Heart normal conduction

The cardiotonics affect the transmission of electrical impulses along the pathway of the conduction system of tiie heart. The conduction system of die heart is a group of specialized nerve fibers consisting of die SA node, die AV node, the bundle of His, and die branches of Purkinje (Fig. 39-2). Each heartbeat (or contraction of tiie ventricles) is tiie result of an electrical impulse tiiat normally starts in tiie SA node, is tiien received by die AV node, and travels down die bundle of His and through tiie Purkinje fibers (see Fig. 39-2). The heartbeat can be felt as a pulse at the wrist and otiier areas of die body where an artery is close to the surface or lies near a bone When the electrical impulse reaches the... 

Inhalation of certain hydrocarbons, including some anesthetics, can make the mammalian heart abnormally sensitive to epinephrine, resulting in ventricular arrhythmias, which in some cases can lead to sudden death (Reinhardt et al. 1971). The mechanism of action of cardiac sensitization is not completely understood but appears to involve a disturbance in the normal conduction of the electrical impulse through the heart, probably by producing a local disturbance in the electrical potential across cell membranes. The hydrocarbons themselves do not produce arrhythmia the arrhythmia is the result of the potentiation of endogenous epinephrine (adrenalin) by the hydrocarbon. 

The cardiac action potential is normally conducted throughout the heart in a coordinated and predictable pattern (Fig. 2 3-2).5 The action potential originates in the SA node and is conducted throughout both atria via the atrial muscle cells. While spreading through the atria, the action potential reaches the AV node. From the AV node, the action potential... 

As well as their effects on the brain, neuroleptics commonly produce other potentially lethal effects. They are all toxic to the heart, inducing conduction defects and arrhythmias. Olanzapine and clozapine also interfere with normal metabolism, causing what is known as metabolic syndrome. This syndrome has only recently been described and is defined as the occurrence of obesity, diabetes, hypertension and dyslipidaemia6 (Shirzadi Ghaemi 2006). The underlying cause of the syndrome is thought to be resistance to insulin. All these effects... 

An average rate of metabolic activity produces roughly 22,000 mEq acid per day. If all of this acid were dissolved at one time in unbuffered body fluids, their pH would be less than 1. However, the pH of the blood is normally maintained between 7.36 and 7.44, and intracellular pH at approximately 7.1 (between 6.9 and 7.4). The widest range of extracellular pH over which the metabolic functions of the liver, the beating of the heart, and conduction of neural impulses can be maintained is 6.8 to 7.8. Thus, until the acid produced from metabolism can be excreted as CO2 in expired air and as ions in the urine, it needs to be buffered in the body fluids. The major buffer systems in the body are the bicarbonate-carbonic acid buffer system, which operates principally in extracellular fluid the hemoglobin buffer system in red blood cells the phosphate buffer system in all types of cells and the protein buffer system of cells and plasma. 

Pacemaker-mediated tachycardia arises from retrograde conduction via the normal conduction system of the heart of a paced or intrinsic ventricniar event to the atrium. The tracking of the retrogradely conducted atrial complex must occur for PMT to occur. The successive ventricular-paced event that tracks this atrial complex also results in retrograde conduction to the atrinm. 

Electrical impulses don t alwa follow normal conduction pathway in the heart. In WPW syndrome, electrical impulses enter the ventricles from the atria through an accessory pathway that bypasses the AV junction. 

Although blood pressure control follows Ohm s law and seems to be simple, it underlies a complex circuit of interrelated systems. Hence, numerous physiologic systems that have pleiotropic effects and interact in complex fashion have been found to modulate blood pressure. Because of their number and complexity it is beyond the scope of the current account to cover all mechanisms and feedback circuits involved in blood pressure control. Rather, an overview of the clinically most relevant ones is presented. These systems include the heart, the blood vessels, the extracellular volume, the kidneys, the nervous system, a variety of humoral factors, and molecular events at the cellular level. They are intertwined to maintain adequate tissue perfusion and nutrition. Normal blood pressure control can be related to cardiac output and the total peripheral resistance. The stroke volume and the heart rate determine cardiac output. Each cycle of cardiac contraction propels a bolus of about 70 ml blood into the systemic arterial system. As one example of the interaction of these multiple systems, the stroke volume is dependent in part on intravascular volume regulated by the kidneys as well as on myocardial contractility. The latter is, in turn, a complex function involving sympathetic and parasympathetic control of heart rate intrinsic activity of the cardiac conduction system complex membrane transport and cellular events requiring influx of calcium, which lead to myocardial fibre shortening and relaxation and affects the humoral substances (e.g., catecholamines) in stimulation heart rate and myocardial fibre tension. 

Clearly, cardiac function may not be addressed exclusively on the basis of describing the working mechanisms of single cells. Both normal and disturbed heart rhythms are based on a spreading wave of electrical excitation, the meaningful investigation of which requires conduction pathways of at least hundreds if not thousands of cells in length. 

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... 

Several intervals and durations are routinely measured on the ECG. The PR interval represents the time of conduction of impulses from the atria to the ventricles through the AV node the normal PR interval in adults is 0.12 to 0.2 seconds. The QRS duration represents the time required for ventricular depolarization, which is normally 0.08 to 0.12 seconds in adults. The QT interval represents the time required for ventricular repolarization. The QT interval varies with heart rate—the faster the heart rate, the shorter the QT interval, and vice versa. Therefore, the QT interval is corrected for heart rate using Bazett s equation3, which is ... 

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. 

Drugs of this group are calcium channel blockers that inhibit slow transmembrane calcium ion flow in the cell of the conductive system of the heart during depolarization, which causes a slowing of atrioventricular conductivity and increased effective refractive period of atrioventricular ganglia, which eventually leads to the relaxation of smooth muscle of heart musculature and restores normal sinus rhythm during supraventricular tachycardias. 

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... 

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... 

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. 

Schematic representation of the heart and normal cardiac electrical activity (intracellular recordings from areas indicated and ECG). Sinoatrial (SA) node, atrioventricular (AV) 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.

By these mechanisms, antiarrhythmic drugs can suppress ectopic automaticity and abnormal conduction occurring in depolarized cells— rendering them electrically silent—while minimally affecting the electrical activity in normally polarized parts of the heart. However, as... 

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