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BIOC33H3 (127)


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University of Toronto Scarborough
Biological Sciences
Stephen Reid

Chapter 36: Dysrhythmias  The ability to recognize normal and abnormal cardiac rhythms, called dysrhythmias, is an essential skill for the nurse.  Four properties of cardiac cells (automaticity, excitability, conductivity, and contractility) enable the conduction system to initiate an electrical impulse, transmit it through the cardiac tissue, and stimulate the myocardial tissue to contract. o A normal cardiac impulse begins in the sinoatrial (SA) node in the upper right atrium. o The signal is transmitted over the atrial myocardium via Bachmann’s bundle and internodal pathways, causing atrial contraction. o The impulse then travels to the atrioventricular (AV) node through the bundle of His and down the left and right bundle branches, ending in the Purkinje fibers, which transmit the impulse to the ventricles, resulting in ventricular contraction.  The autonomic nervous system plays an important role in the rate of impulse formation, the speed of conduction, and the strength of cardiac contraction. o Components of the autonomic nervous system that affect the heart are the right and left vagus nerve fibers of the parasympathetic nervous system and fibers of the sympathetic nervous system. ECG MONITORING  The electrocardiogram (ECG) is a graphic tracing of the electrical impulses produced in the heart.  ECG waveforms are produced by the movement of charged ions across the semipermeable membranes of myocardial cells.  There are 12 recording leads in the standard ECG. o Six of the 12 ECG leads measure electrical forces in the frontal plane (leads I, II, III, aVR, aVL , and aVF). o The remaining six leads (V thr1ugh V ) me6sure the electrical forces in the horizontal plane (precordial leads). o The 12-lead ECG may show changes that are indicative of structural changes, damage such as ischemia or infarction, electrolyte imbalance, dysrhythmias, or drug toxicity.  Continuous ECG monitoring is done using leads II, V , 1nd MCL . 1 o MCL is a1modified chest lead that is similar to V an1 is used when only three leads are available for monitoring. o Monitoring leads should be selected based on the patient’s clinical situation.  The ECG can be visualized continuously on a monitor oscilloscope, and a recording of the ECG (i.e., rhythm strip) can be obtained on ECG paper attached to the monitor.  ECG leads are attached to the patient’s chest wall via an electrode pad fixed with electrical conductive paste.  Telemetry monitoring involves the observation of a patient’s HR and rhythm to rapidly diagnose dysrhythmias, ischemia, or infarction.  Normal sinus rhythm refers to a rhythm that originates in the SA node and follows the normal conduction pattern of the cardiac cycle. o The P wave represents the depolarization of the atria (passage of an electrical impulse through the atria), causing atrial contraction. o The PR interval represents the time period for the impulse to spread through the atria, AV node, bundle of His, and Purkinje fibers. o The QRS complex represents depolarization of the ventricles (ventricular contraction), and the QRS interval represents the time it takes for depolarization. o The ST segment represents the time between ventricular depolarization and repolarization. This segment should be flat or isoelectric and represents the absence of any electrical activity between these two events. o The T wave represents repolarization of the ventricles. o The QT interval represents the total time for depolarization and repolarization of the ventricles. MECHANISMS OF DYSRHYTHMIAS  Normally the main pacemaker of the heart is the SA node, which spontaneously discharges 60 to 100 times per minute. Disorders of impulse formation can cause dysrhythmias.  A pacemaker from another site can lead to dysrhythmias and may be discharged in a number of ways. o Secondary pacemakers may originate from the AV node or His-Purkinje system. o Secondary pacemakers can originate when they discharge more rapidly than the normal pacemaker of the SA node. o Triggered beats (early or late) may come from an ectopic focus (area outside the normal conduction pathway) in the atria, AV node, or ventricles. EVALUATION OF DYSRHYTHMIAS  Dysrhythmias result from various abnormalities and disease states, and the cause of a dysrhythmia influences the treatment.  Several diagnostic tests are used to evaluate cardiac dysrhythmias and the effectiveness of antidysrhythmia drug therapy. o Holter monitoring records the ECG while the patient is ambulatory and performing daily activities. o Event monitors have improved the evaluation of outpatient dysrhythmias. o Signal-averaged ECG (SAECG) is a high-resolution ECG used to identify the patient at risk for developing complex ventricular dysrhythmias. o Exercise treadmill testing is used for evaluation of cardiac rhythm response to exercise. o An electrophysiologic study (EPS) identifies different mechanisms of tachydysrhythmias, heart blocks, bradydysrhythmias, and causes of syncope. TYPES OF DYSRHYTHMIAS  Sinus bradycardia has a normal sinus rhythm, but the SA node fires at a rate less than 60 beats/minute and is referred to as absolute bradycardia. o Clinical associations. Sinus bradycardia may be a normal sinus rhythm (e.g., in aerobically trained athletes), and it may occur in response to carotid sinus massage, Valsalva maneuver, hypothermia, and administration of parasympathomimetic drugs. o Disease states associated with sinus bradycardia are hypothyroidism, increased intracranial pressure, obstructive jaundice, and inferior wall myocardial infarction (MI). o Treatment consists of administration of atropine (an anticholinergic drug) for the patient with symptoms. Pacemaker therapy may be required.  Sinus tachycardia has a normal sinus rhythm, but the SA node fires at a rate greater than 100 beats/minute as a result of vagal inhibition or sympathetic stimulation. o Clinical associations. Sinus tachycardia is associated with physiologic and psychologic stressors such as exercise, fever, pain, hypotension, hypovolemia, anemia, hypoxia, hypoglycemia, myocardial ischemia, heart failure (HF), hyperthyroidism, anxiety, and fear. It can also be an effect of certain drugs. o Angina may result from sinus tachycardia due to the increased myocardial oxygen consumption that is associated with an increased HR. o Treatment is based on the underlying cause. For example, if a patient is experiencing tachycardia from pain, tachycardia should resolve with effective pain management.  Premature atrial contraction (PAC) is a contraction originating from an ectopic focus in the atrium in a location other than the sinus node. A PAC may be stopped (nonconducted PAC), delayed (lengthened PR interval), or conducted normally through the AV node. o Clinical associations. PACs can result from emotional stress or physical fatigue; from the use of caffeine, tobacco, or alcohol; from hypoxia or electrolyte imbalances; and from disease states such as hyperthyroidism, chronic obstructive pulmonary disease (COPD), and heart disease including coronary artery disease (CAD) and valvular disease. o In healthy persons, isolated PACs are not significant. In persons with heart disease, frequent PACs may indicate enhanced automaticity of the atria or a reentry mechanism and may warn of or initiate more serious dysrhythmias. o Treatment depends on the patient’s symptoms. For example, withdrawal of sources of stimulation such as caffeine or sympathomimetic drugs may be warranted.  Paroxysmal supraventricular tachycardia (PSVT) is a dysrhythmia originating in an ectopic focus anywhere above the bifurcation of the bundle of His. o PSVT occurs because of a reentrant phenomenon (reexcitation of the atria when there is a one-way block) and is usually triggered by a PAC. o In the normal heart, PSVT is associated with overexertion, emotional stress, deep inspiration, and stimulants such as caffeine and tobacco. It is also associated with rheumatic heart disease, digitalis toxicity, CAD, and cor pulmonale. o Prolonged PSVT with HR greater than 180 beats/minute may precipitate a decreased CO, resulting in hypotension, dyspnea, and angina. o Treatment for PSVT includes vagal stimulation and drug therapy (i.e., IV adenosine).  Atrial flutter is an atrial tachydysrhythmia identified by recurring, regular, sawtooth- shaped flutter waves that originate from a single ectopic focus in the right atrium. o Atrial flutter is associated with CAD, hypertension, mitral valve disorders, pulmonary embolus, chronic lung disease, cor pulmonale, cardiomyopathy, hyperthyroidism, and the use of drugs such as digoxin, quinidine, and epinephrine. o High ventricular rates (over 100/minute) and the loss of the atrial “kick” (atrial contraction reflected by a sinus P wave) can decrease CO and cause serious consequences such as chest pain and HF. o Patients with atrial flutter are at increased risk of stroke because of the risk of thrombus formation in the atria from the stasis of blood. o The primary goal in treatment of atrial flutter is to slow the ventricular response by increasing AV block.  Atrial fibrillation is characterized by a total disorganization of atrial electrical activity due to multiple ectopic foci resulting in loss of effective atrial contraction. o Atrial fibrillation usually occurs in the patient with underlying heart disease, such as CAD, rheumatic heart disease, cardiomyopathy, hypertensive heart disease, HF, and pericarditis. It can be caused by thyrotoxicosis, alcohol intoxication, caffeine use, electrolyte disturbances, stress, and cardiac surgery. o Atrial fibrillation can often result in a decrease in CO, and thrombi may form in the atria as a result of blood stasis. An embolized clot may develop and pass to the brain, causing a stroke. o The goals of treatment include a decrease in ventricular response and prevention of cerebral embolic events.  Junctional dysrhythmias refer to dysrhythmias that originate in the area of the AV node, primarily because the SA node has failed to fire or the signal has been blocked. In this situation, the AV node becomes the pacemaker of the heart. o Junctional premature beats are treated in a manner similar to that for PACs. o Other junctional dysrhythmias include junctional escape rhythm, accelerated junctional rhythm, and junctional tachycardia. These dysrhythmias are treated according to the patient’s tolerance of the rhythm and the patient’s clinical condition. o Junctional dysrhythmias are often associated with CAD, HF, cardiomyopathy, electrolyte imbalances, inferior MI, and rheumatic heart disease. Certain drugs (e.g., digoxin, amphetamines, caffeine, nicotine) can also cause junctional dysrhythmias. o Treatment varies according to the type of junctional dysrhythmia.  First-degree AV block is a type of AV block in which every impulse is conducted to the ventricles but the duration of AV conduction is prolonged. o First-degree AV block is associated with MI, CAD, rheumatic fever, hyperthyroidism, vagal stimulation, and drugs such as digoxin, -adrenergic blockers, calcium channel blockers, and flecainide. o First-degree AV block is usually not serious but can be a precursor of higher degrees of AV block. Patients with first-degree AV block are asymptomatic. o There is no treatment for first-degree AV block. Patients should continue to be monitored for any new changes in heart rhythm.  Second-degree AV block, Type I (Mobitz I or Wenckebach heart block) is a gradual lengthening of the PR interval. It occurs because of a prolonged AV conduction time until an atrial impulse is nonconducted and a QRS complex is blocked (missing). o Type I AV block may result from use of drugs such as digoxin or -adrenergic blockers. It may also be associated with CAD and other diseases that can slow AV conduction. o Type I AV block is usually a result of myocardial ischemia or infarction. It is almost always transient and is usually well tolerated. However,
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