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An arrhythmia is a
disruption in the normal
events of the cardiac
cycle.
INTRA ATRAL
PATHWAYS
COMMON DYSRHYTMIAS
Ventricular
 Premature ventricular contractions
 Ventricular bigeminy
 Ventricular fibrillation
 Ventricular tachycardia
VENTRICULAR ARRHYTHMIAS
 VENTRICULAR ESCAPE RHYTHM
 Ventricular Escape Rhythms/
Idioventricular Rhythms
 Failure of SA node and AV node to
fire

results in the Ventricles assuming
the role as Pacemaker
VENTRICULAR ESCAPE RHYTHM
Rate: 20–40 bpm
Rhythm: Regular
P Waves: None or, if visible, have no
consistent relationship to the QRS complex.
PR Interval: None
QRS: Wide (0.10 sec), bizarre appearance
♥ Clinical Tip: Idioventricular rhythm may
also be called agonal rhythm.
VENTRICULAR ARRHYTHMIAS
PREMATURE VENTRICULAR CONTRACTION
(PVC)
 is a relatively common event where the
heartbeat is initiated by the heart ventricles
rather than by the sinoatrial node
 a dysrhythmia that is produced by an ectopic
beat originating in a ventricle and being
discharged at a rate faster than that of the next
normally occurring beat.
PVC’s of 6 /minute or more is
life threatening
Premature Ventricular Complex,
Ventricular Premature Contraction
(or complex or complexes) (VPC),
Ventricular Premature Beat (VPB), or
EXTRASYSTOLE
PREMATURE VENTRICULAR CONTRACTION
 be perceived as a "skipped beat" or felt as
palpitations in the chest
 NORMAL:  the ventricles contract after the atria
have helped to fill them by contracting
 this way the ventricles can pump a maximized
amount of blood both to the lungs and to the
rest of the body .
 PVC, the ventricles contract first
 which means that circulation is inefficient
 Single beat PVC arrhythmias do not usually pose a
danger and can be asymptomatic in healthy
individuals
PREMATURE VENTRICULAR CONTRACTION
 Premature ventricular contraction
can occur in a healthy person of any
age
 Becomes more frequent in the
elderly
 more commonly found in men
 PVC frequently occurs
spontaneously with no cause.
ETIOLOGY
 Ischemia
 Drugs such as cocaine
 Certain medicines such as
 Caffeine









digoxin which increases heart
contraction
Myocarditis
Cardiomyopathy, hypertrophic
or dilated
Myocardial contusion
Hypoxia
Hypercapnia (CO2 poisoning)
Sarcoidosis
Mitral valve prolapse
Smoking
Alcohol
 Tricyclic antidepressants
 Magnesium and potassium







deficiency
Calcium excess;
Thyroid problems
Chemical (electrolyte)
problems in the blood
Heart attack;
Adrenaline excess;
Lack of sleep/exhaustion
Stress
PREMATURE VENTRICULAR CONTRACTION
Usually PVCs result from an irritable ventricular
focus.
■ PVCs may be uniform (same form) or multiform
(different forms).
■ The pause following a PVC may be compensatory
or noncompensatory.
PREMATURE VENTRICULAR CONTRACTION
Rate: Depends on rate of underlying rhythm
Rhythm: Irregular whenever a PVC occurs
P Waves: None associated with the PVC
PR Interval: None associated with the PVC
QRS: Wide (0.10 sec), bizarre appearance
Clinical Tip:
Patients may sense the occurrence of PVCs as
skipped beats. Because the ventricles are only
partially filled, the PVC frequently does not
generate a pulse.
 PREMATURE VENTRICULAR
CONTRACTION:
 UNIFORM (SAME FORM)
PREMATURE VENTRICULAR
CONTRACTION: MULTIFORM
(DIFFERENT FORMS)
PREMATURE VENTRICULAR CONTRACTION
PATHOLOGY
 Normally impulses pass through both
ventricles almost simultaneously
 the depolarization waves of the two
ventricles partially cancel each other out in
the ECG.
 However, when a PVC occurs the impulse
nearly always travels in one direction
therefore there is no neutralization effect
 which results in the high voltage QRS wave
in the electrocardiograph.
PREMATURE VENTRICULAR CONTRACTION
VENTRICULAR BIGEMINY
 a PVC where every other beat is a
ventricular complex
 abnormal heart beats occur every other
concurrent beat.
Following the PVC there is a pause and
then the normal beat returns
only to be followed by another PVC.
The continuation of this pairing of beats
is an example of bigeminy.
PREMATURE VENTRICULAR
CONTRACTION:VENTRICULAR
BIGEMINY
 (PVC EVERY OTHER BEAT)
PREMATURE VENTRICULAR
CONTRACTION:VENTRICULAR
TRIGEMINY
 (PVC EVERY 3RD BEAT)
PREMATURE VENTRICULAR
CONTRACTION:VENTRICULAR
QUADRIGEMINY
 (PVC EVERY 4TH BEAT)
PREMATURE VENTRICULAR
CONTRACTION: COUPLETS
(PAIRED PVCS)
PREMATURE VENTRICULAR
CONTRACTION: TRIPLETS
(3 SUCCESSIVE PVC’S)
PREMATURE VENTRICULAR CONTRACTION
 SYMPTOMS
 Chest pain
 Faint feeling
 Fatigue
 Hyperventilation (after exercise)
 Frequent episodes of continuous PVCs
becomes a form of ventricular tachycardia
(VT),
 which is a rapid heartbeat
 because there is an extra electrical impulse

causing an extra ventricular contraction.
PREMATURE VENTRICULAR CONTRACTION
TREATMENT:
 Isolated PVCs with benign characteristics
require no treatment.
 In healthy individuals, PVCs can often be
resolved by restoring the balance of
MAGNESIUM, CALCIUM and POTASSIUM within
the body.
 The most effective treatment is the elimination
of triggers
  particularly the cessation of the use of
substances such as caffeine and certain drugs
PREMATURE VENTRICULAR CONTRACTION
PHARMACOLOGICAL agents
 ANTIARRHYTHMICS:
 these agents alter the electrophysiologic
mechanisms responsible for PVCs
 LIDOCAINE / IV PUSH, DRIP
 Initial bolus dose: 75 – 100mg then 50 – 100 mg. within 10
– 15 min. as needed.
 Continuous IV drip bolus dose: 300 mg.
 PROCAINAMIDE IV PUSH,
 drip bolus dose: 300mg.
 BRETYLIUM
 continuous infusion if lidocaine and procainamide are
ineffective.
PREMATURE VENTRICULAR CONTRACTION
 ELECTROLYTES REPLACEMENT
 Magnesium supplements (e.g. magnesium
citrate, orotate, Maalox, etc.)
 Potassium supplements
 LIFESTYLE MODIFICATION
 Frequently stressed individuals should
consider therapy, or joining a support group
 Heart attacks can increase the likelihood of
having PVCs
PREMATURE VENTRICULAR CONTRACTION
RADIOFREQUENCY CATHETER ABLATION
TREATMENT (RF)
  electrophysiology study to remove cells
that are issuing abnormal electrical activity
leading to arrhythmia
 used to destroy abnormal electrical pathways in heart
tissue or normal parts that are contributing to a cardiac
arrhythmia
  medical procedure where part of the
electrical conduction system of the heart,
tumor or other dysfunctional tissue is
ablated using high frequency alternating
current to treat arrhythmias
 Schematic view of a pulmonary vein ablation. The
catheter reaches (from below) through the inferior vena
cava, the right atrium and the left atrium, to the orifice
of the left upper pulmonary vein.
PRACTICE EXERCISE:
IDENTIFY THE FOLLOWING
PVC’S
VENTRICULAR
BIGEMINY
VENTRICULAR BIGEMINY
VENTRICULAR TRIGEMINY
VENTRICULAR TRIGEMINY
VENTRICULAR
QUIADRIGEMINY
SINGLE PVC
VENTRICULAR BIGEMINY
VENTRICULAR TRIGEMINY
VENTRICULAR TRIGEMINY
VENTRICULAR TRIGEMINY
VENTRICULAR TRIGEMINY
VENTRICULAR ARRHYTHMIAS
 VENTRICULAR TACHYCARDIA
 a life threatening dysrhythmia that originates
for an irritable focus within the ventricle
 It is an emergency catastrophe
 Can degenerate into Ventricular Fibrillation
 Almost always occur in diseased hearts
 VENTRICULAR PACEMAKER
 It is an ineffective rhythm for maintaining cardiac
output.
 Associated hypotension
Ventricular Tachycardia (VT):
Monomorphic
Monomorphic ventricular tachycardia means that
the appearance of all the beats match each other in
each lead of a surface electrocardiogram(ECG).
Rate: 100–250 bpm
Rhythm: Regular
P Waves: None or not associated with the QRS
PR Interval: None
QRS: Wide (0.10 sec), bizarre appearance
♥ Clinical Tip: It is important to confirm the
presence or absence of pulses because
monomorphic VT may be perfusing or nonperfusing.
♥ Clinical Tip: Monomorphic VT will probably
deteriorate into VF or unstable VT if sustained
and not treated.
Ventricular Tachycardia (VT):
Polymorphic
QRS complexes in polymorphic VT vary in shape
and amplitude.
■ The QT interval is normal or long.
Rate: 100–250 bpm
Rhythm: Regular or irregular
P Waves: None or not associated with the QRS
PR Interval: None
QRS: Wide (0.10 sec), bizarre appearance
Clinical Tip: It is important to confirm the presence
or absence of pulses because
polymorphic VT may be perfusing or nonperfusing.
♥ Clinical Tip: Consider electrolyte abnormalities as
a possible etiology.
Torsades de Pointes
*from the French for “twisting of the
points”
demonstrates a rapid, POLYMORPHIC
VENTRICULAR TACHYCARDIA with a characteristic
twist of the QRS complex around the isoelectric
baseline
Torsades de Pointes
The QRS reverses polarity and the strip shows a
spindle effect.
■ This rhythm is an unusual variant of polymorphic
VT with normal or long QT intervals.
Rate: 200–250 bpm
Rhythm: Irregular
P Waves: None
PR Interval: None
QRS: Wide (0.10 sec), bizarre appearance
Clinical Tip: Torsade de pointes may deteriorate to
VF or asystole.
♥ Clinical Tip: Frequent causes are drugs that
prolong QT interval and electrolyte
abnormalities such as hypomagnesemia.
Torsades de Pointes
The pattern is called "twisting" because when
the peaks are at their smallest in one lead,
they are generally at their largest in another,
as if a vibrating string were having its plane
of vibration slowly rotated about the long axis
of the string.
Torsades de Pointes
CAUSES:
•
•
•
•
•
•
•
•
•
•
•
•
Class IA antiarrhythmics
Class III antiarrhythmics
Hypomagnesemia
Hypokalemia
Hypocalcemia
Hypoxia
Acidosis
Heart failure
Slow heart rate
Female gender
Hypothermia
Subarachnoid hemorrhage
TORSADES DE POINTES
 CLINICAL MANIFESTATIONS:
 SIGNS AND SYMPTOMS OF ↓ CARDIAC
OUTPUT:
 Hypotension
 Exercise limitations
 Syncope
 Dizziness
 Restlessness
 ↓ LOC
TORSADES DE POINTES
TREATMENT
 Treatment is directed at withdrawal of the
offending agent
1. Infusion of MAGNESIUM SULFATE
2. ANTIARRHYTHMIC DRUGS - Lidocaine
3. Treat Ischemia
4. Electrical therapy as needed.
DEFIBRILLATION
Because of the polymorphic nature of
TORSADES DE POINTES, synchronized
cardioversion MAY NOT BE POSSIBLE, and the
patient may require an unsynchronized shock
or defibrillation
TORSADES DE POINTES
DEFIBRILLATION
 consists of delivering a therapeutic dose of
electrical energy to the affected heart with a
device called a defibrillator.
 This depolarizes a critical mass of the heart
muscle, terminates the arrhythmia,
 allows normal sinus rhythm to be
reestablished by the body's natural
pacemaker  SA NODE
 can be external, transvenous, or implanted,
depending on the type of device used or
needed
TORSADES DE POINTES
 CARDIOVERSION
 a medical procedure by which an abnormally fast
heart rate or cardiac arrhythmia is converted to a
normal rhythm, using electricity or drugs
 SYNCHRONIZED ELECTRICAL CARDIOVERSION
  uses a therapeutic dose of electric current to
the heart, at a specific moment in the cardiac
cycle
 PHARMACOLOGIC CARDIOVERSION
 AKA chemical cardioversion, uses antiarrhythmia
medication instead of an electrical shock
SYNCHRONIZED ELECTRICAL
CARDIOVERSION
 a reversion shock, by way of the pads, of a
selected amount of electric current over a
predefined number of milliseconds at the
optimal moment in the cardiac cycle which
corresponds to the R WAVE of the QRS
complex on the ECG.
 Timing the shock to the R wave prevents the
delivery of the shock during the vulnerable
period (or relative refractory period) of the
cardiac cycle, which could induce ventricular
fibrillation
DIRECT CURRENT
VENTRICULAR TACHYCARDIA
VENTRICULAR TACHYCARDIA
VENTRICULAR FIBRILLATION
 a condition in which there is uncoordinated
contraction of the cardiac muscle of the ventricles
in the heart
 making them quiver rather than contract properly.
 characterized by the random and chaotic discharging of
impulses within the ventricle at rates that exceed 300
beats per minute.
 While there is activity, it is undetectable by palpation
(feeling) at major pulse points of the carotid and
femoral arteries especially by the lay person.
 Such an arrhythmia is only confirmed by ECG.
VENTRICULAR FIBRILLATION
 It produces clinical death and must be
reversed immediately
 Ventricular fibrillation is a medical emergency
that requires prompt Basic Life Support
interventions
 because should the arrhythmia continue for more
than a few seconds, it will likely degenerate further
into asystole ("flatline").
 This dysrhythmia results in the absence of
cardiac output.
 Almost always occurs with serious heart disease,
especially acute MI.
VENTRICULAR FIBRILLATION
 The condition results in cardiogenic shock, cessation of
effective blood circulation, and sudden cardiac death
(SCD) will result in a matter of minutes.
 If however the patient is revived after a sufficient period
(at room temperature, roughly 5 minutes) of cerebral
hypoxia,
 the patient could sustain irreversible brain damage
and possibly be left brain dead
 death often occurs if normal sinus rhythm is not
restored within 90 seconds of the onset of VF,
especially if it has degenerated further into asystole
VENTRICULAR FIBRILLATION
Rate
P wave
QRS
Conduction
Rhythm
unattainable
may be present, but obscured by
ventricular waves
not apparent
chaotic electrical activity
chaotic electrical activity
VENTRICULAR FIBRILLATION
Chaotic electrical activity occurs with no ventricular
depolarization or contraction.
■ The amplitude and frequency of the fibrillatory
activity can be used to define the type of
fibrillation as coarse, medium, or fine.
Clinical Tip: There is no pulse or cardiac output.
Rapid intervention is critical. The longer the
delay, the less the chance of conversion.
VENTRICULAR FIBRILLATION
CLINICAL MANIFESTATIONS:
1. PULSE DISAPPEARS WITH
ONSET OF VF
2. SYNCOPE,
UNCONSCIOUSNESS
NO CARDIAC OUTPUT
3. RAPID DETERIORATION OF
PHYSIOLOGIC STATUS
VENTRICULAR FIBRILLATION
 TREATMENT:
1. Defibrillation
 Electric defibrillator
 The condition can often be reversed by the electric
discharge of direct current from a defibrillator
 Although a defibrillator is designed to correct the
problem, and its effects can be dramatic,
 it is not always successful.
 Implantable electric defibrillator
 In patients at high risk of ventricular fibrillation, the
use of an implantable cardioverter defibrillator has
been shown to be beneficial.
VENTRICULAR FIBRILLATION
 Precordial thump
 If no defibrillator is available, a precordial thump
can be delivered at the onset of VF
 for a small chance to regain cardiac function.
 However, research has shown that the precordial
thump releases no more than 30 joules of energy.
 This is far less than the 200–360 J typically used to
bring about normal sinus rhythm.
 Consequently, in the hospital setting, this
treatment is not used.
VENTRICULAR FIBRILLATION
 Antiarrhythmic agents
 AMIODARONE OR LIDOCAINE
 can help, but,
 unlike atrial fibrillation ventricular fibrillation
rarely reverses spontaneously in large adult
mammals.
 Drug therapy with antiarrhythmic agents in
ventricular fibrillation does not replace
defibrillation and is not the first priority
 but is sometimes needed in cases where initial
defibrillation attempts are not successful.
Pulseless Electrical Activity (PEA)
Monitor shows an identifiable electrical
rhythm, but no pulse is detected.
■ Rhythm may be sinus, atrial, junctional,
or ventricular in origin.
■ PEA is also called electromechanical
dissociation (EMD).
Rate, rhythm, P waves, P-R interval, and
QRS: Reflect underlying rhythm.
Clinical Tip: Potential causes of PEA are
pulmonary embolism, MI, acidosis, tension
pneumothorax, hyper- and hypokalemia, cardiac
tamponade, hypovolemia, hypoxia,
hypothermia, and drug overdose (i.e., cyclic
antidepressants, beta blockers, calcium channel
blockers, digoxin).
ASYSTOLE
 a state of no cardiac electrical activity
 hence no contractions of the myocardium
 and no cardiac output or blood flow.
 Asystole is one of the conditions required for a
medical practitioner to certify death
 In asystole, the heart will generally not respond to
defibrillation because it is already depolarized
 the treatment of choice is an injection of
EPINEPHRINE and ATROPINE (VASOPRESSIN may
also be used) and chest compressions
ASYSTOLE
Electrical activity in the ventricles is
completely absent.
Rate: None
Rhythm: None
P Waves: None
PR Interval: None
QRS: None
Clinical Tip: Always confirm asystole by checking
the ECG in two different leads. Also,
search to identify underlying ventricular fibrillation.
♥ Clinical Tip: Seek to identify the underlying cause
as in PEA.
CAUSES
NON-SHOCKABLE RHYTHMS
 1. PEA
 2. AYSTOLE
VENTRICULAR FIBRILLATION AND PEA
DRUG
INITIAL
SUBSEQUENT
INTERVAL
MAXIMUM
EPINEPHRINE
1 mg
1 mg
3-5 min.
None
VASOPRESSI
N
40 units
None
None
40 units
AMIODARON
E
300 mg
150 mg
10 min
2.2 G in 24
Hours
1-1.5 mg/kg
0.5-0.75
mg/kg
5-10 min.
3 mg/kg
LIDOCAINE
VENTRICULAR TACHYCARDIA WITH PULSE
DRUG
INTERVAL
MAXIMUM
6 mg
SUBSEQUEN
T
12 mg
2 min
3rd dose
AMIODARONE
150 mg
150
10 min
2.2 G in 24
Hours
LIDOCAINE
1-1.5
mg/kg
0.5-0.75
mg/kg
5-10 min.
3 mg/kg
20
mg/min
0.5-0.75
mg/kg
5-10 min.
3 mg/kg
ADENOSINE
PROCAINAMIDE
INITIAL