24. Drugs Used to Treat Dysrhythmias



Drugs Used to Treat Dysrhythmias


Objectives



Key Terms


conduction system (image) (p. 386)


dysrhythmia (image) (p. 386)


atrial flutter (image) (p. 387)


atrial fibrillation (image) (p. 387)


paroxysmal supraventricular tachycardia (PSVT) (image image image) (p. 387)


atrioventricular blocks (image) (p. 387)


tinnitus (image) (p. 393)


Dysrhythmias


image http://evolve.elsevier.com/Clayton


The function of the heart is to sustain life by rhythmically pumping blood to all the vital organs and the rest of the body’s tissues. The conduction system, or electrical system, of the heart is the anatomic structure that controls the sequence of muscle contractions so that an optimal volume of blood is pumped from the heart with each beat (Figure 24-1).image The conduction system is composed of nerve fibers that carry the electrical impulses to the cardiac muscle, causing it to contract.



In the normal heart, a contraction of the heart muscle begins in the pacemaker cells of the sinoatrial (SA) node. The electrical wave passes through the conduction system in the atrial muscle and causes it to contract, forcing blood from the atrial chambers into the ventricles below. The electrical current then enters the atrioventricular (AV) node, which focuses and conducts an electrical current through the bundle of His and Purkinje fibers to the ventricular muscle tissue. The muscle contracts from the apex upward, causing blood to be pumped from the right ventricle into the pulmonary artery to the lungs and from the left ventricle into the aorta to the rest of the body.


A dysrhythmia (sometimes called an arrhythmia) occurs when there is a disturbance of the normal electrical conduction, resulting in an abnormal heart muscle contraction or heart rate. All people have an occasional irregular contraction of the heart. The danger is the frequency with which the dysrhythmia occurs because the heart muscle loses its efficiency in pumping an adequate volume of blood. Thus certain types of dysrhythmias can produce additional dysrhythmias that can stop the heart from pumping even though it continues to beat for a short time (fibrillation). A person may sense an abnormal contraction (dysrhythmia) because of a flip-flop or racing of the heart. A nurse may also suspect that a patient is having dysrhythmia because of an irregular pulse. Dysrhythmias, however, must be identified with the aid of an electrocardiogram (ECG), which provides a tracing of the electrical activity of the heart.


Dysrhythmias are caused by the firing of abnormal pacemaker cells, blockage of normal electrical pathways, or a combination of both. Normally, the rate and rhythm of electrical activity and muscle contraction are regulated by the pacemaker cells of the SA node. High emotional stress, ischemia (see Chapter 25), or heart failure (see Chapter 28) may trigger normally quiet pacemaker cells in areas of the heart other than the SA or AV nodes to fire. This sends an electrical impulse out of sequence with those from the normal pacemaker cells, causing an irregular muscular contraction, sometimes sensed as a flip-flop of the heart. The second cause of a dysrhythmia is a partial obstruction of the normal conduction pathway, causing an irregular flow of electrical impulses that results in an irregular pattern of muscle contractions. This is sometimes called a reentrant dysrhythmia. Normally, healthy heart tissue has mechanisms that protect against reentrant dysrhythmias. Various forms of heart disease cause changes in the conduction pathways that allow continuous reentrant dysrhythmias.


Dysrhythmias are most commonly classified by origin within the heart tissues. Those that develop above the bundle of His (see Figure 24-1) are called supraventricular. Examples of supraventricular dysrhythmias are atrial flutter, atrial fibrillation, premature atrial contractions(PACs), sinus tachycardia, sinus bradycardia, and paroxysmal supraventricular tachycardia (PSVT). Junctional dysrhythmias are those developing near or within the AV node. Dysrhythmias developing below the bundle of His are referred to as “ventricular dysrhythmias.” These include premature ventricular contractions (PVCs), ventricular tachycardia (VT), and ventricular fibrillation (VF). Dysrhythmias that result from obstruction of conduction pathways are described by location (e.g., supraventricular or ventricular, left or right bundle branches). Atrioventricular blocks can be subclassified by degree of block: first degree = partial block, delayed AV conduction; second degree = partial block, with occasional blocked beats; and third degree = complete block, in which the atria and ventricles function independently of each other. Another method of classification is based on heart beat rate: bradyarrhythmia (more than 60 beats/min) or tachyarrhythmia (more than 100 beats/min).


The tissues of the electrical system can be classified by conduction rate depending on whether calcium or sodium ions create the stimulus for muscle contraction. The SA and AV nodes depend on calcium ions for electrical conduction and are referred to as “slow conduction fibers.” The atrial muscle, His-Purkinje system, and ventricular muscle depend on sodium for contraction and are sometimes referred to as “fast conduction fibers.”


Treatment for Dysrhythmias


When a dysrhythmia is suspected, a patient is often admitted to a coronary care unit, where wire leads are placed in appropriate locations to provide continuous electrocardiographic monitoring (telemetry). A combination of the physical examination, patient history, and electrocardiographic pattern is used to diagnose the underlying cause of the dysrhythmia. The goal of treatment is to restore normal sinus rhythm and normal cardiac function and prevent recurrence of life-threatening dysrhythmias.


Drug Therapy for Dysrhythmias


Actions


Antidysrhythmic agents are complex agents with multiple mechanisms of action. They are classified according to their effects on the electrical conduction system of the heart (Table 24-1). Class I agents act as myocardial depressants by inhibiting sodium ion movement. The Class Ia agents prolong the duration of the electrical stimulation on cells and the refractory time between electrical impulses. Class Ib agents shorten the duration of the electrical stimulation and the time between the electrical impulses. Class Ic antidysrhythmics are the most potent myocardial depressants and slow the conduction rate through the atria and the ventricles.



Class II agents are beta-adrenergic blocking agents (beta blockers). Many dysrhythmias are caused by stimulation of the beta cells of the sympathetic nervous system of the heart. Class III agents slow the rate of electrical conduction and prolong the time interval between contractions by blocking potassium channels. Class IV agents block calcium ion flow, prolonging duration of the electrical stimulation and slowing AV node conduction.


Uses


See individual drug monographs for uses of antidysrhythmic agents.


imageNursing Implications for Antidysrhythmic Agents


The information that nurses assess relative to the cardinal signs of cardiovascular disease can provide a basis for subsequent evaluation of the patient’s response to the therapeutic modalities prescribed.


Assessment

Dysrhythmias are initially assessed by electrocardiographic monitoring. Various types of telemetry monitoring equipment are available. It is vitally important for the nurse not to rely completely on computerized systems, but rather to perform frequent patient assessments while viewing the telemetry system as an adjunct to astute nursing observations. A 24-hour ambulatory ECG (Holter monitor), electrophysiologic studies (EPS), exercise electrocardiography, and laboratory values are used to analyze and diagnose the patient’s myocardial status.


Patients are usually admitted to the coronary care unit, where specialized monitoring equipment is available for continuous surveillance of the patient. The nurses in this care unit have advanced education in cardiac physiology and the nursing care of these individuals. (See a general medical-surgical nursing text or critical care textbook for an in-depth explanation of care of the patient with a dysrhythmia.)


Medication History.

Obtain details of all medications prescribed and being taken. Tactfully find out if the prescribed medications are being taken regularly and if not, why.


History of Six Cardinal Signs of Cardiovascular Disease


• Dyspnea (difficulty in breathing): Record if dyspnea occurs while resting or during exertion. Is the patient affected by position, such as lying down? Does he or she awaken from sleep at night?


• Chest pain: Record data as to the time of onset, frequency, duration, and quality of the chest pain. Note any conditions that the patient has found that either aggravate or relieve the chest pain. Are there any associated symptoms with the pain such as sweating, ashen gray or pale skin, heart skipping a beat, shortness of breath, nausea or vomiting, or racing of the heart? (Not all patients with a dysrhythmia have chest pain.)


• Fatigue: Determine whether fatigue occurs only at specific times of the day, such as evening. Ask the patient if fatigue decreases in relation to a decrease in activity level or if it is present at about the same time daily. Can he or she keep up with family and coworkers?


• Edema: Record the presence or absence of edema. If present, record location of edema, assessment data (e.g., degree of pitting present; ankle, mid-calf, or thigh circumference), and any measures that the patient has used to eliminate edema. Chart the time of day that the edema is present (e.g., when rising in the morning, later in the evening) and the specific parts where it is present on the body. When performing daily weights, use the same scale, at the same time of day, with the patient in a similar type of clothing.


• Syncope: Ask the patient about conditions surrounding any episodes of syncope (faintness or dizziness). Record the degree of symptoms such as general muscle weakness, inability to stand upright, feeling of faintness, or loss of consciousness. Record what activities, if any, bring on these syncopal episodes.


• Palpitations: Record the patient’s description of palpitations, such as “my heart skips some beats” or “it began to feel as if it were racing.” Ask if these conditions are preceded by mild or strenuous exercise and how long the palpitations last.


Basic Mental Status.

Identify the person’s level of consciousness and clarity of thought. Both of these factors are indicators of adequate or inadequate cerebral perfusion. Subsequent regular observations for these data should be made so that apparent improvement or deterioration can be assessed. Schedule basic neurologic assessments at least once per shift.


Vital Signs.

Vital signs should be taken as often as necessary to monitor the patient’s status.



• Blood pressure: Blood pressure readings should be performed at least twice daily in stable cardiac patients and more often if indicated by the patient’s symptoms or the health care provider’s orders. Be sure to use the proper-sized blood pressure cuff and have the patient’s arm at heart level.


• Record the blood pressure in both arms: A systolic pressure variance of 5 to 10 mm Hg is normal; readings reflecting a variance of more than 10 mm Hg should be reported for further evaluation. Always report a narrowing pulse pressure (difference between systolic and diastolic readings).


• Pulse: Assess bilaterally the rhythm, quality, equality, and strength of the pulses (carotid, brachial, radial, femoral, popliteal, posterior tibial, and dorsalis pedis). If any pulse is diminished or absent, record the level at which initial changes are noted. The usual words to describe the pulse are absent, weak, normal, increased, or bounding. Report irregular rate, rhythm, and patient-reported palpitations. Check for delayed capillary refill.


• Respirations: Observe and chart the rate and depth of respirations. Check breath sounds at least every shift, making specific notations regarding the presence of abnormal breath sounds such as crackles or wheezes. Observe the degree of dyspnea that occurs and whether it happens with or without exertion.


• Temperature: Record the patient’s temperature at least every shift.


• Oxygen saturation: Record the patient’s O2 saturation using a pulse oximeter with each vital sign measurement.


Auscultation and Percussion.

Nurses with advanced skills can perform auscultation and percussion to note changes in heart size and heart and lung sounds. (See a medical-surgical nursing text for details about performing these skills.) As appropriate to nursing skills, note changes in cardiac rhythm, heart rate, changes in heart sounds, or murmurs.


Laboratory and Diagnostic Tests.

Review laboratory tests and report abnormal results to the health care provider promptly. Such tests may include levels of serum electrolytes, especially potassium, calcium, magnesium, and sodium; arterial blood gases such as pH, PO2, PCO2, and HCO3−; coagulation studies to evaluate the blood clotting; serum enzyme levels, including aspartate aminotransferase (AST), creatine kinase (CK-MB), troponin, D-dimer, and lactic dehydrogenase (LDH); serum lipid levels (e.g., cholesterol, triglycerides); electrocardiography; chest radiography; nuclear cardiography; cardiac catheterization; EPS testing; and exercise treadmill.


Examine urinalysis reports and perform hourly monitoring of intake and output (I&O) as ordered. Report output that is less than intake or is below 30 to 50 mL per hour for the adult patient. Monitor other renal function tests such as the blood urea nitrogen (BUN) and serum creatinine. Abnormalities of these tests or insufficient hourly output may indicate inadequate renal perfusion.


Implementation


• Monitor electrocardiographic tracings on a continuum (telemetry).


• Perform physical assessments of the patient in accordance with the clinical setting’s policies (e.g., every 4 to 8 hours, depending on the patient’s status).


• Assist the patient, as needed, to perform activities of daily living (ADLs). Make note of the degree of impairment or dyspnea seen with and without exertion.


• Administer oxygen as ordered and as necessary (PRN).


• Be aware of the policy for calling “codes,” location of the emergency cart, and procedures used to check the emergency cart supplies. Know the procedure for defibrillation and cardioversion.


• Administer prescribed medications and treatments per Advanced Cardiac Life Support(ACLS) protocol that can best alleviate the patient’s symptoms and provide maximum level of comfort.


• Encourage physical activity as prescribed. Do not allow the patient to overexert or become fatigued.


• Institute measures to reduce anxiety. Support the patient in a calm manner, even if he or she responds in a hostile or confrontational way.


image Patient Education and Health Promotion


Fostering Health Maintenance


Written Record.

Enlist the patient’s aid in developing and maintaining a written record of monitoring parameters (e.g., pulse rate, blood pressure, degree of dyspnea and precipitating causes, chest pain, edema) (see Patient Self-Assessment Form for Cardiovascular Agents on the Evolve Webimage site for this text). Complete the Premedication Data column for use as a baseline to track response to drug therapy. Ensure that the patient understands how to use the form and instruct the patient to bring the completed form to follow-up visits. During follow-up visits, focus on issues that will foster adherence to the therapeutic interventions prescribed.


Drug Class: Class Ia Antidysrhythmic Agents



disopyramide (image)


Norpace (image)


Actions


Disopyramide is a class Ia antidysrhythmic agent.


Uses


Disopyramide is used to treat life-threatening premature ventricular tachycardia and ventricular tachycardia. It may be used in digitalized and nondigitalized patients. It is a useful drug alternative to quinidine or procainamide when patients develop an intolerance to, or serious adverse effects from, these agents. It should not be used in cardiogenic shock, second- or third-degree block (without a pacemaker already in place), or Q-T prolongation.


Therapeutic Outcome


The primary therapeutic outcome expected from disopyramide therapy is conversion of dysrhythmia to normal sinus rhythm.


imageNursing Implications for Disopyramide


Premedication Assessment


Availability

PO: 100- and 150-mg capsules; 100- and 150-mg controlled-release capsules.


Dosage and Administration

PO: Dosage is individualized but is usually 400 to 800 mg/day. Initial dosage is 100 mg every 6 to 8 hours. Making adjustments gradually, the recommended adult dosage schedule is 150 mg every 6 hours. If body weight is less than 110 lb (50 kg), the recommended dosage is 100 mg every 6 hours. Therapeutic blood level is 2 to 4 mg/L.


Monitoring

Common Adverse Effects

Oropharyngeal


Dry Mouth, Nose, Throat.


Suggest frequent mouth rinses or sucking on ice chips or hard candy to relieve symptoms.


Serious Adverse Effects

Cardiovascular


Myocardial Toxicity.


Hold the medication and report bradycardia or increasing signs of heart failure. Monitoring of the ECG for various types of dysrhythmias may be indicated as ordered by the physician.


Genitourinary


Urinary Hesitancy.


Tell the patient that hesitancy in starting to urinate may occur. Suggest running tap water or immersing hands in water as a means to stimulate urination. Report decreased urinary output and bladder distention. In the hospitalized patient, record input and output. Palpate the area of the symphysis pubis to assess for distention.


Gastrointestinal


Constipation With Distension and Flatus.


Report difficulties in defecation to the physician. Assess distention by measuring abdominal girth, as appropriate. Assess ability to expel flatus.


Drug Interactions

Drugs That Enhance Therapeutic and Toxic Effects.

These include procainamide, quinidine, digoxin, erythromycin, clarithromycin, fluoroquinolones (e.g., ciprofloxacin), ziprasidone, and beta blockers (e.g., propranolol, atenolol). Monitor for increases in severity of drug effects such as bradycardia and hypotension.


Drugs That Enhance Therapeutic and Toxic Effects.

Do not administer disopyramide within 48 hours before or 24 hours after administration of verapamil.


Drugs That Reduce Therapeutic Effects.

These include phenytoin, barbiturates, primidone, and rifampin. Monitor for an increase in the frequency of the patient’s dysrhythmia.


Drugs That Increase Hypotensive Effects.

These include diuretics and antihypertensive agents. Instruct the patient to rise slowly from a supine position. If symptoms become more severe, report to the health care provider.



procainamide hydrochloride (image)


image Do not confuse procainamide with prochlorperazine.


Actions


Procainamide is an effective synthetic class Ia antidysrhythmic agent that has many cardiac effects similar to those of quinidine but generally with fewer adverse effects.


Uses


Procainamide is used to treat a wide variety of life-threatening ventricular and supraventricular dysrhythmias, atrial fibrillation, and flutter. It is usually not as effective as quinidine in atrial fibrillation. Procainamide is not recommended for the treatment of asymptomatic PVCs.


Therapeutic Outcome


The primary therapeutic outcome expected from procainamide therapy is conversion of dysrhythmia to normal sinus rhythm.


imageNursing Implications for Procainamide


Premedication Assessment

Obtain data relating to the six cardinal signs of cardiovascular disease and assess cardiac rhythm, vital signs, and oxygen saturation to be used as a baseline for subsequent evaluation of response to therapy.


Availability

IV: 100 mg/mL in 10-mL vials and 500 mg/mL in 2-mL vials. (High-alert medication).


Dosage and Administration

Adult: IV: 50 mg/kg/day in four to eight divided doses (every 3 to 6 hours) or by continuous infusion of 2 to 6 mg/min to maintain control of the dysrhythmia.



image Medication Safety Alert


Do not use procainamide in complete AV block, and use with extreme caution in partial AV block.


Patients should have monitoring of the ECG and blood pressure when receiving IV doses of procainamide. If dysrhythmia recurs, suppress the dysrhythmia with bolus therapy, as above, and increase the rate of infusion.


Serum levels of procainamide are determined to measure the amount of procainamide and N-acetyl procainamide (an active metabolite) in the bloodstream. It is important to be consistent in the time of drawing the blood and administering the dose if more than one serum level is to be determined in the same patient. Therapeutic blood levels are 4 to 8 mg/L.


Monitoring

Common Adverse Effects

Neurologic


Drowsiness, Sedation, Dizziness.


Tell patients that they may experience these symptoms early in therapy as the dosage is being adjusted. Instruct patients to use caution in operating power equipment or driving.


Cardiovascular


Hypotension.


Hypotension may be observed while therapy is being initiated, particularly by the IV route. Hypotension is usually transient and can be avoided by rising slowly from supine and sitting positions. However, should the systolic blood pressure fall 15 mm Hg or more, hold the medication and notify the prescriber.


Serious Adverse Effects

Immunologic


Fever, Chills, Joint and Muscle Pain, Skin Eruptions.


Tell patients to report the development of these symptoms. Monitor laboratory reports for leukocyte counts and the antinuclear antibody (ANA) titer.


Drug Interactions

Drugs That Enhance Therapeutic and Toxic Effects.

These include digoxin, cimetidine, ranitidine, quinidine, trimethoprim, amiodarone, fluoroquinolones (e.g. ciprofloxacin), ziprasidone, and beta-adrenergic blocking agents (e.g., nadolol, propranolol). Monitor for an increase in severity of adverse effects such as bradycardia and hypotension.


Neuromuscular Blockade, Respiratory Depression.

Procainamide may potentiate the neuromuscular blockade induced by these agents. These agents include surgical muscle relaxants (e.g., tubocurarine, succinylcholine) and aminoglycoside antibiotics (e.g., tobramycin, gentamicin, amikacin). Monitor the patient’s respiratory rate and depth. Observe for signs of cyanosis and additional dysrhythmia.


Patients who are on respirators may require additional time to be weaned off ventilatory assistance.


Hypotension With Diuretics and Antihypertensive Agents.

Instruct patients to rise slowly from a supine position. If symptoms begin to recur more frequently, report to the physician.



quinidine (image)


image Do not confuse quinidine with quinacrine on quinine.


Actions


Quinidine, originally obtained from cinchona bark, has been used as an antidysrhythmic agent for several decades. It is classified as a class Ia antidysrhythmic agent, working on the muscle of the heart and stabilizing the rate of conduction of impulses. It slows the heart and changes a rapid irregular pulse to a slow regular pulse.


Uses


Quinidine is used most often to suppress atrial fibrillation, atrial flutter, PSVT and ventricular tachycardia, and life-threatening PVCs. Use with extreme caution in patients with digitalis intoxication or heart block.


Therapeutic Outcome


The primary therapeutic outcome expected from quinidine therapy is conversion of dysrhythmia to normal sinus rhythm.


imageNursing Implications for Quinidine


Premedication Assessment

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Jul 11, 2016 | Posted by in NURSING | Comments Off on 24. Drugs Used to Treat Dysrhythmias

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