4. A. Cellular atrial and ventricular action potentials. Phases 04 are the rapid upstroke,
early repolarization, plateau, late repolarization, and diastole, respectively. The ionic
currents and their respective genes are shown above and below the action potentials.
The major currents that underlie the action potentials vary in atrial and ventricular
myocytes.
B. A ventricular action potential with a schematic of the ionic currents flowing during
the phases of the action potential. Potassium current (IK1) is the principal current
during phase 4 and determines the resting membrane potential of the myocyte.
5. phase 0 - Sodium current generates the upstroke of the action
potential
phase 1- activation of Ito with inactivation of the Na current
inscribes early repolarization
phase 2 - the plateau is generated by a balance of repolarizing
potassium currents and depolarizing calcium current
phase 3 repolarization - inactivation of the calcium current
with persistent activation of potassium currents
(predominantly I Kr and IKs)
phase 4 - depolarization results from the concerted action of a
number of ionic currents, including K+ currents, Ca2+
currents, electrogenic Na, K-ATPase, the Na-Ca exchanger, and
the so-called funny, or pacemaker, current (If ); however, the
relative importance of these currents remains controversial.
6. An irregular heartbeat is an arrhythmia (also called
dysrhythmia).
A normal heart rate is 50 to 100 beats per minute.
Arrhythmias and abnormal heart rates don't
necessarily occur together.
Arrhythmias can occur with a normal heart rate, or
with heart rates that are slow (called
bradyarrhythmias -- less than 50 beats per minute).
Arrhythmias can also occur with rapid heart rates
(called tachyarrhythmias -- faster than 100 beats per
minute).
Introduction to Arrhythmia
7. Cardiac arrhythmias result from abnormalities of electrical impulse
generation, conduction, or both.
Bradyarrhythmias typically arise from disturbances in impulse formation
at the level of the SA node or from disturbances in impulse propagation at
any level, including exit block from the sinus node, conduction block in the
AVN, and impaired conduction in the His-Purkinje system.
Tachyarrhythmias can be classified according to mechanism, including
enhanced automaticity (spontaneous depolarization of atrial, junctional,
or ventricular pacemakers), triggered arrhythmias (initiated by
afterdepolarizations occurring during or immediately after cardiac
repolarization, during phase 3 or 4 of the action potential), or reentry
(circus propagation of a depolarizing wavefront).
A variety of mapping and pacing maneuvers typically performed during
invasive electrophysiologic testing can often determine the underlying
mechanism of a tachyarrhythmia
MECHANISMS OF CARDIAC ARRHYTHMIAS
9. The evaluation of patients with suspected cardiac
arrhythmias is highly individualized; however, two
key featuresthe history and ECGare pivotal in
directing the diagnostic workup and therapy.
Patients with cardiac arrhythmias exhibit a wide
spectrum of clinical presentations that range from
asymptomatic ECG abnormalities to survival from
cardiac arrest.
Evaluation
10. Arrhythmias may be caused by many
different factors, including:
Coronary artery disease.
Electrolyte imbalances in your blood (such as sodium
or potassium).
Changes in your heart muscle.
Injury from a heart attack.
Healing process after heart surgery.
Irregular heart rhythms can also occur in "normal,
healthy" hearts.
What causes an arrhythmia?
12. Other symptoms
Fatigue
Dyspnea (shortness of breath)
Poor exercise tolerance
Generalized weakness
Confusion
Chest pain
In addition to these classic
symptoms, cardiac arrhythmias
may also produce several less
specific symptoms that may not
necessarily point a healthcare
provider toward considering an
arrhythmia as the cause.
Most of these other symptoms
are related to an arrhythmia
causing a relative reduction in
the ability of the heart to pump
blood to the bodys organs.
14. { Premature atrial contractions (PACs) are extra
heartbeats that start in the upper chambers of your
heart. When the premature, or early, signal tells the
heart to contract, there may not be much blood in the
heart at that moment. That means there's not much
blood to pump out
Premature atrial contractions
15. {
Premature ventricular
contractions (PVCs) are extra
heartbeats that begin in one
of the heart's two lower
pumping chambers
(ventricles). These extra
beats disrupt the regular
heart rhythm, sometimes
causing a sensation of a
fluttering or a skipped beat
in the chest
Premature ventricular
contractions(PVCs)
16. {
Atrial fibrillation happens
when abnormal electrical
impulses suddenly start
firing in the atria. These
impulses override the
heart's natural pacemaker,
which can no longer
control the rhythm of the
heart. This causes you to
have a highly irregular
pulse rate.
Atrial fibrillation
17. {
Atrial flutter is a type of
abnormal heart rhythm,
or arrhythmia. It occurs
when a short circuit in the
heart causes the upper
chambers (atria) to pump
very rapidly. Atrial flutter
is important not only
because of its symptoms
but because it can cause a
stroke that may result in
permanent disability or
death.
Atrial flutter
19. Paroxysmal supraventricular tachycardia
PSVT
A normal heartbeat begins with an electrical impulse from
the sinus node, a small area in the heart's right atrium (upper
chamber).
PSVT occurs because of a short circuit an abnormal
electrical pathway made of heart cells that allows electricity
to speed around in a circle and repeat the signal over and
over.
As a result, the chambers contract rapidly, which may impair
heart function and cause symptoms such as lightheadedness
or shortness of breath.
There are two main types: accessory path tachycardias and
AV nodal reentrant tachycardias.
20. { Example of PSVT with arrows showing the location of P-
waves in the ST segment. Note that the P-waves are
negative in lead I. Also, seen is alternation in the
amplitude of QRS amplitude best seen in C3.
PSVT
22. {
Risks possibly associated with an accessory pathway.
A. During sinus rhythm there is conduction via the atrioven AV node
and accessory pathway. The delta wave in the ECG represents the
ventricular pre-excitation caused by the conduction via the accessory
pathway. The size of the delta wave and the PR interval depend on
the location of the accessory pathway and the conduction properties
of the AV node and accessory pathway.
B. A retrograde conduction of the accessory pathway bears the risk of
an orthodromic AV re-entrant tachycardia with antegrade
conduction via the AV node and retrograde conduction via the
accessory pathway.
C. During atrial fibrillation there is a risk of a fast conduction via the
accessory pathway to the ventricles depending on the conduction
properties of the accessory pathway. As most accessory pathways
have no decremental conduction in contrast to the AV node, the
conduction via the accessory pathway can be much faster than via
the AV node. This can lead to ventricular fibrillation and sudden
cardiac death
23. { Wolff-Parkinson-White (WPW) syndrome is a relatively
common heart condition that causes the heart to beat
abnormally fast for periods of time. The cause is an extra
electrical connection in the heart. This problem with the heart
is present at birth (congenital), although symptoms may not
develop until later in life.
WolffParkinsonWhite syndrome
25. Atrioventricular reentrant
tachycardias
Atrioventricular nodal reentry tachycardia
(AVNRT) is the most common type of
supraventricular tachycardia.
People with AVNRT have episodes of an
irregularly fast heartbeat (more than 100 beats
per minute) that often start and end suddenly.
27. Associated with Fast AV nodal pathway for anterograde conduction and Slow
AV nodal pathway for retrograde conduction.
The retrograde P wave appears after the corresponding QRS
ECG
QRS -P-T complexes
P waves are visible between the QRS and T wave
29. Ventricular tachycardia (VT) is three or more consecutive beats at a
rate faster than 100 beats/min. Three or more consecutive beats at
slower rates are designated an idioventricular rhythm .
VT that terminates spontaneously within 30 s is designated non-
sustained whereas sustained VT persists >30 s or is terminated by
an active intervention, such as administration of an intravenous
medication, external cardioversion, or pacing or a shock from an
implanted cardioverter defibrillator.
30. Ventricular fibrillation
Ventricular Fibrillation is a
very fast, irregular heartbeat
that is caused by abnormal
firing of electrical signals in the
ventricles of the heart.
In ventricular fibrillation,
disorganized electrical
impulses in the hearts lower
chambers cause the heart to
stop beating (cardiac arrest).
The ventricles quiver uselessly,
instead of pumping blood.
32. Long QT syndrome is a heart rhythm disorder
caused by changes in the heart's electrical
recharging system. It doesn't affect the heart's
structure.
In long QT syndrome, the heart's electrical
system takes longer than usual to recharge
between beats. This delay is called a prolonged
QT interval.
Long QT syndrome
33. Congenital long QT syndrome. Some forms of
long QT syndrome result from altered DNA
that is passed down through families
(inherited).
Acquired long QT syndrome - this type of long
QT syndrome is usually reversible when the
underlying cause is identified and treated.
Long QT syndrome is often grouped into two
main categories, depending on the cause.
34. There are two forms of congenital long QT syndrome:
Romano-Ward syndrome (autosomal dominant
form). This more common form occurs in people
who inherit only a single gene variant from one
parent.
Jervell and Lange-Nielsen syndrome (autosomal
recessive form). Episodes of this rare form
of LQTS usually occur very early in life and are more
severe. In this syndrome, children receive the altered
gene variants from both parents. The children are
born with long QT syndrome and deafness.
Causes of congenital long QT
syndrome
35. Causes of acquired long QT syndrome
Drug-induced long QT
syndrome. Medications that can
cause LQTS include:
Certain antibiotics, such as erythromycin
(Eryc, Erythrocin, others), azithromycin
(Zithromax) and others
Antifungal drugs
Diuretics that cause an electrolyte imbalance
(low potassium, most commonly)
Anti-arrhythmics that lengthen the QT interval
Some antidepressant and antipsychotic
medications
Some anti-nausea medications
Health conditions that
can lead to acquired
long QT syndrome
include:
Hypothermia
Hypocalcemia
Hypomagnesemia
Hypokalemia
Pheochromocytoma
Stroke or intracranial bleeding
Hypothyroidism
36. Bradyarrhythmia is a type of heart arrhythmia. It
is characterized by an abnormally slow and
irregular heart beat. It may be a warning sign of
an underlying heart health issue or another
serious health problem.
Bradyarrhythmias
38. { {
Sinus node dysfunction
Sinus node dysfunction,
previously known as sick
sinus syndrome,
describes disorders related to
abnormal conduction and
propagation of electrical
impulses at the sinoatrial
node. An abnormal atrial rate
may result in the inability to
meet physiologic demands,
especially during periods of
stress or physical activity.
Heart block
A heart block is when the
electrical impulses that
control the beating of the
heart muscle are disrupted.
The most serious type of
heart block known as a
complete, or third degree,
heart block will have
symptoms, but often those
with less serious heart block
can have symptoms too.
Types of bradyarrhythmias
#3: The ECG waveforms are labeled alphabetically, beginning with the P wave, which represents atrial depolarization. The QRS complex represents ventricular depolarization, and the ST-T-U complex (ST segment, T wave, and U wave) represents ventricular repolarization. The J point is the junction between the end of the QRS complex and the beginning of the ST segment. Atrial repolarization waveforms (ST-Ta) are usually of too low in amplitude to be detected, it may become apparent in acute pericarditis, atrial infarction, and AV heart block.
#8: Cardiac arrhythmias result from abnormalities of electrical impulse generation, conduction, or both. Bradyarrhythmias typically arise from disturbances in impulse formation at the level of the SA node or from disturbances in impulse propagation at any level, including exit block from the sinus node, conduction block in the AVN, and impaired conduction in the His-Purkinje system. Tachyarrhythmias can be classified according to mechanism, including enhanced automaticity (spontaneous depolarization of atrial, junctional, or ventricular pacemakers), triggered arrhythmias (initiated by afterdepolarizations occurring during or immediately after cardiac repolarization, during phase 3 or 4 of the action potential), or reentry (circus propagation of a depolarizing wavefront). A variety of mapping and pacing maneuvers typically performed during invasive electrophysiologic testing can often determine the underlying mechanism of a tachyarrhythmia