EKG Extravaganza!
Michele Ritter, M.D.
Argy Resident – Feb. 2007
Normal Conduction of the Heart
SA node Left/Right atrium Atrial Contraction AV node Bundle of His Purkinjie fibers Endocardium Epicardium Ventricular
contraction
Generation of EKG
Generation of EKG
P wave: = depolarization/contraction of both atria
QRS complex: = depolarization/contraction of ventricles
T wave = rapid phase of ventricular repolarization
ST segment = plateau phase of ventricular repolarization
QT interval = ventricular systole
ECG Leads
Limb Leads Bipolar
Lead I – left arm (+) and right arm (-)
Lead II – left leg (+) and right arm (-)
Lead III – left leg (+) and right leg (-)
Unipolar aVR -
right arm potentials aVL – left arm
potentials aVF – left leg
potentials
Precordial Leads V1 V2 V3 V4 V5 V6
Precordial Leads
Reading EKGs
1. Rate
2. Rhythm
3. Axis
4. Hypertrophy
5. Infarction
Rate
Large Box = 0.2 seconds Small Box = 0.04 seconds
Rate
300-150-100-75-60-50 Rule If one box between R-waves, then rate is 300;
If two boxes between, then rate 150, etc. Rate = 1500/(mm between R waves)
What is the rate?
Rhythm
Is the rhythm regular (distance between QRS complexes equal)?
Is there a P-wave before every QRS complex?
Is the PR interval normal? 0.12 sec - 0.20 sec
Is the QRS duration normal? 0.04 sec to 0.12 sec
Irregular Rhythms
Usually caused by multiple, active automaticity sites that causes irregular atrial and ventricular activity
Include: Wandering Pacemaker Multifocal Atrial Tachycardia Atrial Fibrillation
Irregular Rhythms
Wandering Pacemaker Have P’ waves (not true P waves because
pacemaker activity is wandering from SA node to a nearby atrial automaticity foci)
Atrial Rate less than 100 Irregular shape to P waves and irregular
ventricular rhythm.
Irregular Rhythms (cont.)
Multifocal Atrial Tachycardia Think of it as tachycardic wandering pacemaker P’ waves again Atrial rate excees 100 Irregular ventricular rhythm Irregular morphology of P’ waves Occurs in:
COPD Heart Disease
Irregular Rhythm (cont.)
Atrial Fibrillation No P waves (because there are multiple atrial automaticity
foci sending impulses – no single impulse depolarizes atria completely)
Irregular ventricular rhythm Caused by:
Heart disease (CAD, CHF) Thyroid disease Pericardial effusion Alcohol
Tachy-arrhythmias
Rapid rhythms originating in a very irritable foci that paces rapidly.
Includes:
Rate Range
Paroxysmal Tachycardia 150 to 250
Flutter 250 to 350
Fibrillation 350 to 450
Atrial Tachyarhythmias
Supraventricular tachycardia Includes paroxysmal junctional tachycardias
Paroxysmal Atrial Tachycardia and Paroxysmal Junctional Tachycardia
Caused by very irritable automaticity foci that originate above the ventricles.
Narrow QRS complex tachycardia Have P’ waves – often get lost in QRS.
Supraventricular arrhythmias
Atrial Tachyarrhythmias (cont.)
Torsades de Pointes Rate is usually 250 to 350 beats/min. The amplitude of each successive complex gradually
increases and then gradually decreases – “party streamer”
Caused by: Severe hypokalemia Medications that block potassium channels Congenital abnormality (Long QT syndrome)
Atrial Tacchyarrhythmia
Atrial Fibrillation Rapid Ventricular Response = increased heart
rate, putting patient at risk for hypotension.
Atrial Tachyarrhythmias (cont.)
Atrial Flutter Extremely irritable atrial focus produces a
rapid series of atrial depolarizations (250-350 beats/min.)
Ventricular tacchyarrythmias (cont.)
Paroxysmal Ventricular Tachycardia Is like a run of PVC’s Irritable (hypoxic) ventricular focus results in
rapid rate that is too fast for heart to function effectively.
WIDE QRS COMPLEX tachycardia
Ventricular Tacchyarhythmia (cont.)
Ventricular Fibrillation Caused by rapid-rate discharges from many irritable,
parasystolic entricular automaticity foci. An erratic, rapid twitching of the ventricles, with
ventricular rate reaching 350 to 450 beats/min. Tracing is totally erratic, without identifiable waves.
Tacchyarrhythmia Wolff-Parkinson-White syndrome
A ventricular “pre-excitation” arrhythmia An abnormal, accessory AV conduction pathway, the bundle
of Kent, can “short circuit” the usual delay of ventricular conduction in the AV node.
Results in Shortened PR interval (< 0.12 sec) Widened QRS (> 0.12 sec) Delta waves
Can result in several tachyarrhythmias including supraventricular tachycardia, atrial flutter, atrial fibrillation
Blocks
Sinus Block AV Block Bundle Branch Block
Sinus Block
SA node fails to pace for at least complete cycle. Occurs in:
Sick Sinus Syndrome (SSS) SA node dysfunction resulting recurrent episodes of
sinus block or sinus arrest Frequently occurs in elderly patients with heart
disease. Bradycardia-Tachycardia Syndrome
Patients with SSS who develop episodes of supraventricular tachycardia mingled with sinus bradycradia.
AV Block
1° (first degree) AV Block Prolongs AV node conduction Prolonged PR interval (>0.2 sec – one big
box) The PR interval is consistently prolonged the
same amount in every cycle P-QRS-T sequence is normal in every cycle.
AV Block (cont.)
2° (second degree) AV Block Wenckebach (Mobitz Type I)
Gradually prolongs the PR interval , until the final P wave fails to produce a QRS response.
This cycle then repeats itself. Usually non-pathologic
Mobitz (Mobitz Type II) Totally blocks a number of paced atrial depolarizations (P
waves) before conduction to the ventricles is successful. Can be:
2:1 – two P waves to every QRS 3:1 – three P waves to every QRS
Usually permanent, and can progress to complete heart block
2° AV Block – “Wenckebach”
2° AV Block - Mobitz
2:1
3:1
AV Block - 2° AV block (cont.)
If see 2:1 AV block and uncertain if Wenckebach or Mobitz… Do vagal maneuver If Wenckebach, there is an increase the
number of cycles/series (increasing to 2:3 or 4:3)
If Mobitz (Type II), it becomes a 1:1 AV conduction.
AV Block (cont.)
3° (third degree) AV block: “Complete Heart Block” Complete block of the conduction to the ventricles, so
atrial depolarizations are not conducted to the ventricles.
See a sinus-paced atrial (P wave) rate and a totally independent, focus-pased, slow ventricular (QRS rate) – AV dissociation.
Can have: Junctional Focus
Normal (narrow) QRS Ventricular rate: 40-60/min.
Ventricular Focus PVC-like QRS’s Ventricular rate: 20-40/min.
AV Block (cont.)
3° (third degree) AV Block
Bundle Branch Block
Bundle Branch Blocks
Caused by block of conduction in the right or left bundle branch.
The bundle branch delays depolarization to the ventricles that it supplies.
Left Bundle Branch Block (LBBB) Associated with cardiovascular disease! Incidence increases greatly with age. Think – V5, V6!!
Right Bundle Branch Block (RBBB) Associated with structural heart disease, increased
age, sometimes iatrogenic (cardiac cath.) Think – V1, V2!!
Bundle Branch Block
Left Bundle Branch Block
Widened QRS (> 0.12 sec, or 3 small squares)
Two R waves appear – R and R’ in V5 and V6, and sometimes Lead I, AVL.
Have predominately negative QRS in V1, V2, V3 (reciprocal changes).
Right Bundle Branch Block
Widened QRS (> 0.12 sec or 3 small squares)
R and R’ in V1V1 and V2, often with ST depression and T wave inversion.
Reciprocal changes (big negative S) in V5,V6, I and AVL.
Right Bundle Branch Block
Bundle Branch Block
Final Note: If you have the above changes with R and R’,
but a normal (not widened) QRS, it is referred to as an incomplete bundle branch block.
Axis
The direction of depolarization as it passes through the heart.
A vector towards a lead results in a positive deflection on the ECG, while a deflection away from a lead results in a negative deflection.
If hypertrophy is present, the overall vector (axis) points towards the hypertrophied part.
Axis
Frontal Plane Horizontal Plane
Axis
Normal Axis: QRS vector pointed downard and to the patient’s left, in the 0 to 90° Range.
Right axis Deviation: > 100° Left axis Deviation: < 0°
Axis – the nitty gritty
QRS net positive in Lead I and AVF: normal axis QRS net positive in Lead I and net negative in AVF: Left axis Deviation QRS net negative in Lead I and net positive in AVF: Right axis Deviation
AVF
Axis
Left Axis Deviation: Can occur in:
Left Ventricular Hypertrophy (hypertension!) Inferior myocardial infarction
Right Axis Deviation: Can occur in:
Right ventricular overload (cor pulmonale) Left pneumothorax Lateral myocardial infarction.
Hypertrophy – we’re going to essentials only. Left Ventricular Hypertrophy
Important because it is often a sign of long- standing hypertension!
Calculation: mm of S in V1
+ mm of R in V5 If sum is more than 35 mm, you have LVH!!!
Remember, you usually see Left axis deviation with LVH.
Now the most important….
MYOCARDIAL
INFARCTION !!!!
EKG in Myocardial Infarction
Gives information about: Duration — hyperacute/acute versus
evolving/chronic Extent — transmural versus subendocardial Size — amount of myocardium affected Localization (which area of heart affected)
Difficult to use EKG in certain situations: Left bundle branch block Paced rhythm
EKG in myocardial infarction
Ischemia: T wavesInjury: ST changesNecrosis: Q waves
Myocardial Ischemia
Represented by inverted T waves. Should be symmetrically inverted. Can be marker of OLD infarction Wellens syndrome: Marked T wave inversion in V2
and V3, which alerts to stenosis of the left anterior descending coronary artery (LAD)
Myocardial Injury
Injury = “acute” or “recent” ischemia.
ST changes show that the episode is acute.
Transmural injury ST Elevation
Subendocardial injury ST Depression
ST elevation
ST depression
Myocardial Necrosis Q wave:
Diagnostic for myocardial infarction. Can have MI in its absence (non Q-wave MI) Can be acute or old! (Use ST changes to determine if
acute) Is significant if at least one small square (1 mm or 0.4
seconds in duration) Is usually at least 1/3 of the QRS amplitude
Location of Infarction Posterior
Right Coronary Artery Large R, ST depressions in V1, V2,
V3 Inferior
R or L coronary artery ST changes/Q waves in II, III, AVF May have reciprocal ST depressions
in I and AVL Lateral
Circumflex artery ST changes/Q waves in I and AVL,
V5, V6 May have reciprocal ST depressions
in II, III, AVF. Anterior
Left Anterior Descending artery ST changes/Q wave in V1, V2, V3,
V4
Where’s the MI?
Where’s the MI?
Where’s the MI?
Final one…
EKG - Conclusion
1. Rate
2. Rhythm1. Regular, irregular, irregularly irregular?
2. P waves? PR interval? QRS duration?
3. Axis
4. Hypertrophy
5. Ischemic Changes 1. T wave changes?
2. ST changes?
3. Q waves
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