When the heart rate , rhythm, conduction or contour of any of the individual wave is

abnormal the disorder is called arrhythmia.

Development of arrhythmia is one of the most common complication in patients with acute
myocardial infection . Nearly half of the deaths from myocardial infarction are due to
arrhythmia. These death can be prevented by recognizing and treating arrhythmias at an early
stage. The letha arrhythmias seldom occur abruptly ; instead they are almost always precede
by less severe( warning) arrhythmias. The nurse in ICCU , should therefore , be familiar with
the identification of such arrhythmias.
How the interpret arrhythmias from ECG:
1. Rate:
I. Atrial rate: since the P wave is indicative of atrial activity , identify the P wave count
the number of small squares between two consecutive P waves and divided 1500 by
this number. This will give the atrial rate.
II. Ventricular rate: couat the number of small squares between the R waves of two
consecutive QRS complexes and divided 1500 by this number. This will give the
ventricular rate. Normally atrial and ventricular rates are identical.
2. Rhythm
I. Atrial rhythm: measure the distance between the two consecutive P waves ( P-P
interval) . if the distance between all the P wave is the same, the atrial rhythm is
regular.
II. Ventricular rhythm: Normally all the R waves should occur at regular intervals.
When there is a difference of more than 0.12 second ( 3 small squares) in RR
intervals the rhythm is said to be irregular.
3. Conduction:
I. P_R interval: count the number of small squares from the beginning of P wave to the
beginning of QRS complex. Multiply this number by 0.004 second. Normally this
interval should be between 0.10 and 0.20 second. Prolongation of P-R interval
indicates a defeat a conduction system between atria and ventricles( first degree AV
block).
II. QRS duration: count the number of small squares from the beginning of Q wave to
the beginning of S-T segment and multiply by 0.04 second. If the duration is more
than 0.12 second, it indicates a bundle branch block.
4. configuration and location:
I. P wave: look at all the P waves and find out whether these are upright or inverted ,
whether P appears regularly before each QRS complex or whether it is necessary to T
wave . look for any absence of P waves.
II. QRS complexes: are these of normal shape or notched or M shaped? Examine the Q
wave and S waves. Are these larger than normal.
III. S-T segment: normally , it is a flat line. If the ST segment is elevated or segment or
depressed more than 1mm from the base line. It indicates myocardial ischaemia or
injury . this is one of the earliest signs of myocardial infarction.
IV. T wave: each QRS complex is followed by a T wave . normally all T waves should be
of the same size and shape and point in the same direction as the QRS complex.
Pathophysiology of ECG changes after MI:
The main changes that are noticed in the ECG after myocardial infarction are S-T elevation /
depression , T inversion and appearance of Q waves. These changes due to pathological
alteration taking place in the myocardium during the first few hours and days of myocardial
infarction.
Inverted T waves represent myocardial ischaemia.
Elevation/ depression of the S-T segment represents myocardial injury
Deep and wide Q waves represent myocardial necrosis. Q waves may be considered
abnormally if it is more than 0.04 second wide and greater in depth than 1/3 of the height of
R waves.
I- normal ECG tracing
II- hours after infarction S-T segment becomes elevated
III- hours to days after infarction , T wave inverts and Q wave appears
IV- days to weeks infarction , Q wave deepens , ST and T waves return towards normal
V- weeks to months later, T wave becomes upright again, but the Q wave persists a sign of
old infarction.
Cause of arrhythmia:
One or more of the following factors may give rise to arrhythmia.
Direct damage to portion of conduction system or myocardium
Irritation or inflammation of the conduction system
Electrical inability of the myocardium
Release of toxic substances from damaged myocardium. E.g- enzyme
Distension of the heart chambers
Stimulation of the autonomic nervous system ( sympathetic or parasympathetic nerves)
Blood gas abnormalities
Increased or decreased level of electrolyte level in the blood e.g. serum potassium
Over dose of a cardiac drug e.g. digoxin
Classification arrhythmia( according to prognosis)
1. minor arrhythmias ( arrhythmias that usually require no treatment)
Sinus arrhythmia
Sinus tachycardia
Premature atrial contraction
First degree A.V block
Sino- atrial block
2. Major arrhythmia( arrhythmias that require immediate treatment to prevent the
patient developing lethal arrhythmias)
Sinus bradycardia
Atrial tachycardia
Atrial flutter
Atrial fibrillation
Paroxysmal junctional tachycardia
Second degree A.V block ( Mobitz type II)
Second degree A.V block ( Mobitz type II)
Third degree A.V block ( complete heart block)
Premature ventricular contractions ( PVC)
3. Lethal arrhythmias ( arrhythmias that require immediate resuscitative measures)
Ventricular tachycardia
Ventricular fibrillation
Ventricular asystole

1. Rate : 60 – 100 beats per- minute

2. Rhythm: P-P interval and R-R interval are constant
3. Conduction: P-R interval and QRS duration are normal and constant
4. Configuration and location:
P wave is normal and upright
P wave precedes each QRS complex
QRS complex is regular , narrow and normal in shape
S-T segment is normal
T wave is normal
5. Clinical significance: This is a normal electrocardiogram
6. Treatment: since it is normal rhythm, no treatment is indicated.
 Figure Sinus Tachycardia

Characteristics: Heart rate is over 100 per minute with normal PQRS waves

1. Rate: Over 100 beats per minute

2. Rhythm: Normal
3. Conduction: Normal
4. Configuration and location: All waves are fairly normal
P waves are sometimes buried in the preceding T waves and are difficult to recognize when
the heart rate is very rapid.
5. Causes: Pain and anxiety
Fever
Нурохіа
Hyperthyroidism
Congestive heart failure
Pericarditis
Hypotension and shock
latrogenic, e.g. after use of atropine, epinephrine, nor- epinephrine
etc.
6. Clinical significance:
If the heart rate is over 120 to 140 per minute, cardiac output may te
significantly reduced because of the insufficient time during diastole for the ventricles to fill
completely with blood. This causes the blood pressure to fall, sometimes to dangerously low
levels. Consequently, body tissues suffer from lack of oxygen. Very rapid heart rates further
damage the myocardium causing is- chaemia, heart failure and even shock.
7. Treatment:
Treat the underlying cause of tachycardia (pain, anxiety, fever etc) If a drug overdose is
suspected, adjust the dose of the drug Notify the doctor and follow the medical orders.
Characteristics: Heart rate is less than 60 per minute with normal PQRST waves

1. Rate: Less than 60 beats per minute

2. Rhythm: Normal
3. Conduction Normal
4. Configuration and location: All waves are usually normal
5. Causes: Atheletes
Vagal stimulation (Parasympathetic)
Raised intracranial pressure
Hypothermia
Myxoedema
Obstructive jaundice
Iatrogenic, c.g. digitalis
6. Clinical significance: Bradycardia cause a fall in blood pressure due to decreased
cardiac output. Consequently, the body tissues will suffer from lack of oxygen. There is a
possibility of an ectopic focus assuming pacemaker function, thus increasing the risk of
premature ventricular contractions.
7. Treatment: a. Treatment is indicated if one or more of the following signs are
present:
Systolic blood pressure 80 90 mm Hg or less
Weak or absent pulse
Pale, cold and clammy skin
Confusion or mental cloudiness
Premature ventricular contractions

b. Drug therapy:
The drugs used to increase the heart rate are: Atropine 0.6 to 1.2 mg given as 1.V bolus
Isoproterenol (isoprenaline) is given as I.V. infusion (2 ng in in 500 ml of 5% dextrose)

Characteristics: Figure Sinus Arrhythmia

1. Rate: R-R intervals vary hut PQRST waves are normel
2. Rhythm: Normal
Irregular, the heart rate increases during inspiration, and de
creases during expiration
3. Conduction: Normal
4. Configuration and location: All waves are usually normal
5. Mechanism: Norimal breathing causes the heart rate to increase during in-
spiration and decrease during expiration. This change is brought. about by fluctuations in the
parasympathetic activity on S.A node during respiration.
6. Clinical significance: Sinus arrhythmia is a normal phenomena, and generally occurs in
adolescents and young adults.
7. Treatment: No treatment is required. However, patients should be watched for
premature atrial contractions and other atrial arrhythmias.

Figure Premature Atrial Contraction (PAC)

Characteristics: K-R intervals vary with a compensatory pause after PAC
1. Rate: Vanes
Irregular, R-R interval of premature beat is shorter than normal.
2. Rhythm: The R-R interval that follows a PAC may be normal or
prolonged (compensatory pause)
3. Conduction P-R interval varies from 0.12 to 0.20 second depending upon the
relation berween the location of pacemaker site to A.V.junction.
4. Configuration and location: R wave may have abnormal configuration , i.e flat, slurred,
notched, inverted or wide, QRS complex is abnormal.
5. Causes: notched, inverted or wide. QRS complex is normal. PAC can be
a normal phenomena or it may be due to damage to atrial wall, hypoxia, congestive heart
fallure, digitalis overdose, and low serum potassium.
6. Clinical significance: PAC can appear in persons with normal heart, and are insignifi
cant. Frequent PACs indicate atrial irritability and may lead to more serious atrial
arrhythmias, such as, paroxysmal atrial tachycardia, atrial flutter, and atrial fibrillation.
7. Treatment: Monitor the patient continuously and watch for other
arrhythmias Inform doctor if more than 8 to 10 PACs appear per minute, and follow medical
orders.
If digitalis overdose is suspected, withhold the drug; Digoxin may be ordered if there is
congestive heart failure Intravenous potassium may be ordered, if s.potassium level is low
Oral quinidine may be ordered for frequent PACS Verapamil (Isoptin) may be given if PAC
leads to atrial tachycardia.

Figure Paroxysmal Atrial Tachycardia (PAT)

Characteristics: Heart rate is 150 to 250 per minute; P waves are difficult to recognize.
QRS complexes are of normal shape.
1. Rate: 150 to 250 per minute
2. Rhythm: Usually regular
3. Conduction: P-R interval usually constant
4. Configuration and location: P waves are sometimes buried in the precoding T waves and
are difficult to recognize
5. Causes: The etiology of this arrhythmia mayt be obvious in many cases;
some of the known causes are: Damage to the S.A. node or atria Irritability of the atrial
muscles Stimulation of the sympathetic nerves Physical and emotional stress
Нурохіа
Digitalis overdose
Congestive heart failure
6. Clinical significance: Reduced diastolic phase causes results in fall of blood pressure.
congestive heart failure and myocardial damage. reduced cardiac output and this Patient may
go into a state of even shock, or may develop
7. Treatment: The cause of PAT, if known, should be treated e.g. withhold the
digitalis if the cause is digitalis overdose.
The arrhythmia can often be abolished by Valsalva mancouver (increasing intrathoracic
pressure by forcible exhala tion against the closed glottis) or carotid sinus pressure. Drug
therapy includes IV verapamil (Isoptin), LV digitalis or propranolol. If digitalis overdose is
suspected, IV potassium chloride or dilantin sodium is the drug of choice. Rarely, in very
resistant cases, synchronized D.C. shock (elec- tive cardioversion) may be required.

Figure Atrial Flutter

Characteristics: P waves form a saw-tooth patterns; there aremore than one P waves
between two consecutive QRS complexes.
1. Rate: The atrial rate may be between 250 to 350 per minute, but the ventricular rate is
much less because of the atrio-ventricular block (2:1 or 4:1).
2. Rhythm: The rhythm is usually regular
3. Conduction: The P-R interval can not be determined; QRS complex is normal.
4. Configuration and location: No P waves are present; instead, there are flutter waves, and
these resemble (saw-tooth pattern. There are two, three, or four flutter) waves between two
consecutive QRS complexes.
5. Causes: Damage to the S.A, node or atria Increased sympathetic stimulation Hypoxia
Congestive heart failure.
6. Clinical significance: The cardine output is greatly reduced due to incomplete filling of the
ventricles because of (i) rapid heart rate which redus the dia 'olic phase of the heart, (ii)
incoordinated contractions of the atria and ventricles. Consequently, the patient may go into a
state of congestive heart failure or even shock.
7. Treatment: a. Treatment is required if any one of the following signs and
symptoms are present:
Systolic blood pressure is 80 to 90 mm Hg or less
Weak or absent pulse
Pale, cold and clammy.skin
Confusion and unconsciousness of patient
b. Drug treatment consists of digoxin and/or propranolol
c. In resistant cases, synchronized D.C. shock (elective cardiover- sion) may be
required:

Figure Atrial Fibrillation

Characteristics: No regular P waves; P waves appearing as a wavy base line.
1. Rate: Atria contract at 350 to 600 times per minute. Ventricular rate is variable
2. Rhythm: Irregular
3. Conduction: P-R interval cannot be measured
4. Configuration and location: P waves are absent and are replaced by small irregular waves
of variable amplitude and morphology, called 'f waves; QRS complexes are normal.
5. Causes: Cate
Rheumatic heart diseases (RHD), specially mitral valve diseases
Coronary artery diseases (CAD)
Cardiomyopathy
Atrial septal defect
Hypertensive heart diseases
Thyrotoxicosis
Chronic cor pulmonale
Many ectopic foci are present in the atria and give rise to im pulses for atrial contraction.
These impulses range in frequency from 350-600 per minute. Only some of these can
penetrate the A.V.node, and themfore, the ventricular response is irregular.
6. Clinical significance: Same as that of atrial flutter.
7. Treatment: Besides treating the etiological factor, the drug therapy aims chiefly at slowing
the ventricular response (without much affect ing the atrial rate). The most commonly used
drugs aro digitalis and verapamil. selected cases Elective cardioversion is required in selected
cases.

Figure Paroxysmal Junctional Tachycardia

Characteristics: Heart rate is over 150 to 220 per minute; P waves are either absent or
appear inverted.
1. Rate: 150 to 220 beats per minute
2. Rhythm: Regular.
3. Conduction: P-R intervals are shorter than normal, since the pacemaker site is in the A.V.
junction.
4. Configuration and location: P waves may be absent (may be lost in the QRS complexes);
If P waves are visible, these are often identified as inverted P waves. QRS complexes are
normal.
5. Causes: Damage to the S.A. node. Damage to the A.V. junction. Hypoxia Digitalis
overdose, Congestive heart failure, Low serum potassium, Idiopathic.

6. Clinical significance: When the ventricular rate is increased beyond 120/minute, the
cardiac output is reduced, and the effect on the patient will be same as that of paroxysmal
atrial tachycardia.
7. Treatment: Same as that of paroxysmal atrial tachycardia.