Hatem Alsrour


Normal heart rhythm & depolarization. Definition of Atrial Arrhythmias Types of Atrial Arrhythmias & their

characteristics Prehospital & ED management of Atrial Arrhythmias Treatment


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.

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.


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)

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.


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


 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


 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).


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


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.


 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 ratecontrolling 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.


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) 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.


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

 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


 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.
 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)


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 betaadrenergic blockers.


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.

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 betablockers and calcium-channel blockers can also cause sinus bradycardia. Occasionally sinus bradycardia can be caused by impaired conduction of impulses to the atrial muscles.


 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.


 Sinus bradycardia is most often asymptomatic.
 Syncope  Dizziness  Lightheadedness  Chest pain  Shortness of breath  Exercise intolerance

However, symptoms may include the following:

 Pertinent elements of the history include the


 Previous cardiac history (e.g., myocardial infarction,

congestive heart failure, valvular failure)  Medications  Toxic exposures  Prior illnesses


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


 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.


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.


 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.

 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.

 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 nearfainting episodes, and, rarely, fainting episodes.

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.

 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.


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.


 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, 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.

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.

Therapy for Wolff-Parkinson-White

syndrome in the prehospital setting depends upon the patient's degree of stability and the specific dysrhythmia.


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.

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.


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).

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.

Hatem Alsrour


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