Depolarization shock

The depolarization shock can be delivered flirough either a unipolar or bipolar lead. Most older leads utilize the unipolar design (Morley-Davies and Cobbe, et al., 1997), in which a single insulated electrode is placed near the myocardium of the heart and acts as a cathode (Tyers et al., 1997 ... 

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... 

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. 

Q2 A defibrillator administers a large direct current (DC) shock (starting at 200 J) across the chest wall in order to depolarize the whole heart and stop the activity of the dysrhythmic areas, which are producing ectopic (abnormal) beats. It is hoped that this will allow the normal pacemaker, the SA node, to start again and generate the cardiac impulse in a normal rhythm this is known as sinus rhythm. 

Physiological Actions of NE Although, NE clearly plays significant roles in olfactory function, the effects of NE at the cellular and network levels are somewhat discrepant. For example, LC stimulation was reported to have no effect on LOT-evoked field-potentials recorded in the GCL (Perez et al., 1987). A subsequent study reported that LC stimulation initially decreased and then subsequently increased paired-pulse depression of GC field-potential responses to LOT stimulation (Okutani et al., 1998). These effects were attributed to activation of fi receptors. Another field-potential study reported that NE infusion into MOB, acting at al receptors, increased the depolarization of GC dendrites elicited by LOT stimulation. Mitral cell responses to antidromic shocks were not affected, suggesting that NE excites GC (Mouly et al.,... 

Palytoxin CAS 11077-03-5 respiratory distress, diarrhea, convulsions, shock, low body temperature, and death. causes irreversible depolarization of nerve and muscle tissue. It has a very potent effect on the coronary artery and may also cause delayed effects including disintegration of red blood cells. corals. Palytoxin is soluble in water and alcohol. It is stable to heat, and both low and high pH. 

Fromm and Bauer [36] found that action potentials in maize sieve tubes change phloem translocation. Using macro- and microautoradiography in mature leaves of maize, Fromm and Bauer [36] studied the inhibition of phloem translocation caused by electric and cold shock. They stimulated the leaf tip with ice water and found that the velocity of signal transmission was 3-5cm/s. Upon stimulation, the microelectrode recorded a basipetally propagating action potential with a depolarizing amplitude of 80 mV in the sieve tubes (Fig. 2). During electrical stimulation, the action potential was measured in the sieve-tube system with a speed of 5cm/s. 

PO/IV. Well absorbed, 80% metabolized in first pass. 90% protein bound. Metabolites are active. Half-life is 5 hrs but may be up to 20 hrs in patients with cirrhosis. Patient on IV blockers or digitalis. A-V node block, sick sinus syndrome, cardiogenic shock, heart failure, hypotension. Beta blockers or digitalis Increases likelihood of bradycardia or A-V blockade. Quinicfine or prazosin Increases hypotension. Digoxin levels are increased. Cimetidine reduces verapamil clearance. Calcium supplements may inhibit actions of verapamil. Depolarization (leading to contraction) of vascular smooth muscle is dependent on calcium entry. Vasodilation is induced by calcium entry blockers because they inhibit calcium influx. 

As frequency increases higher than 50-60 cycles/s, the danger of electric shock decreases dramatically (Figure 2.11.1). Currents that could cause death at 60 cps are imperceptible at very high frequencies. This is because there is a short time after neural or muscle depolarization during which the nerve or muscle is insensitive to further stimuli (see Section 4.4.3). 

The corrective measure is to extinguish the rapidly occurring waves of excitation by simultaneously depolarizing all or most of the cardiac cells with a strong electric shock. The cells can then simultaneously repolarize themselves, and this will put them back in phase with each other. 

Ventricular tachycardia (VT) is the result of uncontrolled electrical activity in the ventricle. This activity may be coordinated or uncoordinated. The definitive therapy for Ventricular is external stimulation by an electric field sufficiently large to reset the electrical activity of most ventricular cells. This ends the previous (uncontrolled) electrical activity and allows the reestablishment of normal cardiac activity. As explained earlier, this requires depolarization of a critical mass of tissue by a high-voltage discharge. When high-voltage therapy is delivered, an attempt is made to synchronize the delivery with a detected R-wave. A synchronized shock is termed cardioversion, whereas an unsynchronized shock is termed defibrillation because VF has no coherent electrical activity, and therefore no basis for synchronization (Figure 15.6). 

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