CV 468: EKG’s
(a continuum)
“That’s right sportsfan’s,
Willy rides again…”
Disclaimer: The information compiled in this powerpoint presentation do not express the views of anyone on
payroll at VCOM nor do they reflect the views of the College itself. This information was put together for review
and is intended as a high-yield review of EKG interpretation. This information is not complete therefore use this
information merely as a supplement and at your own risk.
George Mueller
Review of Physiology
SAN Conduction
Phase 0 – upstroke, increased Ca
conductance, inward Ca current
Phase 3 – repolarization, increased K
conductance, outward K current
Phase 4 – slow depolarization, accounts for
pacemaker activity, increased Na
conductance, inward Na current (“funny
current, If”)
The PACEMAKER
AVN Conduction
The ionic basis for the AVN is the same
as the SAN (see previous slide)
Ventricular
Conductance
Phase 0 – upstroke, increased Na conductance,
inward Na current
Phase 1 – initial repolarization, increased K
conductance, outward K current
Phase 2 – plateau, transiently increased Ca
+ current (balances outward K)
conductance, inward
gNaCa
Phase 3 – repolarization, decreased Ca conductance,
increased K conductance, outward K current
Phase 4 – resting membrane potential, inward and
outward currents are balanced (IK1), approach K
equilibrium
This applies to the ventricles, atria,
and the purkinje system.
Refractory Periods
Absolute – begins with the upstroke and
ends after the plateau, reflects the time
during which NO AP can be initiated
Effective – slightly longer than ARP,
period during which a CONDUCTED AP
cannot be elicited
Relative – period immediately after the
ARP when repolarization is almost
complete, AP CAN be elicited, but MORE
than the usual inward current is required
Put all this together
Isoelectric line
Waves, Intervals, Complexes, and
Segments…
P wave – atrial depolarization, does not include atrial repolarization (hidden in
QRS)
PR interval – beginning of P wave to beginning of Q wave (initial depolarization of
ventricle), varies with conduction velocity of AVN (if decreased, PRI increases…
heart block?)
QRS complex – ventricular depolarization
QT interval – beginning of Q wave to end of T wave, entire period of
depolarization and repolarization of the ventricles
ST segment – end of S ave to beginning of T wave, isoelectric, period when
ventricles are depolarized
R
T wave – ventricular repolarization
INTERVALS
PRI – 0.12 to 0.20 sec
QRS – 0.04 to 0.11
sec
QTI – 0.3 to 0.4 sec
(or no more than half
to RRI)
OR
QTc = QT / √ RRI
Positive
P
T
Isoelectric
Q
S
Negative
EKG Interpretation (Basics)
•
•
•
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RATE
RHYTHM
AXIS
HYPERTROPHY
INFARCTION
IN THIS
ORDER…
and you
cannot go
wrong!
1) RATE
INTRINSIC RATES
SAN – 60 to 100
Atria – 60 to 80
AV JCT – 40 to 60
R wave on
solid black
line
Pick an R wave that falls on a solid
black vertical line and count until you
reach the next one in sequence.
Ventricles – 20 to 40
300 150 100 75
The next R wave falls just before the 75 mark,
so the rate is just greater than 75, about 80
2) RHYTHM
Is it REGULAR? Is the
RRI at the same distance
every time?
THIS QUESTION BROUGHT TO YOU BY
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1st – check for P waves
2nd – check for QRS complex
3rd – look for a P wave before every
QRS
4th – look for a QRS after every P wave
5th – check PR intervals (for AV blocks)
6th – check QRS intervals (for BBB)
7th – look for anything out of the
ordinary, like extra beats
This is the strip
where you
measure rate and
rhythm
If you are looking at a 12-lead EKG ALL of these measurement
should be done on the long strip (at least 6 sec) at the bottom or
top of the 12-lead EKG. You cannot accurately measure this
from any of the shorter 3 second strips that comprise the 12
leads.
More on the actual rhythms to come later…
3) AXIS
Lead II follows the axis of the heart, thus it
is usually the tallest and best lead to define
all of this
Clinical Tip:
“White on Right,
Smoke over Fire.”
Electrical activity follows the anatomy of the
heart.
Look in Lead I & Lead aVF to determine if there
is positivity (up) or negativity (down) in reference
to the isoelectric line.
NORMAL AXIS = Lead I & Lead aVF ↑
LEFT AXIS = Lead I ↑ & Lead aVF ↓
RIGHT AXIS = Lead I ↓ & Lead aVF ↑
EXTREME RIGHT AXIS = Lead I & Lead aVF ↓
+
Ex-R
LAD
+I
+
Notice the
Normal Axis
follows LEAD II
RAD
Normal
+ aVF
IT HELPS IF
YOU CAN
PICTURE THIS
DIAGRAM ON A
PT’S CHEST
Lead I is UP (+)
Lead aVF is UP (+)
NORMAL AXIS
Lead I is UP (+)
Lead aVF is DOWN (-)
CAUSES OF LAD
LBBB / Left Anterior Hemiblock
LVH
Artificial Cardiac Pacing
Inferior Wall MI (Right Coronary Artery)
LEFT AXIS DEVIATION
Hyperkalemia
WPW (Right-sided accessory pathway)
Pulmonary HTN (Right-sided heart failure)
Tricuspid Atresia (Right side)
ASD
Lead I is DOWN (-)
Lead aVF is UP (+)
RIGHT AXIS DEVIATION
CAUSES OF RAD
RVH
RBBB
Anterior / Lateral Wall MI
Normal Variant (peds, tall adults)
Left Posterior Hemiblock
VSD
Key points about axis deviations 1
Vectors point AWAY from INFARCTIONS
No blood supply, no electrical activity gets through necrotic
tissue, therefore they act as stop signs and the electrical vectors
and pointed in the opposing directions
Key points about axis deviations 2
Vectors point TOWARDS the HYPERTROPHY
More muscle means more electrical activity to
depolarize the whole segment
Axis Rotation (AKA – “R wave progression”)
Think about where the V leads are. V1 is R parasternal border and they move in numerical progression to V6
which is L midaxillary. So if you think about the normal axis (vector) of the heart as going toward the L and
wrapping around your chest to match the anatomy of the heart…the amplitude of the QRS should be increasing
(more positive) from V1 to V6 (R to L).
The TRANSITIONAL ZONE (NORMAL) is between V3 and V4 where the amplitude is most isoelectric (there is
about equal positivity and negativity on either side of the isoelectric line) ---- THIS IS A ROTATION IN THE
HORIZONTAL PLANE!
The same rules apply in the horizontal plane as they do in the frontal plane (axis deviation) ---TOWARD HYPERTROPHY, AWAY FROM INFARCTION.
RIGHTWARD ROTATION – RVH or a LATERAL WALL MI (Isoelectric leads moved to V1/V2)
LEFTWARD ROTATION – LVH or an INFERIOR WALL MI (R coronary a) (Isoelectric leads
moved to V5/V6)
NORMAL EKG
USE THIS AS A REFERENCE TOOL
Each small block = 0.1mm
Each small block horizontally = 0.04 sec (big block = 0.2 s)
Each small block vertically = 0.1mV (big block = 0.5mV)
4) HYPERTROPHY
RIGHT VENTRICULAR HYPERTROPHY
(RVH)
CRITERIA
•
R wave is bigger than the S wave in V1,
but the R wave gets progressively
smaller from V1 to V6
•
S wave persists in V5 and V6
•
Negative (discordant) T wave in V1
•
RAD with wide QRS complex
•
Rightward rotation in the horizontal plane
LOOK FOR A HUGE R WAVE IN V1
Enlarged RV adds more vectors to the right side
1) Rightward R wave Progression
2) Right Axis Deviation
LEFT VENRICULAR HYPERTOPHY
(LVH)
Normally the S wave in V1 is very deep…with
LVHyou have more electricity going down the
patient’s left side (AWAY FROM +V1
electrode), therefore the S wave is even
deeper in V1
Lead V5 is sitting directly over the LV, so
there is more electricity going to the +V5
electrode…HUGE R WAVE IN V5
CRITERIA
•
(S wave in V1) + (R wave in V5) >
35mm
•
LAD with wide QRS complex
•
Leftward rotation of horizontal plane
•
Inverted T wave slants down gradually
but up rapidly
RIGHT ATRIAL HYPERTROPHY
(RAH)
CRITERIA
Large, diphasic P wave with tall
initial component (>2.5mm in
Lead II and/or >1.5mm in V1)
It is often “peaked”
LEFT ATRIAL HYPERTROPHY
(LAH)
CRITERIA
Large, diphasic P wave with a
wide terminal component (often
“notched”) and the P wave
duration is > 0.12 sec in Lead II
5) Ischemia
With ischemia the cells become more positive in their resting voltage
(due to channel leakage of Ca++), making the subendocardium more
positive; since the endocardium is further away from the precordial
leads than the more negative myocardium. This is reflected as a ST
depression.
Ischemia – inverted T waves (typically symmetric inversion) – easier to
see them in the V leads.
5) Injury & Infarction
Injury
Indicates the acuteness of an infarct…ST segment ELEVATION denotes injury.
ST segment elevation (J point elevation) tells you that the MI is ACUTE
Infarction
5) NON-Q-WAVE (Non-transmural) – ST segment elevation without pathologic Q waves
10) Q-WAVE (Transmural) – ST segment elevation with pathologic Q waves
Pathologic Q Waves
1st deflection of QRS that
is greater than 1/3 the
entire QRS amplitude
Q waves can be
normal, they are
just small and
called ‘q’ waves
ANTERIOR
POSTERIOR
INFERIOR
LATERAL
INFERIOR WALL MI
ST ELEVATION – Leads II, III, aVF
Reciprocal Changes???
RIGHT CORONARY ARTERY
RCA SUPPLIES SAN/AVN – BRADYCARDIA?
ANTEROLATERAL WALL MI
ST Elevation – Leads I, aVL, V1-V6
Anterior Component – V1-V4
Lateral Component – I, aVL, V5, V6
LEFT CORONARY A & BRS
POSTERIOR
WALL
MI
We have no leads on the posterior thorax, therefore all you will see is the
reciprocal change in leads V1 (mostly) but up through V3 possibly…what is
reciprocal change? ST segment DEPRESSION.
Posterolateral branch of RCA (75%) or Distal Left Circumflex (25%)
MIRROR TEST????
MI THERAPY
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MONA (Morphine, O2, NTG, ASA)
IV Fluids
Thrombolytics (tPA)
Heparin
Plavix
Metoprolol
Enzymes
CXR
Call the Cath Lab / Cardiologist
ISCHEMIA
THERAPY
NTG
Beta-blockers
Plavix (Clopidrogel)
Heparin (UFH or LMWH)
Glycoprotein IIb/IIIa Inhibitor
Cardiac Cath
PERICARDITIS
Diffuse ST elevation
BUNDLE BRANCH BLOCKS
RIGHT BBB - the right ventricular firing is late so R-R’ is in V1
LEFT BBB - the left ventricular firing is delayed so R-R’ is in the V6
CRITERIA
•
Wide QRS Complex > 0.12
sec must be present
•
RBBB – V1/V2 R-R’
•
LBBB – V5/V6 R-R’
RBBB
LBBB
Also see HUGE DEEP S
waves in V1-3
HYPERKALEMIA
CRITERIA
2) PEAKED T WAVES
3) Flat P waves
4) Wide QRS
Etiology – renal failure,
acidosis, rhabdo
TREATMENT
2) Ca Chloride / Gluconate
3) Glucose
4) Insulin
5) Albuterol
6) Kaexalate
7) NaHCO3
EXTREME HYPERKALEMIA – sinusoidal waves
CRITERIA
2) Flat to inverted T
waves
3) Prominent U
waves
TREATMENT
Ummm…K+ (KCl)
HYPOKALEMIA
RHYTHMS
SINUS/ATRIAL RHYTHMS
Normal Sinus Rhythm
Regular rhythm
P:QRS = 1:1
Rate 60-100
Rate < 60
TX – ATROPINE,
PACING, EPI,
DOPAMINE
Rate > 100
Irregular rhythm but P
waves are of different
morphology and the
PRI varies depending
on where/when it fires
Looks like NSR but is
slightly irregular (all
else applies)
Arrest – this would be an
escape beat (jct/vent)
SAN fires but it can’t
exit the SAN
Sinus Exit
Block/Arrest
SVT
Rate 150-250,
regular, narrow QRS
TX – ADENOSINE, DILT
Flutter waves (sawtooth /
picket fence), can be reg/irreg,
atrial rate usually 300
(ventricular rate 150 for 2:1)
TX – ADENOSINE, DILT, AMIO, VERAPAMIL, DIG
Irregularly-irregular, QRS
is normal
Anything that is irregularly-irregular is AFIB until proven otherwise
Irregular, rate 100-250,
2 or more ectopic P
waves with different
morphologies, PRI
vary, QRS is normal
TX - DILTIAZEM
AKA - PSVT
Sinus rhythm
interrupted by a
period of SVT
Wolff Parkinson White
CRITERIA
2)
QRS < 0.10 sec
3)
PRI < 0.12 sec
4)
Delta Wave
TX – ADENOSINE, PROCAINAMIDE
DO NOT GIVE CALCIUM CHANNEL BLOCKERS
If you do this you will block the inherent conductance
of the AVN which is fine, it just so happens that the
extranodal pathway (Bundle of Kent) is faster and
thus conducts before the normal AVN. If you do this
you set the patient up for nasty rythms (VF/VT, etc)
LONG QT SYNDROME
QTc = QT / √RR
The QTI should
not be more
than ½ the RR
TX – BETA-BLOCKERS
AVN BLOCKS
PRI > 0.20 sec
PRI gets progressively
longer until a P wave gets
blocked thru the AVN
QRS?
Going, going, gone…
PPI are regular, PRI can
be normal/long, but a P
wave will get blocked
QRS?
QRS?
TX (2°AVBII / 3°AVB) – PACING, If brady, follow that algorithm
PPI normal, RRI normal, but
there are no P’s associated
with QRS complexes…atria
not talking to ventricles
P in QRS
JUNCTIONAL RHYTHMS
Junctional means the start
point in the AV junction (not
the SAN)…therefore there
are no P waves OR
retroconducted P waves
(inverted)…and they can
occur anywhere (before,
during, or after the QRS)
TX – ADENOSINE, DILT
Junctional Tachycardia
Normal inherent rate is 40-60, but by definition of
a rate between 60-100 is normal, so it is called
ACCELERATED, and if the rate is greater than
100, it is called TACHYCARDIC
PREMATURE BEATS
Bigeminy – there is 1
PVC for every normal
beat
Trigeminy – 1 per 2
Quadrigeminy – 1 per 3
By definition these
are simply ectopic
beats that occur
early…the cadence
is not affected as
you see normal beat
after the premature
beat is in line where
it should have come
if everything was
normal
ESCAPE BEATS
Atrial
These are usually
benign, unless the
patient is symptomatic.
They occur after a long
hesitation (pause) and
then there is a
spontaneous discharge
from the corresponding
tissue.
It must occur later in the
rhythm than expected
Junctional
VENTRICULAR RHYTHMS
USUALLY BAD!!!
May be irregular, wide and
bizarre QRS complexes,
rate 150-250 (pulses?
mono/polymorphic?)
TX – AMIODARONE, SYNC CARDIOVERSION
(PULSE), DEFIBRILLATION (PULSELESS)
Random electrical
activity (coarse/fine?)
“Twisting of the Points,”
often preceded by a long
QTI
TX – MgSO4
Purkinje cell
discharge at their
intrinsic rate of 20-40
(if faster, can be
accelerated IVR),
wide/bizarre
AKA – “dead”
TX – PACING,
ATROPINE, EPI, or
CALL IT
MISCELLANEOUS
If the P wave hits the AVN during
the absolute refractory period, the
signal will not go any further…no P
gets through means no QRS
Widening and distortion of the
QRS, short PRI usually…these are
typically just smaller in amplitude
than the normal conducted
rhythms (this is just one example)
R on T Phenomenon
T wave here
R wave here
Usually results in very bad rhythms…VF/VT
PACED RHYTHMS
Atrial Pacemaker
Look for the pacing spikes
at the onset of the P wave
or QRS. Make sure there is
a T wave to follow the QRS
to ensure repolarization
(especially important for
external pacing).
Ventricular Pacemaker
CPR
PEA
TACHY
CP
BRADY
PEA