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Dysrhythmias

Dysrhythmias. Objectives. Describe basic heart dysrhythmias Explain the pathophysiology of dysrhythmias Describe nursing interventions in caring for clients with heart dysrhythmias. Terms. Automaticity - The inherent ability of the myocardium to generate it’s own electrical impulse

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Dysrhythmias

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  1. Dysrhythmias

  2. Objectives • Describe basic heart dysrhythmias • Explain the pathophysiology of dysrhythmias • Describe nursing interventions in caring for clients with heart dysrhythmias

  3. Terms • Automaticity- The inherent ability of the myocardium to generate it’s own electrical impulse • Depolarization- Electrical activity that stimulates the heart to contract • Repolarization- Electrical activity that signals the myocardium to relax

  4. The Conduction Pathway Flow of Electricity through the Heart Sinoatrial Node (SA node “sinus”) → Atrioventricular Node (AV node) → Bundle of HIS (Right and Left bundle branches) → Purkinje Fibers Any disturbance in the flow of electricity will cause a change in the heart rhythm and rate.

  5. Dysrhythmias • A regular rate may indicate normal electrical conduction, but could be an arrhythmia; it must be diagnosed by ECG/EKG. Most important is to know the patient’s history and their tolerance. • Example: Atrial Flutter and Ventricular Tachycardia have regular rates

  6. Dysrhythmias • An irregularly irregular rhythm or a regularly irregular rhythm may indicate abnormal conduction which may be benign; must be diagnosed by ECG. Most important is to know the patient’s history and their tolerance. • Examples: Sinus Arrhythmia and Premature Ventricular Contractions

  7. Cardiac Dysrhythmias • The Normal Electrical Impulse • P wave = atrial depolarization • QRS = ventricular depolarization • T wave = ventricular repolarization

  8. Normal Sinus Rhythmaka NSR or SR Normal Sinus Rhythm: HR 60-100

  9. Sinus Tachycardia • Rapid regular rhythm originating in the SA node • HR 100 and up • Multiple causes

  10. Sinus Tachycardia • Causes: • Anxiety • Fever • Exercise • Shock • Medication • Excessive caffeine • Tobacco use • Recreational drugs

  11. Sinus Tachycardia • Clinical Manifestations: • Occasional palpitations • Hypotension • Angina • Other CV disease • Many patients are asymptomatic • Medical Management: directed at the primary cause

  12. Sinus Tachycardia Treatment • Anxiolytics • Fever reducer • Fluids • Beta Blockers • Thyroid workup • Insulin • Avoiding triggering stimulants

  13. Sinus Bradycardia • Slow, regular rhythm (<60 bpm) • Originates in SA node • Multiple causes • Worrisome if patient shows s/s of low cardiac output

  14. Sinus Bradycardia • Causes: • Sleep • Vomiting • Intracranial tumors • MI • Drugs (esp. digitalis toxicity) • Vagal stimulation • Hypothermia • Endocrine disturbances

  15. Sinus Bradycardia • Clinical Manifestations: • Fatigue • Lightheadedness • Syncope • Some patients are asymptomatic • Medical Treatment: directed toward the primary cause and maintain cardiac output • Atropine may be prescribed to ↑ output • Temporary or permanent pacemaker

  16. Sinus Bradycardia Treatment • If related to brain- EMERGENCY- this is a late sign of increased ICP! • Otherwise, treat if symptomatic: • Hold affecting medications • Warm • Atropine or Epinephrine • Pacemaker

  17. Supraventricular Tachycardiaaka SVT • Sudden onset of rapid heartbeat • Rate 150-250 bpm, does not fluctuate with activity • Originates in atria • Multiple causes • May be idiopathic

  18. Supraventricular Tachycardia • Causes: • Drugs, alcohol • Mitral valve prolapse • Emotional stress • Smoking • Hormone imbalance

  19. Supraventricular tachycardia • Clinical manifestations: • Palpitations • Lightheadedness • Dyspnea • Anginal pain • Medical Management: • How well does the pt. tolerate the dysrhythmia • Focus: ↓ HR; eliminate underlying cause

  20. SVT Treatment DO NOT USE CAROTID SINUS PRESSURE or CAROTID MASSAGE! • Vagal Stimulation • Gagging • “Bearing down” • Valsalva maneuver • Holding breath while bearing down • Other maneuvers • Coughing/suctioning • Ice water in face

  21. SVT Treatment • Medications • Adenosine/adenocard, antiarrhythmics, AV node blocking agents • Direct Current Cardioversion • Catheter Ablation

  22. Atrial Fibrillation • Disorganized atrial activity  quivering • Ventricle may respond at various rates • An irregularly irregular rhythm • Risk of blood clot if left untreated • Causes

  23. Atrial Fibrillation • Causes: • Cardiac surgery • Long-standing HTN • Atherosclerosis • Pulmonary embolism • Heart Failure • COPD • cardiomyopathy

  24. Atrial Fibrillation • Clinical Manifestations: • Pulse deficit • Palpitations • Dyspnea • Lightheadedness • Fatigue • Angina

  25. Atrial Fibrillation • Medical management: • Treat the irritability of the atria • Slow the ventricular response • Correct the primary cause • Goal of therapy: PREVENT THROMBI

  26. Treatment of AFib • Prevention of thrombi causing an embolism is a major concern • Heparin/Coumadin • Rate Control • AV node Blocking agents • When threat of thrombi diminished • Conversion • Antiarrhythmics • Direct Current Cardioversion (echo first) • Catheter Ablation

  27. Treatment of AFib • Approximately 60-70% of patients with persistent AFib will be treated with anticoagulants and rate control only • Goal of anticoagulation: maintain the INR between 2-3 • Coumadin therapy is dangerous and at times difficult to manage • Benefit of therapy must outweigh risk of therapy • Benefits • Risks

  28. Coumadin Anticoagulants – Coumadin • Inhibits Vitamin K based synthesis clotting factors in liver • Compliance is extremely important • Measured by Protime and INR • Normal Protime: 12-14 seconds • Normal INR: 1.0

  29. Coumadin • Normal Protime for an anticoagulated patient is 1.5 to 2.5 times normal • Normal INR for an anticoagulated patient should be about 2-3.5 (requires frequent testing) • Onset is 1-3 days, peak 3-5 days, effect wears off 3-5 days • Avoid inconsistent intake of foods with vitamin K (i.e. leafy greens) • Reversal agents: Vitamin K and Plasma

  30. AFib Treatment • Other Factors to consider for coumadin: • Client’s cognitive status and memory, or support system • Client’s mobility status: Fall Risk?!?! • Other medications • Meds affecting coagulation • Fluorquinolones (Levaquin and Cipro) • Antifungals • Depakote • Meds that cause orthostatic hypotension or dizziness

  31. AFib Treatment • Rate Control • Sometimes the ventricular rate (HR) is labile • Dosages of AV Node blocking agents may need to be very high • If the client cannot maintain an appropriate ventricular rate may need pacemaker • Example: • On Metoprolol 50mg BID, client has HR ranging from 85-120. On Metoprolol 75mg BID, client has HR of 40. • Client will receive pacemaker to keep HR above a certain number (60) and metoprolol dose of 75 mg.

  32. Atrioventricular (AV) Block • Impulse is slowed or not received in the ventricles from the SA node • Symptoms can range from none to life threatening First Degree AV Block: PR interval longer than 0.20 Heart rate normal Symptoms: Usually none Treatment: Not necessary Causes: MI, Heart Surgery, or medications that depress the SA node, atherosclerosis, digitalis toxicity First Degree Heart Block: PR=0.28 seconds (Normal = .16-0.2 seconds) Conduction delayed

  33. Second Degree Heart Block Second Degree Heart Block: Conduction fails to reach Ventricles PR interval may progressively become longer until a beat is dropped or the PR interval remains the same, but beats are dropped. HR is usually 40-60 BPM Symptoms range from none to dizzness/lightheadedness, SOB, weakness, or confusion Causes: Medications affecting the SA node or the AV node, MI, heart surgery Treatment: Hold medications, pacemaker if needed

  34. Third Degree Heart Block HR 20’s-40. Intervals vary Symptoms: Low cardiac output! Causes: MI, heart surgery, medications Treatment: Pacemaker Most likely to require a pacemaker Third Degree Heart Block: Signals from the SA node are not reaching the ventricles, so the ventricles have their own escape rhythm. ‘Everyone’ is talking but no one is communicating.

  35. Premature Ventricular Contractions (PVCs) • Abnormal beats originating in the ventricles • Early ventricular beats • Symptoms range from none to life threatening depending on frequency of PVCs

  36. PVC’s • Causes: • Irritability of ventricle musculature • Exercise, stress • Electrolyte imbalance • Digitalis toxicity • Hypoxia • MI

  37. PVC’s • Clinical Manifestations • Some – asymptomatic • Palpitations, lightheadedness, weakness • PVCs may be a single event or may last long enough  Vtach  death • Medical Management • Treat the underlying heart condition • Symptomatic PVC’s: beta-adrenergic blockers such as Coreg; antianginals, Inderol; antidysrhythmics: Amiodarone

  38. Ventricular Tachycardia (V-tach) • 3 or more PVCs in a row • Ventricular rate >100 bpm • Multiple causes Patient may or may not have a pulse with this rhythm

  39. V-tach Management • With pulse: • ABC’s, Vitals • If stable- • Vagal/Valsalva maneuver’s • Antiarrhythmics • Defibrillation • Unstable • Synchronized Defibrillation • Without pulse • BLS • Unsynchronized defibrillation

  40. Ventricular Fibrillation(V-fib) • Quivering of the ventricles • Heart is not beating, therefore there is no pulse • Cause: MI • BLS then Unsynchronized defibrillation is usually the only way to convert this rhythm, although antiarrhythmics are given.

  41. Management of the Dysrhythmia Patient • ABCs (Airway, Breathing, Circulation) first!!! • Management will focus on treatment of the underlying cause if known Goalof any therapy is to preserve and maximize cardiac output

  42. Management of the Dysrhythmia Patient • Implantable cardioverter defibrillator • Device implanted in atrium that will automatically sense and shock VT or VF • Often coupled with a pacemaker • Pacemaker • Can be temporary or permanent (implantable) • Maintains a certain minimal heart rate

  43. Permanent Implanted Devices • STERILE PROCEDURE • Performed by cardiologist • Overnight hospital stay • Affected arm in sling • Do not lift over head • Infection can be EXTREMELY SERIOUS

  44. Management of the Dysrhythmia Patient • Medications (Not a Comprehensive List) • Beta-blockers – metoprolol, propranolol • Calcium channel blockers – diltiazem • Class III antiarrythmic- Amiodarone, Lidocaine • Adenosine • Digoxin

  45. Nursing Interventions Patient Teaching

  46. Assessment • DATA COLLECTION • Subjective • Focus on specific cardiac symptoms • Chest pain, SOB, palpitations, exercise intolerance, nausea • Objective • Vital Signs • 12 lead EKG • Apical Pulse • Observe for signs of decreased cardiac output • Decreased peripheral pulses, decreased capillary refill, respiratory distress, pallor, ashen color, cyanosis

  47. Nursing Interventions • Focus on: • Symptomatic relief (anxiety, pain, cardiac s/sx) • Promote comfort • Emergency action as needed • Patient Teaching • During Nsg. Assessment: • Assess the apical (not radial pulse) to obtain accurate rate Take the pulse for 1 minute

  48. Nursing Interventions • Asses patient’s anxiety and degree of understanding • Note verbal and nonverbal expressions re: dx., procedures, and treatments • Explanations as needed • Medication administration • Oxygen administration prn • Maintain quiet environment

  49. Patient Teaching • Avoid/stop smoking • Medication therapy and its purposes • Taking his/her pulse, BP • Exercise within prescribed limits by MD • Energy conservation techniques • Stress management

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