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

Conditions unrelated to respiration may also produce sinus arrhythmia, including heart disease; inferior wall myocardial infarction (MI); the use of certain drugs, such as digoxin and morphine; and conditions involving increased intracranial pressure.

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, but potentially more serious, phenomenon.

The patient’s peripheral pulse rate increases during inspiration and decreases during expiration. Sinus arrhythmia is easier to detect when the heart rate is slow; it may disappear when the heart rate increases, as with exercise.

If the arrhythmia is caused by an underlying condition, you may note signs and symptoms of that condition. Marked sinus arrhythmia may cause dizziness or syncope in some cases.

Unless the patient is symptomatic, treatment usually isn’t necessary. If sinus arrhythmia is unrelated to respirations, the underlying cause may require treatment.

When caring for a patient with sinus arrhythmia, observe the heart rhythm during respiration to determine whether the arrhythmia coincides with the respiratory cycle. Check the monitor carefully to avoid an inaccurate interpretation of the waveform.

If sinus arrhythmia is induced by medications, such as morphine and other sedatives, the practitioner may decide to continue to give the patient the medications because discontinuing them may be worse for the patient than the rhythm itself.

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. As a result, automaticity (the tendency of cells to initiate their own impulses) in the SA node diminishes. It may occur normally during sleep or in a person with a well-conditioned heart—an athlete, for example.

Sinus bradycardia may be caused by:

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.

Usually, sinus bradycardia doesn’t produce symptoms and is
insignificant. Many athletes develop sinus bradycardia because their well-conditioned hearts can maintain a normal stroke volume with less-than-normal effort. Sinus bradycardia also occurs normally during sleep as a result of circadian variations in heart rate.

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.

In a patient with acute inferior wall MI, sinus bradycardia is considered a favorable prognostic sign, unless it’s accompanied by hypotension. Because sinus bradycardia rarely affects children, it’s considered a poor prognostic sign in ill children.

The patient will have a pulse rate of less than 60 beats/minute, with a regular rhythm. As long as he’s able to compensate for the decreased cardiac output, he’s likely to remain asymptomatic. If compensatory mechanisms fail, however, signs and symptoms of declining cardiac output usually appear, including:

Palpitations and pulse irregularities may occur if the patient experiences ectopy such as premature atrial, junctional, or ventricular contractions. This is because the SA node’s increased relative refractory period permits ectopic firing. Bradycardia-induced syncope (Stokes-Adams attack) may also occur.