ekg review for pa review course - mycmemedia.mycme.com/documents/97/ekg_review_24061.pdf · rutgers...
TRANSCRIPT
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EKG REVIEW for
Rutgers
PANCE/PANRE
EKG Review
Presented by
Carol J. Sadley, M.Ed., PA-C
June 5, 2014
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Normal Cardiac Conduction
www.healcentral.org/content/collections/ECG/ecg_ccs.gif
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Conduction Pathway
Sino atrial (SA) node (in RA) fires
Signal travels across atria to AV node
Slight pause, then signal travels down
Bundle of His
His Bundle branches into Right & Left
bundles (and further into fasicles)
Ending at the Purkinje fibers
Slight pause, then repolarization occurs
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EEKKGEK’s
www.commons.wikimedia.org/wiki/File:EKG_complex.png
EKG Nomenclature
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Normal 12-lead EKG
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Heart Rate determination
Start with a QRS on a heavy black line
Use sequence to label rate at subsequent
lines
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Six Second Strip
(aka 30 big blocks)
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Calculate the rate:
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62 is correct (or just a little faster than 60)
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Rate of Impulse Formation
S-A Node = 60-100 bpm
A-V Node = 40-60 bpm
Ventricle = 20-40 bpm
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Normal Sinus Rhythm
www/healcentral.org/content/collections/ECG/ecg_nsr.gif
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Sinus Bradycardia
www.healtcentral.org/content/collections/ECG/ecg_sb.gif
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Sinus Bradycardia
NSR criteria, but heart rate is < 60
Can be normal especially in well-trained
athletes or people taking B-blockers
Most common rhythm disturbance seen in
early stages of AMI
If symptomatic, treat with Atropine,
consider pacing (TransCutaneous
Pacing/TCP)
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Sick Sinus Syndrome
Associated w/ sinus arrest, s-a exit block,
or persistent sinus bradycardia < 45 bpm
Seen in elderly, @ w/ atrial fibrillation, but
often asymptomatic
Patchy fibrosis of SA node and conduction
May be caused by drug therapy, sarcoid,
amyloidosis, cardiomyopathies
Treat with pacemaker if symptomatic
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Sinus Tachycardia
www.healtcentral.org/content/collections/ECG/ecg_st.gif
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Sinus Tachycardia
NSR criteria, but HR is >100<180
Normal under many conditions: exercise,
fever, hyperthyroid, CHF, COPD, ETOH
Treat cause first
If unstable/pt. symptomatic, immediate
synchronized cardioversion
If stable, try vagal maneuvers,
B-blockers, +/- RFA used definitively Rutgers PANCE/PANRE Review Course
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Sinus Arrhythmia
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Sinus Arrhythmia
Normal physiological mechanism 2o vagal
influence (young and/or old)
Barely detectable rate changes
corresponding to the phases of respiration
Slight increase in rate during inspiration
Slight decrease in rate during expiration
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Sinus Arrhythmia
www.healtcentral.org/content/collections/ECG/ecg_sa.gif
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Premature Atrial Contractions
Arrive earlier than expected next beat
Different shape to p wave (because it comes from a different and irritable focus in the atria)
Normal/narrow QRS complex
Followed by a compensatory pause
Usually benign, provide reassurance
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Premature Atrial Contractions
www.healtcentral.org/content/collections/ECG/ecg_pac.gif
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(P)SVT/Supraventricular Tachycardia
Rate 140-240 and regular, w/ narrow QRS
Sudden/abrupt start/stop
AKA “a-v nodal reentry tachycardia” (AVNRT)
Responds (slows or terminates) to vagal maneuvers, carotid massage (R then L: not both!)
Pharmacologic agents: (IV) adenosine - 6 mg bolus or verapamil - 2.5 mg bolus
+/- Cardioversion (100 j) if symptomatic
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(P)Supraventricular Tachycardia
www.commons.wikimedia.org/wiki/File:SVT_Lead_II.JPG
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Wandering Atrial Pacemaker
Somewhat irregular rate of < 100
Impulses originate from three or more
different foci in the atria, so we see at least
3 different p wave morphologies
Followed by narrow QRS complex
Often not treated
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Wandering Atrial Pacemaker
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Multifocal Atrial Tachycardia
Same as WAP, but rate is 100-140
Impulses originate from three or more
different foci in the atria, so we see at least
3 different p wave morphologies
Followed by narrow QRS complex
Often associated with COPD
Treated with verapamil to slow conduction
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Multifocal Atrial Tachycardia
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Atrial Flutter -sawtooth pattern w/ narrow QRS
-common in COPD patients
-2:1 block most common, but 3:1, 4:1, and
variable block exist
-Treated with antiarrhythmic (ibutilide) or
electrical cardioversion if unstable
-catheter ablation is definitive therapy
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Atrial Flutter with 2:1 block;
ventricular rate is ~150 bpm
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Atrial Flutter with variable block
www.healtcentral.org/content/collections/ECG/ecg_aflutter.gif
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Atrial Fibrillation No common/distinct/visible p waves
Irregularly irregular w/ narrow QRS
New onset: check thyroid function
Treated with b-blocker, Ca blocker, cardioversion or ?permanently with radio frequency ablation (RFA)
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Atrial Fibrillation
www.healtcentral.org/content/collections/ECG/ecg_afib.gif
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Atrial Fibrillation
Common causes: HTN, CHD, myopathy
r/o thyrotoxicosis and ETOH use/abuse
Danger due to potential for blood to
coagulate in RA sending clot to brain: CVA
First goal in AF = rate control
Second goal = Cardioversion or ablation
Third goal in chronic AF = anticoagulation:
(details via CHADS2 scoring system)
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Chronic Atrial Fibrillation Tx
Anticoagulation most commonly treated
with Coumadin (warfarin), Pradaxa
(dabigatran), or Xarelto (rivaroxaban)
Levels must be monitored regularly (PT,
INR) for warfarin only
On occasion, aspirin and/or Plavix
(clopidogrel) is used for this purpose if
ASA allergic
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Normal Cardiac Pacemakers
Atrial: SA Node – rate = 60-100
Junctional: AV Node – rate = 40-60
Ventricular: ventricle – rate = 20-40
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Junctional Rhythm
www.healtcentral.org/content/collections/ECG/ecg_junc.gif
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Junctional Rhythm
Regular rhythm (so NOT a-fib)
Normal/narrow QRS (wide possible)
Absent, retrograde, or inverted p waves
Rate usually 40-60 bpm
Often seen with digitalis toxicity
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Premature Junctional Contraction
(PJC) PJC is early, narrow QRS, followed by
compensatory pause, and with absent,
inverted, or retrograde p wave
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Accelerated Junctional Rhythm
Regular rhythm with narrow/normal QRS
Rate > 60 but < 100
P wave is absent, inverted, or retrograde
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Junctional Tachycardia
Regular rhythm
Rate > 100
P waves are absent, inverted, retrograde
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Normal Cardiac Pacemakers
Atrial: SA Node – rate = 60-100
Junctional: AV Node – rate = 40-60
Ventricular: ventricle – rate = 20-40
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Idioventricular Rhythm– treat with
Pacemaker
www.healtcentral.org/content/collections/ECG/ecg_ivr.gif
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Accelerated IVR (AIVR): common
after MI: do not treat
www.healtcentral.org/content/collections/ECG/ecg_aivr.gif
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PVCs (Premature Ventricular
Contraction)
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Premature Ventricular Contractions
Most common ventricular arrhythmia
Beat is early, wide, bizarre
Sticks out like a “sore thumb”
Followed by a compensatory pause
Rare/occasional PVCs may be normal,
especially if they resolve with activity
Check electrolytes, thyroid, occult heart dz
If symptomatic, look for cause and treat with b-
blockers first then consider ablation
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Unifocal PVC
www.healtcentral.org/content/collections/ECG/ecg_pvc.gif
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Multifocal PVCs
www.healtcentral.org/content/collections/ECG/ecg_pvc.gif
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Ventricular Bigeminy
www.healtcentral.org/content/collections/ECG/ecg_bigem.gif
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Ventricular Couplet
www.healtcentral.org/content/collections/ECG/ecg_pairs.gif
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“Salvo” or 3-beat Run of VT
www.healtcentral.org/content/collections/ECG/ecg_trip.gif
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“R-on-T” phenomenon
Danger: may initiate Torsade/VT/VF
Find cause; Tx with lidocaine or amiodarone
then cardiovert (100-360 J)
www.healtcentral.org/content/collections/ECG/ecg_ront.gif
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Ventricular Tachycardia
A run of > 3 PVCs in a row
Rate regular and > 100 (160-240)
May be mono or polymorphic
Common cause = hypo- K+ or hypo-
magnesemia
Non-sustained: <30 sec., spont. terminate
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Ventricular Tachycardia
Monomorphic: more commonly associated
with a healed infarction
If symptomatic, tx with cardioversion;
drugs = amiodarone or lidocaine; OD
pace if recurrent; definitive therapy = ICD
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Torsades de Pointes
Polymorphic VT
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Polymorphic VT
Torsades de pointes means “twisting of
the points”
Often associated with Long QT intervals
May be congenital, but often results from
electrolyte imbalance (K, Mg, Ca)
Treat with B-blockers or temporary
pacing (if pulse is present)
Do NOT treat with antiarrhythmics as they
prolong the QT interval. Rutgers PANCE/PANRE Review Course
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Ventricular Fibrillation
www.healtcentral.org/content/collections/ECG/ecg_vf.gif
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(Coarse) Ventricular Fibrillation
Most common cause of SCD (sudden cardiac death)
Chaotic, irregular rhythm; no true QRS
No pulse on PE; treat with
CPR/defibrillation/ACLS protocols
With survival, treat with ICD
www.commons.wikimedia.org/wiki/File:EKG_VF.jpg
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Asystole
No electrical activity/no defib; look for
cause and treat specific abnormality
www.healtcentral.org/content/collections/ECG/ecg_asys.gif
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Ventricular Rhythms: compared
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AV Conduction Blocks
An AV Conduction Block is any obstruction
or delay of the normal conduction between
the SA node and the Purkinje fibers.
Most commonly occurs between AV node
and His bundle
3 varieties of AV Block: 1st, 2nd, 3rd
degree
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First Degree AV Block
All normal except PR interval >.2 sec (1
big block); often seen in athletes and with
bradycardia; no treatment required
www.healcentral.org/content/collections/ECG/ecg_1_AV_block
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Second degree AV Block
Wenckebach (aka Mobitz type I)
Gradually lengthening PR interval until a
QRS complex is dropped.
Look for “grouped beating” in the EKG
No treatment required; +/- EP studies
www.healcentral.org/content/collections/ECG/ecg_2A_V_block.gif
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Second Degree AV Block –
Mobitz type II
PR interval remains constant
Intermittent dropping of QRS
Usually @ with organic heart disease
Pacemaker usually indicated
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Third Degree (aka) Complete Heart
Block
www.healtcentral.org/content/collections/ECG/ecg_chb.gif
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Third Degree/Complete Heart Block
No relationship between p waves and
QRS (p waves “marching through”)
More p waves than QRS complexes
Ventricular response often slow (IVR)
Treat with permanent pacemaker
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Third Degree A-V Block with Pace-
maker Insertion Treatment
www.healcentral.org/content/collections/ECG/ecg_3_AV_block
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Pacemakers
A power source connected to electrodes
Most popular type = dual chamber
multiple programmable units
www.commons.wikimedia.org/wiki/File:ECG/pacemaker_dualchamber.jpg
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Single Chamber Pacemaker
www.healtcentral.org/content/collections/ECG/ecg_pacer.gif
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Pacemaker Wire Placement
www.healtcentral.org/content/collections/ECG/ecg_lead_wire.gif
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Dual Chamber Pacing (aka AV
sequential pacing)
www.healtcentral.org/content/collections/ECG/ecg_av_pace.gif
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Pre-excitation Syndromes
Accessory AV conduction pathways
Result in “short circuits” or shortcuts from
SA node to AV node
Usually diagnosed on 12-lead EKG
2 types: Wolff-Parkinson-White Syndrome
and Lown-Ganong-Levine Syndrome
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WPW and LGL: shortcuts in conduction
www.healtcentral.org/content/collections/ECG/ecg517.gif
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Wolff-Parkinson-White Syndrome
Accessory pathway via “bundle of Kent”
Appears as short PR interval (<.08)
Presence of delta wave
Predisposes to tachycardias (A-fib—VF)
Treated with amiodarone or sotalol; if unstable cardiovert, then RFA definitively
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WPW (here, look in V4-V6, delta waves)
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Lown-Ganong-Levine Syndrome
Accessory pathway via “James bundle”
Short PR interval
No delta wave
Beware rapid arrhythmias
Treat as with WPW
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LGL – short PR, no delta wave
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Mean QRS Vector and Axis
Down and to pt.’s left
www.commons.wikimedia.org/wiki/File:ECG_Eomtjpvem_vect0.svg
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EKG Axis Determination
(Who’s triangle?) Dr. Einthoven !
www.commons.wikimedia.org/wiki/File:ECG_Einthoven_vect.2.svg
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Normal 12-lead EKG
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12 Lead EKG Arrangement
I AVR
II AVL
III AVF
Rhythm strip (1-3 leads)
V1 V4
V2 V5
V3 V6
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Axis determination short cut
Look at the QRS deflection
Using leads I and AVF: (up =+; down = -)
Up in I and Up in AVF = Normal Axis
Up in I and Down in AVF = Left Axis Deviation
Down in I and Up in AVF = Right Axis Dev.
Down in I and Down in AVF = Extreme RAD
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Left Axis Deviation (LAD)
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Right Axis Deviation (RAD)
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Bundle Branch Block (BBB)
www.commons.wikimedia.org/wiki/File:Reizeleitungssystem_RSB.png
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LBBB Diagnosis Criteria
Wide (>.12 sec) QRS
RSR’ in V5 or V6 (aka “dog ears”)
Associated with ST depression in I, AVL, V5, and V6
Often associated with CAD
New LBBB (@ w/ CP) = “STEMI equivalent”
BEWARE: Difficult to diagnose MI via EKG in presence of LBBB.
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Left Bundle Branch Block
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Criteria to Diagnose RBBB
Wide QRS (> .12 sec)
RSR’ in V1 or V2 (aka “rabbit ears”)
May have associated ST depression in V1, V2, +/- V3
Can be found in a “normal” EKG (i.e., usually not associated with CAD)
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RBBB: RSR’ in V1/V2
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Right BBB with A-fib
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Hemiblocks
Blocks occurring in either the Anterior or
Posterior Divisions (fascicles) of the Left
Bundle Branch (just distal to the AV node)
Often result from diminished blood supply,
i.e. MI or ischemia
QRS may be normal or wide
Major effect on EKG is axis deviation
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Hypertrophy and Enlargement
Hypertrophy = ventricles; enlargement =
atria
Specific EKG leads show evidence of
these findings
ALL EKG findings of hypertrophy and
enlargement must be verified with
ECHOCARDIOGRAM ! ! !
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Examples of LVH & RVH
www.commons.wikimedia.org/wiki/File:Heart_Left_ventricular_hypertrophy_sa.jpg
www.commons.wikimedia.org/wiki/File:Heart/kabulki_syndrome.jpg
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Left Atrial Enlargement
Look for biphasic p
wave in V1 with large
terminal portion
May be associated
with wide p waves
elsewhere
May result from mitral
stenosis, HTN
LAE:
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Left Atrial Enlargement
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Right Atrial Enlargement
Look for tall (>2.5
mm)peaked p waves
in II, III, AVF
Results from tricuspid
stenosis, pulmonary
HTN, severe lung dz
RAE:
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Right Atrial Enlargement: look for
tall p waves (>2.5mm) in II, III, AVF
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Left Ventricular Hypertrophy
S in V 1/2 + R in V 5/6 > 35 mm
R in I + S in III > 25 mm
R in AVL > 13 mm
Often caused by HTN and valvular dz
Often associated with LAD & depressed ST seg
(aka “ventricular strain” pattern)
Criteria not totally applicable < 35 y/o or thin
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Left Ventricular Hypertrophy: look
for deep S in V1/2 plus tall R in V5/6 > 35 mm
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Right Ventricular Hypertrophy
Tall R wave in V1 (R>S)
Deep S wave in V6 (S>R)
Must be accompanied by RAD
Commonly caused by pulmonary disease
and congenital heart disease
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RVH with RAE, causing RAD
Make changes
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Myocardial Infarction
www.commons.wikimedia.wiki/myocardial_ischemia Rutgers PANCE/PANRE Review Course
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Diagnosing an MI
History and Physical Exam
Cardiac Markers (CK-MB, Troponin)
EKG
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Diagnosing an MI: EKG findings
T wave peaking (rarely seen on EKG;
occurs w/in minutes of MI) followed by
inversion of T wave (hours to days later)
ST segment elevation (STEMI) (w/in
hours)
Appearance of new Q waves (hours to
days)
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Evolving EKG changes of MI
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Evolution of Acute MI ST-changes
www.commons.wikimedia.org/wiki/File:12_Lead_EKG_ST_Elevation_tracing_only..jpg
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Localizing an MI
Anterior Wall MI: Supplied by Left Anterior Descending Artery
Seen as EKG changes in I, V1-V4
Often a very deadly MI
Often associated with “poor R-wave progression”
V1 & V2 are mainly considered “septal” leads, so many MIs are “antero-septal”.
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Leads I, V1-V4 = Anterior MI
www.commons.wikimedia.org/wiki/File: AMI_scheme.png
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Acute Antero-septal wall STEMI
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Inferior Wall MI
Inferior or diaphragmatic portion of the
heart is supplied mostly by the Right
Coronary Artery
Can be associated with Right ventricular
infarction
EKG changes are seen in II, III, AVF
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II, III, AVF( +/- V6 ST elevations) = Inferior MI
www.commons.wikimedia.org/wiki/File:AMI_scheme.png
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Inferior Wall MI
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Lateral Wall MI
Lateral portion of the heart is supplied by
the Left Circumflex Artery.
EKG changes seen in I, AVL, V5 & V6
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I, AVL, V5, V6 = Lateral MI
Often a result of left
circumflex artery occlusion
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Acute LWMI w/ reciprocal changes
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Posterior Wall MI
Posterior cardiac muscle is mainly
supplied by the Right Coronary Artery
Frequently associated with arrhythmias
Since we have no EKG leads there, we
look for ST segment depression and tall R
waves in V1/V2 to diagnose a PWMI
(Or you may invert tracing and use “mirror
test” to see ST elevation in V1/V2)
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Look in V1 for “mirror image”: Tall R wave in V1, +/- ST dep
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Reciprocal Changes
Sometimes, the dramatic EKG changes in
the infarct area produce opposing changes
in distant leads (or those opposite the
infarct location.
In an Acute MI with ST elevations, ST
depression may appear in a distant lead.
These ST depressions are called
“reciprocal changes”
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Non-Q Wave or Non-STEMI MIs
Not all MIs produce Q waves or ST
elevations
On EKG, a non-Q Wave or non-STEMI
only shows: T wave inversion and ST
depression
Must use History and Cardiac Markers to
make diagnosis
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Non STEMI vs. Ischemia: note ST dep.
and flipped T waves in I, II, V3-V6 (lateral wall area)
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EKG findings of “old” MI
ST segments and T wave changes usually
return to “normal” after several days.
Q waves often remain indefinitely
Look for residual Q waves in specific
areas to localize old MIs
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Remember this?
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Old IWMI: note sig. Qs only present
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Ischemia/Angina Pectoris
Angina is the diagnosis given to the typical
chest pain associated with CAD
Classic finding is precordial chest pain
precipitated by stress or exertion and
rapidly relieved by rest or nitrates (NTG)
EKG shows classic ST depressions
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Types of ST Segment Depression
www.healtcentral.org/content/collections/ECG/ecg_st.gif
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Ischemia: EKG w/ ST depression
ST depression > 1 mm = significant
< 1mm – “non-specific ST segment changes”
www.commons.wikimedia.org/wiki/File:StressECG_STDepression.jpg
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Antero(septal) wall Ischemia
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Inferolateral wall ischemia (XST)
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Benign ST changes: Early
repolarization (see diffuse ST elevations)
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Prinzmetal’s (Variant) Angina
Angina-like chest pain often a result of
coronary artery spasm
Associated with ST elevation on EKG
Thought to be a reversible injury, with ST
segments returning to baseline after
treatment with nitroglycerin
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Miscellaneous EKG Diagnoses
Certain effects may be recognized by their
characteristic appearance on EKG
The EKG “alerts us” to the diagnosis—it
does NOT make the diagnosis
It can act as another “clue” in making a
diagnosis
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Brugada Syndrome
Familial condition predisposing to sudden
cardiac death
Young Asian Males more commonly
affected
Classic EKG: RBBB w/ ST elevation in V1,
V2, V3
Treat with b-blocker and ICD
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Brugada Syndrome
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Pulmonary Embolus (PE)
Classic trio: S I, Q III, Inverted T in III
Most common EKG finding in PE = ST
May show T wave inversion in V1-V4
RBBB (complete or incomplete)
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Pulmonary Embolus (PE)
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Hyperkalemia (high potassium)
The potassium ion is critical in the cardiac
conduction cycle at the cellular level
The range of potassium is very narrow
Classic finding is tall, peaked T waves
As the levels increase, the p wave flattens
while the QRS widens – beware!
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Hyperkalemia progression
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Hyperkalemia: (early stage); note tall,
peaked T waves in V1-V4
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Note wide QRS, absent p throughout
EKG in advanced hyperkalemia
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Hypokalemia: Classic findings:
flattened T wave and new U wave
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Hypokalemia: u wave in V2, V3
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Hypocalcemia Levels of calcium drop below normal
QT lengthens—DANGER!
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Hypocalemia with long QT seen in
all leads here
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Long QT Syndrome
May be an inherited syndrome (Romano-
Ward syndrome)
May be due to a variety of drugs
(quinidine, sotalol, abx such as the
quinolones, and antidepressants)
May lead to “R-on-T” or Torsades
Treat with b-blocker, Mg, pacer, ICD
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Hypothermia
J/Osborne wave (usually with bradycardia)
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Digitalis: effect and toxicity
Digitalis effect causes “scooped” ST seg
and is normal
Digitalis excess and toxicity can cause AV
blocks and ventricular rhythms
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Pericarditis: inflammation of the
pericardial sac – acute or chronic
www.commons.wikimedia.org/wiki/File: ChronicInfectivePericarditis.jpg
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Acute pericarditis: diffuse ST elevations
Chronic pericarditis: diffuse ST
depressions
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Acute Pericarditis w/ diffuse ST elevation
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Electrical Alternans
Associated with a large pericardial effusion
Electrical axis of the heart varies with each
beat due to the heart “floating in fluid-filled
sac”
Results in varying amplitude (alternating
large and small) of EKG beats (and pulse
on PE = pulses alternans)
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Electrical Alternans: seen in various
leads here
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Hypertrophic Cardiomyopathy
Previously known as IHSS, may occur as
obstructive (HOCM), dilated, or restrictive
Causes SCD in some instances (young)
EKG may show Q waves in many leads, LVH,
LAD, and some deeply inverted T waves.
Treated (if diagnosed) by placement of ICD
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Hypertrophic Cardiomyopathy
www.commons.wikimedia.org/wiki/File:Heart/left/ventricular/hypertrophy/sa.jpg
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Implantable Cardioverter
Defibrillator (ICD)
www.commons.wikimedia.org/wiki/File:AICD.jpg
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A 27 y/o female with a h/o anxiety presents c/o “a racing heart”. Here is a
rate/rhythm strip taken at presentation. Which of the following is her rhythm?
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1 2 3 4
2% 0%2%
96%
1. Atrial fibrillation
2. Atrial flutter
3. Supraventricular
tachycardia
4. Ventricular
tachycardia
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A 67 y/o female, 1 day post PM presents with severe SOB and
dizziness. What is her rhythm via telemetry?
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1 2 3 4
0%
90%
5%5%
1. Atrial fibrillation
2. Supraventricular
tachycardia
3. Ventricular fibrillation
4. Ventricular tachycardia
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References:
Scheidt, S., Basic Electrocardiography, Vol. 36,
Summit, NJ; CIBA-GEIGY Corp., 1996
Thaler, Malcolm S., The Only EKG Book You’ll
Ever Need, Seventh Edition; LWW, 2012
McPhee, S., Papadakis, M., Rabow, M. Lange
2013 Current Medical Diagnosis & Treatment;
51st Ed., McGraw Hill, 2013
www.healcentral.org
www.commons.wikimedia.org
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Thanks and please drive safely!
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