During inspiration, blood flow to the heart increases. This increase reduces vagal tone, which in turn increases heart rate. During expiration, venous return decreases. This increases vagal tone, slowing the heart rate. (See Breathing and sinus arrhythmia.)

To identify sinus arrhythmia, observe the patient’s heart rhythm during respiration. The atrial and ventricular rates should be within normal limits (60 to 100 beats/minute) but increase during inspiration and slow with expiration. Electrocardiogram (ECG) complexes fall closer together during inspiration, shortening the P-P interval (the time elapsed between two consecutive P
waves). During expiration, the P-P interval lengthens. The difference between the shortest and longest P-P intervals exceeds 0.12 second. (See Recognizing sinus arrhythmia, page 144.)

Check the patient’s peripheral pulse rate. It, too, should increase during inspiration and decrease during expiration. If the arrhythmia is caused by an underlying condition, you may note signs and symptoms of that condition as well.

When evaluating sinus arrhythmia, be sure to check the monitor carefully. A marked variation in P-P intervals in an elderly patient may indicate sick sinus syndrome, a related but more serious phenomenon. (See A longer look at sinus arrhythmia, page 144.)

Sinus bradycardia usually occurs as a 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.

Sinus bradycardia commonly occurs after an inferior-wall MI involving the right coronary artery, which supplies blood to the SA node. Numerous other conditions and the use of certain drugs may also cause sinus bradycardia. (See Causes of sinus bradycardia.)

In sinus bradycardia, the heartbeat is regular with a rate less than 60 beats/minute. All other ECG findings are normal: a P wave precedes each QRS complex and the PR interval, QRS complex, T wave, and QT interval are all normal. (See Recognizing sinus bradycardia, page 146.)

The clinical significance of sinus bradycardia depends on the rate and whether the patient is symptomatic. Most adults can tolerate a sinus bradycardia of 45 to 59 beats/minute.

However, if the rate falls below 45 beats/minute, patients usually have signs and symptoms of decreased cardiac output, such as hypotension, dizziness, confusion, or syncope (Stokes-Adams attack). Keep in mind, too, that patients with underlying cardiac disease may be less tolerant of a drop in heart rate.

Bradycardia may also trigger more serious arrhythmias as well. Ectopic beats, such as premature atrial, junctional, or ventricular contractions, may also occur, causing palpitations and an irregular pulse.

In a patient with acute inferior-wall MI, sinus bradycardia is considered a favorable prognostic sign, unless it’s accompanied by hypotension. That’s because, with a slower heart rate, the heart uses less oxygen and avoids ischemia.

Sinus bradycardia rarely affects children. When it occurs in an ill child, it’s considered an ominous sign.

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 may develop these signs and symptoms:

• hypotension

• cool, clammy skin

• altered mental status

• dizziness

• blurred vision

• crackles, dyspnea, and a third heart sound (S₃), which indicate heart failure

• chest pain

• syncope.

When administering atropine, be sure to give the correct dose: Doses lower than 0.5 mg may have a paradoxical effect, slowing 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.

The clinical significance of sinus tachycardia depends on the underlying cause. (See Causes of sinus tachycardia.)

Sinus tachycardia in a patient who has had an acute MI suggests massive heart damage and is a poor prognostic sign. Persistent tachycardia may also signal impending heart failure or cardiogenic shock.

In sinus tachycardia, atrial and ventricular rhythms are regular. Both rates are equal, generally 100 to 160 beats/minute. As in sinus bradycardia, the P wave is of normal size and shape and precedes each QRS, but it may increase in amplitude. As the heart rate increases, the P wave may be superimposed on the preceding T wave and difficult to identify. The PR interval, QRS complex, and T wave are normal. The QT interval normally shortens with tachycardia. (See Recognizing sinus tachycardia.)

When assessing a patient with sinus tachycardia, look for a peripheral pulse rate of more than 100 beats/minute with a regular rhythm. Usually, the patient will be asymptomatic.

If cardiac output falls and compensatory mechanisms fail, the patient may experience hypotension, syncope, and blurred vision. He may report chest pain and palpitations, commonly described as a pounding chest or a sensation of skipped heartbeats. He may also report a sense of nervousness or anxiety. If heart failure develops, he may exhibit lung crackles, an extra heart sound (S₃), and jugular vein distention. (See What happens in tachycardia, page 150.)

Because the heart demands more oxygen at higher rates, tachycardia can trigger chest pain in patients with coronary artery disease (CAD). An increase in heart rate can also be detrimental for patients with obstructive types of heart conditions, such as aortic stenosis and hypertrophic cardiomyopathy.

If sinus tachycardia leads to cardiac ischemia, treatment may include medications to slow the heart rate. The most commonly used drugs include beta-adrenergic blockers, such as metoprolol (Lopressor) and atenolol (Tenormin), and calcium channel blockers such as verapamil (Isoptin) and diltiazem (Cardizem).

The goal of an intervention for the patient with sinus tachycardia is to maintain adequate cardiac output and tissue perfusion and to identify and correct the underlying cause.

Check the patient’s medication history. Over-thecounter sympathomimetic agents, which mimic the effects of the sympathetic nervous system, may contribute to sinus tachycardia. These agents may be contained in nose drops and cold formulas.

You should also ask about the patient’s use of caffeine, nicotine, herbal supplements, alcohol, and such illicit drugs as cocaine and amphetamines—any of which could trigger tachycardia. Advise him to avoid these substances.

Here are other steps you should take for the patient with sinus tachycardia:

• Because sinus tachycardia can lead to injury of the heart muscle, check for chest pain or angina. Also assess for signs and symptoms of heart failure, including crackles, an S₃ heart sound, and jugular vein distention.

• Monitor intake and output as well as daily weight.

• Check the patient’s level of consciousness (LOC) to assess cerebral perfusion.

• Provide the patient with a calm environment. Help reduce fear and anxiety, which can fuel the arrhythmia.

• Teach about procedures and treatments. Include relaxation techniques in the information you provide.

• Be aware that a sudden onset of sinus tachycardia after an MI may signal extension of the infarction. Prompt recognition is vital so treatment can be started.

Sinus arrest occurs when the SA node fails to generate an impulse. Such failure may result from several conditions, including acute infection, heart disease, and vagal stimulation. Pauses of 2 to 3 seconds normally occur in healthy adults during sleep and occasionally in patients with increased vagal tone or hypersensitive carotid sinus disease. Sinus arrest may be associated with sick sinus syndrome, a collection of sinus arrhythmias that includes sinus bradycardia and other abnormalities of the sinus conduction system. (See Causes of sinus arrest, page 154.)

When assessing for sinus pause, you’ll find on the ECG that atrial and ventricular rhythms are regular except for a missing complex at the onset of atrial standstill. Atrial and ventricular rates are equal and are usually within normal limits. The rate may vary, however, as a result of the pauses. (See Recognizing sinus arrest, page 155.)

A P wave that’s of normal size and shape precedes each QRS complex but is absent during a pause. The PR interval is normal and constant when the P wave is present and not measurable when it’s absent. The QRS complex, the T wave, and the QT interval are normal when present and are absent during a pause.

Junctional escape beats, including premature atrial, junctional, or ventricular contractions, may also be present. With sinus arrest, the length of the pause isn’t a multiple of the previous R-R intervals.

You won’t be able to detect a pulse or heart sounds when sinus arrest occurs. If the pauses are short and infrequent, the patient will most likely be asymptomatic and won’t require treatment. He may have a normal sinus rhythm for days or weeks between episodes of sinus arrest, and he may not be able to feel the arrhythmias at all.

Recurrent and prolonged pauses may cause signs of decreased cardiac output, such as low blood pressure; altered mental status; and cool, clammy skin. The patient may also complain of dizziness or blurred vision. The arrhythmias can produce syncope or near-syncopal episodes within 7 seconds of asystole.

Examine the circumstances under which sinus pauses occur. A sinus pause may be insignificant if detected while the patient
is sleeping. If the pauses are recurrent, assess the patient for evidence of decreased cardiac output, such as altered mental status; low blood pressure; and cool, clammy skin.

Ask him whether he’s dizzy or light-headed or has blurred vision. Does he feel as if he has passed out? If so, he may be experiencing syncope from a prolonged sinus arrest.

Document the patient’s vital signs and how he feels during pauses as well as what activities he was involved in when they occurred. Activities that increase vagal stimulation, such as Valsalva’s maneuver or vomiting, increase the likelihood of sinus pauses.

Assess for a progression of the arrhythmia. Notify the doctor immediately if the patient becomes unstable. Withhold medications that may contribute to sinus pauses and check with the doctor about whether those drugs should be continued.

If appropriate, be alert for signs of digoxin (Lanoxin), quinidine, or procainamide (Pronestyl) toxicity. Obtain a serum digoxin level and a serum electrolyte level.

A patient who develops signs of circulatory collapse needs immediate treatment. As with sinus bradycardia, emergency treatment
includes administration of atropine or epinephrine and the use of a temporary pacemaker. A permanent pacemaker may be implanted for long-term management.

The goal for the patient with sinus arrest is to maintain adequate cardiac output and perfusion. Be sure to record and document the frequency and duration of pauses. Determine whether a pause is the result of sinus arrest or SA block. If a pacemaker is implanted, give the patient discharge instructions about pacemaker care.

Sick sinus syndrome results either from a dysfunction of the sinus node’s automaticity or from abnormal conduction or blockages of impulses coming out of the nodal region. These conditions, in turn, stem from a degeneration of the area’s autonomic nervous system and partial destruction of the sinus node, as may occur with an interrupted blood supply after an inferior-wall MI. (See Causes of sick sinus syndrome.)

In addition, certain conditions can affect the atrial wall surrounding the SA node and cause exit blocks. Conditions that cause inflammation or degeneration of atrial tissue can also lead to sick sinus syndrome. In many patients, though, the exact cause of sick sinus syndrome is never identified.

Look for an irregular rhythm with sinus pauses and abrupt rate changes. Atrial and ventricular rates may be fast, slow, or alternating periods of fast rates and slow rates interrupted by pauses.

The P wave varies with the rhythm and usually precedes each QRS complex. The PR interval is usually within normal limits but varies with changes in the rhythm. The QRS complex and T wave are usually normal, as is the QT interval, which may vary with rhythm changes.

The patient’s pulse rate may be fast, slow, or normal, and the rhythm may be regular or irregular. You can usually detect an irregularity on the monitor or when palpating the pulse, which may feel inappropriately slow and then become rapid.

If you monitor the patient’s heart rate during exercise or exertion, you may observe an inappropriate response to exercise such as a failure of the heart rate to increase. You may also detect episodes of brady-tachy syndrome, atrial flutter, atrial fibrillation, SA block, or sinus arrest on the monitor.

The patient may show signs and symptoms of decreased cardiac output, such as hypotension, blurred vision, and syncope, a common experience with this arrhythmia. The length of a pause significant enough to cause syncope varies with the patient’s age, posture at the time, and cerebrovascular status. Consider any pause that lasts 2 to 3 seconds significant.

Other assessment findings depend on the patient’s condition. For instance, he may have crackles in the lungs, an S₃ heart sound, or a dilated and displaced left ventricular (LV) apical impulse if he has underlying cardiomyopathy.

Unfortunately, medications used to suppress tachyarrhythmias may worsen underlying SA node disease and bradyarrhythmias. The patient may need anticoagulants if he develops sudden bursts, or paroxysms, of atrial fibrillation. The anticoagulants help prevent thromboembolism and stroke, a complication of the condition. Because the syndrome is progressive and chronic, a symptomatic patient needs lifelong treatment.

When caring for a patient with sick sinus syndrome, monitor and document all arrhythmias he experiences and signs or symptoms he develops. Assess how his rhythm responds to activity and pain and look for changes in the rhythm.

Watch the patient carefully after starting calcium channel blockers, beta-adrenergic blockers, or other antiarrhythmic medications. If treatment includes anticoagulant therapy and/or the insertion of a pacemaker, make sure the patient and his family receives appropriate instruction.

PACs commonly occur in a normal heart and are rarely dangerous in a patient who doesn’t have heart disease. In fact, they usually cause no symptoms and can go unrecognized for years. (See Causes of PACs.)

However, in patients with heart disease, PACs may lead to more serious arrhythmias, such as atrial fibrillation and atrial flutter. In a patient who has had an acute MI, PACs can serve as an early sign of heart failure or an electrolyte imbalance. PACs can also result from the release of the neurohormone catecholamine during episodes of pain or anxiety.

The hallmark ECG characteristic of a PAC is a premature P wave with an abnormal configuration (when compared with a sinus P wave). It may be lost in the previous T wave, distorting that wave’s configuration. (The T wave might be bigger or have an extra bump.) Varying configurations of the P wave indicate more than one ectopic site. (See Nonconducted PACs and second-degree AV block, page 162.)

The PR interval is usually normal but may be shortened or slightly prolonged, depending on the origin of the ectopic focus. If no QRS complex follows the premature P wave, a nonconducted PAC has occurred.

PACs may occur in bigeminy (every other beat is a PAC), trigeminy (every third beat is a PAC), or couplets (two PACs at a time). The patient may have an irregular peripheral or apical pulse rhythm when the PACs occur. He may complain of palpitations, skipped beats, or a fluttering sensation. In a patient with heart disease, signs and symptoms of decreased cardiac output—such as hypotension and syncope—may occur.

When caring for a patient with PACs, assess him to help determine what’s triggering the ectopic beats. Tailor your patient teaching to help the patient correct or avoid the underlying cause. For example, the patient might need to avoid caffeine or smoking or learn stress reduction techniques to lessen his anxiety.

If the patient has ischemic or valvular heart disease, monitor him for signs and symptoms of heart failure, electrolyte imbalances, and the development of more severe atrial arrhythmias.

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 rarely occurs in a healthy person. When it does, it may indicate intrinsic cardiac disease. (See Causes of atrial flutter.)

Atrial flutter is characterized by abnormal P waves that lose their distinction because of the rapid atrial rate. The waves blend together, creating a saw-toothed or shark fin appearance and are called flutter waves, or F waves. Varying degrees of AV block produce ventricular rates one-half to one-fourth of the atrial rate. 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. (See Recognizing atrial flutter, page 164.)

The atrial rhythm may vary between fibrillatory waves and flutter waves, an arrhythmia commonly referred to as atrial fibrillation and flutter. Fibrillatory waves are uneven baseline fibrillation waves caused by the initiation of chaotic impulses from multiple ectopic sites in the atria. Depolarization can’t spread in an organized manner because the atria quiver instead of contract.

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 (meaning that for every 2 atrial impulses, 1 is conducted; or for every 4, 1 is conducted)— and the resulting ventricular rate. If the ventricular rate is too slow (less than 40 beats/minute) or too fast (more than 150 beats/minute), cardiac output may 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.

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.)

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.

Synchronized cardioversion delivers an electrical stimulus during depolarization. The stimulus makes part of the myocardium refractory to ectopic impulses and terminates circuit reentry movements.

Drug therapy includes digoxin and calcium channel blockers, which decrease AV conduction time. Quinidine may be given to convert flutter to fibrillation, an easier arrhythmia to treat. If digoxin and quinidine therapy is used, the patient must first be given a loading dose of digoxin. Ibutilide (Corvert) may be used to convert recent-onset atrial flutter to sinus rhythm. If possible, the underlying cause of the atrial flutter should be treated. However, it should only be used if the atrial flutter or fibrillation have been going on for less than 48 hours, and there is a high risk for arrhythmias in patients who show LV dysfunction. If treatment is to be administered, synchronized cardioversion is still the best option, especially for the unstable patient.

Because atrial flutter may be an indication of intrinsic cardiac disease, monitor the patient closely for signs and symptoms of low cardiac output. If cardioversion is indicated, prepare the patient for IV administration of a sedative or anesthetic as ordered. The American Heart Association (AHA) recommends caution with the use of sedation and/or analgesia if the patient is hypotensive (systolic blood pressure [SBP] <90) or has any neurologic compromise; however, it should be remembered that this is an extremely uncomfortable and even painful procedure for most patients. Keep resuscitative equipment at the bedside. Be alert to the effects of digoxin, which depresses the SA node. Also, be alert for bradycardia because cardioversion can decrease the heart rate.

Atrial fibrillation occurs more commonly than atrial flutter or atrial tachycardia. It stems from the firing of several impulses in circuit reentry pathways. (See Causes of atrial fibrillation.)

In atrial fibrillation, small sections of the atria are activated individually. This situation causes the atrial muscle to quiver, or fibrillate, instead of contract. On an ECG, you’ll see uneven baseline F waves rather than clearly distinguishable P waves. Also, when several ectopic sites in the atria fire impulses, depolarization can’t spread in an organized manner, which causes an irregular ventricular response. (See Recognizing atrial fibrillation.)

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

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. Atrial fibrillation is called coarse if the F waves are pronounced; the fibrillation is called fine if they aren’t. Atrial fibrillation and flutter may also occur simultaneously. Look for a configuration that varies between fibrillatory waves and flutter waves.

As with other atrial arrhythmias, atrial fibrillation eliminates atrial systole (also known as 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 or rapid ventricular response—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.