Heart sinoatrial node

Heart Sinoatrial node Decrease in rate (negative chronotropy), but note important reflex response (see text)... 

Skeletal muscle is neurogenic and requires stimulation from the somatic nervous system to initiate contraction. Because no electrical communication takes place between these cells, each muscle fiber is innervated by a branch of an alpha motor neuron. Cardiac muscle, however, is myogenic, or self-excitatory this muscle spontaneously depolarizes to threshold and generates action potentials without external stimulation. The region of the heart with the fastest rate of inherent depolarization initiates the heart beat and determines the heart rhythm. In normal hearts, this "pacemaker region is the sinoatrial node. 

Cyclic nucleotide-modulated ion channels (Table 6-2) are not K+-selective. Nevertheless, their inward current of Na+ and Ca2+ ions is conducted through a channel that is similar in overall architecture to Shaker K+ channels. This protein family includes the CNG channels, which respond only to cyclic nucleotides, and the HCN channels, which are activated synergistically by hyperpolarization and cyclic nucleotide binding [38,40]. The CNG channels are involved in signaling of visual and olfactory information and serve as cyclic nucleotide-gated Ca2+ channels. In contrast, the HCN channels are required for normal rhythmic electrical discharges by the sinoatrial node in the heart and the pacemaker cells of the thalamus. 

Atropine generally increases heart rate, but it may briefly and mildly decrease it initially, due to Ml receptors on postganglionic parasympathetic neurons. Larger doses of atropine produce greater tachycardia, due to M2 receptors on the sinoatrial node pacemaker cells. There are no changes in blood pressure, but arrhythmias may occur. Scopolamine produces more bradycardia and decreases arterial pressure, whereas atropine has little effect on blood pressure (Vesalainen et al. 1997 Brown and Taylor 1996). 

Depolarisation of the membrane of the cardiomyocyte, resulting from the action potential, initiates contraction in cardiac as in skeletal muscle. This depolarisation arises in the sinoatrial node, a small group of cells in the right atrium, and then spreads through the heart causing, first, the muscles in the atria to contract and then the muscles in the ventricles to contract. 

Stimulation of the parasympathetic system releases acetylcholine at the neuromuscular junction in the sinoatrial node. The binding of acetylcholine to its receptor inhibits adenylate cyclase activity and hence decreases the cyclic AMP level. This reduces the heart rate and hence reduces cardiac output. This explains why jumping into very cold water can sometimes stop the heart for a short period of time intense stimulation of the vagus nerve (a parasympathetic nerve) markedly increases the level of... 

The electrical impulse for contraction (propagated action potential p. 136) originates in pacemaker cells of the sinoatrial node and spreads through the atria, atrioventricular (AV) node, and adjoining parts of the His-Purkinje fiber system to the ventricles (A). Irregularities of heart rhythm can interfere dangerously with cardiac pumping func-tioa... 

This group consists of j3-adrenergic receptor blockers, the antiarrhythmic activity of which is associated with inhibition of adrenergic innervation action of the circulatory adrenaline on the heart. Because all 8-adrenoblockers reduce stimulatory sympathetic nerve impulses of catecholamines on the heart, reduce transmembrane sodium ion transport, and reduce the speed of conduction of excitation, sinoatrial node and contractibility of the myocardium is reduced, and automatism of sinus nodes is suppressed and atrial and ventricular tachyarrhythmia is inhibited. 

Conduction system abnormalities are common in chronic heart failure, occurring in 15-30% of the population with low left ventricular ejection fraction (LVEF) [1-3]. The prevalence in ischemic heart disease is roughly similar to that seen in other forms of dilated cardiomyopathy. Conduction system disease can occur both at the time of an acute myocardial infarction as well as slowly progressing in chronic ischemic heart disease. Intraventricular conduction delays are associated with a poor prognosis in heart failure, with up to a 70% increase in the risk of death, and are also more prevalent in patients with advanced symptoms [2,4]. In ischemic heart disease, all components of the conduction system are at risk of ischemic injury, from the sinoatrial node to the His-Pukinje system. These conduction system abnormalities have the potential to impair cardiac function by a number of mechanisms. Since conduction abnormalities impair cardiac function, it is logical that pacing therapies to correct or improve these conduction abnormalities may improve cardiac function. 

Additionally, the isolated heart can be used to measure chronotropic or inotropic effects. There are several additional ex vivo assays like the sinoatrial node preparation [76], left ventricular wedge preparation [77] available which address specific questions. All of the ex vivo studies mentioned above with the... 

Many visceral organs are innervated by both divisions of the autonomic nervous system. In most instances, when an organ receives dual innervation, the two systems work in opposition to one another. In some tissues and organs, the two innervations exert an opposing influence on the same effector cells (e.g., the sinoatrial node in the heart), while in other tissues opposing actions come about because different effector cells are activated (e.g., the circular and radial muscles in the iris). 

Myocytes within the sinoatrial node possess the most rapid intrinsic rate of automaticity therefore, the sinoatrial node serves as the normal pacemaker of the heart. Specialized cells within the atria, atrioventricular (A-V) node, and His-Purkinje system are capable of spontaneous depolarization, albeit at a slower rate. The more rapid rate of depolarization of the sinoatrial nodal cells normally suppresses all of the other cells with the potential for automaticity. The other cells will become pacemakers when their own intrinsic rate of depolarization becomes greater than that of the sinoatrial node or when the pacemaker cells within the sinoatrial node are depressed. When impulses fail to conduct across the A-V node to excite the ventricular myocardium (heart... 

The indirect effect of qutnidine on the sinoatrial node is a result of the drug s potential to exert an anticholinergic action resulting in a slight increase in heart rate. Higher concentrations of quinidine have a direct effect of depressing the rate of spontaneous diastolic depolarization. 

The direct depressant actions of disopyramide on the sinoatrial node are antagonized by its anticholinergic properties, so that at therapeutic plasma concentrations, either no change or a slight increase in sinus heart rate is observed. Both the anticholinergic and direct depressant actions of disopyramide on sinus automaticity appear to be greater than those of quinidine. 

Historically and romantically, the heartbeat is recognized as the quintessential hallmark of life. Normally, the heart beats at 60-100 beats per minute (bpm), with each beat yielding a ventricular contraction that ejects blood out to the body. Each heartbeat is an electrical event that originates from a collection of electrically excitable cells within the heart called the sinoatrial node (SA), anatomically located at the upper pole of the heart. The sinoatrial node is the primary pacemaker of the heart. The electrical impulse generated in the sinoatrial node spreads rapidly downward from the atria chambers of the heart and reaches the atrioventricular node (AV), a collection of electrically excitable cells that constitutes the electrical interface between the atria and ventricles of the heart. Erom the AV node, the impulse propagates throughout the ventricles via an electrical conduction system referred to as the His-Purkinje system. The electrical transmission... 

Transient elevations in blood pressure and heart rate occur with seizures, probably as a result of increased sympathetic stimulation that leads to increases in norepinephrine levels. Hypertension or increased pretreatment heart rate are strongly predictive of peak postictal change in both heart rate and blood pressure ( 38). Increased parasympathetic stimulation decreases the heart rate as a result of inhibition of the sinoatrial node. Stimulation of the adrenal cortex leads to increased plasma corticosteroids and stimulation of the adrenal medulla, which may also contribute to increases in blood pressure and heart rate. 

Direct effects on the heart are determined largely by Bi receptors, although B2 and to a lesser extent a receptors are also involved, especially in heart failure. Beta-receptor activation results in increased calcium influx in cardiac cells. This has both electrical and mechanical consequences. Pacemaker activity—both normal (sinoatrial node) and abnormal (eg, Purkinje fibers)—is increased (positive chronotropic effect). Conduction velocity in the atrioventricular node is increased (positive dromotropic effect), and the refractory period is decreased. Intrinsic contractility is increased (positive inotropic effect), and relaxation is accelerated. As a result, the twitch response of isolated cardiac muscle is increased in tension but abbreviated in duration. In the intact heart, intraventricular pressure rises and falls more rapidly, and ejection time is decreased. These direct effects are easily demonstrated in the absence of reflexes evoked by changes in blood pressure, eg, in isolated myocardial preparations and in patients with ganglionic blockade. In the presence of normal reflex activity, the direct effects on heart rate may be dominated by a reflex response to blood pressure changes. Physiologic stimulation of the heart by catecholamines tends to increase coronary blood flow. 

Lidocaine is one of the least cardiotoxic of the currently used sodium channel blockers. Proarrhythmic effects, including sinoatrial node arrest, worsening of impaired conduction, and ventricular arrhythmias, are uncommon with lidocaine use. In large doses, especially in patients with preexisting heart failure, lidocaine may cause hypotension—partly by depressing myocardial contractility. 

FIGURE 23-2 Schematic representation of the conduction system of the heart. Conduction normally follows the pathways indicated by the dashed lines. Impulses originate in the sinoatrial node and are transmitted to the atrioventricular node. Impulses are then conducted from the atrioventricular node to the ventricles by the bundle of His and bundle branches. 

Schematic representation of the heart and normal cardiac electrical activity (intracellular recordings from areas indicated and ECG). Sinoatrial node, atrioventricular node, and Purkinje cells display pacemaker activity (phase 4 depolarization). The ECG is the body surface manifestation of the depolarization and repolarization waves of the heart. The P wave is generated by atrial depolarization, the QRS by ventricular muscle depolarization, and the T wave by ventricular repolarization. Thus, the PR interval is a measure of conduction time from atrium to ventricle, and the QRS duration indicates the time required for all of the ventricular cells to be activated (ie, the intraventricular conduction time). The QT interval reflects the duration of the ventricular action potential.

Figure 5.8. The conduction system of the heart, a Anatomy, b Electrical rhythm in the sinoatrial node (top), atrioventricular node (center), and the heart muscle (bottom). The dotted line inb (center) represents the own rhythm of the AV node that normally gets overridden by the faster sinoatrial rhythm (solid line).

The sinoatrial node (SA), consisting of spindle-shaped cells, initiates the electrical activity of the heart. From its location in the right atrium in proximity to the superior vena cava, the electrical activity spreads to the atria whose cells are larger than those of the SA. The pulse from the atria spreads to the atrioventricular node (AV), the gateway to the ventricles. The atria and the ventricles are electrically isolated. The AV node also slows down the electrical activity giving the atria time to fill. The bundle of His is the upper end of the electrical path, which through the Purkinje fibers allows the electrical signal to activate the ventricles and thus to pump the blood. 

Purkinje cells is demonstrated in Figure 12.1 and, like all cardiac myocytes, can be divided into four phases. Phase 4 (pacemaker potential) involves the slow influx of sodium ions, depolarizing the cell until the threshold potential is reached. Once the threshold potential is reached, the fast sodium current is activated, resulting in a rapid influx of sodium ions causing cell depolarization (phase 0 rapid depolarization). Phase 1 (partial repolarization) involves the inactivation of sodium channels and a transient outward current. Phase 2 (plateau phase) results from the slow influx of calcium ions. Repolarization (phase 3) occurs as a result of outflow of potassium ions from the cell and restores the resting potential. There are variations between the different areas of the heart, specifically the nodal tissues do not possess fast sodium channels and slow L-t5rpe calcium channels generate phase 0 current (Fig. 12.1). Phase 4 activity varies between nodal areas the sinoatrial node depolarizes more rapidly than the atrioventricular (AV) node. Automaticity is under autonomic nervous system control. Parasympathetic neurons... 

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