oxygenation (ECMO) cannulation strategies to provide adequate oxygen delivery and ventilatory support during a period of rapid physiological change. ECMO provides partial or complete support of oxygenation-ventilation and circulation. The choice of which ECMO modality to use is governed by anatomical (vessel size, cardiovascular anatomy and previous surgeries) and physiological (respiratory and/or cardiac failure) factors. The urgency with which ECMO needs to be implemented (emergency cardiopulmonary resuscitation (eCPR), urgent, elective) and the institutional experience will also influence the type of ECMO provided. Here we describe a 12-year-old schoolgirl who, having been resuscitated with peripheral veno-venous (VV) ECMO for severe hypoxemia due to status asthmaticus in the setting of acute anaphylaxis, required escalation to peripheral veno-arterial (VA) ECMO for precipitous cardiovascular deterioration. Insufficient oxygen delivery for adequate cellular metabolic function and possible cerebral hypoxia due to significant differential hypoxia necessitated ECMO modification. After six days of central (transthoracic) VA ECMO support and 21 days of intensive care unit (ICU) care, she made a complete recovery with no neurological sequelae. The use of ECMO support warrants careful consideration of the interplay of a patient's pathophysiology and extracorporeal circuit dynamics. Particular emphasis should be placed on the potential for mismatch between cardiovascular and respiratory support as well as the need to meet metabolic demands through adequate cerebral, coronary and systemic oxygenation. Cannulation strategies occasionally require alteration to meet and anticipate the patient's evolving needs.
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PMID:Extracorporeal membrane modality conversions. 2507 Aug 98