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chflecture藥理ppt課件-wenkub

2023-01-20 03:19:45 本頁(yè)面
 

【正文】 3. Affects of glycosides to conductive tissues A. Increasing conduction of the atrial muscle fibers, because increasing excitation of vagus nerve (increasing of potassium outward). Increasing resting potential. Elevating rate of phase0 depolarization. Acceleration rate of depolarization phase0 and atrial fibers conduction. B. Slowing (depress) conduction at the atrioventricular (AV) node (inhibiting NaKATPase, reducing resting potential), and increase effctive refractory period atrial fibrillation, atrial flutter, paroxymal (and) or supraventricular tachycardia C. Increasing automaticity of Purkinjie fibres: toxicity A. If Na+K+ATPase was inhibited more than 30%, cardiac glycosides would induce toxicity by the overload of intercellular free calcium concentration in myocardiac. (decreasing inotropic action) B. If intercellular potassium concentration was lower level, cardiac glycosides would easily induce toxicity in myocardiac. (arrhythmia) Mechanism of toxicity act 4. Affects of cardiac glycasides to ECG (electrocardiography) A. Therapeutic dose: Twave can bee low, flat, isoelectric or inverted ST segment falls below the isoelectric line PR interval is lengthened, which is associated with slower or delayed AV conduction QT interval is shortened, ERP and APD is shortened in Purkenje fibers B. Higher dose: arrhythmias The affects on ECG T wave It is characterized by an descend ST segment on the ECG PR QT PP Directly inhibit or reflected decrease sympathetic activity ? Exciting increase the vagal activity ? Inhibit RAAS system, promote the excrete of ANP ? cause arrhythmias (toxic doses) II. Action of cardiac glycosides on vascular and kidney ? Vasoconstriction, increase in peripheral vascular resistance ? Diuretic, increase the blood flow through kidney and inhibit Na+K+ATPase → Na+ decreased reabsorb II. Action of cardiac glycosides on neural and hormone Clinical uses 1. Cardiac glycosides are given for CHF Effects: Best go with atrial fibrillation Better hypertension congenital heart disease not good anaemia lack of vitamin B1 not useful pericarditis 心包炎 2. Some kinds of arrhythmias Atrial fibrillation Atrial flutter Supraventricular Tachycardia Toxic effects 1. Responses of stomachintestines : Anorexia 厭食 , nausea, vomiting , Abdominal pain and diarrhoea 2. CNS: visual disturbaces 3. Arrhythmia: 1) Tachycardia 2)AV block 3)Bradycardia 60 beat/min Prophylaxis and treatment of the toxicity ? Clear the signal of toxic and the indication of withdraw ? Inspect the concentration of digoxin (3ng/ml), digitoxin(45ng/ml) ? If necessary ,potassium supplements and antiarrhythmic drugs ( phenytoin ,lidocaine,atropine )administered ? For severe intoxication ,antibodies specific to cardiac glycosides are available Method of administration ? Classical : whole effect dose quick or slow (have use digoxin within two weeks) The suitable dose to the patients ? Maintain : 4~ 5 t 189。 the heart, veins, and capillaries are therefore generally dilated with blood. Hence the term “congestive(充血性 )” heart failure, since the symptoms include pulmonary congestion with life heart failure, and peripheral edema with right heart failure. Underlying causes of CHF include arteriosclerotic heart disease, hypertensive heart disease, valvular heart disease(心瓣膜病 ), dilated cardiomyopathy(擴(kuò)張性心肌病 ), and congenital heart disease(先天性心臟病 ). Left systolic dysfunction secondary to coronaryartery disease is the most mon cause of heart failure. Treatment of congestive heart failure Heart Failure ? Final
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