1 / 93

ECGs

ECGs. Arrhythmias. Abnormal cardiac rhythms Prompt assessment of abnormal cardiac rhythm and patient’s response is critical. Phases of Cardiac Action Potential. Fig. 35-1. 12-Lead ECG. Fig. 35-3. Assessment of Cardiac Rhythm. Fig. 35-5. Assessment of Cardiac Rhythm. Fig. 35-6.

ecato
Télécharger la présentation

ECGs

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript


  1. ECGs

  2. Arrhythmias • Abnormal cardiac rhythms • Prompt assessment of abnormal cardiac rhythm and patient’s response is critical

  3. Phases of Cardiac Action Potential Fig. 35-1

  4. 12-Lead ECG Fig. 35-3

  5. Assessment of Cardiac Rhythm Fig. 35-5

  6. Assessment of Cardiac Rhythm Fig. 35-6

  7. Assessment of Cardiac Rhythm Fig. 35-9

  8. Sinus Bradycardia • Sinus node discharges at a rate < 60 bpm • Normal rhythm in aerobically trained athletes and during sleep

  9. Sinus Bradycardia Fig. 35-11, A

  10. Sinus Bradycardia Clinical Association • Occurs in response to • Carotid sinus massage • Hypothermia • Increased vagal tone • Administration of parasympathomimetic drugs

  11. Sinus Bradycardia Clinical Association • Occurs in disease states • Hypothyroidism • Increased intracranial pressure • Obstructive jaundice • Inferior wall MI

  12. Sinus Bradycardia Significance • Hypotension with decreased CO may occur • An acute MI may predispose the heart to escape arrhythmias and premature beats

  13. Sinus Bradycardia Treatment • Consists of atropine • Pacemaker may be required

  14. Sinus Tachycardia • Discharge rate from the sinus node is increased as a result of vagal inhibition and is > 100 bpm

  15. Sinus Tachycardia Fig. 35-11, B

  16. Sinus Tachycardia Clinical Associations • Associated with physiologic stressors • Exercise • Hypotension • Hypovolemia • Myocardial ischemia • CHF

  17. Sinus Tachycardia Significance • Patients may have symptoms of dizziness and hypotension may occur • Increased myocardial oxygen consumption is associated with increased HR

  18. Sinus Tachycardia Significance • Angina or increase in infarct size may accompany persistent tachycardia in patient with acute MI

  19. Sinus Tachycardia Treatment • Determined by underlying causes • -adrenergic blockers to reduce HR and myocardial oxygen consumption

  20. Atrial Flutter • Atrial tachyarrhythmia identified by recurring, regular, sawtooth-shaped flutter waves • Associated with slower ventricular response

  21. Atrial Flutter Fig. 35-14, A

  22. Atrial Flutter Clinical Associations Usually occurs with: • CAD • Mitral valve disorders • Pulmonary embolus • Chronic lung disease • Cardiomyopathy

  23. Atrial Flutter Significance • High ventricular rates with atrial flutter can decrease CO and cause serious consequences such as heart failure • Risk for stroke because of risk of thrombus formation in the atria • Coumadin used for atrial flutter > 48h

  24. Atrial Flutter Treatment • Primary goal is to slow ventricular response by increasing AV block • Electrical cardioversion may be used to convert atrial flutter to sinus rhythm in emergency situation

  25. Atrial Flutter Treatment • Diltiazem, digoxin, and -adrenergic blockers used to control ventricular rate • Antiarrhythmic drugs used to convert atrial flutter to sinus rhythm or maintain sinus rhythm • Radiofrequency catheter ablation used as curative therapy

  26. Atrial Fibrillation • Total disorganization of atrial activity without effective atrial contraction • Chronic or intermittent

  27. Atrial Fibrillation Fig. 35-14, B

  28. Atrial Fibrillation Clinical Associations • Usually occurs with • Underlying heart disease, such as rheumatic heart disease • Cardiomyopathy • CHF • Pericarditis

  29. Atrial Fibrillation Clinical Associations • Often acutely caused by • Thyrotoxicosis • Alcohol intoxication • Caffeine use • Electrolyte disturbance • Cardiac surgery

  30. Atrial Fibrillation Significance • Can often result in decrease in CO because of ineffective atrial contractions and rapid ventricular response

  31. Atrial Fibrillation Significance • Thrombi may form in atria and may pass to brain, causing stroke • Risk for stroke increases five-fold in atrial fibrillation • Risk even higher in structural heart disease, HTN, and an age over 65

  32. Atrial Fibrillation Significance • Anticoagulation with Coumadin used to prevent stroke

  33. Atrial Fibrillation Treatment • Goals are decreased in ventricular response and conversion to sinus rhythm • Drugs for rate control include digoxin, - adrenergic blockers, and calcium channel blockers

  34. Atrial Fibrillation Treatment • Antiarrhythmic drugs used for conversion • DC cardioversion may be used to convert atrial fibrillation to normal sinus rhythm

  35. Atrial Fibrillation Treatment • Anticoagulant therapy recommended for 3 to 4 weeks in atrial fibrillation > 48 h before attempt at conversion to sinus rhythm

  36. First-Degree AV Block • Every impulse is conducted to the ventricles, but duration of AV conduction is prolonged

  37. First-Degree AV Block Fig. 35-16, A

  38. First-Degree AV Block Clinical Associations Usually occurs with: • Chronic ischemic heart disease • MI • Rheumatic fever • Vagal stimulation • Drugs such as digitalis, -adrenergic blockers, flecainide, and IV verapamil

  39. First-Degree AV Block Significance • May be a precursor to higher degrees of AV block • No treatment

  40. Second-Degree AV Block, Type 1 • Includes gradual lengthening of the PR interval, which occurs because of prolonged AV conduction time • Most commonly occurs at AV node, but can occur in His-Purkinje system

  41. Second-Degree AV Block, Type 1 Fig. 35-16, B

  42. Second-Degree AV Block, Type 1 Clinical Associations • May result from drugs such as digoxin or -adrenergic blockers • Associated with ischemic cardiac disease and other diseases slowing AV conduction

  43. Second-Degree AV Block, Type 1 Significance • Usually a result of myocardial ischemia on an inferior MI • May be warning signal of impending significant AV conduction disturbance

  44. Second-Degree AV Block, Type 1 Treatment • If symptomatic, atopine is used to increase HR or pacemaker may be needed • If asymptomatic, rhythm closely observed with transcutaneous pacemaker on standby

  45. Second-Degree AV Block, Type 2 • P wave not conducted without progressive antecedent PR lengthening • Almost always occurs when bundle branch block is present • Certain number of impulses from the sinus node are not conducted to the ventricles

  46. Second-Degree AV Block, Type 2 Fig. 35-16, C

  47. Second-Degree AV Block, Type 2 Clinical Associations • Associated with rheumatic heart disease, CAD, acute anterior MI, and digitalis toxicity

  48. Second-Degree AV Block, Type 2 Significance • Often progresses to third-degree and is associated with poor prognosis • May result in decreased CO with subsequent hypotension and myocardial ischemia

  49. Second-Degree AV Block, Type 2 Treatment • Before the insertion of a permanent pacemaker may involve use of temporary transvenous or transcutaneous pacemaker • Temporary drug measures to increase HR until pacemaker is available

  50. Third-Degree AV Heart Block • Complete heart block • Constitutes one-fourth of AV dissociation in which no impulses from atria are conducted to ventricles

More Related