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An arrhythmia is an irregular heartbeat due to a disorder of impulse production, impulse conduction, and
in some instances, both. Arrhythmias result from abnormal electrical conduction or automaticity
that changes heart rate and rhythm. They vary in severity, from those that are mild,
asymptomatic, and require no treatment (such as sinus arrhythmia, in which heart rate increases
and decreases with respiration) to catastrophic ventricular fibrillation, which requires immediate
resuscitation.
In adults, a bradycardia is defined as a ventricular rate of less than 60 bpm; a tachycardia is a rate greater
than 100bpm.
Causes
Arrhythmias may be congenital or may result from myocardial ischemia or infarction, organic
heart disease, drug toxicity, electrolyte imbalance, or degeneration of conductive tissue necessary
to maintain normal heart rhythm (sick sinus syndrome).
Sinus Arrhythmia
Causes
o A normal variation of normal sinus rhythm in athletes, children, and the elderly
o Also seen in digoxin toxicity and inferior myocardial infarction (MI)
TREATMENT
Atropine if rate decreases below 40 beats/minute and the patient is symptomatic
In sinus tachycardia, the rate is 100–150 beats per minute with normal P-waves and PR interval. The rate
rarely exceeds 180bpm. It may be normal physiologic response to fever, exercise, anxiety, pain,
dehydration; may also accompany shock, left-sided heart failure, cardiac tamponade,
hyperthyroidism, anemia, hypovolemia, pulmonary embolism, and anterior MI.
May also occur with atropine, epinephrine, isoproterenol, quinidine, caffeine, alcohol, and
nicotine use
Treatment
May also occur with an anticholinesterase, a beta-adrenergic blocker, digoxin, and morphine use.
It only requires treatment if it causes or threatens hemodynamic compromise.
Figure 3: sinus bradycardia
Treatment
o Acute infection
o Coronary artery disease, degenerative heart disease, acute inferior MI
o Vagal stimulation, Valsalva's maneuver, carotid sinus massage
o Digoxin, quinidine, or salicylate toxicity
o Pesticide poisoning
o Pharyngeal irritation caused by endotracheal (ET) intubation
o Sick sinus syndrome
Treatment
Causes
Treatment
Causes
Treatment
Causes
Treatment
Atrial flutter
Causes
o Heart failure, tricuspid or mitral valve disease, pulmonary embolism, cor
pulmonale, inferior MI, and carditis
o Digoxin toxicity
Treatment
o If the patient's conditin is unstable with a ventricular rate > 150 beats/minute,
immediate cardioversion
o If the patient's condition is stable, drug therapy may include a calcium-channel
blocker, a beta-adrenergic blocker, or an antiarrhythmic
o Anticoagulation therapy (heparin, enoxaparin, or warfarin) may also be necessary
o Radiofrequency ablation to control rhythm
Atrial fibrillation
Causes
Treatment
o If the patient's condition is unstable with a ventricular rate > 150 beats/minute;
immediate cardioversion
o If the patient's condition is stable, follow ACLS protocol for cardioversion and
drug therapy which may include a calcium channel blocker, a beta-adrenergic blocker, or
an antiarrhythmic
o Anticoagulant, such as heparin, enoxaparin, or warfarin.
o Class III antiarrhythmic, dofetilide (Tikosyn) for conversion of atrial fibrillation
and atrial flutter to normal sinus rhythm
o Radiofrequency catheter ablation to the His bundle to interrupt all conduction
between atria and the ventricles (in resistant patients with recurring symptomatic atrial
fibrillation)
o Maze procedure in which sutures are placed in strategic places in the atrial
myocardium to prevent electrical circuits from developing perpetuating atrial fibrillation
Causes
o MI or ischemia
o Digoxin toxicity and excessive caffeine or amphetamine use
Treatment
Junctional rhythm
Figure 11: Junctional rhythm
Causes
Treatment
Junctional tachycardia
Causes
Treatment
Causes
Treatment
What is the QRS rate? Ventricular is usually slower than the atrial rate
Is the QRS rhythm regular? No
What is the QRS duration? Less than 0.12s (three small squares)
Is there atrial activity? Yes
Are there P waves before each QRS? Yes, but some P waves are not followed by a QRS.
What is the PR interval? Progressively lengthening until a QRS is “dropped”
• 2:1 AV block (Figure 15) This is probably a short-cycle Wenkebach-type block. The QRS complexes
are usually narrow, but there are two P waves for every QRS complex.
Causes
o Inferior MI, cardiac surgery, acute rheumatic fever, and vagal stimulation
o Digoxin toxicity; use of propranolol, quinidine, or procainamide
Treatment
o Second degree AV block (Mobitz type 2) (Figure 16) In this type of block the PR interval
is usually normal, but the QRS complexes are prolonged. There are intermittent dropped
beats, often with two or three P waves not conducted to the ventricles. The conduction
abnormality arises in the bundle of His and the bundle branches. This rhythm carries a
risk of progression to complete heart block or ventricular asystole (Narula and Samet,
1970).
Figure 16: Second degree AV block type 2
The importance of first- and second-degree block is that either may presage complete (third-
degree) heart block. This is especially so in the case of Mobitz II block.
Causes
Treatment
This is characterized by complete interruption of conduction between the atria and ventricles. All
impulses from the atria are blocked below the AV node, allowing the atria and ventricles to beat
independently (Wolbrette and Nacarelli, 2007). A secondary pacemaker stimulates the ventricles and the
ventricular rate will be dependent on the site of the secondary pacemaker. If it is situated around the AV
node, the QRS rate may be near to normal and the complexes of normal duration. However, if the
secondary pacemaker is located within the ventricle, the QRS complex will be widened and the
ventricular rate slower (20–40bpm).
Figure 17: Third degree AV block.
Causes
Treatment
Causes
Treatment
Ventricular tachycardia
Causes
Treatment
Ventricular fibrillation
Causes
o Myocardial ischemia or infarction, untreated ventricular tachycardia, R-on-T
phenomenon, hypokalemia, hyperkalemia, hypercalcemia, alkalosis, electric shock,
hypothermia
o Digoxin, epinephrine, or quinidine toxicity
Treatment
Asystole
Causes
Treatment
Symptoms
Arrhythmia might not cause noticeable symptoms. However, a doctor may detect an arrhythmia during a
routine examination or after requesting an electrocardiogram (EKG). Even if an individual notices
symptoms, it does not necessarily mean that they have a severe arrhythmia.
Some people with life threatening arrhythmias may have no symptoms, while others with symptoms may
not have a severe arrhythmia. Symptoms depend on the type of arrhythmia, as follows:
Symptoms of tachycardia
breathlessness
dizziness
chest pain
lightheadedness
sudden weakness
Symptoms of bradycardia
trouble concentrating
confusion
dizziness
tiredness
lightheadedness
palpitations
shortness of breath
profuse sweating
Symptoms of A-fib
When A-fib symptoms occur, they often have a rapid onset and may involve:
angina
breathlessness
dizziness
palpitations
fainting or nearly fainting
weakness
Complications
In a patient with a normal heart, arrhythmias typically produce few symptoms. However, even in
a normal heart, persistently rapid or highly irregular rhythms can strain the myocardium and
impair cardiac output.
Assessment findings
Depending on the arrhythmia, the patient may exhibit signs and symptoms ranging from pallor,
cold and clammy extremities, reduced urine output, palpitations, and weakness to chest pains,
dizziness and, if cerebral circulation is severely impaired, syncope.
Diagnostic tests
Electrocardiography (ECG) allows detection and identification of arrhythmias.
Nursing diagnoses
Activity intolerance
Acute pain
Anxiety
Decreased cardiac output
Deficient fluid volume
Disabled family coping
Fatigue
Impaired gas exchange
Ineffective tissue perfusion: Renal, cerebral, cardiopulmonary
Key outcomes
The patient will perform activities of daily living without excess fatigue or exhaustion.
The patient will express feelings of comfort and decreased pain.
The patient will identify measures to reduce anxiety.
The patient will maintain cardiac output and hemodynamic stability.
The patient will maintain palpable pulses and adequate fluid volume.
The patient and family will demonstrate adaptive coping behaviors.
The patient will verbalize the importance of balancing activity with adequate rest periods.
The patient will maintain adequate ventilation and oxygenation.
The patient will maintain adequate cardiopulmonary, renal, and cerebral perfusion.
Nursing interventions
Carefully assess the patient's cardiac, electrolyte, and overall clinical status to determine the
effect on cardiac output and whether the arrhythmia is life-threatening.
Assess an unmonitored patient for rhythm disturbances. If the patient's pulse rate is abnormally
rapid, slow, or irregular, watch for signs of hypoperfusion, such as hypotension and diminished
urine output.
Document arrhythmias in a monitored patient, and watch for possible causes and effects.
When life-threatening arrhythmias develop, quickly assess the patient's level of consciousness
and pulse and respiratory rates and initiate cardiopulmonary resuscitation, if indicated.
Evaluate patient for altered cardiac output resulting from arrhythmias. Administer medications, as
ordered, and prepare to assist with medical procedures (such as cardioversion), if indicated.
Monitor patient for predisposing factors, such as fluid and electrolyte imbalance, and signs of
toxic reaction, especially if the patient is taking digoxin. If you suspect a toxic reaction, report it
to the physician immediately and withhold the next dose.
To prevent arrhythmias postoperatively, provide adequate oxygen and reduce heart workload
while carefully maintaining metabolic, neurologic, respiratory, and hemodynamic status.
To avoid temporary pacemaker malfunction, install a fresh battery before each insertion.
Carefully secure the external catheter wires and the pacemaker box. Assess the threshold daily.
Watch closely for premature contractions, a sign of myocardial irritation.
After pacemaker insertion, monitor the patient's pulse rate regularly, and watch for signs of
pacemaker failure and decreased cardiac output.
References