CARDIAC ARRHYTHMIAS

Cardiac arrhythmia refers to a group of

conditions that cause the heart to beat
irregular , too slowly ,or too quickly.
Arrhythmias occur when the electrical
signals that coordinate heartbeats are
not working correctly.
 NORMAL AND ABNORMAL CARDIAC CONDUCTION
AND ELECTROPHYSIOLOGY

• The heart functions via mechanical and electrical

activity. Mechanical activity refers to atrial and
ventricular contraction, the mechanism by which
blood is delivered to tissues. When deoxygenated
blood returns to the heart via venous circulation, the
blood enters the right atrium. Right atrial
contraction and right ventricular pressure changes
result in delivery of blood to the right ventricle
through the tricuspid valve.
• Right ventricular contraction pumps blood through
the pulmonic valve and through the pulmonary
arteries to the lungs, where blood becomes
oxygenated. The oxygenated blood then flows
through the pulmonary veins into the left atrium. Left
atrial contraction and left ventricle (LV) pressure
changes result in delivery of blood through the mitral
valve into the LV, contraction of which results in
pumping of blood through the aortic valve and to the
tissues of the body.
Normal sinus rhythm;

The normal cardiac pacemaker is the sinus node . During normal

sinus rhythm , an activation wavefront begins in the sinus node,
a group of cells with pacemaker activity on the upper free wall
of the right atrium. The rate of diastolic depolarisation and
hence the rate of discharge of the sinus node is increased by
sympathetic nerve stimulation, circulating catecholamines or
sympathomimetic drugs mediated by ß1-adrenoreceptors on the
cell membranes of the sinus node myocytes. Parasympathetic
(vagus) nerve stimulation exerts the opposite effect, mediated
by muscarinic cholinergic receptors.
An activation wavefront spreads across the
atrial myocardium, leading to atrial contraction
and generating the P wave on the surface
electrocardiogram . The last part of the atria
to be activated is the atrioventricular (AV)
node, the electrical and structural properties
of which result in a slow conduction velocity,
allowing atrial emptying to be completed before
ventricular contraction begins and represented
by the PR interval on the ECG.
The atria and ventricles are electrically isolated
from each other by the annulus fibrosus, the
electrically non-conductive fibrous tissue
forming the valve rings. In the normal
heart,there is just one electrical connection
between the atria and ventricles, the bundle
of His, which conveys the activation wavefront
from the AV node and penetrates the annulus
fibrosus before dividing into the right and left
bundle branches.
The bundle branches ramify into a sub-endocardial
network of Purkinje fibres, which convey the activation
wavefront rapidly across the ventricles ensuring near-
simultaneous contraction of the ventricular
myocardium, and are represented by the narrow QRS
complex of the ECG. Finally, the activation wavefront
spreads from endocardium to epicardium. A wave of
repolarisation then spreads across the ventricles
resulting in the T wave. The QT interval on the ECG,
therefore, represents
the duration of ventricular depolarisation and
repolarisation.
Pathogensis of arrhythmia:

Arrhythmias can arise from problems in the;

Sinus node
Atrial cells
AV junction
Ventricular cells
Arrhythmias caused by two main mechanism:
-Automaticity
-Re-entry
 *Abnormal automaticity;

Automaticity is another term for pacemaker activity, a

characteristic possessed by all cells of the specialised
cardiac conduction system during health and, potentially, by
other cardiac myocytes during certain disease states.
Abnormal initiation of electrical impulses occurs due to
abnormal automaticity. A decrease in sinus node
automaticity results in a reduced rate of impulse generation
and a slow heart rate (sinus bradycardia). Conversely, an
increase in sinus node automaticity results in an increased
rate of impulse generation and a rapid heart rate (sinus
tachycardia).
• If other cardiac fibers become abnormally
automatic, such that the rate of
spontaneous impulse initiation exceeds that
of the sinus node, or premature impulses
are generated, other tachyarrhythmias
may occur. Many cardiac fibers possess the
capability for automaticity, including atrial
tissue, the AV node, the Purkinje fibers,
and ventricular muscle.
*Re-entry;
Many clinically important arrhythmias
are due to re-entry, in which an
activation wavefront rotates
continuously around a circuit. Re-entry
depends upon a trigger in the form of a
premature beat, and a substrate, that
is, the re-entry circuit itself.
Classification of arrhythmias:
All cardiac rhythms can be described
by a phrase which includes terms that
relate to rate (tachycardia,
bradycardia) ,origin (atrial,sinus,
nodal,ventricular) ,and pattern
(ectopic,flutter,fibrillation,paroxysmal)
• Abnormal atrial automaticity may result in premature
atrial depolarizations or may precipitate atrial
tachycardia or atrial fibrillation (AF).
• Abnormal automaticity in the ventricles may result in
precipitate ventricular tachycardia (VT) or
ventricular fibrillation (VF) or premature ventricular
complexes (PVCs)
• Video
Clinical presentation:

Arrhythmia may not cause noticeable symptoms.It

may be detected during a routine examination .
Symptoms depend on the type of arrhythmia ,as
follows:
-Tachyarrhythmia;
breathlessness,dizziness,fainting,chest pain,sudden
weakness
-Bradyarrhythmia;

angina,confusion,dizziness,tiredness
,SOB, profuse sweating
Risk factors and complications:
The following may increase the risk of arrhythmia;
-Older age >65
-Inherited genetic anomalies
-Underlying heart problem(HF,HTN)
-Thyroid disorder
-Uncontrolled DM and obesity
-Electrolyte imbalance
-Heavy and regular alcohol consumption
While some of these are unavoidable, a
person can take a few steps to reduce
their risk of arrhythmia.These include
staying active(AHA recommend at least
150 minutes of moderately intense
exercise every week),avoiding the
regular use of alcohol and limiting
caffeine intake.
Some people may not experience active
symptoms due to arrhythmia.
However,treatment is still essential for
preventing further complications,which
may include stroke and heart failure.
Stroke; Atrial fibrillation means that
the heart is not pumping effectively.
This cause blood to collect in pools and
form clots
If a clot dislodges,it may travel to a brain
artery causing a potentially fatal blockage,
or stroke.Stroke can cause brain damage
and require emergency treatment.
Heart failure; Prolonged tachycardia or
bradycardia can result in HF.When the
heart is failing ,it cannot pump enough
blood to the body .Treatment can usually
help improve this.
Diagnosis:
A detailed history should be obtained,
covering all of the symptoms listed above.
A characteristic of cardiac arrhythmias
is their random onset. Other key
features of the history include:
• A history of cardiac disease
• Other diagnosed medical conditions
A full drug history, including over-the-
counter medicines and recreational
drugs including alcohol.
A family history of heart disease and of
sudden unexpected death.
Physical examination is essential but
often normal between episodes of
arrhythmia
Mandatory investigation includes a 12-
lead ECG and an echocardiogram to
detect structural heart disease. Other
investigations for structural and
ischaemic heart disease may be
indicated at this stage with the aim of
detecting any underlying structural
heart disease.
If the history does not include sinister
features such as syncope or a family history
of sudden unexpected death at a young age,
and the resting 12-lead ECG and
echocardiogram are normal, then the patient
can be reassured that they are extremely
unlikely to have a serious heart rhythm
disturbance. The extent of further
investigation will be dictated by how
troublesome the symptoms are.
Treatment:
The aim of treatment is to restore
circulation and to prevent further
episodes of poor circulation or distress.
Treatment of arrhythmias is often
disappointing with significant adverse
effects and therefore guidelines for
treatment often emphasize safety above
efficacy.
 Atrial Fibrillation
• multiple reentrant wavelets operating
simultaneously within the atria. AF is
associated with chaotic, disorganized atrial
electrical activity, resulting in no completed
atrial depolarizations and therefore no atrial
contraction. Characterized by the abscence
of P wave on ECG.
-- Atrial fibrillation; is the most common
sustained arrhythmia, affecting about 1%
of the population. AF is rare before the
age of 50. AF is characterized by
extremely rapid and uncoordinated
electrical activity in the atria and
variable conduction through the AV node,
resulting in irregular and usually rapid
ventricular contraction
It Increased risk of thomboembolic
stroke( All patients presenting with AF
or atrial flutter should undergo
assessment of their risk of stroke),and
exacerbate heart failure through its
direct haemodynamic effect and by
causing tachycardia induced
cardiomyopathy
• Symptoms :Approximately 20% to 30% of
patients with AF remain asymptomatic.
Symptoms include fatigue, palpitations,
dizziness, light- headedness, dyspnea, chest
pain (if underlying CAD is present), near-
syncope, and syncope. Patients commonly
complain of palpitations; often the complaint
is “I can feel my heart beating fast” or “I can
feel my heart fluttering” or “It feels like my
heart is going to beat out of my chest”
AF may be classified as:
-Paroxysmal: self-limiting episodes of AF lasting no
more
than 7 days
-Persistent: AF lasting more than 7 days or requiring
cardioversion
-Longstanding persistent: continuous AF for more
than 1 year
-Permanent: where a decision has been made not to
attempt cure of persistent AF.
 Management of Atrial Fibrillation
• Treatment Desired Outcomes :
• (a) ventricular rate control;
• (b) termination of AF and restoration of sinus
rhythm (commonly referred to as “cardioversion” or
“conversion to sinus rhythm”);
• (c) maintenance of sinus rhythm, or reduction in the
frequency of episodes of paroxysmal AF; and/or
• (d) prevention of stroke and systemic embolism.
These goals of therapy do not necessarily apply to all
patients; the specific goal(s) that apply depend on
the patient’s AF classification
 Emergency management; AF associated with unstable
angina, heart failure or hypotension requires emergency
treatment. In most cases, the treatment of choice is d.c.
cardioversion.
Concerns about thromboembolism as the heart returns to sinus
rhythm are valid but should not delay emergency
treatment. Immediate d.c. cardioversion is appropriate
when the onset of AF is clearly identified as within 48 h
of presentation or when the patient is already taking warfarin
and has had a therapeutic INR for at least 4 weeks. If
facilities permit, a trans-oesophageal echocardiogram may be
performed in patients not already on warfarin in order to
exclude intracardiac thrombus.
Anticoagulant therapy should be
continued for at least 3 months
following cardioversion. If d.c.
cardioversion is deemed inappropriate,
rapid ventricular rate control may be
achieved with intravenous ß-
blockers,verapamil or digoxin.
Long-term management of AF;
• Ventricular rate control; The mainstay of a ventricular
rate control strategy is the use of drugs which prolong
the AV nodal refractory period, thus reducing the
ventricular rate. Digoxin may control the ventricular
rate at rest but is less successful at controlling the
rate during exertion. ß-Blockers or calcium channel
blockers (verapamil or diltiazem) are generally
effective both at rest and on exertion, although a
combination of these drugs is occasionally necessary
• digoxin use be reserved for control of
ventricular response rate in AF in patients
with impaired left ventricular function or HF
or for use as an add-on therapy when
treatment with a β-blocker or calcium-
channel blocker provides inadequate rate
control.
If treatment is required on symptomatic
grounds, ß-blockers or verapamil are first
line therapy. Catheter ablation of the sinus
node has been performed in highly
symptomatic drug-resistant inappropriate
sinus tachycardia but with limited success
and risks including symptomatic sinus
bradycardia and phrenic nerve palsy.
• Rhythm control; Rhythm control can be considered
in terms of either restoration or maintenance of
sinus rhythm. The most rapid and effective means of
restoring sinus rhythm is d.c. cardioversion. Where
AF is of short duration, well Tolerated and not
associated with structural heart disease, class IC
antiarrhythmic drugs such as flecainide and class III
drugs such as amiodarone may be used intravenously
in order to achieve chemical cardioversion. Stroke
risk should be managed in the same way as described
for the emergency management of AF.
• When the onset of AF is less than 48 hours,
the likelihood of atrial clot formation is low.
However,when the duration of AF is greater
than 48 hours, or if duration is unknown, then
warfarin should be given for 3 weeks before
cardioversion at doses providing an INR
between 2 and 3.
Maintenance of sinus rhythm
No structural
heart disease Structural heart disease

Dofetilide CAD HF
Dronedaron Catheter
e ablation
propafenon
e sotalol
Amiodarone
flecainide Dofetilide
Dronedaro
Catheter dofetilide
ablation
ne
Sotalol
amiodarone
amiodarone
 Prevention of Stroke and Systemic
Embolism
In general, most patients require oral
anticoagulation; however, in patients
with nonvalvular AF and a CHA2DS2-
VASc score of 0, anticoagulation is not
recommended.
 CHADS-VASC SCORE
• Congestive heart failure 1 point
• Hypertension 1 point
• Age 75 years or more 2 points
• Diabetes mellitus 1 point
• History of stroke,TIAor thromboembolism
2 points
• Vascular disease (prior MI, PAD or aortic plaque)
1 point
• Age 65–74 years 1 point
• Female sex 1 point
• Maximum score 9 points
Antithrombotic is not recommended in 0 and 1 score .
2 or more score require oral anticoagulation.
--Atrial flutter; is a right atrial
tachycardia with a re-entry circuit
around the tricuspid valve annulus.It
confers a risk of thromboembolism
similar to that of AF and this risk
should be managed in the same way
Emergency management of atrial flutter is
dictated by the clinical presentation but may
include d.c. cardioversion or ventricular rate
control with drugs which increase the
refractory period of the AV node such as ß-
blockers, verapamil, diltiazem or digoxin. ß-
Blockers, verapamil and digoxin may be given
intravenously. Catheter ablation of atrial flutter
is highly effective and safe and is increasingly
used in preference to long-term drug treatment.
Outcome Evaluation
• Monitor the patient to determine whether the goal of ventricular
rate control is met. A target heart rate less than 80 beats/min is
recommended for symptomatic patients and those with HFrEF. A
target heart rate of less than 110 beats/min may be reasonable for
patients who remain asymptomatic and have preserved LV systolic
function.
• Monitor ECG to assess continued presence of AF and determine
whether conversion to sinus rhythm has occurred.
• In patients receiving warfarin, monitor INR approximately monthly
to make sure it is therapeutic (target: 2.5; range: 2.0–3.0).
• Monitor for adverse effects of specific drug therapy. Monitor
patients receiving oral anticoagulation for signs and symptoms of
bruising or bleeding.
 CASE
• J.K. a 66-year-old man, His medical history includes type2
diabetes mellitus and systolic HF for the last 5 years,
hypertension, and gout presents with complaints of dyspnea on
exertion (DOE) and palpitations for the last 2 weeks. He
experienced palpitations of shorter duration three times in the
last year, but these were not associated with DOE. On physical
examination, he is found to have rales at both bases. Cardiac
examination reveal san irregularly irregular rhythm . His jugular
veins are distended 4 cm, but no organomegaly is found. His
extremities have 1+ pitting edema. The ECG shows AF , and the
chest radiograph is compatible with mild HF. A cardiac
echocardiogram reveals the atrial size to be less than 5 cm
(normal) and a left ventricular ejection fraction of 30%.
• What clinical findings demonstrated by
J.K. are typically associated with AF?
What are the likely consequences of his
AF? What is the apprioprate rate
control agents?
• Chest palpitation
• HF and Stroke
 What is the apprioprate rate control
agents?
• J.K. has signs of HF, so digoxin is a reasonable
choice. IV verapamil and β-blockers may
worsen the signs and symptoms of HF, and the
β-blockers may mask signs of hypoglycemia in
J.K. The goal of rate control should be a
resting heart rate between 60 and 80
beats/minute and an exercising heart rate
between 90 and 115 beats/minute.
• After loading of digoxin, J.K.’s heart rate is still
120beats/minute and he continues to experience
palpitations. His blood pressure is 100/60 mm Hg, and
his symptoms of heart failure are improving, but he
still complains of mild shortness of breath. The
decision is made to cardiovert J.K. back to normal
sinus rhythm. Is J.K. a good candidate for arhythm
control strategy and if so,why?What is the likelihood
that J.K. will be successfully converted to normal
sinus rhythm?
• rhythm control is adequate rate control, when heart
rate cannot be adequately controlled with currently
available treatments , or if patients cannot tolerate
the adverse effects of rate-controlling medications.
J.K.’s heart rate is not adequately controlled with
digoxin. An oral β-blocker or nondihydropyridine
calcium-channel blocker could also be used to control
his heart rate; however, his blood pressure is likely
too low to allow the use of these agents .
Therefore,pursuit of a rhythm control strategy is
warranted.
• J.K. is discharged after successful DC
conversion. However, when he returns
for a follow- up visit 2 weeks later, he is
found to be in AF again. He again
reports frequent palpitations . His
physician wouldlike to initiate an
antiarrhythmic drug to maintain normal
sinus rhythm. Which agent(s) would be
the best option for this patient?
• The only available options for J.K. would
be either dofetilide or amiodarone,both
of which have been proven safe in
patients with HF.
Any questions?
 Assignment

• Anticoagulant strategy for J.K.?

• What is the difference between atrial
fibrillation and atrial flutter?
• Brief note about new oral anticoagulants
; name, mechanism of action ,dose?