Tachycardias
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
poisoning.
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.
Bradycardias
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
trauma.
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 hypoperfusionc. 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
(ECG)
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
failure
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.
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
understood.
4. Plan in place to meet needs after discharge.
NURSING DIAGNOSIS: risk for decreased Cardiac Output
Risk factors may include
Altered electrical conduction
Reduced myocardial contractility
Possibly evidenced by
(Not applicable; presence of signs and symptoms establishes an actual diagnosis)
Desired Outcomes/Evaluation Criteria—Client Will
Cardiac Pump Effectiveness
Maintain or achieve adequate cardiac output as evidenced by BP and pulse within normal range, adequate urinary output,
palpable pulses of equal quality, and usual level of mentation.
Display reduced frequency or absence of dysrhythmia(s).
Participate in activities that reduce myocardial workload.
ACTIONS/INTERVENTIONS
Dysrhythmia Management
Independent
Palpate radial, carotid, femoral, and dorsalis pedis pulses,
noting rate, regularity, amplitude (full or thready), and symmetry.
Document presence of pulsus alternans, bigeminal
pulse, or pulse deficit.
Auscultate heart sounds, noting rate, rhythm, presence of
extra heartbeats, and dropped beats.
Monitor vital signs. Assess adequacy of cardiac output and
tissue perfusion, noting significant variations in BP, pulse
rate equality, respirations, changes in skin color and temperature,
level of consciousness and sensorium, and urine
output during episodes of dysrhythmias.
Determine type of dysrhythmia and document with rhythm
strip if cardiac or telemetry monitoring is available:
Sinus tachycardia
Sinus bradycardia
Atrial dysrhythmias, such as PACs, atrial flutter, AF, and
atrial supraventricular tachycardias (i.e., paroxysmal atrial
tachycardia [PAT], multifocal atrial tachycardia [MAT], SVT)
Ventricular dysrhythmias, such as PVCs and ventricular premature
beats (VPBs), VT, and ventricular flutter and VF
Heart blocks
Provide calm and quiet environment. Review reasons for
limitation of activities during acute phase.
Demonstrate and encourage use of stress management
behaviors such as relaxation techniques; guided imagery;
and slow, deep breathing.
Investigate reports of chest pain, documenting location,
duration, intensity (0 to 10 scale), and relieving or aggravating
factors. Note nonverbal pain cues, such as facial
grimacing, crying, changes in BP and heart rate.
Be prepared to initiate cardiopulmonary resuscitation (CPR), as
indicated.
Collaborative
Monitor laboratory studies, such as the following:
Electrolytes
Medication and drug levels
Administer supplemental oxygen, as indicated.
Prepare for and assist with diagnostic and treatment procedures
such as EP studies, radiofrequency ablation (RFA), and
cryoablation (CA).
Administer medications, as indicated, for example:
Potassium
Antidysrhythmics, such as the following:
Class I drugs:
Class Ia, such as disopyramide (Norpace), procainamide
(Procan SR), quinidine (Cardioquin), and moricizine
(Ethmozine)
Class Ib, such as lidocaine (Xylocaine), phenytoin
(Dilantin), tocainide (Tonocard), and mexiletine (Mexitil)
Class Ic, such as flecainide (Tambocor) and propafenone
(Rhythmol)
Class II drugs, such as atenolol (Tenormin), propranolol
(Inderal), nadolol (Corgard), acebutolol (Sectral), esmolol
(Brevibloc), sotalol (Betapace), and bisoprolol (Zebeta)
Class III drugs, such as bretylium tosylate (Bretylol), amiodarone
(Cordarone), sotalol (Betapace), ibutilide
(Corvert), and dofetilide (Tikosyn)
Class IV drugs, such as verapamil (Calan), nifedipine
(Procardia), and diltiazem (Cardizem)
Class V drugs, such as atropine sulfate, isoproterenol
(Isuprel), and cardiac glycosides (digoxin [Lanoxin])
Adenosine (Adenocard)
Prepare for and assist with elective cardioversion.
Assist with insertion and maintain pacemaker (external or temporary,
internal or permanent) function.
Insert and maintain intravenous (IV) access.
Prepare for surgery, such as aneurysmectomy, CABG, and
Maze, as indicated.
Prepare for placement of ICD when indicated.
RATIONALE
Differences in equality, rate, and regularity of pulses are
indicative of the effect of altered cardiac output on systemic
and peripheral circulation.
(
Specific dysrhythmias are more clearly detected audibly than
by palpation. Hearing extra heartbeats or dropped beats
helps identify dysrhythmias in the unmonitored client.
Although not all dysrhythmias are life-threatening, immediate
treatment may be required to terminate dysrhythmia in the
presence of alterations in cardiac output and tissue perfusion.
Useful in determining need and type of intervention required.
Tachycardia can occur in response to stress, pain, fever,
infection, coronary artery blockage, valvular dysfunction,
hypovolemia, hypoxia, or as a result of decreased vagal
tone or of increased sympathetic nervous system activity
associated with the release of catecholamines. Although it
generally does not require treatment, persistent tachycardia
may worsen underlying pathology in clients with ischemic
heart disease because of shortened diastolic filling time
and increased oxygen demands. These clients may require
medications.
Bradycardia is common in clients with acute MI (especially
anterior and inferior) and is the result of excessive
parasympathetic activity, blocks in conduction to the SA or
AV nodes, or loss of automaticity of the heart muscle.
Clients with severe heart disease may not be able to
compensate for a slow rate by increasing stroke volume;
therefore, decreased cardiac output, HF, and potentially
lethal ventricular dysrhythmias may occur.
PACs can occur as a response to ischemia and are normally
harmless, but can precede or precipitate AF. Acute and
chronic atrial flutter or fibrillation (the most common dysrhythmia)
can occur with coronary artery or valvular disease
and may or may not be pathological. Rapid atrial flutter
or fibrillation reduces cardiac output as a result of
incomplete ventricular filling (shortened cardiac cycle) and
increased oxygen demand.
PVCs or VPBs reflect cardiac irritability and are commonly
associated with MI, digoxin toxicity, coronary vasospasm,
and misplaced temporary pacemaker leads. Frequent, multiple,
or multifocal PVCs result in diminished cardiac output
and may lead to potentially lethal dysrhythmias, such as VT
or sudden death or cardiac arrest from ventricular flutter or
VF. Note: Intractable ventricular dysrhythmias unresponsive
to medication may reflect ventricular aneurysm.
Polymorphic VT (torsades de pointes) is recognized by
inconsistent shape of QRS complexes and is often related
to use of drugs such as procainamide (Pronestyl), quinidine
(Quinaglute), disopyramide (Norpace), and sotalol
(Betapace).
Reflect altered transmission of impulses through normal conduction
channels (slowed, altered) and may be the result of
MI, CAD with reduced blood supply to SA or AV nodes,
drug toxicity, and sometimes cardiac surgery. Progressing
heart block is associated with slowed ventricular rates,
decreased cardiac output, and potentially lethal ventricular
dysrhythmias or cardiac standstill.
Reduces stimulation and release of stress-related catecholamines,
which can cause or aggravate dysrhythmias
and vasoconstriction, increasing myocardial workload.
Promotes client participation in exerting some sense of control
in a stressful situation.
Reasons for chest pain are variable and depend on underlying
cause. However, chest pain may indicate ischemia due
to altered electrical conduction, decreased myocardial
perfusion, or increased oxygen need, such as impending or
evolving MI.
Development of life-threatening dysrhythmias requires prompt
intervention to prevent ischemic damage or death.
Imbalance of electrolytes, such as potassium, magnesium, and
calcium, adversely affects cardiac rhythm and contractility.
Reveal therapeutic and toxic level of prescription medications
or street drugs that may affect or contribute to presence of
dysrhythmias.
Increases amount of oxygen available for myocardial uptake,
reducing irritability caused by hypoxia.
Treatment for several tachycardia dysrhythmias, including
SVT, atrial flutter, Wolf-Parkinson-White ( WPW) syndrome,
AF, and VT, is often carried out as first-line treatment via
heart catheterization or angiographic procedures. After
rhythm is confirmed with EP study, the client will then often
have either an RFA or CA to terminate or disrupt the dysfunctional
pattern. Medications may be tried first or added
after ablation for increased treatment success.
Correction of hypokalemia may be sufficient to terminate
some ventricular dysrhythmias. Note: Potassium imbalance
is the number one cause of AF.
Class I drugs depress depolarization and alter repolarization,
stabilizing the cell. These drugs are divided into groups a,
b, and c, based on their unique effects.
These drugs increase action potential, duration, and effective
refractory period and decrease membrane responsiveness,
prolonging both QRS complex and QT interval. This also
results in decreasing myocardial conduction velocity and
excitability in the atria, ventricles, and accessory pathways.
They suppress ectopic focal activity. Useful for treatment of
atrial and ventricular premature beats and repetitive dysrhythmias,
such as atrial tachycardias and atrial flutter and
AF. Note: Myocardial depressant effects may be potentiated
when class Ia drugs are used in conjunction with any drugs
possessing similar properties.
These drugs shorten the duration of the refractory period
(QT interval), and their action depends on the tissue
affected and the level of extracellular potassium. These
drugs have little effect on myocardial contractility, AV and
intraventricular conduction, and cardiac output. They also
suppress automaticity in the His-Purkinje system. Drugs of
choice for ventricular dysrhythmias, they are also effective
for automatic and re-entrant dysrhythmias and digoxininduced
dysrhythmias. Note: These drugs may aggravate
myocardial depression.
These drugs slow conduction by depressing SA node
automaticity and decreasing conduction velocity through
the atria, ventricles, and Purkinje’s fibers. The result is
prolongation of the PR interval and lengthening of the QRS
complex. They suppress and prevent all types of ventricular
dysrhythmias. Note: Flecainide increases risk of druginduced
dysrhythmias post-MI. Propafenone can worsen
or cause new dysrhythmias, a tendency called the
“pro-arrhythmic effect.”
Beta-adrenergic blockers have antiadrenergic properties and
decrease automaticity. They reduce the rate and force of
cardiac contractions, which in turn decrease cardiac output,
blood pressure, and peripheral vascular resistance.
Therefore, they are useful in the treatment of dysrhythmias
caused by SA and AV node dysfunction, including SVTs,
atrial flutter and AF. Note: These drugs may exacerbate
bradycardia and cause myocardial depression, especially
when combined with drugs that have similar properties.
These drugs prolong the refractory period and action potential
duration, consequently prolonging the QT interval. They
decrease peripheral resistance and increase coronary blood
flow. They have anti-anginal and anti-adrenergic properties.
They are used to terminate VF and other life-threatening
ventricular dysrhythmias and sustained ventricular tachyarrhythmias,
especially when lidocaine and procainamide
are not effective. Note: Sotalol is a nonselective beta
blocker with characteristics of both class II and class III.
Calcium antagonists, or calcium channel blockers, slow
conduction time through the AV node, prolonging PR interval
to decrease ventricular response in SVTs, atrial flutter
and AF. Calan and Cardizem may be used for bedside
conversion of acute AF.
Miscellaneous drugs useful in treating bradycardia by increasing
SA and AV conduction and enhancing automaticity.
Cardiac glycosides may be used alone or in combination
with other antidysrhythmic drugs to reduce ventricular
rate in presence of uncontrolled or poorly tolerated atrial
tachycardias or atrial flutter and AF.
First-line treatment for PSVT. Slows conduction and interrupts
reentry pathways in AV node. Note: Contraindicated in
clients with second- or third-degree heart block or those
with SSS who do not have a functioning pacemaker.
May be used in AF after trials of first-line drugs, such as atenolol,
metoprolol, diltiazem, and verapamil, have failed to control
heart rate or in certain unstable dysrhythmias to restore
normal heart rate or relieve symptoms of heart failure.
Temporary pacing may be necessary to accelerate impulse
formation in bradydysrhythmias, synchronize electrical
impulsivity, or override tachydysrhythmias and ectopic
activity to maintain cardiovascular function until spontaneous
pacing is restored or permanent pacing is initiated.
These devices may include atrial and ventricular pacemakers
and may provide single chamber or dual chamber
pacing. The placement of implantable cardioverter defibrillators
(ICDs) is on the rise.
Patent access line may be required for administration of emergency
drugs.
Differential diagnosis of underlying cause may be required
to formulate appropriate treatment plan. Resection of
ventricular aneurysm may be required to correct intractable
ventricular dysrhythmias unresponsive to medical therapy.
Surgery such as CABG may be indicated to enhance
circulation to myocardium and conduction system. Note:
A Maze procedure is an open heart surgical procedure
sometimes used to treat refractive AF by surgically redirecting
electrical conduction pathways.
This device may be surgically implanted in those clients with
recurrent, life-threatening ventricular dysrhythmias unresponsive
to tailored drug therapy. The latest generation
of devices can provide multilevel or “tiered” therapy, that
is, antitachycardia and antibradycardia pacing, cardioversion,
or defibrillation depending on how each device is
programmed.
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