Professional Documents
Culture Documents
Compiled By:
DEPARTEMENT OF CARDIOLOGY
H. ADAM MALIK GENERAL HOSPITAL
FACULTY OF MEDICINE
SUMATERA UTARA UNIVERSITY
MEDAN
2013
TABLE OF CONTENTS
REFERENCES ........................................................................ 80
PREFACE
Praise God for his gratitude and blessings so that we can finally be able to
complete the case report entitled "Supraventricular Tachycardia" well. This case report is
written in order to fulfill the duty of senior clinical assistant of clinical rotation in
pediatric department. This paper is expected to increase the knowledge and insight,
especially about SVT.
The authors would also like to thank the supervisor, dr.Nizam Akbar, Sp.JP (K) to
give guidance, suggestions, and assessment for this case report.
Last of all, we realize despite the effort we have put into this case report, there
are still errors and flaws in our work. Therefore we encourage and welcome suggestion,
advice and critics that will facilitate the improvement of this paper. Hopefully this
scientific work can contribute to development of medical science in particular.
CHAPTER I
INTRODUCTION
1.1. Background
In the last few years the fundamental mechanism of each has been
elucidated and many have been shown to be based upon reentry whether
anatomical or functional. As the ultimate inmanagement strategies, curative
radiofrequency ablation has forced a reappraisal of what the aim of treatment
should be and its success has focused attention on our new knowledge of
arrhythmia anatomy. Yet there is much that remains to be established.
1.2. Objective
The aim of this study is to explore more about the theoritical aspects on
arrhythmia supraventricular tachycardia, and to integrate the theory and
application of supraventricular tachycardia cases in daily life.
CHAPTER II
LITERATURE REVIEW
The heart contains muscle cells (fibers) that produce and distribute
excitation impulses (conducting system), as well as working myocardium, which
responds to the excitation by contracting. Contrary to the situation in skeletal
muscle, excitation originates within the organ (autorhythmicity or autonomy of
the heart). Atrial and ventricular myocardium each consists functionally of a
syncytium, i.e., the cells are not insulated from one another but connected through
gap junctions. A stimulus that originates somewhere within the atria or ventricles
thus always leads to complete contraction of both atria or of both ventricles,
respectively (all-or-nothing contraction).10
Normal excitation of the heart originates within the sinus node, the hearts
pacemaker. Excitation spreads from there through both atria to the
atrioventricular node (AV node) and from there, via the His bundle and its two
branches, reaches the Purkinje fibers, which transmit the excitation to the
ventricular myocardium.
The potential in the cells of the sinus node is a pacemaker potential. It has
no constant resting potential, but rises after each repolarization. The most negative
value of the latter is called maximal diastolic potential (MDP: 70 mV). It rises
steadily until the threshold potential (TP:. 40 mV) is reached once more and an
action potential (AP) is again triggered. The following changes in ionic
conductance of the plasma membrane and thus of ionic currents cause these
potentials.
Once the TP has been reached, gCa now rises relatively rapidly, the
potential rising more steeply so that an increased influx of Ca2+ (ICa) produces
the upstroke of the AP. While the potential overshoots to positive values, leading
to an outward K+ flux IK, the pacemaker cell is again repolarized to the MDP.
Each AP in the sinus node normally results in a heart beat, i.e., the impulse
frequency of the pacemaker determines the rate of the heart beat. The rate is lower
if
The rise of the slow depolarization becomes less steep
The TP becomes less negative
The MDP becomes more negative so thatspontaneous depolarization
begins at a lower level
Repolarization in an AP starts later or is slower.
All parts of the excitation/conduction system have the capacity of
spontaneous depolarization, but the sinus node plays the leading role in normal
cardiac excitation (sinus rhythm is ca. 7080 beats per minute). The reason for
this is that the other parts of the conduction system have a lower intrinsic
frequency than the sinus node
Excitation starting from the sinus node will thus arrive at more distal parts
of the conducting system, before their spontaneous depolarization has reached the
TP. However, if conduction of the sinus impulse is interrupted, the intrinsic
frequency of more distal parts of the conduction system take over and the heart
then beats in AV rhythm (4060 beats per minute) or, in certain circumstances, at
the even lower rate of the so-called tertiary (ventricular) pacemakers (2040 beats
per minute).
The more subordinate (more peripheral) parts of the conduction system are
acted on chronotropically only by sympathetic fibers, which gives the latter a
decisive influence in any possible takeover of pacemaker function by the AV node
or tertiary pacemakers.
The parasympathetic fibers of the left vagus slow down while the
sympathetic fibers accelerate impulse transmission in the AV node (negative or
positive dromotropic action, respectively). The main influence is on the MDP and
the steepness of the AP upstroke. Changes in gK and gCa play an important role
here as well.
The term arrhythmia refers to any disturbance in the rate, regularity, site of
origin, or conduction of the cardiac electrical impulse. An arrhythmia can be a
single aberrant beat (or even a prolonged pause between beats) or a sustained
rhythm disturbance that can persist for the lifetime of the patient.
More serious are symptoms of decreased cardiac output, which can occur
when the arrhythmia compromises cardiac function. Among these are light-
headedness and syncope (a sudden faint). Rapid arrhythmias can increase the
oxygen demands of the myocardium and cause angina (chest pain). The sudden
onset of an arrhythmia in a patient with underlying cardiac disease can also
precipitate congestive heart failure.
Sometimes, the first clinical manifestation of an arrhythmia is sudden
death. Patients in the throes of an acute myocardial infarction are at a greatly
increased risk for arrhythmic sudden death, which is why they are hospitalized in
cardiac care units where their heart rate and rhythm can be continuously
monitored.
2.2.2.Pathophysiology of Arrythmia
The heart is capable of only five basic types of rhythm disturbances:9
The electrical activity follows the usual conduction pathways we have
already outlined, but it is either too fast, too slow, or irregular. These are
arrhythmias of sinus origin.
The electrical activity originates from a focus other than the sinus node.
These are called ectopic rhythms.
The electrical activity is trapped within an electrical racetrack whose shape
and boundaries are determined by various anatomic or electrical
myocardial features. These are called reentrant arrhythmias. They can
occur anywhere in the heart.
The electrical activity originates in the sinus node and follows the usual
pathways but encounters unexpected blocks and delays.
The electrical activity follows accessory conduction pathways that bypass
the normal ones, providing an electrical shortcut, or short circuit. These
arrhythmias are termed preexcitation syndromes.
Disorders of rhythm (arrhythmias or dysrhythmias) are changes in the
formation and/or spread of excitation that result in a changed sequence of atrial or
ventricular excitation or of atrioventricular transmission. They can affect rate,
regularity, or site of action potential formation.12
2. Common Arrhythmia
Location Bradyarrhythmias Tachyarrythmias
SA nodes Sinus Bradycardia Sinus tachycardia
Sick sinus syndromes
Atria Atrial premature beats
Atrial flutter
Atrial fibrillation
PSVT
Ventricular tachycardia
Torsades de pointes
Ventricular fibrilation
2.3. Pathophysiology of Supraventricular Tachicardia (SVT)
Supraventricular tachycardias (SVTs) include all tachyarrhythmias that
either originate from or incorporate supraventricular tissue in a reentrant circuit.
The ventricular rate may be the same or less than the atrial srate, depending on the
atrioventricular (AV) nodal conduction.
PSVT is an absolutely regular rhythm, with a rate usually between 150 and
250 beats per minute. There are several types of PSVT. The most common type is
driven by a reentrant circuit looping within the AV node. Retrograde P waves may
sometimes be seen in leads II or III, but your best chance would be to look in lead
V1 for what is called a pseudo-R', a little blip in the QRS complex that represents
the superimposed P wave. More often than not, however, the P waves are so
buried in the QRS complexes that they cannot be identified with any confidence.
As with most supraventricular arrhythmias, the QRS complex is usually narrow.
Another type of PSVT occurs in patients with anomalous conduction pathways
and will be discussed in Chapter 5.
Early descriptions of the AV nodal tissue came from Albert Kent more than
a century ago.12 The AV node is located epicardially, just underlying the right
atrial epicardium, anterior to the nodal artery and between the coronary sinus and
medial tricuspid valve leaflet. It comprises three different components: the
transitional cell zone, the compact node, and the penetrating bundle of His (. The
compact AV node refers to the most easily histologically distinguishable tissue
located at the apex of the triangle of Koch (TOK). A zone of transitional cells is
interposed between the compact node and the atrial myocardium. Transitional
cells enter the triangle of Koch to join the compact node superiorly, inferiorly,
posteriorly, and from the left. At its distal extent, the AV node is distinguished
from the penetrating bundle, not so much by cellular characteristics as by the
presence of a fibrous collar surrounding the specialized cells. Systematic anatomic
investigation of the AV node in patients with AVNRT is lacking. No obvious
histologic abnormalities have been identified among patients with AVNRT versus
patients without AVNRT. Several recent autopsy studies have reported that the
sites of successful slow pathway ablation were clearly away from the histologic
compact AV node, approximately 1 or 2 cm inferior and posterior to it.10
before termination (cool down), does not respond to vagal maneuvers, and often displays an incessant nature. Focal atrial tachycardia caused
by reentry generally can be induced by programmed electrical stimulation. During the arrhythmia the criteria for either manifest or concealed
entrainment usually can be demonstrated, and the interval between the initiating beat and the first beat of the atrial tachycardia is usually
inversely related. Triggered activity is thought to be caused by delayed afterdepolarizations, and includes digitalis toxicity, but catecholamines
Classification
The degree of shortening of the P-R interval and the extent of ventricular
preexcitation depend on several factors, including location of the accessory
pathway, the relationship between antegrade conduction times and refractory
periods of the AV bypass tract, and the normal AV conduction system. A bypass
tract that crosses the AV groove in the left lateral region may also result in
inapparent preexcitation and minimal P-Rinterval shortening during sinus
rhythm due to greater interatrial distance for impulse propagation from the sinus
node to this site of atrial input into the AP. Conversely, an AP on the right side is
more likely to demonstrate marked preexcitation. Preexcitation may be less
apparent during sinus tachycardia, when sympathetic tone is high and vagal tone
low, resulting in faster AV node conduction time than that in the AP. On the other
extreme, during conditions of slowed conduction through the AV node either by
intrinsic nodal factors, withdrawal of sympathetic tone, or increased vagal tone,
the amount of preexcitation apparent on the 12-lead ECG is maximized because of
relatively greater conduction through the AP. Rapid intravenous administration of
adenosine causing blocking or slowing of AV node conduction and exposing the
anterograde AP conduction has been used as a diagnostic maneuver. The degree of
preexcitation can also be enhanced with atrial pacing directly over the AP,
eliminating the intraatrial conduction delay from the sinus node to the atrial
insertion site of AP.
2. Sinus tachycardia
Sinus tachycardia is usually a response to physiological stress such as
exercise or anxiety, and it may be the result of an abnormally heightened
sympathetic tone. Abnormal pathological causes include fever, hypotension,
anemia, thyrotoxicosis, hypovolemia, pulmonary emboli, myocardial ischemia,
and shock. Nicotine, caffeine, alcohol, and some medications (sympathetic
agonists or parasympatholytic agents) are frequently the underlying cause of sinus
tachycardia.The QRS complexes are preceded by P waves of normal morphology,
duration, and axis. Sinus tachycardia alone does not require any treatment, but the
underlyingcause should be determined.
3. Atrial tachycardia
Atrial tachycardia can occur in the presence of cardiac or pulmonary
disease at a rate varying from 140 to 240 bpm. P-wave morphology is generally
different from that during SR, but the PQRS relationship remains 1:1. Some
atrial tachycardias are catecholamine sensitive; in this case, a b-blocker
isappropriate therapy. Curative radiofrequency ablation of atrial tachycardia is e
fective in 70% of cases. For refractory cases, creation of complete heart block by
radiofrequency catheter ablation with implantation of a permanent dual-chamber
pacemaker provides control of the rate and avoids drug toxicity.13
4. Atrial Fibrillation
Atrial fibrillation (AF) is characterized by disorganized atrial electrical activation
and uncoordinated atrial contraction. The surface electrocardiogram
characteristically demonstrates rapid fibrillatory waves with changing
morphology and rate and a ventricular rhythm that is irregularly irregular. Most
AF originates in one or more of the pulmonary veins (PVs), and because of
disparate atrial refractory periods the rapid firing focus in the left atrium (LA)
cannot be conducted in a 1:1 manner to the right atrium, which leads to
fibrillatory conduction. Additionally, it is thought that a driver, perhaps a reentrant
focus in the LA, acts in a similar manner. Although the ECG has the characteristic
appearance of disorganized atrial activation, further analysis may reveal what
appears to be a regular rapid atrial rhythm, often seen best in lead. Careful
measurement will disclose variability in the P-P intervals, and this should not be
misinterpreted as atrial flutter, or so-called atrial fibrillation-flutter. Atrial flutter,
as discussed later, is a very regular rhythm with monotonous repetition of similar
P waves with each cycle.
The ventricular rate during AF can be quite variable, and depends on autonomic
tone, the electrophysiologic properties of the atrioventricular (AV) node, and the
effects of medications that act on the AV conduction system. The ventricular rate
may be very rapid (>300 beats/min) in patients with the Wolff-Parkinson-White
(WPW) syndrome, with conduction over accessory pathways (wide preexcited
QRS complexes) having short antegrade refractory periods. A regular, slow
ventricular rhythm during AF suggests a junctional rhythm, either as an escape
mechanism with complete AV block or as an accelerated junctional pacemaker.
5. Atrial Flutter
There are several types of atrial flutter, all having rapid, regular atrial
rates, generally 240 to 340 beats/min, because of a reentrant mechanism in the
atria. Typical, also called counterclockwise atrial flutter is characterized by
negative sawtooth flutter waves and reverse typical, also called atypical or
clockwise atrial flutter by positive flutter waves in ECG leads II, III, and aVF
These two atrial flutter types share the same right atrial reentrant circuit. In typical
atrial flutter, the reentrant wavefront travels up the interatrial septum and down
the right atrial free wall, and vice versa in reverse atypical atrial flutter. Both types
use the sub-Eustachian or cavotricuspid isthmus (i.e., the isthmus between the
tricuspid annulus on one side and the inferior vena cavaEustachian ridge-
coronary sinus on the other) as a part of the reentrant circuit,
More recently, left atrial flutter, double wave reentry atrial flutter (two
reentrant wave fronts simultaneously circulating in the same reentrant circuit),
lower loop and upper loop reentry atrial flutter (variants of typical atrial flutter),
and atrial flutter caused by reentry around a surgical incision (lesion reentry) have
also been described. Left atrial flutter may be caused by reentry around the mitral
valve annulus, the pulmonary veins, or a region of block (usually anatomic) in the
LA, such as secondary to the presence of a scar caused for any reason, including
prior surgery or an ablation line. Atrial flutter caused by a surgical lesion is
common in patients after repair of congenital heart defects that involve one or
more right atrial free wall incisions. It has now been shown that most
(approximately two thirds) recurrent atrial flutter in patients following open heart
surgical repair of congenital heart defects indeed uses the classical atrial flutter
reentrant circuit.
1
Tachyarrythmias
When the heart rate is 100 bpm for three beats or more, a tachyarrhythmia
is present. Tachyarrhythmias result from one of the three mechanisms: enhanced
automaticity, reentry, or triggered activity. Tachyarrhythmias are categorized into
those that arise above the ventricles (supraventricular) and those that arise within
the ventricles.1
1. Regular Rhythm
A. Sinus Tachycardia
Sinus tachycardia is characterized by an SA node discharge rate
100 bpm to 180 bpm) with normal P waves and QRS complexesThis
rhythm most often results from increased sympathetic and/or decreased
vagal tone. Sinus tachycardia is an appropriate physiologic response to
exercise. However, it may also result from sympathetic stimulation in
pathologic conditions, including fever, hypoxemia, hyperthyroidism,
hypovolemia, and anemia. In disease states, sinus tachycardia is
usually a sign of the severity of the primary pathophysiologic process
and treatment should be directed at the underlying cause.2
B. Atrial Flutter
Atrial flutter is characterized by rapid, regular atrial activity at a
rate of 180 to 350 bpm. Many of these fast impulses reach the AV node
during its refractory period and do not conduct to the ventricles,
resulting in a slower ventricular rate, often an even fraction of the
atrial rate. Thus, if the atrial rate is 300 bpm and 2:1 block occurs at
the AV node (i.e., every other atrial impulse finds the AV node
refractory), the ventricular rate is 150 bpm. Because vagal maneuvers
(e.g., carotid sinus massage) decrease AV nodal conduction, they
increase the degree of block, temporarily slowing the ventricular rate,
which allows better visualization of the underlying atrial activity.
2. Irreguler Rhytm
A. Atrial Fibrillation
AF is a chaotic rhythm with an atrial rate so fast (350 to 600
discharges/min) that distinct P waves are not discernible on the ECG.
As with atrial fl utter, many of the atrial impulses encounter refractory
tissue at the AV node, allowing only some of the depolarizations to be
conducted to the ventricles in a very irregular fashion (indicated by a
characteristic irregularly irregular rhythm). The average ventricular
rate in untreated AF is approximately 140 to 160 bpm. Because
discrete P waves are not visible on the ECG, the baseline shows low-
amplitude undulations punctuated by QRS complexes and T waves.2
Multifocal atrial tachycardia. The rhythm is irregular and each QRS is preceded
by a P
wave of varying morphology.
Typically, the ECG shows rapid, irregular atrial activity, with, in the
case of normal atrioventricular conduction a rapid, irregular rhythm.
Characteristically, the former arrhythmia is found in middle-aged men and
begins at night, during rest, or after a meal. Catecholamine-sensitive atrial
fibrillation is less commonly encountered in clinical practice. The
arrhythmia is most often observed in young women. It is related to stress
and exercise, and can be provoked by caffeine and alcohol. Holter
recordings show the occurrence of the arrhythmia in the daytime, usually
in the morning, and preceded by an increase in sinus rate.1
Electrocardiographically, a supraventricular tachyarrhythmia is more likely
if the morphology of the QRS at the rapid rate
is similar to that on the patients ECG tracing obtained while in sinus
rhythm (i.e., the complex is widened because of an underlying bundle
branch block). Conversely, VT is more likely if:
there is no relationship between the QRS complexes and any observed P
waves (AV dissociation)
- the QRS complexes in each of the chest leads (V1 through V6) have a
similar appearance, with a dominant positive or negative defl ection
(i.e., there is concordance of the precordial QRS complexes).
- Other morphologic ECG features have been used to distinguish VT
from SVT with aberrancy, but the distinction is often very difficult.
Most patients with wide QRS tachycardiashould be managed as though
they have VT until proven otherwise.2
2.5. Differential Diagnose
In a less common scenario, some patients with SVT may present with
chronic cardiac failure and cardiomyopathy. In such cases, patients generally do
not experience palpitations during tachycardia and will have excessive heart rates
until cardiac decompensation occurs. The tachycardia in these patients likely takes
weeks or months to cause heart failure, depending on the patients heart rate and
on the amount of time that the patient experiences tachycardia episodes.
Ventricular dysfunction is usually reversible, even, to some degree, in patients
who have not been treated for long-standing tachycardia.
2.7. INTERPRETATION OF ECG FINDINGS IN PSVT
Most PSVTs are represented on ECGs as narrow QRScomplex
tachycardias, with the QRS duration being less than 90 ms (ie, normal QRS
duration). Tachycardia-contingent BBB (ie, aberrancy) is relatively frequent in
patients with PSVT. Many of these patients may have preexistent BBB,
interventricular conduction delays, or some other QRS abnormality. These
abnormalities carry over to the tachycardia.
Termination.
Tachycardias in which the last event at termination is a P wave are highly
unlikely to be atrial tachycardias. If such conditions were atrial
tachycardias, it would be necessary to postulate that the last atrial beat. Its
more logical to postulate that the block in the AV node caused the
tachycardia to terminate and, consequently, that the condition is an AV
nodedependent tachycardia. Although an atrial tachycardia almost always
terminates with a ventricular complex, this observation may not be helpful
in diagnosis because some AV nodedependent tachycardias also terminate
in this manner.
caused the block in the AV node.
1. Non- Pharmacology
Vagal Maneuvers
Massage of the carotid sinus stimulates baroreceptors, which trigger a
reflexive increase in the activity of the vagal nerve and sympathetic with- drawal,
slowing conduction through the atrioventricular node. If the physical examination
does not reveal a carotid bruit and there is no history suggesting carotid artery
disease, pressure may be applied at the level of the cricoid cartilage for about five
seconds with a firm circular movement. If the tachyarrhythmia persists, the
procedure may be repeated on the opposite side. Other approaches to increasing
vagal tone include having the patient perform a Valsalva maneuver or (primarily
in children) apply an ice pack to the face. A continuous 12-lead ECG recording of
the episode should be obtained during vagal maneuvers, since the way in which
arrhythmias end may provide clues to their mechanism.
2. Pharmacology
Adenosine
As with vagal maneuvers, treatment with intravenous adenosine has both
diagnostic and therapeutic value. Data from randomized trials show that
supraventricular tachycardia is terminated in 60 to 80 percent of patients treated
with 6 mg of adenosine and in 90 to 95 percent of those treated with 12 mg. In
patients with atrial tachycardias, adenosine causes a transient atrioventricular
nodal block or interrupts the tachycardia ECG monitoring is required during the
administration of adenosine, and resuscitation equipment should be available in
the event that the rare complications of bronchospasm or ventricular fibrillation
occur. Adenosine is contraindicated in heart-transplant recipients and should be
used cautiously in patients with severe obstructive lung disease. Adenosine is also
contraindicated in patients with tachycardia with a wide QRS complex (unless the
diagnosis of supraventricular tachycardia with aberrancy is certain).
Other Agents
If supraventricular tachycardia is refractory to adenosine or rapidly recurs,
clinical experience indicates that the tachycardia can usually be terminated by the
administration of intravenous verapamil or a beta-blocker. As a next step,
procainamide, ibutilide, propafenone, or flecainide can be given intravenously if
the patients blood pressure is stable.15 However, sequential trials with different
antiarrhythmic agents should be undertaken only after careful consideration of
their possible negative hypotensive, bradycardic, and proarrhythmic effects. At
any point, electrical cardioversion is an alternative, but this technique is generally
considered in patients in hemodynamically stable condition only if
atrioventricular nodal-blocking agents fail. Table 3 reviews medications used for
acute supraventricular tachycardia. These agents are contraindicated in patients
with severe hypotension, a history of heart block, or congestive heart failure.
Pharmacologic Therapy
Patients with recurrent episodes of supraventricular tachycardia without
preexcitation may be treated with prophylactic antiarrhythmic agents.
Pill-in-the-Pocket Approach
For patients with infrequent (i.e., no more than a few per year) but
prolonged (i.e., lasting more than one to two hours) episodes of supraventricular
tachycardia that are well tolerated hemodynamically, or for patients who have had
only a single episode of supraventricular tachycardia, another option is to
prescribe single-dose pharmacologic therapy (the pill in the pocket) to be taken
when needed for an arrhythmic event. Drugs administered in this fashion include
calcium-channel blockers (e.g., 40 to 160 mg of verapamil), exclusively for
patients without preexcitation; various betablockers; flecainide (100 to 300 mg);
and propafenone (150 to 450 mg). In one study, 80 percent of episodes of
supraventricular tachycardia were in- terrupted within two hours with a
combination of diltiazem and propanolol or with flecainide.
One to four catheter electrodes are introduced into the cavities of the heart
through femoral (or, alternatively, internal jugular or subclavian) venous access
after local anesthesia is administered. Radiofrequency current a low-voltage,
high-frequency (500 kHz) form of electrical energy used for electrocautery in
surgery is delivered through a catheter electrode to create small lesions through
thermal injury in the myocardial tissue, the conduction system, or both, which
have been identified as critical for mediating the cardiac arrhythmia. In patients
with arrhythmias mediated by an abnormal accessory pathway, the catheter is
positioned so that it is in contact with the pathway, and the application of
radiofrequency current blocks conduction over the accessory pathway within a
few seconds. For left-sided accessory pathways, a retrograde approach through the
femoral artery and the aortic valve can be used. Alternatively, a transseptal
puncture can be performed to gain access to the left atrium. Cryothermal ablation
is an effective approach in patients with atrioventricular (AV) nodal reentrant
tachycardia or an accessory pathway close to a His bundle because of the
reversibility of the initial effect and the negligible risk of AV block. Most ablation
procedures take one to three hours. Catheter ablation of supraventricular
tachycardia can be performed as a one-day outpatient procedure, or it may require
overnight hospitalization. Treatment with aspirin is often recommended for
several weeks after ablation that has been performed in the left side of the heart to
reduce the potential risk of emboli. Patients need no special follow-up after the
intervention.
Atrial Flutter
Atrial flutter constitutes approximately 15 percent of all supraventricular
arrhythmias and occurs in 25 to 35 percent of patients with atrial
fibrillation.1 Atrial flutter usually is more symptomatic than atrial
fibrillation because it is often associated with more rapid ventricular rates.
The electrical circuit causing the most common forms of atrial flutter is
anatomically well defined and can be interrupted readily with ablation near
the junction of the inferior vena cava and the right atrium.
Longterm success rates for ablation of typical forms of atrial flutter range
from 88 to 100 percent,14-19 and patients treated with ablation have
lower hospitalization rates than patients treated with antiarrhythmic drugs.
Complications from ablation occur at a rate of 2.5 to 3.5 percent and
include heart block, cardiac perforation with tamponade, thromboembolic
events, and myocardial infarction. Catheter ablation is recommended in
most cases of atrial flutter.
Atrial Fibrillation
Atrial fibrillation is the most common clinically significant arrhythmia,
with an estimated prevalence of 0.4 to 1.0 percent in the general
population. Atrial fibrillation is associated with an increased risk of stroke,
heart failure, and all-cause mortality. Management principles focus on
adequate anticoagulation (to prevent embolic stroke occurrence),
ventricular rate control measures (to prevent symptomatic and pathogenic
tachycardia), and in selected patients, rhythm control strategies (to restore
and maintain sinus rhythm).
Atrial fibrillation ablation seeks to establish and maintain sinus rhythm by
targeting the tissue interface between the pulmonary veins and the left
atrium, an anatomic region that plays a critical role in initiating and
perpetuating atrial fibrillation.
During catheter ablation of atrial fibrillation, a catheter ispassed
into the left atrium and is used to cauterize areas surrounding the orifices
of the pulmonary veins. The resulting scars prevent conductionof the extra
beats arising from the veins, which can trigger atrial fibrillation.
Patient Experience
Typically, a patient will present to his or her family physician with
palpitations. An externally worn, ambulatory ECG monitor commonly is
used to correlate symptoms of palpitations with a specific supraventricular
arrhythmia. These monitors can be worn for up to a month. If an
ambulatory monitor fails to identify a specific arrhythmia, an implantable
monitor can be inserted surgically to screen for arrhythmias for up to
several years. If and when a supraventricular arrhythmia is identified, the
patient is usually referred to a cardiologist, and subsequently, an
electrophysiologist. Ultimately, a decision is made regarding
pharmacologic rhythm control versus an electrophysiology study and
ablation.
During the procedure, the patient lies flat for several hours; the
exact length of time is dependent on the complexity of the arrhythmia.
AVNRT ablations tend to be shorter (less than three hours) than atrial
fibrillation ablations (which can last four to eight hours). During and after
the procedure, patients may have back pain and anxiety.
Chest pressure or pleuritic pain may be experienced during the delivery of
ablation energy (a relatively small percentage of the total procedural time).
On completion of the procedure, the catheters and sheaths are removed
from their insertion sites, and manual pressure is applied to achieve
hemostasis. Typically, the patient is discharged later the same day or the
next day. Full recovery typically takes two or three days, with longer
recuperation times for more complex procedures.
Radiation Exposure
As with cardiac catheterization and angioplasty, fluoroscopy is the
principal means of visualizing and modifying catheter position during an
electrophysiology study and arrhythmia ablation. The duration of
fluoroscopy (and thus, the degree of radiation exposure) varies depending
on the type and sophistication of the ablation procedure.
The measurement for radiation doses used in medical procedures,
including an electrophysiology study and ablation, is the millisievert
(mSv). Millisieverts can be converted into chest radiography equivalent
doses, which is the dose of radiation that is received from a single chest
radiograph. One chest radiography equivalent dose is 0.1 mSv.47 The
radiation doses for an electrophysiology study and ablation are estimated
to be 3.2 mSv (chest radiography equivalent dose = 32) and 15.2 mSv
(chest radiography equivalent dose = 152), respectively,48 with a range of
1.4 mSv (chest radiography equivalent dose = 14) to 49.75 mSv (chest
radiography equivalent dose = 497) for combined electrophysiology study
and ablation reported in several studies.
Presens status:
General state: moderate Sensorium: CM BP:90 /70 mmHg
HR : 101 x/i, irreguler RR: 20 x/i
Temperature: 35,8C Cyanosis : (-)
Ortopnu: (+) Dispnu: (-) Icterus: (+) Edema (-) Pale (-)
Physical Examination
Head : Eye : conjungtiva palpebra inferior anemia (+/+), icteric sclera (+/+),
isochoric pupil,
3 mm, Ear/Nose/Mouth normal in appearance
Neck : JVP : R-2 cmH2O
Thoracic wall :
Inspection : Symmetrical fusiformis
Palpation : Weakend in both lower lung. Ictus (+), anterior axillaris sinistra ICR
VII
Percussion : Dullness in both lower lung
Cardiac border : Superior range : ICR III mid clavicularis sinistra
Medial range : Linea parasternalis dekstra
Lateral range : Linea mid axilaris sinistra
Auscultation :
Heart : S1 (N) S2 (N) S3 (-) S4 (-) regular, HR 101x/irreguler
Murmur : (+), Type : PSM Grade : 3/6
Punctum maximum : anterior axillaris ICR VII Radiation : mid
axillaris
Lung : Respiratory sound : vesicular
Additional sound : ronchi (-/-) wheezing (-/-)
Abdominal : Palpation Hepar/Lien : Soepel, unpalpable acites (-)
Extremity : Superior : cyanosis (-) Clubbing : (-)
Inferior : edema (-) Arterial pulsation : (+/+)
Acral : warm
Carbohydrate Metabolism:
KGDS : 34,5 mg/dL
Kidney
Kreatinin 1.72 mg/dl ; Ureum 55 mg/dL
Elektrolit
Na/K/Cl : 131 mEq/L;6 mEq/L; 105 mEq/L
Differential Diagnosis :
- CHF fc III ec MR severe ec dd. RHD
Treatment :
- Bed Rest, semifowler
- O2 2-4L/i
- IVFD NaCl 0,9% 10 gtt/i (micro)
- Furocemide 20 mg/8 hr
- Inj. Ceftriaxone 2 gr/12 hr
- Ambroxol 3x Ci
- Laxadin syr 1x Ci
- Spironolacton 1x25 mg
- Captopril 3x12,5 mg
Prognosis :
Dubia ad malam
3-12-13 S: Dyspnoe (+) reduce - Post SVT with - Bed Rest, semifowler
Palpitations (-) unstable - O2 2-4L/i
Cough (+) hemodinamic - IVFD NaCl 0,9% 10 gtt/i
- CHF Fc IV ec
Sputum (+) (micro)
MR severe
Blood (+) - Furocemide 5 mg/hr
- Pneumonia
O: Sens: CM - Inj. Ceftriaxone 2 gr/12 hr
BP: 140/70 mmHg HR: 100x/i - Ambroxol 3x Ci
RR: 20 x/i Temp: 36C - Laxadin syr 1x Ci
Head : eye: anemia (-/-), icteric
sclera (-/-) Lab results :
Neck : JVP R + 3 cm H2O RBC : 3,70 g 106/mm3
Heart : S1(N), S2(N), Murmurs : (+) WBC : 13,8 103/mm3
type PSM, grade 3/6 apex, gallop (-) Ht : 35,5 %
Lung : LS : Vesicular Platelet : 50 103/mm3
AS : Crackles basal (+/+) Albumin :2,9
Coarse crackles (+/+) Ur/Cr : 107,2/1,42
Abdomen : Acites (+)
Extremity: warm acral, Oedem (+/+)
UOP : 5500 cc/24 hr, TB : 4700 cc
4-12-13 S: Dyspnoe (+) reduce - Post SVT with - Bed Rest, semifowler
O: Sens: CM unstable - O2 2-4L/i
BP: 140/90 mmHg HR: 104x/i hemodinamic - IVFD NaCl 0,9% 10 gtt/i
- CHF Fc III ec
RR: 20 x/i Temp: 36.8C (micro)
MR severe
Head : eye: anemia (-/-), icteric - Pneumonia - Furocemide 20 mg/8 hr
sclera (+/+) - Inj. Ceftriaxone 2 gr/12 hr
Neck : JVP R + 2 cm H2O - Ambroxol 3x Ci
Heart : S1(N), S2(N), Murmurs : (+), - Laxadin syr 1x Ci
type PSM, grade 3/6 apex - Spironolacton 1x25 mg
Lung : LS : Vesicular - Captopril 3x12,5 mg
AS : Crackles basal (+/+)
Abdomen : Soepel Lab results :
Extremity : warm acral, Oedem (+/+) Na : 130 mEq/L
UOP : 9200 cc/24 hr K : 2,7 mEq/L
5-12-13 S: Dyspnoe (+) reduce - Post SVT with - Bed Rest, semifowler
Cough (+) unstable - O2 2-4L/i
Blood (+) hemodinamic - IVFD NaCl 0,9% 10 gtt/i
- CHF Fc III ec
O: Sens: CM (micro)
MR severe
BP: 100/90 mmHg HR: 110x/i - Furocemide 20 mg/8 hr >
- Pneumonia
RR: 20 x/i Temp: 36.5C - Jaundice ec 20 mg/12 hr
Head : eye: anemia (-/-), icteric ischemic - Inj. Ceftriaxone 2 gr/12 hr
sclera (+/+) hepatitis - Ambroxol 3x Ci
- AKI std injury
Neck : JVP R + 2 cm H2O - Laxadin syr 1x Ci
Heart : S1(N), S2(N), Murmurs : (+), - Spironolacton 1x25 mg
type PSM, grade 3/6 apex - Captopril 3x12,5 mg >
Lung : LS : Vesicular 3x25 mg
AS : Crackles basal (+/-)
Abdomen : Soepel Lab result :
Extremity : warm acral, Oedem (+/+) Albumin : 3,0 g/dl
UOP : 3500 cc/24 hr Echocardiography result :
Mitral valve : MR severe ec
remodeling LV
Aortic valve : normal
Tricuspid valve : TR mild
Pulmonary valve : normal
Immpression : Global LV
systolic function decreases,
LVEF 35% of global
hipokinetik
MR severe ec LV dilatation
6-12-13 S: Dyspnoe (+) reduce - Post SVT with - Bed Rest, semifowler
O: Sens: CM unstable - O2 2-4L/i
BP: 100/70 mmHg HR: 114/i hemodinamic - IVFD NaCl 0,9% 10 gtt/i
- CHF Fc III ec
RR: 20 x/i Temp: 36.5C (micro)
MR severe
Head : eye: anemia (-/-), icteric - Furocemide 20 mg/8 hr >
- Pneumonia
sclera (+/+) - Jaundice ec 20 mg/12 hr
Neck : JVP R + 2 cm H2O ischemic - Inj. Ceftriaxone 2 gr/12 hr
Heart : S1(N), S2(N), Murmurs : (+), hepatitis - Ambroxol 3x Ci
type PSM, grade 3/6 apex AKI std injury - Laxadin syr 1x Ci
Lung : LS : Vesicular - Spironolacton 1x25 mg
AS : Crackles basal (+/-) - Captopril 3x12,5 mg >
Abdomen : Soepel 3x25 mg
Extremity : warm acral, Oedem (+/+) - Liver care 3x1
Hasil lab :
INR 3.7
7-12-13 S: Dyspnoe (+) reduce - Post SVT with - Bed Rest, semifowler
O: Sens: CM unstable - O2 2-4L/i
BP: 100/70 mmHg HR: 98/i hemodinamic - IVFD NaCl 0,9% 10 gtt/i
- CHF Fc III ec
RR: 28 x/i Temp: 36C (micro)
MR severe
Head : eye: anemia (-/-), icteric - Furocemide 20 mg/8 hr >
- Pneumonia
sclera (+/+) - Jaundice ec 20 mg/12 hr
Neck : JVP R + 2 cm H2O ischemic - Inj. Ceftriaxone 2 gr/12 hr
Heart : S1(N), S2(N), Murmurs (+), hepatitis - Ambroxol 3x Ci
type PSM, grade 3/6 apex AKI std injury - Laxadin syr 1x Ci
Lung : LS : Vesicular - Spironolacton 1x25 mg
AS : Crackles basal (+/-) - Captopril 3x12,5 mg >
Abdomen : Soepel 3x25 mg
Extremity : warm acral, Oedem (+/+) - Liver care 3x1
CHAPTER IV
CONCLUSION
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