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An arrhythmia is a
disruption in the normal
events of the cardiac
cycle.
INTRA ATRAL
PATHWAYS
General Information
 Dysrhythmias are disorders of the formation
or conduction (or both) of the electrical
impulse within the heart
 It can cause disturbances of the heart rate, the
heart rhythm or both
 May initially be evident by the hemodynamic
effect they cause
 Diagnosed by analyzing ECG waveforms
 They are named according to:
- the site of origin of the impulse and the
mechanism of formation or
- conduction involved
Example:
Impulse that originate from the SA node
that has a slow rate is called SINUS
BRADYCARDIA
Electrophysiology
 Excitability or Irritability is the ability of
a cardiac muscle cell to respond to an
electrical stimulus.
 Automaticity is the heart’s ability to
generate an electrical impulse.
 Contractility
 Conductivity is the ability of cardiac tissue
to transmit electrical impulses.
Electrophysiology
 Refractory Period
 Absolute refractory period a period of
decreased excitability during which the
cell cannot respond to a new stimulus
 Relative refractory period a period
before the resting membrane potential is
reached, a stimulus greater than normal
can evoke a response in the cell
ECTOPIC FOCI
 When the electrical impulse arises anywhere other
than the SA node, it is an abnormal or ectopic focus
 If the ectopic focus depolarizes at a rate faster than
the SA node, the ectopic focus becomes the dominant
pacemaker.
 Ectopic pacemakers may arise in the atria, AV node,
Purkinje fibers, or ventricular muscle.
 They may be activated by hypoxia,ischemia, or
hypokalemia.
 Ectopic foci indicate myocardial irritability (increased
responsiveness to stimuli) and potentially serious
impairment of cardiac function.
Reentry excitation
 means that an impulse continues to reenter an
area of the heart rather than becoming
extinguished.
 For this to occur, the impulse must encounter
an obstacle in the normal conducting
pathway.
 The obstacle is usually an area of damage,
such as myocardial infarction.
 The damaged area allows conduction in only
one direction and causes a circular movement
of the impulse
NORMAL SINUS RHYTHM
 Rate: Normal (60–100 bpm)
 Rhythm: Regular
 P Waves: Normal (upright and uniform)
 PR Interval: Normal (0.12–0.20 sec)
 QRS: Normal (0.06–0.10 sec)
NORMAL ECG
 1. PR INTERVAL SHOULD BE 3-5 LITTLE SQUARES
 120 TO 200 MILLISECONDS
 2. THE WIDTH OF THE QRS COMPLEX SHOULD
BE LESS THAN 3 LITTLE SQUARES
 NOT EXCEED 110 ms
 3. THE QRD COMPLEX SHOULD BE
DOMINANTLY UPRIGHT IN LEADS I AND II
 4. QRS AND T WAVES TEND TO HAVE THE SAME
GENERAL DIRECTION IN THE LIMB LEADS
 5. ALL LEADS ARE (-) IN THE LEAD AVR
NORMAL ECG
 6. THE R WAVE IN THE PRECORDIAL LEADS




MUST GROW FROM V1 TO AT LEAST V4
7. THE ST SEGMENT MUST START ISOELECTRIC
EXCEPT IN V1 AND V2 WHERE IT MAY BE
ELEVATED
8. THE P WAVES SHOULD BE UPRIGHT IN LEADS
I, II AND V2 TO V6
9. THERE MUST BE NO Q WAVE OR ONLY A
SMALL q LESS THAN 0.04 SECONDS IN WIDTH IN
I, II, V2 TO V6
10. THE T WAVE MUST BE UPRIGHT IN I, II, V2 TO
V6
COMMON DYSRHYTMIAS
Sinus
 Sinus Tachycardia
 Sinus Bradycardia
 Sinus A/Dysrhythmia
 Sick Sinus Syndrome
COMMON DYSRHYTMIAS
Atrial
 Premature atrial contraction
 Paroxysmal atrial tachycardia
 Atrial flutter
 Atrial fibrillation
COMMON DYSRHYTMIAS
Ventricular
 Premature ventricular contractions
 Ventricular bigeminy
 Ventricular fibrillation
 Ventricular tachycardia
COMMON DYSRHYTMIAS
Conduction defects
 First degree AV block
 Second degree AV block
 Third degree AV block
SINUS TACHYCARDIA
A. General Information:
 A heart rate of over 100 beats/min,
originating in the SA node
 generally the result of increased
stimulation of the sympathetic
nervous system and the resulting
release of catecholamines
Etiology
B. May be caused by:
- fever
- anemia
- apprehension
- hyperthyroidism
- physical activity (e.g., exercise)
- myocardial ischemia
- caffeine
- drugs (epinephrine, theophylline)
Assessment findings:





Rate: 100-160 beats /min
Rhythm: regular
P wave: precedes each QRS complex with
normal contour
P-R interval: normal (0.08 sec)
QRS complex: normal (0.06 sec)
SAME CHARACTERISTICS ARE NORMAL SINUS RHYTHM EXECEPT THAT
THE RATE IS GREATER THAN 100 BPM
Signs and symptoms
 Occasional palpitations
 If HR is very rapid = reduction of the cardiac
output will be evident
(due to shorter time for atrial contraction and
ventricular filling)
 Clients with underlying heart disease may not
be able to tolerate this and may experience
hypotension and chest pain
Treatment
1.
2.
3.
4.
Correction of underlying cause
Elimination of stimulants
Administration of sedatives as prescribed for
anxiety such as diazepam
Administration of Beta blockers such as
propranolol (Inderal)
SINUS BRADYCARDIA
A. General Information:
 A slowed heart rate initiated by SA
node
 primarily caused by an excessive
parasympathetic response
Etiology
B. May be Caused by:
- excessive vagal or decreased sympathetic
tone
- Myocardial Infarction
- Intracranial tumors
- meningitis
- myxedema
- cardiac fibrosis
- normal variation of the heart rate in well
trained athletes
- Medications such as digoxin or verapamil
Assessment findings
 Rate: <60 beats/min
 Rhythm: regular
 P wave: precedes each QRS with a normal contour
 P-R interval: normal
 QRS complex: normal
SAME CHARACTERISTICS ARE NORMAL SINUS RHYTHM EXECEPT THAT
THE RATE IS LESS THAN 60 BPM
Signs and symptoms
 s/sx of decreased cardiac output:






weakness,
altered LOC,
low BP,
dizziness
syncope
Pulmonary congestion or heart failure
 The slowed rate of SA discharge may allow junctional
or ventricular pacemakers to take over, thereby
producing ectopic beats sensed as palpitaions
Treatment
Identify the underlying cause
Asymptomatic bradycardia, usually does not need
treatment
3. But if cardiac output is inadequate: (s/sx: dizziness,
weakness, altered LOC, and low BP)
1.
ATROPINE 0.5 MG TO 1 MG IV
4. Chronic symptomatic sinus bradycardia requires
insertion of a permanent pacemaker.
1.
IF S/SX SEVERE; CONSIDER CATECHOLAMINE
INFUSIONS:
1.
DOPAMINE 5 TO 20 ug/kg/min
2.
ISOPROTERENOL E 2 to 10 ug/min
1.
2.
SINUS ARRHYTHMIA
 Defined as a variable rate of impulse discharge
from the SA node, occurs when the rhythm is
irregular and usually corresponds to the
respiratory pattern.
 The rhythm increases with inspiration and
slows with expiration
 Sinus arrhythmia can be a normal variation in
children.
SINUS ARRHYTHMIA
 a normal phenomenon of mild acceleration
and slowing of the heart rate that occurs with
breathing in and out.
 It is usually quite pronounced in children, and
steadily decreases with age.
 This can also be present during meditation
breathing exercises that involve deep inhaling
and breath holding patterns
Etiology
 In response to delayed atrial filling with
inspiration
(during inspiration venous return to RA is delayed
because of increased Intrathoracic pressure)
** quiet respiration HR can dec. about 5%
** deep inspiration HR can dec. up to 30%
 The vagal effect of some medications
(e.g., beta-blockers)
 Conditions that affect vagal tone can also be a
cause.
(e.g., vomiting, suctioning, extreme emotions and
severe pain)
Assessment findings
 Rate: Usually normal (60–100 bpm); frequently




increases with inspiration and decreases with
expiration
Rhythm: Irregular; varies with respiration; The P-P
and R-R interval is irregular.
P Waves: Normal (upright and uniform)
PR Interval: Normal (0.12–0.20 sec)
QRS: Normal (0.06–0.10 sec)
Clinical Tip:The pacing rate of the SA node varies with respiration,
especially in children and elderly people.
Treatment
 Clients with sinus dysrhythmia do not usually
require treatment unless the BLOOD
PRESSURE is affected, particularly with
orthostatic position changes
 If dizziness, presyncope or syncope occurs, the
following interventions might help:
- apply Elastic support stocking
- Na retaining drugs (to expand the vascular
volume
Sick Sinus Syndrome
  a dysrhythmia that is caused by a diseased
sinus node.
 The sinus node conducts at a slow rate or may fail
to conduct at all, producing sinus block or pauses.
 also known as “bradycardia syndrome”.
 SINUS PAUSE/ ARREST
 SINUS BLOCK
SINUS PAUSE/ ARREST
The SA node fails to discharge and then
resumes.
■ Electrical activity resumes either when the SA
node resets itself or when a lower latent
pacemaker begins to discharge.
■ The pause (arrest) time interval is not a
multiple of the normal P-P interval.
3 SECOND PAUSE/ ARREST
SINUS PAUSE/ ARREST
3 SECOND PAUSE/ ARREST
Rate: Normal to slow; determined by duration and
frequency of sinus pause (arrest)
Rhythm: Irregular whenever a pause (arrest) occurs
P Waves: Normal (upright and uniform) except in areas
of pause (arrest)
PR Interval: Normal (0.12–0.20 sec)
QRS: Normal (0.06–0.10 sec)
♥ Clinical Tip: Cardiac output may decrease, causing
syncope or dizziness.
 Normal sinus rhythm, with solid black arrows pointing to
normal P waves representative of normal sinus node
function, followed by a pause in sinus node activity
(resulting in a transient loss of heart beats).
 Note that the P wave that disrupts the pause (indicated by
the dashed arrow) does not look like the previous (normal)
P waves- this last P wave is arising from a different part of
the atrium, representing an escape rhythm.
Sinoatrial (SA) Block
 The block occurs in some multiple of the P-P interval.
 The SA node initiates the impulse, but the propagation over




the atrial tissue is blocked
 ATRIA IS NOT DEPOLARIZED
Therefore, there is NO P WAVE and subsequent QRS
complex
■ After the dropped beat, cycles continue on time.
Underlying rhythm resumes on time following the pause
 THE LENGTH OF THE PAUSE BEING A MULTIPLE OF THE
UNDRLYING P-P INTERVAL OR R-R INTERVAL
The R-R interval returns to the same pattern as if nothing
happened
Sinoatrial (SA) Block
Dropped beat
X
Rate: Normal to slow; determined by duration and
frequency of SA block
Rhythm: Irregular whenever an SA block occurs
P Waves: Normal (upright and uniform) except in
areas of dropped beats
PR Interval: Normal (0.12–0.20 sec)
QRS: Normal (0.06–0.10 sec)
♥ Clinical Tip: Cardiac output may decrease, causing
syncope or dizziness.
Sick Sinus Syndrome
 Treatment
 If ischemia is due to arteriosclerotic
heart disease, MI.
 Pacemaker.
Implanted Transvenous Pacemaker
Transcutaneous Pacemaker
ATRIAL ARRHYTMIAS
 Premature Atrial Contraction (PAC)
  is an ectopic beat that originates in the atria
and is discharge at a rate faster than that of the
sinus node.
  this very rapid repetitive complexes is
originating in the atrial tissue (ectopic foci in the
atrium) and NOT in the SA node
 P WAVES MAY LOOK PEAKED
Premature Atrial Contraction (PAC)
 are not as serious as premature
ventricular contractions (PVCs)
  usually require no medical care.
 Individuals with this condition usually
report feeling that their heart "stops" or
misses a beat.
 Like PVCs, PACs are called HEART
PALPITATIONS.
Premature Atrial Contraction (PAC)
 ETIOLOGY:
 * IDIOPATHIC
 * DISEASED TISSUES
 * INFLAMMATORY/ INFECTIOUS
PROCESS
 POST CARDIOVERSION
Premature Atrial Contraction (PAC)
 A single complex occurs earlier than the next expected
sinus complex.
 ■ After the PAC, sinus rhythm usually resumes.
PAC
PAC
Rate: Depends on rate of underlying rhythm
Rhythm: Irregular whenever a PAC occurs
P Waves: Present; in the PAC, may have a different shape
PR Interval: Varies in the PAC; otherwise normal (0.12–0.20
sec)
QRS: Normal (0.06–0.10 sec)
PAC’S
Premature Atrial Complexes
Premature Atrial Contraction (PAC)
 Prognosis
 In rare cases, a PAC, like a PVC, can trigger a more
serious arrhythmia such as an atrial flutter or atrial
fibrillation
 . This is seldom seen in a healthy heart but if it does
happen medical attention should be sought to see what
caused the problem and what steps can be taken to fix
it.
 Unlike PVCs, PACs generally do not compromise the
hemodynamic system
 because the conduction throughout is via the AV
node and the ventricles of the heart are activated in a
normal sequence
Premature Atrial Contraction (PAC)
 Treatment
 Generally does not require treatment.
 Quinidine or calcium – channel
blocker if it increases in frequency.
Premature Atrial Contraction (PAC)
 Treatment
 If the heart is healthy, simple lifestyle
changes can alter or prevent the
occurrences of PACs.

Exercising
Eating right
 Reducing alcohol and caffeine
consumption
 Lowering stress levels


 most effective ways of reducing these
occurrences
ATRIAL ARRHYTHMIAS
 ATRIAL TACHYCARDIA
 this very rapid repetitive complexes is originating in
the atrial tissue (ectopic foci in the atrium) and
NOT in the SA node
 the heart rate is rapid (approximately 150 beats per
minute) with atrial impulse generation.
 Ventricular rate is also correspondingly increased
and is driven by the atrial impulses
 “PROTECT THE VENTRICLES”
 P WAVES MAY LOOK PEAKED
ATRIAL TACHYCARDIA
 A rapid atrial rate overrides the SA node and
becomes the dominant pacemaker.
 ■ Some ST wave and T wave abnormalities may be
present.
Rate: 150–250 bpm
Rhythm: Regular
P Waves: Normal (upright and uniform) but differ in
shape from sinus P waves
PR Interval: May be short (0.12 sec) in rapid rates
QRS: Normal (0.06–0.10 sec) but can be aberrant at
times
SINUS TACHYCARDIA
ATRIAL TACHYCARDIA
SUPRAVENTRICULAR TACHYCARDIA
 any tachycardic rhythm originating
above the ventricular tissue
 Theoretically, it refers to any tachycardia
that is not ventricular in origin
 This definition includes :
 Abnormal Sinus tachycardia
 Ectopic ParoxysmalAtrial Tachycardia
(PAT/ PSVT)

(that is, not from the sinoatrial node)
 Junctional tachycardia
SUPRAVENTRICULAR TACHYCARDIA
 This arrhythmia has such a fast rate that the P
waves may not be seen
P wave buried in T wave
Rate: 150–250 bpm
Rhythm: Regular
P Waves: Frequently buried in preceding T waves and difficult to see
PR Interval: Usually not possible to measure
QRS: Normal (0.06–0.10 sec) but may be wide if abnormally conducted
through ventricles
♥ Clinical Tip: SVT may be related to caffeine intake, nicotine, stress, or
anxiety in healthy adults.
Holter monitor-Imaging with start (red arrow) and end (blue arrow)
of a SV-tachycardia with a pulse frequency of about 128/min
SUPRAVENTRICULAR TACHYCARDIA
SVT
SUPRAVENTRICULAR TACHYCARDIA
 PAROXYSMAL ATRIAL TACHYCARDIA
(PAT) / PAROXYSMAL SUPRA
VENTRICULAR TACHYCARDIA (PSVT)
  This term refers to those SVTs that
have a sudden, almost immediate onset
and are regular
  a sudden onset of an atrial
tachycardia with rates that vary between
140 and 250 beats per minute.
Paroxysmal Supraventricular Tachycardia
(PSVT)
 In paroxysmal supraventricular tachycardia (PSVT),




abnormal conduction of that electricity causes the
atrium, and secondarily the ventricles, to beat very
rapidly.
It is paroxysmal, because the rapid rate can occur
sporadically and without warning.
It may last a few seconds or many hours.
Often the PSVT resolves before the patient reaches a
healthcare provider.
The abnormal conduction pathways may occur
anywhere in the atrium or around the AV node.
PAROXYSMAL ATRIAL TACHYCARDIA (PAT) / PAROXYSMAL
SUPRA VENTRICULAR TACHYCARDIA (PSVT)
 rapid rhythm of the heart that involves
an accessory pathway
 This is in contrast to the potentially
deadlier ventricular tachycardias which
are rapid rhythms that originate within
the ventricular tissue or atrioventricular
(AV) node
  LIFE THREATENING
PAT/ PSVT
 ■ PSVT is a rapid rhythm that starts and stops
suddenly.
 ■ For accurate interpretation, the beginning or end of
the PSVT must be seen.
Sudden onset of SVT
Rate: 150–250 bpm
Rhythm: Regular
P Waves: Frequently buried in preceding T waves and difficult to
see
PR Interval: Usually not possible to measure
QRS: Normal (0.06–0.10 sec) but may be wide if abnormally
conducted through ventricles
♥ Clinical Tip: The patient may feel palpitations, dizziness,
lightheadedness, or anxiety.
PAT/ PSVT
 A person experiencing PSVT/ PAT may feel
their heart rate go from 60 to 200 beats per
minute INSTANTANEOUSLY,
 often in response to a quick movement
 such as picking something up from the
floor.
 Because physiological sinus tachycardias has
a gradual (i.e. non-immediate) onset and AF
is usually obviously irregular they are
excluded from the PSVT category
PSVT
 often presents with the complaints of
palpitations described as a rapid heart rate
often felt in the throat and may be associated
with:
 lightheadedness,
 Weakness
 Shortness of breath,
 chest pressure.
Paroxysmal Supraventricular Tachycardia (PSVT)
PSVT
SUPRAVENTRICULAR TACHYCARDIA
 JUNCTIONAL RHYTHM
 (nodal rhythm)
  results from the cells at the junction of the atrium
and the AV node depolarizing spontaneously and may
even become the “pacemaker” site determining overall
cardiac rhythm (“Escape beat”).
 Normal anterograde conduction into the ventricles
results in a typical QRS complex
 whereas retrograde conduction into the atria produces a
P wave that is often inverted
 may actually occur after the QRS complex or not at
all.
JUNCTIONAL RHYTHM
The atria and SA node do not perform their normal
pacemaking functions.
■ A junctional escape rhythm begins.
Inverted P wave
Absent P wave
Rate: 40–60 bpm
Rhythm: Regular
P Waves: Absent, inverted, buried, or retrograde
PR Interval: None, short, or retrograde
QRS: Normal (0.06–0.10 sec)
JUNCTIONAL RHYTHM
Absent P wave
Inverted P wave
Absent P wave
Rate: 61–100 bpm
Rhythm: Regular
P Waves: Absent, inverted, buried, or retrograde
PR Interval: None, short, or retrograde
QRS: Normal (0.06–0.10 sec)
♥ Clinical Tip: Monitor the patient, not just the ECG,
for clinical improvement
SUPRAVENTRICULAR
TACHYCARDIA
 Symptoms can come on suddenly and may go
away without treatment.
 They are caused for a reason other than stress,
exercise, or emotion.
 They can last a few minutes or as long as 1 or 2
days, sometimes continuing until treated.
 The rapid beating of the heart during SVT can
make the heart a less-effective pump
 decreasing cardiac output and blood
pressure.
SUPRAVENTRICULAR
TACHYCARDIA
 The following symptoms are typical with a
rapid pulse of 150–270 or more beats per
minute:
 Pounding heart
 Shortness of breath
 Chest pain
 Rapid breathing
 Dizziness
 Loss of consciousness (in serious cases)
 Numbness of various body parts
SUPRAVENTRICULAR
TACHYCARDIA
 TREATMENT
  directed at resetting the electrical conduction
of the heart
 In general, SVT is not life threatening, but
episodes can be treated or prevented
 Physical maneuver
  activation of the parasympathetic nervous
system, conducted to the heart by the vagus
nerve.
SUPRAVENTRICULAR
TACHYCARDIA
 VAGAL MANEUVERS.
 It works by increasing intra-thoracic pressure
and affecting baro-receptors (pressure
sensors) within the arch of the aorta.
 It is carried out by asking the patient to hold
their breath and try to exhale forcibly as if
straining during a bowel movement, or by
getting them to hold their nose and blow out
against it.[5]
SUPRAVENTRICULAR TACHYCARDIA
 OTHER VAGAL MANEUVERS:
 coughing,
 plunging the face into cold water
(via the diving reflex),
drinking a glass of ice cold water,
standing on one's head.
Carotid sinus massage
firmly pressing the bulb at the top of one of the carotid
arteries in the neck
is effective but is often not recommended
 due to risks of stroke in those with plaque in the carotid
arteries.






SUPRAVENTRICULAR TACHYCARDIA
 MEDICATIONS:
 Termination of PSVT following adenosine
 ADENOSINE
 an ultra short acting AV nodal blocking agent, is
indicated if vagal maneuvers are not effective.
 treatment of choice for SV Arrhythmias in
pregnancy
 If this works, follow up therapy with DILTIAZEM,
VERAPAMIL or METOPROLOL may be indicated.
 SVT that does not involve the AV node may respond
to other anti-arrhythmic drugs such as SOTALOL or
AMIODARONE
SVT AFTER ADENOSINE
SUPRAVENTRICULAR
TACHYCARDIA
 CARDIOVERSION
 If the patient is unstable or other
treatments have not been effective
 cardioversion may be used, and is
almost always effective.
Paddle Placement for Defibrillation
Implantable Cardioverter Defibrillator
(ICD)
ICD
A device
that detects
and
terminates
lifethreatening
episodes of
tachycardia
or
fibrillation
ATRIAL FLUTTER
 a dysrhythmia in which an ectopic atrial focus captures
the heart rhythm and discharges impulses at a rate of
between 200 and 400 times per minute.
 A continuous (Saw toothed) rapid sequence of atrial
complexes from a single d rapid firing atrial focus
 IMPULSES TRAVEL IN CIRCULAR COURSE IN
ATRIA
 P WAVES ARE ABSENT
 Flutter waves represents abnormal depolarization
of the atria assuming a “saw-tooth” or picket fence
shape most easily seen in inferior leads II, III and
AVF and in precordial lead V1
ATRIAL FLUTTER
 AV node conducts impulses to the ventricles at a 2:1, 3:1,
4:1, or greater ratio (rarely 1:1).
 ■ Degree of AV block may be consistent or variable
Flutter waves
Rate: Atrial: 250–350 bpm; ventricular: slow or fast
Rhythm: Usually regular but may be variable
P Waves: Flutter waves have a SAW-TOOTHED APPEARANCE
PR Interval: Variable
QRS: Usually normal (0.06–0.10 sec), but may appear
widened if flutter waves are buried in QRS
♥ Clinical Tip: The presence of A-flutter may be the first
indication of cardiac disease.
♥ Clinical Tip: Signs and symptoms depend on ventricular
response rate.
ATRIAL FLUTTER
ATRIAL FLUTTER
ATRIAL FIBRILLATION
 a dysrhythmia that is caused by the rapid
and chaotic firing of atrial impulses by a
multitude of foci.
 the most common cardiac arrhythmia and
involves the (atria) of the heart
 Its name comes from the fibrillating (i.e.,
quivering) of the heart muscles of the atria,
instead of a coordinated contraction.
 IMPULSES HAVE CHAOTIC RANDOM
PATHWAYS IN ATRIA
 produces an irregular ventricular rhythm
ATRIAL FIBRILLATION
 It can often be identified by taking a pulse
and observing that the heartbeats do not
occur at regular intervals. However, a
stronger indicator of AF is the absence of P
waves on an ECG
 which are normally present when there is a
coordinated atrial contraction at the
beginning of each heart beat
ATRIAL FIBRILLATION
 ■ Rapid, erratic electrical discharge
comes from multiple atrial ectopic foci.
 ■ No organized atrial contractions are
detectable
ATRIAL FIBRILLATION
Irregular R-R intervals
Rate: Atrial: 350 bpm or greater; ventricular: slow or fast
Rhythm: Irregular
P Waves: No true P waves; chaotic atrial activity
PR Interval: None
QRS: Normal (0.06–0.10 sec)
♥ Clinical Tip: A-fib is usually a chronic arrhythmia associated
with underlying heart disease.
♥ Clinical Tip: Signs and symptoms depend on ventricular
response rate.
ATRIAL FIBRILLATION
 Atrial fibrillation is often ASYMPTOMATIC
 is not in itself generally life-threatening
 But it may result in:
 Palpitations,
 Fainting
 ANGINA/ chest pain
if the rate is faster and puts the heart under strain
 congestive heart failure.
 shortness of breath , edema
 People with AF usually have a significantly increased risk
of stroke
 up to 7 times that of the general population

The baseline rhythm here is ATRIAL FIBRILLATION with rapid
ventricular response. The QRS axis is at 30 degrees.
The first beat is a premature ventricular contraction (PVC), which is
then followed by two supraventricular beats being aberrantly
conducted.
The right bundle is still refractory after the PVC, and the following
two supraventricular impulses are blocked in the RBB, and are being
conducted aberrantly, thus causing a QRS with RBBB morphology.
ATRIAL FIBRILLATION
ATRIAL FLUTTER/ FIBRILLATION
 COMMON ETIOLOGIES:
 ACS  CAD, CHF
 ACQUIRED VALVULAR DEFECTS/
DISEASES
 HYPOXIA; Pulmonary Embolism
 DRUG INDUCED:  Digoxin/ Quinidine
Toxicity
 Hyperthyroidism
ATRIAL FLUTTER/ FIBRILLATION
 CLINICAL MANIFESTATIONS:
  signs and symptoms are function of
the rate of ventricular response to Atrial
Fibrillatory waves ;

AF WITH RVR
 DOB, SOB  s/sx of Acute Pulmonary
edema
 Palpitations
 Decreased Cardiac output  s/sx of
Arterial insufficiency
ATRIAL FLUTTER/ FIBRILLATION
 MAIN GOALS OF TREATMENT
  to prevent circulatory instability
 Rate or rhythm control
  to prevent circulatory stroke
 Anticoagulation
 If cardiovascularly unstable due to
uncontrolled tachycardia
 immediate CARDIOVERSION is
indicated
ATRIAL FLUTTER/ FIBRILLATION
 TREATMENT:
 1. Treat unstable patients urgently
 2. Control the rate
 3. Convert the rhythm
 4. Provide ANTICOAGULATION
ATRIAL FLUTTER/ FIBRILLATION
 RATE CONTROL
  seeks to reduce the heart rate to one that is
closer to normal, usually 60 to 100 bpm,
without trying to convert to a regular rhythm.
 RHYTHM CONTROL
  seeks to restore with cardioversion the
regular heart rhythm and maintain it with
drugs.
ATRIAL FLUTTER/ FIBRILLATION
 RATE CONTROL
 BETA BLOCKERS
  PREFERABLY THE "CARDIOSELECTIVE" BETA
BLOCKERS
 METOPROLOL, ATENOLOL, BISOPROLOL,
NEBIVOLOL
 CALCIUM CHANNEL BLOCKERS
 . DILTIAZEM OR VERAPAMIL
 CARDIAC GLYCOSIDES
 DIGOXIN
 HAVE LIMITED USE, APART FROM IN THE
SEDENTARY ELDERLY PATIENT
ATRIAL FLUTTER/ FIBRILLATION
 RATE CONTROL
 AMIODARONE
  has some AV node blocking effects
 particularly when administered
intravenously
  can be used in individuals when other
agents are contraindicated or ineffective
 hypotension
 Diltiazem has been shown to be more effective
than either Digoxin or Amiodarone
ATRIAL FLUTTER/ FIBRILLATION
 TREATMENT:
 CARDIOVERSION
  noninvasive conversion of an
irregular heartbeat to a normal
heartbeat using electrical or chemical
means:[5]
ATRIAL FLUTTER/ FIBRILLATION
 Electrical cardioversion
 involves the restoration of normal heart
rhythm through the application of a
electrical shock.
 Chemical cardioversion
 is performed with drugs, such as
Amiodarone, Dronedarone,
Procainamide,
ATRIAL FLUTTER/ FIBRILLATION
 ANTICOAGULATION
  use of Aspirin, Heparin, Warfarin
 PREVENT THROMBOEMBOLISM 
STROKE
  method used depends on :
 cost,
 risk of stroke,
 risk of falls,
 compliance,
 speed of desired onset of anticoagulation.