Sinus Rhythms

“Normal” Sinus Rhythm

Sinus rhythm is the primary physiologic mechanism of the heartbeat. You diagnose it by finding P waves with a predictable polarity (see Chapter 4). When the sinus (also called the sinoatrial or SA) node is pacing the heart, atrial depolarization spreads from right to left and downward toward the AV junction. An arrow representing this depolarization wave points downward and toward the (patient’s) left. Therefore, with normal sinus rhythm, the P wave is always positive in lead II and negative in lead aVR (see Figs. 4-3 and 13-1).

Figure 13-1 The heart rate is about 80 beats/min. Each QRS complex is preceded by a P wave that is negative in lead aVR and positive in lead II. The P wave in lead V₁ is usually biphasic with an initial positive component (right atrial activation) followed by a small negative component (left atrial activation).

Key Point

Recall the following from Chapter 4:

If you state that the rhythm is “normal sinus” and do not mention any AV node conduction abnormalities, listeners will assume that each P wave is followed by a QRS complex and vice versa. The more technical and physiologically unambiguous way of stating this finding is to say: “Sinus rhythm with 1:1 AV conduction.”

However, do not forget that sinus rhythm (i.e., the sinus node is the dominant or sole pacemaker of the atria) can exist not only with normal (1:1) AV conduction but with any degree of AV heart block (including complete or third degree) or even with ventricular tachycardia or asystole.

By convention, normal sinus rhythm in a resting subject is usually defined as sinus rhythm with a heart rate between 60 and 100 beats/min. Sinus rhythm with a heart rate greater than 100 beats/min is termed sinus tachycardia (Fig. 13-2). Sinus rhythm with a heart rate of less than 60 beats/min is called sinus bradycardia (Fig. 13-3). Some authors define sinus bradycardia based on a heart rate of less than 50 beats/min.

Figure 13-2 Sinus tachycardia. The heart rate is close to 150 beats/min. Note the positive (upright) P waves in lead II. There is nonspecific T wave flattening.

Figure 13-3 Sinus bradycardia. Sinus rhythm is present, but at a very slow rate of about 38 beats/min.

Regulation of the Heart Rate

The heart, like other organs, has a special nerve supply from the autonomic nervous system, which controls involuntary muscle action. The autonomic nerve supply to the heart (in particular, the SA and AV nodes) consists of fibers with opposing effects: the sympathetic nerves and the parasympathetic nerves. Sympathetic stimulation increases the heart rate and the strength of myocardial contraction. Sympathetic stimulation also occurs by secretion of circulating hormones called catecholamines (especially, norepinephrine and epinephrine), produced by the adrenal glands.

Parasympathetic stimulation (from the vagus nerve) produces slowing of the sinus rate as well as increased conduction time through the AV nodal area. It can also cause a pacemaker “shift” from the SA node to the low right atrial area producing so-called low atrial rhythm with negative P waves in leads II, III, and aVF (Fig. 13-4).

Figure 13-4 Notice the change in P wave polarity from positive to negative in lead II. This shift from sinus bradycardia here to an ectopic (low) atrial escape rhythm may occur as a normal (physiologic) variant, especially with high vagal tone, or in a variety of pathologic settings.

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) stimulation produces a braking effect. For example, when you become excited or upset, or are exercising, increased sympathetic stimuli (and diminished parasympathetic tone) result in an increased heart rate and increased contractility, producing the familiar sensation of a pounding sensation in the chest (palpitations).

Note that the sensation of “palpitations” may be associated with an entirely normal heartbeat, with isolated premature beats (atrial or ventricular), or, more seriously, with an actual run of ectopic (nonsinus) heartbeats (e.g., from atrial fibrillation, paroxysmal supraventricular tachycardia, or ventricular tachycardia).

Sinus Tachycardia

Sinus tachycardia is 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. Even faster rates, transiently 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 (especially those older than 70 years) rarely show sinus tachycardia at rates above 140 to 150 beats/min even during maximal exertion. Indeed, heart rates above this range in the elderly, especially at rest, 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 sinus P wave is followed by a QRS complex, indicating sinus rhythm with 1:1 AV conduction. Sinus tachycardia (or bradycardia), however, can occur with any degree of AV block. 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 (Box 13-1). Sinus tachycardia may occur with healthy or pathologic states, usually involving increased cardiac output needs or decreased vascular resistance. Recall that systemic cardiac output per minute is the product of stroke volume (how much blood the left ventricle pumps with each beat) multiplied by the heart rate (beats/min).

Treatment of sinus tachycardia associated with a pathologic condition must be directed at the underlying cause (e.g., infection, sepsis, internal bleeding, pulmonary embolism hyperthyroidism, chronic heart failure [CHF], or alcohol withdrawal). Sometimes, more than one cause is present. In other cases, the cause may not be apparent. For example, inappropriate sinus tachycardia is a rare syndrome of unknown etiology, typically found in young females. The heart rate is more than 100 beats/min at rest without the expected decrease during sleep and with very rapid acceleration to 140 to 150 beats/min with minimal exercise. It is often combined with orthostatic hypotension.

Sinus Bradycardia

With sinus bradycardia, sinus rhythm is present and the heart rate is less than 60 beats/min (see Fig. 13-3). This arrhythmia commonly occurs in the conditions listed in Box 13-2.

Moderate sinus bradycardia usually produces no symptoms. If the heart rate is very slow (especially, less than 30 to 40 beats/min in the elderly) lightheadedness and even syncope may occur. Treatment may require adjusting medication doses (e.g., beta blockers, calcium channel blockers; lithium carbonate; donezepil). If inappropriate sinus bradycardia causes symptoms of fatigue, lightheadedness, or syncope (as in the symptomatic sick sinus syndrome), or, if severe, symptomatic sinus bradycardia is due to an essential medication, an electronic pacemaker is usually indicated (see Chapter 21).

When evaluating a patient with sinus bradycardia at rest it is also useful to assess the heart rate response to exercise. Some people are unable to appropriately increase the heart rate during exercise, which can cause symptoms of fatigue and shortness of breath. This condition, when not due to a drug or other reversible factor, is called chronotropic incompetence; an electronic pacemaker might be indicated even when the resting heart rate is within the “normal” range (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. 13-5). When this variability is more accentuated, the term sinus arrhythmia is used.

Figure 13-5 Respiratory sinus arrhythmia. Heart rate normally increases on inspiration and slows down with expiration as a result of changes in vagal tone associated with or induced by the different phases of respiration (increase with inspiration; decrease with expiration). This finding, a key aspect of heart rate variability, is physiologic and is especially noticeable in children, young adults, and athletes.

The most common cause of short-term 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.

Respiration-related variations in heart rate are an important component of heart rate variability, often abbreviated HRV. Measurements of HRV reflect the condition of the autonomic nervous system and are affected by cardiovascular status, age, medications, systemic diseases, and multiple other factors. In the United States currently, HRV is primarily used as a research tool. (For more information on this important topic, see online supplement.)

Sinus Pauses, Sinus Arrest, and Sinoatrial Block

In addition to sustained sinus bradycardia, sinus node dysfunction may occur intermittently, ranging from a delayed beat (sinus pause; see Fig. 13-4) to long periods of asystole (sinus arrest). Two distinct mechanisms of sinus node dysfunction may be responsible for either sinus pauses or frank sinus arrest: sinus pacemaker failure and SA exit block The former is due to an actual failure of the SA node to fire for one or more beats. The latter happens when the SA impulse is blocked from exiting the node and stimulating the atria (Fig. 13-6). SA exit block may produce a pause that equals two or more PP intervals. From the ECG and clinical standpoint there is no significant difference between sinus node exit block or pacemaker failure. Always look for reversible causes of SA node dysfunction: drugs, hyperkalemia, etc. (see Box 13-2).

Figure 13-6 Sinus pause in a patient with sick sinus syndrome. The monitor lead shows sinus bradycardia with a long pause (about 2.4 sec).

Sinus node dysfunction can happen spontaneously (sinus exit block; Fig. 13-7) or be induced by overdrive suppression of the sinus node by atrial fibrillation or flutter resulting in a prolonged postconversion pause when the arrhythmia abruptly terminates or “breaks” (Fig. 13-8). Such pauses are among the most common cause of syncope in patients with paroxysmal atrial arrhythmias (and are often exacerbated by rate-controlling medications such as beta blockers or calcium channel blockers) resulting in a type of brady-tachy syndrome requiring a pacemaker (see Chapter 21).

Figure 13-7 Pause due to 2:1 sinus (SA) exit block. Note the sudden pause which is almost exactly twice the baseline P-P interval. This distinctive finding is consistent with intermittent “exit block” of SA node depolarization, such that a P wave, which denotes atrial depolarization, does not occur even though the sinus pacemaker is firing appropriately. The reason for this “missing” P-QRS-T signal is that the sinus impulse is blocked intermittently from exiting the sinus node.

Figure 13-8 Sinus arrest following abrupt cessation of paroxysmal atrial fibrillation (AF). The mechanism is due to “overdrive suppression” of the SA node during the rapid stimulation of the atria during the AF. Such extended pauses may cause lightheadedness or syncope. This combination is an example of the brady-tachy syndrome. Resumption of sinus rhythm starts to occur after the prolonged sinus arrest.

Secondary Pacemakers and Escape Rhythms

Why isn’t a sinus pause or sinus arrest leading to syncope and sudden cardiac arrest even more prevalent? Recall that sinus node cells undergo spontaneous rhythmic depolarization (firing), making the SA node the primary physiologic pacemaker of the heart. However, almost any heart cell (e.g., atrial and ventricular myocytes, AV node cells, Purkinje fibers) is capable of generating spontaneous depolarizations and, therefore, initiating or maintaining the heartbeat.

Lower level (secondary, ectopic) pacemakers provide an essential backup mechanism when “higher level” pacemakers fail or conduction from them is blocked. The rate of spontaneous firing of the SA node is usually faster than that of secondary pacemakers. Thus, with every SA node firing, the wave of depolarization resets (“suppresses” or overrides) these ectopic pacemakers. However, if the SA node fails to fire, the next in the hierarchy of ectopic pacemakers may “escape” or be uninhibited by this suppressive control and generate an escape beat.

The occasional failure of physiologic escape mechanisms to “rescue” the heart is noteworthy because it may precipitate syncope or even sudden cardiac arrest. This finding suggests that the same factors suppressing the sinus node (drugs, ischemia, profound hypervagotonia, diffuse myocardial injury) may be simultaneously reducing or eliminating the automaticity of these backup pacemakers.

Escape beats (or sustained escape rhythm if sinus arrest persists) can appear (in order of frequency and rate of firing) from atrial cells (60-80 beats/min), AV nodal cells (35-60 beats/min), His-Purkinje cells (25-35 beats/min), and ventricular myocytes (less than 30 beats/min).

Atrial escape rhythms are characterized by regular P waves, slower than underlying sinus rhythm, with nonsinus P wave morphology (so-called “low atrial rhythm;” see Fig 13-4).

In junctional escape rhythm (terms AV junctional, junctional, AV nodal, and nodal are essentially synonymous), the atria are activated in a retrograde fashion, from bottom to top, producing negative P waves in leads II, III, and AVF, and a positive P wave in lead aVR (see Fig. 4-5).

With an AV junctional escape, the QRS complex will be normal (of “narrow” duration) because the ventricles are depolarized normally (unless a bundle branch block is also present). Furthermore, because the atria and ventricles are activated simultaneously during an AV junctional rhythm (not sequentially as with sinus rhythm), the QRS and P waves will occur at nearly the same time. As the result, an inverted P wave in lead II may appear: 1) just before QRS complex (with a very short PR interval), 2) inside the QRS (where the P wave is invisible), or 3) just after the QRS (producing “pseudo-S waves” in leads II, III, and aVF and “pseudo-R′” waves in leads V₁ and aVR (Fig. 13-9).

Figure 13-9 Atrioventricular (AV) junctional (nodal) escape rhythm. Simultaneous recording of lead II and lead V₁. The initial two beats show marked sinus bradycardia (at about 40 beats/min) followed by an even slower junctional escape rhythm (about 35 beats/min) with “retrograde” P waves (negative in lead II, just after the QRS complexes). These retrograde P waves may be confused with S waves in leads II, III, and aVF and with R waves in leads aVR and V₁. Therefore, they are sometimes called “pseudo S” and “pseudo R” waves, respectively. Always look for reversible causes of inappropriate sinus bradycardia and junctional escape rhythms, including certain drugs, hypothyroidism, and hyperkalemia.

Escape rhythms may also originate below the AV junction. Fascicular and idioventricular escape rhythms (Fig. 13-10) are slow wide QRS rhythms that usually indicate a life-threatening situation. They are associated with low blood pressure, are unstable, and can transition abruptly into pulseless electrical activity or asystole with cardiac arrest (see Chapter 19). Emergency treatment of underlying reversible conditions (such as hyperkalemia, digitalis toxicity, or other drug toxicity) is essential and temporary pacing is usually indicated.

Figure 13-10 Idioventricular escape rhythm recorded during a cardiac arrest during attempted rescuscitation. The waveforms marked “X” are chest compression artifacts. The underlying atrial mechanism, if any, cannot be determined. (See also Chapter 19, “Basic ECG Patterns in Cardiac Arrest.”) Note also that the current recommended rate of chest compressions in adults is 100/min.

It is important to understand that escape rhythms are not the primary arrhythmias but rather function as automatic backups or compensatory responses. The primary problem is failure of the higher order pacemakers or of AV conduction block. Therefore, diagnosis and treatment of these primary conditions are the goals (see causes of bradycardia earlier).

In urgent conditions, drugs such as atropine (a parasympathetic blocker) can be used to acutely increase the rate of atrial or junctional pacemakers. Sympathomimetic agents (dopamine or isoproterenol) increase both supraventricular and ventricular ectopic pacemaker rates.