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Clues to symptomatic bradycardia
If a patient can’t tolerate bradycardia, he may develop these signs and symptoms:
•hypotension
•cool, clammy skin
•altered mental status
•dizziness
•blurred vision
•crackles, dyspnea, and an S3 heart sound, which indicate heart failure
•chest pain
•syncope.
Sinus tachycardia
If sinus bradycardia is the tortoise of the sinus arrhythmias, sinus tachycardia is the hare. Sinus tachycardia in an adult is characterized by a sinus rate of more than 100 beats/minute. The rate rarely exceeds 160 beats/minute except during strenuous exercise; the maximum rate achievable with exercise decreases with age.
How it happens
The clinical significance of sinus tachycardia depends on the underlying cause. (See Causes of sinus tachycardia.) The arrhythmia may be the body’s response to exercise or high emotional states and may be of no clinical significance. It may also occur with hypovolemia, hemorrhage, or pain. When the stimulus for the tachycardia is removed, the arrhythmia spontaneously resolves.
Hard on the heart
Sinus tachycardia can also be a significant arrhythmia with dire consequences. Because myocardial demands for oxygen are increased at higher heart rates, tachycardia can bring on an episode of chest pain in patients with coronary artery disease.
An increase in heart rate can also be detrimental for patients with obstructive types of heart conditions, such as aortic stenosis and hypertrophic cardiomyopathy.
Sinus tachycardia occurs in about 30% of patients after acute MI and is considered a poor prognostic sign because it may be associated with massive heart damage. Persistent tachycardia may also signal impending heart failure or cardiogenic shock.
Causes of sinus tachycardia
Sinus tachycardia may be a normal response to exercise, pain, stress, fever, or strong emotions, such as fear and anxiety. It can also occur:
•in certain cardiac conditions, such as heart failure, cardiogenic shock, and pericarditis
•as a compensatory mechanism in shock, anemia, respiratory distress, pulmonary embolism, sepsis, and hyperthyroidism
•when taking such drugs as atropine, isoproterenol (Isuprel), aminophylline, dopamine, dobutamine, epinephrine, alcohol, caffeine, nicotine, and amphetamines.
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What to look for
In sinus tachycardia, atrial and ventricular rhythms are regular. (See Identifying sinus tachycardia.) Both rates are equal, generally 100 to 160 beats/minute. As in sinus bradycardia, the P wave is of normal size and shape and precedes each QRS, but it may increase in amplitude. As the heart rate increases, the P wave may be superimposed on the preceding T wave and difficult to identify.
The PR interval, QRS complex, and T wave are normal. The QT interval normally shortens with tachycardia.
Pulse check!
When assessing a patient with sinus tachycardia, look for a pulse rate of more than 100 beats/minute but with a regular rhythm. Usually, the patient is asymptomatic. However, if his cardiac output falls and compensatory mechanisms fail, he may experience hypotension, syncope, and blurred vision. (See What happens in tachycardia, page 72.)
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.
With sinus tachycardia, look for a pulse rate of more than 100 beats/minute but with a regular rhythm.
Identifying sinus tachycardia
This rhythm strip illustrates sinus tachycardia. Look for these distinguishing characteristics.
A normal |
The rhythm is regular with a rate above 100 beats/minute. |
P wave precedes |
|
each QRS complex. |
|
• Rhythm: Regular |
• PR interval: 0.14 second |
• QT interval: 0.34 second |
• Rate: 120 beats/minute |
• QRS complex: 0.06 second |
• Other: None |
• P wave: Normal |
• T wave: Normal |
|
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What happens in tachycardia
Tachycardia can lower cardiac output by reducing ventricular filling time and the amount of blood pumped by the ventricles during each contraction. Normally, ventricular volume reaches 120 to 130 ml during diastole. In tachycardia, decreased ventricular volume leads to hypotension and decreased peripheral perfusion.
As cardiac output plummets, arterial pressure and peripheral perfusion decrease. Tachycardia worsens myocardial ischemia by increasing the heart’s demand for oxygen and reducing the duration of diastole—the period of greatest coronary flow.
How you intervene
When treating the asymptomatic patient, focus on determining the cause of the sinus tachycardia. Treatment for a symptomatic patient involves maintaining adequate cardiac output and tissue perfusion and identifying and correcting the underlying cause. For example, if the tachycardia is caused by hemorrhage, treatment includes stopping the bleeding and replacing blood and fluid.
Slow it down
If tachycardia leads to cardiac ischemia, treatment may include medications to slow the heart rate. The most commonly used drugs include beta-adrenergic blockers, such as metoprolol (Lopressor) and atenolol (Tenormin), and calcium channel blockers such as verapamil (Calan).
Getting at the history
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. These agents may be contained in nose drops and cold formulas.
You should also ask about the patient’s use of caffeine, nicotine, alcohol, and such recreational drugs as cocaine and amphetamines, any of which can trigger tachycardia. Advise him to avoid these substances if he has used them.
More steps to take
Here are other steps you should take for the patient with sinus tachycardia:
•Because sinus tachycardia can lead to injury of the heart muscle, check for chest pain or angina. Also assess for signs and
symptoms of heart failure, including crackles, an S3 heart sound, and jugular vein distention.
•Monitor intake and output as well as daily weight.
Memory jogger
To help you remember how to identify sinus
bradycardia from sinus tachycardia, think of the b in bradycardia as below. Sinus bradycardia is below 60 beats/ minute, while sinus tachycardia is above 100 beats/ minute. Both have a
normal QRS complex, preceded by a normal P wave.
Advise the patient to avoid caffeine,
nicotine, alcohol, and recreational drugs.
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•Check the patient’s LOC to assess cerebral perfusion.
•Provide the patient with a calm environment. Help to reduce fear and anxiety, which can fuel the arrhythmia.
•Teach about procedures and treatments. Include relaxation techniques in the information you provide.
•Be aware that a sudden onset of sinus tachycardia after an MI may signal extension of the infarction. Prompt recognition is vital so treatment can be started.
•Remember that tachycardia is commonly the first sign of a pulmonary embolism. Maintain suspicion, especially if your patient has risk factors for thrombotic emboli.
Sinus arrest
A disorder of impulse formation, sinus arrest is caused by a lack of electrical activity in the atrium, a condition called atrial standstill. (See Causes of sinus arrest.)
During atrial standstill, the atria aren’t stimulated and an entire PQRST complex will be missing from the ECG strip.
Except for this missing complex, or pause, the ECG usually remains normal. Atrial standstill is called sinus pause when one or two beats aren’t formed and sinus arrest when three or more beats aren’t formed.
Sinus arrest closely resembles third-degree SA block, also called exit block, on the ECG strip. (See Understanding sinoatrial blocks, pages 74 and 75.)
How it happens
Sinus arrest occurs when the SA node fails to generate an impulse. Such failure may result from a number of conditions, including acute infection, heart disease, and vagal stimulation. Sinus arrest may be associated with sick sinus syndrome.
The clinical significance of sinus arrest 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. He may not be able to feel the arrhythmias at all.
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.
Causes of sinus arrest
The following conditions can cause sinus arrest:
•sinus node disease, such as fibrosis and idiopathic degeneration
•increased vagal
tone, as occurs with Valsalva’s maneuver, carotid sinus massage, and vomiting
•digoxin (Lanoxin), quinidine, procainamide and salicylates, especially if given at toxic levels
•excessive doses
of beta-adrenergic blockers, such as metoprolol (Lopressor) and propranolol (Inderal)
•cardiac disorders, such as chronic coronary artery disease, acute myocarditis, cardiomyopathy, and hypertensive heart disease
•acute inferior wall myocardial infarction
•sick sinus syndrome
•acute infection.
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Understanding sinoatrial blocks
In sinoatrial (SA) block, the SA node discharges impulses at regular intervals. Some of those impulses, though, are delayed on their way to the atria. Based on the length of the delay, SA blocks are divided into three categories: first-, second-, and third-degree. Second-degree block is further divided into type I and type II.
First-degree SA block consists of a delay between the firing of the sinus node and depolarization of the atria. Because the ECG doesn’t show sinus node activity, you can’t detect first-degree SA block. However, you can detect the other three types of SA block.
Second-degree type I block
In second-degree type I block, conduction time between the sinus node and the surrounding atrial tissue becomes progressively longer until an entire cycle is dropped. The pause is less than twice the shortest P-P interval.
Eventually, an entire PQRST
complex is
dropped.
The rhythm is irregular, and
the P-P interval gets progressively shorter.
Second-degree type II block
In second-degree type II block, conduction time between the sinus node and atrial tissue is normal until an impulse is blocked. The duration of the pause is a multiple of the P-P interval.
An entire PQRST complex is missing.
The rhythm is regular except for pauses.
SA blocks are divided into three categories based on the
length of the delay.
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Understanding sinoatrial blocks (continued)
Third-degree block
In third-degree block, some impulses are blocked, causing long sinus pauses. The pause isn’t a multiple of the sinus rhythm. On an ECG, third-degree SA block looks similar to sinus arrest but results from a different cause.
Third-degree SA block is caused by a failure to conduct impulses; sinus arrest results from failure to form impulses. Failure in each case causes atrial activity to stop.
In sinus arrest, the pause commonly ends with a junctional escape beat. In thirddegree block, the pause lasts for an indefinite period and ends with a sinus beat.
An entire PQRST
complex is missing.
|
|
Sinus arrest |
|
|
can cause accidents. |
|
|
Motor vehicle |
The rhythm is regular except for pauses. |
The pause ends with a |
accidents are of |
sinus beat. |
particular concern. |
Too many for too long
If sinus arrest is frequent and prolonged, however, the patient will most likely have symptoms. 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 may be just as serious. For example, a symptom-producing arrhythmia that occurs while the patient is driving a car could result in a fatal accident.
What to look for
When assessing for sinus pause, you’ll find that atrial and ventricular rhythms are regular except for a missing complex at the onset of atrial standstill. (See Identifying sinus arrest, page 76.) The atrial and ventricular rates are equal and usually within normal limits. The rate may vary, however, as a result of the pauses.
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Identifying sinus arrest
This rhythm strip illustrates sinus arrest. Look for these distinguishing characteristics.
The rhythm is regular. |
An entire PQRST complex is missing. |
|
The rate is normal.
•Rhythm: Regular, except for the missing PQRST complexes
•Rate: 40 beats/minute
•P wave: Normal; missing during pause
• PR interval: 0.20 second |
• QT interval: 0.40 second, absent |
• QRS complex: 0.08 second, ab- |
during pause |
sent during pause |
• Other: None |
• T wave: Normal; absent during |
|
pause |
|
Of normal size and shape, a P wave precedes each QRS complex but is absent during a pause. The PR interval is normal and constant when the P wave is present and not measurable when absent. The QRS complex, the T wave, and the QT interval are normal when present and are absent during a pause.
You might see junctional escape beats and premature atrial, junctional, or ventricular contractions. With sinus arrest, the length of the pause isn’t a multiple of the previous R-R intervals.
Signs of recurrent pauses
You can’t detect a pulse or heart sounds when sinus arrest occurs. Usually, the patient is asymptomatic. Recurrent pauses may cause signs of decreased cardiac output, such as low blood pressure, altered mental status, and cool, clammy skin. The patient may also complain of dizziness or blurred vision.
How you intervene
An asymptomatic patient needs no treatment. For a patient displaying mild symptoms, treatment focuses on maintaining cardiac output and identifying the cause of the sinus arrest. That
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Syncope and sinus arrest
A patient with sinus arrest is at risk for syncope. Ask your patient whether he has ever passed out or felt as if he were going to pass out.
Also ask about a history of falls. If he has passed out or if he has a history of falls, obtain a detailed description of each episode, including where and how the syncope occurred.
Asking questions
If possible, check with friends and family members who witnessed the episodes to find out what happened and how long the patient remained unconscious each time.
The information you gather may help determine whether a vagal mechanism was involved. The presence of syncope or sinus pauses on an electrocardiogram may indicate the need for further electrophysiologic evaluation.
may involve stopping medications that contribute to SA node suppression, such as digoxin, beta-adrenergic blockers, and calcium channel blockers.
Emergent treatment
If the patient is dizzy or lightheaded, he may be
experiencing syncope.
A patient who develops signs of circulatory collapse needs immediate treatment. As with sinus bradycardia, emergency treatment includes using a temporary pacemaker and administration of atropine or epinephrine. A permanent pacemaker may be implanted for long-term management.
The goal for the patient with sinus arrest is to maintain adequate cardiac output and perfusion. Be sure to record and document the frequency and duration of pauses. Determine whether a pause is the result of sinus arrest or SA block.
Don’t let sleeping pauses lie
Examine the circumstances under which sinus pauses occur. A sinus pause may be insignificant if detected while the patient
is sleeping. If the pauses are recurrent, assess the patient for evidence of decreased cardiac output, such as altered mental status, low blood pressure, and cool, clammy skin.
Ask him whether he’s dizzy or light-headed or has blurred vision. Does he feel as if he has passed out? If so, he may be experiencing syncope from a prolonged sinus arrest. (See Syncope and sinus arrest.)
Document the patient’s vital signs and how he feels during pauses as well as what activities he was involved in when they occurred. Activities that increase vagal stimulation, such as Valsalva’s maneuver or vomiting, increase the likelihood of sinus pauses.