Transcript Ventricular Fibrillation

CARDIAC ARRHYTHMIAS
BY
MRUNMAYI JOGLEKAR
NAMRATA KAUL
Heart Physiology
Heart Physiology
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Closed system
Pressure driven
Supply
nutrients/O2
Remove
metabolites
P - atria depol.
QRS - ventricle
depol.
PR - conduction
A-V
T - ventricle
repol.
QT - duration
ventricle
repolarization
Heart Physiology
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Closed system Pressure
driven
Supply nutrients/Oxygen
Pressure driven
Remove metabolites
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Heart’s Electrical System
•The heart’s rhythm is coordinated by its
own electrical system.
• With each heartbeat, the electrical
impulse begins at the sinus (or sinoatrial,
SA) node, also called the heart’s natural
pacemaker. The SA node is a cluster of
specialized cells,located in the right
atrium. The SA node produces the
electrical impulses.
•The impulse then reaches the
atrioventricular (AV) node, which acts as
an electrical bridge allowing impulses to
travel from the atria to the ventricles.
•From the AV node, the impulse travels
through a pathway of fibers called the
HIS-Purkinje system.
•The SA node fires another impulse and
the cycle begins again.
DEFINATION
&
OCCURRENCE
OF
CARDIAC ARRHYTHMIAS
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DEFINATION of Arrhythmias :
Definitions:
- normal sinus rhythm (60-90bpm), SA node
pacemaker
- arrhythmia; any abnormality of firing rate,
regularity or
site of origin of cardiac impulse or disturbance of
conduction that alters the normal sequence of
activity of atria and ventricles
Occurrence:
- 80% of patients with acute myocardial
infarctions
- 50% of anaesthetized patients
- about 25% of patients on digitalis
MECHANISM
OF
CARDIAC ARRHYTHMIAS
Mechanisms of arrhythmias :
1. Abnormal impulse generation (abnormal automaticity)
a. automaticity of normally automatic cells (SA, AV, His)
b. generation of impulses in normally non-automatic cells
- development of phase 4 depolarization in normally
non-automatic cells
- ‘triggered activity’ due to afterdepolarizations
- early afterdepolarization
- delayed afterdepolarization
2. Abnormal impulse conduction (more common mechanism)
a. AV block – ventricle free to start own pacemaker rhythm
b. Re-entry: re-excitation around a conducting loop, which
produces tachycardia
- unidirectional conduction block
- establishment of new loop of excitation
- conduction time that outlasts refractory period
CLASSIFICATION
OF
CARDIAC ARRHYTHMIAS
Classification of arrhythmia :
1. Characteristics:
a. flutter – very rapid but regular contractions
b. tachycardia – increased rate
c. bradycardia – decreased rate
d. fibrillation – disorganized contractile
activity
2. Sites involved:
a. ventricular
b. atrial
c. sinus
d. AV node
e. Supraventricular (atrial myocardium or AV
node)
Ventricular Arrythmias
*Premature ventricular
contractions (PVCs)
*Ventricular tachycardia (V-tach)
*Ventricular fibrillation (V-fib)
Ventricular tachycardia
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Characterized by rapid ventricular rates generally around 100
to 200 beats per minute
This arrhythmia often results from triggered activity in the
context of other electrophysiological abnormalities, especially
a prolonged QT interval
Premature Ventricular
Contractions
•These are early, extra beats beginning in the lower
chambers of the heart (ventricles).
•PVCs are common,most of the time they cause no
symptoms and require no treatment.
•In some people, they can be related to stress, too much
caffeine or nicotine, or exercise.
• Sometimes, PVCs can be caused by heart disease or an
electrolyte imbalance.
Ventricular Fibrillation
The ventricles are the large lower
chamber of the heart. They are
responsible for moving blood to
the organs and tissues of the
body.
In ventricular fibrillation, the
heart’s ventricles contract in a
rapid and chaotic manner. As a
result, little or no blood is pumped
from the heart. Unless medical
help is provided immediately,
ventricular fibrillation will lead to
cardiovascular collapse and
sudden death.
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Ventricular fibrillation is an immediately life-threatening
arrhythmia in which the heart's electrical activity and associated
contraction become disordered and ineffective. It is characterized by
rapid, irregular activation of the ventricles and thereby prevents an
effective mechanical contraction. Blood pressure instantaneously
drops to zero, leading to death within minutes due to lack of cardiac
output unless successful electrical defibrillation is performed;
spontaneous conversion to sinus rhythm is rare.
During ventricular fibrillation, the ECG has no distinctive QRS
complexes but instead consists of an undulating baseline of variable
amplitude. Although the sinus node continues to function properly, P
waves cannot be discerned in the VF waveform. Ventricular
tachycardia in many cases can degenerate to ventricular fibrillation.
Causes of ventricular
fibrillation
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Inadequate blood flow to the heart due to coronary artery disease
(CAD)
Scar tissue within the heart due to previous injury to heart, such as a
heart attack (myocardial infarction)
Congestive heart failure (CHF)
Infection of the heart muscle ( myocarditis )
Shock
Electrical shock
Drowning
Dangerously low body temperature ( hypothermia )
Electrolyte imbalance (eg, very low levels of potassium or
magnesium in the blood)
Drugs that affect the electrical currents of the heart (eg, sodium or
potassium channel blockers)
Low atmospheric oxygen
Diagnosis
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Ventricular fibrillation is suspected
when a person collapses suddenly and
has no detectable pulse or heartbeat.
The diagnosis is confirmed by
electrocardiography (ECG) . ECG
records the heart’s activity by
measuring electrical currents through
the heart muscle.
Supraventricular
Arrythmias
Arrhythmias that begin above the
ventricles, such as in the upper chambers
or atria.
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Types Of Supraventricular arrythmias
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Atrial tachycardia - a rapid heart rhythm or arrhythmia that originates
in the atria.
Atrial fibrillation - a very common irregular rhythm.
Atrial flutter - an atrial arrhythmia due to one or more rapid circuits in the
atrium. Atrial flutter is usually more organized and regular than atrial
fibrillation
Premature atrial contractions (PACs) - early, extra beats that
originate in the upper chambers of the heart (atria).
Paroxysmal supraventricular tachycardia (PSVT) - a rapid
but regular rhythm that comes from the atria. PSVT begins and ends
suddenly.
Accessory pathway tachycardia (such as WolffParkinson-White syndrome) - a fast heart rhythm due to an extra
abnormal electrical pathway or connection between the atria and ventricles.
AV nodal re-entrant tachycardia (AVNRT) - a fast heart rate
due to having more than one pathway through the atrioventricular (AV) node.
Atrial flutter
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Re-entrant supraventricular arrhythmia
characterized by a rapid "sawtooth"
appearance of the ECG owing to the
presence of multiple P waves between QRS
complexes.
Atrial rates typically fall between 250 and
350 beats per minute
Treatment options for atrial flutter include
direct electrical cardioversion and catheter
ablation
Atrial fibrillation
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Complex arrhythmia characterized by
an extremely rapid atrial rate (350 to
600 beats per minute).
AF can be treated by direct
cardioversion but more frequently is
treated with antiarrhythmic and/or
anti-coagulation drug therapy
1st Degree Heart Block
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First-degree AV block, or PR prolongation, is a
disease of the electrical conduction system of the
heart in which the PR interval is lengthened beyond
0.20 seconds
• The impulse conducting from atria to ventricles through
the AV node is delayed and travels slower than normal
2nd Degree Heart Block
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Also called as ‘Woldemar Mobitz’.
This occurs when 1 or more atrial
impulses fail to conduct to ventricles.
Hence, a complete but intermittent
inhibition of pacing impulse.
ECG w/f—2/3 P waves/QRS
3rd Degree Heart Block
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Complete block of S.A node impulse,
accessory pacemakers conduct to
ventricles.
Hence, total and continuous impulse
blockage
Occurs anywhere in conduction system
ECG w/f- wide QRS.
Causes
The most common causes of first-degree heart block
are:
 An AV nodal disease,
 Myocarditis
 Acute myocardial infarction (especially acute inferior
MI)
 Electrolyte disturbances and medication.
 Drugs like calcium channel blockers, beta-blockers,
cardiac glycosides, and anything that increases
cholinergic activity such as cholinesterase inhibitors.