Nursing care plan dysrhytmias

I. Pathophysiology

a. Abnormal formation or conduction of the electrical impulses
within the heart
i. Bradyarrhythmias: decreased intrinsic pacemaker function
or block in conduction, often at atrioventricular (AV)
junction or His-Purkinje system
ii. Tachyarrhythmias: caused by reentry, often due to
enhanced or abnormal automaticity
b. Causes abnormalities of the heart rate, rhythm, or both
c. Change in conduction may alter pumping action of heart,
affecting blood pressure and perfusion of body organs.

II. Classification: Types of Dysrhythmias (Wedro, 2007)

a. Named according to the site of origination and the mechanism
of conduction involved:
i. Sinus or sinoatrial (SA) node
ii. AV node
iii. Involved heart chamber—atrial or ventricular
iv. Between the atria and ventricles—supraventricular or
junctional dysrhythmias
b. Differentiated by rate
i. Slow: bradycardia, pulse below 60 in adult
ii. Fast: tachycardia, pulse above 100 in adult
c. Rhythm disturbances can be regular (e.g., sinus tachycardia)
or irregular (e.g., atrial fibrillation).

III. Etiology

a. Primary cardiac disorder: coronary artery disease (CAD),
myocardial infarction (MI), heart valve dysfunction, coronary
artery bypass (CABG) surgery, or valve replacement
b. Systemic conditions: hypothyroidism and hyperthyroidism;
fever and dehydration; sepsis; shock states (hypovolemic,
cardiogenic); anemia; pulmonary diseases; brain injury;
catecholamine release, such as occurs in intense emotional
stress or vigorous exercise; anxiety disorders and panic
c. Electrolyte imbalances, such as with potassium
d. Effects of drugs and drug toxicity, such as with digoxin,
aminophylline, atropine, and caffeine
e. Illicit drug use, such as cocaine, methamphetamines

IV. Statistics

a. Atrial fibrillation is a frequent complication of cardiac
surgery, occurring in 30% of patients after CABG surgery
and up to 50% of patients following valve surgery
(Yee, 2006).
b. Mortality: 350,000 to 400,000 Americans die annually
from sudden cardiac death (Coughlin, 2007).



I. Sinus Tachycardia
a. Sinus node creates rate that is faster than normal (greater
than 100)
b. Associated with physiological or psychological stress;
medications, such as catecholamines, aminophylline,
atropine, stimulants, and illicit drugs; enhanced
automaticity; and autonomic dysfunction

II. Atrial Flutter
a. Occurs in the atrium and creates regular atrial rates between
250 and 400. Because AV node cannot keep up with
conduction of all these impulses, not all atrial impulses are
conducted into the ventricle, causing a therapeutic block at
the AV node.

III. Atrial Fibrillation (AF)
a. Rapid, irregular twitching of the atrial musculature with an
atrial rate of 300 to 600 and a ventricular rate of 120 to
200 if untreated
b. Associated with advanced age, valvular heart disease,
hyperthyroidism, pulmonary disorder, pulmonary disease,
alcohol ingestion (“holiday heart syndrome”), hypertension,
diabetes, CAD, or after open-heart surgery

IV. Paroxysmal Supraventricular Tachycardia (PSVT,
also called SVT)
a. Pathways in the AV node or atrium allow an altered
conduction of electricity, causing a regular and fast rate of
sometimes more than 150 to 200.
b. Ventricle, sensing the electrical activity coming through
the AV node, beats along with each stimulation.
c. Rarely a life-threatening event, but most people feel
uncomfortable when PSVT occurs.

V. Ventricular Tachycardia (VT)
a. Rapid heartbeat initiated within the ventricles, characterized
by three or more consecutive premature ventricular
beats with elevated and regular heart rate (such as 160 to
240 beats per minute)
b. Heart rate sustained at a high rate causes symptoms such
as weakness, fatigue, dizziness, fainting, or palpitations
c. Potentially lethal disruption of normal heartbeat that can
degenerate to ventricular fibrillation

VI. Ventricular Fibrillation (VF)
a. Aside from myocardial ischemia, other causes of ventricular
fibrillation may include severe weakness of the heart
muscle, electrolyte disturbances, drug overdose, and
b. Electrical signal is sent from the ventricles at a very fast
and erratic rate, impairing the ability of ventricles to fill
with blood and pump it out, markedly decreasing cardiac
output, and resulting in very low blood pressure and loss
of consciousness.
c. Sudden death will occur if VF not corrected.


I. Sinus Bradycardia
a. Rarely symptomatic until heart rate drops below 50, then
fainting or syncope may be reported
b. Causes include hypothyroidism, athletic training, sleep,
vagal stimulation, increased intracranial pressure, MI, hypovolemia,
hypoxia, acidosis, hypokalemia and hyperkalemia,
hyperglycemia, hypothermia, toxins, tamponade, tension
pneumothorax, thrombosis (cardiac or pulmonary), and
c. Medications, such as beta blockers, calcium channel blockers,
and amiodarone, also slow the heart rate (AHA, 2005).

II. Sick Sinus Syndrome (SSS)
a. Varity of conditions affecting SA node function, including
bradycardia, sinus arrest, sinoatrial block, episodes of
tachycardia, and carotid hypersensitivity
b. Signs and symptoms related to cerebral hypoperfusion
c. May be associated with rapid rate (tachycardia) or alternate
between too fast and too slow (bradycardia-tachycardia
syndrome). A long pause (asystole) may occur between
heartbeats, especially after an episode of tachycardia.

III. Heart Blocks
a. First-degree AV block
i. Asymptomatic; usually an incidental finding on electrocardiogram
b. Second-degree AV (type I and type II)
i. Usually asymptomatic, although some clients can feel
irregularities (palpitations) of the heartbeat, or syncope
may occur, which usually is observed in more advanced
conduction disturbances such as Mobitz II AV block
ii. Medications affecting AV node function, such as digoxin,
beta blockers, calcium channel blockers, may contribute
c. Third-degree AV block (also called complete heart block)
i. May be associated with acute MI either causing the block
or related to reduced cardiac output from bradycardia in
the setting of advanced atherosclerotic CAD
ii. Symptomatic with fatigue, dizziness, and syncope and
possible loss of consciousness
iii. Can be life-threatening, especially if associated with heart

Other Dysrhythmias

I. Premature Atrial Complex (PAC)
a. Electrical impulse starts in the atrium before the next normal
impulse of the sinus node.
b. Causes include caffeine, alcohol, and nicotine use, stretched
atrial myocardium; anxiety; hypokalemia; and hypermetabolic
states (pregnancy), or may be related to atrial ischemia, injury,
or infarction.

II. Premature Ventricular Contraction (PVC)
a. Electrical signal originates in the ventricles, causing them to
contract before receiving the electrical signal from the atria.
b. PVCs not uncommon and are often asymptomatic.
c. Increase to several per minute may cause symptoms such as
weakness, fatigue, dizziness, fainting, or palpitations.
d. Irritability of the heart demonstrated by frequent and or
multiple back-to-back PVCs can lead to VF.
Care Settings
Generally, minor dysrhythmias are monitored and treated in
the community setting; however, potential life-threatening
situations (including heart rates above 150 beats per minute)
may require a short inpatient stay.

Related Concerns
Heart failure: chronic
Myocardial infarction
Psychosocial aspects of care

Nursing Priorities

1. Prevent or treat life-threatening dysrhythmias.
2. Support client and significant other (SO) in dealing with
anxiety and fear of potentially life-threatening situation.
3. Assist in identification of cause or precipitating factors.
4. Review information regarding condition, prognosis, and
treatment regimen.

Discharge Goals
1. Free of life-threatening dysrhythmias and complications
of impaired cardiac output and tissue perfusion.
2. Anxiety reduced and managed.
3. Disease process, therapy needs, and prevention of complications
4. Plan in place to meet needs after discharge.

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