Transcript 12-Lead EKG Interpretation - Mississippi Nurses Association

12-lead EKG Interpretation
Jamie Shedden, MSN, ACNP-BC
12 Lead EKG Interpretation
Objectives
Upon Completion of this program, the participant will be able to:
1. Successfully interpret the 12-lead EKG using a systematic
evaluation of key components
2. Identify EKG rate and rhythm
3. Assess PR interval, QRS interval and QT interval with
identification of significant abnormalities
4. Determine EKG Axis with identification of significant
abnormalities
5. Successfully identify 12 lead EKG abnormalities and identify
significance
6. Differentiate between significant 12 lead EKG changes
7. Identify EKG abnormalities related to artifact and lead
misplacement
12 Lead EKG Interpretation:
Electrode Placement
12 Lead EKG Interpretation
Identification of Key Components
1.
2.
3.
Determine rAte
Determine rHythm
Measure Intervals and
Identify abnormalities
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PR Intervals--AV Blocks,
WPW
QRS Interval--Bundle
Branch Blocks-RBBB,
LBBB, IVCD
QT Interval--Long QT
interval, Long QT
Syndrome
4.
Determination of Axis
•
5.
Normal Axis, Left Axis Deviation, Right
Axis Deviation and Indeterminate Axis
Hypertrophy
•
6.
Diagnosis of chamber enlargement
Infarct
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7.
Assessment of significant QRST changes
Recognition of acute changes on the EKG
(ischemia, injury or infarction)
Recognition of significant
EKG abnormalities related
to:
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Electrolyte disturbances
Pericarditis
Medication effects
Lead misplacement and
Artifact
12 Lead EKG Interpretation
Rate Determination
• Numerous methods for rate determination
• One easy “eyeball” method
– Remember the pneumonic “300-150-100-75-60-50”
– Find the QRS complex closest to the dark vertical line on the EKG paper
– Count forward or backward to the next QRS complex using the
pneumonic
– Estimate the HR based on where the next QRS complex falls in the count
12 Lead EKG Interpretation
Rhythm Determination
4 key questions of rhythm Analysis
Are there P waves?
Is the QRS wide or narrow?
Is the rhythm regular?
Who’s married to Whom?
(is the P related to the QRS?)
12 Lead EKG Interpretation
Rhythm Determination
•
Determinants of Sinus rhythm
– P wave will be upright in Lead II
{IF the P wave is NOT upright in
Lead II, it is not sinus rhythm}
Exceptions: Dextrocardia or lead
reversal
– Heart rate will be between 60-100
bpm
– Rhythm will be regular
– If the P wave is upright in lead II
but either rate or regularity is
lacking, consider other sinus
rhythms such as:
• Sinus bradycardia—heart rate
<60
• Sinus tachycardia—heart rate
>100
• Sinus arrhythmia—rhythm
irregular
12 Lead EKG Interpretation
Practice EKG
12 Lead EKG Interpretation
Rhythm Determination
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Supraventricular Rhythms
Atrial Fibrillation/Atrial Flutter (most common)
MAT (Multifocal Atrial Tachycardia): definite P waves that
appear different and irregular rhythm; wandering atrial pacemaker
PSVT or AVNRT: rate 150-240bpm; atrial activity not evident;
sudden onset
Junctional rhythms: Escape rhythms occur when SA node fails to initiate
the electrical impulse and another pacemaker assumes the function
– AV nodal escape rhythm: rate between 40-60bpm; may or may not see
negative P wave before the QRS in Lead II; QRS will be narrow unless
there is other underlying abnormality of the ventricular conduction system
– Accelerated junctional rhythm: rate 61-99bpm
– Junctional tachycardia: rate >100bpm
Atrial Fibrillation
• Deviation from NSR
– No organized atrial depolarization, so no
normal P waves (impulses are not
originating from the sinus node).
– Atrial activity is chaotic (resulting in an
irregularly irregular rate).
Atrial Fibrillation
• Etiology: theories suggest that it is due to
multiple re-entrant wavelets conducted
between the R & L atria. Either way,
impulses are formed in a totally
unpredictable fashion. The AV node allows
some of the impulses to pass through at
variable intervals (so rhythm is irregularly
irregular).
Atrial Fibrillation
Atrial Flutter
• Deviation from NSR
– No P waves. Instead flutter waves (note
“sawtooth” pattern) are formed at a rate of
250 - 350 bpm.
– Only some impulses conduct through the
AV node (usually every other impulse).
Atrial Flutter
• Etiology: Reentrant pathway in the right
atrium with every 2nd, 3rd or 4th impulse
generating a QRS (others are blocked in the
AV node as the node repolarizes).
Atrial Flutter
12 Lead EKG Interpretation
Rhythm Examples
Atrial Fibrillation
Multifocal Atrial Tachycardia or
Wandering atrial Pacemaker
Rhythm Examples
Rhythm Examples
Rhythm Examples
Rhythm Examples
12 Lead EKG Interpretation
Rhythm Examples
ATRIAL FLUTTER
12 Lead EKG Interpretation
Rhythm Examples
Junctional Tachycardia (P wave negative following QRS complex)
Accelerated Junctional rhythm (P wave negative and precedes the QRS complex)
AV nodal escape rhythm (no evidence of atrial activity)
12 Lead EKG Interpretation
Rhythm Examples
12 Lead EKG Interpretation
Rhythm Examples
12 Lead EKG Interpretation
Rhythm Examples
12 Lead EKG Interpretation
Rhythm Determination
Ventricular (Wide QRS) rhythms
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Slow idioventricular escape rhythm: rate 30-40bpm; no P wave evident; wide
QRS
Accelerated Idioventricluar rhythm: rate 40-110bpm
Ventricular Tachycardia: ventricular rate >120-130bpm; wide QRS
– Regular wide complex Tachycardia is always considered VT until proven
otherwise
Ventricular Fibrillation: totally disorganized and chaotic ventricular rhythm
Premature Beats
– PAC’s
– PJC’s
– PVC’s
12 Lead EKG Interpretation
Rhythm Examples
Idioventricular escape
rhythm
Accelerated
Idioventricular rhythm
Ventricular Tachycardia
Ventricular Fibrillation
12 Lead EKG Interpretation
Rhythm Examples
12 Lead EKG Interpretation
Rhythm Examples
12 Lead EKG Interpretation
Rhythm Examples
12 Lead EKG Interpretation
Rhythm Examples
12 Lead EKG Interpretation
Rhythm Examples
12 Lead EKG Interpretation
Rhythm Examples
12 Lead EKG Interpretation
Rhythm Examples
Junctional Tachycardia (P wave negative following QRS complex)
Accelerated Junctional rhythm (P wave negative and precedes the QRS complex)
AV nodal escape rhythm (no evidence of atrial activity)
12 Lead EKG Interpretation
Rhythm Determination
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Quick Review of Ventricular (Wide QRS) rhythms
Slow idioventricular escape rhythm: rate 30-40bpm; no P wave evident; wide
QRS
Accelerated Idioventricluar rhythm: rate 40-110bpm
Ventricular Tachycardia: ventricular rate >120-130bpm; wide QRS
– Regular wide complex Tachycardia is always considered VT until proven
otherwise
Ventricular Fibrillation: totally disorganized and chaotic ventricular rhythm
Premature Beats
– PAC’s
– PJC’s
– PVC’s
12 Lead EKG Interpretation
Rhythm Examples
Idioventricular escape
rhythm
Accelerated
Idioventricular rhythm
Ventricular Tachycardia
Ventricular Fibrillation
12 Lead EKG Interpretation
Assessment of the PR Interval
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Period that extends from the onset of atrial depolarization (beginning of the P wave) to the
onset of ventricular depolarization (beginning of the QRS complex)
Best lead for measurement is Lead II
Normal range 0.12-0.20 seconds
12 Lead EKG Interpretation
PR Interval Abnormalities
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The Short PR Interval
– Usually occurs when conduction occurs through an accessory pathway
– Consider WPW syndrome characterized by short PR and delta wave
– Other causes include accelerated conduction of the electrical activity or anatomic
shortening of the AV node
– Uncommon for PR to be short, more common for long PR interval
12 Lead EKG Interpretation
PR Interval Abnormalities
12 Lead EKG Interpretation
PR Interval Abnormalities
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The Long PR Interval
– Measures longer than 0.20-0.21 seconds (longer than one large box on EKG paper)
– First Degree AV block—delay of conduction to the ventricle across the AV node—
clinically not significant
– Second Degree AV Block—failure of at least some atrial impulses to conduct to the
ventricles—includes Mobitz I, Mobitz II or 2:1 AV block
– Third Degree AV Block—none of the atrial impulses are conducted to the
ventricle—no relationship between P waves and QRS complexes
12 Lead EKG Interpretation
PR Interval Abnormalities
12 Lead EKG Interpretation
Assessment of the QRS Interval
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Represents the time it takes for ventricular depolarization to occur
Normal QRS measures 0.10 seconds or less
Essential to examine all 12 leads and use the lead in which the QRS complex appears to
be longest
12 Lead EKG Interpretation
Assessment of the QRS Interval
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Only abnormality to consider is WIDE QRS complex
If the rhythm is determined to be sinus or supraventricular and the QRS is
wide, systematic approach should then focus on the type of QRS widening
(not to be considered in Ventricular tachycardia)
12 Lead EKG Interpretation
Diagnosis of Bundle Branch Block
• 3 Key leads used in the diagnosis of the type of BBB
• Leads I and V6 are Left sided leads
• Lead V1 is the single right sided lead
• Normal Ventricular Depolarization—begins with left side of septum,
then left and right ventricles are simultaneously activated
12 Lead EKG Interpretation
Diagnosis of RBBB
QRS widening of at least 0.11 sec
rSr’ or rsR’ in lead V1
Wide terminal S wave in leads I and V6
Considered incomplete RBBB if typical
morphology but complex measures <0.11
sec
12 Lead EKG Interpretation
Diagnosis of LBBB
QRS widening of at least 0.12 sec
Upright (monophasic) QRS complex in
leads I and V6
Predominantly negative QRS complex in
lead V1
Incomplete LBBB is rare and difficult to
recognize
12 Lead EKG Interpretation
Secondary ST-T Wave Changes in BBB
Orientation of the ST segment and the T wave with typical RBBB and LBBB should be
opposite that of the last QRS deflection in each o the 3 key leads
12 Lead EKG Interpretation
Example EKG for Review
12 Lead EKG Interpretation
Clinical Significance of BBB
• If found in asymptomatic adult in ambulatory setting, clinical significance
is minimal except for increasing likelihood that underlying heart disease is
present
• Does this patient need a pacemaker? The chance of developing complete
AV block and therefore need for PPM is quite small in asymptomatic
individuals
• Acute development of BBB may be associated with Acute infarction and
therefore the chance of developing Complete AV block is substantial and
Pacing may be required
• Diagnosis of Myocardial Infarction with BBB is difficult, particularly
LBBB which essentially precludes the diagnosis. There are 2 exceptions:
if Q wave is seen in I or V6, consider old infarct or if primary ST-T wave
changes are present, consider ischemia or infarction
12 Lead EKG Interpretation
Example EKG for Review
12 Lead EKG Interpretation
Example EKG for Review
12 Lead EKG Interpretation
Assessment of the QT Interval
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QT interval is the period from the beginning of ventricular depolarization until
the end of ventricular repolarization—measured from the onset of the Q wave
(or R wave if Q not present) to the end of the T wave
Measure QT in a lead where terminal boundary of the T wave is clear
QT interval may be short, normal or long. Short QT interval is difficult to
distinguish from normal QT. Focus should be on Normal or Long QT interval
For heart rate of 60 bpm, upper limit normal QT is 0.42-0.43 sec
12 Lead EKG Interpretation
Assessment of the QT Interval
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QT interval is affected by heart rate, age and sex of the individual
QTc is the correction made for heart rate, what the QT interval should measure at
a heart rate of 60 bpm
• Determination of QTc is complex, most 12 lead readings give a QTc
• Precise determination of the QTc is usually not necessary
Use General rule for measurement
• QT interval should not measure more than half of the R-R interval
• General rule is not valid if heart rate is >100 and QT interval has little
clinical meaning at this point
Normal
Abnormal
12 Lead EKG Interpretation
Common Causes of Prolonged QT
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Drugs
– Type IA Antiarrhythmic agents
(I.e., quinidine, procainamide,
disopyramide
– Type III Antiarrhythmic agents
(Amiodarone, Sotalol)
– Tricyclic antidepressants
– Phenothiazines
Electrolytes
– Hypokalemia
– Hypomagnesemia
– Hypocalcemia
• CNS Catastrophe
– Stroke
– Intracerebral or brainstem
bleeding
– Coma
– Seizures
• Bundle Branch Block or IVCD
• Ischemia or Infarction
12 Lead EKG Interpretation
Practice EKG
12 Lead EKG Interpretation
Practice EKG
12 Lead EKG Interpretation
Practice EKG
12 Lead EKG Interpretation
Practice EKG
12 Lead EKG Interpretation
Practice EKG
12 Lead EKG Interpretation
Electrolyte Disturbances—Hyperkalemia
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Hallmark for diagnosis is tall, peaked T waves with narrow base
T wave prominence may be normal repolarization variant, tend to be less
pointed with broader base
Ischemia should also be considered with tall peaked T waves in anterior leads,
rule out posterior wall ischemia with mirror test (changes with hyperkalemia
usually diffuse)
Can use EKG to verify initial hyperkalemia findings on lab while waiting on
repeat testing
12 Lead EKG Interpretation
Electrolyte Disturbances—Hypokalemia
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Characteristic sign is the development of U waves predominantly seen in leads
V2 through V5
EKG is not a reliable tool for assessing the presence of severity of
hypokalemia
Similar EKG changes may be present with hypomagnesemia
Both disorders should be considered when these EKG changes are present
12 Lead EKG Interpretation
Electrolyte Disturbances
• Hypercalcemia
– May shorten the QT interval
– Difficult to recognize
– Changes are usually not noticeable until serum calcium elevation is
marked
• Hypocalcemia
– May lengthen the QT interval usually without affecting the ST
segment or T wave morphology, can cause Torsades
• Hypernatremia and Hyponatremia
– Not associated with any EKG changes
12 Lead EKG Interpretation
Hypothermia
• Everything slows down—bradycardia and possible prolongation of
intervals
• J wave or Osborne wave—distinctive and virtually diagnostic ST
segment elevation, abrupt ascent right at the J point and then a sudden
plunge back to baseline
• Various arrhythmias, Slow Atrial Fib most common
• Artifact from muscle tremor
12 Lead EKG Interpretation
Pericarditis
• Diagnosed with history, Physical exam and EKG findings
• Characteristic symptom is chest pain that may is usually pleuritic and
increases with inspiration
• Physical exam may reveal pericardial friction rub
• EKG findings usually occur in 4 stages
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Stage I—generalized ST segment elevation
Stage II—transitional stage, pseudonormalization
Stage III—generalized T wave inversion
Stage IV—normalization
• EKG findings in Stage I may be confused with J point elevation of
early repolarization or acute infarction, History and PE is essential
12 Lead EKG Interpretation
Pericarditis
Stage I
Stage III
12 Lead EKG Interpretation
Pericarditis
12 Lead EKG Interpretation
Medication Effects
• Digitalis—Therapeutic or toxic?
– Digitalis Effect –scooped appearance or gradual downslope of the
ST segment, ST segment depression with flattening or inversion of
the T wave
– Digitalis effect is normal and predictable, does not necessitate
discontinuing the drug, may only be seen in about 60% of patients
12 Lead EKG Interpretation
Medication Effects
• Digitalis—Therapeutic or toxic?
– Digoxin Toxicity can cause
• AV conduction abnormalities
• Tachyarrhythmias—enhances automaticity, Paroxysmal atrial
tachycardia and PVCs are most common, junctional rhythms common
• Sinus node suppression (sinus exit block)
– Most characteristic rhythm disturbance of dig toxicity is PAT with
second-degree AV block
12 Lead EKG Interpretation
Practice EKG
12 Lead EKG Interpretation
Lead Misplacement
Most common problem is interchanging the left and right arm electrodes
which reverses the polarity of the QRS complex in the six standard leads
Clues to diagnosis of lead misplacement
P wave in lead II is inverted
global negativity in lead I
QRS complex in aVR is upright
DX: reversal of L and R arm electrodes
12 Lead EKG Interpretation
Lead Misplacement
Normal R wave progression
Precordial lead placement one
interspace too high causes loss
of R wave and appearance of
anterior infarct
12 Lead EKG Interpretation
Practice EKG
12 Lead EKG Interpretation
Practice EKG