Heart electrophysiology

Platiaum and its alloys are also used as biomedical electrodes, eg, platiaum—indium wires for permanent and temporary pacemaker leads and defibrillator leads. Electrophysiology catheters, which contain platinum electrodes and marker bands, have been used to map the electrical pathways of the heart so that appropriate treatment, such as a pacemaker, can be prescribed. 

The Class I agents decrease excitability, slow conduction velocity, inhibit diastoHc depolarization (decrease automaticity), and prolong the refractory period of cardiac tissues (1,2). These agents have anticholinergic effects that may contribute to the observed electrophysiologic effects. Heart rates may become faster by increasing phase 4 diastoHc depolarization in SA and AV nodal cells. This results from inhibition of the action of vagaHy released acetylcholine [S1-84-3] which, allows sympathetically released norepinephrine [51-41-2] (NE) to act on these stmctures (1,2). 

The electrophysiological effects of amiodarone may be a composite of several properties. In addition to prolonging action potential duration and refractory period in ad tissues of the heart, the compound is an effective sodium channel blocker (49), calcium channel blocker (50), and a weak noncompetitive -adrenoceptor blocking agent (51). Amiodarone slows the sinus rate, markedly prolongs the QT interval, and slightly prolongs the QRS duration (1,2). 

The antimuscarinic drug atropine, and its derivative ipratropiumbromide, can also be used for antiarrhyth-mic treatment. Muscarinic receptors (M2 subtype) are mainly present in supraventricular tissue and in the AV node. They inhibit adenylylcyclase via G proteins and thereby reduce intracellular cAMP. On the other hand, activation of the M2 receptor leads to opening of hyperpolarizing Ik.acii and inhibits the pacemaker current If probably via the (3y-subunit of the Gi protein associated with this receptor. The results are hyperpolarization and slower spontaneous depolarization. Muscarinic receptor antagonists like atropine lead to increased heart rate and accelerated atrioventricular conduction. There are no or only slight effects on the ventricular electrophysiology. 

Cardiac glycosides (CG) are potent and highly specific inhibitors of the intrinsic plasma membrane Na+/K+-ATPase, also known as the sodium pump. They modulate electrophysiological properties of the heart and its contractile functions. 

The individual modules of the in situ heart can be coupled together to compute a whole sequence from ventricular pressure development, coronary perfusion, tissue supply of metabolites, cell energy consumption, and electrophysiology, to contractile activity and ventricular pressure development in the subsequent beat. The starting point (here chosen as ventricular pressure development) can be freely selected, and drug effects on the system can be simulated. Inserted into a virtual torso, these models allow one to compute the spread of excitation, its cellular basis, and the consequences for an ECG under normal and pathological conditions. 

While many biological molecules may be targets for oxidant stress and free radicals, it is clear that the cell membrane and its associated proteins may be particularly vulnerable. The ability of the cell to control its intracellular ionic environment as well as its ability to maintain a polarized membrane potential and electrical excitability depends on the activity of ion-translocating proteins such as channels, pumps and exchangers. Either direct or indirect disturbances of the activity of these ion translocators must ultimately underlie reperfiision and oxidant stress-induced arrhythmias in the heart. A number of studies have therefore investigated the effects of free radicals and oxidant stress on cellular electrophysiology and the activity of key membrane-bound ion translocating proteins. 

Electrophysiological changes take place in the human heart even under the influence of limited doses of caffeine. 

Malik, M. (2001) Problems of heart rate correction in assessment of drug-induced QT interval prolongation. Journal of Cardiovascular Electrophysiology, 12, 411—420. 

Aytemir, K., Maarouf, N., Gallagher, M. M., Yap, Y.G., Waktare, J.E. and Malik, M. (1999) Comparison of formulae for heart rate correction of QT interval in exercise electrocardiograms. Pace-Pacing and Clinical Electrophysiology, 22, 1397—... 

Weissenburger, J., Nesterenko, V.V. and Antzelevitch, C. (2000) Transmural heterogeneity of ventricular repolarization under baseline and long QTconditions in the canine heart in vivo torsades de pointes develops with halothane but not pentobarbital anesthesia. Journal of Cardiovascular Electrophysiology, 11, 290-304. 

Heightened sensory perceptions Stimulates appetite Perceived slower passage of time Panic or anxiety Dissociative symptoms Physiological Effects Increases heart rate Reduces body temperature Slowed gastrointestinal function Electrophysiology... 

The quinolinone derivative, OPC-88117 (73), is yet another compound described as possessing both Class I and Class III electrophysiological activities. Studies in guinea-pig papillary muscle showed that OPC-88117 at 30 increased APDgo by about 15% and decreased F ,ax by only 4% however, at 100 /iM APDgo was prolonged by 23 % and was decreased by 23 % [206]. Further experiments in isolated rabbit hearts demonstrated that OPC-88117 increased atrio-His bundle (A-H) and His bundle-ventricle (H-V) conduction times and refractory periods with a profile that was similar to, but more potent than that of lidocaine [207]. 

The general cardiodynamic effects of cardiac glycosides are quite complex because of the combination of their direct action on the heart and indirect action, which changes the electrophysiological properties of the heart (automatism, conductivity, and excitability). 

As a result of the weight of evidence for ICD therapy in prevention of SCD in patients with ischemic cardiomyopathy, the American College of Cardiology, American Heart Association, and the North American Society for Pacing and Electrophysiology (now Heart Rhythm Society) revised guidelines for ICD implantation in October 2002... 

Chronic heart failure is associated with intrinsic sinus node dysfunction that can be demonstrated on careful electrophysiologic studies [22, 23]. Patients with chronic heart failure have longer intrinsic sinus cycle... 

The side-effects of cardiac glycosides are mostly caused by electrophysiological/neuronal phenomena. Gastro-intestinal adverse reactions are probably triggered by effects on the central nervous system. Various types of cardiac arrhythmias are caused by the influence of the drugs on nodal tissues in the heart. The risk of arrhythmia is strongly enhanced by low plasma potassium concentrations. 

Prystowsky EN, Benson DW, Fuster V, Hart RG, Kay GN, Myerburg RJ et al. Management of patients with atrial fibrillation. A Statement for Healthcare Professionals. From the Subcommittee on Electrocardiography and Electrophysiology, American Heart Association. Circulation 1996 93 1262-77. 

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