NCM118: MEDICAL-SURGICAL NURSING 3
ARRHYTHMIA
PROF. CARLOS HANKINS
DEFINITION:
● An electrocardiogram is a machine used to measure the
electrical activity of the human heart
● It is usually the diagnostic tool of choice in order to
investigate cardiac anomalies in most patients
Causes of cardiac arrhythmias:
● Abnormal rhythmicity of the pacemaker
● Shift of the pacemaker from the sinus node to another
place of the heart
● Blocks of different points in the spread of the impulse
through the heart
● Abnormal pathways of impulse transmission through the
heart
● Spontaneous generation of spurious impulses in almost
any part of the heart.
HEART BLOCK:
Block at the level of AV node
A. First degree heart block:
➢ Every atrial depolarization is followed by conduction to
the ventricle but delay. ECG changes prolongation of
the PR interval to more than 0.22 second.
D.M.S|BSN 4-G
B. Second degree heart block
➢ some P waves conducted but other not. ECG changes
every second or third P wave conducted to the ventricles.
C. Third degree heart block (complete heart block
➢ Rate: Atrial: 60–100 bpm; ventricular: 40–60 bpm
➢ Rhythm: Usually regular, but atria and ventricles act
independently.
➢ It occurs when all atrial activity fails to conduct to the
ventricle so the Bundle of His will be responsible for
generation of impulses.
➢ Caused by: Acute myocardial infarction, calcify aortic
stenosis, cardiomyopathy, drugs (digoxin).
Block below AV node
A. block at Bundle of His
B. Block at the branches (Right or Left branch).
SINUS RHYTHM
➢ It is caused by the changes in the number of impulses
emitted from the SA node.
➢ Heart rate more than 100/min is called (tachycardia), while
less than 60/min is called (bradycardia).
➢ It is usually of two types:
1. Sinus Bradycardia
Causes:
A. Extrinsic causes: hypothermia, hypothyroidism, and
raised intracranial pressure, drugs (beta-blockers, digitalis,
and anti-arrhythmic drugs).
B. Intrinsic causes: acute ischemia, infarction of SA node.
ECG changes: Prolonged R-R interval.
2. Sinus Tachycardia
Causes:
A. acute causes: exercise, emotion, pain, fever, acute heart
failure,
B. chronic causes: pregnancy, anemia, hyperthyroidism,
excess catecholamine. ECG: short R-R interval.
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 Ectopic beat (extrasystoles, premature beat) Causes of re –entry(circus movement)
A premature contraction is contraction of heart before the time that ● Long pathway around the circle
normal contraction would have been expected. Most premature ● Decreased velocity of conduction
contraction results from ectopic foci in the heart, which emits ● Shortened refractory period of the muscle
abnormal impulses at odd times during cardiac rhythm.
The types of tachy-arrhythmias are:
Possible causes of ectopic foci are: I. Atrial tachy-arrhythmias:
1. Local area of ischemia Causes:
2. Small calcified plaques at different points in the heart, which Ischemic heart disease, Mitral valve disease, rheumatic
press against the adjacent cardiac muscle so some fibers are heart disease, hypertension, cardio-myo-pathy,
irritated. thyro-toxicosis, atrial septal defect, acute and chronic
3. Toxic irritation of the AV node, Purkinje system, or myocardium alcohol abuse, pulmonary embolism.
caused by drugs, nicotine, or caffeine. If an irritable ectopic
A. ATRIAL FIBRILLATION:
focus discharges once, the result is ectopic beat. If the ectopic
foci discharge repetitively at rate higher than that of SA node, it
produces rapid, irregular tachycardia.
1. Atrial Ectopic

ECG: normal but irregular QRS, there are no P waves but the base
line may show irregular fibrillation waves.
B. ATRIAL FLUTTER:
The ECG changes are:
● The P wave of this beat occurs too soon in the heart cycle,
● The P-R interval is shortened, indicating that the ectopic
origin of the beat is near the A-V node
● The interval between the premature and the next
succeeding contraction is slightly prolonged, which is
called (compensatory pause).
ECG: regular saw-tooth-like atrial flutters waves (F waves) between
2. Ventricular Ectopic QRST complexes; with rate about 300 beat/min., the QRS
conducted 150 if every other one was conducted.
C. ATRIAL TACHY-CARDIA:

The ECG changes:

● Premature beats that originate in an ectopic ventricular
focus usually have bizarrely shaped prolonged and high
voltage QRS complex
● The P wave is usually buried in the QRS of the
extrasystole An ectopic arial tachycardia due to increase automaticity is rare but
● The T wave has an electrical potential polarity opposite to it sometimes is manifestation of digitalis toxicity.
the QRS . Rate: 150–250 bpm
Tachy-arrhythmia: Rhythm: Regular P Waves: Normal (upright and uniform) but differ in
shape from sinus P waves
Cardiac arrhythmia is a disturbance in electrical rhythm of the heart;
this may be paroxysmal or continuous, and may cause sudden
II. Ventricular tachy-arrhythmias:
death, syncope, heart failure, palpitation, or no symptoms.
A. VENTRICULAR TACHY-CARDIA:
2 MECHANISMS FOR TACHYCARDIA:
1. Increase automaticity (increase slop angle): when the
tachycardia is sustained by repeated spontaneous
de-polarization of an ectopic focus or single cell.

It is usually a serious condition because:

● This type of tachycardia dose not occurs unless
considerable ischemic damage is present in the ventricles
● Ventricular tachycardia frequently initiates the lethal
condition of ventricular fibrillation
● Cardiac output is decreased.
● The ECG changes include: a series of ventricular
premature beats occurring one after another without any
2. Re-entry: when the tachycardia is initiated by an ectopic normal beat interspersed so QRS morphology is regular,
beat but sustained by a closed loop or re-entry circuit. the rate is between (140-220/min).
Most tachy-arrhythmias are due to re-entry.

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 B. VENTRICULAR FIBRILLATION Class III
Mechanism
Class III drugs prolong action potential duration and effective
refractory period. These drugs act by interfering with outward K
currents or slow inward Na currents
Major drug:
● Amiodarone (Cordarone) is structurally related to
thyroxine. It increases refractoriness, and it also depresses
The effects of ventricular fibrillation: sinus node automaticity and slows conduction.
● The fibrillating ventricles, like the fibrillating atria, look like
Class IV
a quivering "bag of worms".
● The fibrillating ventricles cannot pump blood effectively Mechanism:
and circulation of the blood stops. ● Class IV drugs selectively block L-type calcium channels.
● Therefore, in the absence of emergency treatment, ● These drugs prolong nodal conduction and effective
ventricular fibrillation that lasts more than a few minutes is refractory period and have pre­dominate actions in nodal
fatal. tissues
● The most common cause of sudden death in patients with
myocardial infarction is ventricular fibrillation. Major drug:
● The ventricular fibrillation can often be stopped and ● Verapamil (Calan, Isoptin) is a phenylalkylamine that
converted to normal sinus rhythm by means of electrical blocks both activated and inactivated slow cal­cium
shock. channels.
● The ECG changes: it shows undulating waves of varying Other Antiarrhythmic drugs
frequency and amplitude. ● Digoxin: can control ventricular response in atrial flutter or
ANTI-ARRHYTHMIC DRUGS fibrillation.
Classification of antiarrhythmic drugs (Vaughan-Williams ● Digoxin toxicity
classification): ○ Extracardiac manifestations
■ anorexia, nausea, vomiting
GOAL OF THERAPY
■ Diarrhea
1. To restore normal pacemaker activity
○ cardiac manifestations
2. Modify impaired conduction that leads to arrhythmias.
■ Bradycardia
Conduction velocity depends on the size of the inward
■ Multiple ventricular ectopics
current during upstroke of the action potential (↑inward
■ Ventricular bigeminy
current→↑. The evocity of conductance)
Therapeutic effects are achieved by:
Treatment of Brady-arrhythmias:
1. sodium- or calcium-channel blockade
2. prolongation of effective refractory period (it is slightly 1. Atropine
longer than absolute refratory period) ● Atropine blocks the effects of acetylcholine. It elevates
3. blockade of sympathetic effects on the heart. Many sinus rate and AV nodal and sinoatrial (SA) conduction
anti-arrhythmic drugs affect depolarized tissue (ectopic velocity, and it decreases refractory period.
foci) to a greater extent than they affect nor­mally polarized ● Atropine is used to treat bradyarrhythmias that accompany
tissue. MI.
Treatment of tachy-arrhythmias: 2. Isoproterenol [Isuprel]
● Isoproterenol stimulates β-adrenoceptors and increases
Class I
heart rate and contractility.
Major drugs
● Isoproterenol is used to maintain adequate heart rate and
● Quinidine
cardiac output in patients with AV block.
● Disopyramide
● Lidocaine [Xylocaine]
● Flecainide
● Propafenone
Class II
Mechanism
Class II drugs are β-adrenoceptor antagonists, including
propranolol, which act by reducing sympathetic stimulation. They
inhibit phase 4 depolarization, depress automaticity; prolong AV
conduction, and decrease heart rate (except for agents that have
sympathomimetic activity) and contractility.

Major Drugs:
● Propranolol [Inderal],
● Atenolol,
● Metoprolol
● Bisoprolol
● Sotalol