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Chapter: Medical Surgical Nursing: Management of Patients With Dysrhythmias and Conduction Problems

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Dysrhythmias: Normal Electrical Conduction

Dysrhythmias: Normal Electrical Conduction
Dysrhythmias are disorders of the formation or conduction (or both) of the electrical impulse within the heart.

Dysrhythmias

Dysrhythmias are disorders of the formation or conduction (or both) of the electrical impulse within the heart. These disorders can cause disturbances of the heart rate, the heart rhythm, or both. Dysrhythmias may initially be evidenced by the hemodynamic effect they cause (eg, a change in conduction may change the pumping action of the heart and cause decreased blood pressure).Dysrhythmias are diagnosed by analyzing the electrocardiographic waveform. They are named according to the site of origin of the impulse and the mechanism of formation or conduction involved (Chart 27-1). For example, an impulse that originates in the sinoatrial (SA) node and that has a slow rate is called sinus bradycardia.


NORMAL ELECTRICAL CONDUCTION

The electrical impulse that stimulates and paces the cardiac muscle normally originates in the sinus node (SA node), an area located near the superior vena cava in the right atrium. Usually, the elecrical impulse occurs at a rate ranging between 60 and 100 times a minute in the adult. The electrical impulse quickly travels from the sinus node through the atria to the atrioventricular (AV) node (Fig. 27-1). The electrical stimulation of the muscle cells of the atria causes them to contract. The structure of the AV node slows the electrical impulse, which allows time for the atria to contract and fill the ventricles with blood before the electrical impulsetravels very quickly through the bundle of His to the right and left bundle branches and the Purkinje fibers, located in the ventricular muscle. The electrical stimulation of the muscle cells of the ventricles, in turn, causes the mechanical contraction of the ventricles (systole). The cells repolarize and the ventricles then relax (diastole). The process from sinus node electrical impulse generation through ventricular repolarization completes the electro mechanical circuit, and the cycle begins again.

Sinus rhythm promotes cardiovascular circulation. The electrical impulse causes (and, therefore, is followed by) the mechanical contraction of the heart muscle. The electrical stimulation is called depolarization; the mechanical contraction is called systole. Electrical relaxation is called repolarization and mechanical relaxation is called diastole.           


Influences on Heart Rate and Contractility

 

The heart rate is influenced by the autonomic nervous system, which consists of sympathetic and parasympathetic fibers. Sym-pathetic nerve fibers (also referred to as adrenergic fibers) are at-tached to the heart and arteries as well as several other areas in the body. Stimulation of the sympathetic system increases heart rate (positive chronotropy), conduction through the AV node (positive dromotropy), and the force of myocardial contraction (positive inotropy). Sympathetic stimulation also constricts peripheral blood vessels, therefore increasing blood pressure. Parasympathetic nerve fibers are also attached to the heart and arteries. Parasympathetic stimulation reduces the heart rate (neg-ative chronotropy), AV conduction (negative dromotropy), and the force of atrial myocardial contraction. The decreased sym-pathetic stimulation results in dilation of arteries, thereby low-ering blood pressure.

Manipulation of the autonomic nervous system may increase or decrease the incidence of dysrhythmias. Increased sympathetic stimulation—caused, for example, by exercise, anxiety, fever, or administration of catecholamines (eg, dopamine [Intropin], aminophylline, dobutamine [Dobutrex])—may increase the in-cidence of dysrhythmias. Decreased sympathetic stimulation (eg, with rest, anxiety-reduction methods such as therapeutic com-munication or prayer, administration of beta-adrenergic block-ing agents) may decrease the incidence of dysrhythmias.

 

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