RN Expert Guides: Cardiovascular Care, 1st Edition (2008)

Chapter 5. Arrhythmias

The most common types of arrhythmias include:

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sinus node arrhythmias

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atrial arrhythmias

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junctional arrhythmias

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ventricular arrhythmias

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atrioventricular (AV) blocks.

BASIC ELECTROCARDIOGRAPHY

Before you can begin to recognize arrhythmias, you need to know the parts of the electrocardiogram (ECG).

An ECG complex represents the electrical events occurring in one cardiac cycle. A complex consists of five waveforms labeled with the letters P, Q, R, S, and T. The middle three letters—Q, R, and S—are referred to as a unit, the QRS complex. ECG tracings represent the conduction of electrical impulses from the atria to the ventricles. (See ECG waveform components.)

ECG WAVEFORM COMPONENTS

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P wave

The P wave is the first component of a normal ECG waveform. It represents atrial depolarization or conduction of an electrical impulse through the atria. When evaluating a P wave, look closely at its characteristics, especially its location, configuration, and deflection.

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A normal P wave has these characteristics:

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Location: precedes the QRS complex

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Amplitude: 2 to 3 mm high

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Duration: 0.06 to 0.12 second

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Configuration: usually rounded and upright

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Deflection: positive or upright in leads I, II, aVF, and V2 to V6; usually positive but may vary in leads III and aVL; negative or inverted in lead aVR; biphasic or variable in lead V1.

If the deflection and configuration of a P wave are normal—for example, if the P wave is upright in lead II and is rounded and smooth—and if the P wave precedes each QRS complex, you can assume that this electrical impulse originated in the sinoatrial (SA) node. The atria start to contract partway through the P wave, but you won't see this on the ECG. Remember, the ECG records electrical activity only, not mechanical activity or contraction.

Peaked, notched, or enlarged P waves may represent atrial hypertrophy or enlargement associated with chronic obstructive pulmonary disease, pulmonary emboli, valvular disease, or heart failure. Inverted P waves may signify retrograde or reverse conduction from the AV junction toward the atria. Whenever an upright sinus P wave becomes inverted, consider possible retrograde or reverse conduction.

Varying P waves indicate that the impulse may be coming from different sites, as with a wandering pacemaker rhythm, irritable atrial tissue, or damage near the SA node. Absent P waves may signify conduction by a route other than the SA node, as with a junctional or atrial fibrillation rhythm. When a P wave doesn't precede the QRS complex, complete heart block may be present. Absence of a P wave doesn't mean that there is no atrial depolarization; the P wave may be buried or hidden in the T wave or the QRS complex.

PR interval

The PR interval tracks the atrial impulse from the atria through the AV node, bundle of His, and right and left bundle branches. When evaluating a PR interval, look especially at its duration. Changes in the PR interval indicate an altered impulse formation or a conduction delay, as seen in AV block.

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A normal PR interval has these characteristics (amplitude, configuration, and deflection aren't measured):

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Location: from the beginning of the P wave to the beginning of the QRS complex

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Duration: 0.12 to 0.20 second.

Short PR intervals (less than 0.12 second) indicate that the impulse originated somewhere other than the SA node. This variation is associated with junctional arrhythmias and preexcitation syndromes. Prolonged PR intervals (greater than 0.20 second) may represent a conduction delay through the atria or AV junction from digoxin toxicity, common cardiac drugs such as beta-adrenergic receptor and calcium channel blockers, or heart block—slowing related to ischemia or conduction tissue disease.

QRS complex

The QRS complex follows the P wave and represents depolarization of the ventricles, or impulse conduction. Immediately after the ventricles depolarize, as represented by the QRS complex, they contract. That 

When you're monitoring cardiac rhythm, remember that the waveform you see represents the heart's electrical activity only. It doesn't guarantee a mechanical contraction of the heart and a subsequent pulse. The contraction could be weak, as happens with premature ventricular contractions, or absent, as happens with pulseless electrical activity. So, before you treat the strip, check the patient.

Pay special attention to the duration and configuration when evaluating a QRS complex.

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A normal complex has these characteristics:

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Location: follows the PR interval

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Amplitude: 5 to 30 mm high, but differs for each lead used

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Duration: 0.06 to 0.10 second, or half of the PR interval. Duration is measured from the beginning of the Q wave to the end of the S wave, or from the beginning of the R wave if the Q wave is absent.

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Configuration: consists of the Q wave (the first negative deflection, or deflection below the baseline, after the P wave), the R wave (the first positive deflection after the Q wave), and the S wave (the first negative deflection after the R wave). You may not always see all three waves. The ventricles depolarize quickly, minimizing contact time between the stylus and the ECG paper, so the QRS complex typically appears thinner than other ECG components. It may also look different in each lead.

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Deflection: positive (with most of the complex above the baseline) in leads I, II, III, aVL, aVF, and V4 to V6, negative in leads aVR and V12, and biphasic in lead V3.

Remember that the QRS complex represents intraventricular conduction time. That's why identifying and correctly interpreting it is so crucial. If no P wave appears with the QRS complex, then the impulse may have originated in the ventricles, indicating a ventricular arrhythmia.

Deep, wide Q waves may represent myocardial infarction. In this case, the Q wave amplitude (depth) is greater than or equal to 25% of the height of the succeeding R wave, or the duration of the Q wave is 0.04 second or more. A notched R wave may signify a bundle-branch block. A widened QRS complex (greater than 0.12 second) may signify a ventricular conduction delay. A missing QRS complex may indicate AV block or ventricular standstill.

CHANGES IN THE ST SEGMENT

Closely monitoring the ST segment on a patient's electrocardiogram can help you detect ischemia or injury before infarction develops.

ST-segment depression

An ST segment is considered depressed when it's 0.5 mm or more below the baseline. A depressed ST segment may indicate myocardial ischemia or digoxin toxicity.

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ST-segment elevation

An ST segment is considered elevated when it's 1 mm or more above the baseline. An elevated ST segment may indicate myocardial injury.

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ST segment

The ST segment represents the end of ventricular conduction or depolarization and the beginning of ventricular recovery or repolarization. The point that marks the end of the QRS complex and the beginning of the ST segment is known as the J point.

Pay special attention to the deflection of an ST segment.

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A normal ST segment has these characteristics (amplitude, duration, and configuration aren't observed):

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Location: extends from the S wave to the beginning of the T wave

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Deflection: usually isoelectric (neither positive nor negative); may vary from -0.5 to +1 mm in some precordial leads.

A change in the ST segment may indicate myocardial injury or ischemia. An ST segment may become either elevated or depressed. (See Changes in the ST segment.)

T wave

The peak of the T wave represents the relative refractory period of repolarization or ventricular recovery. When evaluating a T wave, look at the amplitude, configuration, and deflection.

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Normal T waves have these characteristics (duration isn't measured):

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Location: follows the ST segment

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Amplitude: 0.5 mm in leads I, II, and III and up to 10 mm in the precordial leads

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Configuration:

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Deflection: usually positive or upright in leads I, II, and V2 to V6; inverted in lead aV1.

The T wave's peak represents the relative refractory period of ventricular repolarization, a period during which cells are especially vulnerable to extra stimuli. Bumps in a T wave may indicate that a P wave is hidden in it. If a P wave is hidden, atrial depolarization has occurred, and the impulse has originated above the ventricles.

Tall, peaked, or “tented” T waves may indicate myocardial injury or electrolyte imbalances such as hyperkalemia. Hypokalemia can cause flattened T waves. Inverted T waves in leads I, II, aVL, aVF, or V2 through V6 may represent myocardial ischemia. Heavily notched or pointed T waves in an adult may indicate pericarditis.

QT interval

The QT interval measures the time needed for ventricular depolarization and repolarization. The length of the QT interval varies according to heart rate. The faster the heart rate, the shorter the QT interval. When checking the QT interval, look closely at the duration.

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A normal QT interval has these characteristics (amplitude, configuration, and deflection aren't observed):

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Location: extends from the beginning of the QRS complex to the end of the T wave

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Duration: varies according to age, sex, and heart rate; usually lasts from 0.36 to 0.44 second; shouldn't be greater than half the distance between the two consecutive R waves (called the R-R interval) when the rhythm is regular.

CORRECTING THE QT INTERVAL

The QT interval is affected by the patient's heart rate. As the heart rate increases, the QT interval decreases; as the heart rate decreases, the QT interval increases. For this reason, evaluating the QT interval based on a standard heart rate of 60 is recommended. This corrected QT interval is known as QTc. The following formula is used to determine the QTc:

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The normal QTc for women is less than 0.46 seconds and for men is less than 0.45 seconds. When the QTc is longer than 0.50 seconds in men or women, torsades de pointes is more likely to develop.

The QT interval measures the time needed for ventricular depolarization and repolarization. Prolonged QT intervals indicate that ventricular repolarization time is slowed, meaning that the relative refractory or vulnerable period of the cardiac cycle is longer. (See Correcting the QT interval.)

This variation is also associated with certain drugs such as class I antiarrhythmics. Prolonged QT syndrome is a congenital conductionsystem defect present in certain families. Short QT intervals may result from digoxin toxicity or electrolyte imbalances such as hypercalcemia.

U wave

The U wave represents repolarization of the His-Purkinje system or ventricular conduction fibers. It isn't present on every rhythm strip. The configuration is the most important characteristic of the U wave.

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When present, a normal U wave has these characteristics (amplitude and duration aren't measured):

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Location: follows the T wave

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Configuration: typically upright and rounded

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upright.

The U wave may not appear on an ECG. A prominent U wave may be from hypercalcemia, hypokalemia, or digoxin toxicity.

RECOGNIZING NORMAL SINUS RHYTHM

Normal sinus rhythm, shown below, represents normal impulse conduction through the heart.

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Rhythm: atrial and ventricular rhythms regular

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Rate: atrial and ventricular rates normal; 60 beats/minute

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normal; precedes each QRS complex; all P waves similar in size and shape

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PR interval: normal; 0.10 second

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QRS complex: 0.06 second

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T wave: normal shape (upright and rounded)

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QT interval: normal; 0.40 second

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Other: no ectopic or aberrantly conducted impulses

NORMAL SINUS RHYTHM

Before you can recognize an arrhythmia, you first need to be able to recognize a normal cardiac rhythm. The term arrhythmia literally means an absence of rhythm. The more accurate term dysrhythmia means an abnormality in rhythm. These terms, however, are frequently used interchangeably.

Normal sinus rhythm (NSR) occurs when an impulse starts in the sinus node and progresses to the ventricles through a normal conduction pathway—from the sinus node to the atria and AV node, through the bundle of His, to the bundle branches, and on to the Purkinje fibers. There are no premature or aberrant contractions. NSR is the standard against which all other rhythms are compared. (See Recognizing normal sinus rhythm.)

Practice the 8-step method, described below, to analyze an ECG strip with NSR. The ECG characteristics of NSR are:

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Rhythm: atrial and ventricular rhythms are regular

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atrial and ventricular rates are 60 to 100 beats/minute, the sinoatrial node's normal firing rate

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P wave: normally shaped (round and smooth) and upright in lead II; all P waves similar in size and shape; a P wave for every QRS complex

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PR interval: within normal limits (0.12 to 0.20 second)

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QRS complex: within normal limits (0.06 to 0.10 second)

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T wave: normally shaped; upright and rounded in lead II

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QT interval: within normal limits (0.36 to 0.44 second)

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Other: no ectopic or aberrant beats.

ff1-b01382759AGE AWARE

Always keep the patient's age in mind when interpreting the ECG. Changes that might be seen in the ECG of an older adult include increased PR, QRS, and QT intervals, decreased amplitude of the QRS complex, and a shift of the QRS axis to the left.

THE 8-STEP METHOD

Analyzing a rhythm strip is a skill developed through practice. You can use several methods, as long as you're consistent. Rhythm strip analysis requires a sequential and systematic approach such as the 8 steps outlined here.

Step 1: Determine rhythm

To determine the heart's atrial and ventricular rhythms, use either the paper-and-pencil method or the caliper method. (See Methods of measuring rhythm.)

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For atrial rhythm, measure the P-P intervals; that is, the intervals between consecutive P waves. These intervals should occur regularly, with only small variations from respirations. Then compare the P-P intervals in several cycles. Consistently similar P-P intervals indicate regular atrial rhythm; dissimilar P-P intervals indicate irregular atrial rhythm.

To determine the ventricular rhythm, measure the intervals between two consecutive R waves in the QRS complexes. If an R wave isn't present, use either the Q wave or the S wave of consecutive QRS complexes. The R-R intervals should occur regularly. Then compare R-R intervals in several cycles. As with atrial rhythms, consistently similar intervals mean a regular rhythm; dissimilar intervals point to an irregular rhythm.

After completing your measurements, ask yourself:

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Is the rhythm regular or irregular? Consider a rhythm with only slight variations, up to 0.04 second, to be regular.

 

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If the rhythm is irregular, is it slightly or markedly irregular? Does the irregularity occur in a pattern?

METHODS OF MEASURING RHYTHM

You can use either of these methods to determine atrial or ventricular rhythm.

Paper-and-pencil method

Place the ECG strip on a flat surface. Then position the straight edge of a piece of paper along the strip's baseline. Move the paper up slightly so the straight edge is near the peak of the R wave.

With a pencil, mark the paper at the R waves of two consecutive QRS complexes, as shown below. This is the R-R interval. Next, move the paper across the strip lining up the two marks with succeeding R-R intervals. If the distance for each R-R interval is the same, the ventricular rhythm is regular. If the distance varies, the rhythm is irregular.

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Caliper method

With the ECG on a flat surface, place one point of the calipers on the peak of the first R wave of two consecutive QRS complexes. Then adjust the caliper legs so the other point is on the peak of the next R wave, as shown below. This distance is the R-R interval.

Now pivot the first point of the calipers toward the third R wave, and note whether it falls on the peak of that wave. Check succeeding R-R intervals in the same way. If they're all the same, the ventricular rhythm is regular. If they vary, the rhythm is irregular.

Using the same method, measure the P-P intervals to determine whether the atrial rhythm is regular or irregular.

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Step 2: Calculate rate

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You can use one of three methods to determine atrial and ventricular heart rates from an ECG waveform. Although these methods can provide accurate information, you shouldn't rely solely on them when assessing your patient. Remember, the ECG waveform represents electrical, not mechanical, activity. Therefore, although an ECG can show you that ventricular depolarization has occurred, it doesn't mean that ventricular contraction has occurred. To calculate heart rate, you must take the patient's pulse. So remember, always check a pulse to correlate it with the heart rate on the ECG.

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Times-ten method. The simplest, quickest, and most common way to calculate rate is the times-ten method, especially if the rhythm is irregular. ECG paper is marked in increments of 3 seconds, or 15 large boxes. To calculate the atrial rate, obtain a 6-second strip, count the number of P waves on it, and multiply by 10. Ten 6-second strips equal 1 minute. Calculate ventricular rate the same way, using the R waves.

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1,500 method. If the heart rhythm is regular, use the 1,500 method, so named because 1,500 small squares equal 1 minute. Count the number of small squares between identical points on two consecutive P waves, and then divide 1,500 by that number to get the atrial rate. To obtain the ventricular rate, use the same method with two consecutive R waves.

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Sequence method.

Step 3: Evaluate P wave

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When examining a rhythm strip for P waves, ask yourself:

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Are P waves present?

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Do the P waves have a normal configuration?

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Do all the P waves have a similar size and shape?

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Is there one P wave for every QRS complex?

Step 4: Determine PR-interval duration

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To measure the PR interval, count the small squares between the start of the P wave and the start of the QRS complex; then multiply the number of squares by 0.04 second. After performing this calculation, ask yourself:

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Does the duration of the PR interval fall within normal limits, 0.12 to 0.20 second (or 3 to 5 small squares)?

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Is the PR interval constant?

Step 5: Determine QRS complex duration

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When determining QRS complex duration, make sure you measure straight across from the end of the PR interval to the end of the S wave, not just to the peak. Remember, the QRS complex has no horizontal components. To calculate duration, count the number of small squares between the beginning and end of the QRS complex, and multiply this number by 0.04 second. Then ask yourself:

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Does the duration of the QRS complex fall within normal limits, 0.06 to 0.10 second?

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Are all QRS complexes the same size and shape? (If not, measure each one and describe them individually.)

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Does a QRS complex appear after every P wave?

Step 6: Evaluate T wave

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Examine the T waves on the ECG strip. Then ask yourself:

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Do all of the T waves have a normal shape?

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Could a P wave be hidden in a T wave?

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Do all T waves have a normal amplitude?

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Do the T waves have the same deflection as the QRS complexes?

Step 7: Determine QT-interval duration

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Count the number of small squares between the beginning of the QRS complex and the end of the T wave, where the T wave returns to the baseline. Multiply this number by 0.04 second. Ask yourself:

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Does the duration of the QT interval fall within normal limits, 0.36 to 0.44 second?

Step 8: Evaluate other components

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Note the presence of ectopic or aberrantly conducted beats or other abnormalities. Also check the ST segment for abnormalities, and look for the presence of a U wave.

Now, interpret your findings by classifying the rhythm strip according to one or all of the following:

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Site of origin of the rhythm: for example, sinus node, atria, atrioventricular node, or ventricles

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Rate: normal (60 to 100 beats/minute), bradycardia (less than 60 beats/minute), or tachycardia (greater than 100 beats/minute)

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Rhythm: normal or abnormal; for example, flutter, fibrillation, heart block, escape rhythm, or other arrhythmias.

SINUS NODE ARRHYTHMIAS

When the heart functions normally, the sinoatrial (SA) node, also called the sinus node, acts as the primary pacemaker. The sinus node assumes this role because its automatic firing rate exceeds that of the heart's other pacemakers. In an adult at rest, the sinus node has an inherent firing rate of 60 to 100 times/minute.

In about half of the population, the SA node's blood supply comes from the right coronary artery, and from the left circumflex artery in the other half of the population. The autonomic nervous system (ANS) richly innervates the sinus node through the vagal nerve, a parasympathetic nerve, and several sympathetic nerves. Stimulation of the vagus nerve decreases the node's firing rate, and stimulation of the sympathetic system increases it.

Changes in the automaticity of the sinus node, alterations in its blood supply, and ANS influences may all lead to sinus node arrhythmias. This chapter will help you to identify sinus node arrhythmias on an electrocardiogram (ECG). It will also help you to determine the causes, clinical significance, signs and symptoms, and interventions associated with each arrhythmia presented.

The 8-step method for analyzing the ECG strip will be used for each of the following arrhythmias.

Sinus arrhythmia

In sinus tachycardia and sinus bradycardia, the cardiac rate falls outside the normal limits. In sinus arrhythmia, the rate stays within normal limits, but the rhythm is irregular and corresponds to the respiratory cycle. Sinus arrhythmia can occur normally in athletes, children, and older adults, but it rarely occurs in infants.

CAUSES

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.)

RECOGNIZING SINUS ARRHYTHMIA

The following rhythm strip illustrates sinus arrhythmia. Look for these distinguishing characteristics.

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heart disease

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inferior wall myocardial infarction

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the use of certain drugs, such as digoxin and morphine

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conditions involving increased intracranial pressure (ICP).

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.

ECG CHARACTERISTICS

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Rhythm: Atrial rhythm is irregular, corresponding to the respiratory cycle. The P-P interval is shorter during inspiration, longer during expiration. The difference between the longest and shortest P-P interval exceeds 0.12 second. Ventricular rhythm is also irregular, corresponding to the respiratory cycle. The R-R interval is shorter during inspiration, longer during expiration. The difference between the longest and shortest R-R interval exceeds 0.12 second.

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Rate: Atrial and ventricular rates are within normal limits (60 to 100 beats/minute) and vary with respiration. Typically, the heart rate increases during inspiration and decreases during expiration.

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P wave: Normal size and configuration; P wave precedes each QRS complex.

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PR interval: May vary slightly within normal limits.

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QRS complex: Normal duration and configuration.

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QT wave: Normal size and configuration.

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QT interval: May vary slightly, but usually within normal limits.

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Other: None.

SIGNS AND SYMPTOMS

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.

INTERVENTIONS

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 drugs, such as morphine and other sedatives, the practitioner may decide to continue to give the patient those medications. If sinus arrhythmia develops suddenly in a patient taking digoxin (Lanoxin), notify the practitioner immediately. The patient may be experiencing digoxin toxicity.

RECOGNIZING SINUS BRADYCARDIA

The following rhythm strip illustrates sinus bradycardia. Look for these distinguishing characteristics.

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BRADYCARDIA AND TACHYCARDIA IN CHILDREN

Evaluate bradycardia and tachycardia in children in context. Bradycardia (less than 90 beats/minute) may occur in the healthy infant during sleep, and tachycardia may occur when the child is crying or otherwise upset. Because the heart rate varies considerably from the neonate to the adolescent, neither bradycardia nor tachycardia can be assigned a single definition to be used for all children.

Sinus bradycardia is characterized by a sinus rate below 60 beats/ minute and a regular rhythm. All impulses originate in the SA node. This arrhythmia's significance depends on the symptoms and the underlying cause. Unless the patient shows symptoms of decreased cardiac output, no treatment is necessary. (See Recognizing sinus bradycardia andBradycardia and tachycardia in children.)

CAUSES

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-onditioned heart—an athlete, for example.

Sinus bradycardia may be caused by:

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noncardiac disorders, such as hyperkalemia, increased ICP, hypothyroidism, hypothermia, and glaucoma

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conditions producing excess vagal stimulation or decreased sympathetic stimulation, such as sleep, deep relaxation, the Valsalva maneuver, carotid sinus massage, and vomiting

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cardiac diseases, such as SA node disease, cardiomyopathy, myocarditis, and myocardial ischemia, can also occur immediately following an inferior wall myocardial infarction (MI) that involves the right coronary artery, which supplies blood to the SA node

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certain drugs, especially beta-adrenergic receptor blockers, digoxin, calcium channel blockers, lithium, and antiarrhythmics, such as sotalol (Betapace), amiodarone (Cordarone), propafenone (Rhythmol), and quinidine (Quinora).

CLINICAL SIGNIFICANCE

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.

ECG CHARACTERISTICS

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Rhythm: Atrial and ventricular rhythms are regular.

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Rate: Atrial and ventricular rates are less than 60 beats/minute.

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P wave: Normal size and configuration; P wave precedes each QRS complex.

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PR interval: Within normal limits and constant.

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QRS complex: Normal duration and configuration.

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T wave: Normal size and configuration.

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QT interval: Within normal limits, but may be prolonged.

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Other:

SIGNS AND SYMPTOMS

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:

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hypotension

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cool, clammy skin

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altered mental status

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dizziness

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blurred vision

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crackles, dyspnea, and an S3 heart sound, indicating heart failure

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chest pain

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syncope.

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.

INTERVENTIONS

If the patient is asymptomatic and his vital signs are stable, treatment generally isn't necessary. Continue to observe his heart rhythm, monitoring the progression and duration of the bradycardia. Evaluate his tolerance of the rhythm at rest and with activity. Review the medications he's taking. Check with the practitioner about stopping medications that may be depressing the SA node, such as digoxin, beta-adrenergic receptor blockers, or calcium channel blockers. Before giving these drugs, make sure the heart rate is within a safe range.

If the patient is symptomatic, treatment aims to identify and correct the underlying cause. Meanwhile, the heart rate must be maintained with transcutaneous pacemaker. Use such drugs as atropine, epinephrine, or dobutamine (Dobutrex) while awaiting a pacemaker or if pacing is ineffective. For the complete ACLS algorithm, see pages 328 and 329.

RECOGNIZING SINUS TACHYCARDIA

The following rhythm strip illustrates sinus tachycardia. Look for these distinguishing characteristics.

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Keep in mind that a patient with a transplanted heart won't respond to atropine and may require pacing for emergency treatment. Treatment of chronic, symptomatic sinus bradycardia requires insertion of a permanent pacemaker.

Sinus tachycardia

Sinus tachycardia is an acceleration of the firing of the SA node beyond its normal discharge rate. Sinus tachycardia in an adult is characterized by a sinus rate of more than 100 beats/minute. The rate rarely exceeds 180 beats/minute except during strenuous exercise; the maximum rate achievable with exercise decreases with age. (See Recognizing sinus tachycardia.)

CAUSES

Sinus tachycardia may be a normal response to exercise, pain, stress, fever, or strong emotions, such as fear and anxiety. Other causes of sinus tachycardia include:

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certain cardiac conditions, such as heart failure, cardiogenic shock, and pericarditis

 

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other conditions, such as shock, anemia, respiratory distress, pulmonary embolism, sepsis, and hyperthyroidism where the increased heart rate serves as a compensatory mechanism

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drugs, such as atropine, isoproterenol (Isuprel), aminophylline, dopamine (Intropin), dobutamine, epinephrine, alcohol, caffeine, nicotine, and amphetamines.

CLINICAL SIGNIFICANCE

The clinical significance of sinus tachycardia depends on the underlying cause. The arrhythmia may be the body's response to exercise or high emotional states and of no clinical significance. It may also occur with hypovolemia, hemorrhage, or pain. When the stimulus for the tachycardia is removed, the arrhythmia generally resolves spontaneously.

Although sinus tachycardia commonly occurs without serious adverse effects, persistent sinus tachycardia can also be serious, especially if it occurs in the setting of an acute MI. Tachycardia can lower cardiac output by reducing ventricular filling time and stroke volume. Normally, ventricular volume reaches 120 to 130 ml during diastole. In tachycardia, decreased ventricular volume leads to decreased cardiac output with subsequent hypotension and decreased peripheral perfusion.

Tachycardia worsens myocardial ischemia by increasing the heart's demand for oxygen and reducing the duration of diastole, the period of greatest coronary blood flow. Sinus tachycardia occurs in about 30% of patients after an acute MI and is considered a poor prognostic sign because it may be associated with massive heart damage.

An increase in heart rate can also be detrimental for patients with obstructive types of heart conditions, such as aortic stenosis and hypertrophic cardiomyopathy. Persistent tachycardia may also signal impending heart failure or cardiogenic shock. Sinus tachycardia can also cause angina in patients with coronary artery disease.

ECG CHARACTERISTICS

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Rhythm: Atrial and ventricular rhythms are regular.

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Rate: Atrial and ventricular rates are greater than 100 beats/minute, usually between 100 and 160 beats/minute.

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P wave: Normal size and configuration, but it may increase in amplitude. The P wave precedes each QRS complex, but as the heart rate increases, the P wave may be superimposed on the preceding T wave and difficult to identify.

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PR interval: Within normal limits and constant.

 

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QRS complex: Normal duration and configuration.

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Normal size and configuration.

·

QT interval: Within normal limits, but commonly shortened.

·

Other: None.

SIGNS AND SYMPTOMS

The patient will have a peripheral pulse rate above 100 beats/minute, but with a regular rhythm. Usually, he'll be asymptomatic. However, if his cardiac output falls and compensatory mechanisms fail, he 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 crackles, an extra heart sound (S3), and jugular vein distention.

INTERVENTIONS

When treating the asymptomatic patient, focus on determining the cause of the tachycardia. The focus of treatment in the symptomatic patient with sinus tachycardia is to maintain adequate cardiac output and tissue perfusion and to identify and correct the underlying cause. For example, if the tachycardia is caused by hemorrhage, treatment includes stopping the bleeding and replacing blood and fluid losses.

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

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

Also question the patient about the use of caffeine, nicotine, and alcohol, each of which can trigger tachycardia. Advise him to avoid these substances. Ask about the use of illicit drugs, such as cocaine and amphetamines, which can also cause tachycardia.

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

·

Because sinus tachycardia can lead to injury of the heart muscle, assess the patient for signs and symptoms of angina. Also assess for signs and symptoms of heart failure, including crackles, an S3

·

Monitor intake and output, along with daily weight.

·

Check the patient's level of consciousness to assess cerebral perfusion.

·

Provide the patient with a calm environment. Help to reduce fear and anxiety, which can aggravate 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.

·

Keep in mind that tachycardia is frequently the initial sign of pulmonary embolism. Maintain a high index of suspicion, especially if your patient has predisposing risk factors for thrombotic emboli.

Sinus arrest and sinoatrial exit block

Although sinus arrest and SA or sinus exit block are two separate arrhythmias with different etiologies, they're discussed together because distinguishing the two can be difficult. In addition, there's no difference in their clinical significance and treatment.

In sinus arrest, the normal sinus rhythm is interrupted by an occasional, prolonged failure of the SA node to initiate an impulse. Therefore, sinus arrest is caused by episodes of failure in the automaticity or impulse formation of the SA node. The atria aren't stimulated, and an entire PQRST complex is missing from the ECG strip. Except for this missing complex, or pause, the ECG usually remains normal. (See Recognizing sinus arrest.)

In sinus exit block, the SA node discharges at regular intervals, but some impulses are delayed or blocked from reaching the atria, resulting in long sinus pauses. Blocks result from failure to conduct impulses, whereas sinus arrest results from failure to form impulses in the SA node. Both arrhythmias cause atrial activity to stop. In sinus arrest, the pause often ends with a junctional escape beat. In sinus exit block, the pause occurs for an indefinite period and ends with a sinus rhythm. (See Recognizing sinoatrial exit block, page 257.)

CAUSES

Causes of sinus arrest and sinus exit block include:

·

acute infection

·

sick sinus syndrome

·

sinus node diseases, such as fibrosis and idiopathic degeneration

·

increased vagal tone, such as with Valsalva's maneuver, carotid sinus massage, and vomiting

·

digoxin, quinidine, procainamide (Procan SR), and salicylate toxicity

 

·

excessive doses of beta-adrenergic receptor blockers, such as metoprolol (Lopressor) and propranolol (Inderal)

·

cardiac disorders, such as coronary artery disease (CAD), acute myocarditis, cardiomyopathy, hypertensive heart disease, and acute inferior wall myocardial infarction.

RECOGNIZING SINUS ARREST

The following rhythm strip illustrates sinus arrest. Look for these distinguishing characteristics.

c5-tt25

CLINICAL SIGNIFICANCE

The clinical significance of these two arrhythmias depends on the patient's symptoms. 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 or sinus exit block, and he may be totally unaware of the arrhythmia. 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.

This rhythm strip illustrates sinoatrial (SA) exit block.

c5-tt26

If either of the arrhythmias is frequent or prolonged, however, the patient will most likely experience symptoms related to low cardiac output. The arrhythmias can produce syncope or near-syncopal episodes usually within 7 seconds of asystole.

During a prolonged pause, the patient may fall and injure himself. Other situations are potentially just as serious. For example, a symptom-producing arrhythmia that occurs while the patient is driving a car could result in a fatal accident. Extremely slow rates can also give rise to other arrhythmias.

ECG CHARACTERISTICS

Sinus arrest and SA exit block share these ECG characteristics:

·

Rhythm: Atrial and ventricular rhythms are usually regular except when sinus arrest or SA exit block occurs.

·

The underlying atrial and ventricular rates are usually within normal limits (60 to 100 beats/minute) before the arrest or SA exit block occurs. The length or frequency of the pause may result in bradycardia.

·

P wave: Periodically absent, with entire PQRST complex missing. However, when present, the P wave is normal in size and configuration and precedes each QRS complex.

 

·

PR interval: Within normal limits and constant when a P wave is present.

·

QRS complex: Normal duration and configuration, but absent during a pause.

·

T wave: Normal size and configuration, but absent during a pause.

·

QT interval: Usually within normal limits, but absent during a pause.

To differentiate between these two rhythms, compare the length of the pause with the underlying P-P or R-R interval. If the underlying rhythm is regular, determine if the underlying rhythm resumes on time following the pause. With sinus exit block, because the regularity of the SA node discharge is blocked, not interrupted, the underlying rhythm will resume on time following the pause. In addition, the length of the pause will be a multiple of the underlying P-P or R-R interval.

In sinus arrest, the timing of the SA node discharge is interrupted by the failure of the SA node to initiate an impulse. The result is that the underlying rhythm doesn't resume on time after the pause and the length of the pause is not a multiple of the previous R-R intervals.

SIGNS AND SYMPTOMS

You won't be able to detect a pulse or heart sounds when sinus arrest or sinus exit block occurs. Short pauses usually produce no symptoms. Recurrent or prolonged pauses may cause signs of decreased cardiac output, such as low blood pressure; altered mental status; cool, clammy skin; or syncope. The patient may also complain of dizziness or blurred vision.

INTERVENTIONS

An asymptomatic patient needs no treatment. Symptomatic patients are treated following the guidelines for patients with symptom-producing bradycardia. Treatment will also focus on the cause of the sinus arrest or sinus exit block. This may involve discontinuation of medications that contribute to SA node discharge or conduction, such as digoxin, beta-adrenergic receptor blockers, and calcium channel blockers.

Examine the circumstances under which the pauses occur. Both SA arrest and SA exit block 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 or sinus exit block.

Document the patient's vital signs and how he feels during pauses as well as the activities he was involved in at the time. 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 practitioner immediately if the patient becomes unstable. If appropriate, be alert for signs of digoxin, quinidine, or procainamide toxicity. Obtain a serum digoxin level and a serum electrolyte level.

Sick sinus syndrome

Also known as sinoatrial (SA) syndrome, sinus nodal dysfunction, and Stokes-Adams syndrome

SSS usually shows up as bradycardia, with episodes of sinus arrest and SA block interspersed with sudden, brief periods of rapid atrial fibrillation. Patients are also prone to paroxysms of other atrial tachyarrhythmias, such as atrial flutter and ectopic atrial tachycardia, a condition sometimes referred to as bradycardia-tachycardia (or “brady-tachy”) syndrome.

Most patients with SSS are over age 60, but anyone can develop the arrhythmia. It's rare in children except after open-heart surgery that results in SA node damage. The arrhythmia affects men and women equally. The onset is progressive, insidious, and chronic. (See Recognizing sick sinus syndrome, page 260.)

CAUSES

SSS 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 ANS and partial destruction of the sinus node, as may occur with an interrupted blood supply after an inferior wall myocardial infarction.

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 SSS. In many patients, though, the exact cause is never identified.

Causes of SSS include:

RECOGNIZING SICK SINUS SYNDROME

The following rhythm strip illustrates sick sinus syndrome. Look for these distinguishing characteristics.

c5-tt27

·

conditions leading to fibrosis of the SA node, such as increased age, atherosclerotic heart disease, hypertension, and cardiomyopathy

     

·

trauma to the SA node caused by open heart surgery (especially valvular surgery), pericarditis, or rheumatic heart disease

·

autonomic disturbances affecting autonomic innervation, such as hypervagotonia or degeneration of the autonomic system

·

cardioactive medications, such as digoxin, beta-adrenergic receptor blockers, and calcium channel blockers.

CLINICAL SIGNIFICANCE

The significance of SSS depends on the patient's age, the presence of other diseases, and the type and duration of the specific arrhythmias that occur. If atrial fibrillation is involved, the prognosis is worse, most likely because of the risk of thromboembolic complications.

If prolonged pauses are involved with SSS, syncope may occur. The length of a pause needed to cause syncope varies with the patient's age, posture at the time, and cerebrovascular status. Any pause that lasts 2 to 3 seconds or more should be considered significant.

ECG CHARACTERISTICS

SSS encompasses several potential rhythm disturbances that may be intermittent or chronic. SSS may include one, or a combination, of these rhythm disturbances:

·

sinus bradycardia

·

SA block

·

sinus arrest

·

sinus bradycardia alternating with sinus tachycardia

·

episodes of atrial tachyarrhythmias, such as atrial fibrillation and atrial flutter

·

failure of the sinus node to increase heart rate with exercise.

SSS displays these ECG characteristics:

·

Rhythm: atrial and ventricular rhythms irregular because of sinus pauses and abrupt rate changes

·

Rate: atrial and ventricular rates are fast or slow or alternate between fast and slow; and interrupted by a long sinus pause

·

P wave: varies with the prevailing rhythm; may be normal size and configuration or may be absent; when present, a P wave usually precedes each QRS complex

·

PR interval: usually within normal limits; varies with change in rhythm

·

QRS complex:

·

T wave: usually normal size and configuration

·

QT interval: usually within normal limits; varies with rhythm changes

·

Other: usually more than one arrhythmia on a 6-second strip.

SIGNS AND SYMPTOMS

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, then 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.

Other assessment findings depend on the patient's condition. For example, he may have crackles in the lungs, S3, or a dilated and displaced left ventricular apical impulse if he has underlying cardiomyopathy. The patient may also show signs and symptoms of decreased cardiac output, such as fatigue, hypotension, blurred vision, and syncope, a common experience with this arrhythmia. Syncopal episodes, when related to SSS, are referred to as Stokes-Adams attacks.

When caring for a patient with SSS, be alert for signs and symptoms of thromboembolism, especially if the patient has atrial fibrillation. Blood clots or thrombi forming in the heart can dislodge and travel through the bloodstream, resulting in decreased blood supply to the lungs, heart, brain, kidneys, intestines, or other organs. Assess the patient for:

·

neurologic changes (such as confusion)

·

vision disturbances

·

weakness

·

chest pain

·

dyspnea

·

tachypnea

·

tachycardia

·

acute onset of pain.

Early recognition allows for prompt treatment.

ff1-b01382759AGE AWARE

Because the older adult with SSS may have mental status changes, be sure to perform a thorough assessment to rule out other disorders, such as stroke, delirium, or dementia.

INTERVENTIONS

As with other sinus node arrhythmias, no treatment is generally necessary if the patient is asymptomatic. If the patient is symptomatic, however, treatment aims to alleviate signs and symptoms and correct the underlying cause of the arrhythmia.

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.

When caring for a patient with SSS, monitor and document all arrhythmias as well as signs or symptoms experienced. Note changes in heart rate and rhythm related to changes in the patient's level of activity.

ATRIAL ARRHYTHMIAS

Atrial arrhythmias, the most common cardiac rhythm disturbances, result from impulses originating in the atrial tissue in areas outside the SA node. These arrhythmias can affect ventricular filling time and diminish atrial kick. The term atrial kick

Atrial arrhythmias are thought to result from three mechanisms: altered automaticity, reentry, and afterdepolarization.

·

Altered automaticity. The term automaticity refers to the ability of cardiac cells to initiate electrical impulses spontaneously. An increase in the automaticity of the atrial fibers can trigger abnormal impulses. Causes of increased automaticity include extracellular factors, such as hypoxia, hypocalcemia, and digoxin toxicity as well as conditions in which the function of the heart's normal pacemaker, the SA node, is diminished. For example, increased vagal tone or hypokalemia can increase the refractory period of the SA node and allow atrial fibers to initiate impulses.

·

Reentry. In reentry, an impulse is delayed along a slow conduction pathway. Despite the delay, the impulse remains active enough to produce another impulse during myocardial repolarization. Reentry may occur with CAD, cardiomyopathy, or MI.

·

Afterdepolarization. Afterdepolarization can occur as a result of cell injury, digoxin toxicity, and other conditions. An injured cell sometimes only partially repolarizes. Partial repolarization can lead to repetitive ectopic firing called triggered activity. The depolarization produced by triggered activity, known as afterdepolarization, can lead to atrial or ventricular tachycardia.

Premature atrial contractions

Premature atrial contractions (PACs) originate in the atria, outside the sinoatrial (SA) node. They arise from either a single ectopic focus or from multiple atrial foci that supersede the SA node as pacemaker for one or more beats. PACs are generally caused by enhanced automaticity in the atrial tissue. (See .)

RECOGNIZING PREMATURE ATRIAL CONTRACTIONS

The following rhythm strip illustrates premature atrial contraction (PAC). Look for these distinguishing characteristics.

c5-tt28

PACs may be conducted or nonconducted (blocked) through the atrioventricular (AV) node and the rest of the heart, depending on the status of the AV and intraventricular conduction system. If the atrial ectopic pacemaker discharges too soon after the preceding QRS complex, the AV junction or bundle branches may still be refractory from conducting the previous electrical impulse. If they're still refractory, they may not be sufficiently repolarized to conduct the premature electrical impulse into the ventricles normally.

When a PAC is conducted, ventricular conduction is usually normal. Nonconducted, or blocked, PACs aren't followed by a QRS complex.

CAUSES

Alcohol, cigarettes, anxiety, fatigue, fever, and infectious diseases can trigger PACs, which commonly occur in a normal heart. Patients who eliminate or control those factors can usually correct the arrhythmia.

PACs may be associated with:

·

hyperthyroidism

·

coronary or valvular heart disease

·

acute respiratory failure

·

hypoxia

·

chronic pulmonary disease

·

digoxin toxicity

·

certain electrolyte imbalances.

PACs may also be caused by drugs that prolong the absolute refractory period of the SA node, including quinidine and procainamide.

CLINICAL SIGNIFICANCE

PACs are rarely dangerous in patients free from heart disease. They usually cause no symptoms and can go unrecognized for years. Patients may perceive PACs as normal palpitations or skipped beats.

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

ECG CHARACTERISTICS

·

Rhythm: Atrial and ventricular rhythms are irregular as a result of PACs, but the underlying rhythm may be regular.

·

Rate: Atrial and ventricular rates vary with the underlying rhythm.

·

P wave: The hallmark characteristic of a PAC is a premature P wave with an abnormal configuration, when compared with a sinus P wave. Varying configurations of the P wave indicate more than one ectopic site. PACs may be hidden in the preceding T wave.

·

PR interval:

·

QRS complex: Duration and configuration are usually normal when the PAC is conducted. If no QRS complex follows the PAC, the beat is called a nonconducted PAC.

·

T wave: Usually normal; however, if the P wave is hidden in the T wave, the T wave may appear distorted.

·

QT interval: Usually within normal limits.

·

Other: PACs may occur as a single beat, in a bigeminal (every other beat is premature), trigeminal (every third beat), or quadrigeminal (every fourth beat) pattern, or in couplets (pairs). Three or more PACs in a row is called atrial tachycardia.

PACs are commonly followed by a pause as the SA node resets. The PAC depolarizes the SA node early, causing it to reset itself and disrupting the normal cycle. The next sinus beat occurs sooner than it normally would, causing a P-P interval between normal beats interrupted by a PAC to be shorter than three consecutive sinus beats, an occurrence referred to as noncompensatory.

SIGNS AND SYMPTOMS

The patient may have an irregular peripheral or apical pulse rhythm when the PACs occur. Otherwise, the pulse rhythm and rate will reflect the underlying rhythm. Patients 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.

INTERVENTIONS

Most asymptomatic patients don't need treatment. If the patient is symptomatic, however, treatment may focus on eliminating the cause, such as caffeine and alcohol. People with frequent PACs may be treated with drugs that prolong the refractory period of the atria. Those drugs include beta-adrenergic receptor blockers and calcium channel blockers.

When caring for a patient with PACs, assess him to help determine factors that trigger ectopic beats. Tailor patient teaching to help the patient correct or avoid underlying causes. For example, the patient may need to avoid caffeine or learn stress-reduction techniques to lessen anxiety.

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

Atrial tachycardia

Atrial tachycardia is a supraventricular tachycardia, which means that the impulses driving the rapid rhythm originate above the ventricles. Atrial tachycardia has an atrial rate from 150 to 250 beats/minute. The rapid rate shortens diastole, resulting in a loss of atrial kick, reduced cardiac output, reduced coronary perfusion, and the potential for myocardial ischemia. (See Recognizing atrial tachycardia.)

There are three forms of atrial tachycardia: atrial tachycardia with block, multifocal atrial tachycardia (MAT, or chaotic atrial rhythm), and paroxysmal atrial tachycardia (PAT). In MAT, the tachycardia originates from multiple foci. PAT is generally a transient event in which the tachycardia appears and disappears suddenly.

RECOGNIZING ATRIAL TACHYCARDIA

The following rhythm strip illustrates atrial tachycardia. Look for these distinguishing characteristics.

c5-tt29

CAUSES

Atrial tachycardia can occur in patients with a normal heart. In those cases, it's commonly related to excessive use of caffeine or other stimulants, marijuana use, electrolyte imbalance, hypoxia, or physical or psychological stress. Typically, however, atrial tachycardia is associated with primary or secondary cardiac disorders, including myocardial infarction (MI), cardiomyopathy, congenital anomalies, Wolff-Parkinson-White syndrome, and valvular heart disease.

Signs of digoxin toxicity, page 268.)

In a healthy person, nonsustained atrial tachycardia is usually benign. However, this rhythm may be a forerunner of more serious ventricular arrhythmias, especially if it occurs in a patient with underlying heart disease.

The increased ventricular rate that occurs in atrial tachycardia results in decreased ventricular filling time, increased myocardial oxygen consumption, and decreased oxygen supply to the myocardium. Heart failure, myocardial ischemia, and MI can result.

SIGNS OF DIGOXIN TOXICITY

With digoxin (Lanoxin) toxicity be alert for the following signs and symptoms, especially if the patient is taking digoxin and his potassium level is low or he's also taking amiodarone (Cordarone) (because both combinations can increase the risk of digoxin toxicity):

·

CNS: fatigue, general muscle weakness, agitation, hallucinations

·

EENT: yellow-green halos around visual images, blurred vision

·

GI: anorexia, nausea, vomiting

·

CV: arrhythmias (most commonly, conduction disturbances with or without AV block, premature ventricular contractions, and supraventricular arrhythmias), increased severity of heart failure, hypotension. (Digoxin's toxic effects on the heart may be life-threatening and always require immediate attention.)

ECG CHARACTERISTICS

·

Rhythm: The atrial rhythm is usually regular. The ventricular rhythm is regular or irregular, depending on the atrioventricular (AV) conduction ratio and the type of atrial tachycardia. (See Recognizing types of atrial tachycardia, pages 270 and 271.)

·

Rate: The atrial rate is characterized by three or more consecutive ectopic atrial beats occurring at a rate between 150 and 250 beats/ minute. The rate rarely exceeds 250 beats/minute. The ventricular rate depends on the AV conduction ratio.

·

P wave: The P wave may be aberrant (deviating from normal appearance) or hidden in the preceding T wave. If visible, it's usually upright and precedes each QRS complex.

·

PR interval: The PR interval may be unmeasurable if the P wave can't be distinguished from the preceding T wave.

·

QRS complex: Duration and configuration are usually normal, unless the impulses are being conducted abnormally through the ventricles.

·

T wave: Usually distinguishable but may be distorted by the P wave; may be inverted if ischemia is present.

·

QT interval: Usually within normal limits but may be shorter because of the rapid rate.

·

Other: None.

The patient with atrial tachycardia will have a rapid apical and peripheral pulse rate. The rhythm may be regular or irregular, depending on the type of atrial tachycardia. A patient with PAT may complain that his heart suddenly starts to beat faster or that he suddenly feels palpitations. Persistent tachycardia and rapid ventricular rate cause decreased cardiac output, resulting in hypotension and syncope.

INTERVENTIONS

Treatment depends on the type of tachycardia and the severity of the patient's symptoms. Because one of the most common causes of atrial tachycardia is digoxin toxicity, assess the patient for signs and symptoms of digoxin toxicity and monitor digoxin blood levels.

Valsalva's maneuver or carotid sinus massage may be used to treat PAT. (See Understanding carotid sinus massage, page 272.) These maneuvers increase the parasympathetic tone, which results in a slowing of the heart rate. They also allow the sinoatrial (SA) node to resume function as the primary pacemaker.

If vagal maneuvers are used, make sure resuscitative equipment is readily available. Keep in mind that vagal stimulation can result in bradycardia, ventricular arrhythmias, and asystole.

ff1-b01382759AGE AWARE

Older adults may have undiagnosed carotid atherosclerosis and carotid bruits may be absent, even with significant disease. As a result, cardiac sinus massage shouldn't be performed in latemiddle-age and older patients.

Drug therapy (pharmacologic cardioversion) may be used to increase the degree of AV block and decrease ventricular response rate. Appropriate drugs include adenosine (Adenocard), amiodarone, beta-adrenergic receptor blockers, calcium channel blockers, and digoxin. When other treatments fail, or if the patient is clinically unstable, synchronized electrical cardioversion may be used. For the complete ACLS algorithm, see pages 332 and 333.

Atrial overdrive pacing (also called rapid atrial pacing or overdrive suppression) may also be used to stop the arrhythmia. This technique involves suppression of spontaneous depolarization of the ectopic pacemaker by a series of paced electrical impulses at a rate slightly higher than the intrinsic ectopic atrial rate. The pacemaker cells are depolarized prematurely and, following termination of the paced electrical impulses, the SA node resumes its normal role as the pacemaker.

Radiofrequency ablation can be used to treat PAT. The ectopic focus is mapped during the electrophysiology study, and then the area is ablated. Because MAT commonly occurs in patients with chronic pulmonary disease, the rhythm may not respond to treatment.

RECOGNIZING TYPES OF ATRIAL TACHYCARDIA

Atrial tachycardia comes in three varieties. Here's a quick rundown of each.

Atrial tachycardia with block

Atrial tachycardia with block is caused by increased automaticity of the atrial tissue. As the atrial rate speeds up and atrioventricular (AV) conduction becomes impaired, a 2:1 block typically occurs. Occasionally a type I (Wenckebach) second-degree AV block may be seen. Look for these distinguishing characteristics.

c5-tt30

·

Rhythm:

·

atrial—140 to 250 beats/ minute, multiple of ventricular rate; ventricular—varies with block

·

P wave: slightly abnormal

·

PR interval: usually normal; may be hidden

·

QRS complex: usually normal

·

Other: more than one P wave for each QRS complex

Multifocal atrial tachycardia (MAT)

In MAT, atrial tachycardia occurs with numerous atrial foci firing intermittently. MAT produces varying P waves on the strip and occurs most commonly in patients with chronic pulmonary disease. The irregular baseline in this strip is caused by movement of the chest wall. Look for these distinguishing characteristics.

·

Rhythm: both irregular

·

Rate: atrial—100 to 250 beats/ minute, usually under 160; ventricular —101 to 250 beats/minute

·

P wave:

·

PR interval: varies

·

Other: none

Paroxysmal atrial tachycardia (PAT)

A type of paroxysmal supraventricular tachycardia, PAT features brief periods of tachycardia that alternate with periods of normal sinus rhythm. PAT starts and stops suddenly as a result of rapid firing of an ectopic focus. It commonly follows frequent premature atrial contractions, one of which initiates the tachycardia. Look for these distinguishing characteristics.

c5-tt31

·

Rhythm: regular

·

Rate: 140 to 250 beats/minute

·

P wave: abnormal, possibly hidden in previous T wave

·

PR interval: identical for each cycle

·

QRS complex: can be aberrantly conducted

·

Other: one P wave for each QRS complex

c5-tt32

UNDERSTANDING CAROTID SINUS MASSAGE

Carotid sinus massage may be used to interrupt paroxysmal atrial tachycardia. Massaging the carotid sinus stimulates the vagus nerve, which inhibits firing of the sinoatrial (SA) node and slows atrioventricular (AV) node conduction. As a result, the SA node can resume its function as primary pacemaker.

Carotid sinus massage involves a firm massage that lasts no longer than 5 to 10 seconds. The patient's head is turned to the left to massage the right carotid sinus, as shown below. Remember that simultaneous, bilateral massage should never be attempted.

Carotid sinus massage is contraindicated in patients with carotid bruits. Risks of the procedure include decreased heart rate, syncope, sinus arrest, increased degree of AV block, cerebral emboli, stroke, and asystole.

c5-tt33

When caring for a patient with atrial tachycardia, carefully monitor the patient's rhythm strips. Doing so may provide information about the cause of atrial tachycardia, which in turn can facilitate treatment. Monitor the patient for chest pain, indications of decreased cardiac output, and signs and symptoms of heart failure or myocardial ischemia.

Atrial flutter

Atrial flutter, a supraventricular tachycardia, is characterized by a rapid atrial rate of 250 to 350 beats/minute, although it's generally around 300 beats/minute. Originating in a single atrial focus, this rhythm results from circus reentry and possibly increased automaticity.

RECOGNIZING ATRIAL FLUTTER

The following rhythm strip illustrates atrial flutter. Look for these distinguishing characteristics.

c5-tt34

On an ECG, the P waves lose their normal appearance due to the rapid atrial rate. The waves blend together in a sawtooth configuration called flutter waves, or F waves. These waves are the hallmark of atrial flutter. (See Recognizing atrial flutter.)

Atrial flutter may be caused by conditions that enlarge atrial tissue and elevate atrial pressures. The arrhythmia is commonly found in patients with:

·

mitral or tricuspid valvular disease

·

hyperthyroidism

·

pericardial disease

·

digoxin toxicity

·

primary myocardial disease.

The rhythm is sometimes encountered in patients following cardiac surgery or in patients with acute myocardial infarction, chronic pulmonary disease, or systemic arterial hypoxia. Atrial flutter rarely occurs in healthy people. When it does, it may indicate intrinsic cardiac disease.

CLINICAL SIGNIFICANCE

Usually the faster the ventricular rate, the more dangerous the arrhythmia. Rapid ventricular rates reduce ventricular filling time and coronary perfusion, which can cause angina, heart failure, pulmonary edema, hypotension, and syncope.

ECG CHARACTERISTICS

·

Rhythm: Atrial rhythm is regular. Ventricular rhythm depends on the AV conduction pattern; it's typically regular, although cycles may alternate. An irregular pattern may signal atrial fibrillation or indicate development of a block.

·

Rate: Atrial rate is 250 to 350 beats/minute. Ventricular rate depends on the degree of AV block; usually it's 60 to 100 beats/ minute, but it may accelerate to 125 to 150 beats/minute.

Varying degrees of AV block produce ventricular rates that are usually one-half to one-fourth of the atrial rate. These are expressed as ratios, for example, 2:1 or 4:1. Usually, the AV node won't accept more than 180 impulses/minute and allows every second, third, or fourth impulse to be conducted. These impulses account for the ventricular rate. At the time atrial flutter is initially recognized, the ventricular response is typically above 100 beats/minute. One of the most common ventricular rates is 150 beats/minute with an atrial rate of 300, known as 2:1 block.

·

P wave: Atrial flutter is characterized by abnormal P waves that produce a sawtooth appearance, referred to as flutter or F waves.

·

PR interval: Unmeasurable.

·

QRS complex: Duration is usually within normal limits, but the complex may be widened if flutter waves are buried within the complex.

·

T wave: Not identifiable.

·

QT interval: Unmeasurable because the T wave isn't identifiable.

·

Other: The patient may develop an atrial rhythm that commonly varies between a fibrillatory line and flutter waves. This variation is referred to as atrial fib-flutter. The ventricular response is irregular.

SIGNS AND SYMPTOMS

When caring for a patient with atrial flutter, you may note that the peripheral and apical pulses are 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. If the ventricular rate is rapid, however, the patient may experience a feeling of palpitations and may exhibit signs and symptoms of reduced cardiac output.

INTERVENTIONS

If the patient is hemodynamically unstable, synchronized electrical cardioversion or countershock should be administered immediately. Cardioversion delivers electrical current to the heart to correct an arrhythmia, but unlike defibrillation, it usually uses much lower energy levels and is synchronized to discharge at the peak of the R wave. This causes immediate depolarization, interrupting reentry circuits and allowing the sinoatrial (SA) node to resume control as pacemaker. Synchronizing the energy current delivery with the R wave ensures that the current won't be delivered on the vulnerable T wave, which could initiate ventricular tachycardia or ventricular fibrillation.

The focus of treatment for hemodynamically stable patients with atrial flutter includes controlling the rate and converting the rhythm. Specific interventions depend on the patient's cardiac function, whether preexcitation syndromes are involved, and the duration (less than or greater than 48 hours) of the arrhythmia. For example, in atrial flutter with normal cardiac function and duration of rhythm less than 48 hours, electrical cardioversion may be considered; for duration greater than 48 hours, don't use electrical cardioversion because it increases the risk of thromboembolism unless the patient has been adequately anticoagulated.

Because atrial flutter may be an indication of intrinsic cardiac disease, monitor the patient closely for signs and symptoms of low cardiac output. Be alert to the effects of digoxin, which depresses the SA node.

Atrial fibrillation

Atrial fibrillation, sometimes called AFib multiple impulses from numerous ectopic pacemakers in the atria. Atrial fibrillation is characterized by the absence of P waves and an irregularly irregular ventricular response.

The atrioventricular (AV) node protects the ventricles from the 350 to 600 erratic atrial impulses that occur each minute by acting as a filter and blocking some of the impulses. The ventricles respond only to impulses conducted through the AV node, hence the characteristic, wide variation in R-R intervals. When the ventricular response rate drops below 100, atrial fibrillation is considered controlled. When the ventricular rate exceeds 100, the rhythm is considered uncontrolled.

Like atrial flutter, atrial fibrillation results in a loss of atrial kick. The rhythm may be sustained or paroxysmal, meaning that it occurs suddenly and ends abruptly. It can either be preceded by or be the result of premature atrial contractions. (See Recognizing atrial fibrillation.)

CAUSES

Atrial fibrillation occurs more commonly than atrial flutter or atrial tachycardia. Atrial fibrillation can occur following cardiac surgery. Other causes of atrial fibrillation include:

·

rheumatic heart disease

·

valvular heart disease (especially mitral valve disease)

·

hyperthyroidism

·

pericarditis

·

coronary artery disease

·

acute myocardial infarction

·

hypertension

·

cardiomyopathy

·

atrial septal defects

·

chronic obstructive pulmonary disease.

The rhythm may also occur in a healthy person who smokes or drinks coffee or alcohol or who is fatigued and under stress. Certain drugs, such as aminophylline and digoxin, may contribute to the development of atrial fibrillation. Endogenous catecholamine released during exercise may also trigger the arrhythmia.

RECOGNIZING ATRIAL FIBRILLATION

The following rhythm strip illustrates atrial fibrillation. Look for these distinguishing characteristics.

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CLINICAL SIGNIFICANCE

The loss of atrial kick from atrial fibrillation can result in the subsequent loss of approximately 20% of normal end-diastolic volume. Combined with the decreased diastolic filling time associated with a rapid heart rate, clinically significant reductions in cardiac output can result. In uncontrolled atrial fibrillation, the patient may develop heart failure, myocardial ischemia, or syncope.

Patients with preexisting cardiac disease, such as hypertrophic cardiomyopathy, mitral stenosis, rheumatic heart disease, or those with mitral prosthetic valves, tend to tolerate atrial fibrillation poorly and may develop severe heart failure.

Left untreated, atrial fibrillation can lead to cardiovascular collapse, thrombus formation, and systemic arterial or pulmonary embolism. (See Risk of restoring sinus rhythm, page 278.)

ECG CHARACTERISTICS

·

Rhythm: Atrial and ventricular rhythms are grossly irregular, typically described as irregularly irregular.

·

Rate: The atrial rate is almost indiscernible and usually exceeds 350 beats/minute. The atrial rate far exceeds the ventricular rate

because most impulses aren't conducted through the AV junction. The ventricular rate usually varies, typically from 100 to 150 beats/ minute but can be below 100 beats/minute.

·

P wave: The P wave is absent. Erratic baseline f waves appear in place of P waves. These chaotic waves represent atrial tetanization from rapid atrial depolarizations.

·

PR interval: Indiscernible.

·

QRS complex: Duration and configuration are usually normal.

·

T wave: Indiscernible.

·

QT interval: Unmeasurable.

·

Other: The patient may develop an atrial rhythm that commonly varies between a fibrillatory line and flutter waves, a phenomenon called atrial fib-flutter.

RISK OF RESTORING SINUS RHYTHM

A patient with atrial fibrillation is at increased risk for developing atrial thrombus and subsequent systemic arterial embolism. In atrial fibrillation, neither atrium contracts as a whole. As a result, blood may pool on the atrial wall, and thrombi may form. Thrombus formation places the patient at higher risk for emboli and stroke.

If normal sinus rhythm is restored and the atria contract normally, clots may break away from the atrial wall and travel through the pulmonary or systemic circulation with potentially disastrous results, such as stroke, pulmonary embolism, or arterial occlusion.

SIGNS AND SYMPTOMS

When caring for a patient with atrial fibrillation, you may find that the radial pulse rate is slower than the apical rate. The weaker contractions that occur in atrial fibrillation don't produce a palpable peripheral pulse; only the stronger ones do.

The pulse rhythm will be irregularly irregular, with a normal or abnormal heart rate. Patients with a new onset of atrial fibrillation and a rapid ventricular rate may demonstrate signs and symptoms of decreased cardiac output, including hypotension and light-headedness. Patients with chronic atrial fibrillation may be able to compensate for the decreased cardiac output. Although these patients may be asymptomatic, they face a greater-than-normal risk of the development of pulmonary, cerebral, or other thromboembolic events.

INTERVENTIONS

Treatment of atrial fibrillation aims to reduce the ventricular response rate to below 100 beats/minute. This may be accomplished either by drugs that control the ventricular response or by a combination of electrical cardioversion and drug therapy, to convert the arrhythmia to normal sinus rhythm. When the onset of atrial fibrillation is acute and the patient can cooperate, vagal maneuvers or carotid sinus massage may slow the ventricular response but won't convert the arrhythmia.

HOW SYNCHRONIZED CARDIOVERSION WORKS

A patient experiencing an arrhythmia that leads to reduced cardiac output may be a candidate for synchronized cardioversion. This procedure may be done electively or as an emergency. For example, it may be an elective procedure in a patient with recurrent atrial fibrillation or an emergency procedure in a patient with ventricular tachycardia and a pulse.

unsynchronized cardioversion, except that synchronized cardioversion generally requires lower energy levels. Synchronizing the energy delivered to the patient reduces the risk that the current will strike during the relative refractory period of a cardiac cycle and induce ventricular fibrillation (VF).

Keep in mind that a slight delay occurs between the time the discharge buttons are depressed and the moment the energy is actually discharged. When using handheld paddles, continue to hold the paddles on the patient's chest until the energy is delivered.

Remember to reset the “sync mode” on the defibrillator after each synchronized cardioversion. Resetting this switch is necessary because most defibrillators will automatically reset to an unsynchronized mode.

If VF occurs during the procedure, turn off sync button, and immediately deliver an unsynchronized defibrillation to terminate the arrhythmia. Be aware that synchronized cardioversion carries the risk of lethal arrhythmia when used in patients with digoxin (Lanoxin) toxicity.

If the patient is hemodynamically unstable, synchronized electrical cardioversion should be administered immediately. Electrical cardioversion is most successful if used within the first 48 hours after onset and less successful the longer the duration of the arrhythmia. Conversion to normal sinus rhythm will cause forceful atrial contractions to resume abruptly. If a thrombus forms in the atria, the resumption of contractions can result in systemic emboli. (See How synchronized cardioversion works.)

The focus of treatment for hemodynamically stable patients with atrial fibrillation includes:

·

controlling the rate

·

converting the rhythm

·

providing anticoagulation if indicated.

Specific interventions depend on the patient's cardiac function, whether preexcitation syndromes are involved, and the duration of the arrhythmia.

Beta-adrenergic receptor blockers and calcium channel blockers are the drugs of choice to control the ventricular rate. Patients with reduced left ventricular function typically receive digoxin. Anticoagulation is crucial in reducing the risk of thromboembolism. Heparin and warfarin (Coumadin) are used for anticoagulation and to prepare the patient for electrical cardioversion. Symptomatic atrial fibrillation that doesn't respond to routine treatment may be treated with radiofrequency ablation therapy.

When assessing a patient with atrial fibrillation, assess the peripheral and apical pulses. If the patient isn't on a cardiac monitor, be alert for an irregular pulse and differences in the radial and apical pulse rates.

Assess for symptoms of decreased cardiac output and heart failure. If drug therapy is used, monitor serum drug levels, and observe the patient for evidence of toxicity. Tell the patient to report pulse rate changes, syncope or dizziness, chest pain, and signs of heart failure, such as dyspnea and peripheral edema.

Wandering pacemaker, also called wandering atrial pacemaker, is an atrial arrhythmia that results when the site of impulse formation shifts from the sinoatrial (SA) node to another area above the ventricles. The origin of the impulse may wander beat to beat from the SA node to ectopic sites in the atria or to the atrioventricular (AV) junctional tissue. The P wave and PR interval vary from beat to beat as the pacemaker site changes. (See Recognizing wandering pacemaker)

CAUSES

In most cases, wandering pacemaker is caused by increased parasympathetic (vagal) influences on the SA node or AV junction. It can also be caused by chronic pulmonary disease, valvular heart disease, digoxin toxicity, and inflammation of the atrial tissue.

RECOGNIZING WANDERING PACEMAKER

The following rhythm strip illustrates wandering pacemaker. Look for these distinguishing characteristics.

c5-tt36

CLINICAL SIGNIFICANCE

The arrhythmia may be normal in young patients and is common in athletes who have slow heart rates. The arrhythmia may be difficult to identify because it's often transient. Although wandering pacemaker is rarely serious, chronic arrhythmias are a sign of heart disease and should be monitored.

ECG CHARACTERISTICS

·

Rhythm: The atrial rhythm varies slightly, with an irregular P-P interval. The ventricular rhythm varies slightly, with an irregular R-R interval.

·

Rate: Atrial and ventricular rates vary but are usually within normal limits, or below 60 beats/minute.

·

P wave: Altered size and configuration are due to the changing pacemaker site (SA node, atria, or AV junction). The P wave may also be absent, inverted, or may follow the QRS complex if the impulse originates in the AV junction. A combination of these variations

may appear, with at least three different P-wave shapes visible.

·

PR interval: The PR interval varies from beat to beat as the pacemaker site changes but usually less than 0.20 second. If the impulse originates in the AV junction, the PR interval will be less than 0.12 second. This variation in PR interval will cause a slightly irregular R-R interval. When the P wave is present, the PR interval may be normal or shortened.

·

QRS complex: Ventricular depolarization is normal, so duration of the QRS complex is usually within normal limits and is of normal configuration.

·

T wave: Normal size and configuration.

·

QT interval: Usually within normal limits, but may vary.

·

Other: None.

SIGNS AND SYMPTOMS

Patients are generally asymptomatic and unaware of the arrhythmia. The pulse rate may be normal or below 60 beats/minute, and the rhythm may be regular or slightly irregular.

INTERVENTIONS

Usually, no treatment is needed for asymptomatic patients. If the patient is symptomatic, however, the patient's medications should be reviewed and the underlying cause investigated and treated. Monitor the patient's heart rhythm, and assess for signs of hemodynamic instability, such as hypotension and changes in mental status.

JUNCTIONAL ARRHYTHMIAS

Junctional arrhythmias originate in the atrioventricular (AV) junction—the area in and around the AV node and the bundle of His. The specialized pacemaker cells in the AV junction take over as the heart's pacemaker if the sinoatrial (SA) node fails to function properly or if the electrical impulses originating in the SA node are blocked. These junctional pacemaker cells have an inherent firing rate of 40 to 60 beats/minute.

In normal impulse conduction, the AV node slows transmission of the impulse from the atria to the ventricles, which allows the ventricles to fill as much as possible before they contract. However, these impulses don't always follow the normal conduction pathway. (See Conduction in Wolff-Parkinson-White syndrome.)

Because of the location of the AV junction within the conduction pathway, electrical impulses originating in this area cause abnormal depolarization of the heart. The impulse is conducted in a retrograde (backward) fashion to depolarize the atria, and antegrade (forward) to depolarize the ventricles.

CONDUCTION IN WOLFF-PARKINSON-WHITE SYNDROME

Electrical impulses in the heart don't always follow normal conduction pathways. In preexcitation syndromes, electrical impulses enter the ventricles from the atria through an accessory pathway that bypasses the atrioventricular junction. Wolff-Parkinson-White (WPW) syndrome is a common type of preexcitation syndrome.

WPW syndrome commonly occurs in young children and in adults ages 20 to 35. The syndrome causes the PR interval to shorten and the QRS complex to lengthen as a result of a delta wave. Delta waves, which in WPW occur just before normal ventricular depolarization, are produced as a result of the premature depolarization or preexcitation of a portion of the ventricles.

WPW is clinically significant because the accessory pathway—in this case, Kent's bundle—may result in paroxysmal tachyarrhythmias by reentry and rapid conduction mechanisms.

c5-tt37

Depolarization of the atria can precede depolarization of the ventricles, or the ventricles can be depolarized before the atria. Depolarization of the atria and ventricles can also occur simultaneously. (See Locating the P wave, page 284.)

Retrograde depolarization of the atria results in inverted P waves in leads II, III, and aVF, leads in which you would normally see upright P waves appear.

Remember that arrhythmias causing inverted P waves on an ECG may originate in the atria or AV junction. Atrial arrhythmias are sometimes mistaken for junctional arrhythmias because impulses are generated so low in the atria that they cause retrograde depolarization and inverted P waves. Looking at the PR interval will help you determine whether an arrhythmia is atrial or junctional.

LOCATING THE P WAVE

When the specialized pacemaker cells in the atrioventricular junction take over as the dominant pacemaker of the heart:

·

depolarization of the atria can precede depolarization of the ventricles

·

the ventricles can be depolarized before the atria

·

simultaneous depolarization of the atria and ventricles can occur.

The rhythm strips shown here demonstrate the various locations of the P waves in junctional arrhythmias, depending on the direction of depolarization.

Inverted P wave

If the atria are depolarized first, the P wave will occur before the QRS complex.

c5-tt38

Inverted P wave

If the ventricles are depolarized first, the P wave will occur after the QRS complex.

c5-tt39

Inverted P wave (hidden)

If the ventricles and atria are depolarized simultaneously, the P wave will be hidden in the QRS complex.

c5-tt40

Premature junctional contractions

Recognizing a PJC.)

CAUSES

PJCs may be caused by digoxin toxicity, excessive caffeine intake, amphetamine ingestion, excessive alcohol intake, excessive nicotine intake, stress, coronary artery disease, myocardial ischemia, valvular heart disease, pericarditis, heart failure, chronic obstructive pulmonary disease, hyperthyroidism, electrolyte imbalances, or inflammatory changes in the AV junction after heart surgery.

RECOGNIZING A PJC

The following rhythm strip illustrates premature junctional contraction (PJC). Look for these distinguishing characteristics.

c5-tt41

CLINICAL SIGNIFICANCE

PJCs are generally considered harmless unless they occur frequently—typically defined as more than six/minute. Frequent PJCs indicate junctional irritability and can precipitate a more serious arrhythmia, such as junctional tachycardia. In patients taking digoxin, PJCs are a common early sign of toxicity.

ECG CHARACTERISTICS

·

Rhythm: Atrial and ventricular rhythms are irregular during PJCs; the underlying rhythm may be regular.

·

Rate: Atrial and ventricular rates reflect the underlying rhythm.

·

P wave: The P wave is usually inverted. It may occur before or after the QRS complex or may appear absent when hidden in the QRS

complex. Look for an inverted P wave in leads II, III, and aVF

·

PR interval: If the P wave precedes the QRS complex, the PR interval is shortened (less than 0.12 second); otherwise, it can't be measured.

·

QRS complex: Because the ventricles are usually depolarized normally, the QRS complex usually has a normal configuration and a normal duration of less than 0.12 second.

·

T wave: Usually has a normal configuration.

·

QT interval: Usually within normal limits.

·

Other:

SIGNS AND SYMPTOMS

The patient is usually asymptomatic. He may complain of palpitations or a feeling of “skipped heart beats.” You may be able to palpate an irregular pulse when PJCs occur. If PJCs are frequent enough, the patient may experience hypotension from a transient decrease in cardiac output.

INTERVENTIONS

PJCs don't usually require treatment unless the patient is symptomatic. In those cases, the underlying cause should be treated. For example, in digoxin toxicity, the medication should be discontinued and serum drug levels monitored.

Monitor the patient for hemodynamic instability as well. If ectopic beats occur frequently, the patient should decrease or eliminate his caffeine intake.

Junctional escape rhythm

A junctional escape rhythm, also referred to as junctional rhythm, is an arrhythmia originating in the atrioventricular (AV) junction. In this arrhythmia, the AV junction takes over as a secondary, or “escape” pacemaker. This usually occurs only when a higher pacemaker site in the atria, usually the sinoatrial (SA) node, fails as the heart's dominant pacemaker.

Remember that the AV junction can take over as the heart's dominant pacemaker if the firing rate of the higher pacemaker sites falls below the AV junction's intrinsic firing rate, if the pacemaker fails to generate an impulse, or if the conduction of the impulses is blocked.

In a junctional escape rhythm, as in all junctional arrhythmias, the atria are depolarized by means of retrograde conduction. The

Recognizing junctional escape rhythm.)

RECOGNIZING JUNCTIONAL ESCAPE RHYTHM

The following rhythm strip illustrates junctional escape rhythm. Look for these distinguishing characteristics.

c5-tt42

CAUSES

A junctional escape rhythm can be caused by a condition that disturbs normal SA node function or impulse conduction. Causes of the arrhythmia include:

·

SA node ischemia

·

hypoxia

·

electrolyte imbalances

·

valvular heart disease

·

heart failure

·

cardiomyopathy

·

myocarditis

·

sick sinus syndrome

·

increased parasympathetic (vagal) tone.

Drugs, such as digoxin, calcium channel blockers, and beta-adrenergic receptor blockers, can also cause a junctional escape rhythm.

CLINICAL SIGNIFICANCE

The clinical significance of junctional escape rhythm depends on how well the patient tolerates a decreased heart rate (40 to 60 beats/ minute) and associated decrease in cardiac output. In addition to a decreased cardiac output from a slower heart rate, depolarization of the atria either after or simultaneously with ventricular depolarization results in loss of atrial kick. Remember that junctional escape rhythms protect the heart from potentially life-threatening ventricular escape rhythms.

·

Rhythm: Atrial and ventricular rhythms are regular.

·

Rate: The atrial and ventricular rates are 40 to 60 beats/minute.

·

P wave: The P wave is inverted (look for inverted P waves in leads II, III, and aVF). The P wave may occur before or after the QRS complex or may appear absent when hidden within QRS complex.

·

PR interval: If the P wave precedes the QRS complex, the PR interval is shortened (less than 0.12 second); otherwise, it can't be measured.

·

QRS complex: Duration is usually within normal limits; configuration is usually normal.

·

T wave: Usually normal configuration.

·

QT interval:

·

Other: None.

SIGNS AND SYMPTOMS

A patient with a junctional escape rhythm will have a slow, regular pulse rate of 40 to 60 beats/minute. The patient may be asymptomatic. However, pulse rates under 60 beats/minute may lead to inadequate cardiac output, causing hypotension, syncope, or blurred vision.

INTERVENTIONS

Treatment for a junctional escape rhythm involves identification and correction of the underlying cause, whenever possible. If the patient is symptomatic, atropine may be used to increase the heart rate, or a temporary (transcutaneous or transvenous) or permanent pacemaker may be inserted. Because junctional escape rhythm can prevent ventricular standstill, it should never be suppressed.

RECOGNIZING ACCELERATED JUNCTIONAL RHYTHM

The following rhythm strip illustrates accelerated junctional rhythm. Look for these distinguishing characteristics.

c5-tt43

Monitor the patient's serum digoxin and electrolyte levels, and watch for signs of decreased cardiac output, such as hypotension, syncope, and blurred vision.

Accelerated junctional rhythm

An accelerated junctional rhythm is an arrhythmia that originates in the atrioventricular (AV) junction and is usually caused by enhanced automaticity of the AV junctional tissue. It's called accelerated because it occurs at a rate of 60 to 100 beats/minute, exceeding the inherent junctional escape rate of 40 to 60 beats/minute.

Because the rate is below 100 beats/minute, the arrhythmia isn't classified as junctional tachycardia. The atria are depolarized by means of retrograde conduction, and the ventricles are depolarized normally. (See Recognizing accelerated junctional rhythm.)

CAUSES

Digoxin toxicity is a common cause of accelerated junctional rhythm. Other causes include:

·

electrolyte disturbances

 

·

valvular heart disease

·

rheumatic heart disease

·

heart failure

·

myocarditis

·

cardiac surgery

·

inferior- or posterior-wall myocardial infarction.

CLINICAL SIGNIFICANCE

Patients experiencing accelerated junctional rhythm are generally asymptomatic because the rate corresponds to the normal inherent firing rate of the sinoatrial node (60 to 100 beats/minute). However, symptoms of decreased cardiac output, including hypotension and syncope, can occur if atrial depolarization occurs after or simultaneously with ventricular depolarization, which causes the subsequent loss of atrial kick.

ECG CHARACTERISTICS

·

Atrial and ventricular rhythms are regular.

·

Rate: Atrial and ventricular rates range from 60 to 100 beats/ minute.

·

P wave:F. It may precede, follow, or be hidden in the QRS complex.

·

PR interval: If the P wave occurs before the QRS complex, the PR interval is shortened (less than 0.12 second). Otherwise, it can't be measured.

·

QRS complex: Duration is usually within normal limits. Configuration is usually normal.

·

T wave: Usually within normal limits.

·

QT interval: Usually within normal limits.

·

Other: None.

SIGNS AND SYMPTOMS

The pulse rate will be normal with a regular rhythm. The patient may be asymptomatic because accelerated junctional rhythm has the same rate as sinus rhythm. However, if cardiac output is decreased, the patient may exhibit symptoms, such as hypotension, changes in mental status, and weak peripheral pulses.

INTERVENTIONS

Treatment for accelerated junctional rhythm involves identifying and correcting the underlying cause. Assessing the patient for signs and symptoms related to decreased cardiac output and hemodynamic instability is key, as is monitoring serum digoxin and electrolyte levels.

RECOGNIZING JUNCTIONAL TACHYCARDIA

The following rhythm strip illustrates junctional tachycardia. Look for these distinguishing characteristics.

c5-tt44

Junctional tachycardia

In junctional tachycardia, three or more premature junctional contractions (PJCs) occur in a row. This supraventricular tachycardia generally occurs as a result of enhanced automaticity of the atrioventricular (AV) junction, which causes the AV junction to override the sinoatrial node as the dominant pacemaker.

In junctional tachycardia, the atria are depolarized by retrograde conduction. Conduction through the ventricles is normal. (See Recognizing junctional tachycardia.)

CAUSES

·

inferior- or posterior-wall infarction or ischemia

·

inflammation of the AV junction after heart surgery

·

heart failure

 

·

electrolyte imbalances

·

valvular heart disease.

CLINICAL SIGNIFICANCE

The clinical significance of junctional tachycardia depends on the rate and underlying cause. At higher ventricular rates, junctional tachycardia may reduce cardiac output by decreasing ventricular filling time. A loss of atrial kick also occurs with atrial depolarization that follows or occurs simultaneously with ventricular depolarization.

ECG CHARACTERISTICS

·

Rhythm: Atrial and ventricular rhythms are usually regular. The atrial rhythm may be difficult to determine if the P wave is hidden in the QRS complex or preceding T wave.

·

Rate: Atrial and ventricular rates exceed 100 beats/minute (usually between 100 and 200 beats/minute). The atrial rate may be difficult to determine if the P wave is hidden in the QRS complex or the preceding T wave.

·

P wave: The P wave is usually inverted in leads II, III, and aVF. It may occur before or after the QRS complex or be hidden in the QRS complex.

·

PR interval: If the P wave precedes the QRS complex, the PR interval is shortened (less than 0.12 second); otherwise, the PR interval can't be measured.

·

QRS complex: Duration is within normal limits; configuration is usually normal.

·

T wave: Configuration is usually normal but may be abnormal if the P wave is hidden in the T wave. The fast rate may make T waves indiscernible.

·

QT interval: Usually within normal limits.

·

Other: None.

SIGNS AND SYMPTOMS

The patient's pulse rate will be above 100 beats/minute and have a regular rhythm. Patients with a rapid heart rate may experience signs and symptoms of decreased cardiac output and hemodynamic instability including hypotension.

INTERVENTIONS

The underlying cause should be identified and treated. If the cause is digoxin toxicity, the drug should be discontinued. In some cases of digoxin toxicity, a digoxin-binding drug may be used to reduce serum digoxin levels. Vagal maneuvers and drugs, such as adenosine, may slow the heart rate for symptomatic patients. Patients with recurrent junctional tachycardia may be treated with ablation therapy, followed by permanent pacemaker insertion.

Monitor patients with junctional tachycardia for signs of decreased cardiac output. In addition, check digoxin and potassium levels, and administer potassium supplements as ordered.

VENTRICULAR ARRHYTHMIAS

Ventricular arrhythmias originate in the ventricles below the bifurcation of the bundle of His. These arrhythmias occur when electrical impulses depolarize the myocardium using a different pathway from normal impulse conduction.

Ventricular arrhythmias appear on an ECG in characteristic ways. The QRS complex in most of these arrhythmias is wider than normal because of the prolonged conduction time through, and abnormal depolarization of, the ventricles. The deflections of the T wave and the QRS complex are in opposite directions because ventricular repolarization, as well as ventricular depolarization, is abnormal. The P wave in many ventricular arrhythmias is absent because atrial depolarization doesn't occur. If the P wave does occur, it usually doesn't have any relationship to the QRS complex.

When electrical impulses come from the ventricles instead of the atria, atrial kick is lost and cardiac output can decrease by as much as 30%. This is one reason why patients with ventricular arrhythmias may show signs and symptoms of heart failure, including hypotension, angina, syncope, and respiratory distress.

Although ventricular arrhythmias may be benign, they're generally considered the most serious arrhythmias, because the ventricles are ultimately responsible for cardiac output. Rapid recognition and treatment of ventricular arrhythmias increase the chances of successful resuscitation.

Premature ventricular contractions

Premature ventricular contractions (PVCs) are ectopic beats that originate in the ventricles and occur earlier than expected. PVCs may occur in healthy people without being clinically significant.

When PVCs occur in patients with underlying heart disease, however, they may herald the development of lethal ventricular arrhythmias, including ventricular tachycardia (VT) and ventricular fibrillation (VF).

RECOGNIZING PVCS

The following rhythm strip illustrates premature ventricular contraction (PVC) on beats 1, 6, and 11. Look for these distinguishing characteristics.

c5-tt45

PVCs may occur singly, in pairs (couplets), or in clusters. PVCs may also appear in patterns, such as bigeminy or trigeminy. (See Recognizing PVCs.)

In many cases, PVCs are followed by a compensatory pause. (See Compensatory pause.) PVCs may be uniform in appearance, arising from a single ectopic ventricular pacemaker site, or multiform, originating from different sites or originating from a single pacemaker site but having QRS complexes that differ in size, shape, and direction.

PVCs may also be described as unifocal or multifocal. Unifocal PVCs originate from the same ventricular ectopic pacemaker site, whereas multifocal PVCs originate from different ectopic pacemaker sites in the ventricles.

CAUSES

PVCs are usually caused by enhanced automaticity in the ventricular conduction system or muscle tissue. The irritable focus results from a disruption of the normal electrolyte shifts during cellular depolarization and repolarization. Possible causes of PVCs include:

COMPENSATORY PAUSE

You can determine if a compensatory pause exists by using calipers to mark off two normal P-P intervals. Place one leg of the calipers on the sinus P wave that comes just before the premature ventricular contraction. If the pause is compensatory, the other leg of the calipers will fall precisely on the P wave that comes after the pause.

·

anesthetics

·

electrolyte imbalances, such as hypokalemia, hyperkalemia, hypomagnesemia, and hypocalcemia

·

enlargement or hypertrophy of the ventricular chambers

·

hypoxia

·

 

·

infection

·

irritation of the ventricles by pacemaker electrodes or a pulmonary artery catheter

·

metabolic acidosis

·

mitral valve prolapse

·

myocardial ischemia and infarction

·

 

·

sympathomimetic drugs, such as epinephrine and isoproterenol (Isuprel)

·

tobacco use

·

caffeine or alcohol ingestion

·

drug intoxication, particularly with cocaine, amphetamines, digoxin (Lanoxin), phenothiazines, and tricyclic antidepressants.

CLINICAL SIGNIFICANCE

PVCs are significant for two reasons. First, they can lead to more serious arrhythmias, such as VT or VF. The risk of developing a more serious arrhythmia increases in patients with ischemic or damaged hearts.

PVCs also decrease cardiac output, especially if ectopic beats are frequent or sustained. The decrease in cardiac output with a PVC stems from reduced ventricular diastolic filling time and the loss of atrial kick for that beat. The clinical impact of PVCs hinges on the body's ability to maintain adequate perfusion and the duration of the abnormal rhythm.

PATTERNS OF POTENTIALLY DANGEROUS PVCS

Some premature ventricular contractions (PVCs) are more dangerous than others. Here are examples of patterns of potentially dangerous PVCs.

Paired PVCs

Two PVCs in a row, called paired PVCs or a ventricular couplet (see shaded areas), can produce ventricular tachycardia (VT). That's because the second contraction usually meets refractory tissue. A burst, or a salvo, of three or more PVCs in a row is considered a run of VT.

c5-tt46

Multiform PVCs

Multiform PVCs, which look different from one another, arise from different sites or from the same site with abnormal conduction (see shaded areas). Multiform PVCs may indicate severe heart disease or digoxin toxicity.

c5-tt47

Bigeminy and trigeminy

PVCs that occur every other beat (bigeminy) or every third beat (trigeminy) may indicate increased ventricular irritability, which can result in VT or ventricular fibrillation (see shaded areas). The rhythm strip shown below illustrates ventricular bigeminy.

c5-tt48

R-on-T phenomenon

In R-on-T phenomenon, a PVC occurs so early that it falls on the T wave of the preceding beat (see shaded area). Because the cells haven't fully repolarized, VT or ventricular fibrillation can result.

c5-tt49

To help determine the seriousness of PVCs, ask these questions:

·

How often do they occur? In patients with chronic PVCs, an increase in frequency or a change in the pattern of PVCs from the baseline rhythm may signal a more serious condition.

·

What's the pattern of PVCs? If the ECG shows a dangerous pattern—such as paired PVCs, PVCs with more than one focus, a bigeminal rhythm, or R-on-T phenomenon (when a PVC strikes on the down slope of the preceding normal T wave)—the patient may require immediate treatment. (See Patterns of potentially dangerous PVCs.)

·

Are they really PVCs? Make sure the complex is a PVC, not another, less dangerous arrhythmia. PVCs may be mistaken for ventricular escape beats or normal impulses with aberrant ventricular conduction.

Ventricular escape beats serve as a safety mechanism to protect the heart from ventricular standstill. Some supraventricular impulses may follow an abnormal (aberrant) conduction pathway causing an abnormal appearance to the QRS complex. In any event, never delay treatment if the patient is unstable.

ECG CHARACTERISTICS

·

Rhythm: Atrial and ventricular rhythms are irregular during PVCs; the underlying rhythm may be regular.

·

Rate: Atrial and ventricular rates reflect the underlying rhythm.

·

P wave:

·

PR interval: Not measurable except in the underlying rhythm.

 

·

QRS complex: Occurrence is earlier than expected. Duration exceeds 0.12 second, with a bizarre and wide configuration. Configuration of the QRS complex is usually normal in the underlying rhythm.

·

T wave:

·

QT interval: Not usually measured, except in the underlying rhythm.

·

Other: A PVC may be followed by a compensatory pause, which can be full or incomplete. The sum of a full compensatory pause and the preceding R-R interval is equal to the sum of two R-R intervals of the underlying rhythm. If the sinoatrial (SA) node is depolarized by the PVC, the timing of the SA node is reset, and the compensatory pause is called incomplete. In this case, the sum of an incomplete compensatory pause and the preceding R-R interval is less than the sum of two R-R intervals of the underlying rhythm. A PVC occurring between two normally conducted QRS complexes without greatly disturbing the underlying rhythm is referred to as interpolated. A full compensatory pause, usually accompanying PVCs, is absent with interpolated PVCs.

Sometimes it's difficult to distinguish PVCs from aberrant ventricular conduction.

SIGNS AND SYMPTOMS

The patient experiencing PVCs usually has a normal pulse rate with a momentarily irregular pulse rhythm when a PVC occurs.

With PVCs, the patient will have a weaker pulse wave after the premature beat and a longer-than-normal pause between pulse waves. If the carotid pulse is visible, however, you may see a weaker arterial wave after the premature beat. When auscultating for heart sounds, you'll hear an abnormally early heart sound with each PVC.

A patient with PVCs may be asymptomatic; however, patients with frequent PVCs may complain of palpitations. The patient may also exhibit signs and symptoms of decreased cardiac output, including hypotension and syncope.

INTERVENTIONS

If the PVCs are infrequent and the patient has normal heart function and is asymptomatic, the arrhythmia probably won't require treatment. If symptoms or a dangerous form of PVCs occur, the type of treatment given will depend on the cause of the problem. If PVCs have a purely cardiac origin, drugs to suppress ventricular irritability, such as procainamide (Procan SR), amiodarone (Cardarone), or lidocaine, may be used. When PVCs have a noncardiac origin, treatment is aimed at correcting the cause. For example, drug therapy may be adjusted because of the patient's acidosis, or an electrolyte imbalance may be corrected.

Patients who have recently developed PVCs need prompt assessment, especially if they have underlying heart disease or complex medical problems. Patients with chronic PVCs should be closely observed for the development of more frequent PVCs or more dangerous PVC patterns.

Until effective treatment is begun, patients with PVCs accompanied by serious symptoms should have continuous ECG monitoring and ambulate only with assistance. If the patient is discharged on antiarrhythmic medications, family members should know how to contact the emergency medical system and perform cardiopulmonary resuscitation.

Idioventricular rhythm

ventricular escape rhythm, originates in an escape pacemaker site in the ventricles. The inherent firing rate of this ectopic pacemaker is usually 20 to 40 beats/minute. The rhythm acts as a safety mechanism by preventing ventricular standstill, or asystole—the absence of electrical activity in the ventricles. When fewer than three QRS complexes arising from the escape pacemaker occur, they're called ventricular escape beats or complexes. (See Recognizing idioventricular rhythm, page 300.)

When the rate of an ectopic pacemaker site in the ventricles is less than 100 beats/minute but exceeds the inherent ventricular escape rate of 20 to 40 beats/minute, it's called accelerated idioventricular rhythm (AIVR). (See Recognizing AIVR, page 301.) The rate of AIVR isn't fast enough to be considered ventricular tachycardia. The rhythm is usually related to enhanced automaticity of the ventricular tissue. AIVR and idioventricular rhythm share the same ECG characteristics, differing only in heart rate.

CAUSES

Idioventricular rhythms occur when all of the heart's higher pacemakers fail to function or when supraventricular impulses can't reach the ventricles because of a block in the conduction system. Idioventricular

RECOGNIZING IDIOVENTRICULAR RHYTHM

The following rhythm strip illustrates idioventricular rhythm. Look for these distinguishing characteristics.

c5-tt50

·

myocardial ischemia

·

myocardial infarction

·

digoxin toxicity, beta-adrenergic receptor blockers, calcium channel blockers, and tricyclic antidepressants

·

pacemaker failure

·

metabolic imbalances

·

sick sinus syndrome

·

 

CLINICAL SIGNIFICANCE

Idioventricular rhythm may be transient or continuous. Transient ventricular escape rhythm is usually related to increased parasympathetic effect on the higher pacemaker sites and isn't generally clinically significant. Although idioventricular rhythms act to protect the heart from ventricular standstill, a continuous idioventricular rhythm presents a clinically serious situation.

RECOGNIZING AIVR

An accelerated idioventricular rhythm (AIVR) has the same characteristics as an idioventricular rhythm except that it's faster. The rate shown here varies between 40 and 100 beats/minute.

c5-tt51

The slow ventricular rate of this arrhythmia and the associated loss of atrial kick markedly reduce cardiac output. If not rapidly identified and appropriately managed, idioventricular arrhythmias can cause death.

ECG CHARACTERISTICS

·

Rhythm: Usually, atrial rhythm can't be determined. Ventricular rhythm is usually regular.

·

Rate: Usually, atrial rate can't be determined. Ventricular rate is 20 to 40 beats/minute.

·

P wave: Absent.

·

PR interval: Not measurable because of the absent P wave.

·

QRS complex: Because of abnormal ventricular depolarization, the QRS complex has a duration longer than 0.12 second, with a wide and bizarre configuration.

·

T wave: The T wave is abnormal. Deflection usually occurs in the opposite direction from that of the QRS complex.

·

QT interval: Usually prolonged.

·

Other: Idioventricular rhythm commonly occurs with third-degree atrioventricular block.

TRANSCUTANEOUS PACEMAKER

Transcutaneous pacing, also referred to as external pacing or noninvasive pacing, involves the delivery of electrical impulses through externally applied cutaneous electrodes. The electrical impulses are conducted through an intact chest wall using skin electrodes placed either in anteriorposterior or sternal-apex positions. (An anteriorposterior placement is shown here.)

Transcutaneous pacing is the initial pacing method of choice in emergency situations because it's the least invasive technique and can be instituted quickly.

c5-tt52

SIGNS AND SYMPTOMS

The patient with continuous idioventricular rhythm is generally symptomatic because of the marked reduction in cardiac output that occurs with the arrhythmia. Blood pressure may be difficult or impossible to auscultate or palpate. The patient may experience dizziness, light-headedness, syncope, or loss of consciousness.

INTERVENTIONS

Treatment should be initiated immediately to increase the patient's heart rate, improve cardiac output, and establish a normal rhythm. Atropine may be administered to increase the heart rate.

If atropine isn't effective or if the patient develops hypotension or other signs of clinical instability, a pacemaker may be needed to reestablish a heart rate that provides enough cardiac output to perfuse organs properly. A transcutaneous pacemaker may be used in an emergency until a temporary or transvenous pacemaker can be inserted. (See Transcutaneous pacemaker.)

Remember that the goal of treatment doesn't include suppressing the idioventricular rhythm because it acts as a safety mechanism to protect the heart from ventricular standstill. Idioventricular rhythm should never be treated with lidocaine or other antiarrhythmics that would suppress the escape beats.

Patients with idioventricular rhythm need continuous ECG monitoring and constant assessment until treatment restores hemodynamic stability. Keep atropine and pacemaker equipment available at the bedside. Enforce bed rest until an effective heart rate has been maintained and the patient is clinically stable.

Be sure to tell the patient and his family about the serious nature of this arrhythmia and the treatment it requires. If the patient needs a permanent pacemaker, teach the patient and family how it works, how to recognize problems, when to contact the practitioner, and how pacemaker function will be monitored.

Ventricular tachycardia

Ventricular tachycardia (VT), also called V-tach, occurs when three or more premature ventricular contractions (PVCs) strike in a row and the ventricular rate exceeds 100 beats/minute. This life-threatening arrhythmia may precede ventricular fibrillation and sudden cardiac death, especially in patients who aren't in a health care facility.

VT is an extremely unstable rhythm and may be sustained or non-sustained. When it occurs in short, paroxysmal bursts lasting less than 30 seconds and causing few or no symptoms, it's called non-sustained. When the rhythm is sustained, however, it requires immediate treatment to prevent death, even in patients initially able to maintain adequate cardiac output. (See Recognizing ventricular tachycardia, page 304.)

CAUSES

This arrhythmia usually results from increased myocardial irritability, which may be triggered by enhanced automaticity, reentry within the Purkinje system, or by PVCs occurring during the downstroke of the preceding T wave.

Other causes of VT include:

·

myocardial ischemia

·

myocardial infarction

·

coronary artery disease

·

valvular heart disease

 

·

heart failure

·

cardiomyopathy

·

electrolyte imbalances such as hypokalemia

·

drug intoxication from digoxin (Lanoxin), procainamide, quinidine (Quinora), or cocaine

·

proarrhythmic effects of some antiarrhythmics.

RECOGNIZING VENTRICULAR TACHYCARDIA

The following rhythm strip illustrates ventricular tachycardia. Look for these distinguishing characteristics.

c5-tt53

CLINICAL SIGNIFICANCE

VT is significant because of its unpredictability and potential for causing death. A patient may be hemodynamically stable, with a normal pulse and blood pressure; clinically unstable, with hypotension and poor peripheral pulses; or unconscious, without respirations or pulse.

Because of the reduced ventricular filling time and the drop in cardiac output that occurs with this arrhythmia, the patient's condition can quickly deteriorate to ventricular fibrillation (VF) and complete cardiovascular collapse.

ECG CHARACTERISTICS

·

Rhythm: Atrial rhythm can't be determined. Ventricular rhythm is usually regular but may be slightly irregular.

·

Rate: Atrial rate can't be determined. Ventricular rate is usually rapid (100 to 250 beats/minute).

·

P wave: The P wave is usually absent. It may be obscured by the QRS complex; P waves are dissociated from the QRS complexes. Retrograde P waves may be present.

·

PR interval: Not measurable because the P wave can't be seen in most cases.

·

QRS complex: Duration is greater than 0.12 second; it usually has a bizarre appearance with increased amplitude. QRS complexes in monomorphic VT have a uniform shape. In polymorphic VT, the shape of the QRS complex constantly changes.

·

T wave: If the T wave is visible, it occurs in the opposite direction of the QRS complex.

·

QT interval: Not measurable.

·

Other: Ventricular flutter and torsades de pointes are two variations of this arrhythmia. Torsades de pointes is a special variation of polymorphic VT. (See Torsades de pointes, page 306.)

SIGNS AND SYMPTOMS

Although some patients have only minor symptoms initially, they still require rapid intervention to prevent cardiovascular collapse. Most patients with VT have weak or absent pulses. Low cardiac output will cause hypotension and a decreased level of consciousness (LOC), quickly leading to unresponsiveness if left untreated. VT may prompt angina, heart failure, or a substantial decrease in organ perfusion.

INTERVENTIONS

Treatment depends on the patient's clinical status. Is the patient conscious? Does the patient have spontaneous respirations? Is a palpable carotid pulse present?

Patients with pulseless VT are treated the same as those with VF and require immediate defibrillation and cardiopulmonary resuscitation (CPR). Treatment for patients with a detectable pulse depends on whether they're unstable or stable.

Unstable patients generally have ventricular rates greater than 150 beats/minute and have serious signs and symptoms related to the tachycardia, which may include hypotension, shortness of breath, chest pain, or altered LOC. These patients are usually treated with immediate synchronized cardioversion.

TORSADES DE POINTES

Torsades de pointes, which means “twisting about the points,” is a special form of polymorphic ventricular tachycardia. The hallmark characteristics of this rhythm, shown below, are QRS complexes that rotate about the baseline, deflecting downward and upward for several beats.

The rate is 150 to 250 beats/minute, usually with an irregular rhythm, and the QRS complexes are wide with changing amplitude. The P wave is usually absent.

Paroxysmal rhythm

This arrhythmia may be paroxysmal, starting and stopping suddenly, and may deteriorate into ventricular fibrillation. It should be considered when ventricular tachycardia doesn't respond to antiarrhythmic therapy or other treatments.

Reversible causes

The cause of this form of ventricular tachycardia is usually reversible. The most common causes are drugs that lengthen the QT interval, such as amiodarone (Cordarone), ibutilide (Covert), erythromycin (E-Mycin), haloperidol (Haldol), droperidol, and sotalol (Betapace). Other causes include myocardial ischemia and electrolyte abnormalities, such as hypokalemia, hypomagnesemia, and hypocalcemia.

Cause-based treatment

Torsades de pointes is treated by correcting the underlying cause, especially if the cause is related to specific drug therapy. The practitioner may order mechanical overdrive pacing, which overrides the ventricular rate and breaks the triggered mechanism for the arrhythmia. Magnesium sulfate may also be effective. Electrical cardioversion may be used when torsades de pointes doesn't respond to other treatment.

c5-tt54

A clinically stable patient with VT and no signs of heart failure is treated differently.

Treatment for these patients is determined by whether the rhythm is regular or irregular. If the rhythm is regular (monomorphic), the patient is treated with amiodarone and possible synchronized cardioversion. If the rate is irregular (polymorphic), look at the length of the T interval when the rhythm is in sinus rhythm. If the QT interval is long, the polymorphic rhythm is most likely torsades de pointes. The treatment for polymorphic VT is to stop medications that may cause a long QT, correct electrolyte imbalances, and administer antiarrhythmics, such as magnesium or amiodarone. If at any point the patient becomes clinically unstable, immediate synchronized cardioversion is the best treatment. For the complete ACLS algorithms, see pages 332 and 333.

Patients with VT or VF not from a transient or reversible cause may need an implanted cardioverter-defibrillator (ICD). This device is a permanent solution to recurrent episodes of VT.

A 12-lead ECG and all other available clinical information is critical for establishing a specific diagnosis in a stable patient with wide QRS complex tachycardia of unknown type but regular rate. If a definitive diagnosis of SVT or VT can't be established, use amiodarone to control the rate and elective synchronized cardioversion.

If a patient will be discharged with an ICD or a prescription for long-term antiarrhythmics, make sure that family members know how to use the emergency medical system and how to perform CPR.

Ventricular fibrillation

Ventricular fibrillation, commonly called V-fib or VF, is characterized by a chaotic, disorganized pattern of electrical activity. The pattern arises from electrical impulses coming from multiple ectopic pacemakers in the ventricles.

The arrhythmia produces no effective ventricular mechanical activity or contractions and no cardiac output. Untreated VF is the most common cause of sudden cardiac death in people outside of a health care facility. (See Recognizing ventricular fibrillation, page 308.)

CAUSES

Causes of VF include:

RECOGNIZING VENTRICULAR FIBRILLATION

The following rhythm strips illustrate coarse ventricular fibrillation (first strip) and fine ventricular fibrillation (second strip). Look for these distinguishing characteristics.

c5-tt55

·

coronary artery disease

·

myocardial ischemia

·

myocardial infarction

·

untreated ventricular tachycardia

·

underlying heart disease such as dilated cardiomyopathy

·

acid-base imbalance

·

electric shock

·

severe hypothermia

·

drug toxicity, including digoxin, quinidine, and procainamide

·

electrolyte imbalances, such as hypokalemia, hyperkalemia, and hypercalcemia

·

environmental.

CLINICAL SIGNIFICANCE

With VF, the ventricular muscle quivers, replacing effective muscular contraction with completely ineffective contraction. Cardiac output falls to zero and, if allowed to continue, leads to ventricular standstill and death.

ECG CHARACTERISTICS

·

Rhythm: Atrial rhythm can't be determined. Ventricular rhythm has no pattern or regularity. Ventricular electrical activity appears as fibrillatory waves with no recognizable pattern.

·

Rate: Atrial and ventricular rates can't be determined.

·

P wave: Can't be determined.

·

PR interval: Can't be determined.

·

QRS complex: Duration can't be determined.

·

T wave: Can't be determined.

·

QT interval: Not applicable.

·

Other: Coarse fibrillatory waves are generally associated with greater chances of successful electrical defibrillation than smaller amplitude waves. Fibrillatory waves become finer as hypoxemia and acidosis progress, making the VF more resistant to defibrillation.

SIGNS AND SYMPTOMS

The patient in VF is in full cardiac arrest, unresponsive, and without a detectable blood pressure or central pulses. Whenever you see an ECG pattern resembling VF, check the patient immediately and initiate definitive treatment.

INTERVENTIONS

When faced with a rhythm that appears to be VF, always assess the patient first. Other events can mimic VF on an ECG strip, including interference from an electric razor, shivering, or seizure activity.

Immediate defibrillation and cardiopulmonary resuscitation (CPR) are the most effective treatments for VF. CPR must be performed until the defibrillator arrives to preserve oxygen supply to the brain and other vital organs. Drugs such as epinephrine and vasopressin (Pitressin) may be used for persistent VF if the first two attempts at electrical defibrillation fail to correct the arrhythmia. Antiarrhythmic agents, such as amiodarone, lidocaine, and magnesium, may also be considered. For the complete ACLS algorithm, see pages 330 and 331.

In defibrillation, two electrode pads are applied to the chest wall. Current is then directed through the pads and, subsequently, the patient's chest and heart. The current causes the myocardium to completely depolarize, which, in turn, encourages the sinoatrial node to resume normal control of the heart's electrical activity.

One electrode pad is placed to the right of the upper sternum, and one is placed over the fifth or sixth intercostal space at the left anterior axillary line. During cardiac surgery, internal paddles are placed directly on the myocardium.

Automated external defibrillators (AEDs) are increasingly being used, especially in the out-of-hospital setting, to provide early defibrillation. After a patient is confirmed to be unresponsive, breathless, and pulseless, the AED power is turned on and the electrode pads and cables attached. The AED can analyze the patient's cardiac rhythm and provide the caregiver with step-by-step instructions on how to proceed. These defibrillators can be used by people without medical experience as long as they're trained in the proper use of the device.

For the patient in VF, successful resuscitation requires rapid recognition of the problem and prompt defibrillation. Many health care facilities and emergency medical systems have established protocols so that health care workers can initiate prompt treatment. Make sure you know the location of your facility's emergency equipment and that you know how to use it.

You'll also need to teach the patient and family how to use the emergency medical system following discharge from the facility. Family members may need instruction in CPR and in how to use the AED. Teach them about long-term therapies that help prevent recurrent episodes of VF, including antiarrhythmic drug therapy and implantable cardioverter-defibrillators.

Asystole

Ventricular asystole, also called asystole and ventricular standstill, is the absence of discernible electrical activity in the ventricles. Although some electrical activity may be evident in the atria, these impulses aren't conducted to the ventricles. (See Recognizing asystole

Asystole usually results from a prolonged period of cardiac arrest without effective resuscitation. It's important to distinguish asystole from fine ventricular fibrillation, which is managed differently. Therefore, asystole must be confirmed in more than one ECG lead.

CAUSES

Possible reversible causes of asystole include:

·

hypovolemia

·

myocardial infarction (coronary thrombosis)

P.311

·

severe electrolyte disturbances, especially hyperkalemia and hypokalemia

·

massive pulmonary embolism

·

hypoxia

·

severe, uncorrected acid-base disturbances, especially metabolic acidosis

·

drug overdose

·

hypothermia

·

cardiac tamponade

·

tension pneumothorax.

RECOGNIZING ASYSTOLE

The following rhythm strip illustrates asystole, the absence of electrical activity in the ventricles. Except for a few P waves or pacer spikes, nothing appears on the waveform, and the line is almost flat.

c5-tt56

CLINICAL SIGNIFICANCE

Without ventricular electrical activity, ventricular contractions can't occur. As a result, cardiac output drops to zero, and vital organs are no longer perfused. Asystole has been called the arrhythmia of death and is typically considered to be a confirmation of death, rather than an arrhythmia to be treated.

The patient with asystole is completely unresponsive, without spontaneous respirations or pulse (cardiopulmonary arrest). Without immediate initiation of cardiopulmonary resuscitation (CPR) and rapid identification and treatment of the underlying cause, the condition quickly becomes irreversible.

PULSELESS ELECTRICAL ACTIVITY

Pulseless electrical activity (PEA) defines a group of arrhythmias characterized by the presence of some type of electrical activity without a detectable pulse. Although organized electrical depolarization occurs, no synchronous shortening of the myocardial fibers occurs. As a result, no mechanical activity or contractions take place.

Causes

The most common causes of PEA include hypovolemia, hypoxia, acidosis, tension pneumothorax, cardiac tamponade, massive pulmonary embolism, hypothermia, hyperkalemia and hypokalemia, massive acute myocardial infarction, and overdoses of drugs such as tricyclic antidepressants.

Rapid identification and treatment of underlying reversible causes is critical for treating PEA. For example, hypovolemia is treated with volume expansion. Tension pneumothorax is treated with needle decompression.

Institute cardiopulmonary resuscitation, tracheal intubation, and I.V. administration of epinephrine or atropine.

ECG CHARACTERISTICS

·

Rhythm:

·

Rate: Atrial rate is usually indiscernible; no ventricular rate is present.

·

P wave: May be present.

·

PR interval: Not measurable.

·

QRS complex: Absent or occasional escape beats.

·

T wave: Absent.

·

QT interval: Not measurable.

·

Other: On a rhythm strip, asystole looks like a nearly flat line (except for changes caused by chest compressions during CPR). In a patient with a pacemaker, pacer spikes may be evident on the strip, but no P wave or QRS complex occurs in response to the stimulus.

SIGNS AND SYMPTOMS

The patient will be unresponsive and have no spontaneous respirations, discernible pulse, or blood pressure.

INTERVENTIONS

Immediate treatment for asystole includes effective CPR and supplemental oxygen. Resuscitation should be attempted unless evidence exists that these efforts shouldn't be initiated, such as when a do-notresuscitate order is in effect.

Remember to verify the presence of asystole by checking more than one ECG lead. Priority must also be given to searching for and treating identified potentially reversible causes, such as hypovolemia, cardiac tamponade, and tension pneumothorax. Early CPR is vital, and I.V. or intraosseous epinephrine or a one-time dose of vasopressin and atropine is given. For the complete ACLS algorithm, see pages 330 and 331.

Be aware that pulseless electrical activity can appear as any cardiac rhythm, including asystole. Know how to recognize this problem and treat it. (See .)

With persistent asystole (despite appropriate management), consider terminating resuscitation.

ATRIOVENTRICULAR BLOCKS

Atrioventricular (AV) heart block refers to an interruption or delay in the conduction of electrical impulses between the atria and the ventricles. The block can occur at the AV node, the bundle of His, or the bundle branches. When the site of the block is the bundle of His or the bundle branches, the block is referred to as infranodal AV block. AV block can be partial, where some or all of the P waves are conducted to the ventricle (first or second degree), or complete, where no P waves conduct to the ventricle (third degree).

The heart's electrical impulses normally originate in the sinoatrial node, so when those impulses are blocked at the AV node, atrial rates are usually normal (60 to 100 beats/minute). The clinical significance of the block depends on the number of impulses completely blocked and the resulting ventricular rate. A slow ventricular rate can decrease cardiac output and cause symptoms such as light-headedness, hypotension, and confusion.

Causes

A variety of factors may lead to AV block, including underlying heart conditions, use of certain drugs, congenital anomalies, and conditions that disrupt the cardiac conduction system.

Typical causes of AV block include:

·

myocardial ischemia, which impairs cellular function so that cells repolarize more slowly or incompletely. The injured cells, in turn,

may conduct impulses slowly or inconsistently. Relief of the ischemia may restore normal function to the AV node.

·

myocardial infarction, in which cellular necrosis or death occurs. If the necrotic cells are part of the conduction system, they may no longer conduct impulses, and a permanent AV block occurs.

·

excessive serum levels of, or an exaggerated response to, a drug. This response can cause AV block or increase the likelihood that a block will develop. The drugs may increase the refractory period of a portion of the conduction system. Although many antiarrhythmics can have this effect, the drugs more commonly known to cause or exacerbate AV blocks include digoxin (Lanoxin), amiodarone (Cordarone), beta-adrenergic receptor blockers, and calcium channel blockers.

·

lesions, including calcium and fibrotic, along the conduction pathway.

·

congenital anomalies such as congenital ventricular septal defects that involve cardiac structures and affect the conduction system. Anomalies of the conduction system, such as an AV node that doesn't conduct impulses, can also occur in the absence of structural defects.

AV block can also be caused by inadvertent damage to the heart's conduction system during surgery. Damage is most likely to occur in operations involving the aortic, mitral, or tricuspid valve or in the closure of a ventricular septal defect. If the injury involves tissues adjacent to the surgical site and the conduction system isn't physically disrupted, the block may be temporary. If a portion of the conduction system is severed, permanent block results.

Similar disruption of the conduction system can occur from a procedure called radiofrequency ablation. In this invasive procedure, a transvenous catheter is used to locate the area in the heart that participates in initiating or perpetuating certain tachyarrhythmias. Radiofrequency energy is then delivered to the myocardium through this catheter to produce a small area of necrosis at that spot. The damaged tissue can no longer cause or participate in the tachyarrhythmia. If the energy is delivered close to the AV node, bundle of His, or bundle branches, however, AV block can result, and the patient may need a permanent pacemaker.

Classification of atrioventricular block

Atrioventricular (AV) blocks are classified according to the site of block and the severity of the conduction abnormality. The sites of AV block include the AV node, bundle of His, and bundle branches.

Severity of AV block is classified in degrees: first-degree AV block; second-degree AV block, type I (Wenckebach or Mobitz I); second-degree AV block, type II (Mobitz II) AV block; and third-degree (complete) AV block. The classification system for AV blocks aids in the determination of the patient's treatment and prognosis.

First-degree atrioventricular block

First-degree atrioventricular (AV) block occurs when there's a delay in the conduction of electrical impulses from the atria to the ventricles. This delay usually occurs at the level of the AV node, or bundle of His. First-degree AV block is characterized by a PR interval greater than 0.20 second. This interval remains constant beat to beat. After the impulse is slowed down, it is then conducted through the normal conduction pathway.

CAUSES

First-degree AV block may result from:

·

myocardial ischemia or myocardial infarction (MI)

·

myocarditis

·

hyperkalemia

·

rheumatic fever

·

degenerative changes in the heart associated with aging.

The condition may also be caused by such drugs as digoxin (Lanoxin), calcium channel blockers, and beta-adrenergic receptor blockers.

CLINICAL SIGNIFICANCE

First-degree AV block may cause no symptoms in a healthy person. The arrhythmia may be transient, especially if it occurs secondary to drugs or ischemia early in the course of an MI. The presence of first-degree block, the least dangerous type of AV block, indicates a delay in the conduction of electrical impulses through the normal conduction pathway. In general, a rhythm strip with this block looks like normal sinus rhythm except that the PR interval is longer than normal.

RECOGNIZING FIRST-DEGREE AV BLOCK

The following rhythm strip illustrates first-degree atrioventricular (AV) block. Look for these distinguishing characteristics.

c5-tt57

Because first-degree AV block can progress to a more severe type of AV block, the patient's cardiac rhythm should be monitored for changes. (See Recognizing first-degree AV block.)

ECG CHARACTERISTICS

·

Rhythm: Atrial and ventricular rhythms are regular.

·

Rate: Atrial and ventricular rates are the same and within normal limits.

·

P wave: Normal size and configuration; each P wave followed by a QRS complex.

·

PR interval: Prolonged (greater than 0.20 second) but constant.

·

QRS complex: Duration usually remains within normal limits if the conduction delay occurs in the AV node. If the QRS duration exceeds 0.12 second, the conduction delay may be in the His-Purkinje system.

·

T wave: Normal size and configuration unless the QRS complex is prolonged.

·

QT interval: Usually within normal limits.

 

·

Other:

SIGNS AND SYMPTOMS

The patient's pulse rate will usually be normal and the rhythm will be regular. Most patients with first-degree AV block are asymptomatic because cardiac output isn't significantly affected. If the PR interval is extremely long, a longer interval between S1 and S2 may be noted on cardiac auscultation.

INTERVENTIONS

Treatment generally focuses on identification and correction of the underlying cause. For example, if a drug is causing the AV block, the dosage may be reduced or the drug discontinued. Close monitoring can help detect progression of first-degree AV block to a more serious form of block.

Evaluate a patient with first-degree AV block for underlying causes that can be corrected, such as drugs or myocardial ischemia. Observe the ECG for progression of the block to a more severe form. Administer digoxin (Lanoxin), calcium channel blockers, and beta-adrenergic receptor blockers cautiously.

Second-degree atrioventricular block

Second-degree atrioventricular (AV) block occurs when some of the electrical impulses from the AV node are blocked and some are conducted through normal conduction pathways. Second-degree AV block is subdivided into type I second-degree AV block and type II second-degree AV block.

TYPE I SECOND-DEGREE AV BLOCK

Also called Wenckebach or Mobitz I block, type I second-degree AV block occurs when each successive impulse from the sinoatrial (SA) node is delayed slightly longer than the previous impulse. (See Recognizing type I second-degree AV block, page 318.) This pattern of progressive prolongation of the PR interval continues until an impulse fails to be conducted to the ventricles.

Usually only a single impulse is blocked from reaching the ventricles, and following this nonconducted P wave or dropped beat the pattern is repeated. This repetitive sequence of two or more consecutive beats followed by a dropped beat result in “group beating.” Type I second-degree AV block generally occurs at the level of the AV node.

RECOGNIZING TYPE I SECOND-DEGREE AV BLOCK

The following rhythm strip illustrates type I second-degree atrioventricular (AV) block. Look for these distinguishing characteristics.

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Causes

Type I second-degree AV block frequently results from increased parasympathetic tone or the effects of certain drugs. Coronary artery disease (CAD), inferior-wall myocardial infarction (MI), and rheumatic fever may increase parasympathetic tone and result in the arrhythmia. It may also be caused by cardiac medications, such as beta-adrenergic receptor blockers, digoxin, and calcium channel blockers.

Clinical significance

Type I second-degree AV block may occur normally in an otherwise healthy person. Almost always transient, this type of block usually resolves when the underlying condition is corrected. Although an asymptomatic patient with this block has a good prognosis, the block may progress to a more serious form, especially if it occurs early in an MI.

ECG characteristics

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Rhythm:

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Rate: The atrial rate exceeds the ventricular rate because of the nonconducted beats, but both usually remain within normal limits.

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P wave: Normal size and configuration; each P wave is followed by a QRS complex except for the blocked P wave.

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PR interval: The PR interval is progressively longer with each cycle until a P wave appears without a QRS complex. The variation in delay from cycle to cycle is typically slight. The PR interval after the nonconducted beat is shorter than the interval preceding it. The phrase commonly used to describe this pattern is long, longer, dropped.

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QRS complex: Duration usually remains within normal limits because the block commonly occurs at the level of the AV node. The complex is absent when the impulse isn't conducted.

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T wave: Normal size and configuration.

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QT interval: Usually within normal limits.

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Other: The arrhythmia is usually distinguished by “group beating,” referred to as the footprints of Wenckebach. Frederik K. Wenckebach was a Dutch internist who, at the turn of the century and long before the introduction of the ECG, described the two forms of what's now known as second-degree AV block by analyzing waves in the jugular venous pulse. Following the introduction of the ECG, German cardiologist Woldemar Mobitz clarified Wenckebach's findings, identifying two types of second-degree AV block, type I and type II.

When you're trying to identify type I second-degree AV block, think of the phrase “longer, longer, drop,” which describes the progressively prolonged PR intervals and the missing QRS complexes. The QRS complexes are usually normal because the delays occur in the AV node

Signs and symptoms

Usually asymptomatic, a patient with type I second-degree AV block may show signs and symptoms of decreased cardiac output, such as light-headedness or hypotension. Symptoms may be especially pronounced if the ventricular rate is slow.

Interventions

Treatment is rarely needed because the patient is generally asymptomatic. A transcutaneous pacemaker may be required for a symptomatic patient until the arrhythmia resolves.

For a patient with serious signs and symptoms related to a low heart rate, atropine may be used to improve AV node conduction.

When caring for a patient with this block, assess the tolerance for the rhythm and the need for treatment to improve cardiac output. Evaluate the patient for possible causes of the block, including the use of certain medications or the presence of myocardial ischemia.

Check the ECG frequently to see if a more severe type of AV block develops. Make sure the patient has a patent I.V. line. Provide patient teaching about a temporary pacemaker if indicated.

TYPE II SECOND-DEGREE AV BLOCK

Type II second-degree AV block (also known as Mobitz II block) is less common than type I, but more serious. It occurs when impulses from the SA node occasionally fail to conduct to the ventricles. This form of second-degree AV block occurs below the level of the AV node, either at the bundle of His, or more commonly at the bundle branches.

One of the hallmarks of this type of block is that, unlike type I second- degree AV block, the PR interval doesn't lengthen before a dropped beat. (See Recognizing type II second-degree AV block.) In addition, more than one nonconducted beat can occur in succession. (See 2:1 AV block.)

Causes

Unlike type I second-degree AV block, type II second-degree AV block rarely results from increased parasympathetic tone or drug effect. Because the arrhythmia is usually associated with organic heart disease, it's usually associated with a poorer prognosis, and complete heart block may develop.

Type II second-degree AV block is commonly caused by

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an anterior-wall MI

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degenerative changes in the conduction system

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The arrhythmia indicates a conduction disturbance at the level of the bundle of His or bundle branches.

Clinical significance

Second-degree AV block type II is more severe than type I. The patient does not tolerate this rhythm well and usually exhibits signs of decreased cardiac output, such as hypotension and syncope. If the block is a result of an anterior wall MI, the block is likely to be permanent because of the tissue damage to the conduction system.

RECOGNIZING TYPE II SECOND-DEGREE AV BLOCK

The following rhythm strip illustrates type II second-degree atrioventricular (AV) block. Look for these distinguishing characteristics.

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2:1 AV BLOCK

In 2:1 second-degree atrioventricular (AV) block, every other QRS complex is dropped, so there are always two P waves for every QRS complex. The resulting ventricular rhythm is regular.

To help determine whether a rhythm is type I or type II AV block, look at the width of the QRS complexes. If they're wide and a short PR interval is present, the block is probably type II.

Keep in mind that type II block is more likely to impair cardiac output, lead to symptoms such as syncope, and progress to a more severe form of block. Be sure to monitor the patient carefully.

In type II second-degree AV block, the ventricular rate tends to be slower than in type I. In addition, cardiac output tends to be lower and symptoms are more likely to appear, particularly if the sinus rhythm is slow and the ratio of conducted beats to dropped beats is low such as 2:1.

ECG characteristics

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Rhythm: The atrial rhythm is regular. The ventricular rhythm can be regular or irregular. Pauses correspond to the dropped beat. When the block is intermittent or when the conduction ratio is variable, the rhythm is often irregular. When a constant conduction ratio occurs, for example, 2:1 or 3:1, the rhythm is regular.

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The atrial rate is usually within normal limits. The ventricular rate, slower than the atrial rate, may be within normal limits.

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P wave: The P wave is normal in size and configuration, but some P waves aren't followed by a QRS complex. The R-R interval containing a nonconducted P wave equals two normal R-R intervals.

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PR interval: The PR interval is within normal limits or prolonged but generally always constant for the conducted beats.

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QRS complex: Duration is within normal limits if the block occurs at the bundle of His. If the block occurs at the bundle branches, however, the QRS will be widened and display the features of bundle-branch block. The complex is absent periodically.

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T wave:

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QT interval: Usually within normal limits.

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Other: The PR and R-R intervals don't vary before a dropped beat, so no warning occurs. For a dropped beat to occur, there must be complete block in one bundle branch with intermittent interruption in conduction in the other bundle as well. As a result, this type of second-degree AV block is commonly associated with a wide QRS complex. However, when the block occurs at the bundle of His, the QRS may be narrow because ventricular conduction is undisturbed in beats that aren't blocked.

Signs and symptoms

Most patients who experience occasional dropped beats remain asymptomatic as long as cardiac output is maintained. As the number of dropped beats increases, the patient may experience signs and symptoms of decreased cardiac output, including fatigue, dyspnea, chest pain, or light-headedness. On physical examination, you may note hypotension and a slow pulse, with a regular or irregular rhythm.

Interventions

If the patient doesn't experience serious signs and symptoms related to the low heart rate, he may be prepared for transvenous pacemaker insertion. Alternatively, the patient may be continuously monitored, with a transcutaneous pacemaker readily available.

If the patient is experiencing serious signs and symptoms due to bradycardia, treatment goals include improving cardiac output by increasing the heart rate. Transcutaneous pacing, I.V. dopamine (Intropin), I.V. epinephrine, or I.V. atropine may be used to increase cardiac output. Use atropine cautiously because it can worsen ischemia during an MI and may induce ventricular tachycardia or fibrillation in patients with this form of second-degree AV block and complete heart block. Because this form of second-degree AV block occurs below the level of the AV node—either at the bundle of His or, more commonly, at the bundle branches—transcutaneous pacing should be initiated quickly, when indicated. For this reason, type II second-degree AV block may also require placement of a permanent pacemaker. A temporary pacemaker may be used until a permanent pacemaker can be inserted.

When caring for a patient with type II second-degree block, assess tolerance for the rhythm and the need for treatment to improve cardiac output. Evaluate for possible correctable causes such as ischemia.

Keep the patient on bed rest, if indicated, to reduce myocardial oxygen demands. Administer oxygen therapy as ordered. Observe the patient's cardiac rhythm for progression to a more severe form of AV block. Teach the patient and family about the use of pacemakers if the patient requires one.

Third-degree atrioventricular block

Also called complete heart block, third-degree atrioventricular (AV) block indicates the complete absence of impulse conduction between the atria and ventricles. There's no correlation between the conduction of the P waves and the QRS complex. In complete heart block, the atrial rate is generally faster than the ventricular rate.

Third-degree AV block may occur at the level of the AV node, the bundle of His, or the bundle branches. The patient's treatment and prognosis vary depending on the anatomic level of the block.

RECOGNIZING THIRD-DEGREE AV BLOCK

The following rhythm strip illustrates third-degree atrioventricular (AV) block. Look for these distinguishing characteristics.

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When third-degree AV block occurs at the level of the AV node, ventricular depolarization is typically initiated by a junctional escape pacemaker. This pacemaker is usually stable with a rate of 40 to 60 beats/minute. (See Recognizing third-degree AV block.) The sequence of ventricular depolarization is usually normal because the block is located above the bifurcation of the bundle of His, which results in a normal-appearing QRS complex.

CAUSES

Third-degree AV block occurring at the anatomic level of the AV node can result from increased parasympathetic tone associated with inferior wall myocardial infarction (MI), AV node damage, or toxic effects of such drugs as digoxin and propranolol (Inderal).

Third-degree AV block occurring at the infranodal level is usually associated with extensive anterior MI. It generally isn't the result of increases in parasympathetic tone or drug effect.

CLINICAL SIGNIFICANCE

Third-degree AV block occurring at the AV node, with a junctional escape rhythm, is usually transient and generally associated with a favorable prognosis. In third-degree AV block at the infranodal level, however, the pacemaker is unstable and episodes of ventricular asystole are common. Third-degree AV block at this level is generally associated with a less favorable prognosis.

Because the ventricular rate in third-degree AV block can be slow and the decrease in cardiac output so significant, the arrhythmia usually results in a life-threatening situation. In addition, the loss of AV synchrony results in the loss of atrial kick, which further decreases cardiac output.

ECG CHARACTERISTICS

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Rhythm: Atrial and ventricular rhythms are usually regular.

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Rate: Acting independently, the atria, generally under the control of the sinoatrial node, tend to maintain a regular rate of 60 to 100 beats/minute. The atrial rate exceeds the ventricular rate. With intranodal block, the ventricular rate is usually 40 to 60 beats/ minute (a junctional escape rhythm). With infranodal block, the ventricular rate is usually below 40 beats/minute (a ventricular escape rhythm).

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P wave: The P wave is normal in size and configuration. Some P waves may be buried in QRS complexes or T waves.

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PR interval: Not applicable or measurable because the atria and ventricles are depolarized from different pacemakers and beat independently of each other.

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QRS complex: Configuration depends on the location of the escape mechanism and origin of ventricular depolarization. When the block occurs at the level of the AV node or bundle of His, the QRS complex will appear normal. When the block occurs at the level of the bundle branches, the QRS complex will be widened.

 

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Normal size and configuration unless the QRS complex originates in the ventricle.

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QT interval: May be within normal limits.

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Other: None.

Most patients with third-degree AV block experience significant signs and symptoms, including severe fatigue, dyspnea, chest pain, light-headedness, changes in mental status, and changes in the level of consciousness. Hypotension, pallor, and diaphoresis may also occur. The peripheral pulse rate will be slow, but the rhythm will be regular.

A few patients will be relatively free of symptoms, complaining only that they can't tolerate exercise and that they're typically tired for no apparent reason. The severity of symptoms depends to a large extent on the resulting ventricular rate and the patient's ability to compensate for decreased cardiac output.

INTERVENTIONS

If the patient is experiencing serious signs and symptoms related to the low heart rate, or if the patient's condition seems to be deteriorating, interventions may include transcutaneous pacing or I.V. atropine, dopamine, or epinephrine. Atropine isn't indicated for third-degree AV block with new wide QRS complexes. In such cases, a permanent pacemaker is indicated because atropine rarely increases sinus rate and AV node conduction when AV block is at the His-Purkinje level.

Asymptomatic patients in third-degree AV block should be prepared for insertion of a transvenous temporary pacemaker until a decision is made about the need for a permanent pacemaker. If symptoms develop, a transcutaneous pacemaker should be used until the transvenous pacemaker is placed.

Because third-degree AV block occurring at the infranodal level is usually associated with extensive anterior MI, patients are more likely to have permanent third-degree AV block, which most likely requires insertion of a permanent pacemaker.

Third-degree AV block occurring at the anatomic level of the AV node can result from increased parasympathetic tone associated with an inferior wall MI. As a result, the block is more likely to be short-lived. In these patients, the decision to insert a permanent pacemaker is often delayed to assess how well the conduction system recovers.

When caring for a patient with third-degree AV block, immediately assess the patient's tolerance of the rhythm and the need for interventions to support cardiac output and relieve symptoms. Make sure the patient has a patent I.V. line. Administer oxygen therapy as ordered. Evaluate for possible correctable causes of the arrhythmia, such as drugs or myocardial ischemia. Minimize the patient's activity and maintain bed rest.

ACLS ALGORITHMS

Shown on the next pages are the American Heart Association ACLS algorithms for bradycardia, pulseless arrest, and tachycardia.

BRADYCARDIA

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PULSELESS ARREST

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TACHYCARDIA

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