Dysrrhythmia, major arrhythmias and management, bascs of ECG.

PRASANTH.K
POST GRADUATION IN CARDIOTHORACIC NURSING,
NARAYANA HRUDAYALAYA HOSPITAL AND COLLEGE OF
NURSING
BANGALURU
12/6/2013

1

PHYSIOLOGY BEHINED
THE ECG

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PRASANTH.K, CARDIOTHORACIC NURSING,
NARAYANA HRUDAYALAYA

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Limb electrodes
1. Augmented limb leads/unipolar leads
2. Bipolar leads
Chest leads / precordial leads

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See chest leads

V2
V3
V6
V5
V4

V1

Lead 1

aVR

aVL

Lead 2

RL(-)
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Lead 3

aVF

Show lead
placement
from
9
beginning

Mid
clavicular
line
V3- mid way between V2
and V4

V1 fourth intercostal
space at right sternal
margin
Anterior
axillary
line

V4 fifth intercostal space
at mid clavicular line

Mid
axillary
line
V2 fourth intercostal
space left sternal
margin

V6 mid axillary line
horizontal level of V4 and
V5

V5 anterior axillary line at

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NARAYANA HRUDAYALAYA horizontal level of lead 4

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ECG waves …

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ECG GRAPH PAPER

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paper

.1 mv

Voltage

.5 mv

.04 seconds

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Time

.20 seconds


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THE DIFFERENT PARTS OF THE ECG
ECG machines run at a standard rate of 25mm/s
5mm = 0.2 seconds
There are 5 squares / seconds = 300/mnt

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Intervals show timing of cardiac cycle
–
–
–
–

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P-P = one cardiac cycle
P-Q = time for atrial depolarization
Q-T = time for ventricular depolarization
T-P = time for relaxation


16

SEE THE TIME INTERVALS
R
ST
segment

PR
segment

T

P

U
Q
S

.12 - .20
sec

<.10
sec

.35 - .45
sec

QT
PR
QRS
interval
interval width

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P -1st wave of ECG
Due to atrial contraction

 Not >2-3 mm in height

 Not >0.11 sec in duration
 Shape – gently rounded

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Abnormalities of P wave
 Inverted: ectopic atrial or A-V junctional rhythm.

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Increased amplitude: atrial hypertrophy
or dilatation

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Absence of P wave:A-V junctional
rhythm & SA block or atrial fibrilation
.

• It is an atrial fibrilation here we cannote
identify any P waves.

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QRS– Complex- The ventricular mass is large so
there is a large deflection of the ECG when ventricles
are depolarized

 Duration - 0.05 to 0.1 sec

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Abnormalities of QRS Complex
 Duration :- More than 0.12 sec – abnormal intra
ventricular conduction

In this strip a normal QRS complex is followed by and
abnormal QRS complex ,that is widened .
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Amplitude :- Low – diffuse coronary
disease, cardiac failure, pericardial
effusion.

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Amplitude :- High – Left or right
Ventricular Hypertrophy.

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ST segment :-. ST” ELEVATION
 Acute / post myocardial infarction
 Prinzmetal’s angina.
 Hyperkalemia.

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A rhythm with ST elevation

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T- Wave
The return of the
ventricular mass to its resting
electrical state (repolarization )
Recovery period of ventricles.

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ABNORMALITIES
Inversion: myocardial ischemia

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Notching: Pericarditis

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Unusually tall T waves: Acute Myocardial
Infarction ,hyperkalemia, myocardial ischemia.

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U wave - In some ECGs an extra wave
can be seen on the end of the T wave.
Usually not seen unless patients serum
potassium level is low.

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NORMAL RHYTHM

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CALCULATION OF HEART RATE FROM
AN ECG STRIP

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The 1500 Method

• Count the number of small boxes between
two R waves and divide this number into
1500 to obtain the HR/min.

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‹#›

SINUS NODE DYSRHYTHMIAS

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SINUS BRADYCARDIA.
• Sinus bradycardia
• Relative bradycardia

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CAUSES
• Lower metabolic needs
eg, sleep, athletic training,
hypothermia, hypothyroidism
• Vagal stimulation
eg, from vomiting, suctioning,
severe pain, extreme emotions
• Medications
eg, calcium channel blockers,
amiodarone, beta-blockers
• Increased intracranial pressure.
• Myocardial infarction (MI), especially of the
inferior wall.
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• Ventricular and atrial rate: Less than 60 in the
adult
• PR interval: Consistent interval between 0.12
and 0.20 seconds.

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Sign and symptoms
Decrease in heart rate
Shortness of breath
Decreased LOC
Angina
Hypotension
ST-segment changes
Premature ventricular complexes.

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Treatment
• Treatment is directed toward increasing the
heart rate.
• If the bradycardia is from a medication such as
a beta-blocker, the medication may be with
held.
• Atropine, 0.5 to 1.0 mg given rapidly as an
intravenous (IV) bolus.
• Pace make therapy may be required.
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SINUS TACHYCARDIA

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Etiology
Acute blood loss
Anemia
Shock

Hypervolemia
Hypovolemia

Congestive heart failure
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Pain
Hypermetabolic states
Fever,
Exercise
Anxiety

Sympathomimetic medications.
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• Medicine – epinephrine, atropine,
theophilline, nifedipine , or hydralazine .

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1.Ventricular and atrial rate: Greater than 100 in
the adult
2.P wave: Normal and consistent shape; always
in front of the
QRS, but may be buried in the preceding T
wave

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Sign and symptoms
• Reduced cardiac output

• syncope and low blood pressure.
• Acute pulmonary edema.

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Treatment
• Calcium channel blockers (reduce HR and
decrease myocardial oxygen consumption)
– Nifedipine
– Nicardipine
– Verapamil

• beta-blockers
-propanolol
- Atenolol
• I/V- Adenosine
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ATRIAL DYSRHYTHMIAS

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PREMATURE ATRIAL COMPLEX.

Premature – term refers to the
incompleteness of the electrical
activity from the SA node
The P wave can form premature and
early
Some time P wave will be hidden
also.
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PAC is a single ECG
complex that occurs when an
electrical impulse starts in the atrium
before the next normal impulse of the
sinus node.

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Etiology
1. Alcohol
2. Nicotine
3. Stretched atrial myocardium (as in hypervolemia)
4. Anxiety
5. Hypokalemia (low potassium level)
6. Hypermetabolic states, or atrial ischemia, injury,
or infarction.
7. Often seen with sinus tachycardia.
8. COPD
9. CAD
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ECG characteristics
Ventricular and atrial rate: Depends on the

underlying rhythm (eg, sinus tachycardia)
Ventricular and atrial rhythm: Irregular due to

early P waves, creating a PP interval that is
shorter than the others.

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P wave: An early and different P wave may be
seen or may be hidden in the T wave
PR interval: The early P wave has a shorterthan-normal PR interval, but still between 0.12
and 0.20 seconds.

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Sign and symptoms
• PACs are common in normal hearts. The
patient may say,“My heart skipped a beat.”
• A pulse deficit may exist.

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Treatment
• If PACs are infrequent, no treatment is
necessary.
• Caffeine or sympathomimetic drugs may be
warrented.
• Treatment is directed toward the cause.

• Beta adrenergic blockers may be used to
decrease PACs.
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ATRIAL FLUTTER.
Atrial flutter occurs when the
atrium creates impulses at rate of 250 - 400
times per minute.
Here atrial rate is faster than the
AV node can conduct so not all atrial impulses
are conducted into the ventricle causing a
therapeutic block at the AV node.

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The atrial rate is
faster than the AV node can
conduct, not all atrial impulses
are conducted into the
ventricle, causing a therapeutic
block at the AV node.
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• There will be single recurring saw toothed
waves which originates from a single ectopic
focus in the right atrium.

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Etiology
•
•
•
•
•
•
•
•

CAD
HTN
Mitral valve disorders
Pulmonary embolus
Cor pulmonale
Cardiomyopathy
Hyperthyroidism
Drugs- digoxine, quinidine, epinephrine.

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7. Pulmonary disease

8. Acute moderate to heavy ingestion
of alcohol (“holiday heart”
syndrome)

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ECG characteristics
1.Atrial rate -220 - 430;
2.ventricular rate -75 – 150
(< 300).
3. QRS shape and duration:
Usually normal/ but may be
abnormal /may be absent

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4. P wave: Saw-toothed shape.
(F waves.)
5.PR interval: Multiple F

waves may make it difficult
to determine the PR

interval.
6.P: QRS ratio: 2:1, 3:1, or

4:1
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Sign and symptoms
• Chest pain
• Shortness of breath
• Low blood pressure.

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Treatment
• For unstable patient - electrical cardioversion .
• For stable patient –
Diltiazem ,verapamil
beta-blockers, or digitalis I/V - to slow the
ventricular rate.
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ATRIAL FIBRILLATION.
Atrial fibrillation causes
a rapid, disorganized ,and
uncoordinated twitching of atrial
musculature . It may start and stop
suddenly.
Atrial fibrillation may
occur for a very short time
(paroxysmal), or it may be chronic.

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Etiology
•
•
•
•
•
•

Causes are similar to atrial flutter.
Cardiomyopathy
RHD
HTN
HF
Pericarditis

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•
•
•
•
•
•
•

Thyrotoxication
CAD
Alcohol intoxication
Caffeine use
Electrolyte disturbence
Stress
Cardiac surgery

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ECG characteristics
1. Atrial rate is 350 to 650.
2. Ventricular rate - slow to rapid.
3. Ventricular and atrial rhythm: Highly irregular
4. P wave: irregular undulating waves referred as fibrillatory
waves (f waves)
5. PR interval: Cannot be measured

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Treatment
• Usually converts to sinus rhythm within 24 hours

without treatment.
• Calcium channel blocker. - ditiazem

• Beta adrenergic blockers.- metoprolol,
• Digoxin

• Cardioversion.
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• Antidysrhythmia medication- propafenone,
procainamid,amiodarone.
• HF/LV dysfunction<40% - amiodarone, DC
cardioversion.
• Trans esophageal echocardiogram
• >48 hrs – warferin-3-4 weeks before
cardioversion
4-6 hrs after cardioversion
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• Radiofrequency catheter ablation
(MAZE procedure)
cryoablation
High intensity ultrasound

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JUNCTIONAL DYSRHYTHMIAS

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JUNCTIONAL RHYTHM
Junctional or idionodal
rhythm occurs when the AV node,
instead of the sinus node, becomes
the pacemaker of the heart.
When the sinus node
slows or when the impulse cannot be
conducted through the AV node , the
AV node automatically discharges an
impulse.

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ETIOLOGY
• RHD
• IWMI
• Electrolyte imbalance
• CAD
• Drugs
Digoxin,amphetmines,caffeine,nicotine.
• Cardiomyopathy
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SA node failed
to produce
AV node start
acting as the
natural pace
maker

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ECG characteristics
1.Ventricular rate 40 to 60; atrial rate also 40
to 60
2.P wave: May be absent, after the QRS
complex, or before the QRS; may be

inverted,
3.PR interval: If P wave is in front of the

QRS, PR interval is less than 0.12 second.
4.P: QRS ratio: 1:1 or 0:1
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Sign and symptoms
• Junctional rhythm may produce signs and
symptoms of reduced cardiac output

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Treatment
The treatment is the same as for sinus
bradycardia.
 Emergency pacing may be needed.

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• Accelerated junctional rhythm and junctinal
tachycardia –digoxin toxycity
With held Digoxin

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ATRIOVENTRICULAR NODAL
REENTRY TACHYCARDIA.

AV nodal re-entry tachycardia
occurs when an impulse is
conducted to an area in the AV
node that causes the impulse to be
rerouted back into the same area
over and over again at a very fast
rate.
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Each time the impulse
is conducted through this area,
it is also conducted down into
the ventricles, causing a fast
ventricular rate.
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AV nodal reentry tachycardia. In
yellow, is evidenced the P wave that
falls after the QRS complex.
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ECG CHARACTERISTICS
1.Atrial rate - 150 to 250; ventricular rate - 75 to
250
2.QRS shape and duration: normal or abnormal
3.P wave: Usually very difficult to discern

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Sign and symptoms
 Palpitations

 Restlessness
 Chest pain
 Shortness of breath
 Pallor
 Hypotension

 Loss of consciousness.
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Treatment
• Treatment is aimed at breaking the reentry of the

impulse.
• Vagal maneuvers.
• If the vagal maneuvers are ineffective, a bolus of
adenosine, verapamil, or diltiazem.
• Cardioversion for the unstable or unresponsive patient.

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VAGALMANEUVERS
• Valsalva maneuver
The Valsalva maneuver or Valsalva manoeuvre
is performed by moderately forceful
attempted exhalation against a closed airway,
usually done by closing one's mouth and
pinching one's nose shut.

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• It works by increasing intra-thoracic pressure
and affecting baro-receptors (pressure
sensors) within the arch of the aorta. It is
carried out by asking the patient to hold their
breath and try to exhale forcibly as if straining
during a bowel movement, or by getting them
to hold their nose and blow out against it

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• Holding ones breath for a few seconds,
coughing, plunging the face into cold water,
(via the diving reflex), drinking a glass of ice
cold water, and standing on one's head.
• Carotid sinus massage, carried out by firmly
pressing the bulb at the top of one of the
carotid arteries in the neck, is effective but is
often not recommended due to risks of stroke
in those with plaque in the carotid arteries.
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VENTRICULAR DYSRHYTHMIAS

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PREMATURE VENTRICULAR
COMPLEX
(PVC) is an impulse that starts in a ventricle and
is conducted through the ventricles before the
next normal sinus impulse.

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• Normally impulses pass through both
ventricles almost simultaneously, the
depolarisation waves of the two ventricles
partially cancel each other out in the ECG.

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• However, when a PVC occurs the impulse
nearly always travels in one direction
therefore there is no neutralisation effect
which results in the high voltage QRS wave in
the electrocardiograph.

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•
•
•
•

Multifocal
Unifocal
Bigeminy
Trigeminy

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PHYSIOLOGICAL EXPLANATIONS FOR
PREMATURE VENTRICULAR
CONTRACTIONS:
• Re-entrant signaling
or
• Enhanced automaticity in some ectopic focus.

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ETIOLOGY
1.Caffeine, nicotine, or alcohol.
2. Cardiac ischemia or infarction.
3.Digitalis toxicity.
4.Hypoxia.
5.Acidosis.
6.Electrolyte imbalances, especially
hypokalemia.
7.Valve prolapse
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ECG characteristics
• (1) more frequent than 6 per minute,AV nodal reentry

tachycardia in lead II.
• (2) multifocal or polymorphic (having different shapes)

• (3) occur two in a row (pair).
• (4) Occur on the T wave have not been found to be
precursors of VT

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In a rhythm called bigeminy, every
other complex is a PVC.

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Trigeminy is a rhythm in which every
third complex is a PVC.

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Quadrigeminy is a rhythm in which
every fourth complex is a PVC.

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1.QRS -Duration is 0.12 seconds or longer;
shape is bizarre and abnormal

2.P wave: Visibility of P wave depends
3.PR interval: If the P wave is in front of the

QRS, the PR interval is less than 0.12 seconds.
4.P: QRS ratio: 0:1; 1:1

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Sign and symptoms
The patient may feel a “skipped heart beat.”
Complaints of angina and heart failure

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Treatment
• Initial treatment is aimed at correcting the
cause.
• Beta adrenergic blockers
• Lidocaine - as short-term therapy .

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VENTRICULAR TACHYCARDIA.
Three or more PVCs in a row, occurring at a rate
exceeding 100 beats per minute.

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MONOMORPHIC VT

POLYMORPHIC VT(torsades de
points)

QRS complex are same in Different shape direction
shape, size and direction
and size.

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ETIOLOGY
Causes are similar to PVC
Usually associated with coronary artery disease

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ECG CHARACTERISTICS

1.Ventricular rate - 100 to 200 beats per minute
2.QRS : Duration is 0.12 seconds or more;
bizarre, abnormal shape
3.P wave: Very difficult to detect, so atrial rate

and rhythm may be indeterminable
4.PR interval: Very irregular.

5.P: QRS ratio: Difficult to determine
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Treatment
• VT is an emergency because the patient is
usually unresponsive and pulseless.

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• Monomorphic + hemodynamicaly stable +
preserved left ventricular function –
IV procainamide
Sotalol
Amidarone
lidocaine

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• Hemodynamically unstable + poor left
ventricular function –
IV amiodarone/lidocaine
Cardioversion

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• Hemodynamically unstable + polymorphic VT
+ nomal base line QT intervl
Beta adrenergic blockers
Lidocaine
Amidarone
Procainamide
sotalol
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• Hemodynamically unstable + polymorphic VT
+ nomal base line QT intervl
Beta adrenergic blockers
Lidocaine
Amidarone
Procainamide
sotalol
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• Polymorphic VT + prolonged baseline QT
interval
IV magnesium
Isoproterenol
Phenytoin
Lidocaine
Antitachycardia pacing
cardioversion
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• VT with out pulse
Life tretening situation
CPR
Rapid defibrillation
Epinephrine.

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PAROXYSMAL SUPRAVENTRICULAR
TACHYCARDIA.
• PSVT originates in an ectopic focus anywhere
above the bifurcation of the bundle of his.
• Reentrant phenomenon

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ETIOLOGY
•
•
•
•
•

Wolff parkinson- white (WPW)/preexcitation
Overexertion
Emotional stress
Deep inspiration
Stimulants

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•
•
•
•
•
•

Caffeine
Tobacco
RHD
Digitalis toxicity
CAD
Cor pulmonale

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TREATMENT
•
•
•
•
•
•
•
•

Vagal maneuvers – valsalva and coughing
IV adenosine(Half life – 10sec)
IV adrenergic blockers
Calcium channel blockers – diltiazem
Digoxin
Amidarone (WPW)
If not again stable – DC cardioversion
Radiofrequency catheter ablation

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VENTRICULAR FIBRILLATION.
Rapid but disorganized ventricular rhythm
Causes ineffective quivering of the ventricles.
With out any atrial activity on the ECG.

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Etiology
• Causes of ventricular fibrillation are the same
as for VT

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ECG CHARACTERISTICS
1. Ventricular rate: Greater than 300 per minute

2. Ventricular rhythm: Extremely irregular, without
specific pattern
3. QRS shape and duration: Irregular, undulating waves

without recognizable QRS complexes
4. This dysrhythmia is always characterized by the
absence of an audible heartbeat, a palpable pulse, and

respirations.
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Treatment
CPR
ACLS measures
Defibrillation

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VENTRICULAR
ASYSTOLE/COMMONLY CALLED
FLATLINE

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ETIOLOGY
• Advanced cardiac disease
• End stage HF
• Severe conduction system disturbences

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ECG CHARACTERISTICS
• Absent QRS complexes
• P waves may be apparent for a short duration

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Sign and symptoms
• There is no heartbeat, no palpable pulse, and
no respiration

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Treatment
A fatal condition.
• Cardiopulmonary resuscitation
• Transcutaneous pacing

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• A bolus of intravenous epinephrine should be
administered and repeated at 3- to 5-minute
intervals
Followed by 1-mg boluses of atropine at 3- to 5minute intervals.

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CONDUCTION ABNORMALITIES

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AV BLOCKS
AV blocks occur when the conduction of the
impulse through the AV nodal area is decreased
or stopped.

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COMMON ETIOLOGICAL
FACTORES
• Medications like digitalis, calcium channel
blockers, beta-blockers.
• Myocardial ischemia and infarction
• Valvular disorders, or myocarditis.

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AV block

1st degree

3RD degree
2nd degree

M1
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M2

157

first-degree AV block
• rarely causes any hemodynamic effect.
• First-degree heart block occurs when all the
atrial impulses are conducted through the AV
node into the ventricles at a rate slower than
normal.

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ECG characteristics
• PR interval: Greater than 0.20 seconds
• P: QRS ratio: 1:1

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SECOND-DEGREE
ATRIOVENTRICULAR BLOCK
• Type I. Second-degree,
•

type I heart block occurs when all but one

of the atrial impulses are not conducted through
the AV node into the ventricles.

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type1
• The RR interval reflects a pattern of change.
• Starting from the RR that is the longest, the
RR interval gradually shortens until there is
another long RR interval.

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• PR interval: PR interval becomes longer
with each succeeding

• ECG complex until there is a P wave not
followed by a QRS.

• The changes in the PR interval are
repeated between each “dropped” QRS.

• P: QRS ratio: 32, 43, 54, and so forth
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SECOND-DEGREE
ATRIOVENTRICULAR BLOCK,
TYPE II.
• Second-degree,type II heart block occurs when
only some of the atrial impulses are conducted
through the AV node into the ventricles.

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ECG characteristics
• PR interval: PR interval is constant for those P
waves just before QRS complexes.
• P: QRS ratio: 2:1, 3:1, 4:1, 5:1, and so forth

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THIRD-DEGREE ATRIOVENTRICULAR
BLOCK.
• No atrial impulse is conducted through the AV
node into the ventricles.
• P waves may be seen, but no QRS complex.
This is called AV dissociation.

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CHARACTERISTICS
• PR interval: Very irregular

• P: QRS ratio: More P waves than QRS
complexes

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1st degree HB

•No treatement
•Modifications
to causative
medications
•Continuous
montoring

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2nd degree HB

MORBITZ 1
SYMPTOMATIC
PATIENT/MI
Atropine
ASYMPTOMATIC
PATIENT
Close
observation with
subcutaneous
pace maker
stand by

3rd degree HB

MORBITZ 2
Temporary
transcutaneous /
transvenous
pacing

SYMPTOMATIC
PATIENT
Transcutaneous
pase maker untll
transvenous pase
maker
Permanent pace Atropine
maker
epinephrine
adenosin


172

12/6/2013


173

12/6/2013


174

Dysrrhythmia, major arrhythmias and management, bascs of ECG.

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