Dysrrhythmia Monitoring Intervening Key Points Cardiac electrical activity

Dysrrhythmia Monitoring & Intervening

Key Points Cardiac electrical activity can be monitored by using an electrocardiogram (ECG); a standard 12 -lead ECG (resting ECG), ambulatory ECG (Holter monitoring), continuous cardiac monitoring, or by telemetry Cardiac dysrhythmias are heartbeat disturbances (beat formation, beat conduction, myocardial response to beat). Dysrhythmias are classified by the: Site of origin: SA node, atria, atrioventricular (AV) node, or ventricle. Effect on heart’s rate and rhythm: Bradycardia, tachycardia, heart block, premature beat, flutter, fibrillation, or asystole.

Key Points Dysrhythmias may be benign or life-threatening; decreased cardiac output and ineffective tissue perfusion. Cardiac dysrhythmias are 1 ry cause of death in clients suffering acute MI, and other sudden death disorders. Therefore, rapid Dx & Rx of serious dysrhythmias is essential to preserve life. Dysrhythmia treatment is based on the client’s symptoms and the cardiac rhythm. Cardioversion is the delivery of synchronized direct countershock to the heart for the elective treatment of atrial dysrhythmias or ventricular tachycardia with pulse. Defibrillation is the delivery of an unsynchronized, direct countershock to the heart during ventricular fibrillation or pulseless ventricular tachycardia. Defibrillation stops all electrical activity of the heart, allowing the sinoatrial (SA) node to take over and reestablish a perfusing rhythm.

Dysrhythmia Medication Electrical Management Bradycardia (any rhythm < 60 beats/min) Treat if client is symptomatic Atropine, isoproterenol Pacemaker Atrial Fibrillation, Supraventricular Tachycardia (SVT), or Ventricular Tachycardia with pulse Amiodarone, adenosine, verapamil Synchronized cardioversion Ventricular Tachycardia without pulse or Ventricular Fibrillation Amiodarone, lidocaine, epinephrine Defibrillation

Risk Factors for Dysrhythmias Cardiovascular disease MI Hypoxia Acid-base imbalances Electrolyte disturbances Chronic renal, hepatic, or lung disease Pericarditis Drug use or abuse Hypovolemia Shock

Nursing Interventions Perform 12 -lead ECG by: Monitor for S & Sx of decreased perfusion (chest pain, decreased level of consciousness, SOB) and hypoxia. Prevention Reduce risk factors for CAD. Correct electrolyte imbalances. Treat substance abuse. Manage stress, fever, and anxiety. Assess/monitor for signs of decreased cardiac output (hypotension, irregular heart beats, fatigue, dyspnea, chest pain, syncope). Monitor for pulmonary or systemic emboli following cardioversion. Administer oxygen.

Nursing Interventions Administer prescribed antidysrhythmic agent or other prescribed medications. Perform CPR for cardiac asystole or other pulseless rhythms. Defibrillate immediately for ventricular fibrillation Prepare the client for cardioversion if prescribed. Cardioversion is the treatment of choice for symptomatic clients. Clients with atrial fibrillation of unknown duration must receive adequate anticoagulation prior to cardioversion therapy. Administer oxygen and sedation as prescribed. Cardioversion requires activation of the synchronizer button in addition to charging the machine. Failure to synchronize can lead to development of a lethal dysrhythmia, such as ventricular fibrillation. After defibrillation or cardioversion, check vital signs, assess airway patency, and obtain an ECG. Provide reassurance and emotional support to the client and family.

Nursing Interventions Documentation: Client’s condition prior to intervention Pre- and postprocedure rhythm Number of defibrillation or cardioversion attempts, energy settings, time, and response Vital signs Emergency medications administered including times and dosages The client’s condition and state of consciousness following the procedure Teach the client and family regarding the need for compliance with prescribed medication regimen. Teach the client and family how to assess pulse.

Complications and Nursing Implications Embolism PE – dyspnea, chest pain, air hunger, decreasing Sa. O 2 CVA – decreased level of consciousness, slurred speech, muscle weakness/paralysis MI – chest pain, ST segment depression or elevation Provide therapeutic anticoagulation for clients with dysrhythmias. Decreased Cardiac Output and Heart Failure Monitor for signs of decreased cardiac output (hypotension, syncope, increased heart rate) and of heart failure (dyspnea, productive cough, edema, distention). Provide medications to increase output (inotropic agents) and to decrease cardiac workload.

Heart Failure and Cardiomyopathy

Key Points v. HF: inability of the heart to maintain adequate circulation to meet tissue needs for oxygen and nutrients. v. Heart failure occurs when the heart muscle is unable to pump effectively, resulting in: v inadequate cardiac output, v myocardial hypertrophy, and v pulmonary/systemic congestion. v. Heart failure is the result of: an acute or chronic cardiopulmonary problem, such as systemic HTN, PE, pulmonary HTN, dysrhythmias, valvular heart disease, pericarditis, and cardiomyopathy.

Key Points v Severity of heart failure is graded on classification scale indicating how little, or how much, activity it takes to make the client symptomatic (chest pain, SOB). Class I: Client exhibits no symptoms with activity. Class II: Client has symptoms with ordinary exertion. Class III: Client displays symptoms with minimal exertion. Class IV: Client has symptoms at rest. Cardiomyopathy is a change in the structure of cardiac muscle fibers that causes impaired cardiac function leading to heart failure. Blood circulation is impaired to the lungs or body when the cardiac pump is compromised. There are three main types: Dilated – decreased contractility and increased ventricular filling pressures. Hypertrophic – increased thickness of ventricular and/or septal muscles. Restrictive – ventricles become rigid and lose their compliance.

Key Points Low output heart failure can initially occur on either Lt/Rt side of the heart. Left-sided heart (ventricular) failure results in inadequate left ventricle (cardiac) output and consequently in inadequate tissue perfusion. Right-sided heart (ventricular) failure results in inadequate right ventricle output and systemic venous congestion (for example, peripheral edema).

Key Factors Risk Factors/Causes: Left-Sided Heart (Ventricular) Failure Hypertension CAD, angina, myocardial infarction (MI) Valvular disease (mitral and aortic) Risk Factors/Causes: Right-Sided Heart (Ventricular) Failure Left-sided heart (ventricular) failure Right ventricular myocardial infarction Pulmonary problems (COPD, ARDS) Risk Factors/Causes: Cardiomyopathy Coronary artery disease Infection or inflammation of the heart muscle Various cancer treatments Prolonged alcohol abuse Heredity

Diagnostic Procedures and Nursing Interventions Hemodynamic Monitoring: Increased CVP, increased right arterial pressure, increased pulmonary artery pressure (PAP), and decreased cardiac output (CO) Ultrasound (echocardiogram): 2 D or 3 D to measure both systolic and diastolic function of the heart. Chest x-ray can reveal cardiomegaly and pleural effusions. Electrocardiogram (ECG), cardiac enzymes, electrolytes, and arterial blood gases: Assess factors contributing to heart failure and/or the impact of heart failure.

Therapeutic Procedures and Nursing Interventions A ventricular assist device (VAD) is a mechanical pump that assists a heart that is too weak to pump blood through the body. A VAD is used in clients who have severe end-stage congestive heart failure and are not candidates for heart transplants. Heart transplantation is the treatment of choice for clients with severe dilated cardiomyopathy. Heart transplantation is a possible option for clients with end-stage heart failure. Immunosuppressant therapy is required post transplantation to prevent rejection.

Assessments S & Sx of Left-sided failure Dyspnea, orthopnea, nocturnal dyspnea Fatigue Displaced apical pulse (hypertrophy) S 3 heart sound (gallop) Pulmonary congestion (dyspnea, cough, bibasilar crackles) Frothy sputum (may be blood-tinged) Altered mental status Symptoms of organ failure, such as oliguria Hemodynamic findings: CVP/right atrial pressure (normal = 1 to 8 mm Hg): Normal or elevated Pulmonary Artery Pressure (normal = 15 to 26 mm Hg/5 to 15 mm Hg): Elevated CO (normal = 4 to 7 L/min): Decreased

Assessments Right-sided failure Jugular vein distention Ascending dependent edema (legs, ankles, sacrum) Abdominal distention, ascites Fatigue, weakness Nausea and anorexia Polyuria at rest (for example, nocturnal) Liver enlargement (hepatomegaly) and tenderness Weight gain Hemodynamic findings CVP/right atrial pressure (normal = 1 to 8 mm Hg): Elevated

Assessments Cardiomyopathy Fatigue, weakness Heart failure (left with dilated type, right with restrictive type) Dysrhythmias (for example, heart block) S 3 gallop Cardiomegaly

Assess/Monitor Oxygen saturation VS Heart rhythm Lung sounds for crackles, wheezes Level of dyspnea upon exertion Serum electrolytes (especially potassium if receiving diuretics) Daily Wt Changes in LOC I&O For signs of drug toxicity Coping ability of client and family

NANDA Nursing Diagnoses Impaired gas exchange Decreased cardiac output Activity intolerance Excess fluid volume Ineffective tissue perfusion (cerebral) Risk for ineffective tissue perfusion (renal)

Nursing Interventions Place the client in high-Fowler’s, if a client is experiencing respiratory distress O 2 as prescribed. Encourage bed rest until the client is stable. Encourage energy conservation by assisting with care and ADL Maintain dietary restrictions (restricted fluid intake, restricted sodium intake). Administer medications as prescribed. Diuretics: To decrease preload Loop diuretics, such as furosemide (Lasix), bumetanide (Bumex) Thiazide diuretics, such as hydrochlorothiazide (Hydro. DIURIL) Potassium-sparing diuretics, such as spironolactone (Aldactone) Teach the client taking loop or thiazide diuretics to ingest foods and drinks that are high in potassium to counter hypokalemia effect. Potassium supplementation may be required. Administer IV furosemide (Lasix) no faster than 20 mg/min.

Nursing Interventions Afterload-Reducing Agents ACE inhibitors, such as enalapril (Vasotec), captopril (Capoten); monitor for initial dose hypotension. Beta-blockers, such as carvedilol (Coreg), metoprolol (Lopressor XL) Angiotensin receptor II blockers, such as losartan (Cozaar) Inotropic agents, such as digoxin (Lanoxin), dopamine, dobutamine (Dobutrex), milrinone (Primacor): To increase contractility and thereby improve cardiac output Vasodilators, such as nitrates: To decrease preload and afterload

Nursing Interventions Anticoagulants, such as warfarin (Coumadin), heparin, clopidogrel: To prevent thrombus formation (risk associated with congestion/stasis and associated atrial fibrillation) Teach clients who are self-administering digoxin (Lanoxin) to: Count pulse for one full minute before taking the medication. If the pulse rate is irregular or less than 60 or greater than 100), instruct the client to hold the dose and to contact the primary care provider. Take digoxin (Lanoxin) dose at same time each day. Do not take digoxin at the same time as antacids (Separate by 2 hr). Report signs of toxicity, including fatigue, muscle weakness, confusion, and loss of appetite. Regularly have digoxin and potassium levels checked. Provide emotional support to the client and family.

Client Education Take medications as prescribed. Take diuretics in early morning and early afternoon. Maintain fluid and sodium restriction – a dietary consult may be useful. Increase dietary intake of potassium (? ) if taking potassiumlosing diuretics such as loop diuretics and thiazide diuretics. Weigh self daily at the same time and notify the primary care provider for weight gain of 1 kg in 24 hr or 2. 5 in 1 week. Schedule regular follow-ups with the primary care provider. Get vaccinations (pneumococcal vaccine and yearly influenza vaccine).

Complications and Nursing Implications Acute pulmonary edema is a life-threatening medical emergency, ( anxiety, tachycardia, ARDS, dyspnea at rest, change in LOC, and an ascending fluid level within lungs (crackles, cough productive of frothy, blood-tinged sputum). Urgent Rx: Positioning the client in high-Fowler’s position. Administration of oxygen, positive airway pressure, and/or intubation and mechanical ventilation. IV morphine (to decrease anxiety, respiratory distress, and decrease venous return). IV administration of rapid-acting loop diuretics, such as furosemide (Lasix). Effective intervention should result in diuresis (carefully monitor output), reduction in respiratory distress, improved lung sounds, and adequate oxygenation.

Complications and Nursing Implications Cardiogenic shock is a serious complication of pump failure. It is a class IV heart failure. Symptoms include tachycardia, hypotension (BP less than 90 mm Hg or less than 30 mm Hg from baseline BP), inadequate urinary output (less than 30 m. L/hr), altered LOC, respiratory distress (crackles, tachypnea), cool clammy skin, decreased peripheral pulses, and chest pain. Intervention oxygen; possible intubation and ventilation; IV administration of morphine, diuretics, and/or nitroglycerin to decrease preload; and IV administration of vasopressors and/or positive inotropes to increase cardiac output and to maintain organ perfusion. Other possible emergency interventions include use of an intra-aortic balloon pump and/or emergency coronary artery bypass surgery CABAG.

Complications and Nursing Implications Pericardial effusion and pericardial tamponade is an accumulation of fluid within the pericardial sac. Immediate intervention, such as a pericardiocentesis, sternotomy, and creation of a pericardial window, may be necessary in addition to measures to improve cardiac output. Administer anti-inflammatory medications as prescribed. Systemic and pulmonary emboli are possible complications due to decreased cardiac output and systemic congestion. New onsets of atrial fibrillation need to be reported. Organ failure, such as renal failure, is possible due to tissue ischemia