Cardiac electrical activity, normal

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.

Undoubtedly, the most promising modehng of the cardiac dynamics is associated with the study of the spatial evolution of the cardiac electrical activity. The cardiac tissue is considered to be an excitable medium whose the electrical activity is described both in time and space by reaction-diffusion partial differential equations [519]. This kind of system is able to produce spiral waves, which are the precursors of chaotic behavior. This consideration explains the transition from normal heart rate to tachycardia, which corresponds to the appearance of spiral waves, and the fohowing transition to fibrillation, which corresponds to the chaotic regime after the breaking up of the spiral waves, Figure 11.17. The transition from the spiral waves to chaos is often characterized as electrical turbulence due to its resemblance to the equivalent hydrodynamic phenomenon. 

Repolarization of the ventricle leads to the T wave. The T wave usually goes in the same direction as the QRS complex. The normal axis of the ECG is 30 degrees (above the horizontal) to 4-110 degrees (away from the horizontal) (Fig. 11-5). The six frontal plane (A) and the six horizontal plane (B) leads provide a three-dimensional representation of cardiac electrical activity. 

An arrhythmia may occur as a result of heart disease or from a disorder that affects cardiovascular function. Conditions such as emotional stress, hypoxia, and electrolyte imbalance also may trigger an arrhythmia An electrocardiogram (ECG) provides a record of the electrical activity of the heart. Careful interpretation of the ECG along with a thorough physical assessment is necessary to determine the cause and type of arrhythmia The goal of antiarrhythmic drug therapy is to restore normal cardiac function and to prevent life-threatening arrhythmias. 

An arrhythmia can be broadly defined as any significant deviation from normal cardiac rhythm.6 Various problems in the origination and conduction of electrical activity in the heart can lead to distinct types of arrhythmias. If untreated, disturbances in normal cardiac rhythm result in impaired cardiac pumping ability, and certain arrhythmias are associated with cerebrovascular accidents, cardiac failure, and other sequelae that can be fatal.1,2 16 Fortunately, a variety of drugs are available to help establish and maintain normal cardiac rhythm. 

The cardiac conduction system of the horse shares many features with other species but also has some important differences. The function of the heart relies upon the presence of cells capable of spontaneous activity these form the pacemaker areas of the heart. These nodal areas generate the normal cardiac rhythm. The electrical activity of the... 

Recent studies demonstrate that cardiac resynchronization therapy (CRT) offers a promising approach to selected patients with chronic heart failure. Delayed electrical activation of the left ventricle, characterized on the ECG by a QRS duration that exceeds 120 ms, occurs in approximately one-third of patients with moderate to severe systolic heart failure. Since the left and right ventricles normally activate simultaneously, this delay results in asynchronous contraction of the left and right ventricles, which contributes to the hemodynamic abnormalities of this disorder. Implantation of a speciahzed biventricular pacemaker to restore synchronous activation of the ventricles can improve ventricular contraction and hemodynamics. Recent trials show improvements in exercise capacity, NYHA classification, quality of life, hemodynamic function, and hospitalizations. A device that combined CRT with an implantable cardioverter-defibrillator (ICD) improved survival in addition to functional status. CRT is currently indicated only in NYHA class ni-IV patients receiving optimal medical therapy (ACE inhibitors, diuretics, -blockers, and digoxin) and... 

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). 

Cardiac arrest occurs when the heart s electrical activity becomes disrupted, causing it to beat irregularly (ventricular fibrillation) or to stop beating altogether. In either case, the heart cannot adequately pump blood to the brain and other vital organs. Often defibrillation is the only way to restore the heart s normal rhythm — particularly with ventricular fibrillation. 

A rhythm that can look normal electrically but there is no cardiac output and the patient is in cardiac arrest (Fig. 6.37). In this instance the electrical activity in the heart is working but there is no mechanical action taking place. As with asystole there is a poor outcome. Treatment consists of correcting reversible canses and CPR. 

Cardiac glycosides (CG) bind to the extracellular side of Na+/lC-ATPases of cardiomyocytes and inhibit enzyme activity. The Na+/lC-ATPases operate to pump out Na+ leaked into the cell and to retrieve 1C leaked from the cell. In this manner, they maintain the transmembrane gradients for 1C and Na+, the negative resting membrane potential, and the normal electrical excitability of the cell membrane. When part of the enzyme is occupied and inhibited by CG, the unoccupied remainder can increase its level of activity and maintain Na and 1C transport The effective stimulus is a small elevation of intracellular Na concentration (normally approx. 7 mM). 

In the undamaged myocardium, cardiac impulses travel rapidly antegrade through the Purkinje hbers to deliver the excitatory electrical impulse to the ventricular myocardium. During the normal activation sequence, retrograde conduction from ventricular myocardium to the conducting hbers is prevented by the longer duration of the membrane action potential and thus the refractory period in the Purkinje hbers. 

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. 

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