Download Free Medical Advanced EKG Interpretation PowerPoint Presentation

Advanced EKG Interpretation PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : Check out this medical presentation on Arrhythmia, which is titled "Advanced EKG Interpretation", to know how to interpret EKG.

Tags : Arrhythmia, Advanced EKG Interpretation, electrocardiogram, ECG

Published on : Jun 02, 2021 | Views : 2729 | Downloads : 28

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

ADVANCED EKG INTERPRETATION Micelle J. Haydel, M.D. LSU New Orleans Emergency Medicine
Slide 2-

Image Sources My patients www.ecglibrary.com The Alan E. Lindsay Ecg Learning Center http://medlib.med.utah.edu/kw/ecg/intro.html The EKG of the week from NCEMI http://www.ncemi.org Emergency Medicine Education http://www.emedu.org
Slide 3-

Normal EKG Axis determination Blocks Bundle branch blocks Nodal blocks Dysrhythmias Patterns of Infarction EKG CASES
Slide 4-

Normal Electrical Pathway AV AV node SA node Bundle of His Bundle Branches SA HIS BB
Slide 5-

NORMAL EKG P wave: atrial activity Q wave: first downward deflection from isoelectric line (t-p) R wave: first upward deflection from isoelectric line S wave: second downward deflection
Slide 6-

NORMAL EKG rS: small upward deflection, and large downward deflection Qr: large downward deflection, and small upward deflection qRs: small downward deflection, large upward deflection, and small downward deflection Rs: large upward deflection, and small downward deflection
Slide 7-

AXIS: NORMAL EKG - positive polarity(tall R) in inferior and lateral leads with increasing positive polarity (r-wave progression) across the precordium V1-6 AVF I II III AVL V1 V2 V3 V4 V5 V6 AVR
Slide 8-

In a “normal” patient the only leads that should have negative polarity are AVR and V1-2 AVF I II III AVL V1 V2 V3 V4 V5 V6 AVR ---To determine axis: Look at leads I and AVF
Slide 9-

LAD - negative polarity (rS) in AVF
Slide 10-

RAD: negative polarity(rS) in lead I
Slide 11-

Severe RAD, negative polarity(rS) in 1& AVF
Slide 12-

Left axis deviation - negative QRS in lead AVF Right axis deviation - negative QRS in lead I Severe Right axis deviation negative QRS in BOTH lead I and AVF Quick & Easy AXIS DETERMINATION AVF AVF AVF I I I I I I
Slide 13-

Why do we care about axis determination in the ER? Differential Diagnosis LAD : LBBB, LAFB, Mechanical shift due to ascites or elevated diaphragm, left atrial hypertrophy RAD : RBBB, LPFB, right ventricular hypertrophy, dextrocardia, Pulmonary Embolism Both RAD and LAD can be caused by COPD, Hyperkalemia, MI, WPW
Slide 14-

LAD Note negative polarity in AVF
Slide 15-

RAD Note negative polarity (rS) in I Severe RAD Note negative polarity (rS) in I & AVF
Slide 16-

BUNDLE BRANCH BLOCKS Unifascicular Right BBB Left Hemiblocks Left anterior OR Left posterior Bifascicular Left BBB (implies both hemiblocks present) Right BBB PLUS Left anterior Left posterior Trifascicular Bifasicular PLUS AV nodal block
Slide 17-

Right Bundle Branch Block QRS > 0.12 sec Predominantly positive rSR’ in V 1-2 Wide slurred S in lead I
Slide 18-

LEFT BUNDLE BRANCH BLOCK Left bundle branch block (Both fascicles are blocked) QRS > 0.12 sec Deep S in V 1-3 Tall R and RsR’ in lateral leads: I, AVL, & V 5-6
Slide 19-

Left bundle divides into anterior and posterior branches Left anterior fascicular block Left axis deviation: negative polarity (rS) of AVF rS waves in Inferior leads Small Q in I (qR)
Slide 20-

Left posterior fascicular block Right axis deviation RAD = negative polarity (rS) of Lead I Small Q in III (qR)
Slide 21-

BIFASCICULAR BLOCKS Right bundle branch block associated with Left anterior fascicular block rS in AVF qR in I
Slide 22-

BIFASCICULAR BLOCKS Right bundle branch block associated with Left posterior fascicular block -- uncommon RBBB RAD – rS I plus qR III
Slide 23-

SA BLOCK Sinus pause : 1 - 2 second pause sinus beat resumes Sinus arrest : > 2 seconds junctional escape beat intervenes at 40-55 bpm ventricular escape beat at 20 -40 bpm
Slide 24-

AV-BLOCKS 1st degree - PR > 0.2 sec
Slide 25-

AV-BLOCKS 2nd degree Mobitz I (Wenckebach) PR increases until a QRS is blocked dropped
Slide 26-

AV-BLOCKS 2nd degree Mobitz II - blocked QRS (2:1, 3:1, 4:1) PR interval is fixed and usually normal, then p-waves with dropped beats
Slide 27-

AV-BLOCKS 3rd degree - disassociation of PP and RR, the PP intervals and RR intervals are constant. RR PP
Slide 28-

PEARLS Differential diagnosis for slow irregularly irregular rhythm Second Degree heart block : wenckebach Third Degree heart block If you see Left Axis Deviation, think about LAFB If you see Right Axis Deviation, think about LPFB
Slide 29-

TYPES OF DYSRHYTHMIAS Re-entry (SVT, WPW) Two parallel pathways with different rates and refractory periods Something alters the refractory period and the alternative pathway becomes dominant This causes a unidirectional conduction block, and a circuitous conduction pathway forms.
Slide 30-

TYPES OF DYSRHYTHMIAS Enhanced or Triggered (PACs, PVCs, Afib, MFAT) Conduction cells act as Pacemaker cells Conduction cells can be enhanced and become dominant in the setting of ischemia, sepsis, electrolyte imbalance or toxins. Some dysrhythmias start with enhanced or triggered activity, but follow a circuitous pathway seen in re-entry. (Atrial flutter, Vtach)
Slide 31-

A 60 yo with COPD c/o palpitations & SOB. The EKG shows: a. Atrial Fibrillation b. Premature Atrial Complexes c. Multi-Focal Atrial Tachycardia d. Paroxismal Atrial Tachycardia with block
Slide 32-

MULTIFOCAL ATRIAL TACHYCARDIA (MFAT) P waves of at least 3 different shapes No dominant atrial pacemaker Rate greater than 100 bpm Varying PR, RR, and PP intervals Enhanced or triggered automaticity
Slide 33-

MFAT - CLINICAL SIGNIFICANCE Hypoxia COPD Methylxanthene toxicity CHF or sepsis Treat the underlying disease process causing the triggered automaticity OXYGENATION and PERFUSION Magnesium Sulfate Calcium channel blocker for rate control prn
Slide 34-

MULTIFOCAL ATRIAL TACHYCARDIA (MFAT) P waves of at least 3 different shapes No dominant atrial pacemaker Rate greater than 100 bpm Varying PR, RR, and PP intervals
Slide 35-

A 56 year old presents with palpitations. EKG shows: a. Atrial fibrillation b. Atrial flutter c. Left anterior fasicular block d. RBBB
Slide 36-

B. ATRIAL FLUTTER : Rapid, regular flutter (F) waves at 250-350 per minute (ventricular conduction 1:2, ie ~150bpm) Sawtooth pattern of F waves in leads 2, 3 and AVF Little evidence of atrial activity in lead 1 AV conduction variable, QRS typically normal width Enhanced automaticity leading to circuitous conduction/reentry
Slide 37-

ATRIAL FLUTTER - TREATMENT Atrial flutter is the most electrosensitive of all dysrhythmias therefore cardioversion is the treatment of choice for conversion to sinus rhythm. Drug of choice for rate control is Calcium channel blockers. Drug of choice for diagnostic purposes is Adenosine (as long as QRS is narrow
Slide 38-

Atrial flutter with 2:1 conduction is often confused with SVT But, look for the sawtooth flutter waves in the inferior leads.
Slide 39-

Same patient after adenosine, showing prominent flutter waves.
Slide 40-

A 46 year old presents with palpitations. EKG shows: a. Atrial fibrillation b. Atrial flutter c. Left anterior fasicular block d. RBBB
Slide 41-

EKG shows: a. Atrial fibrillation Prominent fibrillatory waves in V 1-3 & AVF Irregular ventricular response, greater than 100 / min Ventricular rate less than 100 implies AV block Triggered/enhanced automaticity
Slide 42-

ATRIAL FIBRILLATION - treatment Cardiovert if unstable Ca Channel Blocker- Drug of choice for rate control Beta blocker Digitalis ASA alone for afib < 48h ASA & Anti-coagulate all others, if unknown or >48h the longer the patient has been in afib, the less likely you will be able to convert to NSR
Slide 43-

Ashman’s phenomenon – short runs of wide complex tachycardia during rapid atrial fibrillation. The refractory period is rate-related, and when erratic changes in rate occur, an impulse conducted during the refractory period will have an aberrant (RBBB) pattern.
Slide 44-

The most common dysrhythmia associated with digitalis toxicity is: A. Paroxysmal atrial tachycardia with AV nodal block B. Premature ventricular contractions C. Second degree AV nodal blocks D. Ventricular tachycardia E. Junctional tachycardia
Slide 45-

DIGITALIS TOXICITY - DYSRHYTHMIAS Most common : b. PVCs Most pathognomonic : PAT w/block Others AV nodal blocks sinus bradycardia, pause, SA block junctional escape beats or tachycardia Ectopic SVT, V-tach, V-fib
Slide 46-

Paroxysmal atrial tachycardia with block is pathognomonic for digitalis toxicity. Note the p waves at a rate > 100 & blocked QRS complexes. (Don’t mistake for aflutter with variable conduction or 3rd degree block) Note the blocked Impulses!!
Slide 47-

A 23 yo male with c/o palpitations, EKG shows: a. Atrial fibrillation b. MFAT c. SVT d. PAT with block
Slide 48-

His EKG shows c. SVT or AV nodal reentry tachycardia with a rapid, regular rate, absent p waves & narrow QRS complexes
Slide 49-

AV nodal Re-entry tachycardia/SVT Two parallel pathways with different rates and refractory periods Something alters the refractory period and the alternative pathway becomes dominant This causes a unidirectional conduction block, and a circuitous conduction pathway forms.
Slide 50-

AV nodal Re-entry tachycardia/SVT The circuitous impulse is typically transmitted anterograde (forward) over the relatively slow AV nodal fibers, limiting the rate to 200bpm. WHAT’S THE BIG DEAL??? Treat by blocking the AV node and allowing the normal pacemaker to resume. Adenosine Ca channel blocker Beta blocker
Slide 51-

SVT with aberrancy is a supraventricular tachycardia with a wide-complex QRS due to a rate-related bundle branch block. SVT with Aberrancy (rate-related block)
Slide 52-

SVT with aberrancy is treated by blocking the AV node and allowing the normal pacemaker to resume Adenosine Ca ch blocker Beta blocker It is very difficult to differentiate from Vtach if unsure, treat as stable Vtach amiodarone procainamide SVT with Aberrancy (rate-related block)
Slide 53-

44yo with complaint of palpitations and shortness of breath, ekg shows: SVT with aberrancy Ashman’s phenomenon WPW V-tach
Slide 54-

C. The EKG is WPW w/ retrograde conduction causing wide QRS. Because the etiology of a wide complex tachydysrhythmia is often unknown in the ER, treat with amiodarone, procainamide, lidocaine or cardioversion. (avoid procainamide in TCA OD or prolonged qt toursades)
Slide 55-

Pre-Excitation Syndromes-WPW & LGL Accessory pathway connects atria to the ventricles, bypassing the AV node Wolff-Parkinson-White: short PR (< 0.12 s), Delta wave (slurred upstroke QRS), slight wide QRS >0.10s, and frequently a psuedoinfarction pattern in the inferior leads and RBBB pattern. Lown-Ganong-Levine: short PR (< 0.12 s), NO Delta wave, normal QRS & episodes of tachydysrhythmias LGL WPW
Slide 56-

Delta waves, short pr interval, wide QRS The underlying ECG in WPW is a fusion of the accessory pathway (delta wave) and normal pathway of the QRS. During tachy-dysrhythmias, the electrical impulse follows only the accessory pathway in a circuitous fashion.
Slide 57-

Underlying ECG Fusion of accessory & normal pathways Accessory pathway with circuitous impulses traveling retrograde (wide QRS)
Slide 58-

Accessory Pathways-WPW If narrow QRS d/t forward conduction, treat as SVT (Adenosine) Wide QRS b/c retrograde conduction –10%
Slide 59-

Accessory Pathways-WPW Wide QRS if retrograde conduction Amiodarone and procainamide affect the forward and retrograde pathways as well as the ventricles and are safe in wide-complex tachydysrhythmias. (Caveat: Procainamide and Amiodarone not to be used in Toursades) Adenosine, Ca channel blockers, B blockers and digitalis block the forward conduction, not the retrograde conduction. In a wide complex WPW (retrograde impulses) most AV nodal blockers stop only anterograde conduction and can allow the rate of retrograde conduction to speed up and deteriorate into Vfib! This is seen in wide complex WPW with Afib or Aflutter.
Slide 60-

Evaluation of Re-entry Tachycardias - QRS Width Wide or Narrow If the QRS is narrow, it MUST have atrial origin and conduct through the AV node in a forward manner. If the QRS is wide, more than 0.12 seconds, consider : Bypass tract (WPW) with retrograde conduction SVT with aberrancy (rate-related bundle branch block) Junctional origin Ventricular origin
Slide 61-

Re-entry Tachycardias - Treatment Modalities Based on hemodynamic stability & QRS width Unstable : synchronized cardioversion Stable : Narrow complex – vagal maneuvers, adenosine, calcium channel blockers or beta blockers Wide complex – Amiodarone, Lidocaine or Procainamide to treat both anterograde and retrograde impulses and ventricular dysrhythmias Beware: it is very difficulty to tell the difference between the wide-complex tachy-dysrhythmias. It is safer to treat as presumed V-tach.
Slide 62-

PEARLS Wide complex QRS tachydysrhythmias of unknown etiology – use amiodorone, procainamide, lidocaine Differential diagnosis for rapid, irregularly irregular rhythm MFAT Atrial Fib Atrial flutter with variable conduction SVT at 150 or 300, consider Atrial flutter
Slide 63-

DYSRHYTHMIAS OF VENTRICULAR ORIGIN Idioventricular rhythms Ventricular Tachycardia Ventricular Fibrillation Torsades de pointes
Slide 64-

VENTRICULAR DYSRHYTHMIAS - Etiology V Tach, V Fib & Idioventricular rhythms – typically caused by an ischemic focus which allows a rapid reentry dysrhythmia Torsades de pointes - caused by a prolonged QT interval Brugada syndrome – sodium ion channel-apathy
Slide 65-

IDIOVENTRICULAR RHYTHMS Mechanism : re-entry with unidirectional block due to myocardial ischemia QRS width > 0.12 sec and rate 40 - 140 T waves typically have opposite polarity to QRS Treatment : Controversial, tends to be self-limited Supportive care & close observation
Slide 66-

VENTRICULAR TACHYCARDIA Mechanism : re-entry with unidirectional block due to myocardial ischemia (Monomorphic) QRS width > 0.12 sec and rate > 140 bpm T waves have opposite polarity to QRS Treatment : Stable : Amiodarone, Procainamide, Sotolol, Lidocaine, Mag Unstable : Unsynchronized defibrillation plus meds
Slide 67-

VENTRICULAR FIBRILLATION Chaotic ventricular depolarization with loss of organized QRS complexes Life-threatening Immediate loss of consciousness Loss of blood pressure & death Treatment : immediate unsynchronized defibrillation at 200, 300, then 360 joules (if Biphasic use ½ dose or 150j)
Slide 68-

Brugada Syndrome: ST elevation V1-3 with RBBB-like pattern which predisposes to ventricular dysrhythmias. 30% mortality within 3 years. Brugada P & Brugada J. J Am Coll Cardiol 1992;20:1391-6
Slide 69-

Brugada Syndrome: Look for ST elevation V1-3 part of the syncope or palpitation work-up immediate cardiology referral for ICD placement
Slide 70-

CARDIOVERSION PEARLS Atrial flutter is the most electro-responsive dysrhythmia 10-50 joules ~ treatment of choice SVT and STABLE ventricular tachycardia often respond to 50 joules Atrial and Ventricular FIBRILLATION require 100 joules or more Biphasic defibrillators use half the joules or 150j
Slide 71-

TORSADES DE POINTES V-tach due to prolonged QT interval, in which the QRS axis alternates between positive and negative (Polymorphic) Often self-limited, but may deteriorate into ventricular fibrillation Treatment of Choice : Magnesium Overdrive pacing & Isoproterenol can be used to speed the heart and decrease QT interval Avoid procainamide and amiodarone, as can worsen QT prolongation If refractory, defibrillate
Slide 72-

QUESTION ~ All of the following cause Torsades de pointes, except: A. Hypomagnesemia B. Tricyclic antidepressant overdose C. Procainamide D. Hyperkalemia E. Quinidine
Slide 73-

CAUSES OF PROLONGED QT INTERVAL Hypo -Mg, -Ca, -K, Type Ia antidysrhythmics - quinidine, procainamide Tricyclic antidepressant overdose drug reactions-EES, antihistamines, antifungals d is incorrect, hyperkalemia does not cause prolonged QT
Slide 74-

Prolonged qt interval
Slide 75-

Shortened qt: hypercalcemia
Slide 76-

Hyperkalemia Peaked T waves ( > 1/3 QRS) Prolonged PR interval Widening of QRS Sine Wave
Slide 77-

U waves in Hypokalemia Potassium 3.5mEq/L Potassium 3mEq/L Potassium 2mEq/L Potassium 1mEq/L
Slide 78-

Osborne J wave in hypothermia: notching at end of a slurred downstroke of QRS
Slide 79-

Tricyclic Antidepressant Overdose tall r in AVR slurring of the terminal portion of the rS in AVR
Slide 80-

Patterns of Infarction The LAD supplies the septal V1-2 and anterior leads V2-4 The RCA supplies the Inferior leads: II, III & AVF The Circumflex supplies the high and low Lateral leads: V5-6 and I &AVL
Slide 81-

Inferior Wall MI – ST segment elevation in II, III & aVF
Slide 82-

Anterior Wall MI – ST segment elevation in V2-4 Septal MI – ST segment elevation V1-2
Slide 83-

Lateral Wall MI – ST segment elevation in V5-6 and/or I & aVL
Slide 84-

Posterior Wall MI - Tall R in V1 & ST segment depression in V1-2
Slide 85-

Pericarditis – diffuse ST segment elevation & PR depression, with PR elevation in AVR
Slide 86-

EKG PEARLS When you see a “normal” looking EKG on a test, start looking for: Hyperkalemia :Peaked T waves Hypokalemia : U waves Hypomagnesimia : Prolonged QT Hypercalcemia: Shortened QT WPW : short PR, slurring of upstroke qrs Hypothermia : Osborne J waves (notched downstroke QRS; reversed delta waves) TCA overdose : stach, widening QRS, slurring of the terminal rS in aVR Axis deviation & Hemiblocks : LAFB, LPFB
Slide 87-

EKG PEARLS Usefulness of aVR & V1 Tall R wave in V1 RBBB WPW Posterior wall MI Severe RV strain: PE, pneumothorax, severe COPD aVR is normally flipped/negative polarity slurring terminal rS in TCA OD PR elevation in pericarditis Diffuse ST elevation: think pericarditis
Slide 88-

?