Clinical electrocardiography . l complex afterthe attack, showing that retrogression has not occurred. Theindividual waves of these electrocardiograms are unaltered. ,^!;*^/l •^: . -.,. , Fig. 48.—Paroxysmal sinus tachycardia. Rate 55 to 136. Electrocardiogram in Derivation II. Figure 47 represents this disorder and Fig. 48, the termina-tion of a paroxysm. PAROXYSMAL AURICULAR TACHYCARDIA In auricular tachycardia the ectopic focus of stimulus produc-tion is at some point in the auricular musculature. Each auricular X ^muuu Fig. 49.—Schematic graph of paroxysmal auricular tachycardia. beat i
Clinical electrocardiography . l complex afterthe attack, showing that retrogression has not occurred. Theindividual waves of these electrocardiograms are unaltered. ,^!;*^/l •^: . -.,. , Fig. 48.—Paroxysmal sinus tachycardia. Rate 55 to 136. Electrocardiogram in Derivation II. Figure 47 represents this disorder and Fig. 48, the termina-tion of a paroxysm. PAROXYSMAL AURICULAR TACHYCARDIA In auricular tachycardia the ectopic focus of stimulus produc-tion is at some point in the auricular musculature. Each auricular X ^muuu Fig. 49.—Schematic graph of paroxysmal auricular tachycardia. beat is followed by a ventricular beat, and the rate does not attain200 a minute. Figure 49 schematically represents a paroxysm ECTOPIC RHYTHMS AND TACHYCARDIAS 79 of auricular tachycardia. Figure 50 is an electrocardiogram of aparoxysm. It is apparent that 1 : 1 auriculoventricular associa-tion occurs. The P wave is inverted,which is indicative of auricular impulseproduction outside the sino-auricularnode. AURICULAR FLUTTER. .2 •- CJ u oo bpO S *3 Auricular flutter may be describedas an acceleration of the auricles to arate beyond 200 a minute. This ac-celeration is accompanied by partialheart-block, giving a ventricular rateof one-half, one-third, or one-fourth ofthe auricular rate, or a complete au-riculoventricular dissociation (completeheart-block), or varying degrees ofpartial block, causing a gross ventric-ular arhythmia. The partial blockis apparently due to the inability ofthe auriculoventricular bundle to con-duct impulses so rapidly, or to theinability of the ventricle to respond sorapidly. There is no known pathologic dif-ference between an auricular rate of lessthan 200 and one exceeding this figure,yet the clinical manifestations are so dif-ferent as to justify the classification of flutter as a clinical entity. The fundamental clinical differenceslie in the fact that flutter tends to persist indefinitely, whereasauricular paroxysmal tachycardia rarely reaches s
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