Cardiac Arrhythmias and Their Electrocardiographic Interpretation

Tachycardia

The term tachycardia means fast heart rate, which usually is defined as faster than 100 beats/min in an adult. An electrocardiogram (ECG) recorded from a patient with tachycardia is shown in Figure 13-1 . This ECG is normal except that the heart rate, as determined from the time intervals between QRS complexes, is about 150 beats/min instead of the normal 72 beats/min. Some causes of tachycardia include increased body temperature, dehydration, blood loss anemia, stimulation of the heart by the sympathetic nerves, and toxic conditions of the heart.

The heart rate usually increases about 10 beats/min for each degree Fahrenheit increase in body temperature (with an increase of 18 beats/min for each degree Celsius), up to a body temperature of about 105°F (40.5°C). Beyond this, the heart rate may decrease because of progressive debility of the heart muscle as a result of the fever. Fever causes tachycardia because an increased temperature increases the rate of metabolism of the sinus node, which in turn directly increases its excitability and rate of rhythm.

Many factors can cause the sympathetic nervous system to excite the heart, as discussed in this text. For example, when a patient sustains severe blood loss, sympathetic reflex stimulation of the heart may increase the heart rate to 150 to 180 beats/min. Simple weakening of the myocardium usually increases the heart rate because the weakened heart does not pump blood into the arterial tree to a normal extent, causing reductions in blood pressure and eliciting sympathetic reflexes to increase the heart rate.

Bradycardia

The term bradycardia means a slow heart rate, usually defined as fewer than 60 beats/min. Bradycardia is shown by the ECG in Figure 13-2 .

Sinus Arrhythmia

Figure 13-3 shows a cardiotachometer recording of the heart rate, at first during normal respiration and then, in the second half of the record, during deep respiration. A cardiotachometer is an instrument that records the duration of the interval between the successive QRS complexes in the ECG by the height of successive spikes . Note from this record that the heart rate increased and decreased no more than 5% during quiet respiration (shown on the left half of the record). Then, during deep respiration, the heart rate increased and decreased with each respiratory cycle by as much as 30%.

Sinus arrhythmia can result from any one of many circulatory conditions that alter the strengths of the sympathetic and parasympathetic nerve signals to the heart sinus node. The respiratory type of sinus arrhythmia results mainly from the spillover of signals from the medullary respiratory center into the adjacent vasomotor center during inspiratory and expiratory cycles of respiration. The spillover signals cause alternate increases and decreases in the number of impulses transmitted through the sympathetic and vagus nerves to the heart.

Sinoatrial Block

In rare cases, the impulse from the sinus node is blocked before it enters the atrial muscle. This phenomenon is demonstrated in Figure 13-4 , which shows sudden cessation of P waves, with resultant standstill of the atria. However, the ventricles pick up a new rhythm, with the impulse usually originating spontaneously in the atrioventricular (A-V) node, so the rate of the ventricular QRS-T complex is slowed but not otherwise altered. Sinoatrial block can be due to myocardial ischemia affecting the sinus node, inflammation or infection of the heart, or side effects from certain medications, and it can be observed in well-trained athletes.

Atrioventricular Block

The only means whereby impulses ordinarily can pass from the atria into the ventricles is through the A-V bundle, also known as the bundle of His. Conditions that can either decrease the rate of impulse conduction in this bundle or block the impulse entirely are as follows:

• 1.

  Ischemia of the A-V node or A-V bundle fibers often delays or blocks conduction from the atria to the ventricles. Coronary insufficiency can cause ischemia of the A-V node and bundle in the same way that it can cause ischemia of the myocardium.

• 2.

  Compression of the A-V bundle by scar tissue or by calcified portions of the heart can depress or block conduction from the atria to the ventricles.

• 3.

  Inflammation of the A-V node or A-V bundle can depress conduction from the atria to the ventricles. Inflammation results frequently from different types of myocarditis that are caused, for example, by diphtheria or rheumatic fever.

• 4.

  Extreme stimulation of the heart by the vagus nerves in rare cases blocks impulse conduction through the A-V node. Such vagal excitation occasionally results from strong stimulation of the baroreceptors in people with carotid sinus syndrome, discussed earlier in relationship to bradycardia.

• 5.

  Degeneration of the A-V conduction system, which is sometimes seen in older patients.

• 6.

  Medications such as digitalis or beta-adrenergic antagonists can, in some cases, impair A-V conduction.

Incomplete Atrioventricular Block

First-Degree Block—Prolonged P-R Interval

The usual lapse of time between the beginning of the P wave and the beginning of the QRS complex is about 0.16 second when the heart is beating at a normal rate. This so-called P-R interval usually decreases in length with a faster heartbeat and increases with a slower heartbeat. In general, when the P-R interval increases to more than 0.20 second, the P-R interval is said to be prolonged, and the patient is said to have first-degree incomplete heart block.

Figure 13-5 shows an ECG with a prolonged P-R interval; the interval in this case is about 0.30 second instead of the normal 0.20 second or less. Thus, first-degree block is defined as a delay of conduction from the atria to the ventricles but not actual blockage of conduction. The P-R interval seldom increases above 0.35 to 0.45 second because, by that time, conduction through the A-V bundle is depressed so much that conduction stops entirely. One means for determining the severity of some heart diseases, such as acute rheumatic heart disease, for example, is to measure the P-R interval.

Second-Degree Block

When conduction through the A-V bundle is slowed enough to increase the P-R interval to 0.25 to 0.45 second, the action potential is sometimes strong enough to pass through the bundle into the ventricles and sometimes not strong enough to do so. In this case, there will be an atrial P wave but no QRS-T wave, and it is said that there are “dropped beats” of the ventricles. This condition is called second-degree heart block.

There are two types of second-degree A-V block— Mobitz type I (also known as Wenckebach periodicity ) and Mobitz type II . Type I block is characterized by progressive prolongation of the P-R interval until a ventricular beat is dropped and is then followed by resetting of the P-R interval and repeating of the abnormal cycle. A type I block is almost always caused by abnormality of the A-V node. In most cases, this type of block is benign, and no specific treatment is needed.

In type II block, there is usually a fixed number of nonconducted P waves for every QRS complex. For example, a 2:1 block implies that there are two P waves for every QRS complex. At other times, rhythms of 3:2 or 3:1 may develop. In contrast to type I block, with type II block the P-R interval does not change before the dropped beat; it remains fixed. Type II block is generally caused by an abnormality of the bundle of His–Purkinje system and may require implantation of a pacemaker to prevent progression to complete heart block and cardiac arrest.

Figure 13-6 shows progressive P-R interval prolongation typical of type I (Wenckebach) block. Note prolongation of the P-R interval preceding the dropped beat, followed by a shortened P-R interval after the dropped beat.

Complete A-V Block (Third-Degree Block)

When the condition causing poor conduction in the A-V node or A-V bundle becomes severe, complete block of the impulse from the atria into the ventricles occurs. In this case, the ventricles spontaneously establish their own signal, usually originating in the A-V node or A-V bundle distal to the block. Therefore, the P waves become dissociated from the QRS-T complexes, as shown in Figure 13-7 . Note that the rate of rhythm of the atria in this ECG is about 100 beats/min, whereas the rate of ventricular beat is less than 40 beats/min. Furthermore, there is no relationship between the rhythm of the P waves and that of the QRS-T complexes because the ventricles have “escaped” from control by the atria and are beating at their own natural rate, controlled most often by rhythmical signals generated distal to the A-V node or A-V bundle where the block occurs.

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