Depolarization, of myocardial

Supraventricular arrhythmias arising from accessory conduction pathways include Wolff-Parkinson-White syndrome (re-entrant arrhythmias). In this case, a depolarization and conduction occur in an accessory pathway, which circumvents the upper portion of the AV node and weakly depolarizes AV nodal tissue. Then, because the tissue is quickly repolarized, it is able to rapidly depolarize the upper portion of the AV node after depolarization of myocardial tissue, causing a re-entrant loop or circus rhythm. (The nodal tissue is normally refractory to stimulus, and thus serves as the termination stimulus for ventricular conduction.) The therapy of supraventricular arrhythmias involves partial blockade of the AV node. 

The mechanical activity of the heart (contraction of the atria and ventricles) occurs as a result of the electrical activity of the heart. The heart possesses an intrinsic electrical conduction system (Fig. 6-1). Normal myocardial contraction cannot occur without proper and normal function of the heart s electrical conduction system. Electrical depolarization of the atria results in atrial contraction, and ventricular depolarization is... 

Ventricular premature depolarizations occur with variable frequency, depending on underlying comorbid conditions. The prevalence of complex or frequent VPDs is approximately 33% and 12% in men with and without CAD, respectively 34 in women, the prevalence of complex or frequent VPDs is 26% and 12% in those with and without CAD, respectively.35 Ventricular premature depolarizations occur more commonly in patients with ischemic heart disease, a history of myocardial infarction, and HF due to LV dysfunction. They may also occur as a result of hypoxia, anemia, and following cardiac surgery. 

Tachyarrhythmias (sinus rate more than 100 per minute) are produced by a disturbances of impulse generation or of impulse conduction in the heart. Tachyarrhythmias due to disturbed impulse formation are associated with irregular and rhythmic discharge from ectopic pacemaker activity in areas of the heart other than the SA node. The characteristic of myocardial cells, which enables them to generate spontaneous depolarization, is called automaticity. 

The electrical activity produced by either the depolarization or the repolarization of myocardial tissue, specifically the nerve fibre cells, may be identified conveniently by the help of suitable electrodes and this may be plotted as a graph showing intensity (mV millivolts) along the Y-axis and time (seconds) along the X-axis, as shown in Fig. 12.1(a), also known as the electro-cardiogram (ECG). 

Failure to Capture. The absence of myocardial depolarization despite appropriate stimulus delivery from the pulse generator defines failure to capture. Failure to capture is usually diagnosed fiom the ECG by the occurrence of visible pacing artifact without resultant paced P-waves or QRS complexes (Fig. 16.2). Failure to capture can, however, result in no visible stimulus artifact despite stimulus output from the generator when there is complete lead fracture (see above). Failure to capture results from lead failure, lead-tissue interface problems, and increases in myocardial stimulation threshold (Fig. 16.3). 

Electrical depolarization, but no synchronous shortening of myocardial fibers and no mechanical activity or contractions in the heart... 

Direct current cardioversion is the process of administering a synchronized electrical shock to the chest. The purpose of DCC is to simultaneously depolarize all of the myocardial cells, resulting in interruption and termination of the multiple reentrant circuits and restoration of normal sinus rhythm. The initial energy level of the shock is 100 joules (J) if the DCC attempt is unsuccessful, successive cardioversion attempts maybe made at 200,300, and 360 J.14 Delivery of the shock is synchronized to the ECG by the cardioverter machine, such that the electrical charge is not delivered during... 

Ventricular premature depolarizations occur as a result of abnormal ventricular automaticity, as a result of enhanced activity of the sympathetic nervous system and altered electro-physiologic characteristics of the heart during myocardial ischemia and following myocardial infarction. 

Direct current cardioversion The process of administering a synchronized electrical shock to the chest to simultaneously depolarize all of the myocardial cells, resulting in restoration of normal sinus rhythm. 

The answer is d. (Hardman, pp 865-867.) Lidocaine usually shortens the duration of the action potential and, thus, allows more time for recovery during diastole. It also blocks both activated and inactivated Na channels. This has the effect of minimizing the action of lidocaine on normal myocardial tissues as contrasted with depolarized ischemic tissues. Thus, lidocaine is particularly suitable for arrhythmias arising during ischemic episodes such as myocardial infarction (Ml). 

Mecfianism of Action An antiarrhythmic that decreases sodium influx during depolarization, potassium efflux during repolarization, and reduces calcium transport across the myocardial cell membrane.Decreases myocardial excitability, conduction velocity, and contractility Therapeutic Effect Suppresses arrhythmias. Pharmacokinetics Almost completely absorbed after PO administration. Protein binding 80%-90%. Metabolized in liver. Excreted in urine. Removed by hemodialysis. Half-life 6-8 hr. 

Cardiac arrhythmias are a common problem in clinical practice, occurring in up to 25% of patients treated with digitalis, 50% of anesthetized patients, and over 80% of patients with acute myocardial infarction. Arrhythmias may require treatment because rhythms that are too rapid, too slow, or asynchronous can reduce cardiac output. Some arrhythmias can precipitate more serious or even lethal rhythm disturbances for example, early premature ventricular depolarizations can precipitate ventricular fibrillation. In such patients, antiarrhythmic drugs may be lifesaving. On the other hand, the hazards of antiarrhythmic drugs—and in particular the fact that they can precipitate lethal arrhythmias in some patients—has led to a reevaluation of their relative risks and benefits. In general, treatment of asymptomatic or minimally symptomatic arrhythmias should be avoided for this reason. 

There are two forms of arrhythmia in acute myocardial ischemia. Type-la arrhythmias occur 2-10 min after the onset of ischemia with a peak at 5-6 min. These arrhythmias are often of the reentrant type and are caused by diastolic bridging (details see chapter 1). It is also possible that premature ventricular depolarizations occur in this phase and initiate reentry. 

Recently, both hirsutine (85) and dihydrocorynantheine (86) were found to be active when the effects of these compounds on the action potentials of sino-atrial node, atrium and ventricle tissues were studied with standard microelectrode techniques [65]. In sino-atrial node preparations, both compounds concentration-dependently increased cycle length, decreased the slope of the pacemaker depolarization, decreased the maximum rate of rise and prolonged action potential duration. Thus, it was for the first time shown that hirsutine and dihydrocorynantheine have direct inhibitory effects on the cardiac pacemaker. In atrial and ventricular preparations, both compounds concentration-dependently decreased the maximum rate of rise and prolonged action potential duration. Although stereochemically different, these two alkaloids exhibited no difference in their effects on various myocardial action potential parameters. Dihydrocorynantheine also displays potent a-adrenoceptor blocking activity, while hirsutine is inactive [66]. Experiments with ion channels indicate that the mechanisms for these two phenomena probably differ. The direct effects of hirsutine and dihydrocorynantheine on the action potential of cardiac muscle through inhibition of multiple ion channels may explain the negative chronotropic and antiarrhythmic activities of these two alkaloids. 

---