Nodal contraction

The second-order thermodynamics for orientation-independent w(l 2) is embodied in (94), with (94a) giving the full SOGA result, (94b) the result after nodal contraction, and (94c) the result after nodal approximation. 

Abnormal initiation of electrical impulses occurs as a result of abnormal automaticity. If the automaticity of the SA node increases, this results in an increased rate of generation of impulses and a rapid heart rate (sinus tachycardia). If other cardiac fibers become abnormally automatic, such that the rate of initiation of spontaneous impulses exceeds that of the SA node, other types of tachyarrhythmias may occur. Many cardiac fibers possess the capability for automaticity, including the atrial tissue, the AV node, the Purkinje fibers, and the ventricular tissue. In addition, fibers with the capability of initiating and conducting electrical impulses are present in the pulmonary veins. Abnormal atrial automaticity may result in premature atrial contractions or may precipitate atrial tachycardia or atrial fibrillation (AF) abnormal AV nodal automaticity may result in junctional tachycardia (the AV node is also sometimes referred to as the AV junction). Abnormal automaticity in the ventricles may result in ventricular premature depolarizations (VPDs) or may precipitate ventricular tachycardia (VT) or ventricular fibrillation (VF). In addition, abnormal automaticity originating from the pulmonary veins is a precipitant of AF. 

Verapamil (Class IV antiarrhythmic drug) is an effective agent for atrial or supraventricular tachycardia. A Ca++ channel blocker, it is most potent in tissues where the action potentials depend on calcium currents, including slow-response tissues such as the SA node and the AV node. The effects of verapamil include a decrease in heart rate and in conduction velocity of the electrical impulse through the AV node. The resulting increase in duration of the AV nodal delay, which is illustrated by a lengthening of the PR segment in the ECG, reduces the number of impulses permitted to penetrate to the ventricles to cause contraction. 

The a wave This is caused by atrial contraction and is, therefore, seen before the carotid pulsation. It is absent in atrial fibrillation and abnormally large if the atrium is hypertrophied, for example with tricuspid stenosis. Cannon waves caused by atrial contraction against a closed tricuspid valve would also occur at this point. If such waves are regular they reflect a nodal rhythm, and if irregular they are caused by complete heart block. 

During arrhythmias Atrial tachycardia, atrial fibrillation AV nodal tachycardia, AV blockade Premature ventricular contractions, bigeminy, ventricular tachycardia, ventricular fibrillation... 

In equation (42), the quantities j denote the vailues of the function / or those of its derivative / jj and / z. The details of the basis functions, the quantities j and the nodes of an element have been presented elsewhere [26], The first and second derivatives of the mapping function / can be obtained from derivatives of the basis fimctions. To compute the pressiure p and tensor components, the four nodal values at points A, B, C and D of each element are chosen as unknowns. Their derivatives are evaluated by using finite-difference formulae. In Fig 14 we present computed streamlines for 4/1 and 8/1 axisymmetric contractions, and the computed shear stress along the computed streamlines, for a K-BKZ fluid of the form given by Papanastasiou et al [19]. 

Patients frequently complain of intermittent episodes of rapid heart rate/palpitations that start and stop abruptly, usually without provocation (but occasionally during exercise). Severe symptoms include syncope. Often (in particular, those with AV nodal reentry) patients complain of a chest pressure or a fullness in the neck sensation. This is due to simultaneous AV contraction with the right atrium contracting against a closed tricuspid valve. Life-threatening symptoms (syncope, hemodynamic collapse) are associated with extremely rapid rate (e.g., >200 beats per minute) and atrial fibrillation associated with an accessory AV pathway. 

Voltage-sensitive Ca + channels (L-type or slow channels) mediate the entry of extracellular Ca + into smooth muscle and cardiac myocytes, and sinoatrial (SA) and atrioventricular (AV) nodal cells, in response to electrical depolarization. In both smooth muscle and cardiac myocytes, Ca + is a trigger for contraction, albeit by different mechanisms. Ca +-channel antagonists, also called Ca +-entry mockers, inhibit Ca +-channel function. In vascular smooth muscle, this leads to relaxation, especially in arterial beds. These drugs also may produce negative inotronic and chronotropic effects in the heart. 

Arrhythmias arise from ectopic foci in the cardiac tissue. Recall that all cardiac myocytes have the potential for spontaneous depolarization because of their smooth muscle-like properties and the close proximity of the cell membrane to depolarization threshold. Normally, these foci are eliminated by the powerful depolarization of the SA nodal cells. Unopposed, these foci generate depolarizations that cause small premature contractions and inhibit full contraction of cardiac muscle in response to the normal SA nodal depolarization. This is of primary importance in ventricular tissue. 

Iso > Epi = NE Dobutamine Metoprolol CGP 20712A Juxtaglomerular cells Heart Increased renin secretion Increased force and rate of contraction and AV nodal conduction velocity... 

By increasing the rates of ventricular contraction and relaxation, Epi preferentially shortens systole and usually does not reduce the duration of diastole. Epi speeds the heart by accelerating the slow depolarization of sinoatrial (SA) nodal cells that takes place during phase 4 of the action potential (see Chapter 34). The amplitude of the AP and the maximal rate of depolarization (phased) also are increased. A shift in the location of the pacemaker within the SA node often occurs, owing to activation of latent pacemaker cells. In Purkinje fibers, Epi accelerates diastolic depolarization and may activate latent pacemakers. If large doses of Epi are given, premature ventricular contractions occur and may herald more serious ventricular arrhythmias. Conduction through the Purkinje system depends on the level of membrane potential at the time of excitation. Epi often increases the membrane potential and improves conduction in Purkinje fibers that have been excessively depolarized. 

An analogous explanation at the molecular level can be proposed for the spontaneous emergence of the cardiac rhythm at a precise stage of embryonic development. This appearance of one of the most remarkable biological rhythms results from the fact that in the course of development cells in nodal tissues of the heart acquire the capability to generate periodically, in an autonomous manner, the electrical signal that initiates cardiac contraction (Fukii, Hirota Kamino, 1981). As for the neurons, the variation of certain ionic conductances would endow these cells with the property of oscillating spontaneously, while other cardiac cells would only be excitable (DeHaan, 1980). 

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