MANAGEMENT OF PATIENTS WITH DYSRHYTHMIAS  The electrical stimulation is called

AND CONDUCTION PROBLEMS depolarization, and the mechanical contraction

JEFF THOMAS B. SYDIONGCO JR. M.D is called systole.
DYSRHYTHMIAS  Electrical relaxation is called repolarization, and
 are disorders of the formation or conduction (or mechanical relaxation is called diastole.
both) of the electrical impulse within the heart.  The process from sinus node electrical impulse
 These disorders can cause disturbances of the generation through ventricular repolarization
heart rate, the heart rhythm, or both. completes the electromechanical circuit, and
 Dysrhythmias may initially be evidenced by the the cycle begins again.
hemodynamic effect they cause (e.g., a change INFLUENCES ON HEART RATE AND CONTRACTILITY
in conduction may change the pumping action  The heart rate is influenced by the autonomic
of the heart and cause decreased blood nervous system, which consists of sympathetic
pressure), and are diagnosed by analyzing the and parasympathetic fibers.
electrocardiographic (ECG) waveform.  Sympathetic nerve fibers (also referred to as
 Their treatment is based on the frequency and adrenergic fibers) are attached to the heart and
severity of symptoms produced. arteries as well as several other areas in the
 Dysrhythmias are named according to the site body.
of origin of the electrical impulse and the  Stimulation of the sympathetic system increases
mechanism of formation or conduction heart rate (positive chronotropy), conduction
involved. through the AV node (positive dromotropy),
 For example, an impulse that originates in the and the force of myocardial contraction
sinoatrial (SA) node and at a slow rate is called (positive inotropy).
sinus bradycardia  Sympathetic stimulation also constricts
NORMAL ELECTRICAL CONDUCTION peripheral blood vessels, therefore increasing
 The electrical impulse that stimulates and paces blood pressure. Parasympathetic nerve fibers
the cardiac muscle normally originates in the SA are also attached to the heart and arteries.
node, also called the sinus node, an area  Parasympathetic stimulation reduces the heart
located near the superior vena cava in the right rate (negative chronotropy), AV conduction
atrium. (negative dromotropy), and the force of atrial
 In the adult, the electrical impulse usually myocardial contraction.
occurs at a rate of 60 to 100 times a minute.  The decreased sympathetic stimulation results
 The electrical impulse quickly travels from the in dilation of arteries, thereby lowering blood
SA node through the atria to the pressure.
atrioventricular (AV) node; this process is  Manipulation of the autonomic nervous system
known as conduction. may increase or decrease the incidence of
 The electrical stimulation of the muscle cells of dysrhythmias.
the atria causes them to contract.  Increased sympathetic stimulation (e.g., caused
 The structure of the AV node slows the by exercise, anxiety, fever, or administration of
electrical impulse, giving the atria time to catecholamines, such as dopamine [Intropin],
contract and fill the ventricles with blood. aminophylline, or dobutamine [Dobutrex]) may
 This part of atrial contraction is frequently increase the incidence of dysrhythmias.
referred to as the atrial kick and accounts for  Decreased sympathetic stimulation (e.g., with
nearly one third of the volume ejected during rest, anxiety reduction methods such as
ventricular contraction (Fuster, Walsh, & therapeutic communication or meditation, or
Harrington, 2011). administration of beta-adrenergic blocking
 The electrical impulse then travels very quickly agents) may decrease the incidence of
through the bundle of His to the right and left dysrhythmias
bundle branches and the Purkinje fibers,
located in the ventricular muscle
THE ELECTROCARDIOGRAM  The QRS complex represents ventricular
 The electrical impulse that travels through the depolarization. Not all QRS complexes have all
heart can be viewed by means of three waveforms.
electrocardiography, the end product of which  The Q wave is the first negative deflection after
is an electrocardiogram (ECG). the P wave.
 Each phase of the cardiac cycle is reflected by  The Q wave is normally less than 0.04 seconds
specific waveforms on the screen of a cardiac in duration and less than 25% of the R-wave
monitor or on a strip of ECG graph paper amplitude. The R wave is the first positive
COMPONENTS OF THE ELECTROCARDIOGRAM deflection after the P wave, and the S wave is
 The ECG waveform reflects the function of the the first negative deflection after the R wave.
heart’s conduction system in relation to the  The T wave represents ventricular
specific lead. repolarization (when the cells regain a negative
 The ECG offers important information about the charge; also called the resting state).
electrical activity of the heart and is useful in  It follows the QRS complex and is usually the
diagnosing dysrhythmias. same direction (deflection) as the QRS complex.
 ECG waveforms are printed on graph paper that  Atrial repolarization also occurs but is not visible
is divided by vertical and horizontal lines at on the ECG because it occurs at the same time
standard intervals. as ventricular depolarization (i.e., the QRS).
 Time and rate are measured on the horizontal  The U wave is thought to represent
axis of the graph, and amplitude or voltage is repolarization of the Purkinje fibers; although
measured on the vertical axis. this wave is rare, it sometimes appears in
 When an ECG waveform moves toward the top patients with hypokalemia (low potassium
of the paper, it is called a positive deflection. levels), hypertension, or heart disease.
 When it moves toward the bottom of the paper,  If present, the U wave follows the T wave and is
it is called a negative deflection usually smaller than the P wave.
WAVES, COMPLEXES, AND INTERVALS
 The ECG is composed of waveforms (including NORMAL SINUS RHYTHM
the P wave, the QRS complex, the T wave, and  Electrical conduction that begins in the SA node
possibly a U wave) and of segments and generates a sinus rhythm.
intervals (including the PR interval, the ST  Normal sinus rhythm occurs when the electrical
segment, and the QT interval) impulse starts at a regular rate and rhythm in
 The P wave represents the electrical impulse the SA node and travels through the normal
starting in the SA node and spreading through conduction pathway.
the atria. NORMAL SINUS RHYTHM HAS THE FOLLOWING
 Therefore, the P wave represents atrial CHARACTERISTICS:
depolarization.  Ventricular and atrial rate: 60 to 100 bpm in the
adult Ventricular and atrial rhythm: Regular
 QRS shape and duration: Usually normal, but
may be regularly abnormal
 P wave: Normal and consistent shape; always in
front of the QRS
 PR interval: Consistent interval between 0.12
and 0.20 seconds
 P:QRS ratio: 1:1
 Although normal sinus rhythm is generally
indicative of good cardiovascular health,
patients with an average resting heart rate that
exceeds 90 bpm over a 24-hour period should
receive a full medical workup for potential
 underlying causes (Sheldon, Grubb, Olshansky,  The patient is assessed to determine the
et al., 2015). hemodynamic effect and the possible cause of
TYPES OF DYSRHYTHMIAS the dysrhythmia.
 Dysrhythmias include sinus, atrial, junctional,  If the decrease in heart rate results from
and ventricular dysrhythmias and their various stimulation of the vagus nerve, such as with
subcategories, as well as conduction bearing down during defecation or vomiting,
abnormalities. Sinus Node Dysrhythmias attempts are made to prevent further vagal
 Sinus node dysrhythmias originate in the SA stimulation.
node; these include sinus bradycardia, sinus  If the bradycardia is caused by a medication
tachycardia, and sinus arrhythmia. such as a beta-blocker, the medication may be
withheld.
 If the slow heart rate causes significant
hemodynamic changes resulting in shortness of
breath, acute alteration of mental status,
angina, hypotension, ST-segment changes, or
premature ventricular complexes (PVCs),
treatment is directed toward increasing the
heart rate.
 Slow heart rate may be due to sinus node
dysfunction (previously known as sick sinus
syndrome), which has a number of risk factors
including increased age; white race; obesity;
SINUS BRADYCARDIA hypertension; lower heart rate; and a history of
 Sinus bradycardia occurs when the SA node a cardiovascular event, such as myocardial
creates an impulse at a slower-than-normal infarction, heart failure, or stroke (Jensen,
rate. Gronroos, Chen, et al., 2014).
Causes include:  Tachy-brady syndrome is the term used when
 lower metabolic needs (e.g., sleep, athletic bradycardia alternates with tachycardia.
training, hypothyroidism), MEDICAL MANAGEMENT
 vagal stimulation (e.g., from vomiting,  Management depends on the cause and
suctioning, severe pain), symptoms. Resolving the causative factors may
 medications (e.g., calcium channel blockers be the only treatment needed.
(e.g., nifedipine [Procardia]),  If the bradycardia produces signs and symptoms
 amiodarone [Cordarone], of clinical instability (e.g., acute alteration in
 betablockers (e.g., metoprolol [Lopressor]), mental status, chest discomfort, or
 idiopathic sinus node dysfunction, hypotension), 0.5 mg of atropine may be given
 increased intracranial pressure, and rapidly as an intravenous (IV) bolus and
 coronary artery disease, especially myocardial repeated every 3 to 5 minutes until a maximum
infarction (MI) of the inferior wall. dosage of 3 mg is given.
 Unstable and symptomatic bradycardia is  Rarely if the bradycardia is unresponsive to
frequently due to hypoxemia. atropine, emergency transcutaneous pacing can
 Other possible causes include acute altered be instituted, or catecholamines, such as
mental status (e.g., delirium) and acute dopamine or epinephrine, are given (Link,
decompensated heart failure (Fuster et al., Berkow, Kudenchuk, et al., 2015)
2011). SINUS TACHYCARDIA
 All characteristics of sinus bradycardia are the  Sinus tachycardia occurs when the sinus node
same as those of normal sinus rhythm, except creates an impulse at a faster-than-normal rate.
for the rate.
Causes may include the following:
 Physiologic or psychological stress (e.g., acute
blood loss, anemia, shock, hypervolemia,
hypovolemia, heart failure, pain,
hypermetabolic states, fever, exercise, anxiety)
 Medications that stimulate the sympathetic
response (e.g., catecholamines, aminophylline,
atropine), stimulants (e.g., caffeine, nicotine),
and
 illicit drugs (e.g., amphetamines, cocaine,
Ecstasy)
 Enhanced automaticity of the SA node and/or
 If the tachycardia has a wide QRS, then
excessive sympathetic tone with reduced
adenosine is considered only if the QRS is
parasympathetic tone that is out of proportion
monomorphic (uniform shape) and the
to physiologic demands, a condition called
ventricular rhythm is regular.
inappropriate sinus tachycardia Autonomic
 Otherwise, procainamide (Pronestyl),
dysfunction, which results in a type of sinus
amiodarone, and sotalol (Betapace) are the
tachycardia referred to as postural orthostatic
options in wide QRS tachycardia.
tachycardia syndrome (POTS).
 Catheter ablation of the SA node may be used in
 POTS is characterized by tachycardia (increase
cases of persistent inappropriate sinus
in heart rate greater than 30 bpm) without
tachycardia unresponsive to other treatments.
hypotension when moving to a standing
 Treatment for POTS often involves a
position, or with frequent symptoms such as
combination of approaches, with treatment
palpitations, lightheadedness, weakness, and
targeted at the underlying problem.
blurred vision that occur with standing (Sheldon
 For example, patients with hypovolemia may be
et al., 2015)
advised to increase their fluid and sodium
MEDICAL MANAGEMENT
intake, or use salt tablets if necessary (Sheldon
 Medical management of sinus tachycardia is
et al., 2015).
determined by the severity of symptoms and
SINUS ARRHYTHMIA
directed at identifying and abolishing its cause.
 Sinus arrhythmia occurs when the sinus node
 If the tachycardia is persistent and causing
creates an impulse at an irregular rhythm; the
hemodynamic instability, synchronized
rate usually increases with inspiration and
cardioversion is the treatment of choice.
decreases with expiration.
 Otherwise, vagal maneuvers, such as carotid
 Non-respiratory causes include heart disease
sinus massage, gagging, bearing down against a
and valvular disease, but these are rare.
closed glottis (as if having a bowel movement),
 Medical Management Sinus arrhythmia does
forceful and sustained coughing, and applying a
not cause any significant hemodynamic effect
cold stimulus to the face (such as immersing the
and therefore is not typically treated
face in ice water), or administration of
adenosine (Adenocard) may be considered to
interrupt the tachycardia.
 These increase parasympathetic stimulation,
causing slower conduction through the AV node
and blocking the reentry of the rerouted
impulse (Smith, Fry, Taylor, et al., 2015).
 Beta-blockers (Class II antiarrhythmic) and
calcium channel blockers (Class IV
antiarrhythmic) although rarely used, may also
be considered in a narrow-QRS tachycardia.
ATRIAL DYSRHYTHMIAS
  Atrial dysrhythmias originate from foci within  Atrial fibrillation causes electrophysiologic
the atria and not the SA node. changes in the atrial myocardium (remodeling
 These include aberrancies such as: of the atrial electrical circuit) and structural
❑ premature atrial complexes (PACs) remodeling (fibrosis), which provides the basis
❑ atrial fibrillation and for continuance of the dysrhythmia (January,
❑ atrial flutter. Wann, Alpert, et al., 2014; Stavrakis, Nakagawa,
Premature Atrial Complex Po, et al., 2015).
 A premature atrial complex (PAC) is a single ECG  Atrial fibrillation can result from diverse
complex that occurs when an electrical impulse pathophysiologic etiologies and risks.
starts in the atrium before the next normal  Atrial fibrillation results from abnormal impulse
impulse of the sinus node. formation that occurs when structural or
 The PAC may be caused by caffeine, alcohol, electrophysiological abnormalities alter the
nicotine, stretched atrial myocardium (e.g., as in atrial tissue causing a rapid, disorganized, and
hypervolemia), anxiety, hypokalemia (low uncoordinated twitching of the atrial
potassium level), hypermetabolic states (e.g., musculature (January et al., 2014).
with pregnancy), or atrial ischemia, injury, or  Both the extrinsic (central) and intrinsic cardiac
infarction. autonomic nervous systems (CANS) are thought
 PACs are common in normal hearts. to play an important role in the initiation and
 The patient may say, “My heart skipped a beat.” continuance of atrial fibrillation (Stavrakis et al.,
A pulse deficit (a difference between the apical 2015).
and radial pulse rate) may exist.  Separate from the extrinsic (central) nervous
MEDICAL MANAGEMENT system, which includes the brain and spinal
 If PACs are infrequent, no treatment is cord, the CANS consists of a highly
necessary. interconnected network of autonomic ganglia
 If they are frequent (more than six per minute), and nerve cell bodies embedded within the
this may herald a worsening disease state or the epicardium, largely within the atrial
onset of more serious dysrhythmias, such as myocardium and great vessels (pulmonary
atrial fibrillation. veins).
 Medical management is directed toward  Hyperactive autonomic ganglia in the CANS are
treating the underlying cause (e.g., reduction of thought to play a critical role in atrial fibrillation,
caffeine intake, correction of hypokalemia) resulting in impulses that are initiated from the
pulmonary veins and conducted through to the
AV node.
 The ventricular rate of response depends on the
conduction of atrial impulses through the AV
node, presence of accessory electrical
conduction pathways, and therapeutic effect of
medications.
 Lack of consistency in describing patterns or
types of atrial fibrillation has led to the use of
numerous labels (e.g., paroxysmal [i.e., it has a
sudden onset and terminates spontaneously],
persistent, and permanent).
Patients with atrial fibrillation are at increased risk of:
ATRIAL FIBRILLATION ❑ heart failure,
 Atrial fibrillation is the most common sustained ❑ myocardial ischemia, and
dysrhythmia, affecting as many as 6.1 million ❑ embolic events such as stroke (January et al., 2014)
Americans (Mozaffarian, Benjamin, Go, et al., A rapid and irregular ventricular response reduces the
2015).
time for ventricular filling, resulting in a smaller stroke examination that identifies the onset and
volume. nature of signs and symptoms, including their
 Because atrial fibrillation causes a loss in AV frequency, duration and any precipitating
synchrony (the atria and ventricles contract at factors, and any response to medications.
different times), the atrial kick (the last part of  Whether or not the patient has a known history
diastole and ventricular filling, which accounts of heart disease or other risks is identified.
for 25% to 30% of the cardiac output) is also  A 12-lead ECG is performed to verify the atrial
lost. fibrillation rhythm, as well as to identify the
 As a consequence, although some patients with presence (or absence) of left ventricular
atrial fibrillation are asymptomatic, others hypertrophy, bundle branch block, prior
experience palpitations and clinical myocardial ischemia, or other dysrhythmias.
manifestations of heart failure (e.g., shortness  The RR, QRS, and QT intervals are analyzed to
of breath, hypotension, dyspnea on exertion, verify the effectiveness of any prescribed
fatigue). antiarrhythmic medications (January et al.,
In addition, a high ventricular rate of response during 2014). A transthoracic echocardiogram (TEE)
atrial fibrillation (greater than 80 bpm) can eventually can:
lead to:  identify the presence of valvular heart disease,
❑ mitral valve dysfunction,  provide information about left ventricular (LV)
❑ mitral regurgitation, and right ventricular (RV) size and function, RV
❑ intraventricular conduction delays, and pressures (to identify pulmonary hypertension,
❑ dilated ventricular cardiomyopathy. which may exist concomitant with atrial
 Patients with atrial fibrillation may exhibit a fibrillation), LV hypertrophy, and presence of
pulse deficit—a numeric difference between left atrial thrombi (January et al., 2014)
apical and radial pulse rates.  Blood tests to screen for diseases that are
 The shorter time in diastole reduces the time known risks for atrial fibrillation, including
available for coronary artery perfusion, thereby thyroid, renal, and hepatic function, are
increasing the risk of myocardial ischemia with assessed in the patient with a new onset of
the onset of anginal symptoms. atrial fibrillation, as well as when the ventricular
 Decreasing the ventricular rate may avoid and rate is difficult to control (January et al., 2014).
correct these effects.  Additional tests may include a chest x-ray (to
 The erratic nature of atrial contraction, evaluate pulmonary vasculature in a patient
alterations in ventricular ejection, and atrial suspected of having pulmonary hypertension),
myocardial dysfunction promote the formation exercise stress test (to exclude myocardial
of thrombi, especially within the left atrium, ischemia or reproduce exerciseinduced atrial
increasing the risk of an embolic event. fibrillation), Holter or event monitoring and an
 The origin of embolisms resulting in stroke for EP study (January et al., 2014)
patients with nonvalvular atrial fibrillation is MEDICAL MANAGEMENT
most often the left atrial appendage (LAA)  Treatment of atrial fibrillation depends on
(Masoudi, Calkins, Kavinsky, et al., 2015). the cause, pattern, and duration of the
dysrhythmia, the ventricular response rate,
as well as the presence of structural or
valvular heart disease and other cardiac
conditions such as coronary artery disease
or heart failure.
 Strategies for both rhythm control (i.e.,
conversion to sinus rhythm) and rate
ASSESSMENT AND DIAGNOSTIC FINDINGS control are dependent on shared clinical
 The clinical evaluation of atrial fibrillation decision making between the patient and
should include a history and physical primary provider.
  In some cases, atrial fibrillation MEDICATIONS THAT CONVERT THE HEART RHYTHM OR
spontaneously converts to sinus rhythm PREVENT ATRIAL FIBRILLATION
within 24 to 48 hours and without ► For patients with atrial fibrillation lasting 48 hours or
treatment. longer, anticoagulation is recommended prior to
 However, in instances where atrial attempts to restore sinus rhythm, which may be
fibrillation is concomitant with significant achieved through pharmacological or electrical
other morbid conditions (e.g., severe heart cardioversion (January et al., 2014).
failure), the atrial fibrillation may be ► In the absence of therapeutic anticoagulation, TEE
classified as “permanent,” meaning that the may be performed prior to cardioversion to identify left
patient and primary provider have made a atrial thrombus formation, including in the LAA (January
joint decision to stop further attempts to et al., 2014).
restore or maintain sinus rhythm. ► If no thrombus is identified, cardioversion can
 Therefore, management of atrial fibrillation proceed.
may not only be different in different MEDICATIONS THAT MAY BE GIVEN TO ACHIEVE
patients, but it also may change over time PHARMACOLOGIC CARDIOVERSION TO SINUS RHYTHM
for any one patient. INCLUDE:
Medical management revolves around: ❑ flecainide (Tambocor),
❑ preventing embolic events such as stroke with ❑ dofetilide (Tikosyn),
antithrombotic drugs, ❑ propafenone (Rythmol),
❑ controlling the ventricular rate of response with ❑ amiodarone, and
antiarrhythmic agents, and ❑ IV ibutilide (Corvert)
❑ treating the dysrhythmia as indicated so that it is • These medications are most effective if given within 7
converted to a sinus rhythm (i.e., cardioversion) days of the onset of atrial fibrillation.
• It is recommended that patients who were prescribed
dofetilide be hospitalized so that the QT interval and
renal function both may be monitored.
• Despite a degree of risk, dofetilide is a preferred
medication because it is highly effective at converting
atrial fibrillation to sinus rhythm, has fewer drug-to-
drug interactions, and is better tolerated by patients
than other medications.
►Prevention of atrial fibrillation following cardiac
surgery is best achieved through administration of beta-
blockers for at least 24 hours prior to surgery (Shi,
2016).
► Cholesterol-lowering drugs such as the HMG-CoA
reductase inhibitors (also called “statins,”) may also be
prescribed for primary prevention of new-onset atrial
MEDICATIONS THAT CONTROL THE HEART RATE fibrillation following cardiac surgery (January et al.,
► A strategy to control the ventricular rate of response 2014).
so that the resting heart rate is less than 80 bpm is ► Therapy with angiotensin-converting enzyme (ACE)
recommended in order to manage symptoms of atrial inhibitors and angiotensin receptor blockers (ARBs) may
fibrillation (January et al., 2014). decrease the incidence of atrial fibrillation for patients
► To decrease the ventricular rate in patients with with concomitant hypertension, although the use of
paroxysmal, persistent, or permanent atrial fibrillation, these drugs is not found to be beneficial as a primary
a beta-blocker (Class II antiarrhythmic) or non- prevention strategy for patients without hypertension
dihydropyridine calcium channel blocker (Class IV (January et al., 2014).
antiarrhythmic) is generally recommended (January et • If symptomatic, paroxysmal atrial fibrillation is
al., 2014). refractory to at least one Class I or Class III
antiarrhythmic medication , and rhythm control is • Ablation may also be accomplished using a special
desired, catheter ablation may be indicated (January et catheter to apply extremely cold temperature to
al., 2014) destroy selected cardiac cells, called cryoablation.
ELECTRICAL CARDIOVERSION FOR ATRIAL • The goal of each of these ablation procedures is to
FIBRILLATION eliminate the dysrhythmia, by preventing the ectopic
 Electrical cardioversion is indicated for patients activity arising from the pulmonary veins from reaching
with atrial fibrillation that is hemodynamically the atria, thereby stopping fibrillation (Stavrakis et al.,
unstable (e.g., acute alteration in mental status, 2015)
chest discomfort, hypotension) and does not • An EP study may be performed to induce the
respond to medications (January et al., 2014). dysrhythmia prior to the catheter ablation.
 Flecainide, propafenone, amiodarone, • During the ablation procedure, defibrillation pads, an
dofetilide, or sotalol may be given prior to automatic blood pressure cuff, and a pulse oximeter are
cardioversion to enhance the success of used.
cardioversion and maintain sinus rhythm • The patient is usually given moderate sedation and IV
(January et al., 2014). heparin to reduce the risk of periprocedural
 Because atrial function may be impaired for thromboembolism.
several weeks after cardioversion, warfarin is • Immediately post-ablation, the patient is monitored
indicated for at least 4 weeks after the for another 30 to 60 minutes and then retested to
procedure (January et al., 2014). Repeated ensure that the dysrhythmia does not recur.
attempts at electrical cardioversion may be • Successful ablation is achieved when the dysrhythmia
made, following administration of an cannot be induced.
antiarrhythmic medication. MAJOR RISKS OF CATHETER ABLATION INCLUDE:
CARDIAC RHYTHM THERAPIES  AV block,
Atrial fibrillation that does not respond to medications  pericardial tamponade,
or electrical cardioversion may be treated by cardiac  phrenic nerve injury,
rhythm therapies, including  stroke,
❑ catheter ablation,  hematoma,
❑ maze or mini-maze procedure, or  retroperitoneal bleeding,
❑ convergent procedure.  pulmonary vein stenosis, and
CATHETER ABLATION  atrioesophageal fistulas
► Therapy Catheter ablation destroys specific cells that  Obstructive sleep apnea is one known risk
are the cause of a tachydysrhythmia. factor associated with the recurrence of atrial
► Catheter ablation is performed most often today for fibrillation after catheter ablation (Shukla, Aizer,
atrial fibrillation, although it may also be useful in Holmes, et al., 2015).
treating atrioventricular nodal reentry tachycardia NURSING MANAGEMENT
(AVNRT) and recurrent ventricular tachycardia (VT). • Postprocedural care on a step-down unit for the
• Recent evidence demonstrates that the pathogenesis patient who has had ablation is similar to the nursing
of atrial fibrillation is associated with intrinsic cardiac management of a patient who has had a cardiac
autonomic nervous system activity to the pulmonary catheterization;
veins (Stavrakis et al., 2015). • the patient is monitored closely to ensure recovery
• Ablation involves a procedure similar to a cardiac from sedation.
catheterization; however, in this instance, a special • Postprocedural nursing interventions include frequent
catheter is advanced at or near the origin of the monitoring for dysrhythmias and for signs and
dysrhythmia, where high-frequency, low-energy sound symptoms of a stroke, vascular access site
waves are passed through the catheter, causing thermal complications, and fluid imbalance (Hoke & Steletsky,
injury, localized cell destruction, and scarring. 2015).
•The tissue damage is more specific to the dysrhythmic • Because of the prolonged time required for the
tissue, with less trauma to the surrounding cardiac procedure as well as the time needed in bed to obtain
tissue.
hemostasis at the vascular access site, it is not unusual same manner as atrial fibrillation (January et al.,
for the patient to have back discomfort. 2014).
• In addition to administering any pain medications, the  Electrical cardioversion is often successful in
nurse may help to alleviate this pain by placing rolled converting atrial flutter to sinus rhythm.
towels under the patient’s knees and waist VENTRICULAR DYSRHYTHMIAS VENTRICULAR
ATRIAL FLUTTER DYSRHYTHMIAS ORIGINATE FROM FOCI WITHIN THE
 Atrial flutter occurs because of a conduction VENTRICLES; THESE MAY INCLUDE:
defect in the atrium and causes a rapid, regular ❑ premature ventricular complexes
atrial impulse at a rate between 250 and 400 ❑ VT
bpm. ❑ ventricular fibrillation, and
 Because the atrial rate is faster than the AV ❑ idioventricular rhythms.
node can conduct, not all atrial impulses are ► Technically, ventricular asystole is characterized by
conducted into the ventricle, causing a an absence of rhythm formation.
therapeutic block at the AV node. \ PREMATURE VENTRICULAR COMPLEX
 This is an important feature of this dysrhythmia. • A PVC is an impulse that starts in a ventricle and is
If all atrial impulses were conducted to the conducted through the ventricles before the next
ventricle, the ventricular rate would also be 250 normal sinus impulse.
to 400 bpm, which would result in ventricular • PVCs can occur in healthy people, especially with
fibrillation, a life-threatening dysrhythmia. intake of caffeine, nicotine, or alcohol.
 Atrial flutter risk factors mirror those for atrial • PVCs may be caused by cardiac ischemia or infarction,
fibrillation (Fuster et al., 2011) increased workload on the heart (e.g., heart failure and
tachycardia), digitalis toxicity, hypoxia, acidosis, or
electrolyte imbalances, especially hypokalemia.
• In a rhythm referred to as bigeminy, every other
complex is a PVC.
• In trigeminy, every third complex is a PVC, and in
quadrigeminy, every fourth complex is a PVC.
•The patient may feel nothing or may say that the heart
“skipped a beat.”
• The effect of a PVC depends on its timing in the
MEDICAL MANAGEMENT cardiac cycle and how much blood was in the ventricles
 Atrial flutter can cause serious signs and when they contracted. Initial treatment is aimed at
symptoms, such as chest pain, shortness of correcting the cause.
breath, and low blood pressure. MEDICAL MANAGEMENT
 Medical management involves the use of vagal • PVCs usually are not serious.
maneuvers or a trial administration of • PVCs that are frequent and persistent may be treated
adenosine, which causes sympathetic block and with amiodarone or sotalol, but long-term
slowing of conduction through the AV node. pharmacotherapy for only PVCs is not usually indicated.
 This may terminate the tachycardia; optimally, • In patients with an acute MI, studies have found that
it will facilitate visualization of flutter waves for PVCs are not associated with sudden cardiac death and
diagnostic purposes. do not warrant more aggressive therapy (Mann et al.,
 Adenosine is given intravenously by rapid 2015).
administration, and immediately followed by a • PVCs are not considered a warning for ensuing VT.
20-mL saline flush and elevation of the arm with • However, a recent study reported a higher frequency
the IV line to promote rapid circulation of the of PVCs preceded the development of cardiomyopathy,
medication. with an increased incidence of heart failure and
 Atrial flutter is treated with antithrombotic increased mortality (Dukes, Dewland, Vittinghoff, et al.,
therapy, rate control, and rhythm control in the 2015)
 • Procainamide may be used for monomorphic stable
VT in patients who do not have acute MI or severe HF
(Link et al., 2015).
• IV amiodarone is the medication of choice for a
patient with impaired cardiac function or acute MI. •
Sotalol may also be considered for stable monomorphic
VT.
• Although lidocaine had been the medication most
commonly used for immediate, short-term therapy,
especially for patients with impaired cardiac function, it
has no proven short- or long-term efficacy in cardiac
arrest (Link et al., 2015).
VENTRICULAR TACHYCARDIA ► CARDIOVERSION is the treatment of choice for
► VT is defined as three or more PVCs in a row, monophasic VT in a symptomatic patient.
occurring at a rate exceeding 100 bpm. ► DEFIBRILLATION is the treatment of choice for
► The causes are similar to those of PVC. pulseless VT.
► Patients with larger MIs and lower ejection fractions ► Any type of VT in a patient who is unconscious and
are at higher risk of lethal VT. without a pulse is treated in the same manner as
► VT is an emergency because the patient is nearly ventricular fibrillation: immediate defibrillation is the
always unresponsive and pulseless. action of choice.
► The patient’s tolerance or lack of tolerance for this ► For long-term management, patients with an
rapid rhythm depends on the ventricular rate and ejection fraction less than 35% should be considered for
severity of ventricular dysfunction. an implantable cardioverter defibrillator (ICD).
► However, hemodynamic stability does not predict • Those with an ejection fraction greater than 35% may
mortality risk (Mann et al., 2015) be managed with amiodarone.
• A small percentage of patients with VT have
structurally normal hearts and respond well to
medications and catheter ablation, and they have an
excellent prognosis (Russo, Stainback, Bailey, et al.,
2013).
MEDICAL MANAGEMENT
• If the ventricular rate is above 200 bpm, then the
 Several factors determine the initial treatment,
presence of an accessory pathway should be suspected.
including the following:
• If the ventricular rhythm is irregular, atrial fibrillation
 identifying the rhythm as monomorphic (having
should be suspected and treated appropriately (Mann
a consistent QRS shape and rate) or
et al., 2015)
polymorphic (having varying QRS shapes and
►TORSADES DE POINTES is a polymorphic VT preceded
rhythms),
by a prolonged QT interval, which could be congenital
 determining the existence of a prolonged QT
or acquired.
interval before the initiation of VT,
COMMON CAUSES INCLUDE:
 any comorbidities, and
► central nervous system disease;
 ascertaining the patient’s heart function
► certain medications (e.g., ciprofloxacin [Cipro],
(normal or decreased).
erythromycin [Zmax, Zithromax, Biaxin], haloperidol
• If the patient is stable, continuing the assessment,
[Haldol], lithium (Eskalith, Lithobid), methadone
especially obtaining a 12-lead ECG, may be the only
[Dolophine, Methadose]); or
action necessary.
► low levels of potassium, calcium, or magnesium.
• However, the patient may need antiarrhythmic
► Congenital QT prolongation is another cause.
medications, anti-tachycardia pacing, or direct
• Because this rhythm is likely to cause the patient to
cardioversion or defibrillation.
deteriorate and become pulseless, immediate
treatment is required and includes correction of any
electrolyte imbalance, such as administration of IV • Idioventricular rhythm commonly causes the patient
magnesium, and with IV isoproterenol (Isuprel) or to lose consciousness and experience other signs and
pacing if associated with bradycardia (Link et al., 2015) symptoms of reduced cardiac output.
VENTRICULAR FIBRILLATION • In such cases, the treatment is the same as for
► The most common dysrhythmia in patients with asystole and pulseless electrical activity (PEA) if the
cardiac arrest is ventricular fibrillation, which is a rapid, patient is in cardiac arrest or for bradycardia if the
disorganized ventricular rhythm that causes ineffective patient is not in cardiac arrest.
quivering of the ventricles. • Interventions include identifying the underlying cause;
► No atrial activity is seen on the ECG. administering IV epinephrine, atropine, and vasopressor
► The most common cause of ventricular fibrillation is medications; and initiating emergency transcutaneous
coronary artery disease and resulting acute MI. pacing.
► Other causes include untreated or unsuccessfully • In some cases, idioventricular rhythm may cause no
treated VT, cardiomyopathy, valvular heart disease, symptoms of reduced cardiac output.
several proarrhythmic medications, acid–base and VENTRICULAR ASYSTOLE
electrolyte abnormalities, and electrical shock. ► Commonly called flatline, ventricular asystole is
► Another cause is Brugada syndrome, in which the characterized by absent QRS complexes confirmed in
patient (frequently of Asian descent) has a structurally two different leads, although P waves may be apparent
normal heart, few or no risk factors for coronary artery for a short duration.
disease, and a family history of sudden cardiac death ► There is no heartbeat, no palpable pulse, and no
(Aizawa, Takatsuki, Sano, et al., 2013; Tokioka, Kusano, respiration.
Morita, et al., 2014). ► Without immediate treatment, ventricular asystole is
MEDICAL MANAGEMENT fatal.
► Ventricular fibrillation is always characterized by the
absence of an audible heartbeat, a palpable pulse, and
respirations.
► Because there is no coordinated cardiac activity,
cardiac arrest and death are imminent if the
dysrhythmia is not corrected.
► Early defibrillation is critical to survival, with
administration of immediate bystander *always check two different leads to confirm rhythm
cardiopulmonary resuscitation (CPR) until defibrillation MEDICAL MANAGEMENT
is available. • Ventricular asystole is treated the same as PEA,
► For refractory ventricular fibrillation, administration focusing on high-quality CPR with minimal interruptions
of amiodarone and epinephrine may facilitate the and identifying underlying and contributing factors. The
return of a spontaneous pulse after defibrillation (Link key to successful treatment is a rapid assessment to
et al., 2015) identify a possible cause, which is known as the Hs and
IDIOVENTRICULAR RHYTHM Ts:
► Idioventricular rhythm, also called ventricular escape  hypoxia,
rhythm, occurs when the impulse starts in the  hypovolemia,
conduction system below the AV node.  hydrogen ion (acid–base imbalance),
► When the sinus node fails to create an impulse (e.g.,  hypo- or hyperglycemia,
from increased vagal tone) or when the impulse is  hypo- or hyperkalemia,
created but cannot be conducted through the AV node  hyperthermia,
(e.g., due to complete AV block), the Purkinje fibers  trauma,
automatically discharge an impulse.  toxins,
 tamponade (cardiac),
MEDICAL MANAGEMENT  tension pneumothorax, or thrombus (coronary
or pulmonary)
• After the initiation of CPR, intubation and
establishment of IV access are the next recommended
actions, with no or minimal interruptions in chest
compressions
CONDUCTION ABNORMALITIES
► When assessing the rhythm strip, the underlying
rhythm is first identified (e.g., sinus rhythm, sinus
arrhythmia).
► Then, the PR interval is assessed for the possibility of SECOND-DEGREE ATRIOVENTRICULAR BLOCK, TYPE I
an AV block. (WENCKEBACH)
► AV blocks occur when the conduction of the impulse • Second-degree AV block, type I, occurs when there is a
through the AV nodal or bundle of His area is decreased repeating pattern in which all but one of a series of
or stopped. atrial impulses are conducted through the AV node into
► These blocks can be caused by medications (e.g., the ventricles (e.g., every four of five atrial impulses are
digitalis, calcium channel blockers, beta-blockers), Lyme conducted).
disease, myocardial ischemia and infarction, valvular • Each atrial impulse takes a longer time for conduction
disorders, cardiomyopathy, endocarditis, or myocarditis than the one before, until one impulse is fully blocked.
(Mann et al., 2015). • Because the AV node is not depolarized by the
► If the AV block is caused by increased vagal tone blocked atrial impulse, the AV node has time to fully
(e.g., long-term athletic training, sleep, coughing, repolarize so that the next atrial impulse can be
suctioning, pressure above the eyes or on large vessels, conducted within the shortest amount of time.
anal stimulation), it is commonly accompanied by sinus
bradycardia.
► AV block may be temporary and resolve on its own,
or it may be permanent and require permanent pacing.
• The clinical signs and symptoms of a heart block vary
with the resulting ventricular rate and the severity of
any underlying disease processes.
• Whereas first-degree AV block rarely causes any
hemodynamic effect, the other blocks may result in
SECOND-DEGREE ATRIOVENTRICULAR BLOCK, TYPE II
decreased heart rate, causing a decrease in perfusion to
► Second-degree AV block, type II, occurs when only
vital organs, such as the brain, heart, kidneys, lungs, and
some of the atrial impulses are conducted through the
skin.
AV node into the ventricles.
• A patient with third-degree AV block caused by
digitalis toxicity may be stable; another patient with the
same rhythm caused by acute MI may be unstable.
• Health care providers must always keep in mind the
need to treat the patient, not the rhythm.
• The treatment is based on the hemodynamic effect of
the rhythm
FIRST-DEGREE ATRIOVENTRICULAR BLOCK
► First-degree AV block occurs when all the atrial
impulses are conducted through the AV node into the
ventricles at a rate slower than normal.
THIRD-DEGREE ATRIOVENTRICULAR BLOCK
•Third-degree AV block occurs when no atrial impulse is
conducted through the AV node into the ventricles.
• In third-degree AV block, two impulses stimulate the
heart: one stimulates the ventricles, represented by the
QRS complex, and one stimulates the atria, represented ► The choice of medication depends on the specific
by the P wave. dysrhythmia and its duration, the presence of structural
• P waves may be seen, but the atrial electrical activity heart disease (e.g., heart failure), and the patient’s
is not conducted down into the ventricles to cause the response to previous treatment.
QRS complex, the ventricular electrical activity. ► The nurse is responsible for monitoring and
• Having two impulses stimulate the heart results in a documenting the patient’s responses to the medication
condition referred to as AV dissociation, which may also and for ensuring that the patient has the knowledge
occur during VT and ability to manage the medication regimen.
• If medications alone are ineffective in eliminating or
decreasing the dysrhythmia, certain adjunctive
mechanical therapies are available.
• The most common therapies are elective
cardioversion and defibrillation for acute
tachydysrhythmia, and implantable devices
(pacemakers for bradycardias and ICDs for chronic
tachydysrhythmias).
MEDICAL MANAGEMENT OF CONDUCTION • Surgical treatments, although less common, are also
ABNORMALITIES available.
► Based on the cause of the AV block and the stability • The nurse is responsible for assessing the patient’s
of the patient, treatment is directed toward increasing understanding of and response to mechanical therapy,
the heart rate to maintain a normal cardiac output. as well as the patient’s self-management abilities.
► If the patient is stable and has no symptoms, no • The nurse explains that the purpose of the device is to
treatment may be indicated or it may simply consist of help the patient lead a life that is as active and
decreasing or eliminating the cause (e.g., withholding productive as possible.
the medication or treatment). CARDIOVERSION AND DEFIBRILLATION
► If the causal medication is necessary for treating ► Cardioversion and defibrillation are used to treat
other conditions and no effective alternative is tachydysrhythmias by delivering an electrical current
available, pacemaker implantation may be indicated. that depolarizes a critical mass of myocardial cells.
► The initial treatment of choice is an IV bolus of ► When the cells repolarize, the SA node is usually able
atropine, although it is not effective in second-degree to recapture its role as the heart’s pacemaker.
AV block, type II, or third-degree AV block. ► The same type of device, called a defibrillator, is used
• If the patient does not respond to atropine, has for both cardioversion and defibrillation.
advanced AV block, or has had an acute MI, temporary ► The electrical voltage required to defibrillate the
transcutaneous pacing may be started. heart is usually greater than that required for
• If the patient has no pulse, treatment is the same as cardioversion and may cause more myocardial damage.
for ventricular asystole (Link et al., 2015). • Only biphasic types of defibrillators are now
• A permanent pacemaker may be necessary if the manufactured; these deliver an electrical charge from
block persists. one paddle that then automatically redirects its charge
ADJUNCTIVE MODALITIES AND MANAGEMENT back to the originating paddle.
► Dysrhythmia treatments depend on whether the • Because the delivery of the electrical charge varies
disorder is acute or chronic, as well as on the cause of among devices, the manufacturer’s recommended dose
the dysrhythmia and its actual or potential should be followed for the first and subsequent
hemodynamic effects. defibrillations (Link et al., 2015)
► Acute dysrhythmias may be treated with medications • The electrical current may be delivered externally
or with external electrical therapy (emergency through the skin with the use of paddles or with
defibrillation, cardioversion, or pacing). conductor pads.
► Many antiarrhythmic medications are used to treat • The paddles or pads may be placed on the front of the
atrial and ventricular tachydysrhythmias. chest (standard placement), or one pad may be placed
on the front of the chest and the other pad placed
under the patient’s back just left of the spine • When the synchronizer is on, no electrical current is
(anteroposterior placement). delivered if the defibrillator does not discern a QRS
•Defibrillator multifunction conductor pads contain a complex.
conductive medium and are connected to the • Therefore, it is important to ensure that the patient is
defibrillator to allow for hands-off defibrillation. connected to the monitor and to select a lead (not
• This method reduces the risk of touching the patient “paddles”) that has the most appropriate sensing of the
during the procedure and increases electrical safety. QRS.
• Automated external defibrillators (AEDs), which are • Because there may be a short delay until recognition
now found in many public areas, use this type of of the QRS, the discharge buttons of an external manual
delivery for the electrical current. defibrillator must be held down until the shock has
• Whether using pads or paddles, the nurse must been delivered.
observe two safety measures. • In most monitors, the synchronization mode must be
• First, good contact must be maintained between the reactivated if the initial cardioversion was ineffective
pads or paddles and the patient’s skin (with a and another cardioversion is needed (i.e., the device
conductive medium between them) to prevent defaults to unsynchronized defibrillation mode).
electrical current from leaking through the air (arcing) If the cardioversion is elective and the dysrhythmia has
when the defibrillator is discharged. lasted longer than 48 hours, anticoagulation for a few
• Second, no one is to be in contact with the patient or weeks before cardioversion may be indicated (January
with anything that is touching the patient when the et al., 2014).
defibrillator is discharged, to minimize the chance that ► Digoxin is usually withheld for 48 hours before
electrical current is conducted to anyone other than the cardioversion to ensure the resumption of sinus rhythm
patient. with normal conduction.
► The patient is instructed not to eat or drink for at
least 4 hours before the procedure.
► Gel-covered paddles or conductor pads are
positioned front and back (anteroposteriorly) for
cardioversion.
• Before cardioversion, the patient receives moderate
sedation IV as well as an analgesic medication or
anesthesia.
ELECTRICAL CARDIOVERSION • Respiration is then supported with supplemental
► Electrical cardioversion involves the delivery of a oxygen delivered by a bag-valve mask device with
“timed” electrical current to terminate a suction equipment readily available.
tachydysrhythmia. • Although patients rarely require intubation,
► In cardioversion, the defibrillator is set to equipment is nearby in case it is needed.
synchronize with the ECG on a cardiac monitor so that • The amount of voltage used varies from 50 to 360
the electrical impulse discharges during ventricular joules, depending on the defibrillator’s technology, the
depolarization (QRS complex). type and duration of the dysrhythmia, and the size and
► The synchronization prevents the discharge from hemodynamic status of the patient (Link et al., 2015).
occurring during the vulnerable period of repolarization INDICATIONS OF A SUCCESSFUL RESPONSE ARE:
(T wave), which could result in VT or ventricular ❖ conversion to sinus rhythm,
fibrillation. ❖ adequate peripheral pulses, and
► The ECG monitor connected to the external ❖ adequate blood pressure.
defibrillator usually displays a mark or line that indicates ► Because of the sedation, airway patency must be
sensing of a QRS complex. maintained and the patient’s state of consciousness
• Sometimes the lead and the electrodes must be assessed.
changed for the monitor to recognize the patient’s QRS ► Vital signs and oxygen saturation are monitored and
complex. recorded until the patient is stable and recovered from
sedation and analgesic medications or anesthesia.
► ECG monitoring is required during and after
cardioversion.
DEFIBRILLATION
► Defibrillation is used in emergency situations as the
treatment of choice for ventricular fibrillation and
pulseless VT, the most common cause of abrupt loss of
cardiac function and sudden cardiac death.
► Defibrillation is not used for patients who are
conscious or have a pulse.
► The energy setting for the initial and subsequent
shocks using a monophasic defibrillator should be set at
360 joules (Link et al., 2015).
► The energy setting for the initial shock using a
biphasic defibrillator may be set at 150 to 200 joules,
with the same or an increasing dose with subsequent
shocks (Link et al., 2015).
► The sooner defibrillation is used, the better the
survival rate (Kronick, Kurz, Lin, et al., 2015; Link et al.,
2015).
• Several studies have demonstrated that early
defibrillation performed by lay people in a community
setting can increase the survival rate (Kronick et al.,
2015).
• If immediate CPR is provided and defibrillation is
performed within 5 minutes, more adults in ventricular
fibrillation may survive with intact neurologic function
(Link et al., 2015).
• The availability and the use of AEDs in public places,
especially exercise facilities, shorten the interval from
collapse to rhythm recognition and defibrillation, which
can significantly increase survival (Page, Husain, White,
et al., 2013)
► Epinephrine is given after initial unsuccessful
defibrillation to make it easier to convert the
dysrhythmia to a normal rhythm with the next
defibrillation.
► This medication may also increase cerebral and
coronary artery blood flow.
► Antiarrhythmic medications such as amiodarone,
lidocaine, or magnesium may be given if ventricular
dysrhythmia persists.
► This treatment with continuous CPR, medication
administration, and defibrillation continues until a
stable rhythm resumes or until it is determined that the
patient cannot be revived.
Pls do self-study on:
► Electrophysiology Studies
► Pacemaker Therapy
► Implantable Cardioverter Defibrillator (ICD