1. Monitoring & Intervening
Dysrrhythmia
Monitoring & Intervening

3. 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.

4. 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.

5. Key Points
Cardioversion is the delivery of synchronized direct counter shock to the heart for the elective treatment of atrial dysrhythmias or ventricular tachycardia with pulse.
Defibrillation is the delivery of an unsynchronized, direct counter shock 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.

6. Electrical Management
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

7. 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

8. 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.

9. 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.

10. 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.

11. Complications and Nursing Implications
Embolism
PE – dyspnea, chest pain, air hunger, decreasing SaO2
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.

13. Heart Failure and Cardiomyopathy

14. Key Points
HF: inability of the heart to maintain adequate circulation to meet tissue needs for oxygen and nutrients.
Heart failure occurs when the heart muscle is unable to pump effectively, resulting in:
inadequate cardiac output,
myocardial hypertrophy, and
pulmonary/systemic congestion.
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.

15. Key Points
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.

16. 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).

17. 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

18. 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): 2D or 3D 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.

19. 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.

20. Assessments S & Sx of Left-sided failure Hemodynamic findings:
Dyspnea, orthopnea, nocturnal dyspnea
Fatigue
Displaced apical pulse (hypertrophy)
S3 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

21. 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

22. Assessments Cardiomyopathy Fatigue, weakness
Heart failure (left with dilated type, right with restrictive type)
Dysrhythmias (for example, heart block)
S3 gallop
Cardiomegaly

23. Assess/Monitor Oxygen saturation V S 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

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

25. Nursing Interventions
Place the client in high-Fowler’s, if a client is experiencing respiratory distress
O2 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 (HydroDIURIL)
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.

26. 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

27. Nursing Interventions
Anticoagulants, such as warfarin (Coumadin), heparin: 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.

28. 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 potassium-losing 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 1kg 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).

29. 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.

30. 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 mL/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.

31. 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