Arrhythmia

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.

Arrhythmias are classified according to their origin as ventricular, atrial (supraventricular), or

junctional. Their effect on cardiac output and blood pressure, partially influenced by the site of
origin, can be used to determine their clinical significance.

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

Figure 1: Sinus Arrhythmia

o Irregular atrial and ventricular rhythms

o Normal P wave preceding each QRS complex

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

Sinus tachycardia (Figure 2)

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

Figure 2: Sinus tachycardia.

Treatment

o Correction of underlying cause

o Beta-adrenergic blocker or calcium channel blocker for symptomatic patients

Sinus bradycardia (Figure 3)

In sinus bradycardia, the rate is less than 60 beats per minute with normal complexes. This is common in
a well-conditioned heart, as in an athlete, in young healthy individuals especially if they are physically
fit, and patients taking beta-blockers. It also occurs in patients with raised intracranial pressure or
sinoatrial (SA) node disease (‘sick-sinus syndrome’), and is common during myocardial infarction,
especially inferior territory myocardial infarction, since this area contains the SA node.

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

What is the QRS rate? Less than 60bpm

Is the QRS rhythm regular? Yes
what is the QRS duration? Less than 0.12s (three small squares)
Is there atrial activity? P waves
Are there P waves before each QRS? Yes
What is the PR interval? 0.12–0.20s (three to five small squares)

Treatment

o Correction of underlying cause

o For low cardiac output, dizziness, weakness, altered level of consciousness, or
low blood pressure; advanced cardiac life support (ACLS) protocol for administration of
atropine
o Temporary pacemaker or permanent pacemaker
o Dopamine or epinephrine infusion

Sinoatrial (SA) arrest or block (sinus arrest)

Figure 4: SA arrest or block (sinus arrest)

o Regular atrial and ventricular rhythms, except for missing complex

o Normal P waves preceding each QRS complex; missing during pause
o Pause not equal to a multiple of the previous sinus rhythm
Causes

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

o Correction of underlying cause

o Treat symptoms with atropine I.V.
o Temporary or permanent pacemaker for repeated episodes

Wandering atrial pacemaker

Figure 5: wandering atrial pacemaker

o Slightly irregular atrial and ventricular rhythms

o PR interval varies
o Irregular P waves with changing configuration, indicating that they aren't all from
SA node or single atrial focus; may appear after the QRS complex
o QRS complexes uniform in shape but irregular in rhythm

Causes

o Rheumatic carditis due to inflammation involving the SA node

o Digoxin toxicity
o Sick sinus syndrome

Treatment

o No treatment if the patient is asymptomatic

o Treatment of underlying cause if the patient is symptomatic
Premature atrial contraction (PAC)

Figure 6: Premature atrial contraction (PAC)

o Premature, abnormal-looking P waves that differ in configuration from normal P

waves
o QRS complexes after P waves, except in very early or blocked PACs
o P wave often buried in the preceding T wave or identified in the preceding T
wave

Causes

o Coronary or valvular heart disease, atrial ischemia, coronary atherosclerosis, heart

failure, acute respiratory failure, chronic obstructive pulmonary disease (COPD),
electrolyte imbalance, and hypoxia
o Digoxin toxicity; use of aminophylline, an adrenergics, or caffeine
o Anxiety

Treatment

o Usually no treatment needed

o Treatment of underlying cause

Paroxysmal supraventricular tachycardia

Figure 7: Paroxysmal supraventricular tachycardia

o Regular atrial and ventricular rhythms

o Heart rate > 160 beats/minute; rarely exceeds 250 beats/minute
 o P waves regular but aberrant; difficult to differentiate from preceding T wave
o P wave preceding each QRS complex
o Sudden onset and termination of arrhythmia

Causes

o Intrinsic abnormality of atrioventricular (AV) conduction system

o Physical or psychological stress, hypoxia, hypokalemia, cardiomyopathy,
congenital heart disease, MI, valvular disease, Wolff-Parkinson-White syndrome, cor
pulmonale, hyperthyroidism, and systemic hypertension
o Digoxin toxicity; use of caffeine, marijuana, or other central nervous system
stimulant

Treatment

o If the patient's condition is unstable, immediate cardioversion

o If the patient's condition is stable, vagal stimulation, Valsalva's maneuver, and
carotid sinus massage
o If cardiac function is preserved, treatment priority: calcium channel blocker, beta-
adrenergic blocker, digoxin, and cardioversion; then consider procainamide, amiodarone,
or sotalol if each preceding treatment is ineffective in rhythm conversion
o If the ejection fraction is < 40% or if the patient is in heart failrue, treatment
order: digoxin, amiodarone, then diltiazem

Atrial flutter

Figure 8: Atrial flutter

o Regular atrial rhythm; rate 250 to 400 beats/minute

o Ventricular rate variable, depending on degree of AV block (usually 60 to 100
beats/minute)
o Sawtooth P-wave configuration possible (F waves)
o QRS complexes uniform in shape but commonly irregular in rate

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

Figure 9: Atrial fibrillation

o Grossly irregular atrial rhythm; rate > 400 beats/minute

o Grossly irregular ventricular rate
o QRS complexes of uniform configuration and duration
o No discernible PR interval
o No P waves, or P waves that appear as erratic, irregular, baseline fibrillatory
waves

Causes

o Heart failure, COPD, thyrotoxicosis, constrictive pericarditis, ischemic heart

disease, sepsis, pulmonary embolus, rheumatic heart disease, hypertension, mitral
stenosis, atrial irritation, complication of coronary bypass or valve replacement surgery
o Nifedipine and digoxin use

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

Premature junctional contractions (junctional premature beats)

Figure 10: Premature junctional contractions (junctional premature beats)

o Irregular atrial and ventricular rhythms

o P waves inverted; may precede, be hidden within, or follow QRS complex
o PR interval < 0.12 second if P wave precedes QRS complex
o QRS complex configuration and duration normal

Causes

o MI or ischemia
o Digoxin toxicity and excessive caffeine or amphetamine use

Treatment

o Correction of underlying cause

o Discontinuation of digoxin if appropriate

Junctional rhythm
 Figure 11: Junctional rhythm

o Regular atrial and ventricular rhythms; atrial rate 40 to 60 beats/minute;

ventricular rate usually 40 to 60 beats/minute (60 to 100 beats/minute is accelerated
junctional rhythm)
o P waves preceding, hidden within (absent), or after QRS complex; inverted if
visible
o PR interval (when present) < 0.12 second
o QRS complex configuration and duration normal, except in aberrant conduction

Causes

o Inferior MI or ischemia, hypoxia, vagal stimulation, sick sinus syndrome

o Acute rheumatic fever
o Valve surgery
o Digoxin toxicity

Treatment

o Correction of underlying cause

o Atropine for symptomatic slow rate
o Pacemaker insertion if the patient doesn't respond to drugs
o Discontinuation of digoxin if appropriate

Junctional tachycardia

Figure 12: Junctional tachycardia

o Regular atrial and ventricular rhythms

 o Atrial rate > 100 beats/minute; however, P waves may be absent, hidden in QRS
complex, or preceding T wave
o Ventricular rate > 100 beats/minute
o Inverted P wave; may occur before or after QRS complex, may be hidden in QRS
complex, or may be absent
o QRS complex configuration and duration normal

Causes

o Myocarditis, cardiomyopathy, inferior MI or ischemia, acute rheumatic fever,

complication of valve replacement surgery
o Digoxin toxicity

Treatment

o Correction of underlying cause

o Beta-adrenergic blocker, calcium channel blocker, or amiodarone
o Discontinuation of digoxin if appropriate

Atrioventricular (AV) blocks

The SA node may be generating impulses causing the atria to contract at a normal rate, but not every
impulse passes through the AV node to the ventricles. Heart blocks may be congenital or acquired, for
example following an ischaemic event. There are various types of AV block.
First degree AV block (Figure 13)
This is simply a delay in conduction through the conducting system. It is diagnosed by a prolonged PR
interval, beyond the normal 0.20s. Importantly, each P wave is followed by a QRS complex.

Figure 13: First degree AV block

  What is the QRS rate? Dependent on the underlying rhythm
 Is the QRS rhythm regular? Yes
 What is the QRS duration? Less than 0.12s (three small squares)
 Is there atrial activity? Yes, P waves
 Are there P waves before each QRS? Yes
 What is the PR interval? Greater than 0.20s (five small squares)

Causes

o May be seen in a healthy person

o Inferior MI or ischemia, hypothyroidism, hypokalemia, hyperkalemia
o Digoxin toxicity; use of quinidine, procainamide, or a beta-adrenergic blocker, a
calcium channel blocker, or amiodarone

Treatment

o Correction of underlying cause

o Possibly atropine if severe bradycardia develops and the patient is symptomatic
o Cautious use of digoxin, a calcium channel blocker, and a beta-adrenergic blocker

Second degree AV block

Here, the rhythm is characterized by an intermittent failure or interruption of AV node conduction. The P
wave is blocked within the AV conducting system, and in effect is “dropped” and hence not followed by a
QRS complex.

o Second degree AV block (Mobitz type 1 – Wenkebach phenomenon) (Figure 14)

Cellular depolarisation in the AV node becomes more prolonged, usually due to
ischaemia in these tissues. As a result, the refractory period is prolonged. On the surface
ECG, this rhythm has an initially normal PR interval, with each subsequent PR interval
becoming more prolonged. The cycle is complete when atrial activation occurs while the
AV node is refractory, and no ventricular conduction occurs, resulting in a “dropped”
QRS complex. The PR interval following the dropped beat will be normal, as AV nodal
tissue will have recovered. The sequence then continues to repeat itself.

Figure 14: Second degree AV block, type 1(Mobitz I)

 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.

Figure 15: 2:1 AV block.

 What is the QRS rate? Slow

 Is the rhythm regular? Yes
 What is the QRS duration? Usually Less than 0.12s (three small squares)
 Is there atrial activity? Yes, P waves
 Are there P waves before each QRS? Yes, but every second P wave is not followed by a QRS
complex
 What is the PR interval? Normal for conducted beats

Causes

o Inferior MI, cardiac surgery, acute rheumatic fever, and vagal stimulation
o Digoxin toxicity; use of propranolol, quinidine, or procainamide

Treatment

o Treatment of underlying cause

o Atropine or temporary pacemaker for symptomatic bradycardia
o Discontinuation of digoxin if appropriate

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

 What is the QRS rate? May be normal

 Is the QRS rhythm regular? No
 What is the QRS duration? Greater than 0.12s (three small squares)
 Is there atrial activity? Yes, P waves
 Are there P waves before each QRS? Yes, but some P waves are not followed by a QRS
 What is the PR interval? Less than 0.20s for conducted beats

 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

o Severe coronary artery disease, anterior MI, acute myocarditis

o Digoxin toxicity

Treatment

o Temporary or permanent pacemaker

o Atropine, dopamine, or epinephrine for symptomatic bradycardia
o Discontinuation of digoxin if appropriate

Third degree AV block (complete heart block) (Figure 17)

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.

 What is the QRS rate? Slow

 Is the QRS rhythm regular? Yes
 What is the QRS duration? Dependent on pacemaker site: close to the AV node, normal.
Within the ventricles, wide
 Is there atrial activity? Yes
 Are there P waves before each QRS? Unrelated. More P waves than QRS complexes
 What is the PR interval? Variable

Causes

o Inferior or anterior MI, congenital abnormality, rheumatic fever, hypoxia,

postoperative complication of mitral valve replacement, Lev's disease (fibrosis and
calcification that spreads from cardiac structures to the conductive tissue), Lenegre's
disease (conductive tissue fibrosis)
o Digoxin toxicity

Treatment

o Atropine, dopamine, or epinephrine for symptomatic bradycardia

o Temporary or permanent pacemaker

Premature ventricular contraction (PVC)

 Figure 18: Premature ventricular contraction (PVC)

o Regular atrial rhythm

o Irregular ventricular rhythm
o QRS complex premature, usually followed by a complete compensatory pause
o QRS complex wide and distorted, usually > 0.14 second
o Premature QRS complexes occurring singly, in pairs, or in threes, alternating with
normal beats; focus from one or more sites
o Ominous when clustered, multifocal, with R wave on T pattern

Causes

o Heart failure; old or acute MI, ischemia, or contusion; myocardial irritation by

ventricular catheter or a pacemaker; hypercapnia; hypokalemia; hypocalcemia
o Drug toxicity (cardiac glycoside, aminophylline, tricyclic antidepressant, beta-
adrenergic blocker [isoproterenol or dopamine])
o Caffeine, tobacco, or alcohol use
o Psychological stress, anxiety, pain, exercise

Treatment

o If warranted, procainamide, lidocaine, or amiodarone I.V.

o Treatment of underlying cause
o Discontinuation of drug causing toxicity
o Potassium chloride I.V. if PVC induced by hypokalemia
o Magnesium sulfate I.V. if PVC induced by hypomagnesemia

Ventricular tachycardia

Figure 19: Ventricular tachycardia

 o Ventricular rate 140 to 220 beats/minute; regular or irregular rhythm
o QRS complexes wide, bizarre, and independent of P waves
o Indiscernible P waves
o May start and stop suddenly

Causes

o Myocardial ischemia, infarction, or aneurysm; coronary artery disease; rheumatic

heart disease; mitral valve prolapse; heart failure; cardiomyopathy; ventricular catheters;
hypokalemia; hypercalcemia; pulmonary embolism
o Digoxin, procainamide, epinephrine, or quinidine toxicity
o Anxiety

Treatment

o Pulseless: Initiate cardiopulmonary resuscitation (CPR); follow ACLS protocol

for defibrillation, ET intubation, and administration of epinephrine or vasopressin,
followed by amiodarone or lidocaine; if ineffective, magnesium sulfate or procainamide
o With pulse: If hemodynamically stable monomorphic VT, follow ACLS protocol
for administration of procainamide, sotalol, amiodarone, or lidocaine. If drugs are
ineffective, initiate synchronized cardioversion
o If polymorphic VT, follow ACLS protocol for administration of a beta-adrenergic
blocker, lidocaine, amiodarone, procainamide, or sotalol; if drugs are ineffective, initiate
synchronized cardioversion
o If torsades: Administer magnesium, then overdrive pacing; if rhythm persists,
isoproteronol, phenytoin, or lidocaine may also be given.
o Implanted cardioverter defibrillator, if recurrent VT

Ventricular fibrillation

Figure 19: Ventricular fibrillation

o Ventricular rhythm chaotic; rate rapid

o QRS complexes wide and irregular; no visible P waves

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

o Pulseless: Initiate CPR; follow ACLS rotocol for defibrillation, ET intubation,

and administration of epinephrine or vasopressin, lidocaine or amiodarone; if ineffective,
magnesium sulfate or procainamide.
o Implantable cardioverter defibrillator, if risk for recurrent VT

Asystole

Figure 20: Asystole

o No atrial or ventricular rate or rhythm

o No discernible P waves, QRS complexes, or T waves

Causes

o Myocardial ischemia or infarction, aortic valve disease, heart failure, hypoxia,

hypokalemia, severe acidosis, electric shock, ventricular arrhythmia, AV block,
pulmonary embolism, heart rupture, cardiac tamponade, hyperkalemia, electromechanical
dissociation
o Cocaine overdose

Treatment

o Continue CPR, follow ACLS protocol for ET intubation, transcutaneous pacing,

and administration of epinephrine and atropine

Torsades de pointes (polymorphic VT) (Figure 21)

In this variant ventricular tachycardia, each QRS complex is a different shape to the one preceding it, the
net effect on the surface ECG being that the QRS complex appears to twist around the baseline. The QRS
complexes are bizarre and multiform, with the sharp points directed one way for a few seconds and then
directed in another way, hence the term (Schamroth, 1990). As with monomorphic VT, this arrhythmia
may cause syncope or cardiac arrest. It is a rare arrhythmia, and may be caused by QT prolongation.

Figure 21: Torsades de pointes

 What is the QRS rate? Greater than 120bpm

 Is the QRS rhythm regular? No
 What is the QRS duration? Prolonged, greater than 0.12s (three small squares)
 Is there atrial activity? Not discernable
 Are there P waves before each QRS? Not discernable
 What is the PR interval? Not discernable

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

Symptoms of a rapid heartbeat include:

 breathlessness

 dizziness

 fainting or nearly fainting

 fluttering in the chest

 chest pain
  lightheadedness

 sudden weakness

Symptoms of bradycardia

Bradycardia can cause the following symptoms:

 angina, or chest pain

 trouble concentrating

 confusion

 finding exercise more difficult than usual

 dizziness

 tiredness

 lightheadedness

 palpitations

 shortness of breath

 fainting or nearly fainting

 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

1. A Nursing Process Approach to Excellent Care, 4th Edition

Copyright ©2006 Lippincott Williams & Wilkins