By

Teddie Joe Snodgrass, RN, MBA, MSN

Revised: 09 April 2009

http://www.HeartyHealth.com/CV/training/a-flutter.html

Atrial Flutter

Atrial Flutter is an arrhythmia generated by a rapid, irritable focus in the atria which is the result of a flawed reentry circuit within the atria. It’s characterized by an atrial rate of 220-350 beats per minute. The atrial rate is greater than the ventricles can contract.

With atrial flutter, the transmission of the rapidly firing impulses is intermittently blocked at the AV node. Impulses that pass through may do so at consistent or variable intervals.

On the ECG, the “P” waves lose their distinction due to the rapid atrial rate. The waves blend together in a saw-tooth appearance and are called flutter waves; the saw-tooth distinction is also referred to by some practitioners’ as a picket fence. These waves are the hallmark of the atrial flutter arrhythmia. The rhythm is a result of a circular (circus) course or movement pathway (reentry) around the atria - enhanced automaticity has been suggested.

The Conduction System: Normal Electrical Activity

During normal electrical activity, the Sino-Atrial (SA) node which is located in the right atrium (RA) and which is also known as the major pacemaker of the heart fires at the intrinsic rate of 60-100 beats per minutes in a normal conduction environment.

The Atrio-Ventricular (AV) node is the backup pacemaker and gatekeeper of the electrical conduction system of the heart. Its intrinsic rate is rated at 40-60 beats per minutes.

The Bundle of HIS, right and left bundle branches, Purkinje fibers deliver the impulses to the ventricles. This area within the hearts “Conduction System” also acts as a backup pacemaker allowing for a ventricular backup intrinsic rate of 20-40 beats per minute.

A normal conduction pathway begins with electrical impulses that originate in the SA node and spread through the atria (causing the atria to contract), then are delayed slightly at the AV node before rapidly spreading to the Bundle of HIS, down the right & left Bundle Branches to the Purkinje fibers (which are like small fingerlike projections into the myocardium causing the ventricles to contract).

The Conduction System: Abnormal Electrical Activity (Atrial Flutter)

Atrial flutter is determined by the number of impulses conducted through the node – expressed as a conduction ratio, for example 2:1 or 4:1 – and the resulting ventricular rate. The atria are beating too rapidly for the ventricles to respond, so the AV node blocks some of the impulses and may be described as 4:1, 5:1 et cetera conduction pattern of, for example, 4 flutter waves to 1 QRS. If the ventricular rate is too slow (fewer than 40 beats per minute) or too fast (more than 150 beats per minute), cardiac output can be seriously compromised.

Usually the faster the ventricular rate, the more dangerous the arrhythmia. The rapid rate reduces ventricular filling time and coronary perfusion time.

Some Common Etiologies or Precipitating Factors of Atrial Flutter

·         Irritable atrial tissue

·         Acute or chronic cardiac disease

·         Inferior wall MI (transient)

·         Coronary Artery Disease (CAD)

·         Congestive Heart Failure (CHF)

·         Cardiomyopathy

·         Acute pulmonary embolism

·         Sick sinus syndrome,

·         Hyperthyroidism

·         Hypoxia

·         Hypertension

·         Digitalis toxicity

·         Pericarditis

·         Mitral and tricuspid value disorders (valvular disease) such as rheumatic heart disease

·         Enhanced automaticity

·         Drug-induced: digoxin or quinidine; beta-blockers agonists, theophylline

What to Look For:

The AV node usually won’t accept more than 180 impulses per minute and allows every second, third, or fourth impulse to be conducted, the ratio of which determines the ventricular rate. One of the most common rates is 150 beats per minute. With an atrial rate of 300, that rhythm is referred to as a 2:1 block.

The AV node is a protective mechanism. Imagine the atria depolarizing at a rate of 220-350 beat per minute. If all of these atrial depolarizing beats made it through to the ventricles, then they would more than likely begin to fibrillate. Think of the AV node as an air traffic control station where an enormous amount of runways merge. The air traffic controller is only going to allow some of the planes (atrial depolarization’s) through at any given time to avoid a crash (the ventricles starting to fibrillate i.e., Ventricular Fibrillation (VF)). So, the AV node helps in protecting the ventricles from a crash by only allowing some of that atrial depolarization’s to make down through the bundle of His into the bundle branches and on to the ventricles.

Controlled atrial flutter is when the ventricular rate is less than 100 beats per minute.

Uncontrolled atrial flutter is when the ventricular rate is greater than 100 beats per minute.

It’s important to remember that the ventricles have more time to fill during diastole when the heart is beating at less than 100 beats per minute. So, our goal is to keep the atrial flutter under control. This is normally accomplished by drug therapy.

As in atrial fibrillation, coordinated contraction of the atria is also absent with atrial flutter. Here again, as with atrial fibrillation, we are losing our “atrial kick” that will normally result in a loss of cardiac output and in a lower blood pressure.

Atrial kick is defined as an additional 10% to 30% of ventricular filling of blood that occurs during atrial contraction at the end of diastolic filling of the ventricles.

How to Intervene: What You Should Do!

Atrial flutter with a rapid ventricular response and reduced cardiac output requires immediate intervention. Therapy aims to control the ventricular rate and convert the atrial ectopic rhythm to a normal sinus rhythm. Cardioversion is the treatment of choice. If possible, treatment includes removal of the precipitating factor.

Note: Anticoagulants should be administered first before cardioversion to prevent emboli from forming.

The following drugs may be used to control the ventricular rate:

• Digitalis
• Verapamil (Isoptin)
• Beta-adrenergic blockers (esmolol, metoprolol or propranolol)
• Procainamide (Pronestyl)
• Quinidine Sulfate*

* Never administer Quinidine Sulfate to a patient in Atrial Flutter without first administering Digoxin.

It’s also important to note that drugs “ARE NOT” to be used to manage a patient with unstable tachycardia. Immediate cardioversion is recommended. If the patient is awake and conscious, consider administering sedative drugs for comfort. However, do not delay immediate cardioversion in the unstable patient.

Nursing Priorities:

• Ensure patient is oxygenated appropriately.
• Monitor your patient's blood pressure – look for a low blood pressure.
• Assess for syncope.
• Assess for palpitations.
• Assess for Shortness Of Breath (SOB).

Remember, your patient may have a lower blood pressure due to the loss of atrial kick.

ECG Findings:

·         Rate: The atrial rate 220 to 350 per minute. Ventricular response is a function of the AV node block or conduction of atrial impulses. Ventricular response rarely is > 150 to 180 beats because of the AV nodal conduction limits.

·         Rhythm: Regular (unlike atrial fibrillation). Ventricular is also often regular. Set ratio to atrial rhythm, for example 2-to-1 or 4-to-1.

·         P-Wave: Configuration: No true “P” waves are seen. Flutter waves appear in “saw tooth” pattern are a classic hallmark sign. Rate: The atrial rate may vary from 220 to 350 beats per minute. Rhythm: Flutter or saw tooth waves are continuous.

·         P-R Interval: No “P” waves are identifiable, so no “P-R” interval can be measured. Flutter waves outnumber QRS complexes, but it is difficult to determine which flutter wave caused the QRS complex.

·         QRS Complex: Configuration: QRS complexes remain less than or equal to 0.10 to 0.12 seconds unless QRS complex is distorted by flutter waves or by conduction defects through the ventricles. QRS complexes however do appear normal. Rate: The ventricular rate will vary, depending on the number of impulses conducted through the AV node. Rhythm: The R-R interval may be regular or irregular. Duration: The QRS duration is usually normal ranging from 0.04 – 0.12 when measured.

Effects on the Patient:

With a diminishing of synchronous atrial and ventricular contractions comes a loss of atrial input or atrial kick. This loss of atrial input or atrial kick reduces cardiac output by 10% to 30% therefore Congestive Heart Failure (CHF) may develop. Atrial flutter may also produce rapid ventricular rates that further reduce cardiac output.

Treatments:

Atrial Flutter that does not respond to medication, or is creating an acute or rapid ventricular rhythm may be treated with synchronized cardioversion.

Drug therapy includes: Digoxin*, Cardizem, Propranolol, Verapamil, Quinidine Sulfate**, and Procainamide.

Cardioversion may also be used if drugs fail or the patients condition is acute.

* Cardioversion occurring after Digoxin administration may result in bradycardia or asystole due to the depression of the SA node.

** Never administer Quinidine Sulfate to a patient in Atrial Fibrillation without first administering Digoxin.

Nursing Implications:

·         Ensure patient is adequately oxygenated.

·         Assess the patient for signs or symptoms of CHF

·         Monitor serum digoxin levels

·          Monitor your patient's blood pressure.

·          Assess for syncope.

·          Assess for palpitations.

·          Assess for Shortness Of Breath (SOB).

For a review of the hearts conduction system with this article click the following link: