12-lead EKG Interpretation Jamie Shedden, MSN, ACNP-BC.

12-lead EKG Interpretation

Jamie Shedden, MSN, ACNP-BC

12 Lead EKG InterpretationObjectives

Upon Completion of this program, the participant will be able to:1. Successfully interpret the 12-lead EKG using a systematic

evaluation of key components2. Identify EKG rate and rhythm3. Assess PR interval, QRS interval and QT interval with

identification of significant abnormalities4. Determine EKG Axis with identification of significant

abnormalities5. Successfully identify 12 lead EKG abnormalities and identify

significance6. Differentiate between significant 12 lead EKG changes7. Identify EKG abnormalities related to artifact and lead

misplacement

12 Lead EKG Interpretation:Electrode Placement

12 Lead EKG InterpretationIdentification of Key Components

1. Determine rAte

2. Determine rHythm

3. Measure Intervals and Identify abnormalities

• 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• Normal Axis, Left Axis Deviation, Right

Axis Deviation and Indeterminate Axis

5. Hypertrophy• Diagnosis of chamber enlargement

6. Infarct• Assessment of significant QRST changes• Recognition of acute changes on the EKG

(ischemia, injury or infarction)

7. Recognition of significant EKG abnormalities related to:

• Electrolyte disturbances• Pericarditis• Medication effects• Lead misplacement and

Artifact

12 Lead EKG InterpretationRate 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 InterpretationRhythm 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?)


• 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 InterpretationPractice EKG


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 InterpretationRhythm Examples

Atrial Fibrillation

Multifocal Atrial Tachycardia or

Wandering atrial Pacemaker

Rhythm Examples


ATRIAL FLUTTER


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)


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


Idioventricular escape rhythm

Accelerated Idioventricular rhythm

Ventricular Tachycardia

Ventricular Fibrillation


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)


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


Idioventricular escape rhythm

Accelerated Idioventricular rhythm

Ventricular Tachycardia

Ventricular Fibrillation

12 Lead EKG InterpretationAssessment of the PR Interval

• 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

• 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

• 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


• 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 InterpretationAssessment of the QRS Interval

12 Lead EKG InterpretationAssessment of the QRS Interval

• 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 InterpretationDiagnosis 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 InterpretationDiagnosis 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 InterpretationDiagnosis 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 InterpretationSecondary 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 InterpretationExample EKG for Review

12 Lead EKG InterpretationClinical 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 InterpretationExample EKG for Review

12 Lead EKG InterpretationAssessment of the QT Interval

• 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 InterpretationAssessment of the QT Interval

• 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 InterpretationCommon Causes of Prolonged QT

• 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 InterpretationElectrolyte Disturbances—Hyperkalemia

• 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 InterpretationElectrolyte Disturbances—Hypokalemia

• 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 InterpretationElectrolyte 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 InterpretationHypothermia

• 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 InterpretationPericarditis

• 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– 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


Stage I Stage III

12 Lead EKG InterpretationMedication 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 InterpretationMedication 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 InterpretationLead 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 InterpretationLead 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 Jamie Shedden, MSN, ACNP-BC.

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