Routine ECG

Normal Sinus Rhythm (NSR)

• Rate: Normal (60–100 bpm)
• Rhythm: Regular
• P Waves: Normal (upright and uniform)
• PR Interval: Normal (0.12–0.20 sec)
• QRS: Normal (0.06–0.10 sec)
 Sinus Bradycardia
Results from slowing of the SA node
• Rate: Slow (<60 bpm) • Sinus bradycardia is normal in
• Rhythm: Regular athletes and during sleep. In
• P Waves: Normal (upright and acute MI, it may be protective
uniform) and beneficial, or the slow rate
may compromise cardiac output.
• PR Interval: Normal (0.12–0.20
Certain drugs , such as beta
sec)
blockers, CCB may also cause
• QRS: Normal (0.06–0.10 ec)
sinus bradycardia
 Sinus Tachycardia
Results from increased SA node discharge.
• Rate: Fast (>100 bpm) • Clinical Tip: Sinus tachycardia
• Rhythm: Regular may be caused by exercise,
• P Waves: Normal (upright and anxiety, fever, hypoxemia,
uniform) hypovolemia, or cardiac failure.
• PR Interval: Normal (0.12–0.20
sec)
• QRS: Normal (0.06–0.10 sec)
  Premature Atrial Contraction (PAC)
■ A single complex occurs earlier than the next expected sinus
complex. After the PAC, sinus rhythm usually resumes
• Rate: Depends on rate of underlying • Clinical Tip: In patients with
rhythm
• Rhythm: Irregular whenever a PAC
heart disease, frequent
occurs PACs may precede
• P Waves: Present; in the PAC, may paroxysmal supraventricular
have a different shape tachycardia (PSVT), A-fib, or
• PR Interval: Varies in the PAC;
otherwise normal (0.12–0.20 sec) A-flutter.
• QRS: Normal (0.06–0.10 sec)
 Supraventricular Tachycardia (SVT)
■ This arrhythmia has such a fast rate that the P waves may not be
seen.
• Rate: 150–250 bpm • Clinical Tip: SVT may be related
• Rhythm: Regular to caffeine intake, nicotine, stress,
• P Waves: Frequently buried in or anxiety in healthy adults
preceding T waves and difficult to see
• PR Interval: Usually not possible to
measure
• QRS: Normal (0.06–0.10 sec) but may
be wide if abnormally conducted
through ventricles
 Atrial Flutter (A-flutter)
■ AV node conducts impulses to the ventricles at a 2:1, 3:1, 4:1,
or greater ratio (rarely 1:1).
■ Degree of AV block may be consistent or variable.
• Rate: Atrial: 250–350 bpm; Clinical Tip
ventricular: slow or fast • The presence of A-flutter may be
• Rhythm: Usually regular but may the first indication of cardiac
be variable disease.
• P Waves: Flutter waves have a • Signs and symptoms depend on
saw-toothed appearance ventricular response rate.
• PR Interval: Variable
• QRS: Normal (0.06–0.10 sec)
 Atrial Fibrillation (A-fib)
■ Rapid, erratic electrical discharge comes from
multiple atrial ectopic foci.
■ No organized atrial contractions are detectable
• Rate: Atrial: 350 bpm or greater;
Clinical Tip: A-fib is usually a
ventricular: slow or fast
chronic arrhythmia associated
• Rhythm: Irregular
• P Waves: No true P waves;
with underlying heart disease.
chaotic atrial activity • Signs and symptoms
• PR Interval: None depend on ventricular
• QRS: Normal (0.06–0.10 sec) response rate.
 Premature Ventricular Contraction (PVC)
■ Usually PVCs result from an irritable ventricular focus.
■ PVCs may be uniform (same form) or multiform (different
forms).
• Rate: Depends on rate of underlying • Clinical Tip: Patients may
rhythm
• Rhythm: Irregular whenever a PVC
sense the occurrence of
occurs PVCs as skipped beats.
• P Waves: None associated with the Because the ventricles are
PVC only partially filled, the PVC
• PR Interval: None associated with the
PVC
frequently does not
• QRS: Wide (0.10 sec), bizarre generate a pulse.
appearance
 Premature Ventricular Contraction:
Uniform (same form) Multiform (different forms)
 PVC
Bigeminy (PVC every other beat)
Trigeminy (PVC every 3rd beat)
Quadrigeminy (PVC every 4th beat)
 Ventricular Tachycardia (VT): Monomorphic
■ QRS complexes in monomorphic VT have the same
shape and amplitude.
• Rate: 100–250 bpm • Clinical Tip: It is important to
confirm the presence or absence of
• Rhythm: Regular pulses because monomorphic VT may
• P Waves: None or not be perfusing or nonperfusing.
• Monomorphic VT will probably
associated with the QRS deteriorate into VF or unstable VT if
• PR Interval: None sustained and not treated.
• QRS: Wide (0.10 sec),
bizarre appearance
 Ventricular Fibrillation (VF)
■ Chaotic electrical activity occurs with no ventricular depolarization or contraction.
■ The amplitude and frequency of the fibrillatory activity can be used to define the
type of fibrillation as coarse, medium, or fine.

• Rate: Indeterminate • Clinical Tip: There is no

pulse or cardiac output.
• Rhythm: Chaotic
Rapid intervention is
• P Waves: None critical. The longer the
• PR Interval: None delay, the less the chance of
conversion.
• QRS: None
 Primary Causes of ST Segment Elevation

• ST segment elevation 1 mm in the limb leads and 2 mm in the

chest leads indicates an evolving acute MI until there is proof
to the contrary. Other primary causes:
◆ Early repolarization (normal variant in young adults)
◆ Pericarditis
◆ Ventricular aneurysm
◆ Pulmonary embolism
◆ Intracranial hemorrhage
 Primary Causes of ST Segment Depression

■ Myocardial ischemia
■ Left ventricular hypertrophy
■ Intraventricular conduction defects
■ Medication (e.g., digitalis)
■ Reciprocal changes in leads opposite the
area of acute injury
 Anterior Myocardial Infarction
• Clinical Tip: Anterior MI frequently involves
a large area of the myocardium and can
present with cardiogenic shock, second-degree
AV block type II, or third-degree AV block.
 Inferior Myocardial Infarction
■
ECG changes: ST segment elevation in leads II, III, and aVF
Clinical Tip: Be alert for symptomatic sinus bradycardia,
AV blocks, hypotension, and hypoperfusion.
IWMI
 L

Lateral wall myocardial infarction

• ECG changes: ST segment elevation in leads I,

aVL, V5, and V6
• Clinical Tip: Lateral MI is often associated with
anterior or inferior wall MI. Be alert for
changes that may indicate cardiogenic shock
or congestive heart failure
 Septal wall myocardial infarction
■ ECG changes: Pathological Q waves ;
ST elevation in V2, V3, V4, V5
 LBBB
■ QRS >0.10 sec • Clinical Tip: Patients
■ QRS predominantly negative may have underlying
in leads V1 and V2 heart disease, including
■ QRS predominantly positive coronary artery disease,
in V5 and V6 and often
hypertension, cardio
notched
myopathy, and
■ Absence of small, normal Q
waves in I, aVL, V5, and V6 ischemia.
■ Wide monophasic R waves
in I, aVL, V1, V5, and V6
o ST-T segment in opposite
direction to QRS complex
Complete LBBB

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 Right Bundle Branch Block
• QRS 0.10 sec • Clinical Tip: Patients
• ■ QRS normal or may have underlying
deviated to the right right ventricular
• ■ Slurred S wave in • hypertrophy, pulmonary
leads I and V6 edema,
• ■ RSR’ pattern in lead cardiomyopathy,
V1 with R’ taller than R congenital
• heart disease, or
rheumatic heart disease
Complete RBBB

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Right Ventricular Hypertrophy

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 Right Ventricular Hypertrophy

• Tall R in V1 with R >> S, or R/S ratio

>1
• Deep S waves in V4, V5 and V6
• The DD is RVH, Posterior MI, Anti-
clock wise rotation of Heart
• Associated Right Axis Deviation, RAE
• Deep T inversions in V1, V2 and V3
• Absence of Inferior MI
 Criteria and Causes of RVH
Criteria of RVH
• Tall R in V1 with R >> S, or R/S ratio > 1
• Deep S waves in V4, V5 and V6
• The DD is RVH, Posterior MI, Rotation
• Associated Right Axis Deviation, RAE
• Deep T inversion in V1, V2 and V3
Cause of RVH
• Long standing Mitral Stenosis
• Pulmonary Hypertension of any cause
• VSD or ASD with initial L to R shunt
• Congenital heart with RV over load
• Tricuspid regurgitation, Pulmonary
stenosis
Left Ventricular Hypertrophy

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 Left Ventricular Hypertrophy

• High QRS voltages in limb leads

• R in Lead I + S in Lead III > 25 mm
• S in V1 + R in V5 > 35 mm
• R in aVL > 11 mm or S V3 + R aVL > 24 ♂, >
20 ♀
• Deep symmetric T inversion in V4, V5 & V6
• QRS duration > 0.09 sec
• Associated Left Axis Deviation, LAE
• Cornell Voltage criteria, Estes point scoring
 Causes and Criteria of LVH
Causes of LVH
• Pressure overload - Systemic Hypertension, Aortic Stenosis
• Volume overload - AR or MR - dilated cardiomyopathy
• VSD - cause both right & left ventricular volume overload
• Hypertrophic cardiomyopathy – No pressure or volume
overload
Criteria of LVH
• High QRS voltages in limb leads
• R in Lead I + S in Lead III > 25 mm or S in V1 + R in V5 > 35
mm
• R in aVL > 11 mm or S V3 + R aVL > 24 ♂, > 20 ♀
• Deep symmetric T inversion in V4, V5 & V6
• QRS duration > 0.09 sec, Associated Left Axis Deviation, LAE
 AV Block
• First Degree AV Block
• Second Degree AV Block
• Third Degree AV Block
 First Degree AV Block
• Delay in the conduction through the conducting system
• Prolong P-R interval
• All P waves are followed by QRS
• Associated with : AC Rheumatic Carditis, Digitalis, Beta
Blocker, excessive vagal tone, ischemia, intrinsic disease in
the AV junction or bundle branch system.
 Second Degree AV Block
• Intermittent failure of AV conduction
• Impulse blocked by AV node
• Types:
• Mobitz type 1 (Wenckebach Phenomenon)
• Mobitz type 2
 Mobitz type 1 (Wenckebach Phenomenon)

The 3 rules of "classic AV Wenckebach"

1. Gradually increasing PR interval
2. Finally P wave not followed by QRS complex
3. Same cycle starts all over again
Mobitz type 1 (Wenckebach Phenomenon)
 •Mobitz type 2

• Fixed PR interval followed by a drop beat

•One of the branches should be completely blocked;
(most likely blocked in the right bundle)
•P waves may blocked somewhere in the AV junction, the His
bundle.
 Third Degree Heart Block

•CHB evidenced by the AV dissociation

•A junctional escape rhythm at 45 bpm.
•The PP intervals vary because of ventriculophasic sinus arrhythmia;
 Third Degree Heart Block

3rd degree AV block with a left ventricular escape rhythm,

'B' the right ventricular pacemaker rhythm is shown.