Post on 07-Mar-2016
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Lead I + lead III = Lead II (Einthovens Law)
Lead I - LA RA
Lead II - LL RA
Lead III - LL LA
Kirchoffs Law The sum of the potentials of AVR + AVL + AVF = 0
NORMAL
P wave
Amplitude normally 0.5 to 2.5 mm (2.5 squares) (in limb
leads)
Duration not over 110 msec (3 squares) (in limb leads) In sinus rhythms, P wave is upright in Lead II and inverted in
aVR. If not, SA node is not pacemaker
Normal axis (frontal plane) is 0 to +90 , usually +30 to +60
Left axis 0 to -30
Right axis beyond +75
PR interval
Normal value in adults is 0.12 sec to 0.20 sec (ventricular preexcitation < 3-5 squares < 1st degree AV
block)
QRS
60-100ish ms (1.5-2.5 squares)
ST segment
Usually isoelectric, but may normally deviate between 0.5 and +1.0 mm from baseline in standard and
unipolar extremity leads
Upward displacement of 2 or 3 mm may be normal particularly in right precordial leads
T wave - 10% of amplitude of QRS is normal.
U wave
Polarity usually same as T wave
Most prominent in lead V3
Maximum amplitude should not exceed 1 mm
Alterations in automaticity of the SA node
Sinus tachycardia - sinus rhythm > 100 beats/min
Sinus bradycardia - sinus rhythm < 60 beats/min
Sinus arrhythmia - increased sinus rate with inspiration.
withdrawal of parasympathetic tone during inspiration
Sinus arrest - pause. SA node fails to fire.
can be caused by increased parasympathetics, hypersensitive carotid sinus, damage to SA node, digitalis
Irregular Rhythms
Wandering Pacemaker - pacemaker activity wanders from SA node to nearby atrial automaticity foci
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P shape varies
Atrial rate 100 then becomes multifocal atrial tachycardia) Irregular ventricular rhythm
Multifocal Atrial Tachycardia - Chaotic Atrial Rhythm
P wave shape varies (Three or more ectopic P-waves with different configurations/morphologies because P
waves come from different areas in the atrium.)
Isoelectric line between P-P intervals
Frequent occurrence of varying PR intervals
Atrial rate >100 (100-250 bpm)
Irregular ventricular rhythm
Seen in COPD
Atrial Fibrillation
Irregular rhythm and irregular ventricular rhythm
Chaotic atrial spikes
Escape beat - an automaticity focus transiently escapes overdrive suppression to emit one beat (A beat originating from a site
other than the SA node). Long pause followed by escape beat (versus premature beat where there is no pause before)
Escape Rhythm - an automaticity focus escapes overdrive suppression to pace at its inherent rate (another normal pacemaker
takes over) a sequence of similar ectopic beats (many ectopic beats). When SA node pacemaker activity is impaired
Atrial escape rhythm 60-80/min
P waves are not identical to previous P waves which are from the SA node. (The same is for the escape
beat)
Junctional escape rhythm40-60/min
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Conducts mainly to ventricles series of lone QRS complexes.
Retrograde atrial depolarization leads to an inverted P
can be immediately before the QRS
can be buried in the QRS
can be after the QRS
Ventricular escape rhythm20-40/min
large ventricular complexes can be so slow that it causes Stokes-Adams Syndrome where not enough blood reaches the brain.
Premature Beatsirritable focus spontaneously fires a single stimulus
Premature atrial beatearly P wave which can be hidden in the T wave with normal QRS following.
P can depolarize the ventricles leading to a wide QRS in the PAC beat only.
If not conducted, lone P wave with no QRS following.
Irritated by (same for premature junctional beat) - epi, increased SNS stimulation, caffeine, amphetamines,
cocaine, other beta1 stimulants, excess digitalis, toxins, etoh (sometimes), hyperthyroid, stretch
Premature junctional beatpremature irritable stimulation from AV junction which depolarizes the ventricles and
sometimes in a retrograde fashion, will depolarize the atria.
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P wave can be before, during or after the QRS.
Upper AV Junctional Rhythm
AV node not pacemaker. Retrograde/inverted P waves precede the QRS complexes by short P-R intervals (start pacemake
near AV node travels faster because shorter distance) in leads II, III, and aVF
Middle AV Junctional Rhythm
P waves cannot be identified since they are buried in the QRS complexes. Atrial fibrillation is ruled
out since the base line shows no oscillations.
Lower AV Junctional Rhythm
Retrograde P waves follow QRS complexes. They are best seen in leads II, III, and aVF
Atria depolarized AFTER the ventricles depolarize.
Premature ventricular beatirritate the ventricles
Wide and tall QRS with opposite polarity of the normal QRS Only depolarizes the ventricles, not the SA node.
Irritated by - airway obstruction, hypoxia, reduced CO, low potassium, mitral valve prolapse, stretch,
myocarditis
Ventricular Parastolefrom an entrance block but not irritable PVCs coupled to long series of normal cycles
Multifocal PVCseach focus is own unique identifiable PVC
R on TPVC falls on a T wave/falls on a vulnerable period and starts shit
from hypoxia and low serum potassium.
Tachyarrhythmiasrapid ventricular rhythms originating in a very irritable automaticity foci
Paroxysmal (sudden) tachycardia150-250 (sinus tachycardia is not sudden like paroxysmal)
Paroxysmal Atrial Tachycardia (PAT)
rapid rate, spike P waves
2:1 ratio P:QRS
(suspect digitalis excess or toxicity - digitalis can inhibit the AV node)
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PAT with AV block more than one P wave for every QRS response
Paroxysmal Junctional Tachycardia (PJT)- sudden rapid pacing of a very irritable automaticity foci in the
AV junction
inverted P before, during, or after the QRS - can depolarize the atria in a retrograde fashion from
below
Wide QRS from depolarizing left before right
Junctional Tachycardia AV nodal reentry tachycardia
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continuous reentry circuit rapidly paces the atria and ventricles. Each pacing stimulus records in
an origin near the coronary sinus.
Supraventricular tachycardia irritable automaticity foci that produce both paroxysmal atrial and
junctional tachycardia (above the ventricles)
Paroxysmal Ventricular Tachycardia resembles a series of PVCs
SA node still paces atria independent pacing of the atria and ventricles (AV dissociation)
Indicates coronary insufficiency leading to poor O2 to the heart.
Distinguishing wide QRS insufficiency complex SVT from VTach.
SVT VTach
Pt with coronary disease or infarction uncommon very common
QRS width (duration) 0.14s
AV dissociation showing captures orfusions
rare yes
Axis - extreme RAD rare yes
Torsades de Pointes (250-350)
caused by low potassium, meds that block the K+ channels, congenital abnormalities,
long/lengthened QT segment.
Possibly from two irritable foci in different ventricular areas.
Flutter250-350
Atrial flutter- saw-tooth shape
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Originates in the atrial automaticity focus
Ventricular Flutter
single ventricular automaticity focus
Sine waves of similar amplitude
Tends to go to VFib.
Fibrillation350-450 (multiple foci discharge rapidly)
atrial fibrillation
many irritable parasystolic atrial foci
causes many irregular spokes on the EKG
No identifiable P or P waves with irregular QRS response.
Ventricular Fibrillation
Many irritable parasystolic ventricular automaticity foci pacing rapidly (entrance block)
Wolff-Parkinson-White Syndrome
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Delta wave = area of preexcitation
Can have paroxysmal tachycardia
rapid conduction - SVT (atrial flutter and afib) can be rapidly conducted through the
accessory pathway
some bundles have automaticity foci that can initial paroxysmal tachycardia
Re-entry - ventricular depolarization may immediately re-stimulate the atria in a
retrograde fashion via the accessory pathway causing a theoretical circus reentry loop
Lown-Ganong-Levine Syndrome (LGL)
AV node is bypassed by an extension of the anterior internodal tract (James Bundle) which
conducts atrial depolarizations directly to the Bundle of His without delay
No significant PR interval delay
P waves are adjacent to the QRSs on EKG.
Sinus Block
SA node may temporarily fail to pace for at least one cycle then resumes pacing
The pause can induce an escape beat from an automaticity foci
Sick Sinus Syndrome
seen in the elderly with heart disease
Marked sinus bradycardia without normal escape mechanisms or atrial and junctional foci
can develop bradycardia-tachycardia syndromeintermittent episodes of SVT (a flutter or afib)
AV Block
First Degree AV block
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lengthened PR interval > 0.2 s (1 large square) No wide QRS
Second degree AV block
Wenckebach lengthening of PR interval until QRS is dropped.
Mobitz 2 1 normal cycle preceded by a series of paced P waves that fail to conduct through the
AV node
Third degree AV block
block of the conduction of atrial stimuli to ventricles. Atria and ventricles pace at different rates.
Bundle Branch Block/Intraventricular Conduction Delay
block of one bundle branch which produces a delay of depolarization of the ventricle it supplies.
Wide QRS with rabbit ears (>0.12s) (3 squares or more in any lead) -- RSR
RBBB- rabbit ears in V1, V2
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Deep and round S-waves in I, aVL and V4-6
Secondary S-T, T-wave change in V1-3
abnormal depolarization and repolarization
Complete RBBB with RVH > 15 mm. Can Dx only with RBBB.
LBBB - rabbit ears in V5, V6
Absence of septal q-waves in V4-6 (small q from septal activation not seen)
RSR or M pattern of QRS in I, aVL and V4-6
Secondary S-T, T-wave change in I, aVL and V4-6
Septal activation in opposite direction (R L)
If RSR of normal QRS duration incomplete BBB
Intermittent mobitz - occasional dropped QRS due to permanent BBB with intermittent BBB of other side.
Hemiblock
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Anterior Hemiblock
LADusually associated with an MI (or other heart dz)
Normal or slightly widened QRS (0.10-0.12s)
Q1S3Q in I or wise/deep S in III)
Left Anterior block
Mean and terminal QRS vectors are directed to the left of -30 in frontal plane
Initial 0.02-second QRS vector
Directed right and inferiorly and produces a small 0.02-second Q-wave in Lead I and
AVL Small 0.02-second R-wave in Leads II, III and AVF
Other causes of abnormal left axis deviation are ruled out i.e., inferior wall myocardial infarction
Anterior hemiblock with RBBB
RBBB - mean QRS vector is within normal range or shows minimal RAD
RBBB + LAD = anterior hemiblock
Posterior hemiblock
RAD (usually associated with an MI)
normal or slightly widened QRS
S1Q3 - Wide S in I and Q in III
Posterior block
This condition is very difficult to diagnose - right ventricular enlargement and lateral infarctions
Mean and terminal QRS vectors in frontal plane show right axis deviation
Initial 0.02-second QRS vector
Directed slightly leftward and superiorly and produces a small 0.02-second R-wave in
Lead I and AVL (r/o anterolateral infarction)
Small 0.02-second Q-wave in Leads II, III and AVF
Bifascicular block
RBBB + anterior hemiblock
RBBB + posterior hemiblock
Intermittent block
continuous EKG pattern with intermittent wide QRS characteristic of intermittent BBB or with intermittent
changes of QRS axis.
Incomplete Trifascicular Block
First-degree A-V block plus a right bundle branch block plus either a left anterior hemiblock or posterior
hemiblock
Axis- direction of depolarization as it passes through the heart origin of mean QRS vector is the AV node = tail of the
vector. 0-90 is normal
Mean QRS vector will point toward hypertrophy and away
from infarct
V1, V2 = rightward rotation
V5, V6 = leftward rotation
Hypertrophy
Diphasic wave = atrial enlargement
Right atrial enlargement - initial large deflection in V1. Tall
P wave
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if height > 2.5mm in II and >0.12s, suspect right atrial enlargement
pointed P wave greater than 2.5 mm, which is best seen in leads perpendicular to the heart bottom wall (II,
III, aVF) and chest leads V1 and V2
Left atrial enlargement- large terminal deflection in V1. Long P wave
P wave is a prolonged and biphasic (bifid). It is best seen in leads I, II and aVL and sometimes possibly in
leads V5 and V6. (http://www.health-tutor.com/p-mitrale-ecg.html)
Right ventricular hypertrophy
http://www.google.com/url?q=http%3A%2F%2Fwww.health-tutor.com%2Fp-mitrale-ecg.html&sa=D&sntz=1&usg=AFQjCNE-yV6j2gKLbnTH6EbcBDGK-onpXQ7/21/2019 Cardio Ekg
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Large R wave in V1, S wave is much smaller
The large R wave in V1 progressively becomes smaller in V2, V3, V4
RVH causes RAD + rightward shift.
Left ventricular hypertrophy
QRS complexes are exaggerated in amplitude eps. in chest leads.
Very tall R waves in V5
Height/depth of S in V1 + height of R in V5 > 35 mmLVH.
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Can see an asymmetrical inverted T wave (ideal leads V5/V6)
ventricular strain
V1 provides the most information regarding hypertrophy -- diphasic waves, R wave in V1, S wave in V1, R
wave in V5
Accompanied by
left atrial abnormality
>0.11s
Left axis deviation 0-30
ST segment T wave changes left ventricular strain pattern (systolic overload)
Extremity leads
Amplitude of R-wave in Lead I and/or AVL > 15 mm Amplitude of R-wave in AVF > 21 mm
Sum of R-wave in Lead I plus S-wave in
Lead III > 25 mm
Precordial leads
SV1 + RV5 or SV1 + RV6 > 35 mm
R-wave in V5 or V6 > 26 mm
R-wave in V6 taller than R-wave in Lead V5
Infarction
Ischemia - reduced blood supply
characterized by symmetric inverted T waves
Leads V2-V6 is pathological
Marked T wave inversion in leads V2, V3 is Wellens SyndromeStenosis of anterior descending
artery.
Injury - acute or recent
if no Q waves, can be non-Q wave infarction
ST elevation is infarct. Depression in reciprocal changes.
Pericarditis
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ST segment is elevated (diffuse) and usually flat or concave (middle sags down).
Entire T wave may be elevated off baseline
Subendocardial infarction
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Necrosis - dead tissue
Q wave indicates necrosis can Dx infarction
Insignificant Q waves < 0.04s (1mm)
Significant Q waves > 0.04s (or QRS amplitude - old criterion)
Anterior Infarct
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elevated ST segments and Q waves in V1, V2, V3, V4anterior descending of left coronary
artery
Posterior Infarct
Mirror image of anterior infarct
ST depression in V1, V2
Large R waves, maybe Q in V6
Lateral infarct
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I, AVL Q waves
Circumflex left coronary artery
Inferior Infarct
II, III, AVF Q waves
right/left coronary artery Cannot Dx infarction with LBBB
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hyperkalemia
wide, flat P
peaked T
wide QRS
Hypokalemia
T/U wave fusion. Flat T wave
Prominent U wave
Hypercalcemia
short QT interval
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Hypocalcemia
prolonged QT interval
Digitalis
positive inotrope - Improve contractility of the failing heart (mechanical effect)
Prolong the refractory period of the AV node in patients with supraventricular arrhythmias (electrical effect)
inhibits the cell membrane sodium-potassium ATPase pump
Therapeutic use for treating Atrial fibrillation
Salvador Dalis mustache
Toxicity - Sinus bradycardia, AV block, VTach secondary to ectopic beats
Quinidine
Class IA antiarrhythmic (blocks Na and K channels)
retards and repolarizes
Long QT interval can lead to Torsades
Wide, notched P
Wide QRS
depression ST
U wave