Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0231835 (tachypnea)
 2,543 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Malignant hyperthermia has been an iatrogenic syndrome which was usually fatal. The syndrome occurs when certain physiologically active compounds act on defective skeletal and cardiac muscle cells. The syndrome consists of a soaring fever, severe acidosis, tachycardia, tachypnea, and usually myoclonic spasms. Cardiac arrhythmias, shock, bleeding disorders, and death soon follow. Malignant hyperthermia has characteristically complicated the administrations of anesthesiologists, but is being triggered by drugs used in other diagnostic and therapeutic activities. This paper reports a fatal case which followed the infusion of iodinated contrast media. The increased release of epinephrine and the production of fibrin split products seen in an iodinated contrast media reaction suggest certain commonalities between it and a malignant hyperthermia reaction which may be triggered be epinephrine and is complicated by disseminated vascular clotting and bleeding disorders. The potential for successful treatment has greatly improved with the availability of dantrolene. Increased awareness of the syndrome, temperature monitoring, early diagnosis, and rapid treatment should make this malignant disorder less threatening.
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PMID:Malignant hyperthermia following intravenous iodinated contrast media. Report of a fatal case. 701 55

A major determinant of survival in patients with advanced viral or bacterial infection, or following severe trauma or burns complicated by multiple organ failure, is the combination of clinical signs termed the systemic inflammatory response syndrome (SIRS). SIRS is characterized by hypotension, tachypnea, hypo- or hyperthermia and leukocytosis as well as other clinical signs and symptoms, including a depression in myocardial contractile function. Heart failure complicating systemic sepsis or other causes of SIRS is usually not accompanied by coronary artery ischemia due to hypotension, myocardial necrosis, or marked cardiac interstitial inflammatory infiltrates, and thus the cause of cardiac contractile dysfunction in this syndrome has remained unclear. However, recent evidence has implicated an endogenous nitric oxide (NO) signalling pathway within cardiac myocytes and other cellular constituents of cardiac muscle, including the microvascular endothelium, as a possible contributor to the pathogenesis of heart failure in this syndrome. Cardiac myocytes are now known to express both constitutive NO synthase (cNOS) and inducible NO synthase (iNOS) activities. Activation of cNOS appears to modulate cardiac myocyte responsiveness to muscarinic cholinergic and beta-adrenergic receptor stimulation. Induction of iNOS by soluble inflammatory mediators, including cytokines, causes a marked depression in myocyte contractile responsiveness to beta-adrenergic agonists. Thus, inappropriate activation of cNOS or excessive or prolonged induction of iNOS in the myocardium may contribute to cardiac dysfunction complicating SIRS.
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PMID:Myocardial contractile dysfunction in the systemic inflammatory response syndrome: role of a cytokine-inducible nitric oxide synthase in cardiac myocytes. 753 82

This report describes a case of cardiac right auricle rupture (RAR) in a flock of 11,500 broilers that were 14 days old. The birds were housed at an altitude of 300 m, with an external temperature of -10 degrees C and an internal temperature of 15 degrees C. There was 3.6% mortality, due to sudden deaths, from 10 to 14 days of age. All necropsied birds had haemopericardium due to RAR at the point of the junction with the vena cava, and 85% of them had blood in the oral cavity and external acoustic meatus. The vena cava and its caudal branches, the intestinal vessels, and the sinus durae matris and sinus saggitalis were distended. Histological examination showed haemorrhages into the myocardium, degeneration of the cardiac muscle fibres, as well as oedema of the lungs and hypertrophy of the smooth muscle bundles of the parabronchial walls. Blood in the mouth of the broilers may have been due to haemoptysis, which in humans is caused mainly by mitral stenosis. In broilers, mitral stenosis and/or insufficiency, and left ventricular failure with consequent pulmonary hypertension (PH) were considered as possible triggers for right ventricular failure. The alarm reaction in hypoxaemia, due to secondary factors such as cold, caused tachycardia and tachypnoea, may have induced further elevation of PH, and acute myocardial infarction causing cardiac rupture and haemopericardium in this case. Hypertension and PH, due to possible mitral stenosis/insufficiency in association with acute myocardial ischaemia, were probably the determinant factors causing this acute episode. This opens the possibility that the RAR may be cardiogenic.
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PMID:Rupture of the right auricle in broiler chickens. 1623 69