Clinical Electrocardiography: A Simplified Approach, 7th Edition (2006)

Part II. CARDIAC RHYTHM DISTURBANCES

Chapter 13. Sinus Rhythms

NORMAL SINUS RHYTHM

Normal sinus rhythm is the reference physiologic rhythm of the heart. The diagnosis of normal sinus rhythm was described in Chapter 3 . When the sinus (or sinoatrial [SA]) node is pacing the heart, atrial depolarization spreads from right to left and downward toward the atrioventricular (AV) junction. An arrow representing this depolarization wave points downward and toward the left. Therefore, with normal sinus rhythm, the P wave is negative in lead aVR and positive in lead II (Figs. 13-1 to 13-4 [1] [2] [3] [4]; see also Fig. 4-3 ).

FIGURE 13-1  Each QRS complex is preceded by a P wave that is negative in lead aVR and positive in lead II.

FIGURE 13-2  Sinus tachycardia.

FIGURE 13-3  Sinus bradycardia. Notice the negative P waves, because this is lead aVR.

FIGURE 13-4  Respiratory sinus arrhythmia. Normally, the heart rate increases slightly with inspiration and decreases slightly with expiration.

By convention, normal sinus rhythm is usually defined as sinus rhythm with a heart rate between 60 and 100 beats/min. Sinus rhythm with a heart rate of less than 60 beats/min is called sinus bradycardia.[*] Sinus rhythm with a heart rate greater than 100 beats/min is termed sinus tachycardia.

*  Some authors define sinus bradycardia based on a heart rate of less than 50 beats/min.

 

REGULATION OF THE HEART RATE

The heart, like the other organs of the body, has a special nerve supply from the autonomic nervous system, which controls involuntary muscle action. The autonomic nerve supply to the heart (the SA and AV nodes in particular) consists of two opposing groups of fibers: the sympathetic nerves and the parasympathetic nerves. Sympathetic stimulation produces an increased heart rate and also increases the strength of myocardial contraction. Parasympathetic stimulation (from the vagus nerve) produces a slowing of the heart rate as well as a slowing of conduction through the AV nodal area. In this way, the autonomic nervous system exerts a counterbalancing control of the heart rate.

The sympathetic nervous system acts as a cardiac accelerator, whereas the parasympathetic (vagal) system produces a braking effect. For example, when you become excited or upset, increased sympathetic stimuli (and diminished parasympathetic tone) result in an increased heart rate and increased contractility, producing the familiar sensation of a pounding heart (palpitations). Palpitations may be associated with a normal heartbeat, isolated premature beats (atrial or ventricular), or an actual run of ectopic (nonsinus) heartbeats (e.g., from atrial fibrillation, paroxysmal supraventricular tachycardia, or ventricular tachycardia).

 

SINUS TACHYCARDIA

Sinus tachycardia is simply sinus rhythm with a heart rate exceeding 100 beats/min. In adults, the heart rate with sinus tachycardia is generally between 100 and 180 beats/min. Somewhat faster rates, up to 200 beats/min or so, can be observed in healthy young adults during maximal exercise.

Aging decreases the capacity to generate very rapid sinus rates. Elderly individuals (more than 70 years) rarely show sinus tachycardia at rates above 140 to 150 beats/min. Indeed, heart rates above this range in the elderly usually indicate the presence of a nonsinus tachycardia (e.g., atrial fibrillation or flutter, or a paroxysmal supraventricular tachycardia).

Figure 13-2 shows an example of sinus tachycardia. Each QRS complex is preceded by a P wave. Notice that the P waves are positive in lead II. With sinus tachycardia at very fast rates, the P wave may merge with the preceding T wave and become difficult to distinguish.

In general, sinus tachycardia occurs with any condition that produces an increase in sympathetic tone or a decrease in vagal tone. The following conditions are commonly associated with sinus tachycardia:

 

   

Anxiety, excitement, exertion, and pain

 

   

Drugs that increase sympathetic tone (e.g., epinephrine, dopamine, tricyclic antidepressants, isoproterenol, and cocaine)

 

   

Drugs that block vagal tone (e.g., atropine and other anticholinergic agents)

 

   

Fever, many infections, and septic shock

 

   

Congestive heart failure (CHF) (Sinus tachycardia caused by increased sympathetic tone is generally seen with pulmonary edema.)

 

   

Pulmonary embolism (As noted in Chapter 11 , sinus tachycardia is the most common arrhythmia seen with acute pulmonary embolism.)

 

   

Acute myocardial infarction (MI), which may produce virtually any arrhythmia (Sinus tachycardia persisting after an acute MI is generally a bad prognostic sign and implies extensive heart damage.)

 

   

Hyperthyroidism (Sinus tachycardia occurring at rest may be an important diagnostic clue.)

 

   

Pheochromocytoma

 

   

Intravascular volume loss because of bleeding, vomiting, diarrhea, acute pancreatitis, dehydration, and related conditions

 

   

Alcohol intoxication or withdrawal

Treatment of sinus tachycardia associated with a pathologic condition must be directed at the underlying cause (e.g., infection, hyperthyroidism, CHF, or alcohol withdrawal).[*]

*  A small subset of patients who complain of palpitations (typically young adults) is found to have inappropriate sinus tachycardia. The causes of this syndrome are not certain. In some cases, autonomic factors may play a role; in others, a reentrant tachycardia originating in or very near the SA node is discovered.

 

SINUS BRADYCARDIA

With sinus bradycardia, sinus rhythm is present and the heart rate is less than 60 beats/min ( Fig. 13-3 ). This arrhythmia commonly occurs in the following conditions:

 

   

Normal variant (Many people have a resting pulse rate of less than 60 beats/min, and trained athletes may have a resting or sleeping pulse rate as low as 35 beats/min.)

 

   

Drugs that increase vagal tone (e.g., digitalis or edrophonium) or that decrease sympathetic tone (e.g., beta blockers) (In addition, calcium channel blockers such as diltiazem and verapamil may cause marked sinus bradycardia.)

 

   

Hypothyroidism

 

   

Hyperkalemia

 

   

Sick sinus syndrome (Some patients, particularly elderly ones, have marked sinus bradycardia without obvious cause, probably from degenerative disease of the SA node or surrounding tissue. Sick sinus syndrome is discussed further at the end of this chapter and in Chapter 20 ; see also Fig. 13-5 .)

 

   

Sleep apnea syndromes

 

   

Carotid sinus hypersensitivity syndrome

 

   

Vasovagal reactions

FIGURE 13-5  Sinus pause in a patient with sick sinus syndrome. The monitor lead shows sinus bradycardia with a long pause (about 2.4 sec).

Moderate sinus bradycardia usually produces no symptoms. If the heart rate is very slow (especially if it is less than 40 to 50 beats/min), light-headedness and even syncope may occur. Treatment may require adjusting medication doses (e.g., beta blockers, calcium channel blockers). If inappropriate sinus bradycardia causes symptoms (as in sick sinus syndrome), or if severe sinus bradycardia is due to an essential medication, an electronic pacemaker is indicated (see Chapter 21 ).

 

SINUS ARRHYTHMIA

In healthy people, especially younger subjects, the SA node does not pace the heart at a perfectly regular rate. Instead, a slight beat-to–beat variation is present ( Fig. 13-4 ). When this variability is more accentuated, the term sinus arrhythmia is used.

The most common cause of sinus arrhythmia is respiration. Respiratory sinus arrhythmia (RSA) is a normal finding and may be quite marked (up to 10 to 20 beats/min or more), particularly in children and young adults. The heart rate normally increases with inspiration and decreases with expiration because of changes in vagal tone that occur during the different phases of respiration (see Fig. 13-4 ).

 

SINUS PAUSES, SINUS ARREST, AND ESCAPE BEATS

Normal sinus rhythm, sinus tachycardia, sinus bradycardia, and sinus arrhythmia have been considered. Now suppose that the sinus node fails to stimulate the atria for one or more beats. Such dysfunction may occur intermittently, with simply a missed beat (no P wave or QRS complex) at occasional intervals, or it may be more extreme.[*] An example of the latter is sinus pause or sinus arrest,in which the SA node fails to stimulate the atria for a prolonged period ( Fig. 13-5 ). This leads to syncope or even cardiac arrest with asystole unless the sinus node regains function or some other pacemaker (escape pacemaker) takes over. Fortunately, other parts of the cardiac conduction system are capable of producing electrical stimuli and functioning as an escape pacemaker in these circumstances. Escape beats may come from the atria, the AV node, or the ventricles. Figure 13-6 shows a junctional escape beat. (The characteristics of escape beats are described in Chapter 14 .)

FIGURE 13-6  The monitor strip shows a sinus pause interrupted by a junctional escape (JE) beat. The wide QRS complex is due to an underlying bundle branch block.

SA block or arrest can be caused by numerous acute factors, including the following:

 

   

Hypoxemia

 

   

Myocardial ischemia or infarction

 

   

Hyperkalemia

 

   

Digitalis toxicity

 

   

Toxic responses to drugs such as beta blockers and calcium channel blockers (e.g., diltiazem and verapamil)

 

   

Vagal hyperreactivity (e.g., severe vasovagal episode)

Particularly in elderly persons, the SA node may undergo chronic degenerative changes, with periods of SA dysfunction and bradycardia leading at times to light-headedness and syncope. The term sick sinus syndrome refers to this type of irreversible SA node dysfunction (see Figs. 13-5 and 20-13 ).

The next few chapters describe important arrhythmias in which the cardiac pacemaker is located outside the SA node—in the atria, AV junction, or ventricles.

*  The two distinct mechanisms for sinus node dysfunction are sinus pacemaker failure and SA block. The former is due to actual failure of the SA node to fire electrically (depolarize) for one or more beats. The latter results when the SA node fires but the impulse is apparently blocked from exiting the node and stimulating the atria. From a clinical viewpoint, distinguishing between SA pacemaker dysfunction and SA (exit) block is not usually essential.

 

REVIEW

With normal sinus rhythm, each heartbeat originates in the sinus (or sinoatrial [SA]) node. The P wave is always negative in lead aVR and positive in lead II. The heart rate is between 60 and 100 beats/min.

The heart rate is greater than 100 beats/min with sinus tachycardia and is less than 60 beats/min with sinus bradycardia. Sinus bradycardia and sinus tachycardia have multiple causes, and both rhythms may occur normally.

Beat-to-beat variation of the sinus rate occurs with sinus arrhythmia. The rate variation is typically phasic with respiration (respiratory sinus arrhythmia). SA node dysfunction (because of either pacemaker cell failure or exit block) may lead to sinus pauses or, in extreme cases, SA arrest. Prolonged sinus arrest causes fatal asystole unless normal sinus rhythm resumes or escape beats from other foci in the atria, AV junction, or ventricles take over. SA dysfunction may be seen, particularly in elderly people, as a consequence of sick sinus syndrome. Digitalis toxicity or toxic responses to other drugs (e.g., beta blockers, calcium channel blockers, amiodarone) must always be excluded in patients with marked sinus bradycardia, SA pauses, or sinus arrest.

 

QUESTIONS

 

1.   

Is normal sinus rhythm present in the ECG shown below?

 

 

2.   

Is normal sinus rhythm present in this ECG?

 

 

3.   

Which one of the following drugs is not a cause of sinus bradycardia?

 

a.   

amiodarone

 

b.   

metoprolol

 

c.   

verapamil

 

d.   

isoproterenol

 

e.   

edrophonium

 

4.   

True or false: Respiratory sinus arrhythmia is a normal, expected finding in healthy young adults.