The hemodynamic consequences of cardiac arrhythmias depend on various factors, including the ventricular rate and the duration of the abnormal rate, the temporal relationship btween atrial and ventricular activity, the sequence of ventricular activation, the functional state of the heart, the irregularity of the cycle length, associated drug therapy, the peripheral vascular vasomotor system, disease in organ systems other than the heart, and the degree of anxiety caused by the disease processes. Sinus bradycardia, even with rates as low as 40 beats/min, may not be associated with significant hemodynamic consequences unless the stroke volume is limited by myocardial or valvular disease, as in acute myocardial infarction. Cardiac output usually, but not invariably, falls when atrial fibrillation replaces normal sinus rhythm, even at comparable ventricular rates, both at rest and during exercise. Similar observations have been made during the development of atrial flutter despite the persistence of effective mechanical atrial activity in at least some cases. Marked hemodynamic changes are frequent in the course of ventricular tachycardia with systemic arterial hypotension, a decrease in cardiac output, and evidence of cerebral, coronary, and renal vascular insufficiency. Cyclic variations in systemic and pulmonary arterial pressures are common during atrioventricular dissociation. Cardiac output is generally depressed during the severe bradycardia of acquired complete heart block with evidence of atrioventricular valvular insufficiency. Increase of the heart rate by ventricular pacing reverses all or some of these abnormalities. The changes in congenital complete heart block are considerably less severe because myocardial insufficiency is less frequently seen in congenital complete heart block.
|Title of host publication||AMER.HEART ASS.MONOGR.|
|Number of pages||9|
|State||Published - Dec 1 1973|
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