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Internal Medicine

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INTERNAL MEDICINE

CARDIOLOGY

ECG

Prepared by : Dr. Abdullahi Muktar Abdikadir


GROSS ANATOMY
ELECTROCARDIOGRAM
An ECG provides an assessment of the electrical
activity of the heart. The heart rate, rhythm, axis,
intervals, ischemia, and chamber enlargement can
be evaluated
ECG LEADS
1: Chest leads
2: Limb leads
LIMB LEADS
NORMAL ECG
Rate
Normal adult heart rate (HR) is 60–100 beats/min
(bpm). HR <60 bpm is bradycardia.
Heart rate >100 bpm is tachycardia.
Common causes of sinus bradycardia are
1: physical fitness, sick sinus syndrome, drugs,
vasovagal attacks, acute myocardial infarction (MI), and
↑ intracranial pressure.
Common causes of sinus tachycardia are anxiety,
anemia, pain, fever, sepsis, congestive heart failure
(CHF), pulmonary embolism, hypovolemia,
thyrotoxicosis,
carbon dioxide (CO2) retention, and sympathomimetics.
Rhythm
Sinus rhythm: Normal rhythm that originates from
the sinus node. It is characterized by a P wave
(upright in leads II, III, and aVF; inverted in lead
aVR) preceding every QRS complex and a QRS
complex following every P wave.
Sinus arrhythmia is a sinus rhythm originating
from the sinoatrial (SA) node with cyclical beat-to-
beat variation (>120 milliseconds [msec]) in the P-
P interval and a constant P-R interval, which
results in an irregular ventricular rate. It is
common in young adults and is considered a
normal variant.
Axis The QRS axis represents the direction in which the mean QRS
current flows. It can be determined by examining the QRS in leads I, II,
and aVF
Intervals
PR interval: Normally 120 to 200 msec (3–5 small
boxes). Prolonged = delayed atrioventricular (AV)
conduction (eg, first-degree heart block).
Short = fast AV conduction down accessory
pathway (eg, Wolff-Parkinson-White [WPW]
syndrome).
QRS interval: Normally <120 msec. A normal Q
wave is <40 msec wide and <2 mm deep.
Ventricular conduction defects can cause a widened
QRS complex (>120 msec)
Left bundle-branch block (LBBB): Deep S wave and
no R wave in V1 (“W” shaped); wide, tall and
broad, or notched (“M”-shaped) R waves in I, V5,
and V6 . A new LBBB is pathologic, and it may be
suggestive of acute MI. However, this is not
diagnostic in isolation. Rather, the Modified
Sgarbossa Criteria (see key fact) should be used for
the ECG diagnosis of acute MI in this situation
(higher sensitivity and specificity).
KEY FACT
Smith-Modified Sgarbossa Criteria are used to
diagnose MI in the presence of LBBB should be
suspected in a patient with LBBB and the following
ECG findings:
Concordant ST elevation (STE) ≥1 mm in ≥1 lead
Concordant ST depression ≥1 mm in ≥1 lead of V1–
V3
Excessive discordant STE in ≥1 lead with ≥1 mm
STE, where excessive discordance is defined as STE
to the maximum QRS amplitude ratio ≥25%
Right bundle-branch block (RBBB): RSR′ complex
(“rabbit ears;” “M”-shaped); qR or R morphology
with a wide R wave in V1; QRS pattern with a wide
S wave in I, V5, and V6
QT interval: Normally QTc (the QT interval
corrected for extremes in heart rate) is 380 to 440
msec (QTc = QT/√RR). QTc may be prolonged (QTc
>440 msec) due to acquired causes, including
electrolyte derangements (↓ K+, ↓ Ca2+, ↓ Mg2+)
and medications (macrolides, fluroquinolones,
opioids, ondansetron, Classes Ia [quinidine,
procainamide] and III [sotalol, amiodarone]
antiarrhythmic drugs). Congenital causes include
long QT syndrome (LQTS), an underdiagnosed
disorder that predisposes to ventricular
tachyarrhythmias (eg, torsade de pointes) and
sudden cardiac death (SCD, see later).
Within hours, peaked T-waves and ST-segment
changes (either depression or elevation). Within
24 hours, T-wave inversion and ST-segment
resolution. Within a few days, pathologic Q waves
(>40 msec or more than one-third of the QRS
amplitude). Q waves usually persist, but may
resolve in 10% of patients. Because of this,
Q waves signify either acute or prior ischemic
events. Non–Q-wave infarcts (also known as
subendocardial infarcts) have ST and T changes
without Q waves. In a normal ECG, R waves
increase in size compared to the S wave between
leads V1 and V5. Poor R-wave progression refers to
abnormalities in this pattern (eg, reversed
progression [R in V2 > V3], transition point beyond
V4, R in V3 <3 mm) and can be a sign of new or
prior anterior infarction, although it is not specific.
Chamber Enlargement
Atrial enlargement: Right atrial abnormality (P
pulmonale): Generally, the right atrium (RA)
depolarizes before the left. Right atrial
enlargement (due to pulmonary hypertension [eg,
chronic obstructive, pulmonary disease, tetralogy
of Fallot, tricuspid atresia]) causes slowed
conduction; therefore peak right atrial
depolarization coincides with left. This results in
increased P-wave amplitude (>2.5 mm in lead II).
Left atrial abnormality (P mitrale): Left atrial
enlargement causes prolonged left atrial (LA)
depolarization, increased P-wave duration (>120
msec in lead II), and sometimes a V-shape occurs in
P wave (also in lead II) .
Also, the P wave in lead V1 may have a large
negative deflection (>1 small square wide and 1
small square deep in a standard tracing).
Commonly seen in isolation in mitral stenosis or
associated with LV hypertrophy
Amplitude of S in V1 + R in V5 or V6 is >35 mm.
Alternative criteria: The amplitude of R in aVL + S in
V3 is >28 mm in men or >20 mm in women.
Usually associated with ST depression and T-wave
changes.
Causes include hypertension (most common),
aortic stenosis/regurgitation, mitral regurgitation,
coarctation of the aorta, and hypertrophic
cardiomyopathy.
Right ventricular hypertrophy (RVH):
Right-axis deviation and an R wave in V1 >7 mm.
Causes
pulmonary hypertension, pulmonary embolism,
chronic lung disease (cor pulmonale), mitral
stenosis, and congenital heart disease (eg, tetralogy
of Fallot, pulmonary stenosis).
KEY FACT
Axis deviation can be a sign of ventricular enlargement
MNEMONIC
“D ARMS PITS” Diastolic Murmurs Aortic
Regurgitation Mitral Stenosis Pulmonary
Insufficiency Tricuspid Stenosis
END OF THE LECTURE

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