ECG Flashcards
Limb lead reversal
negative p-wave, qrs and twave in lead 1
Low voltage
def
<5mm Limb leads
<10mm in ALL precordial leads
Hypocalcemia
prolonged QT
because of lengthened flat ST segment without change in duration or morphology of T wave
Prolonged QT
> 1/2 RR interval
not reliable with tachycardia (>100bpm)
Aflutter with pause
can see aflutter which spontaneously breaks -> sinus pause and suddenly a junctiona escape beat followed by sinus node recover (ie sinus bradycardia etc) - sinus node dysfunction has prolonged sinus node recovery time
Digitalis toxicity
Regularized afib
aflutter with 3rd deg AVB and junctional tachycardia
prominent U-waves
Junctional rhythm
40-60bpm
Jnc Tach
> 60bpm
more likely to occur with inferior MI
Normally conducted beat after paced beat
can have twave inversion and not sensitive for ischemia so do not code ischemia changes
Failure to sense
look for premature v-pace beat (
T wave memory
T wave changes looking like ischemia persist for several days after patietn returns to normal AV conduction and v activation after prolonged 100% pacing time (or after WPW with pathway ablation now conducting through normal AV conduction system
RVH with pulm HTN/PE
Tall R wave V1
Acute PE
S wave in I (RAD from LPFB)
Q wave III
inverted T in III
Accessory pathway localization
Step 1: QRS Transition
-R/S transition before V1 (Tall R wave V1)/RBBB pattern = left sided pathway
-later than V2 (>V2) S wave in V1, LBBB = right sided pathway
-Transition V1-V2=septal
Step 2: Delta wave polarity
-positive in 2/3 leads = anterior
-negative in 2/3 lead= posterior/inferior
Brugada pattern
h/o syncope
Type I pattern (dx of brugada): J-point elevation >2mm with COVED donwloping ST segments
Type 2: J-point nelevation >2mm and saddleback shaped ST segment elevation >1mm
SCN5A
a/w threating VT arrythmias and SCD
Resemble RBBB but lacks QRS morphology c/w RBBB in other leads ie wide slurred S waves in I and V6
Electrical alternans in patient with cancer
code electrical alternans
pericardial effusion,
SR
LPFB
RAD
small r wave in I, aVL
small q in lead III
RBBB
QRS>120ms
rsR’ complex V1
wide slurred S waves I, V6
RBBB
QRS>120ms
rsR’ complex V1
wide slurred S waves I, V6
T wave inversion opposite to terminal deflection of QRS in V1, V2 - not case with V3-6 - suggests ischemia
does not interfere with ECG dx LVH or Q wave MI
LBBB
QRS >120ms
V1 - rS (tiny R, big S - wide) with ST elev and discordant twave ie upright while S is down)
or deep QS (no r)
R waves in lateral leads (I, V5,6) M shaped, notched, monophasic or RS)
Dextrocardia vs limb lead reversal
Limb lead reversal - normal R-wave progression
Dextrocardia - REVERSE R wave pgoression (starts out big)
DO NOT CODE AXIS
Dextrocardia vs limb lead reversal
Limb lead reversal - normal R-wave progression
DO NOT CODE AXIS - technical error with lead placement
Dextrocardia - REVERSE R wave pgoression (starts out big gets smaller)
DO CODE RAD…neg qrs I, postiive in aVF
R&L Arm lead reversal
transposition of leads II, III
Transposition of leads avR and avL
Precordial lead reversal
Unexplained decrease in R wave voltage in 2 consecutuive leads (ie V1, V2) with return to normal progression in following leads (V3-6)
Mobitz I - wenkebach
PR interval immediatly before non-conducted P-wave is longer than PR interval immediately following non-conducted P-wave
at level of AV node - narrow QRS
Group beating -> RR interval constant, PR interval prolongs till drops a QRS then resets…
Mobitz II
PR intervals constant with random drops of conduction
below level of node - wide QRS
LOOK FOR GROUPED BEATING…
Posterior wall MI
horizontal or downsloping ST segemnt depression with upright T waves in V1-3 with or without prominent R wave in these same leads (with or without equivalent of Q waves for posterior wall)
Digoxin toxicity
DO NOT CODE without
sagging ST depression with upward concavity -> digitalis effect
Junctional rhythm/tach
regular R-R interval no p-waves, NARROW complex
more likely with inferior MI
Prolonged QTc
> 470ms male
480ms female
Normal QT <1/2 preceeding R-R for HR 60-100 -
When measuring use lead with longest QT
WPW
if v-rate >200, QRS >120ms
Posterior MI
can’t be coded with RBBB
LAD
can’t be coded with Q wave MI (inferior?)
SVT
r’ at end of QRS complex = retrograde atrial depolarization -> best seen in V1
Acute cor pulmonale
needs sinus tach/afib - ie change in rhythm AND
right ventricular strain ie T wave inversions V1-3, ST dep
RAE
Upright 2 wave >2mm in leads II, III and aVF or >1.5mm V1,V2, RAD
LAE
notched p-wave duration >120ms
Terminal portion of p-wave in V1 >1mm deep >0.04s (1 box) duration
LAD
positive in I, neg in aVF
RAD
negative I, positive in aVF
RVH
RAD Dom R wave V1 >7mm R V1 +S V5/6 >10.5 rSR' V1 R'>10mm Secondary downsloping ST dep and T wave inversion in RIGHT precordial leads right atrial abnormality (RAE) R/S ratio in V1 or V3r >1 or R/S in v5/6 <1
Lateral MI
I, aVL
Anterior/anteroseptal
V1, V2 AND V3
ST changes of ischemia/injury
DO NOT CODE if other Q wave MI coded
LAFB
LAD qR I, avL rS in II, III, aVF QRS 80-110 ms aVL R wave >45ms avL R wave can be >11mm but no LV strain pattern so no LVH
VPC
look for compensatory pause after
QRS initial direction DIFF from QRS during SR
Sinus arrhythmia
PP intervals vary by >0.16 sec (4 small boxes)
LVH
S V1 + R V5 >35 R wave aVL+ S wave V3 >28 M >20 F S wave V1 or V2 > 30 R wave in V5 or V6>30 Max R wave + Swave in precordial leads >45
Prominent U wave
check II, V5 >1.5mm HYPOKALEMIA LVH CAD Drugs
WPW with afib
do not coce LVH, Q wave MI, ST-T chages, axis shift or IVCD
irregularity with delta wave
Afib
atrial activity seen in right precordial/inferior leads
WPW
think WPW if v rate >200/min and QRS > 120ms
initial slurring QRS
QRS>120ms
DO NOT CODE LVH/RVH
myocardial ischemia/infrction (if need to code non-specific ST changes)
PR<120
QRS >120
secondary ST chagnes opp direction of QRS
THINK WPW if afib/flutter is a/w QRS that is variabl ein width and rate >200
Dextrocardia
neg P-QRS-T in I, avL, positive P-QRS-T in avR
BUT
Reverse precordial R wave progression -> gets smaller
CODE RAD
Torsades
Find prolonged QT
Find QRS superimposed on T started NSVT (R on T)
V-rate 150-300 (200-280)
sinisoidal cycle of changing amplitude and polarity (twisting)
QRS morphology varies beat to beat
Ashman’s Phenomenon
Single wide QRS beat with RBBB morphology occuring in afib after short RR preceeded by long RR -> beat encountered a bundle that wasn't repolarized (refractory) so Wide QRS Afib Aberrant conduction (Ashman's) Aberrant conduction usually RBBB since RBB has longer refractory period than LBB
Hyperkalemia
narrow based tall peaked T wave QT shortening >6.5 1st deg AVB flat wide P wave, pwave dissappearance ST dep >7.5 - no p waves, LBBB/RBBB IVCD -> sinisoid (sinoventricular conduction) VT/VF/IV rhythm, asystole
Anterior or anteroseptal
V1-3
Anterolat
V4-6
Lateral
high lateral - I, aVL
ST/T changes c/w myocardial ischemia
ST dep WITHOUT Q waves
Anterior or anteroseptal
V1-3
Q in V1 makes it anteroseptal
Q wave MI acute or recent
Q waves and ST elev or depression
Lateral
high lateral - I, aVL
Q wave in JUST aVL does NOT qualify as lateral MI
When coding acute Q wave MI or ST-t of Injury
DO NOT CODE ST/T wave of ischemia (don’t code for ST depressions if concurrent ST elev alone or ST elev and Q waves
When coding acute Q wave MI or ST-t of Injury
DO NOT CODE ST/T wave of ischemia (don’t code for ST depressions if concurrent ST elev alone or ST elev and Q waves
Acute cor pulmonale
NEED RV strain to code this!
RAD - down in I, up in aVF
RAE - P wave in III >2.5mm
RVH - tall dominant R wave in V1 (R>S, R wave >7mm), R wave in V1 + S wave in V5 or 6 >10.5
rSR’ in V1 with R’>10mm
Secondary downloping ST depression and twave inversion in right precordia leads
RAE
ST/T changes of RVH -
RV Strain ST seg depression V1-3,
borderline LAE
S1Q3T3 (deep prom Swave in I, W wave in III, Twave inversion or lfat in III
Acute cor pulmonale
NEED RV strain to code this!
RAD - down in I, up in aVF
RAE - P wave in III >2.5mm
RVH - tall dominant R wave in V1 (R>S, R wave >7mm), R wave in V1 + S wave in V5 or 6 >10.5
rSR’ in V1 with R’>10mm
Secondary downloping ST depression and twave inversion in right precordia leads
RAE
ST/T changes of RVH -
RV Strain ST seg depression V1-3,
borderline LAE
S1Q3T3 (deep prom Swave in I, W wave in III, Twave inversion or lfat in III
Sinus tach, afib, aflutter, atach and first deg AVB
PE vs IWMI
PE doesn’t have Q wave in II (just in III)
Juvenile T waves
Younger women (healthy) <20yo
right precordial leads (V1-3)
relatively shallow
Juvenile T waves
Younger women (healthy) <20yo
right precordial leads (V1-3)
relatively shallow
Failure to sense
pacemaker spike FOLLOWING QRS complexes (or on Twaves that are premature relaive to V-V interval (ie interval between first and 2nd PPM spike)
Failure to capture
pacemaker spike not followed by QRS complex
Ventricular escape rhythm
QRS>120ms
DO NOT CODE RBBB - RBBB pattern is due to abnormal ventricular activation from ventricular escape rhythm not ture BBB due to IV conduction abnormality
20-50bpm
QRS similar to VPCs
CHB
SR and ventricular escape independent of one another (Sinus rate > V-escape rate)
PR interval varies
PP and RR intervals are CONSTANT
Atrial rate > ventricular rate
CHB
SR and ventricular escape independent of one another (Sinus rate > V-escape rate)
PR interval varies
PP and RR intervals are CONSTANT
Atrial rate > ventricular rate
DO NOT ALSO CODE AV DISSOCIATION if CHB coded
CHeck for 2:1 AVB…
CHB with AWMI
block due to extensive damage to LV - usually preceeded by mobitz II or bifascibular block - high mortality
Dig toxicity
reversible CHB - usually associated with acceleratd JNC rhythm
RBBB
QRS>120ms rsR' V1 wide slurred S waves in I, V6 DO NOT CODE RAD with RBBB DO NOT CODE RVH with RBBB
LPFB
RAD (down in I, up in avF)
small r in I, aVL
q in III
DO NOT CODE RAD with LPFB
LPFB
RAD (down in I, up in avF)
small r in I, aVL
q in III
DO NOT CODE RAD with LPFB
LBBB
QRS>120
QS V1 (spear down)
broad monophasic R in I, V5, V6 (spear up)
rS or QS in right precordial leads
DO NOT CODE LAD with LBBB
interferes with dx of LVH/RVH, myocardial sichemia, Q wave MI
Mean QRS duration greater than or equal to 120 ms in adults,greater than 100 ms in children 4 to 16 years of age, andgreater than 90 ms in children less than 4 years of age
Late forces of QRS complex should be negative (i.e terminal S wave) in V1
Broad notched or slurred R wave in leads I, aVL, V5, and V6 and an occasional RS pattern in V5 and V6 attributed to displaced transition of QRS complex
Absent q waves in leads I, V5, and V6, but in the lead aVL,a narrow q wave may be present in the absence of myocardial pathology
Delayed onset of intrinsicoid deflection (> 60 ms from beginning of QRS complex to peak of R wave) in leads V5 and V6 but normal in leads V1, V2, and V3, when small initial r waves can be discerned in these leads.
Aflutter
Saw tooth flutter waves best seen in II
artifact from tremor can look like flutter waves
Scarbossa
ST elev >1mm in leads where QRS vector positive
>1mm ST dep in V1-3
>5mm elevation in leads where QRS vector negative
Aflutter 1:1 conduction
conducts aberrantly - wide QRS can resemble VT
VT
starts with VPC, gradually slowing of rate then termination
SVT with LBBB aberrancy
starts wtih APC with long PR and narrow QRS
Aritfact
ususally due to tremor
Parkinson’s tremmor simulates atrial flutter rate of 4-6/s
Skeletal muscle/physiolligc tremor 7-9/s
Rapid arm moviement (bushing teeth/hair - looks like VT
RBBB
WRS >120
rsR’ V1
wide slurred S waves I, V6
LAFB (total opposite of LPFB)
LAD (up in I, down in aVF)
Small q waves in I, aVL
Small r in III
Mobitz I
PP interval constant, PR interval increases until a beat drops (and doesn’t conduct one QRS)
LOOK FOR GROUPED BEATING
Mobitz II
PP interval constant, PR interval constant
LOOK FOR GROUPED BEATING - string of conducted QRS after constant P-P intervals then all of a sudden one QRS drops out (though P’s keep going)
Group beating
Mobitz I
Mobitz II
frequent blocked APCs
J-wave/osborn wave
left precordial leads
HYPOTHERMIA
extra postive deflection in terminal end of QRS
don’t code IVCD or LAE
Biventricular hypertrophy
LVH S V1 + R V6>35
RVH R V1 + S in V5 or 6
Equiphasic large amplitude R & S waves in id precordial leads
R>Q wave in aVR and S wave >R wave in V5 and T wave insersion in V1
VF
rapid chaotic irregular deflections of VARYING AMPLITUDE without distinct P waves, QRS complexes or T waves
SHOCK
Course VF - large amplitude fibillatory waves
Fine VF - small amplitude fibrillary waves
Mobitz I vs II
compare PR interval immediately before and after blocked p wave - if there is a difference it is mobitz I - if same it is mobitz II
LAFB
LAD qR I, avL rS in II, III, aVF QRS 80-110 ms aVL R wave >45ms avL R wave can be >11mm but no LV strain pattern so no LVH
LPFB
RAD (down in I, up in avF)
small r in I, aVL
small q in III
DO NOT CODE RAD with LPFB
Atrial tachycardia
atrial rate >100
P waves that may precede, be buried wthin or follow QRS complex
P-wave morphology that is NON-sinus
(ie not upright in I&II, inverted in aVR)
CNS bleed/event
Deep T wave inversions (or upright) across precordial leads
AND QT prolongation
AND VPCs
Posterior MI
Dominent R wave with ST depression and twave inversion in V2/V3
DO NOT CODE RBBB in setting of posterior wall MI
APC/tachycardia
Look for dominant p-waves - that is sinus rate - other morphologies are APCs
Only code RAE if on dominant p-waves ->APCs can show RAE but this is not reliable
incomplete RBBB
rsR’ V1 with QRS 100ms…not >120
Lateral
I, aVL
Anterior/anteroseptal
V3-5
Anterolateral
V4-5
Failure to capture
DOESN’t COUNT if tries to pace on Twave in refractory period -> this is failure to sense ONLY not failure of pacing…
ST/T myocardial ischemia
If see extensive ST depression and see a q-wave somewhere -> likely on one Q and then do not code MI -> just code ST/T myocardial ischemia ONLY
VT
Concordance of QRS (all QRS deflections positive)
AV dissociation (ventric rate > atrial rate)
capture beats
fusion beats
Aflutter
SVT that is regular with rate of 150 is aflutter with 2:1 AV block
Flutter 1:1 conduction
conducts aberrantly - wide QRS complexes looking like VT
Biventricular pacing
Diff than LBBB pacing seen with RV lead pacing
Q waves I, aVL
+R waves in V1-3
Torasades
200-280bpm
DO NOT CODE if myocardial injury suspected (this is polymorphic VT not TdP)
QT interveal prolonged…
Posterior MI (old)
In context of inferior or lateral MI
with dominant R wave in V1-3 (R wave > S wave) consider posterior infarct old…
SVT
regular rhythm Rate >100 QRS narrow P waves SOMETIMES seen If rate >150 consider aflutter with 2:1 block
Hypercalcemia
Short QT secondary to short ST segment
Early repolarization
Normal variant
Borderline normal/normal variant ECG
subtle notching of J-topoint (II, III, aVF, V2-6
tall upright twaves concave upward ST elev
no PR depression - sepearates from pericarditis
HCM
LVH voltage
deeply inverted T waves in precordial leads
=apical HCM
AV dissociation
similar sinus and ventricular rates with a slightly varying relationship between p wave and paced QRS complexes
Do not confuse with DDD where has a fixed AV interval (ie tracks atrial beats and if doesn’t conduct paces V)
VVI vs DDD
VVI - varying AV interval
DDD - fixed AV interval
VVI demand vs VOO asynchronous
VVI demand is INHIBITED by native ventricular beat
Asynchronous V-pace (VOO) does not sense any ventricular beats - just paces V at set rate…
Dx of VVI demand requires evidence of appropriate inhibition of PPM output in response to a native QRS
acute RV infarct
ST elev in V1-3 in setting of acute inferior MI -> think RV infarction…
Digitalis toxicity
Sinus pause/arrest
sagging salvidore ST seg depression
prominent U-wave
AV junctional rhythm or afib with CHB, pAF with block, SVT or VT with alternating BBB
Sinus pause vs sinoatrial exit block
Resumption of sinus rhythm at PP interva that IS multiple of basic sinus PP interval = sinus pause
Sinus rhythm resumption at multiple of basic PP interval -> sinoatrial exit block
Prominent U wave
presense of preceding isoelectric baseline
QT interval
II, V5 best
RVH
Tall dominant R waves in V1 (R>S R>7mm)
S/T wave changes c/w hypertrophy V1-3 -> elsewhere would be ischemia/injury
CAN CODE RAD
Don’t code Q wave MI - changes associated with thickening of septum from RVH NOT MI
Sinus arrythmia
diff in PP intervals >0.16s (almost one big box)
Do not also code SR
AIVR
regular ventricular rhythm similar to VPCs that occurs when ectopic ventricular pppm fires at 55-110 and exceeds sinus rate -> AV dissociation
Tdp
R on T triggers rapid polymorphic tachycardia
twistin garound isoelectric baseline
prolonged QT (ventricle more suseptible to malignant ventr arrhythmias such as Tdp kicked off by critcally timed VPC on T wave
DO NOT CODE VT with TdP (implied)
Heart block
Check for group beating -> check for constant PR interval -->if variable -> mobitz I -->if constant-> mobitz II CONSIDER blocked APCs
If no blocked APCs then consider 3rd deg AVB with ventricular or junctional escape…PR interval varies…
LVH
Cornell criteria R aVL S V3 >28
prominent U-wave common
ST changes a/w hypertrophy
LAFB vs LPFB
LAFB - small q I,aVL, small r III + LAD
LPFB - small r in I,aVL, small q in III + RAD (do not code LPFB if other causes of RAD ie ASD)
Non conducted APCs
Check for deformed Twave in regular pattern near earlier conducted P -> bigeminy atrial rhythm… causes sinus pause on ecg mimicking sinus brady
Look for deformed T wave immediately before pause to ID non-conducted APC
Pseudo-sinus brady cardia
conducted APCs
most commonly RBBB pattern
AIVR
regular wide QRS rhythm
AV dissocitation and sinus brady present
LBBB pattern exists but do not code with AIVR
LAD also but do not code with AIVR
Acute cor pulmonale/PE
S1Q3T3
RAD
Sinus tach, afib, aflutter, atach, first dev AVB
No qwave in II (if so then consider IWMI)
?iRBBB
ST changes non-specific (ST elev V1, ST dep V4-6)
QT int can’t be assessed with STach
CHB vs AV dissociation
V rate similar to or greater than atrial rate (isorhythmic)
capture beat rules out CHB
Vpace beats
can interpret ST elev by scarbosa CANNOT interpret ST depressions as ST secondary changes can occur with vpacing Can't interpret Q wave MI Can't code LBBB/RBBB Can't code prolonged QT Can't code LVH/RVH
SVT vs VT
Wide QRS - usually VT
unless it is SVT with aberrant conduction (ie RBBB/LBBB)
RVOT VT
inferior axis - QRS complex positive in inferior leads
Atach
look for abnormal p-wave morphology - ie neg in II, III, aVF (NSR p wave positive in II, III, aVF)
Upper rate behavior
PPM tracks high rate atach and progressively increases AV delay to an upper limit and then drops a pacing spike
VVI demand
need to see inhibition in at least one beat with native QRS to tell if it is VVI demand??
VVI demand
need to see inhibition in at least one beat with native QRS to tell if it is VVI demand??
VT
monophasic R wave in AVR
Sinoatrial exit block
First Degree is not detectable on the surface ECG
Second Degree Mobitz Type I is characterized by group beating, a shortening P-P interval with a constant P-R interval, and a P-P pause interval less than twice the usual P-P interval
Second Degree Mobitz Type II is characterized by a constant P-P interval with a P-P pause interval being approximately a precise multiple (within 0.10 seconds) of the usual P-P interval
Third Degree is not detectable on the surface ECG
Sinoatrial exit block
Grouped-beating is seen here with every third P-wave being dropped. This is suggestive of sinoatrial exit block. Many types of sinoatrial exit block exist. A shortening P-P interval with the longest P-P interval (the interveal between the dropped P-wave) being less than twice the standard P-P interval is known as sinoatrial exit block, second degree, Mobitz type I.
AV junctional escape complex
Usually narrow QRS complex following a previously conducted beat at a coupling interval that corresponds to a rate of 40 to 60 per minute
A P wave, with typically a superior and leftward axis, if seen, may be seen immediately before or after the QRS complex
Termed ‘escape’ complexes because they act as a backup pacemaker of the heart in the setting of severe sinus node dysfunction, sinus pauses, or high degree AV block
Sinus Arrhythmia
Normal P wave axis (0 to 75 degrees; i.e. upright in leads I and II)
P-P interval varies by > 10% or 0.16 seconds
AIVR
Regular or mildly irregular ventricular rhythm with a rate of 60 to 110 per minute
Morphology of QRS complex is typically wide and similar to that of premature ventricular contractions
Often will be seen in the setting of myocardial reperfusion following infarction and is felt to be benign
Hyperkalemia
narrow based tall peaked T wave QT shortening** >6.5 1st deg AVB flat wide P wave, pwave dissappearance ST dep >7.5 - no p waves, LBBB/RBBB IVCD -> sinisoid (sinoventricular conduction) VT/VF/IV rhythm, asystole
Hypokalemia
Prominent U waves sometimes long QT ST seg depression, flat t waves various AVB VT/VF
Hypercalcemia
Short QT
maybe long PR
Renal cell CA (paraneoplastic syndrome)
Hypocalcemia
prolonged QT (narrow t wave)** because of lengthened flat ST segment without change in duration or morphology of T wave
Bivi pacing
Dual ventricular pacing spikes, typically occurring within 80 msec of each other, resulting from two separate pacing leads (one in the right ventricle and the other placed epicardially via the coronary sinus)
May result in a paced right-bundle branch block QRS morphology if the epicardial lead is being activated first (usually standard RV apical pacing results in a paced left bundle-branch block QRS morphology)
LBBB, complete
Mean QRS duration greater than or equal to 120 ms in adults,greater than 100 ms in children 4 to 16 years of age, andgreater than 90 ms in children less than 4 years of age
Late forces of QRS complex should be negative (i.e terminal S wave) in V1
Broad notched or slurred R wave in leads I, aVL, V5, and V6 and an occasional RS pattern in V5 and V6 attributed to displaced transition of QRS complex
Absent q waves in leads I, V5, and V6, but in the lead aVL,a narrow q wave may be present in the absence of myocardial pathology
Delayed onset of intrinsicoid deflection (> 60 ms from beginning of QRS complex to peak of R wave) in leads V5 and V6 but normal in leads V1, V2, and V3, when small initial r waves can be discerned in these leads.
RBBB Complete
*Prolonged QRS duration greater than or equal to 120 ms in adults, greater than 100 ms in children ages 4 to 16 years, and greater than 90 ms in children less than 4 years of age
*rsR’, rsr’, or rSR’ complexes in V1 or V2, with the secondary R wave (r’ or R’) usually wider than the initial R wave (r); a minority of patients may have a wide and often notched R wave pattern in lead V1 and/or V2
*S wave of greater duration than R wave or > 40 ms in leads I and V6 in adults
**Normal R peak time in leads V5 and V6 but > 50 ms in lead V1
Of the above criteria, the first 3 should be present to make the diagnosis. When a pure dominant R wave with or without a notch is present in V1, the 4th criteria should be satisfied.
Note: A right bundle branch block results in secondary ST-T segment changes (ST depression or T wave inversion), unrelated to ischemia, in V1-V2. A right bundle branch block can be seen in normal adults without structural heart disease; however, in the setting of known coronary artery disease, a right bundle branch block carries a 2-fold increase in mortality.
LAFB
Mean QRS axis between -45 degrees and -90 degrees with mean QRS duration < 120 ms
Typically qR complex in lead I and rS complexes in leads II and III
qR pattern in lead aVL with delay of > 45 ms from beginning of QRS complex to peak of R wave in lead aVL
Absence of other causes of marked left axis deviation such as inferior myocardial infarction or left ventricular hypertrophy
Note: The entire left bundle conduction system of the heart is made up of two fascicles, one anterior and one posterior. The left anterior fascicle supplies fibers to the anterior and lateral walls of the left ventricle. The above criteria of left anterior fascicular block do not apply to patients with congenital heart disease in whom left-axis deviation is present in infancy.
IVCD
Mean QRS duration greater than 110 ms in adults, greater than 90ms in children 8 to 16 years of age, and greater than 80 ms in children less than 8 years of age
Specific criteria for right or left bundle branch block (e.g. delayed onset of intrinsicoid deflection) are not met
WPW
Short P-R interval (< 120 ms during sinus rhythm in adults and < 90 ms in children)
Slurring of the QRS complex (delta wave), resulting in the QRS complex being > 120 ms in adults and > 90 ms in children (the widened QRS complex results from fusion of two electrical impulses, one through the normal AV node and the other through the bypass tract)
Secondary ST-T wave changes (ST-T segment deviation opposite in directon of main QRS deflection)
Note: Wolff-Parkinson White (WPW) syndrome exists due to an abnormal muscular network of conduction tissue that connects the atrium to the ventricle and affectively bypasses the AV node. Most patients with WPW have no structural heart disease, although the syndrome is more prevalent in Epstein’s anomaly (anomalous attachment and downward displacement of the tricuspid valve leaflets), hypertrophic cardiomyopathy, mitral valve prolapse, and dilated cardiomyopathy. Most tachyarrhythmias are from AV re-entry tachycardia and typically result in a symptomatic narrow-complex tachycardia. However, the real concern with WPW exists if atrial fibrillation or flutter were to spontaneously occur. In that setting, abnormal conduction down the bypass tract with retrograde conduction back up the AV node could result in a rapid, wide-complex and irregular tachycardia that could potentially be life-threatening.
Atrial tach
Abnormal P waves different in morphology from sinus P waves
Differs from atrial premature complexes in that there are at least 3 beats in succession
Typical atrial rate is 100 to 180 beats per minute
Usually results in a normal QRS complex (similar to that seen in sinus rhythm) following each P wave, unless the QRS complex is aberrantly conducted
Atrial tach
Abnormal P waves different in morphology from sinus P waves
Differs from atrial premature complexes in that there are at least 3 beats in succession
Typical atrial rate is 100 to 180 beats per minute
Usually results in a normal QRS complex (similar to that seen in sinus rhythm) following each P wave, unless the QRS complex is aberrantly conducted
Pathologic Q’s
30ms wide, 0.1mV deep
ventricular escape complexes and rhythm
Regular or mildly irregular ventricular rhythm with a rate of 20 to 40 per minute
Morphology of QRS complex is typically wide and similar to that of premature ventricular contractions
AV Junctional escape complexes
Usually narrow QRS complex following a previously conducted beat at a coupling interval that corresponds to a rate of 40 to 60 per minute
A P wave, with typically a superior and leftward axis, if seen, may be seen immediately before or after the QRS complex
Termed ‘escape’ complexes because they act as a backup pacemaker of the heart in the setting of severe sinus node dysfunction, sinus pauses, or high degree AV block
RVH
Mean QRS axis greater than or equal to 100 degrees (i.e. Right Axis Deviation)
R/S ratio in V1 > 1, R/S ratio in V5 or V6 < 1, qR complex in V1, or R wave > 7mm in V1
Secondary ST-T segment changes (ST depression or T wave inversion) in right precordial leads
ST changes from hypertrophy
Results in ST-T segment displacement opposite in direction to the QRS complex
Note: Left ventricular hypertrophy results in downsloping ST-segment depression and T wave inversion in leads I, V5, and V6, and subtle ST-segment elevation (< 1mm) in V1-V2. Rigth ventricular hypertrophy results in ST-T segment depression and T wave inversion in V1-V3.
RVH in setting of RBBB
In the setting of a right bundle branch block, an R-prime in V1 greater than or equal to 15 mm suggests right ventricular hypertrophy.
HCM
Abnormal QRS complex characterized by large amplitude QRS (left ventricular hypertrophy), pathological Q waves (pseudoinfarct pattern in the inferior, anterior, or lateral leads), or a tall R wave in V1 simulating right ventricular hypertrophy
Left axis deviation in approximately 20% of patients
Nonspecific ST-T segment abnormalities or ST-T segment changes secondary to ventricular hypertrophy
Left atrial abnormalities
Note: Apical variant of hypertrophic cardiomyopathy gives deep T wave inversions in V4-V6.
LVH
LAE
