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Sinus node arrhythmias

Just the facts

In this chapter, you’ll learn:

the proper way to identify the various sinus node arrhythmias

the role of the sinoatrial node in arrhythmia formation

the causes, significance, treatment, and nursing implications of each arrhythmia

assessment findings associated with each arrhythmia

interpretation of sinus node arrhythmias on an electrocardiogram.

A look at sinus node arrhythmias

When the heart functions normally, the sinoatrial (SA) node, also called the sinus node, acts as the primary pacemaker. The sinus node assumes this role because its automatic firing rate exceeds that of the heart’s other pacemakers. In an adult at rest, the sinus node has an inherent firing rate of 60 to 100 times/minute.

The SA node’s blood supply comes from the right coronary artery or the left circumflex artery. The autonomic nervous system richly innervates the sinus node through the vagus

nerve, a parasympathetic nerve, and several sympathetic nerves. Stimulation of the vagus nerve decreases the node’s firing rate, and stimulation of the sympathetic system increases it.

SINUS NODE ARRHYTHMIAS

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Sinus arrhythmia

In sinus arrhythmia, the pacemaker cells of the SA node fire irregularly. The cardiac rate stays within normal limits, but the rhythm is irregular and corresponds with the respiratory cycle. Sinus arrhythmia can occur naturally in athletes and children, but it rarely occurs in infants. Conditions unrelated to respiration may also produce sinus arrhythmia, including inferior wall myocardial

infarction (MI), advanced age, use of digoxin (Lanoxin) or morphine, and conditions involving increased intracranial pressure.

How it happens

Sinus arrhythmia, the heart’s normal response to respirations, results from an inhibition of reflex vagal activity, or tone. During inspiration, an increase in the flow of blood back to the heart reduces vagal tone, which increases the heart rate. ECG complexes fall closer together, which shortens the P-P interval, the time elapsed between two consecutive P waves.

During expiration, venous return decreases, which in turn increases vagal tone, slows the heart rate, and lengthens the P-P interval. (See Breathing and sinus arrhythmia.)

Breathing and sinus arrhythmia

When sinus arrhythmia is related to respirations, you’ll see an increase in heart rate with inspiration and a decrease with expiration, as shown here.

Sick sinus

Sinus arrhythmia usually isn’t significant and produces no symptoms. A marked variation in P-P intervals in an older adult, however, may indicate sick sinus syndrome, a related, potentially more serious phenomenon.

What to look for

When you look for sinus arrhythmia, you’ll see that the rhythm is irregular and corresponds to the respiratory cycle. (See Identifying sinus arrhythmia.) The difference between the shortest

and longest P-P intervals—and the shortest and longest R-R inter- vals—exceeds 0.12 second.

The atrial and ventricular rates are within normal limits (60 to 100 beats/minute) and vary with respiration—faster with inspiration, slower with expiration. All other parameters are normal, except for the QT interval, which may vary slightly but remains normal.

It’s all in the breath

Look for a peripheral pulse rate that increases during inspiration and decreases during expiration. If the arrhythmia is caused by an underlying condition, you may note signs and symptoms of that condition.

Identifying sinus arrhythmia

This rhythm strip illustrates sinus arrhythmia. Look for these distinguishing characteristics.

The cyclic irregular rhythm varies with the respiratory cycle.

How it happens

Sinus bradycardia usually occurs as the normal response to a reduced demand for blood flow. In this case, vagal stimulation increases and sympathetic stimulation decreases. (See Causes of sinus bradycardia.) As a result, automaticity (the tendency of cells to initiate their own impulses) in the SA node diminishes.

A tolerable condition?

Sinus bradycardia commonly occurs after an inferior wall MI that involves the right coronary artery, which supplies blood to the SA node. It can also result from numerous other conditions and the use of certain drugs.

The clinical significance of sinus bradycardia depends on how low the rate is and whether the patient is symptomatic. For example, most adults can tolerate a sinus bradycardia of 45 to 59 beats/minute but are less tolerant of a rate below 45 beats/ minute.

No symptoms? No problem.

Usually, sinus bradycardia produces no symptoms and is insignificant. Unless the patient shows symptoms of decreased cardiac output, no treatment is necessary. (See the appendix ACLS algorithms.)

Symptoms? Problem!

When sinus bradycardia produces symptoms, however, prompt attention is critical. The heart of a patient with underlying cardiac disease may not be able to compensate for a drop in rate by increasing its stroke volume. The resulting drop in cardiac output produces such signs and symptoms as hypotension and dizziness. Bradycardia may also predispose some patients to more serious arrhythmias, such as ventricular tachycardia and ventricular fibrillation.

Causes of sinus bradycardia

Identifying sinus bradycardia

This rhythm strip illustrates sinus bradycardia. Look for these distinguishing characteristics.

Atropine is given as a 0.5 mg dose by rapid injection. The dose may be repeated every 3 to 5 minutes up to a maximum of 3 mg total. If atropine proves ineffective, administer an epinephrine infusion at a rate of 2 to 10 mcg/minute. If low blood pressure accompanies bradycardia, administer a dopamine infusion at 2 to 10 mcg/kg/minute. Treatment of chronic, symptom-producing sinus bradycardia requires insertion of a permanent pacemaker.

Check the ABCs

If the patient abruptly develops a significant sinus bradycardia, assess his airway, breathing, and circulation (ABCs). If these are adequate, determine whether the patient has an effective cardiac output. If not, he’ll become symptomatic. (See Clues to symptomatic bradycardia, page 70.)

When administering atropine, be sure to give the correct dose: Doses lower than 0.5 mg can have a paradoxical effect, slow-

ing the heart rate even further. Keep in mind that a patient with a transplanted heart won’t respond to atropine and may require pacing for emergency treatment.