Introduction to the basics of 12-Lead EKG Interpretation

1. Introduction to the basics of 12-Lead EKG Interpretation Jennifer Rodgers, MSN, ARNP Wichita State University Summer 2006

2. INTRODUCTION 12-Lead EKG machine developed in 1903 timeless invention Inexpensive, easily accessible Goals 1. Review basic cardiac physiology 2. Develop systematic approach to 12-Lead interpretation 3. Practice interpreting EKG strips Remarkable clinical power One glance>diagnose evolving MI, arrhythmia, re-assurance for patient wanting to start exercise program, OR chronic effects of HTN Only a tool>reliable as userRemarkable clinical power One glance>diagnose evolving MI, arrhythmia, re-assurance for patient wanting to start exercise program, OR chronic effects of HTN Only a tool>reliable as user

3. 12-Lead EKG Electrical recording of the heart�s electrical activity Cardiac cells �resting state polarized (negative inside positive outside) Ensure appropriate distribution of ions (potassium, sodium, chloride, calcium) Depolarization-fundamental electrical event of the heart, stimulation>muscle begins to work Propagated from cell to cell>wave throughout entire heart>flow of electricity Currents can be detected by external electrodes All the various waves seen on EKG>manifestations of depolarization and polarizationCurrents can be detected by external electrodes All the various waves seen on EKG>manifestations of depolarization and polarization

4. TYPES OF CELLS PACEMAKER-electrical source ELECTRICAL CONDUCTING-hard wiring MYOCARDIAL-contractile machinery

5. PACEMAKER CELLS Small 5-10 cm in length Depolarize spontaneously @ particular rate Located in Right Atrium-Sinoatrial (sinus) node Typical 60-100 beats/minute Dependent on autonomic nervous system and body demands Anything that affects cardiac output Cycle polarization-depolarization>action potentialAnything that affects cardiac output Cycle polarization-depolarization>action potential

6. ELECTRICAL CONDUCTING CELLS Long-Thin cells Rapidly carry currents to distant regions of heart

7. Myocardial Cells Heavy labor cells Constantly contracting & relaxing> delivering blood to the periphery Contain contractile proteins> actin & myosin Depolarization>myocardial cell>calcium released within cell>contract

8. Time & Voltage Waves on EKG primarily reflect electrical activity>myocardial cells Waves-3 characteristics 1. Duration-measured fraction/second 2. Amplitude-measured millivolts (mV) 3. Configuration-shape/appearance

9. EKG PAPER Light lines small squares- 1 X 1 mm Bold lines large squares 5 X 5 mm Horizontal axis=time 1. Distance across small square=0.04 sec. 2. Distance across large square=0.2 sec. Vertical axis=voltage 1. Distance across small square=0.1 mV 2. Distance across large square=0.5 mV 6 second strip to figure rate (X 10) (30 lg=6)

10. SINUS NODE STARTS EACH CARDIAC CYCLE OF CONTRACTION & RELAXATION BY SPONTANEOUS DEPOLARIZATION THIS IS NOT SEEN ON THE EKG SA NODE FIRES>DEPOLARIZATION BEGINS>ATRIAL CONTRACTION (LIKE PEBBLE IN POND) ELECTRODES MEASURES ATRIAL POLARIZATION/DEPOLARIZATION> P WAVESA NODE FIRES>DEPOLARIZATION BEGINS>ATRIAL CONTRACTION (LIKE PEBBLE IN POND) ELECTRODES MEASURES ATRIAL POLARIZATION/DEPOLARIZATION> P WAVE

11. ATRIOVENTRICULAR (AV) NODE Electrical Gatekeeper between atria and ventricles Allows atrial contraction to end & empty contents into the ventricle before ventricular contraction begins ELECTRICAL GATEKEEPER JUNCTION ATRIA & VENTRICLES AV NODE> SLOWS CONDUCTION TO A HALT> ALLOWS ATRIAL CONTRACTION END & EMPTY CONTENTS INTO VENTRICULE BEFORE VENTRICULAR CONTRACTION BEGINSELECTRICAL GATEKEEPER JUNCTION ATRIA & VENTRICLES AV NODE> SLOWS CONDUCTION TO A HALT> ALLOWS ATRIAL CONTRACTION END & EMPTY CONTENTS INTO VENTRICULE BEFORE VENTRICULAR CONTRACTION BEGINS

12. VENTRICULAR DEPOLARIZATION WAVE DEPOLARIZATION SPREADS THROUGH THE 3 PARTS-Bundle of His (intrinsic 40-60 bpm)> Bundle Branches> Purkinje Fibers (intrinsic 20-40 bpm) & out into the ventricular myocardium Beginning ventricular depolarization>QRS complex Amplitude QRS much greater than P wave>ventricles are much larger First deflection Q WAVE First upward deflection R WAVE Next downward deflection S WAVE Amplitude QRS much greater than P wave>ventricles are much larger First deflection Q WAVE First upward deflection R WAVE Next downward deflection S WAVE

13. VENTRICULAR REPOLARIZATION Brief refractory period Restore electro negativity of their interiors �T wave� Atrial repolarization is not seen

14. PR INTERVAL Includes P wave & the first straight line connecting it to the QRS interval Measures the time from the start of atrial depolarization to the start of ventricular depolarization Normal 0.12-0.20 sec >0.20 delay in AV conduction <0.12 shortens as HR increases

15. ST SEGMENT The straight line connecting the end of the QRS complex with the beginning of the T wave Measures the time from the end of ventricular depolarization to the start of ventricular depolarization

16. QT INTERVAL Includes the QRS complex, ST segment, & T wave Measures the time from the beginning of ventricular depolarization to the end of ventricular repolarization Normal duration QRS 0.06-0.10 seconds

17. RATE MEASURMENT 1. COUNT THE # OF QRS COMPLEXES IN 6 SECONDS X 10, MOST COMMON 2. COUNT # OF LG. BOXES BETWEEN 2 R WAVES /BY 300 3. COUNT # OF SM. BOXES BETWEEN 2 R WAVES /BY 150 1. EASIEST CAN BE USED WITH ANY TYPE RHYTHM , SIMPLE, QUICKEST1. EASIEST CAN BE USED WITH ANY TYPE RHYTHM , SIMPLE, QUICKEST

18. STEPWISE APPROACH STRIP INTERPRETATION A. Determine Atrial & Ventricle Rate 1. V-measure R-R, A-measure P-P 2. >100 Tachycardia, <60 Bradycardia B. R-R Interval Regular? C. P wave Formation 1. Precede QRS, occur regularly, similar size 2. P wave + (SA Node) OR -/absent (AV Junction) D. QRS wide or narrow

19. SINUS NODE DYFUNCTION SINUS ARRHYTHMIA SINUS TACHYCARDIA SINUS BRADYCARDIA

20. SINUS ARRHYTHMIA A. Rate 60-100 bpm B. *R-R irregular C. *Normal P wave D. Normal PR interval 0.12-0.20 sec. E. Normal QRS complex </=0.10 sec. Phasic slowing & quickening, benign, normal response to respirations, asymptomatic Except in elderly>Sick Sinus Syndrome, not usually seen in infants INSPIRATION>INCREASE BLOOD FLOW>HR INCREASE, EXPIRATION>DECREASED VENOUS RETURN>HR SLOWSINSPIRATION>INCREASE BLOOD FLOW>HR INCREASE, EXPIRATION>DECREASED VENOUS RETURN>HR SLOWS

21. SINUS BRADYCARDIA Usual response to reduced demand for blood flow A. *Rate < 60 bpm B. R-R Regular C. Normal P wave D. Normal PR interval E. Normal QRS Complex Asymptomatic Vs. Symptomatic EXAMPLE: NORMAL ATHLETES>CONDITIONED, AMI INFERIOR >FAVORABLE UNLESS HYPOTENSION , OFTEN MEDICATION INDUCED >BBEXAMPLE: NORMAL ATHLETES>CONDITIONED, AMI INFERIOR >FAVORABLE UNLESS HYPOTENSION , OFTEN MEDICATION INDUCED >BB

22. SINUS TACHYCARDIA ACCELERATION SA NODE A. *Rate >110 bpm (110-160) B. R-R Regular C. Normal P wave D. Normal PR Interval 0.12-0.20 sec E. Normal QRS Complex </=0.10 sec Response to exercise/stress, OR response illness (hypovolemia/hypotension)>resolves once cause fixed EXAMPLE 67 FEMALE (TURNER) LUNG CA> ST 150�S, HYPOXEMIA, BP 80/40, ABG>ACUTE RESP. FAILURE, CXR>RML INFILTRATE + BACTEREMIA >BIPAP>30 MINUTES HR 110 EXAMPLE 67 FEMALE (TURNER) LUNG CA> ST 150�S, HYPOXEMIA, BP 80/40, ABG>ACUTE RESP. FAILURE, CXR>RML INFILTRATE + BACTEREMIA >BIPAP>30 MINUTES HR 110 EXAMPLE 67 FEMALE (TURNER) LUNG CA> ST 150�S, HYPOXEMIA, BP 80/40, ABG>ACUTE RESP. FAILURE, CXR>RML INFILTRATE + BACTEREMIA >BIPAP>30 MINUTES HR 110 EXAMPLE 67 FEMALE (TURNER) LUNG CA> ST 150�S, HYPOXEMIA, BP 80/40, ABG>ACUTE RESP. FAILURE, CXR>RML INFILTRATE + BACTEREMIA >BIPAP>30 MINUTES HR 110

23. ATRIAL DYSRHYTHMIAS Most common cardiac rhythm disturbance Originate in/around SA Node �above ventricle� Can diminish atrial �kick� >20% ventricular volume PSVT-Paroxysmal Supraventricular Tachycardia Atrial Fibrillation Atrial Flutter

24. PSVT A. Rate 150-250 bpm B. *Regular R-R interval C. P wave can be buried D. PR interval may be hard to find E. *Normal �narrow� QRS complex Treatment LVEF50%>CCB, BB, Dig., possible cardioversion, <40% No Cardioversion!, Dig., Amiodorone, Diltiazem

25. ATRIAL FLUTTER A. Atrial Rate 250-350 bpm B. R-R Irregular C. *P wave �classic saw tooth OR flutter� D. PR interval immeasurable E. QRS complex narrow May have palpitations, OR s/sx reduced C.O. If symptomatic>cardioversion, BB, Sotalol, Dig.

26. ATRIAL FIBRILLATION Chaotic, asynchronous electrical activity in atrial tissue>multiple impulses numerous eptopic pacemakers A. Atrial Rate-indiscernible, V-Rate 60-160 (RVR-Rapid Ventricular Response) B. *R-R Irregular C. *No P wave D. No PR interval E. QRS narrow PREVELANCE 8-10% >75, RESPONSIBLE 15-20% CVA�S, LEADING CAUSE CVA ELDERLY KNOW TREATMENT, DON�T FORGET ANTICOAGULATIONPREVELANCE 8-10% >75, RESPONSIBLE 15-20% CVA�S, LEADING CAUSE CVA ELDERLY KNOW TREATMENT, DON�T FORGET ANTICOAGULATION

27. JUNCTIONAL ESCAPE RHYTHM Originates in AV junction �escape pacemaker� A. Rate 40-60 bpm B. R-R Regular C. *Inverted P wave, preceding each QRS D. *PR Interval short 0.10 sec. E. QRS normal How is patient tolerating? Loss of �atrial kick�> can reduce C.O. by 20%

28. PREMATURE BEATS Premature Atrial Contractions (PAC�s)-originate outside AV node, single/multiple ectopic focus supersede SA node Premature Ventricular Contractions (PVC�s)-ectopic beats that originate in ventricles & occur earlier, singles, pairs or in clusters

29. VENTRICULAR DYSRHYTHMIAS VENTRICULAR TACHYCARDIA VENTRICULAR FIBRILLATION

30. VENTRICULAR TACHYCARDIA (V-TACH) Defined as: Vent. Rate > 100 bpm & when 3 OR more PVC�s strike in a row Life threatening, unstable, sustained OR unsustained A. A-rate can�t be determined, V-rate100-250 bpm B. R-R regular or slightly irregular C. P wave usually absent, dissociated D. PR Interval-immeasurable E. *WIDE QRS >0.12 sec. Bizarre appearance Don�t want to miss unpredictableDon�t want to miss unpredictable

31. VENTRICULAR FIBRILLATION (V-FIB) VF-Full cardiac arrest, no pulse/BP, always check patient first>Defibrillate>CPR/ACLS A. Rate-can�t be determined pulseless B. R-R can�t determine C. P wave can�t be determined D. PR interval can�t be determined E. QRS complex can�t be determined Ventricular electrical activity >fibrillatory waves with no recognizable pattern

32. A-V BLOCKS Interruption/delay in the conduction of electrical impulses between the atria & ventricles Classified site of block/severity of conduction abnormality 1st degree, 2nd degree Mobitz I (Wenkebach), 2nd degree Mobitz II, 3rd degree (Complete heart block)

33. 1st Degree AV Block Characterized by PR Interval > 0.20 seconds Delay in conduction AV Node Prolonged PR Interval constant Usually asymptomatic Least concerning of the blocks

34. 2nd Degree Mobitz I (Wenkebach) Successive impulses from SA node delayed slightly longer than the previous impulse Characterized by prolonged PR interval that continues until the P wave is dropped (impulse doesn�t reach ventricle) May have hypotension or lightheadedness

35. 2nd Degree Mobitz II Less common, more serious Impulses from SA node fail to conduct to ventricles Hallmark PR Interval constant normal or prolonged, doesn�t prolong before dropping, not followed by QRS, can have > 1 dropped in a row Precursor to 3rd Degree Heart Block P-P CONSTANT EVEN IN DROPPED BEATP-P CONSTANT EVEN IN DROPPED BEAT

36. 3RD DEGREE �COMPLETE HEART BLOCK� Indicates complete absence of impulse between the atria & ventricle Atrial rate > or = ventricular rate Occur @ AV node 40-60 bpm Occur @ bundle branches < 40 bpm wide QRS complex Decreased C.O., P-P & R-R disassociated

37. EKG INTERPRETATION LET�S PRACTICE!!!!