A Common Sense Approach to ECGs

Transcription

A Common Sense
Approach to ECGs
Vikram Gurtu
Cardiology Resident
University of Alberta
Mazankowski Cardiology Update
May 2, 2015
Objectives
• Briefly discuss the usefulness of ECGs
and when they should be ordered.
• Review some basic ECG interpretation
skills systematically
• Go over some key tips for differentiating
between diagnoses (eg. Arrhythmias,
ischemia)
• Review some example ECGs with must
not miss diagnoses
What is an ECG?
• Electrocardiogram
– Shows electrical activity of the heart in
multiple planes
– Two major planes:
• Coronal plane – Limb leads
• Horizontal plane – Precordial leads
– Allows you to “see” the electrical activity of
the heart in two planes thereby inferring which
way electrical activity is going
Precordial Leads
Mirvis DM and Goldberger AL (2015) from Electrocardiography. In Braunwald’s Heart Disease: A
Textbook of Cardiovascular Medicine
The Limb Leads
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When Should an ECG be
Done?
When there are new symptoms concerning for a cardiac
cause (ischemia, arrhythmia, etc.)
When there have been changes in symptoms
Prior to and following drug treatment that may have cardiac
side effects (eg. QT prolongation)
Preoperatively in those deemed to be at a higher
cardiovascular risk
Baseline screening for those in occupations that require high
cardiovascular performance (eg. firefighters) or linked to
safety (eg. pilots)
Follow up of patients with pacemakers
Follow up of patients with known cardiac disease (at
appropriate time intervals)
Should ECGs be Used for
Screening of Coronary Disease?
US Preventative Task Force (2012):
• In the low risk population, asymptomatic patients should
not be screened with regular ECGs
• There is insufficient evidence to determine the balance
of benefits and harms in the asymptomatic intermediate
or high risk populations .
Moyer, VA. Ann Intern Med. 2012;157:512-518.
A Systematic Approach to the ECG
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Name, date and previous ECGs
Standardization
Lead placement
Rate
Rhythm
Axis
Intervals
P-Q-RS-ST-T-U
Conclusion
1. Name, Date, Previous ECGs
• Ensure correct patient – use of incorrect
ECG for clinical decisions can lead to
adverse outcomes
• Always look at previous ECGs
– The most reassuring ECG is one that looks
the same as an ECG from 1 month ago
• ST elevation or T-wave inversion that was there
one month ago is not due to an acute infarct
2. Standardization
• Paper speed
– 25 mm / second
– One small square is 40 ms
– One large square is 200 ms or 0.2 seconds
– Five large squares is 1 second
– Whole ECG strip is 10 seconds
– Beats per minute = 60,000 / milliseconds
• Amplitude
– 10 mm/mV
3. Appropriate lead placement
• Limb leads appropriately placed
– aVR completely negative
• Precordial leads appropriately placed
– Appropriate R-wave progression from V1 to
V6
4. Rate
• If a ten second ECG, can count QRS
complexes and multiply by 6
• Divide 300 by the number of large boxes
between consecutive R-Rs (300, 150, 100,
75, 60, 50 rule…)
• HR = 60,000 / (R-R interval in ms)
Nathanson L A, McClennen S, Safran C, Goldberger AL. ECG Wave-Maven: Self-Assessment Program for Students and Clinicians. http://ecg.bidmc.harvard.edu.
5. Rhythm
• Sinus Rhythm
– Only requires upright P waves in leads I and II
• Tachycardias
– Narrow QRS – Sinus Tach, Afib, Aflutter, MAT, AVRT,
AVNRT
– Wide Complex – VT, VF, SVT with aberrancy
• Bradycardias
– Look for AV nodal blocks
– Escape rhythms
5. Rhythm
• Is there normal atrial / ventricular association?
– P-wave before every QRS
– QRS after every P-wave
• If more P-waves than QRS
– 2nd and 3rd degree AV blocks
– Atrial fibrillation
– Atrial flutter
• If less P-waves than QRS
– Junctional rhythms
– Ventricular tachycardia, ventricular flutter, ventricular
fibrillation
7. Axis ‐ The Limb Leads
7. Axis
• Normal axis is -30 to +90
• Normal axis if positive QRS in leads I and
II
• Generally if:
– Lead I positive, lead II negative – LAD
– Lead I negative, lead II positive – RAD
– Both negative – EAD
QRS Axis
Source: ECGpedia.org
Originally from Goldberger AL: Clinical Electrocardiography: A Simplified
Approach. 7th ed. St. Louis, CV Mosby, 2006.
8. Intervals
• PR interval (normal 120-200 ms)
– < 120 ms – think about accessory pathways (eg. WolffParkison White); look for delta wave
– > 200 ms – 1st degree AV block
• QRS  If > 120 ms – Bundle Branch Block
– LBBB
• Right sided precordial leads (V1, V2) has wide S wave
• Left sided precordial leads (V5,V6) has broad slurred R
wave
– RBBB
• Right sided precordial leads (V1, V2) has wide R wave
• Left sided precordial leads (V5,V6) has broad S wave
8. Intervals
• QTc interval
– Long QT
• > 440 ms in males
• > 460 ms in females
– Short QT
• < 340 ms
• Long QT
– Ischemia
– Hypokalemia, hypomagnesemia, hypocalcemia
– Congetial LQTS
– Drugs
• Short QT < 320 ms (sudden cardiac death)
9. Morphologies
• P-wave
• PR Segment
– Can be depressed in pericarditis
– aVR elevated in pericarditis
• Q waves
– Presence of infarct if in two contiguous leads
• RS – check for RVH and LVH
9. Morphologies
• ST Segment
– ST elevation - Acute transmural ischemia
– ST depression - Acute nontransmural ischemia
• T-waves
– Inversion - Ischemia as well as many other
causes
– Hyperacute – eg. hyperkalemia
• U-waves
– Large U-wave 1.5 mm (eg. Hypokalemia)
Originally from Goldberger AL: Clinical Electrocardiography: A Simplified
Approach. 7th ed. St. Louis, CV Mosby, 2006.
Rhythm
• Important therapeutic implications based
on the rhythm
– Atrial fibrillation and atrial flutter  need to
assess for the need for anticoagulation
– Other tachycardias may require urgent
cardioversion or defibrillation
– Bradycardias or heart blocks may be a side
effect of excess medication, or may require
monitoring or pacemaker
Rhythm
• When assessing rhythm, it is important to
separately assess for
– Atrial activity – regular, irregular, tachycardic?
– Ventricular activity – regularity, narrow or wide
complex, bradycardic vs tachycardic
– AV association - relationship between atrial
waves and QRS complexes
Normal Sinus Rhythm
• Upright P waves in leads I and II (also
often upright in aVF)
• Rate 60-100
– Sinus tachycardia if > 100 bpm
– Sinus bradycardia if < 60 bpm
• *IF there is normal A-V conduction, there
will also be:
– P wave before every QRS
– QRS after every P wave
Examples of Abnormal Rhythms
Atrial Fibrillation
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Irregularly irregular
Can see fibrillatory waves
Absence of P waves
Atrial rate 350-600 bpm
Atrial Flutter
• Atrial rate of 250-350
• Ventricular rate of usually 140-160 (not
always)
• Can have 2:1, 3:1, 4:1 block etc or a
variable block
• Classic saw tooth pattern (best seen in
lead II but also look in lead V1)
Is this Afib or A Flutter?
Artifact
• Make sure to look at all of the leads.
• The previous ECG clearly shows regular
p-waves in V2-V4 with the other waves
being artifact
• This patient has a Parkinsonian tremor
Wide Complex Tachycardias
• Can be ventricular arrhythmias
– Ventricular Tachycardia
– Ventricular Fibrillation
• Can also be supraventricular tachycardias
(e.g. Atrial fibrillation) with aberrant
conduction (e.g. LBBB)
• If hemodynamically unstable  SHOCK
Ventricular Tachycardia
• Clues to differentiate VT from SVT with aberrancy
– Look for an extreme axis (VT is coming from
bottom of ventricle)
– Positive in aVR (VT axis is from bottom to top)
– Precordial concordance (VT goes in one
direction)
– Signs of AV dissociation with QRS rate > P rate
• Capture beats / Fusion beats
• Obvious p-waves separated from QRS
– Atypical looking RBBB or LBBB (eg very wide >
150ms, or very abnormal looking)
– Ventricular rate faster than an atrial rate
Ventricular Tachycardia
• Monomorphic – (eg. scar related VT) prior MI,
cardiomyopathy, arrhythmogenic RV dysplasia,
RVOT VT, idiopathic LV VT
• Polymorphic VT – ischemia, cardiomyopathy,
torsades de pointes with long QT, Brugada
syndrome (looks like pseudo RBBB with ST
elevation V1-V3)
Ventricular Fibrillation
• No clear QRS or P, can have a wandering
baseline
• Bizarre, irregular waveforms
• Rate > 350, disorganized
• Treatment  Defibrillation
Case
• An 87 year old female with a history of
hypertension presents to the emergency room
with an episode of suddenly passing out while
sitting at a table.
• Her ECG is shown
AV Nodal Blocks
• 1º AV Block – PR prolongation > 200ms
• 2º AV Block
– Mobitz Type I (Wenckebach)
• Increasing PR lengths then dropped QRS
– Mobitz Type II
• occasionally or repeatedly dropped QRS complexes,
with consistent PR interval
• Often progresses in to 3ºAVB
• 3º AV Block
– complete heart block, no AV conduction.
– P and QRS completely disassociated
Source: ECGPedia.org
Case
• A 59 year old female presents with
lightheadedness and palpitations
• Her ECG is shown
Abnormal PR - Pre-excitation
• Normal PR 120-200 ms
• PR > 200 ms = 1st degree AV Block
• PR < 120 ms = pre-excitation
• In this case, suspecting pre-excitation is important
clinically. Giving AV nodal blockers like metoprolol or
diltiazem could increase conduction down the bypass
tract  can degenerate into VT or VF
• Drug of choice would be IV procainamide, or DC
cardioversion if unsuccessful or if patient is
hemodynamically unstable.
Ischemia / Coronary Disease
Localizing changes:
When are Q waves significant?
• Presence of two or more in contiguous
leads means “infarct”
• Can be localizing
• Always pathologic in leads V1-V4
• Usually need to be greater than 30 ms in
width or more than 1/3 height of QRS in
inferior and lateral leads
Q Waves
• Anterior MI
– any Q is significant in V1-V3 (shouldn’t be there)
• Lateral MI
– Q in I, aVL, V5, or V6 > 30ms is significant
– R/Q ratio in I or aVL < 1 (bigger Q and smaller R)
• Inferior MI
– Qs generally pathologic if > 40ms in inferior leads
(though> 30ms cutoff also specific, but not as
sensitive)
– Always look for POSTERIOR involvement
• Posterior MI → R/S ratio > 1 in V1
• Tall wide R wave, like a reciprocal Q wave (>40ms in V1 or
>50ms in V2)
ST Elevation
• Current of injury. Is localizing.
• Generally need at least 1mm elevation in 2
contiguous leads
• Evolution of ST Elevation:
– J point elevation, with ST remaining concave
– Compare to the flat TP segment (BEFORE the P wave)
– ST segment becomes more elevated and more
convex or rounded upward.
– The ST segment may eventually be
indistinguishable from T wave
Old ECGs
• Ventricular aneurysm, not acute MI
• Always look at previous ECGs
ST Elevation - Differential
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Early repolarization
Pericarditis: ST elevation in all leads except aVR
P.E.: ST elevation in V1 and aVR
Hypothermia: ST elevation in V3-V6, II, III and aVF
LVH, Hypertrophic CM, Paced/idioventricular
rhythms
Hyperkalemia: V1-V2 (V3)
Acute neurologic events: all leads, primarily V1-V6
Acute sympathic stress: all leads, especially V1-V6
Brugada syndrome.
Cardiac aneurysm, or cardiac contusion
Is it a STEMI?
• Measure at the J-point
• Look for reciprocal changes – PAILS mnemonic
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Posterior ST Elevation - Anterior ST depression
Anterior ST Elevation - Inferior ST depression
Inferior ST Elevation - Lateral ST depression
Lateral ST Elevation - Septal ST depression
Septal ST Elevation - Posterior ST depression
Is it a STEMI?
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Take into account the clinical scenario
Look at previous ECGs (if available)
Look for dynamic changes
If any doubt at all, consult cardiology (it is better to
be overcautious!)
Early Repolarization
ST Depression
• Can see reciprocal changes  ST
depression on opposite side of where you
see ST elevation
• If no ST elevation, ST depression can still
indicate ischemia (but not localizing)
• Generally nonspecific if < 0.5mm in depth
(>0.5mm consider ischemia)
ST Depression Differential
• Reciprocal ST segment depression.
• Left ventricular hypertophy with "strain" or
depolarization abnormality
• Drugs - Digoxin effect
• Metabolic – low K+ / low Mg2+
• Heart rate-induced changes (post
tachycardia)
• During acute neurologic events.
T Wave Flattening/Inversion
• Nonspecific repolarization abnormalities, eg
due to metabolic changes.
• Hyperkalemia
• Neurological disorders (eg. stroke, SAH)
• Pericarditis/myocarditis
• Cardiac contusion
• Mitral valve prolapse (MVP)
• Digoxin
• RVH and LVH with strain
• Can be inverted in ischemia.
• More indicative of ischemia if deep,
symmetric T wave inversions, and also
deemed more significant if > 2mm
Hyperacute T-waves
• Greater than 1/3 height of QRS complex
• Occur in:
– Hyperkalemia
– Hyperacute ischemia (before ST elevation)
Hyperkalemia
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Peaked T waves “uncomfortable to sit on”
Increased PR interval
QRS widens, fusion of QRS-T
Increased QRS width → sine waves
Loss of ST segment
AF and VF can occur with K > 7.5
Summary
• Try to follow the systematic approach to
ECGs
• Always try to compare the current ECG to
previous
• Use serial ECGs
– Can be helpful for example when looking for
dynamic ischemic changes, ruling out artifacts
• When in doubt call for help
References and Resources
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ECG Wave Maven - ECG Self Assessment Program:
Nathanson L A, McClennen S, Safran C, Goldberger AL. ECG Wave-Maven: SelfAssessment Program for Students and Clinicians. http://ecg.bidmc.harvard.edu.
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Mirvis DM and Goldberger AL (2015). Chapter 12: Electrocardiography. In DL Mann
et al (Eds) Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine Tenth
Edition (pp. 114-154). Philadelphia, PA: Elsevier Saunders.
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ECGpedia.org
–A fantastic resource with cases and examples
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ACC Cardiovascular Board Review
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Gupta R, et al (2011) Cardiology. In MS Sabatine (Ed) Pocket Medicine Fourth
Edition. Philadelphia, PA: Lippincott, Williams & Wilkins.
Acknowledgments
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Dr. Janek Senaratne

A Common Sense Approach to ECGs

Transcription

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