ECG Basics Sonia Samtani 7/2017 UCI Resident Lecture Series

Transcription

1 ECG Basics Sonia Samtani 7/2017 UCI Resident Lecture Series

2 Agenda I. Introduction II.The Conduction System III.ECG Basics IV.Cardiac Emergencies V.Summary

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5 The Conduction System

6 Lead Placement avf

7 Precordial Leads

8 Electrical Leads: Limb Leads (Frontal): I, II, III, AV F, AV R, AV L Precordial Leads (Transverse): V 1 V 6 Providing a 2-D view of the hearts electrical activity Depolarization towards lead = + deflection Depolarization away from lead = - deflection

9 Anatomy of an ECG:

10 Interpretation Develop a systematic approach to reading EKGs and use it every time The system we will learn is: Rate Rhythm (including intervals and blocks) Axis Hypertrophy Ischemia

11 Rate Rule of 300- Divide 300 by the number of boxes between each QRS = rate Number of big boxes Rate Start

12 Rhythm: Normal Sinus Rhythm Originating from SA node P wave before every QRS P wave in same direction as QRS P wave has same morphology each beat Upright P wave in I, II

13 Intervals PR 0.20 sec (less than one large box) QRS sec (1-2 small boxes) QT 450 ms in men, 460 ms in women Based on sex / heart rate Half the R-R interval with normal HR

14 Blocks AV blocks First degree block PR interval fixed and > 0.2 sec Second degree block, Mobitz type 1 PR gradually lengthened, then drop QRS Second degree block, Mobitz type 2 PR fixed, but drop QRS randomly Type 3 block PR and QRS dissociated

15 QRS Duration QRS > 0.10sec indicates conduction system disease, usually in the bundles (LAFB, LPFB, Incomplete RBBB) QRS > 0.12sec indicates Bundle Branch Block, either RBBB, LBBB or IVCD

16 Right Bundle Branch Block Look for characteristic R-S-R morphology in V 1 (aka bunny ears) Where R is larger than R Look for broad terminal S-waves in V 5, V 6, I & AV L

17 Right Bundle Branch Block

18 Left Bundle Branch Block Look for wide QRS > 0.12sec Absence of RBBB No S-wave or Q-wave in Lead I or V 6 Dominate S-wave in V 1 with small Q or small R-wave May see R-S-R in V 5 or V 6

19 LBBB

20 QT & QT c Intervals Normal QT interval represents time to repolarization of ventricles (T-wave) The QT maybe prolonged with slow heart rates or short with fast heart rates. As a result,use QT c. Bazett s Formula: QT c = QT / RR Normal is ~0.42sec, concern > 0.46sec and higher, usually >0.5sec at risk for

21 The QRS Axis Overall Direction of Heart s Electrical Activity. Axis of 30 to +90 degrees is normal Extreme Right Axis

22 Causes of Left Axis Deviation Left anterior hemiblock most common!! Not typically caused by LVH Inferior myocardial infarction with Q- waves Artificial cardiac pacing Emphysema Hyperkalemia Wolff-Parkinson-White syndrome - right sided accessory pathway Tricuspid atresia Ostium primum ASD Injection of contrast into left coronary artery

23 Causes of Right Axis Deviation Normal finding in children and tall thin adults Right ventricular hypertrophy Chronic lung disease even without pulmonary hypertension Lateral wall myocardial infarction with Q-waves Left posterior hemiblock Pulmonary embolus (remember S 1 Q 3 T 3) Wolff-Parkinson-White syndrome - left sided accessory pathway Atrial septal defect Ventricular septal defect

24 Causes of Extreme Right Axis Lead transposition someone placed the leads wrong (happens very commonly) Artificial cardiac pacing Ventricular tachycardia Emphysema Hyperkalemia

25 Hypertrophy Limb Leads R wave in lead I + S wave in lead III > 25 mm R wave in avl > 11 mm R wave in avf > 20 mm S wave in avr > 14 mm Precordial Leads R wave in V4, V5 or V6 > 26 mm R wave in V5 or V6 plus S wave in V1 > 35 mm Largest R wave plus largest S wave in precordial leads > 45 mm Non Voltage Criteria: Increased R wave peak time > 50 ms in leads V5 or V6 ST segment depression and T wave inversion in the left-sided leads: AKA the left ventricular strain pattern

26 Ischemia: Q-ST-T Changes Q-waves indicate myocardial infarction, or scar tissue Pathologic Q waves - usually need to be >0.04 sec wide & > 25% of subsequent R-wave ST segment elevations represent myocardial infarction ST segment depression represents myocardial ischemia Compare ST segment to baseline TP segment Group Q-ST-T wave changes by groups of leads that correspond to left ventricular walls

27 Grouped Leads

28 Cardiac Emergencies

29 Mr. Jones is Tachycardic

30 History and Physical Exam: History of prior myocardial infarction (MI) has a 98% positive predictive value of VT History of congestive heart failure and recent angina pectoris has a 100% positive predictive value for VT. Age greater than 35 has a sensitivity of 92% Hemodynamic instability can be seen with VT VT does not respond to carotid sinus massage Cannon A-waves in presence of AV dissociation strongly suggests VT.

31 Atrioventricular Dissociation Detected in the lead where the p wave is most prominent. QRS variability can indicate AV dissociation.

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34 Doctor, the patient is hypotensive with SBP 80s

35 HPI/Physical Exam: Symptoms can be chest pain, shortness of breath, or near syncope Beck s Triad: Hypotension with a Narrowed Pulse Pressure Jugular Venous Distention Muffled heart Sounds Pulsus Paradoxsus

36 Pulsus Paradoxsus

37 Treatment: IV Fluids for Temporizing Pericardiocentesis Pericardial Window (not acutely)

38 Our patient in Trauma B is having chest pain

39 ACS Unstable angina vs. NSTEMI vs. STEMI Unstable Angina = Normal troponin, CK- MB with nml ECG or non-specific ECG findings. (But will have symptoms). NSTEMI = +troponin/ckmb, without ECG changes. STEMI= +troponin/ckmb and ST segment elevation in two or more contiguous leads or ST elevation equivalents (i.e. new LBBB).

40 ECG localization of Acute MI Anatomic Location ECG leads Inferior II, III, avf RCA Ateroseptal V1-V3 LAD Coronary Lateral and apical Posterior I, avl, V4- V6 ST depression with tall R waves in V1-V3. LAD, left circumflex posterior descending artery

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42 Doctor, our patient who was admitted with UTI has this rhythm strip.

43 Torsades de Pointes Prolonged QT is a risk factor for Torsades de Pointes (turning of points) Torsades is a polymorphic ventricular tachycardia POINTS POINTS

44 What causes prolonged QT? Congenital defect in K-channels Hypocalcemia, Hypokalemia, Hypomagnesemia Hypothermia HIV Connective tissue disease: SLE, Sjogren s Myocardial Ischemia Anorexia Nervosa Intracranial Pathology

45 QT Prolonging Medication:

46 Treatment 2 grams IV Magnesium Sulfate Stop the medication Defibrillate if torsades deteriorates into ventricular fibrillation or unstable Keep K + > 5.0 and Mg 2+ > 3.0

47 Summary: Work to develop a systematic way of reading ECGs: Rate Rhythm (including intervals and blocks) Axis Hypertrophy Ischemia Wide based tachycardia is VT until proven otherwise A New LBBB is a STEMI equivalent Many, Many medications prolong the QT Torsades de Pointes is treated with magnesium

48 Last Word: You may not be able to change the circumstances of your training but you can change your attitude, it s the only thing you can control Dr. George Ruiz

49 Thanks so much for your kind attention!