Cardiac electrophysiology presentation part two


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Cardiac electrophysiology presentation part two

  1. 1. Cardiac ElectrophysiologyRhythm Interpretation: PART TWO Kathleen Brownrigg, BSc, RN, MSN Pediatric Nurse Educator May 2011
  2. 2. Sino-atrial Node Arrhythmias• Arrhythmias that originate in the SA Node are the following • Sinus bradycardia • Sinus tachycardia • Sinus arrhythmia • Sinus arrest
  3. 3. Sinus Bradycardia Characteristics: •Can be in normal health individuals, such as athletes •Can be found in people with heart disease, such as MI •HR < 60 bpm •Regular rhythm •PR intervals 0.12 – 0.20 sec and are constant •QRS < 0.12 sec •May be caused by: B-blockers, anesthesia, hypothermia Treatment •If HR very low and S & S of low CO or HF •Meds: Atropine, Isuprel •Pacemaker (temporary, permanent)
  4. 4. Sinus Tachycardia Characteristics •Can be present in healthy individuals, for example with exercise, anxiety, fever, hyperthyroidism, pain and stress. •May be early sign of CHF. •HR between 100-160 bpm in adults, age dependent in pediatric patients. •PR intervals 0.12 – 0.20 sec and constant. •QRS < 0.12 sec •Regular rhythm Treatment
  5. 5. Sinus arrhythmia Characteristics •Variations in sinus rhythm. •Found in children and associated with respiration; HR speeds up with inspiration and slows with expiration. •Rate 60 – 100 bpm •PR interval 0.12 – 0.20 sec and constant •QRS < 0.12 sec Treatment •Digoxin
  6. 6. Sinus Arrest Characteristics •Failure of SA node momentarily so that no impulse is initiated •May be related to vagal stimulation, carotid sinus massage, deep inspiration as in Valsalva’s maneuver. •No atrial activity since no stimulus for atria to contract. •May occur with large doses of Digoxin or Quinidine •Usually, person has no symptoms, BUT with decreased CO, fainting, dizziness or syncope may occur.
  7. 7. Atrial Arrhytmias• Atrial arrhythmias originate from the atria when an ectopic focus in the atria assumes reponsibility for pacing the heart, either by irritability or escape.• Four types of atrial arrhythmias are: – Premature atrial contractions – Atrial tachycardia – Atrial flutter – Atrial fibrillation
  8. 8. Premature Atrial Contraction Characteristics •Single beats originating in the atria and coming early in the cardiac cycle. •Rhythm is irregular d/t ectopic beats (ectopic means originating outside the SA node). •P wave of PAC different from other P waves •PR Interval 0.12 – 0.20 sec; could also be > 0.20 sec. •QRS < 0.12 sec. •Person may complain of heart “skiping”beats. •Can be caused by digitalis intake, vagus nerve stimulation, heart disease (i.e., rheumatic heart carditis).
  9. 9. Atrial Tachycardia (SVT) Characteristics •Occurs in healthy individuals. •In cardiac patients, may be precursor to more serious atrial arrhythmias. •Rapid, regular heartbeat, which begins suddenly, and was likely preceded by frequent PACs. •Can be short-runs or last for hours. •Can be due to the toxic effects of digitalization. •Can lead to CHF with prolonged periods. •Rhythm is regular •Rate 150 – 250 bpm •P waves different from sinus P waves •PR Interval 0.12 – 0.20 sec •QRS < 0.12 sec
  10. 10. Atrial Flutter Characteristics •Impulse from single or multiple ectopic foci in atria. •Occurs in presence of organic heart disease. •Many impulses fail to pass though AV node to the ventricles b/c of chaotic atrial activity. •Digoxin and Inderal usually effective in treating. •Some cases may beed cardioversion or atrial pacin •Rhythm can be regular or irregular. •Atrial rate is 250 – 350 bpm •P waves have saw-toothed appearance •Unable to determine PR Interval •QRS < 0.12 sec
  11. 11. Atrial Fibrillation Characteristics •Impulse originates in one or more irritable atrial ectopic areas. •Ventricular rhythm highly irregular. •Atrial rate constantly changing due to the fibrillation wave •Atrial rate > 350 bpm •P waves not distinguishable, therefore PR Interval unmeasurable. •QRS < 0.12 sec •May have unknown etiology •Can be treated with Digoxin, Quinidine, Inderal •Elective cardioversion or temparary pacemaker for low ventricular rates due to possible
  12. 12. Junctional Arrhythmias• Rhythms that originate from the AV node.• They replace the activity of the SA node when he latter fails, therefore are the heart’s secondary pacemaker.• P waves may be inverted because the atria are depolarized via retrograde conduction. P waves can be closer, lost in or follow the QRS complex, and the PR Intervals are < 0.12 sec in the P wave precedes the QRS complex.• Junctional arrythmias can occur in cases of organic heart disease, atrial ischemia, myocardial infarction, or exessive digitalization.
  13. 13. Junctional Escape Rhythm Characteristics •Ventricular rate 40-60 bpm •QRS duration < 0.12 sec •May lead to heart failure and decreased cardiac output.
  14. 14. Junctional Tachycardia Characteristics •Rate 100 – 180 bpm •Occurs when the AV junction becomes irritable, speeds up and overrides higher pacemaker sites. •Rhythm is regular
  15. 15. Premature Junctional Contraction Characteristics •Can be caused by excess digitalization or Quinidine, or organic heart disease. •PR Interval < 0.12 sec •Also called premature nodal contraction.
  16. 16. Ventricular Arrythmias• Ventricular arrythmias are the most serious arrythmias because the heart is less effective than usual, and because the heart is functioning on its last level of backup support. Usually they occur suddenly and are often rapidly fatal despite vigorous treatment.• Occasionally they can be benign.• Types of ventricular arrythmias are: – Premature ventricular contractions (PVCs) – Ventricular tachycardia – Ventricular fibrillation – Idioventricular rhythm – Asystole/ventricular standstill
  17. 17. Premature Ventricular ContractionUnifocal PVCUnifocalPVC, Bigeminy Multifocal PVCs
  18. 18. Premature Ventricular ContractionsCharacteristics• Originate in an ectopic focus of the ventricular myocardium.• Have wide bizarre-shaped QRS complex with no preceding P wave, and T wave is in opposite direction• QRS can be in opposite direction of person’s normal QRS complexes.• Can occur in healthy people but are more common when the heart is disease or injured.• Can arise from a single focus (unifocal) or several foci (multifocal) in the ventricles.• Can occur alone, in pairs (couplets), or in runs of three or more.• Multifocal PVCs are often signs of difitalis toxicity or severe myocardial diseases.Treatment• Lidocaine to quiet an irritable myocardium• Procainamide and Quinidine can also be given• PVCs are often associated with poor cardiac output, therefore, temporary pacemakers may be required with severe bradycardia.
  19. 19. Premature Ventricular Contractions Unifocal PVCs Multifocal PVCs
  20. 20. Ventricular Tachycardia Characteristics •Looks like an uninteruupted series of PVCs •Rhythm usually regular, but could be irregular •Rate 150 – 250 bpm •Often preceded by a PVC that occurs in the vulnerable period of he ventricular repolarization cycle. Treatment •Must be initiated since person unable tolerate high ventricular rates for long (decreased cardiac output). •Lidocaine, procainamide or Quinidine for short runs of V tach. •Cardioversion needed for sustained runs of V tach.
  21. 21. Ventricular Fibrillation Characteristics •Appears on monitored as an uncoordinated tracing with no discernible waves or complexes. •Indication of extreme myocardial irritability with many ventricular foci initiating impulses in a chaotic fashion. •Patient may appear dead, complete loss of sensorium and possible tremors and seizures. Treatment •Defibrillation •If defibrillation not effective after a few shocks, START CPR!
  22. 22. Idioventricular RhythmCharacteristics•HR 20 – 40 bpm and usually regular•Because rate so slow, cardiac output very low.•As with other ventricular arrhythmias, QRS complex wideand bizarre
  23. 23. Torsade de PointesCharceteristics:• Type of ventricular tachycardia• Characterized by a gradual twisting of the direction of the QRS complexes around the isoelectric line.• Associated with R on T phenomenon and a unique mechanism of initiation with a long-short cycle length.• D Precipitating factors: – Class I antiarrythmic agents – Electrolyte imbalances – Altered ventricular refractoriness related to prolonged QT intervals, brady-arrythmias or ischemia.• Treatment – Correct underlying abnormality or stop Class I antiarrythmics
  24. 24. AsystoleCharacteristics•Signifies ventricular standstill, meaning there is no electrical conductionthroughout the heart. Therefore, no contraction occurs.•Can be caused by various problems, cardiac and non-cardiac, i.e., impairedrespiratory function, drug overdose, hemorrhage, anaphalactic reactions, …Treatment•EMERGENCY•Initiate CPR
  25. 25. Atrio-ventricular Blocks• AV blocks are conduction delays or blocks through the AV node.• Three categories: 1. First Degree AV Blocks 2. Second Degree AV Blocks Mobitz Type I (Wenckebach) Mobitz Type II (Classical) 3. Third Degree AV Block- Complete heart block
  26. 26. First Degree AV Block Characteristics •Most common conduction disturbance •Can appear in healthy individuals and those with diseasaed hearts. •In many elderly patients, chronic degeneration of the conduction system causes this arrythmia. •Can be caused by Quinidine and Procainamide. •Impulse carried normally from SA node through atria but are delayed when reach AV node. •PR Interval > 0.20 sec and usually constant across the strip.
  27. 27. Second Degree AV Block:Mobitz Type I (Wenckebach) Characteristics •Characterized by occasional dropped ventricular beats, meaning the impulse conducted through the atria, but was blocked at the AV node. •Irregular rhythm; R-R interval gets progressively shorter as PR interval gets longer unitl one P wave is not conducted. •Occurs with digitalis toxicity or with inferior wall MI •Can be caused by acute rheumatic fever, electrolyte imbalance, vagal stimulation, Quinidine or Procainamide therapy. •Generally, does not affect CO since V rate remains almost normal
  28. 28. Second Degree AV Blocks:Mobitz Type II (Classical 2:1 AV Block) Characetristics •There are 2, 3, or 4 P waves for every QRS complex because AV node blocks out many of the impulses. •Rhythm can be regular or irregular. •Rate is usually bradycardic. •PR Interval is regular and ALWAYS constant.
  29. 29. Third Degree AV Block Characteristics •Total block at the AV node, resulting in AV dissociation, meaning that the atria and ventricles are totally dissociated from each other. •Venricles can be controlled by either junctional or ventricular escape rhythm. •Atrial rate faster than ventricle. •Can be due to digitalis toxicity; acute rheumatic fever, acute MI or diffuse fibrosis throughout the conduction system. Can be congenital also. •May also occur after open-heart surgery, especially in patients with septal defects. •With slow ventricular rates may cause low CO. •Rhythm is regular •No relationship between P waves and QRS complexes.
  30. 30. Bundle Branch BlocksCharacterstics•Caused by a block ofdepolarization in the right or leftBundle Branch.•A block to either of the bundlebranches creates a delay of theelectrical impulse to that side, sothat the ventricles are notdeolarized at the same time,•Individual depolarization of bothventricles are still of normalduration, but because bothventricles do not firesimultaneously, a widened QRS isseen on the ECG since the two areout of sync.
  31. 31. Bundle Branch BlockCharacteristics•QRSs are superimposed on each other; as seenin diagram•Occasionally, occur in healthy individuals, butmore commonly in people with coronary arterydisease or hypertension.Treatment•Usually directed toward the associated heartdisease rather than the block.