Arrhythmias

PAROXYSMAL
SUPRAVENTRICULAR
TACHYCARDIA

Definition:
 group of arrhythmias that generally originate
as re-entrant rhythm from the AV node and
are characterized by sudden onset and abrupt
termination. AV nodal re-entrant tachycardia is
the most common type (60%) of
supraventricular tachycardia, 30% are due to
an AV reentry circuit mediated by an
accessory pathway (a short muscle bundle
directly connecting the atria and ventricles),
10% are due to atrial tachycardia

Etiology
 Re-enterant tract
 Pre excitation syndrome(WPW syndrome)
 ASD
 Acute MI

Check for triggers
 Alcohol
 Caffiene
 drugs

presentation
 Sinus tachycardia:
 accelerates and decelerates gradually.
 Supraventricular tachycardia:
 Sudden onset and termination.

ECG
 Absolutely regular rhythm at rate of 150 to 220
bpm

 P waves may or may not be seen (the presence of
P waves depends on the relationship of atrial to
ventricular depolarization). Atrial P waves may be
observed that differ from sinus P waves.

 In supraventricular tachycardia, the QRS duration
is < 0.10 second unless an intraventricular
conduction delay exists.

 Wide QRS complex (>0.12 second with initial slurring [de lta
wave ] during sinus rhythm) and short PR interval (≥ 0.12
second) is characteristic of WPWsyndrome
 ; the syndrome is caused by an accessory AV pathway
(bundle of Kent), which preexcites the ventricular muscle
earlier than would be expected if the impulse reached the
ventricles by way of the normal conduction system;
arrhythmias associated with WPW are narrow-complex
supraventricular tachycardia, atrial fibrillation, and ventricular
fibrillation; digoxin and verapamil use should be avoided
because they can lead to arrhythmia acceleration through
the accessory pathway. Radiofrequency catheter ablation of
accessory pathways (performed in conjunction with
diagnostic electrophysiology testing) is a safe and effective
treatment of patients with WPW syndrome.

Symptoms:
 the patient may be aware of "fast heartbeat" or
palpitations; lightheadedness, near syncope, and
neck pounding may occur during paroxysms.
 May precipitate CHF or hypotension during acute
MI.

Therapy:
 Valsalva maneuver in the supine position is the
most effective way to terminate supraventricular
tachycardia; carotid sinus massage (after excluding
occlusive carotid disease [absence of carotid bruit
and no history suggestive of carotid artery
disease]) or application of an ice pack to the face in
children is also commonly used to elicit vagal
efferent impulses.

Therapy
 Synchronized DC shock if patient shows signs of
cardiogenic shock (is hypotensive), angina, or
CHF.

Therapy
 Adenosine (Adenocard), an endogenous nucleoside, is useful
for treatment of paroxysmal supraventricular tachycardia that
is unresponsive to vagal maneuvers; the dose is 6 mg given
as a rapid IV bolus under ECG monitoring; tachycardia is
usually terminated within a few seconds in 60% to 80% of
patients; if necessary, the drug can be given again with a 12
mg IV bolus (effective in terminating the supraventricular
tachycardia in > 90% of patients). Contraindications are
second- or third-degree AV block, sick sinus syndrome, atrial
fibrillation, and ventricular tachycardia. Adenosine is also
contraindicated in heart transplant patients and should be
used with caution in COPD patients. It may also cause
bronchospasm in asthmatic patients. Patients receiving
theophylline (a competitive antagonist of adenosine
receptors) are usually refractory to treatment. Dipyridamole
enhances the effect of adenosine; therefore, lower doses of
adenosine should be given to patients receiving dipyridamole.

Therapy
 If adenosine is not effective, verapamil, 2.5 to 5 mg IV
every 5 minutes to a maximum of 15 mg is generally
effective
 Verapamil should be used cautiously in patients with
supraventricular tachycardia and history of hypotension. If
the patient is truly hypotensive with SVT, immediate
synchronized cardioversion is indicated.
 Slow injection of calcium chloride (10 mL of a 10% solution)
given over 5 to 8 minutes before verapamil administration
may decrease the hypotensive effect without compromising
its antiarrhythmic effect.
 Repeat carotid massage after IV verapamil if
supraventricular tachycardia persists.

Therapy
 β-Blockers (metoprolol [5 mg IV q2min up to 15 mg]
or esmolol [500 mg/kg IV bolus, then 50
mg/kg/min]) or IV diltiazem, IV procainamide, IV
propafenone, IV flecainide, or IV ibutilide may also
be effective in the treatment of supraventricular
tachycardia; however, these agents generally have
little role in acute management of paroxysmal
supraventricular tachycardia. Digoxin should also
be avoided in patients with WPW syndrome and
narrow QRS tachycardia (because of increased
risk for atrial fibrillation during AV re-entrant
tachycardia).

Definition
 chaotic, irregular atrial activity at rates of 100
to 180 bpm.

Etiology
 COPD
 Metabolic disturbances (hypoxemia, hypokalemia,
hypomagnesemia)
 Sepsis
 Theophylline toxicity
 CHF
 Acute MI

ECG:
 Variable P-P intervals
 Morphology of the P wave varies from beat to
beat , with a minimum of three different forms of P
wave in addition to those from the sinus node.
 Each QRS complex is preceded by a P wave.
 Atrial rate of 100 to 150 bpm

Therapy:
 Treat the underlying cause (e.g., improve
oxygenation, correct electrolyte abnormalities).
 Verapamil 5 mg IV at a rate of up to 1 mg/min
(may repeat after 20 minutes). Calcium
gluconate, 1 g IV given 5 minutes before
treatment with verapamil, may reduce drug-
induced hypotension without influencing the
antiarrhythmic effect.
 Metoprolol or esmolol has also been used in
absence of COPD, CHF, or bronchospasm.
 Amiodarone may be useful in refractory cases.

Definition
 totally chaotic atrial activity caused by
simultaneous discharge of multiple atrial foci.
The prevalence of atrial fibrillation increases
with age, from 2% in the general population to
5% in patients older than 60 years.

Etiology:
 CAD
 Mitral stenosis, mitral regurgitation, aortic stenosis, aortic regurgitation.
 Left atrial enlargement from any cause
 Thyrotoxicosis
 Pulmonary embolism, COPD
 Pericarditis
 Myocarditis, cardiomyopathy
 Tachycardia-bradycardia syndrome
 Alcohol abuse
 MI
 Hypertension
 WPW syndrome
 Other causes: left atrial myxoma, atrial septal defect, carbon monoxide poisoning,
pheochromocytoma, idiopathic, hypoxia, hypokalemia, sepsis, pneumonia

Clinical presentation:
 The most common presenting complaint is
palpitations.
 Fatigue, dizziness, and lightheadedness may also
be present.
 A few patients may be completely asymptomatic.

Diagnostic studies of new-onset
atrial fibrillation
 echocardiography to evaluate left atrial size
and detect valvular disorders.
Transesophageal echo has a greater than
95% sensitivity and specificity for detection of
left atrial thrombi and is useful prior to
cardioversion to identify patients with thrombi
who need prolonged anticoagulation after
cardioversion. Laboratory evaluation should
include thyroid function studies to rule out
thyrotoxicosis.

Diagnostic studies of new-onset
atrial fibrillation
 ECG reveals the following:
 Irregular, nonperiodic wave forms (best seen in
V1) reflecting continuous atrial reentry
 Absence of P waves
 Conducted QRS complexes show no periodicity

Treatment of new-onset atrial
fibrillation
 If the patient is hemodynamically unstable,
perform synchronized cardioversion. If the
patient is hemodynamically stable, treatment
options include the following:

Forcontrol of a rapid ventricular
rate:
 Ibutilide (Corvert), an antiarrhythmic drug with
predominantly class III properties, is approved for the
rapid conversion of atrial fibrillation or atrial flutter of
recent onset to sinus rhythm. Dose is 1 mg (10 mL) IV
over 10 minutes; if first dose is not effective, give a
second infusion 10 minutes later. This medication should
be administered only under continuous ECG monitoring
and by personnel trained in arrhythmia recognition and
treatment. Ibutilide use is followed by oral dofetilide
(Tikosyn), another class III agent. Dofetilide dose is 0.1 to
0.5 mg every 12 hours.

 Other medications useful for converting atrial
fibrillation to sinus rhythm are flecainide (Tambocor),
propafenone (Rythmol), disopyramide (Norpace),
amiodarone (Cordarone), and quinidine sulfate or
quinidine gluconate.

 Digoxin is not a very potent AV nodal blocking agent and
cannot be relied upon for acute control of the ventricular
response. When used, give 0.5 mg IV loading dose
(slow), then 0.25 mg IV 6 hr later. A third dose may be
needed after 6 to 8 hr; daily dose varies from 0.125 to
0.25 mg (decrease dosage in patients with renal
insufficiency and elderly patients). Digoxin should be
avoided in WPW patients with atrial fibrillation.
Procainamide is the preferred pharmacologic agent in
these patients.

 Procainamide is the preferred agent for pharmacologic
cardioversion in the presence of WPW. Usual dose is 100
mg over 5 minutes (20 mg/min). Maximum dose is 17
mg/kg. Procainamide (total dose of 15 mg/kg given IV at
15 to 20 mg/kg) will restore sinus rhythm in 60% of
patients with AF of < 1 week duration. AV nodal blocking
agents should be administered prior to using
procainamide or any other primary antiarrhythmic agent to
prevent conversion of atrial fibrillation into atrial flutter.

Cont. Treatment of new-onset atrial
fibrillation
 Radiofrequency catheter modification of an
atrioventricular condition, followed by ablation, may
be necessary if drug therapy does not successfully
control the heart rate. The need for a pacemaker
frequently arises with this form of therapy.

Cardioversion
 Cardioversion is indicated if the ventricular
rate is >140 bpm and the patient is
symptomatic with acute MI, chest pain,
dyspnea, or CHF.

 Cardioversion will restore sinus rhythm in 90% of
patients. However, there is no advantage of
cardioversion over control of rate medically if the
patient is stable.
 If left atrial size is ≥ 4.5 cm, there is little chance
of achieving or maintaining normal sinus rhythm.
 In patients receiving digoxin, hold digoxin and
check serum digoxin level on morning of
cardioversion.
 The patient should be NPO for 8 hours before
cardioversion (unless done emergently).

 Anticoagulation with warfarin (target INR, 2.5) is
advisable for 3 weeks before and at least 4 weeks
after cardioversion, particularly in patients with
mitral valve disease or a history of
thromboembolism. Longer anticoagulation
therapy (>3 months) after cardioversion may be
necessary in patients at risk for recurrence of
atrial fibrillation (see following section).

 Early cardioversion (within 24 hours of new-onset
atrial fibrillation) may be performed if heparin is
started immediately and transesophageal
echocardiography has ruled out atrial thrombus.
For these patients, adjusted-dose warfarin therapy
anticoagulation should be continued until normal
sinus rhythm has been maintained for at least 4
weeks.

Complications of cardioversion:
 Ventricular fibrillation (if shock is applied on T waves)
 Thromboembolism (seen mainly in nonanticoagulated
patients with long-standing atrial fibrillation)
 Myocardial damage secondary to the current (rare)
 Erythema on the chest wall
 Recurrence of prior arrhythmia; factors associated
with maintenance of sinus rhythm are left atrium
diameter of < 60 mm, absence of mitral valve disease,
short duration of atrial fibrillation, and conversion to
normal sinus rhythm with drug therapy alone.

Long-term anticoagulation with
warfarin
 Long-term anticoagulation with warfarin (adjusted to maintain
an INR of 2 to 3) to decrease risk for thromboembolism is
indicated in all patients with atrial fibrillation and associated
cardiovascular disease, including the following:
 Rheumatic valvular disease (mitral stenosis, mitral regurgitation,
aortic insufficiency)
 Aortic stenosis
 Prosthetic mitral valve (any type)
 History of previous embolism
 Known cardiac thrombus
 CHF
 Cardiomyopathy with poor left ventricular function
 Nonrheumatic heart disease (e.g., hypertensive cardiovascular
disease, CAD, ASD).

 Anticoagulation is not recommended in younger
patients with chronic lone atrial fibrillation (no
associated cardiovascular disease).
 Aspirin 325 mg/day may be a suitable alternative
to warfarin in patients older than 70 years of age
with increased risk for bleeding and falls and in
low-risk patients (no recent CHF, previous
thromboembolism, or systolic blood pressure >
160 mm Hg) between 65 and 75 years of age.

Surgical treatment of atrial
fibrillation:
 The Maz e pro ce dure with its recent modifications,
which create electrical barriers to macro-re-
entrant circuits that are thought to underlie atrial
fibrillation, is being performed with good results in
several medical centers (preservation of sinus
rhythm in more than 95% of patients without the
use of long-term antiarrhythmic medication).

Surgical treatment of atrial
fibrillation
 Generally, surgery is reserved for patients with
rapid heart rate refractory to pharmacologic
therapy or who cannot tolerate pharmacologic
therapy.

Catheter-based radiofrequency
ablation
 Catheter-based radiofrequency ablation
procedures designed to eliminate atrial
fibrillation and development of an implantable
atrial defibrillator represent newer approaches
to atrial fibrillation. Restoration and
maintenance of sinus rhythm by catheter
ablation without the use of drugs in patients
with congestive heart failure and atrial
fibrillation significantly improves cardiac
function, symptoms, exercise capacity, and
quality of life.

Cont. Treatment AF
 Implantable pacemakers and defibrillators that
combine pacing and cardioversion therapies
both to prevent and to treat atrial fibrillation are
likely to have an increasing role in the future
management of atrial fibrillation.

 Amiodarone therapy should be considered for
patients with recent atrial fibrillation and
structural heart disease, particularly those with
left ventricular dysfunction. Amiodarone
should also be considered for patients with
refractory conditions who do not have heart
disease, before therapies with irreversible
effects such as AV nodal ablation are
attempted. Pulmonary function must be
closely monitored in patients on chronic
amiodarone therapy.

 Rate control with chronic anticoagulation is the
recommended strategy for the majority of patients with
atrial fibrillation. Rhythm control has not been shown
to be superior to rate control (with chronic
anticoagulation) in reducing morbidity and mortality
and may be inferior in some patient subgroups to rate
control. Rhythm control is appropriate when based on
other special considerations, such as patient
symptoms, exercise tolerance, and patient preference.
Ultimately, rhthym control fails in most patients,
dependent upon the underlying cause of the atrial
fibrillation, and thromboembolic risk might be higher in
these patients, as asymptomatic episodes are likely
under-recognized.

 For patients with atrial fibrillation, the following
drugs are recommended for their
demonstrated efficacy in rate control during
exercise and while at rest: atenolol,
metoprolol, diltiazem, and verapamil (drugs
listed alphabetically by class). Digoxin is
effective for rate control only at rest and,
therefore, should only be used as a second-
line agent for rate control in atrial fibrillation.

 Most patients converted to sinus rhythm from
atrial fibrillation should not be placed on rhythm
maintenance therapy because the risks outweigh
the benefits. In a selected group of patients
whose quality of life is compromised by atrial
fibrillation, the recommended pharmacologic
agents for rhythm maintenance are amiodarone,
disopyramide, propafenone, and sotalol (drugs
listed in alphabetical order). The choice of agent
depends on specific risk for side effects based on
patient characteristics.

Definition
 Ectopic atrial rhythm in which an irritable site
depolarizes regularly at a rapid rate. It is
characterized by a rapid atrial rate of 250 to
450 bpm with varying degrees of
atrioventricular block. The ventricular rate is
variable (determined by AV blockade). It
generally does not exceed 180 bpm because
of the intrinsic conduction rate of the AV
junction. But, it is commonly 150 bpm and a
narrow-complex regular tachycardia is atrial
flutter until proven otherwise.

Etiology:
 Atherosclerotic heart disease
 MI
 Thyrotoxicosis
 Pulmonary embolism
 Mitral valve disease
 Cardiac surgery
 COPD

ECG:
 Regular "sawtooth" or "F wave" pattern best seen in
II, III, and aVF and secondary to atrial depolarization
(Fig. 3-13)
 AV conduction block (2:1, 3:1, or varying)
 QRS duration usually <0.10 second but may be
widened if flutter waves are buried in the QRS
complex or an intraventricular conduction delay exists
 Valsalva maneuver or carotid sinus massage usually
slows the ventricular rate (increases grade of AV
block) and may make flutter waves more evident.

Therapy:
 Use electrical cardioversion at low energy levels (20 to 25
J). More than 85% of patients convert to regular sinus
rhythm following cardioversion. Because atrial flutter is
frequently associated with intermittent atrial fibrillation, it
may be prudent to perform anticoagulation on patients with
atrial flutter and coexisting medical disorders (e.g.,
diabetes mellitus, hypertension, cardiac disease) prior to
cardioversion. Sedation of a conscious patient is highly
recommended before cardioversion is performed. The use
of external defibrillators having biphasic waveforms
decreases the amount of energy required for cardioversion
and improves cardioversion success rate.

Therapy:
 In the absence of cardioversion, intravenous
diltiazem or digitalization may be tried to slow the
ventricular rate and convert flutter to fibrillation.
Esmolol, verapamil, and adenosine may also be
effective. In patients with atrial flutter, it is
essential to pre-administer AV nodal blocking
agents prior to using procainamide or ibutilide.

Therapy:
 Overdrive pacing in the atrium may also terminate
atrial flutter. This method is especially useful in
patients who have recently undergone cardiac
surgery and still have temporary atrial pacing
wires.

ATRIOVENTRICULAR
CONDUCTION DEFECTS

FIRST-DEGREE
ATRIOVENTRICULAR
BLOCK

Definition:
 prolongation of the PR interval > 0.2 second
(at a rate of 70 bpm), which remains constant
from beat to beat

Etiology:
 Vagal stimulation. First degree AV block may be a normal finding
in individuals with no history of cardiac disease, especially in
athletes.
 Degenerative changes in the AV conduction system
 Ischemia at the AV nodes (seen particularly in cases of inferior
wall MI)
 Drugs (digitalis, quinidine, procainamide, adenosine, calcium
channel blockers, β-blockers, digitalis, amiodarone)
 Cardiomyopathies
 Aortic regurgitation
 Lyme carditis
 Hyperkalemia
 Complication of bacterial endocarditis

SECOND-DEGREE
ATRIOVENTRICULAR
BLOCK

Definition:
 blockage of some (but not all) impulses from
the atria to the ventricles.

SECOND-DEGREE
ATRIOVENTRICULAR
BLOCK
Mobitz type I (Wenckebach)

Definition:
 Progressive prolongation of the PR interval before an
impulse is completely blocked; the cycle repeats
periodically.
 Cycle with dropped beat is less than two times the
previous cycle.

Site of block
 usually AV nodal (proximal to the bundle of
His)

Etiology:
 Vagal stimulation.
 Degenerative changes in the AV conduction system
 Ischemia at the AV nodes (seen particularly in cases
of inferior wall MI)
 Drugs (digitalis, quinidine, procainamide, adenosine,
calcium channel blockers, β-blockers, digitalis,
amiodarone)
 Cardiomyopathies
 Aortic regurgitation
 Lyme carditis
 Hyperkalemia
 Complication of bacterial endocarditis

ECG:
 Gradual prolongation of PR interval leading to a
blocked beat
 Shortened PR interval after the dropped beat.

Therapy:
 Usually transient; no treatment is necessary.
 If symptomatic (e.g., dizziness), atropine 1 mg (may repeat
once after 5 minutes) can be tried to increase AV
conduction; if no response, insert temporary pacemaker.
 If block is secondary to drug (e.g., digitalis), discontinue the
drug.
 If associated with anterior wall MI and wide QRS escape
rhythm, consider insertion of a temporary pacemaker.
 Significant AV block post MI may be caused by adenosine
produced by the ischemic myocardium. These arrhythmias,
which may be resistant to conventional therapy, such as
atropine, may respond to theophylline (adenosine
antagonist).

SECOND-DEGREE
ATRIOVENTRICULAR
BLOCK
Mobitz type II

Definition:
 sudden interruption of AV conduction without
previous prolongation of the PR interval

Etiology:
 Degenerative changes in His-Purkinje system and any
cause of first degree AV block
 Acute anterior wall MI more commonly but any MI can
cause the block
 Calcific aortic stenosis
 Complication of bacterial endocarditis
 Lyme carditis

ECG:
 Fixed duration of PR interval
 Sudden appearance of blocked beats

Therapy:
 pacemaker insertion, because this type of
block is usually permanent and often
progresses to complete AV block.

THIRD-DEGREE
ATRIOVENTRICULAR
BLOCK (COMPLETE
ATRIOVENTRICULAR
BLOCK)

Definition:
 all AV conduction is completely blocked, and
the atria and ventricles have separate
independent rhythms.

Etiology:
 Same as for Mobitz II. Incidence is 5.8% in early
MI (greater in inferior/posterior infarctions)
 Cardiomyopathy
 Trauma
 Cardiovascular surgery
 Congenital
 Any cause of first-degree AV block and Mobitz I

ECG:
 There is no relationship between the P-waves
and the QRSs. P waves constantly change their
relationship to the QRS complexes.
 Ventricular rate usually < 50 bpm (may be higher
in congenital forms).
 Ventricular rate generally lower than the atrial
rate.
 QRS wide.

Symptoms:
 Dizziness, palpitations
 Stokes-Adams syncopal attacks
 CHF
 Angina

Therapy:
 immediate pacemaker insertion unless the
patient has congenital third-degree AV block
and is completely asymptomatic. A temporary
pacer could be used until a permanent pacer
is inserted.

Definition
 Long QT syndrome is an inherited disease
predisposing to cardiac arrhythmias and
sudden death. The electrocardiographic
abnormality is characterized by a corrected
QT interval longer than 0.44 sec.

Diagnostic Criteria for the Congenital Long
QT Syndrome
Diagnostic Criteria for the
Congenital Long QT Syndrome

ECG criteria:
 Corrected QT >480 ms-3 points
 Corrected QT 460 to 480 ms-2 points
 Corrected QT 450 to 460 ms-1 point (males)
 Torsades de pointes-2 points
 T-wave alternans-1 point
 Notched T wave in 3 leads-1 point
 Bradycardia-0.5 point

History:
 Syncope with stress-2 points
 Syncope without stress-1 point
 Congenital deafness-0.5 point
 Definite family history-1 point of long QT
 Unexplained cardiac death in first-degree relative-
0.5 point under age 30
 Total score ≥ 4: definite long QT syndrome
 Total score 2 to 3: intermediate probability
 Total score ≤ 1: low probability

Etiology
 Cardiac repolarization abnormality
 Congenital cause (chromosome 3 or chromosome 7
abnormality)
 Acquired causes:
 Drugs (dofetilide, ibutilide, bepridil, quinidine, procainamide,
sotalol, amiodarone, disopyramide, phenothiazines and
antiemetic agents [droperidrol, domperidone], tricyclic
antidepressants, methadone, quinolones, astemizole or
cisapride given with ketoconazole or erythromycin,
clarithromycin, and antimalarials), particularly among patients
with asthma or those using potassium-lowering medications
 Hypokalemia, hypomagnesemia
 Liquid protein diet
 CNS lesions
 Mitral valve prolapse

Physical Findings and Clinical
Presentation
 Syncope caused by ventricular tachycardia
 Sudden death
 Abnormal ECG (prolonged QT) in
asymptomatic relatives of known case. Bazett
formula; QTc5QT/vRR. Calculated QTc should
be < 440 ms. If patient has atrial fibrillation,
take the average of the longest and shortest
QTc intervals.

Work-Up
 In relatives of patients with known long-QT syndrome or in
young patients with syncope:
 Stress test may prolong the QT interval or cause T-wave
alternans
 Valsalva maneuver: may prolong the QT interval or cause T-
wave alternans
 Prolonged ECG monitoring with various stimulations aimed at
increasing catecholamines (perform in a setting that can provide
resuscitation)
 Epinephrine-induced prolongation of the 2T interval (epinephrine
infusion QT stress test)
 Genetic analysis
 LQT1 locus of KCNQ1 potassium channel gene
 LQT2 locus of KCNH2 potassium channel gene
 LQT33 locus of SCN5A sodium channel gene

Treatment
 Asymptomatic sporadic forms with no complex
ventricular arrhythmias: no treatment

Treatment
 Risk stratification
 High risk (>50% of cardiac event): QTc > 500 ms
and LQT1 and LQT2 or male with LQT3
 Moderate risk (30% to 50%): QTc > 500 ms in
female with LQT3 or L QTc < 500 ms in male with
LQT3 or in female with LQT2 or 3
 Low risk (<30%): QTc < 500 ms and LQT1 and or
male OQT2

Treatment
 General recommendations:
 Avoid competitive sports.
 β-blocker at maximum tolerated dose
 Pacemaker and implantable defibrillator may be
advised.
 Antiarrthymics (mexelitine) may be useful in a
subset of patients.
 Cardiac sympathetic denervation is uncommonly
used in the United States, but is sometimes
performed for this.

Definition:
 three or more consecutive beats of ventricular origin
(wide QRS) at a rate between 100 and 200 bpm .
 When the QRS complexes of the ventricular
tachycardia (VT) are of the same shape and
amplitude, the rhythm is termed m o no m o rphic VT;
when the QRS complexes vary in shape and
amplitude, the rhythm is known as po lym o rphic VT.
 Polymorphic VT can be further subclassified based on
its association with a normal or prolonged QT interval.
Polymorphic VT occurring in the presence of a long
QT is called to rsade s de po inte s

Differentiation between ventricular beats and
supraventricular tachycardia with aberrant
ventricular conduction
 may be very difficult; because most wide
complex tachycardias are VT, wide-QRS
tachycardia in the conscious adult should be
considered as VT until proven otherwise,
especially in the presence of underlying heart
disease.

Factors favoring ventricular
tachycardia:
 Similar morphology to PVC
 Initiating event is a PVC
 Usually no response to vagal maneuvers
 Presence of AV dissociation (P waves marching through QRS)
 QRS duration >140 milliseconds with an RBBB pattern and > 160
milliseconds with an LBBB pattern
 Extreme left axis deviation (less than -90 to ± 180 degrees)
 Combination of LBBB and right axis deviation
 Different QRS pattern during tachycardia compared with a baseline
ECG in patients with preexisting bundle branch block
 QRS concordance (QRS waves are in same direction in all precordial
leads)
 Left peak ("rabbit ear") of the QRS complex is taller than the right in
lead V1.
 QS v6

Factors favoring supraventricular
rhythm:
 Morphology is similar to baseline rhythm.
 Initiating event is a premature atrial contraction.
 Rhythm can slow or break with vagal stimuli.
 Physical examination demonstrates ventriculoatrial
dissociation (e.g., variation in loudness of S1 and
systolic blood pressure on successive beats).
 ECG may reveal biphasic or monophasic QRS in V1
with RBBB, QRS >0.14 second, left axis deviation.

VENTRICULAR
TACHYCARDIA
Torsades de pointes

Torsades de pointes
 is a form of ventricular tachycardia manifested
by episodes of alternating electrical polarity
with the amplitude of the QRS complex
twisting around an isoelectric baseline
resembling a spindle; rhythm usually starts
with a PVC and is preceded by widening of the
QT interval.

cause
 electrolyte disturbances (hypokalemia, hypomagnesemia, hypocalcemia),
 antiarrhythmic drugs
 that prolong the QT interval (procainamide, quinidine, disopyramide),
 N-acetylprocainamide,
 droperidol,
 amiodarone,
 phenothiazines,
 haloperidol,
 tricyclic antidepressants,
 terfenadine,
 astemizole,
 ketoconazole,
 erythromycin,
 trimethoprim-sulfamethoxazole,
 high-dose methadone, or cocaine.
 Torsades de pointes is also associated with hereditary long QT interval syndromes.

Treatment of Torsades de pointes
 Electrical termination of the tachycardia with
cardioversion when the ventricular tachyarrhythmia is
sustained.

 Intravenous infusion of isoproterenol to decrease the
QT interval and prevent recurrences.

 Elimination of contributing factors (correction of
electrolyte abnormalities, discontinuation of suspected
drugs); early diagnosis of hereditary long-QT
syndromes and treatment of them with β1-adrenergic
receptor blocking agents. Surgical sympathectomy
and use of implantable cardioverter-defibrillators
should also be considered in high-risk patients with
hereditary long-QT syndrome.

 Intravenous magnesium sulfate may be helpful even if
magnesium levels are normal. Magnesium sulfate
(10% solution) may be administered by bolus (1-2 g
given IV over 1 to 2 minutes and repeated 5 to
15minutes later if no response) or by infusion (50
mg/min over 2 hours).
 Sequential overdrive pacing if the episodes of
torsades are sustained and appear to be precipitated
by bradycardia.

Therapy of VT:
 Check ACLS algorythms on ACC guidelines.

Therapy of VT:
 Electrophysiologic mapping followed by
surgical treatment can be performed for
recurrent tachycardia, generally in
combination with CABG. Currently, the use of
transvenous implantable cardioverter-
defibrillators is the most common
nonpharmacologic intervention in patients with
life-threatening arrhythmias.

Therapy of VT:
 The American College of Cardiology and the
American Heart Association indications fortherapy
with an automatic implantable cardioverter-
defibrillator are as follows:
 Spontaneous sustained VT.
 Cardiac arrest related to ventricular fibrillation (VF) or VT
not resulting from a transient or reversible cause.
 Syncope of undetermined origin with clinically relevant,
hemodynamically significant sustained VT, or VF induced
at electrophysiologic study when drug therapy is ineffective,
not tolerated, or not preferred.
 Nonsustained VT with CAD, previous MI, left ventricular
dysfunction, and inducible VF or sustained VT at
electrophysiologic study that is not suppressed by a class I
antiarrhythmic drug.

Ventricular Fibrillation
 VF is the most common cause of out-of-hospital cardiac
arrest. Fatality rate is > 95%.
 VF is characterized by a chaotic ventricular rhythm with
disorganized spread of impulses throughout the ventricles .
 VF with low-amplitude waves (<3 mm) is called fine VF.
 Waves that are more easily visible are described as co arse .
 The current guidelines recommend considering the use of
either amiodarone or lidocaine for shock-resistant VF. Recent
trials (ALIVE trial) indicate that the survival rate is
considerably higher with the use of amiodarone instead of
lidocaine.

Ventricular Fibrillation
 Check ACLS guidelines for VF

Pulseless Electrical Activity
 Pulseless electrical activity is an organized
rhythm on the monitor (other than VT) that
does not produce a palpable pulse.

 It is most commonly due to hypovolemia and myocardial
contractile failure from ischemia or metabolic injury. The
acronym PATCH-4-MD can be used to memorize the causes
of pulseless electrical activity:
 Pulmonary embolism
 Acidosis
 Tension pneumothorax
 Cardiac tamponade
 Hypovolemia
 Hypoxia
 Hypothermia/hyperthermia
 Hypokalemia/hyperkalemia
 Myocardial infarction
 Drug overdose

 Check ACLS for PEA

Asystole
 May be due to multiple causes (e.g., MI, hypoxia,
electrolyte abnormalities, trauma, drug overdose)
 ECG: ventricular rhythm is not discernible, atrial
rhythm may be discernible. Whenever a "flat line"
is observed on an ECG, the rhythm should be
confirmed in two leads because ventricular
fibrillation may be masquerading as asystole.
 Vasopressin is superior to epinephrine in patients
with asystole. Vasopressin followed by
epinephrine may be more effective than
epinephrine alone in the treatment of refractory
cardiac arrest.

Asystole
 Check ACLS algoryths for ASYSTOLE

ACCELERATED
IDIOVENTRICULAR
RHYTHM

Accelerated Idioventricular Rhythm
 Ventricular rate of 60 to 100 bpm, at times interspersed with
brief runs of sinus rhythm .
 QRS > 0.12 second,
 T wave frequently in opposite direction of QRS complex,
 P waves usually absent.
 Usually seen in acute MI during the first 12 hours and also
particularly common following successful reperfusion therapy.
 It can also be seen with digitalis toxicity and subarachnoid
hemorrhage.
 Generally benign and transient, not requiring any therapy.
 Atrioventricular sequential pacing may be necessary if the
dissociation between atria and ventricles impairs ventricular
filling and decreases cardiac output.

Arrhythmias

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