Hatem Alsrour

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Normal heart rhythm & depolarization.
Definition of Atrial Arrhythmias
Types of Atrial Arrhythmias & their
characteristics
Prehospital & ED management of Atrial
Arrhythmias
Treatment

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The electrical discharge for each cardiac cycle
normally starts in special area of the right
atrium called the sinoatrial SA node.
 Depolarization then spread s through the
atrial muscle fibers.
There is delay while depolarization spreads
through another special area in the atrium
called atrioventricular AV node, thereafter the
electrical discharge rapidly bundle of his & in
that to two pathway: left & right bundle
branch that divide into it.
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An arrhythmia is a change in the heart's
normal rate or rhythm, normally between 60
and 100 beats per minute.
Arrhythmias are classified by their location in
the heart and by their speed or rhythm.
 An atrial arrhythmia is an abnormality that
occurs in one of the left or right atrium.

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Atrial fibrillation
Atrial flutter
Premature atrial contraction (PAC or
premature atrial impulses)
Sinus tachycardia
Sinus bradycardia
Supraventricular tachycardia (SVT) or
Proximal Supraventricular tachycardia (PSVT)
Sick sinus syndrome (SSS)
Wolff-Parkinson-White syndrome (WPW)

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The electrical signal that circles uncoordinated
through the muscles of the atria, causing
them to quiver without contracting.
The ventricles do not receive regular impulses
and contract out of rhythm, and the heartbeat
becomes uncontrolled and irregular.

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Atrial fibrillation is the result of multiple wavelets
of depolarization (shown by arrows) moving
around the atria chaotically, rarely completing a
re-entrant circuit

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 Important cardiovascular causes include the following:
 Long-standing hypertension
 Ischemic heart disease
 CHF
 Any form of carditis
 Cardiomyopathy
 Infiltrative heart disease of any type
 Sick sinus syndrome
 Noncardiovascular causes of atrial fibrillation include the following:
 Hyperthyroidism
 Low levels of potassium, magnesium, or calcium
 Pheochromocytoma
 Sympathomimetic drugs, alcohol, electrocution
 Noncardiovascular respiratory causes include the following:
 Pulmonary embolism
 Pneumonia
 Lung cancer
 Idiopathic
 Hypothermia 8
 Palpitations
 Fatigue or poor exercise tolerance
 Dyspnea
 Chest pain (true angina)
 Presyncope or syncope
 Generalized weakness
 Irregular pulse.
 Hypotension and poor perfusion.
 Congestive heart failure, jugular venous distension,
peripheral edema, and a gallop.
 Signs of embolization, including transient ischemic
attack (TIA), stroke, and peripheral arterial
embolization (e.g., cold, pulseless extremities).

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Laboratory Studies
 CBC
 Electrolytes and BUN/creatinine levels
 Cardiac enzymes - CK and/or troponin Atrial fibrillation waves seen in lead V1
 Thyroid function studies
 Digoxin level
 Toxicology testing
Rhythm strip in atrial fibrillation
Imaging Studies
 Chest radiography
 Echocardiography
 Transthoracic and transesophageal echocardiography (TEE).

Other Tests
 ECG: Absent P waves, replaced by irregular, chaotic fibrillatory F waves, in the
setting of irregular QRS.
 Holter monitoring
 Exercise testing
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ACLS protocols, including direct current (DC)
cardioversion.
Symptomatic patients may benefit from
intravenous (IV) rate-controlling agents, either
calcium-channel blockers or beta-adrenergic
blockers.

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 Urgently assess need for interventions, including
the following:
 Airway and oxygenation (pulse oximetry); O2
supplementation as needed
 Blood pressure support (often difficult until rate is
controlled)
 A patient with hemodynamic instability, mental
status changes, preexcitation, or angina will require
urgent synchronized DC cardioversion.
 Obtain emergent laboratory and imaging studies (ECG,
chest radiography).
 control ventricular tachycardia by administration a rate-
controlling agent (most typically a beta-blocker or a
calcium-channel blocker).
 If the patient persists in AF, anticoagulation should be
initiated with either intravenous or subcutaneous heparin.
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Electrical cardioversion
 Atrial fibrillation with a rapid ventricular response
and acute hemodynamic deterioration should be
treated with synchronized cardioversion. Over 60
percent can be converted with 100 J, and over 80
percent with 200 J.
 Pharmacologic cardioversion
Diltiazem 20 mg (0.25 mg/kg) IV over 2 min is
extremely effective. An infusion of 10 mg/h is
usually started after the initial dose to maintain
control, and a second dose of 25 mg (0.35 mg/kg)
can be given at 15 min if rate control is not
achieved. Alternatives include digoxin (0.5 mg IV)
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and verapamil (5 to 10 mg IV).
 Differentiated from atrial fibrillation by its
coordinated, regular pattern, atrial flutter is a
coordinated rapid beating of the atria.
 Atrial flutter is classified into two types, according
to the pathways responsible for it:
o Type I normally causes the heart rate to increase to
and remain at 150 beats per minute. Rarely, the
rate may reach 300 beats per minute; sometimes it
decreases to 75 beats per minute.
o Type II increases the atrial rate faster, so the
ventricular rate may be 160 to 170 beats per
minute. As with atrial fibrillation, atrial flutter
increases the risk of stroke.

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Atrial flutter is usually the result of a single re-
entrant circuit in the right atrium (top); atrial
flutter showing obvious flutter waves (bottom)

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 long-standing hypertension
 valvular heart disease (rheumatic)
 left ventricular hypertrophy
 coronary artery disease
 Pericarditis
 pulmonary embolism
 Hyperthyroidism
 Diabetes
 CHF
 Additional causes include the following:
 Postoperative revascularization
 Digitalis toxicity

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History
 Symptomatic atrial flutter is typically a manifestation of the rapid
ventricular rate that decreases cardiac output.
 Palpitations
 Fatigue or poor exercise tolerance
 Mild dyspnea
 Presyncope
 Less common symptoms include angina, profound dyspnea, or
syncope. Symptomatic embolic events are rare, but must be
considered.
Physical finding
 Tachycardia, Cardiac rate, often approximately 150 PBM, regular or
slightly irregular heartbeat
 Hypotension is possible, but normal blood pressure is observed
more commonly.
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 Peripheral embolization
 Imaging Studies
 Chest radiographic
 Thyroid function studies.
 Serum electrolyte and digoxin levels if appropriate.
 CBCs
 Consider obtaining blood gases in patients with
hypoxia, or carbon monoxide intoxication.

 Transthoracic Echocardiogram
 Exercise Testing
 Holter Monitoring
 Electrocardiography (ECG) Rhythm strip in atrial flutter (rate
150 beats/min)

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In general in the prehospital setting is safest
because of possible induction of 1:1
conduction. Generally, the rate can be slowed
safely with calcium channel blockers or beta-
adrenergic blockers.

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Assess airway, breathing, and circulation.
Hemodynamic concerns will dictate initial
treatment.
Blood pressure can be supported and rate
controlled with medication.
Look for underlying causes. At times,
treatment of the underlying disorder (e.g.,
thyroid disease, valvular heart disease) is
necessary to effect conversion to sinus
rhythm.

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Associated with impaired impulse generation in
the SA node, it causes the heart rate to
decrease to fewer than 60 beats per minute.
Commonly caused by SSS, drugs like beta-
blockers and calcium-channel blockers can
also cause sinus bradycardia. Occasionally
sinus bradycardia can be caused by impaired
conduction of impulses to the atrial muscles.

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 the sick sinus syndrome.
 therapeutic and supratherapeutic doses of
digitalis glycosides, beta-blockers, and calcium
channel-blocking agents.
 class I antiarrhythmic agents and amiodarone.
 lithium, paclitaxel, toluene, dimethyl sulfoxide
(DMSO), topical ophthalmic acetylcholine,
fentanyl, alfentanil, sufentanil, reserpine, and
clonidine.
 hypothermia, hypoglycemia, and sleep apnea.
 Less commonly, the sinus node may be affected
as a result of diphtheria, rheumatic fever, or viral
myocarditis. 22
 Sinus bradycardia is most often asymptomatic.
However, symptoms may include the following:
 Syncope
 Dizziness
 Lightheadedness
 Chest pain
 Shortness of breath
 Exercise intolerance
 Pertinent elements of the history include the
following:
 Previous cardiac history (e.g., myocardial infarction,
congestive heart failure, valvular failure)
 Medications
 Toxic exposures
 Prior illnesses 23
Palpation of peripheral pulses reveal a slow,
regular heart rate.
The physical examination is generally
nonspecific, although it may reveal the
following signs:
 Decreased level of consciousness
 Cyanosis
 Peripheral edema
 Pulmonary vascular congestion
 Dyspnea
 Poor perfusion
 Syncope

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 Laboratory Studies
 Reasonable screening studies, especially if the patient
is symptomatic and this is the initial presentation,
include the following:
 Electrolyte levels
 Glucose level
 Calcium level
 Magnesium level
 Thyroid function tests
 Toxicologic screen
 Imaging Studies
 Other Tests
 12-lead ECG may be performed to confirm the diagnosis.
 The long, flat line between impulses indicates an
abnormally slow heartbeat.

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Intravenous access, supplemental oxygen,
and cardiac monitoring should be initiated in
the field.
In symptomatic patients, intravenous atropine
may be used.
In rare cases, transcutaneous pacing may
need to be initiated in the field.

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 Care in the ED should first rapidly ensure the stability
of the patient's condition. This is followed by an
investigation into the underlying cause of the
bradycardia.
 Patients in unstable condition may require immediate
endotracheal intubation and transcutaneous or
transvenous pacing.
 Patients should have continuous cardiac monitoring
and intravenous access.
 In hemodynamically stable patients, attention should
be directed at the underlying cause of the bradycardia.
 In sick sinus syndrome, drug therapy approaches have
been relatively disappointing. While atropine has aided
some patients transiently, most patients ultimately
require placement of a pacemaker.

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 In patients with sinus bradycardia secondary to
therapeutic use of digitalis, beta-blockers, or
calcium channel blockers, simple discontinuation
of the drug, along with monitored observation, are
often all that is necessary
 In patients with hypothermia who have confirmed
sinus bradycardia with a pulse, atropine and
pacing are usually not recommended because of
myocardial irritability. Rewarming and supportive
measures are the mainstays of therapy.
 Sleep apnea is usually treated with weight loss,
nasal bi-level positive airway pressure (BiPAP)
and, occasionally, surgery.
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 Characterized by a rapid heart rate that ranges
between 100 and 240 beats per minute, SVT
usually begins and ends suddenly. SVT occurs
when an electrical impulse 're-enters' the atrial
muscles.
 A disorder that a person may have at birth, SVT is
commonly caused by a variation in the electrical
system of the heart.
 SVT often begins in childhood or adolescence and
can be triggered by exercise, alcohol, or caffeine.
SVT is rarely dangerous, but can cause a drop in
blood pressure, causing lightheadedness or near-
fainting episodes, and, rarely, fainting episodes.
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History should include:
time of onset any triggers, any previous
episodes or arrhythmia, and previous
treatment.
Patients who are hemodynamically unstable
should be resuscitated immediately with
cardioversion. An ECG should be performed as
soon as possible.
Many patients with frequent episodes of PSVT
tend to avoid activities such as exercising and
driving due to past episodes of syncope or
near-syncope.
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 PSVT may present with mild symptoms or severe
cardiopulmonary complaints. Some common presenting
symptoms are listed below:
 Palpitation - Greater than 96%
 Dizziness - 75%
 Shortness of breath - 47%
 Syncope - 20%
 Chest pain - 35%
 Fatigue - 23%
 Diaphoresis - 17%
 Nausea - 13%
 Quite distressed.
 Tachycardia.
 Patients who have limited hemodynamic reserve may be tachypneic and
hypotensive.
 Crackles may be auscultated secondary to heart failure.

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Laboratory Studies
 A cardiac enzyme.
 Electrolyte
 A complete blood cell count
 thyroid studies.
 digoxin level.
Imaging Studies
 Chest cardiography
 A transthoracic echocardiogram
 Cardiac MRI.
Other Tests
 ECG findings allow classification of the tachyarrhythmia, and they
may allow a precise diagnosis. P waves may not be visible; when
present, they may be normal or abnormal depending on the
mechanism of atrial depolarization.

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 Adenosine, initially 6 mg rapid IV bolus. If there
is no effect within 2 min, a second dose of 12 mg
can be given.
 Verapamil, 0.075 to 0.15 mg/kg (3 to 10 mg) IV
over 15 to 60 s, with a repeat dose in 30 min, if
necessary. Hypotension may occur but can be
treated and/or prevented with calcium chloride,4
mL of a 10% solution.
 Diltiazem, 20 mg (0.25 mg/kg) IV over 2 min.
 Further alternatives include esmolol (300
g/kg/min), propranolol (0.5 to 1 mg IV), or
digoxin (0.5mg IV).
 Synchronized cardioversion should be done in
any unstable patient with hypotension, 33
pulmonary edema, or severe chest pain. The
 WPW syndrome occurs when electrical signals fail
to pause in the atrioventricular node because an
extra pathway allows the impulse to "bypass" the
normal pathway; and the syndrome is sometimes
called bypass tract. WPW syndrome causes heart
rates approaching 240 beats per minute.
 Occasionally, impulses can go down one extra
pathway and up another, creating a "loop" or
"short circuit," (called SVT because of WPW).
Patients with WPW syndrome may develop atrial
fibrillation and are at increased risk for developing
a dangerous ventricular arrhythmia when this
occurs.

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History
 mild chest discomfort or palpitations with or without syncope to
severe cardiopulmonary compromise or cardiac arrest.
 disease is discovered on routine electrocardiography (ECG),
independent of a concurrent tachydysrhythmia.
 rapid heart rates in the 250 (bpm) range, often with associated
hypotension.
 Many patients are not aware of their underlying condition.
Physical
 WPW has no specific examination features except for those that
may accompany symptomatic dysrhythmias.
 Many young patients appear minimally symptomatic (e.g.,
palpitations, weakness, mild dizziness) despite exceedingly fast
heart rates.
 On physical examination, the patient may be cool, diaphoretic, and
hypotensive.
 Crackles in the lungs are common, as the rapid heart rate may
cause pulmonary vascular congestion due congestive heart failure.
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Therapy for Wolff-Parkinson-White
syndrome in the prehospital setting depends
upon the patient's degree of stability and the
specific dysrhythmia.

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Upon presentation, immediately place an IV
line in the patient and connect him or her to
cardiac, blood pressure, and pulse oximetry
monitors.
 Administer oxygen if the patient is hypoxic.
 Immediately perform cardioversion on a
patient who is grossly unstable. Otherwise, a
defibrillator should be readily available.
 If a patient is in cardiac arrest, treat
according to advanced cardiac life support
(ACLS) guidelines.
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The sinus node emits abnormally fast
electrical signals, which increases the heart
rate to between 100 beats per minute to 140
beats per minute at rest, and 200 beats per
minute during exercise.
 A normal response to exercise or stress, it
can also be caused by: Adrenaline;
Consumption of caffeine, nicotine, or alcohol;
and Heart conditions.

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Sick sinus syndrome (SSS) is a type of
bradycardia in which the sinoatrial node is not
functioning as it should. This means that the
electrical signal that starts a heartbeat either
moves too slowly through the SA node
(sinoatrial block) or that there are pauses in
delivery of the electrical signal (sinus arrest).
 SSS can also cause tachycardia (heart rates
that are too fast) or bradycardia-tachycardia
syndrome (heart rates that fluctuate between
being too slow and too fast).
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• occurs when an ectopic atrial impulse discharges prematurely
and, in most cases, is conducted in a normal fashion through the
AV conducting system to the ventricles.

• Individuals of all ages experience PACs. PACs may occur in healthy

individuals as a result of various stimuli, such as emotions,
tobacco, alcohol, and caffeine.
• PACs also may be associated with rheumatic heart disease,
ischemic heart disease, mitral stenosis, heart failure, hypokalemia,
hypomagnesaemia, medications, and hyperthyroidism.
• No treatment is necessary in many cases. The patient should be
monitored and frequency of premature beats documented. In
addition, the patient should be assessed for underlying conditions
and treated.
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Hatem Alsrour

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