Which cell type is recorded by the EKG?

Waves that appear on an EKG primarily reflect the electrical activity of the
myocardial cells, which compose the vast bulk of the heart. Pacemaker activity and transmission by the conducting
system are generally not seen on the EKG; these events simply do not generate sufficient voltage to be recorded
by surface electrodes.

Segment or Interval? A segment is a straight line connecting two waves, whereas an interval encompasses at least
one wave plus the connecting straight line.

Guide to Limb Choice: Leads II, III, and aVF are called the inferior leads
because they most effectively view the inferior surface of the heart. The inferior
surface, or wall, of the heart is an anatomic term for the bottom of the heart,
the portion that rests on the diaphragm. Leads I and aVL are often called the
left lateral leads because they have the best view of the left lateral wall of the
heart. aVR is pretty much a loner. It is considered the only true rightsided limb
lead.

V: Lead V1 lies directly over the right ventricle, V2 and V3 over the
interventricular septum, V4 over the apex of the left ventricle, and V5 and V6
over the lateral left ventricle.

Leads V1 through V4 are often referred to as the anterior leads, and V5

and V6 join I and aVL as left lateral leads. To summarise:

Leads Group
V2, V3, V4 Anterior
I, aVL, V5, V6 Left Lateral
II, III, aVF Inferior
aVR, V1 Right Lateral
R Progression: Lead V1 has the smallest R wave; lead V5, the largest (the R wave in lead V6 is usually a little smaller
than that in lead V5). We also speak of a transition zone, the precordial lead or leads in which the QRS complex
goes from being predominantly negative to predominantly positive. The normal transition zone occurs at leads
V3 and V4.

T & QRS Polarity: It is typical and normal to find positive T waves in the same leads that have tall R waves.

Enlargement: Dilation of a chamber caused by volume overload, usually resulting from valve insufficiency

Hypertrophy: Enlargement of muscular mass because of pressure overload, resulting from elevated systemic
pressure or valve stenosis

These two usually coexist, resulting from a need for increased cardiac output. They also aren’t distinguished very
well by an EKG, but it’s usual to speak of atrial dilation and ventricular hypertrophy.

What Changes? Duration increase/ Amplitude increase/ Wave axis change

Normal QRS Axis: if 0˚-90˚ is taken as the normal range for the QS axis, then a
positive QRS voltage in leads I and aVF means a normal QRS axis.

Examining Method for Determining QRS Axis: Find the lead in which QRS is
biphasic. The axis IS perpendicular to that axis. Find a lead in which QRS is positive
to see which one of the two perpendicular axes the QRS axis actually is.

Geometric Method for Determining QRS Axis: Draw lines with a length relative to
QRS amplitude on each lead, find the vectorial sum of the two.

RAH: increased P amplitude in lead II and higher amplitude of the first peak in lead
V1. Possible axis deviation

LAH: two-peaked P wave in lead II and higher amplitude of the second peak in
lead V1. No axis deviation because LA is already dominant in normal conditions.

RVH: lead III QRS largest among I, II, III, slightly negative lead I QRS. R progression is somewhat reversed, with
leads V1 to V3 having the largest QRS, and leads V5 & V6 having smaller QRS. R>S in V1, R<S in V6. Mostly caused
by pulmonary disease or congenital heart disease.

LVH: More complex diagnosis than RVH. Common criterion is increased R amplitude in left-lateral leads and
increased S amplitude in right-lateral leads. Precordial leads: R+S amplitude more than 35mm in V1 & V2. Limb
leads: I QRS largest among I, II & III, negative (?) aVL QRS. The sensitivity of EKG for LVH is not high, but the
specificity is.

Repo Abnormalities: down sloping ST depression and T inversion. Indicates possible hypertrophied ventricle failure.
Most distinguishable EKG in leads w/ the tallest R wave.
Definition: Any deviation from the normal sinus rhythm. May be an aberrant beat or sustained for prolonged times.
Some dangerous, some not.

HISDEBS: The main causes of arrhythmia are: Hypoxia, Ischemia and Irritability, Sympathetic Stimulation, Drugs,
Electrolyte disturbances, Bradycardia, Stretch

5 Basic Types of Arrhythmias: Arrhythmias of Sinus Origin: usual conduction pathways, but either too fast or too
slow, or irregular. Ectopic Rhythms. Reentrant Arrhythmias: caused by a closed circuit, can occur anywhere in the
heart. Conduction Blocks: usual pathways but encountering unusual blocks or delays. Preexcitation Syndromes:
accessory pathways that bypass the normal ones, causing short circuit.

Arrhythmias of Sinus Origin

Sinus Tachycardia and Sinus Bradycardia: Normal heart rate is in the range
60-100. Plain deviation from this range is called sinus
tachycardia/bradycardia.

Sinus Arrhythmia: The rhythm is normal in all aspects except that it’s
irregular. Expiration slows heart rate, inspiration accelerates it.

Sinus Arrest, Asystole, and Escape Beats: If the SA node stops firing, sinus
arrest has occurred. Were there no other pacemakers, asystole would
follow, meaning a flat line for the EKG. But escape usually happens, because
of other pacemakers in the heart. These pacemakers include, in the order
of how high their rate is, atrial pacemakers, junctional pacemakers (near
the AV node), and ventricular pacemakers. The most common type of
escape is junctional escape, mediated by the junctional pacemakers, which
means normal ventricular depo (except that it’s slow), but abnormal atrial
depo. The P wave is either absent, or inverted because of retrograde
conduction.

Sinus Arrest & Sinus Exit Block: Because the EKG doesn’t record SA node
depo, these two can’t be recognized, but functionally they mean the same
thing, the SA node either falls silent or fails to conduct its depo to the conduction pathway.

Hint: sinus bradycardias and tachycardia usually involve altered T waves, taller in tachy and of lower height in
brady.

Reentrant Arrhythmias:

The Four Questions: 1. Are normal P waves present? 2. Are the QRS complexes narrow or wide? 3. What is the
relationship between P waves and the QRS complexes? 4. Is the rhythm regular or irregular?

The Answers for a Normal Rhythm: The normal sinus rhythm has specific answers for all four, and they’re obvious.
Atrial and Junctional Premature Beats: Can be recognized by
abnormal/absent P waves, atrial premature beat involves an
altered P wave, and junctional premature beat doesn’t have any P
waves. The factors for an abnormal P wave are early onset and
altered contour. Trace A shows an atrial premature beat and trace
B shows a junctional (AV nodal) premature beat.

Junctional Escape/Premature Beat: One occurs prematurely, the

other occurs lately, after a
delay. However, both are
conducted normally to the
ventricles, resulting in normal, narrow QRS complexes.

Paroxysmal Supraventricular Tachycardia: Caused by a supraventricular

reentrant loop, very high rate. Sometime w/ visible retrograde P waves as a
pseudo-Rʹ.

Atrial Flutter: Very high atrial rate caused by a large reentrant circuit,
accompanied by type a Mobitz type II AV block. The RR interval shows a saw-
toothed pattern with no
straight lines in between,
because of the high atrial
rate.

Atrial Fibrillation: Blitz-like atrial depo rate causing RR intervals with no distinct
pattern, sometimes even the ventricular rate is so high that there no distinct
RR interval, making the irregularly irregular QRS rhythm the only useful clue
to distinguish it from PSVT.

Multifocal Atrial Tachycardia and Wandering Atrial Pacemakers: involves random firing of multiple ectopic atrial
pacemakers, characteristic multiple types of P wave contour and irregular rhythm occurring in the same EKG.
Paroxysmal Atrial Tachycardia: Caused by ectopic foci or
reentrant loop, regular rhythm w/ P wave characteristics very
similar to paroxysmal atrial tachycardia. The distinction is a
warm-up and cool-down period in PAT.

Supraventricular versus Ventricular Arrhythmias

The distinction between the two is very important, and usually

easy, ventricular arrhythmias produce a wide QRS, whereas
supraventricular arrhythmias are associated w/ a narrow QRS
complex. There is one exception, in which supraventricular
beats are conducted abnormally in the ventricles. It looks VERY
similar to PVC. Therefore, a wide QRS can have one of two
reasons: a beat originating in the ventricles, or a
supraventricular beat conducted aberrantly. The trace
can be showing a VT or PSVT conducted aberrantly. You CAN’T know for sure.

Definition: Any obstruction or delay in the flow of electricity in normal conduction pathways

2nd degree AV blocks: Mobitz types I & II. The first one is in the AV node itself, the second one is in the His bundle

Hint: Watch out for a 2:1 ratio. You can’t tell which 2nd degree AV block type it is!

3rd Degree AV Block: Abnormal and widened QRSs w/ low rate, look similar to a PVC. The difference is that a PVC
occurs before you expect it, whereas the 3rd degree blocked ventricular beat occurs after a delay. The diagnosis
requires AV dissociation w/ a ventricular rhythm slower than the atrial.

Bundle Branch Block (General): Normal QRSs are narrow w/ an axis lying in 0˚-90˚. All of this changes completely
in a bundle branch block.

RBBB: RV depo occurs after LV depo is almost

complete, resulting in a wide QRS, w/ a
characteristic rabbit-ears-like RSR in right lateral
leads such as V1, and a deep S in left lateral
leads, such as V4.
LBBB: Wide QRS, but not rabbit-ears-like RSR, w/ a
deeper S in all leads, or a prolonged QRS w/ two
peaks.

Repo & BBB: Both RBBB & LBBB cause ST

depression and T inversion in the corresponding
lateral leads. The EKG below shows an RBBB.

Hemiblock: left anterior hemiblock >> left axis deviation, left posterior hemiblock >> right axis deviation. The QRS
is not widened, and the ST segment & T wave are normal (unlike complete branch block). Hemiblock is diagnosed
for by axis deviation in the limb leads
Combined Blocks: How many
different types of block do you see in
the EKG to the left?

Example of Pacemaker: An RV pacemaker will result in EKG characteristics similar to LBBB, widened, PVC-like QRS
w/ delayed depo of the LV. Generally, artificial pacemaker beats generate very sharp, spike-like waves.

Definition: In contrast to conduction blocks, preexcitation syndromes occur when the electrical current is conducted
more quickly than usual. This happens mainly through accessory pathways that bypass the AV node. The two
major types are Wolff-Parkinson-White and Lown-Ganong-Levine, both of which are easily diagnosed in the EKG.
WPW: The accessory pathway may be left sided (LA to LV) or right-sided (RA to
RV), and is called the Kent bundle. Diagnosis criteria include PR interval less than
0.12 seconds and prolonged QRS because of preexcitation rather than delayed
conduction, w/ a characteristic delta wave (therefore it’s a fusion beat). Check all
the leads for the delta wave, it might be inconspicuous in some.

LGL: In the LGL syndrome, the bypass only short-circuits the AV node, and
nothing else. There is no small patch of the ventricles that depos independently
from the rest, there’s no delta wave, there is no prolonged QRS, only shortened
PR interval (less than 0.12 seconds).

Associated Arrhythmias: The most common arrhythmias associated

w/ WPW are PSVT & atrial fibrillation:

PSVT in WPW: In WPW, PSVT occurs because of reentry (as is the case usually). The Kent bundle is a very good
substrate for reentry, as it conducts faster than the AV node, but has a longer refractory period. If the atrial depo
catches the Kent bundle refractory, the depo from the AV-conducted ventricular depo will depo it instead. The
Kent bundle will proceed to depo the atria. The circular pathway is thus established, resulting in PSVT. Note that
the QRSs are not wide, as they are conducted normally through the AV bundle to the ventricles. Another, less
common occurrence is the reverse of the former pathway, resulting in VT-like tachycardia.

Atrial Fibrillation in WPW: The characteristic thing about WPW atrial fibrillation is the lack of 2nd degree AV block,
causing very high ventricular rate, resulting in the chaotic atrial rhythm becoming invisible.
Definition: The complete cessation of blood supply to an area of the heart, leading to local necrosis of that area.

EKG Diagnosis: T wave peaking,

followed by inversion (A & B); ST
segment elevation (C); Appearance of
new Q waves (D)

T Inversion: The important thing to remember about MI T inversion is that it’s symmetric.

Recognizing MI ST Elevation from J point elevation: The elevated J point is an elevated segment; it’s quite flat, the
MI elevated ST is not flat, it fuses to the T wave at its end.

New Q Wave: The ischemic part is electrically inactive, so the mean depo vector is deviated away from it, leading
to an altered QRS axis and therefore Q wave contour. Its length should be at least 1/3 of the R wave in the same
lead to be regarded as significant. Never check aVR for a significant Q wave.

Localizing the Infarct: Each type of infarct produces the changes in the corresponding leads, w/ reciprocal changes
in the opposing leads. Inferior Infarction: II, III, & aVF; (Left) Lateral Infarction: I, aVL, V5, V6. Anterior Infarction: any
of the precordial leads may show the changes; Posterior
Infarction: Reciprocal changes in the precordial leads,
especially V1.

Angina: EKG symptoms similar to MI, except no new Q-

waves. Angina is usually the result of atherosclerotic
cardiac disease.

Causes of ST elevation: MI, angina, J-point elevation, hyperkalemia, hypothermia

Hyperkalemia: Produces a progressive set of symptoms. The first one is T wave peaking (the difference w/ acute
MI is that it’s diffuse, not confined to a specific area). A more severe case involves PR prolonging, P wave
disappearance and T waves becoming taller than QRS complexes. Ultimately, the QRS widens until it merges w/
the T wave, producing a sinus wave pattern and possible ventricular fibrillation.

Hypokalemia: Produces symptoms that are somewhat the reverse of hyperkalemia’s, incl. ST depression, T wave
flattening, and U wave appearance.

Calcium Disorders: Too much calcium shortens the QT interval, and vice versa (possibly because of NCX). The
prolonged QT can cause torsades de pointes.

Hypothermia: Everything slows down, w/ a characteristic type of ST elevation, called J wave that produces an
incisor-like J point, followed by a possibly inverted T wave. Muscle tremor may produce atrial fibrillation-like EKG,
but the TP interval is much more ordered (but not straight!)

Athletes’ Heart: Profound bradycardia, resulting in a variety of symptoms, but these are of no concern. The only
downside is that they’re at an increased risk of lethal, sudden arrhythmias.

Step by Step method: Intervals, QRS axis, Rhythm [P waves, QRS length, P-QRS relation, regular or irregular?], AV
block, BBB, Preexcitation, Hypertrophy & Dilation, MI

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