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asystole. If vagal maneuvers are used, make sure that resuscitative equipment is readily available.

Optimal treatment options

Drug therapy may be used, including digoxin, beta-adrenergic blockers, and calcium channel blockers. When other treatments fail, or if the patient is clinically unstable, synchronized cardioversion may be used.

Atrial overdrive pacing may also be used to stop the arrhythmia. This treatment helps suppress the depolarization of the ectopic pacemaker and permits the SA node to resume its normal role.

Monitor the strip

When caring for a patient with atrial tachycardia, carefully monitor his rhythm. Doing so may provide information about the cause of atrial tachycardia, which can facilitate treatment. In addition, monitor the patient for chest pain, indications of decreased cardiac output, and signs and symptoms of heart failure or myocardial ischemia.

Atrial flutter

Atrial flutter, a supraventricular tachycardia, is characterized by an atrial rate of 250 to 350 beats/minute, although it’s generally around 300 beats/minute. Originating in a single atrial focus, this rhythm results from circus reentry and possibly increased automaticity.

On an ECG, the P waves lose their distinction due to the rapid atrial rate. The waves blend together in a

saw-toothed appearance and are called flutter waves, or f waves. These waves are the hallmark of atrial flutter.

How it happens

Atrial flutter is commonly associated with second-degree block. In that instance, the AV node fails to allow conduction of all the impulses to the ventricles. As a result, the ventricular rate is slower. Atrial flutter may be caused by conditions that enlarge atrial tissue and elevate atrial pressures. It’s commonly found in patients

with severe mitral valve disease, hyperthyroidism, pericardial disease, and primary myocardial disease. The rhythm is also sometimes encountered in patients after cardiac surgery or in patients with acute MI, chronic obstructive pulmonary disease (COPD), and systemic arterial hypoxia. Atrial flutter rarely occurs

Atrial flutter is commonly associated with second-degree block.

in healthy people. When it does, it may indicate intrinsic cardiac disease.

Rating the ratio

The clinical significance of 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. If the ventricular rate is too slow (fewer than 40 beats/minute) or too fast (more than 150 beats/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, which can cause angina, heart failure, pulmonary edema, hypotension, and syncope.

What to look for

Atrial flutter is characterized by abnormal P waves that produce a saw-toothed appearance, the hallmark flutter-wave appearance. (See Identifying atrial flutter.) Varying degrees of AV block produce ventricular rates one-half to one-fourth of the atrial rate.

Saw-toothed P waves are the hallmark of atrial flutter.

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The AV node usually won’t accept more than 180 impulses/ 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/minute. With an atrial rate of 300, that rhythm is referred to as a 2:1 block. (See

Atrial flutter and sinus tachycardia.)

The QRS complex is usually normal but may be widened if flutter waves are buried in the complex. You won’t be able to identify a T wave, nor will you be able to measure the QT interval.

The atrial rhythm may vary between fibrillatory waves and flutter waves, an arrhythmia commonly referred to as atrial fibrillation and flutter.

Misleading pulses

When caring for a patient with atrial flutter, you may note that his peripheral or apical pulse is normal in rate and rhythm. That’s because the pulse reflects the number of ventricular contractions, not the number of atrial impulses.

If the ventricular rate is normal, the patient may be asymptomatic. However, if the ventricular rate is rapid, the patient may exhibit signs and symptoms of reduced cardiac output and cardiac decompensation.

How you intervene

If the patient is hemodynamically unstable, synchronized electrical cardioversion should be administered immediately. Cardioversion delivers electric current to the heart to correct an arrhythmia. It’s synchronized to discharge at the peak of the R wave. Synchronizing the energy current delivery with the R wave ensures that the current won’t be delivered on the vulnerable T wave, which could initiate ventricular tachycardia or ventricular fibrillation.

Control and convert operation

The focus of treatment for hemodynamically stable patients includes controlling the rate and converting the rhythm. Specific interventions depend on the patient’s cardiac function, whether preexcitation syndromes are involved, and the duration (less than or greater than 48 hours) of the arrhythmia.

For example, in atrial flutter with normal cardiac function and duration, direct current (DC) cardioversion may be considered; for duration greater than 48 hours, DC cardioversion wouldn’t be considered because it increases the risk of thromboembolism unless the patient has been adequately anticoagulated.

Mixed signals

Atrial flutter and sinus tachycardia

Whenever you see sinus tachycardia with a rate of 150 beats/minute, take another look. That rate is a common one for atrial flutter with 2:1 conduction. Look closely for flutter waves, which may be difficult to see if they’re hidden in the QRS complex. You may need to check another lead to clearly see them.

Atrial fibrillation

Atrial fibrillation, sometimes called A-fib, is defined as chaotic, asynchronous, electrical activity in atrial tissue. It’s the most common arrhythmia, affecting an estimated 2 million people in the United States. Atrial fibrillation stems from the firing of a number of impulses in reentry pathways. As with atrial flutter, atrial fibrillation results in a loss of atrial kick. The ectopic impulses may fire at a

rate of 400 to 600 times/minute, causing the atria to quiver instead of contract.

The ventricles respond only to those impulses that make it through the AV node. On an ECG, atrial activity is no longer represented by P waves but by erratic baseline waves called fibrillatory waves, or f waves. This rhythm may be either sustained or paroxysmal (occurring in bursts). It can be either preceded by or be the result of PACs.

The irregular conduction of impulses through the AV node produces a characteristic irregularly irregular ventricular response. If you see R waves that look irregularly irregular, suspect atrial fibrillation.

How it happens

Atrial fibrillation occurs more commonly than atrial flutter or atrial tachycardia. Atrial fibrillation can occur following cardiac surgery, or it can be caused by long-standing hypotension, pulmonary embolism, COPD, electrolyte imbalances, mitral insufficiency, mitral stenosis, hyperthyroidism, infection, coronary artery disease, acute MI, pericarditis, hypoxia, and atrial septal defects.

The rhythm may also occur in a healthy person who uses coffee, alcohol, or nicotine to excess or who’s fatigued and under stress. Certain drugs, such as aminophylline and digoxin, may contribute to the development of atrial fibrillation. Catecholamine release during exercise may also trigger the arrhythmia.

Whenever

I lose my kick, I jump start it with a little exercise. Loss of atrial kick may require something else!

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Where have all the atrial kicks gone?

As with other atrial arrhythmias, atrial fibrillation eliminates atrial kick. That loss, combined with the decreased filling times associated with rapid rates, can lead to clinically significant problems.

If the ventricular response is greater than 100 beats/minute—a condition called uncontrolled atrial fibrillation—the patient may develop heart failure, angina, or syncope.

Patients with preexisting cardiac disease, such as hypertrophic obstructive cardiomyopathy, mitral stenosis, rheumatic heart disease, and mitral prosthetic valves, tend to tolerate atrial fibrillation poorly and may develop shock and severe heart failure.

Left untreated, atrial fibrillation can lead to cardiovascular collapse, thrombus formation, and systemic arterial or pulmonary embolism. (See Risk of restoring sinus rhythm.)

What to look for

Atrial fibrillation is distinguished by the absence of P waves and an irregular ventricular response. When several ectopic sites in the atria fire impulses, depolarization can’t spread in an organized manner. (See Identifying atrial fibrillation.)

Small sections of the atria are activated individually, which results in the atrial muscle quivering instead of contracting. On an ECG, you’ll see uneven baseline f waves rather than clearly distinguishable P waves.

That fabulous filter

The AV node protects the ventricles from the 400 to 600 erratic atrial impulses that occur each minute by acting as a filter and blocking some of the impulses. The AV node itself doesn’t receive all the impulses, however. If muscle tissue around the AV node is in a refractory state, impulses from other areas of the atria can’t reach the AV node, which further reduces the number of atrial impulses conducted through to the ventricles.

Those two factors help explain the characteristic wide variation in R-R intervals in atrial fibrillation.

Barely measurable

The atrial rate is almost indiscernible but is usually greater than 400 beats/minute. The ventricular rate usually varies from 100 to 150 beats/minute but can be lower. When the ventricular response rate is below 100, atrial fibrillation is considered controlled. When it exceeds 100, the rhythm is considered uncontrolled.

Atrial fibrillation is called coarse if the f waves are pronounced and fine if they aren’t. Atrial fibrillation and flutter may also

Risk of restoring sinus rhythm

A patient with atrial fibrillation is at increased risk for developing atrial thrombus and systemic arterial embolism. Because the atria don’t contract, blood may pool on the atrial wall, and thrombi can form.

If normal sinus rhythm is restored and the atria contract normally, clots can break away and travel through the pulmonary or systemic circulation with potentially disastrous results.

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response or by cardioversion and drugs in combination to convert the rhythm to sinus.

Atrial fibrillation is treated following the same guidelines as atrial flutter.

Timing is everything

Electrical cardioversion is most successful if used within the first 48 hours of treatment and less successful if the rhythm has existed for a long time. If the patient shows signs of more severe angina or of decreased cardiac output, emergency measures are necessary.

When the onset of atrial fibrillation is acute and the patient can cooperate, vagal maneuvers or carotid sinus massage may slow the ventricular response but won’t convert the arrhythmia.

Cardioversion

A symptomatic patient needs immediate synchronized cardioversion. The patient should receive appropriate anticoagulation therapy first because cardioversion can cause emboli to form, especially in a patient with chronic or paroxysmal atrial fibrillation.

A conversion to normal sinus rhythm will cause forceful atrial contractions to resume abruptly. If a thrombus forms in the atria, the resumption of contractions can result in systemic emboli. (See

How synchronized cardioversion works.)

Immediate synchronized cardioversion reestablishes normal sinus rhythm in a symptomatic patient. Rhythm is very important!