Arrhythmia

• The term “Arrhythmia” refers to any disturbance in the rate, rhythm, site of origin or conduction of the cardiac
electrical impulse.
• The only normal rhythm of the heart is a normal sinus rhythm. In this rhythm, an impulse is generated in the sinoatrial
node, which is conducted through and slowed down while passing through the atrioventricular node. It is then
conducted through the bundle of His, to the left and right bundle branches, and eventually into the Purkinje fibers. Any
deviation from this conduction pathways results in arrhythmia.
• Normal heart rate is 60-100 bpm.
 Causes of Cardiac arrhythmias
• Abnormal rhythmicity of the pacemaker
• Another part of the heart taking over as
pacemaker (sinoatrial node is natural
pacemaker of heart)
• Blocks at different points through
conduction system of the heart
• Abnormal pathways of impulse
transmission through the heart
• Spontaneous of spurious impulses in
almost any part of the heart
• Excessive exertion, strain or stress
• An imbalance of fluids, hormones, or
electrolytes in the blood
• Certain heart medications
• Changes to heart tissue cause by changes in
blood flow, damage to the heart`s electrical
system or stiffening or scarring of the heart
tissue.
 Classification
The most widely used classification of arrhythmia is based on their origin. They can be categorized as
supraventricular, junctional, ventricular

Supraventricular arrhythmia:
1. Sinus origin:
a. sinus tachycardia
b. sinus bradycardia
c. sinus arrhythmia
2. Reentrant origin:
a. PSVT
b. atrial flutter
c. atrial fibrillation
3. Premature atrial contractions

Ventricular arrhythmia:
1. Premature ventricular
contractions
2. Ventricular tachycardia
3. Ventricular fibrillation
 Tachycardia
Fast heart rate (a heart rate over 100bpm)
Some causes of tachycardia:
INCREASED BODY TEMPERATURE:
• The heart rate increases about 18 bpm for each degree of Celsius
(or 10 bpm per degree Fahrenheit)
• Beyond temperature 45.5*C heart rate may decrease Normal Sinus Rhythm (HR=75 bpm)
• Fever increases the metabolism of sinus node, which in return
increases its excitability and rate of rhythm.
STIMULATION OF HEART BY SYMPATHETIC NERVES:
• When a person passes into a state of shock or semishock  heart
rate increases up to 150-180 bpm Sinus Tachycardia (HR= 108 bpm)
• Heart failure (weakening of the myocardium  low ejection
fraction  activation of sympathetic system
• Very low blood pressure
OTHER CAUSES:
• Anemia
• Hyperthyroidism Sinus Tachycardia (HR= 158 bpm)
• Certain medication (Beta-agonists, leukotriene modifiers, ect)
• Illegal drugs (cocaine, amphetamines)
 Bradycardia
Slow heart rate (a heart rate fewer than 60 bpm) Intrinsic Causes Extrinsic Causes
Some causes of bradycardia: Sick Sinus syndrome Athletic heart

BRADYCARDIA IN ATHLETES: Conduction system disease Autonomic influences

• The athlete`s heart is larger and stronger  their heart pump a
Coronary artery disease Electrolyte disturbances
large volume output per beat  excessive amount of blood into
arterial tree  activation of parasympathetic system  Cardiomyopathy Hypothyroidism

bradycardia Infiltrative disorders Increased intracranial

pressure
VAGAL STIMULATION: Collagen vascular disease Hypothermia
• Stimulation of vagus nerves causes release of acetylcholine at the
Inflammatory processes Sepsis
vagal endings in the heart, giving a parasympathetic effect.
• Example: carotid sinus syndrome (baroreceptors in the carotid Surgical trauma Drugs
sinus region of the carotid artery walls are excessively sensitive)

Normal Sinus Rhythm (HR=75 bpm) Bradycardia (HR=38 bpm)

 An easy way to
calculate heart rate
using an EKG
 Sinus Arrhythmia

• Sinus arrhythmia characteristically presents

inspiration
with an irregular rate in which the variation in
the R-R interval is greater than 0.12 sec.
expiration

• Heart rate increases during inspiration and

decreases during expiration

• It is generated from stimulation of the vagus

nerve and changes in cardiac filling pressures
during respiration
 Premature Contractions/ Extrasystole

Definition: An extrasystole is a contraction of the heart that occur

earlier than expected in the heart’s natural rhythm.

Causes 1. Local areas of ischemia

2. Small calcified plaques
3. Toxic irritation of the A-V node, Purkinje system, or
myocardium caused by drugs, nicotine, cafeine

Types 1. Premature Atrial Contractions

2. Premature Junctional Contractions
3. Premature Ventricular Contractions
 Premature Atrial Contractions
• Premature atrial contractions are early depolarization of the atria that are triggered by the atrial myocardium
but have not originated from the sinoatrial node.
• These early depolarization initiate an untimely contraction that flows through the atrium and then down into
the ventricles, creating an early beat with a malformed P wave, through relatively normal QRS complex.
• Asymptomatic, but may cause palpitations
• Triggered by: alcohol, nicotine, anxiety, fatigue, fever, anxiety…
• Associated with: coronary or valvular heart disease, acute respiratory failure, hypoxia, pulmonary disease,
digoxin toxicity, electrolyte imbalance

• P-R interval is shortened

• Compensatory pause (the interval between
the premature contraction and the next
succeeding contraction is slightly
prolonged)
• Rhythm is irregular
• Premature P-wave with an abnormal shape
• QRS complex appears to be similar to the
underlying QRS complex
 Premature Junctional Contractions

• Early beats initiated by AV junction

• P-wave may or may not be present – if present will be inverted
• Cardiac impulse is initiated by AV node and travel backward into the atria at the same time it travel
forward into the ventricles.
• PR interval is shorter than normal
 Premature Ventricular Contractions
Missing P
wave
• P wave usually does not precede the QRS complex.
It may be seen after the QRS complex (retrograde)

QRS Complex
• Wide QRS, and bizarre in appearance.
• The QRS complex has a high voltage for the following reasons:
impulse travels in only one direction, so there is no such
neutralization effect  this cause large electrical potentials

ST segment +
T wave • ST segment and T wave are opposite in direction to the
QRS complex

RR interval RR interval
• Usually followed by a full compensatory pause that’s slightly
longer than the normally conducted R-R interval
Compensatory\ Non-compensatory
Pause

Compensatory Pause: The two sinus cycles

containing the ventricular ectopic (three P waves) are
identical to two sinus cycles without an ectopic.

Non-compensatory Pause: The two sinus cycles

containing the ventricular ectopic is shorter than the
two sinus cycles without an ectopic. A partial
compensatory pause may be only a few ms shorter
than a full one.
 Paroxysmal
tachycardia
Paroxysmal
Paroxysmal tachycardia accounts for atrial
intermittent episodes of tachycardia with Paroxysmal tachycardia
sudden onset and termination. 1. Supraventricula
r tachycardia Paroxysmal
junctional
Some irritable focus in different portions of tachycardia
the heart (atria, Purkinje system, ventricles)
can cause rapid rhythmical discharge of
impulses that spread in all directions
throughout the heart. 2. Paroxysmal ventricular
tachycardia
In most cases this is due to re-entrant circus
pathways that set up local repeated self-re-
excitation
 Paroxysmal supraventricular
tachycardia

• Usually occurs in young, otherwise

healthy people

• Recent consummation of alcohol or

coffee

• May cause weakness during paroxysm,

but only seldom does permanent harm
come from the attack
Mechanism for reentrant paroxysmal supraventricular tachycardia.
(A) A premature atrial complex (PAC) occurs and is blocked in a fast • Regular rhythm, with narrow QRS
pathway, but it can propagate down the slower pathway. (B) By the complex, with a rate 150-250 bpm
time the electrical signal reaches the end of the slow pathway, the fast
pathway has repolarized, and retrograde conduction of the wave
occurs. (C) The wave then returns down the slow pathway, setting up
a closed circuit that is self-sustaining.
Paroxysmal supraventricular tachycardia

Rate & Rhythm

- heart rate >150 bpm
- regular rhythm
P wave
- rarely visible
-partial or completely buried within or the end of preceding T wave
QRS
-usually normal\narrow (less than 0.12 sec)
-may be widened if there is a pre-existing bundle branch block
Paroxysmal ventricular tachycardia

• Short paroxysm of ventricular

tachycardia
• A series of ventricular
premature beats occurring one
after another without any
normal beats interspersed
• Occurs in patients with
ischemic damage of ventricles
• Frequently initiates ventricular
fibrillation
Atrial fibrillation

• Atrial fibrillation is the most prevalent cardiac

arrhythmia

• It is characterized by rapid and disorganized

atrial activation leading to impaired atrial
activation

• Can be defined as paroxysmal (converts to

sinus rhythm within 7 days), persistent
(converts to sinus rhythm after 7 days) and
permanent (does not convert to sinus rhythm)

• AF is associated with increased morbidity and

mortality and is a risk factor for embolic stroke
and worsening heart failure.
Atrial fibrillation (Mechanisms)

AF occurs because of complex electrical defects in the atria,

which include:
1. Rapidly firing focus (ectopic atrial foci)
2. Complex multiple reentrant circuit (occur due to
(a)reduced refractoriness, (b)slow conduction,
(c)conduction barriers.
3. Rotors (localized electrical spiral waves), are a result of
complex substrate changes leading to a stable disease
wave.

These electrical defects are dependent upon remodeling

mechanisms, which can be grouped:
4. Structural remodeling mechanisms
5. Autonomic remodeling mechanisms
6. Electrical remodeling mechanisms
 Atrial fibrillation (EKG)

Rate & Rhythm

- heart rate 125-150 bpm
- irregular rhythm
P wave
- not-visible
QRS
-usually normal\narrow (less than 0.12 sec)
* Atrial muscle mass is separated from ventricular muscle mass by fibrous tissue  they are connected only by
conducting pathway through the A-V bundle  atrial fibrillation often occurs without ventricular fibrillation
* Atria will not pump blood during fibrillation  atria become useless as primer pumps for the ventricles  blood passes
passively into the ventricles (the efficiency of ventricular pumping is decreased only 20-30%.
 Atrial Flutter

Rate & Rhythm

Typical atrial flutter involves a single reentrant
circuit with circus activation in the right atrium
around the tricuspid valve annulus. The
electrical wavefront most often propagates in a
counterclockwise direction.
- heart rate 200-350 bpm
- regular rhythm (Ratio may be 2:1, 3:1, 4:1 or vary)
P wave
- f wave (classical saw-tooth appearance)
QRS
-usually narrow\normal (less than 0.12 sec)
 Ventricular Fibrillation
Ventricular fibrillation is a life threating cardiac arrhythmia in which the coordinated contraction of the ventricular
myocardium is replaced by high-frequency, disorganized excitation, resulting in failure of the heart to pump blood.

• Ventricular fibrillation occurs due to erratic cardiac impulses within

the ventricular muscle mass.
• These impulses stimulate different portions of the ventricular
muscle in a disorganized manner.
• The stimulation occurs sequentially, first affecting one portion, then
another, and so on.
• Eventually, the impulses feed back onto themselves, continuously
re-exciting the same ventricular muscle.
• Resulting in many small portions of the ventricular muscle
contracting simultaneously.
• Meanwhile, an equal number of portions are relaxing, leading to a
lack of coordinated contraction.
• The absence of coordinated contraction prevents the heart from
completing a pumping cycle effectively.