FAKULTAS KEDOKTERAN

UNIVERSITAS MUSLIM INDONESIA Makassar, 8 April 2019

LAPORAN PBL
MODUL BERDEBAR-DEBAR
BLOK KARDIOVASKULAR

OLEH:
KELOMPOK 15
M. Farizan Atjo (11020160032)
Ainunnisa Muhammad (11020170003)
Miftahul Janna (11020170042)
Moh. Yusril (11020170052)
Muhammad Fakhri (11020170069)
Muh. Fadil Asrar (11020170055)
Jihan Adjdjibiyan S. Azzubaidi (11020170105)
Indah Setiyani Ulum (11020170134)
Andi Bau Syatirah Ninnong M (11020170138)
Hernita (11020170152)
TUTOR: dr. Dwi Anggita M,Kes
FAKULTAS KEDOKTERAN
UNIVERSITAS MUSLIM INDONESIA
MAKASSAR
2019
SCENARIO 3
An 18 years-old women came to the clinic complaining of chest palpitation and
discomfort on the last 3 month. The patient says his heart sometimes suddenly beats
very fast so that the patient felt discomfort on his chest. Suddenly patient suddenly
wakeup in the middle of the naight sand feel thei heartbeat is irregular and rather
fast.
Complaints are raised at night, especially before going to bed. Patient regularly
drink coffe and tea everyday. There is no history of fainting. There is no family
history with the same complaint. There is no history of hypertension or diabetes
mellitus. From physical ecxamination, blood pressure was 110/60 mmHg, pulse
was 70x/minute, irregular, repiratory rate 22x/minute, temperature 36.5oC. there is
no murmur
Keywords
1. An 18 years-old women complaining of chest palpitation and discomfort on
the last 3 month
2. Her heart sometimes suddenly beats very fast, suddenly wakeup in the
middle of the naight sand feel thei heartbeat is irregular
3. Complaints are raised at night, especially before going to bed
4. Patient regularly drink coffe and tea everyday.
5. There is no family history and hypertension or diabetes mellitus
6. Blood pressure was 110/60 mmHg, pulse was 70x/minute, irregular,
repiratory rate 22x/minute, temperature 36.5oC. there is no murmur
Questions
1. What is the etiology and mechanism of palpitation?
2. What is the relation between consumption coffe with herat palpitation?
3. What is classification of aritmia?
4. What are the factor that influence cardiac conduction that can make heart
palpitation?
5. what is the definition of ECG and classification of tachycardia and
bradycardia?
6. How to diagnose the patient based on the scenario?
7. What is the differential diagnose?
Answer
1. What is the etiology and mechanism of palpitation?
Palpitation is a perceived abnormality of the heartbeat characterized by
awareness of heart muscle contractions in the chest: hard beats, fast beats,
irregular beats, and/or pauses. It is both a symptom reported by the patient
and a medical diagnosis. Palpitation is frequently associated with anxiety and
does not necessarily indicate a structural or functional abnormality of the
heart, but it can be a symptom arising from an objectively rapid or irregular
heartbeat. Palpitation can be intermittent and of variable frequency and
duration, or continuous. Associated symptoms include dizziness, shortness of
breath, sweating, headaches, and chest pain.
Palpitations are the perception of cardiac activity. They are often described
as a fluttering, racing, or skipping sensation. They are common; some patients
find them unpleasant and alarming. Palpitations can occur in the absence of
heart disease or can result from life-threatening heart disorders. Some patients
simply have heightened awareness of normal cardiac activity, particularly
when exercise, febrile illness, or anxiety increases heart rate. However, in
most cases, palpitations result from arrhythmia. Arrhythmias range from
benign to life threatening.2
The most common arrhythmias include
• Premature atrial contractions (PACs)
• Premature ventricular contractions (PVCs)
• Paroxysmal supraventricular tachycardia (PSVT)
• Atrioventricular nodal reentrant tachycardia
• Atrial fibrillation or flutter
• Ventricular tachycardia
Some arrhythmias (eg, PACs, PVCs, PSVT) often occur spontaneously in
patients without serious underlying disorders, but others are often caused by
a serious cardiac disorder.
 o Serious cardiac causes include myocardial ischemia or other
myocardial disorders, congenital heart disease (eg, Brugada
syndrome, arrhythmogenic right ventricular cardiomyopathy,
congenital long QT syndrome), valvular heart disease, and
conduction system disturbances (eg, disturbances that cause
bradycardia or heart block). Patients with orthostatic hypotension
commonly sense palpitations caused by sinus tachycardia upon
standing.
o Noncardiac disorders that increase myocardial contractility (eg,
thyrotoxicosis, pheochromocytoma, anxiety) may cause
palpitations.
o Some drugs, including digitalis, caffeine, alcohol, nicotine, and
sympathomimetics (eg, albuterol, amphetamines, cocaine,
dobutamine, epinephrine, ephedrine, isoproterenol, norepinephrine,
and theophylline), frequently cause or exacerbate palpitations.
o Metabolic disturbances, including anemia, hypoxia, hypovolemia,
and electrolyte abnormalities (eg, diuretic-induced hypokalemia),
can trigger or exacerbate palpitations.1
The mechanisms responsible for the sensation of palpitations are unknown.
Ordinarily, sinus rhythm at a normal rate is not perceived, and palpitations
thus usually reflect changes in cardiac rate or rhythm. In all cases, it is the
abnormal movement of the heart within the chest that is felt. In cases of
isolated extrasystoles, the patient may actually perceive the augmented
postextrasystolic beat as the “skipped” beat rather than the premature beat
itself, probably because the extrasystole blocks the next sinus beat and allows
longer ventricular filling and thus a higher stroke volume.
The clinical perception of cardiac phenomena is highly variable. Some
patients are aware of virtually every premature ventricular beat, but others
are unaware of even complex atrial or ventricular tachyarrhythmias.
Awareness is heightened in sedentary, anxious, or depressed patients and
reduced in active, happy patients. In some cases, palpitations are perceived
 in the absence of any abnormal cardiac activity. Some structural heart
diseases can give rise to palpitations in the absence of true rhythm disorders.
These include, among others, mitral valve prolapse, severe mitral and aortic
regurgitation, congenital heart disease with significant shunt, hypertrophic
cardiomyopathy, and mechanical prosthetic valves3
2. What is the relation between consumption coffe with herat palpitation?
Higgins concluded that in healthy individuals aged 22 to 59 years who
consume 200 to 300 mg of caffeine, indirect tests indicate improved ECF
and vasodilation at rest. So adults consuming this much caffeine during
activities of daily living are likely safe, provided they are not caffeine
sensitive, pregnant, or taking medication that interacts with caffeine or do
not have a medical condition that is worsened by caffeine. For those who
consume caffeine immediately before or during exercise, however, there
could be harmful results. It appears that caffeine may attenuate the normal
physiological mechanisms that help increase myocardial blood flow that
occur during the increased demand of exercise. Researchers know that
caffeine blocks adenosine receptors, thus reducing the ability of the
coronary arteries to improve their flow commensurate with the increased
myocardial demand of exercise. This could perhaps result in supply-demand
ischemia. In healthy individuals aged 21 to 71 years who consume 200 to
300 mg of caffeine and then perform aerobic exercise 1 hour later, indirect
tests indicate reduced ECF as measured by reduced myocardial blood flow.
Finally, in healthy individuals aged 20 to 47 years who consume energy
drinks, indirect tests indicate reduced ECF at rest.4

Higgins called for more research on the effects of caffeine and energy drinks
on ECF and the mechanisms underlying those effects and for more research
on the safety of high-dose caffeine and energy drinks in younger individuals,
caffeine-naïve individuals, and individuals who exercise 1 to 2 hours after
consumption. In the 6 cases that he was aware of in which deaths were
associated with energy drink consumption, affected individuals were
between 12 and 19 years of age. He identified that age group as a potentially
vulnerable population.4

In recent years, clinical and observational studies reported that caffeine

consumption was associated with cardiac arrhythmias, affected heart rate
variability, and subsequently increased cardiovascular risk. Moderate
intake of caffeine seems to have protective effects on arrhythmias, on
contrary high intake of caffeine seems to be associated with increased risk
of atrial fibrillation. There is a deep difference when we analysed intake
of caffeine from coffee compared to other sources. In very recent time an
increase in caffeinated beverages, namely energy drinks, has been reported
in young people and several arrhythmic complications has been observed.
Lifestyle factors, particularly dietary intake, have been recognized as
important, modifiable risk factors for cardiovascular disease. The majority
of studies analyzed the relationship between lifestyle and atherosclerosis,
whereas little is know about influence of lifestyle on arrhythmias. Atrial
fibrillation (AF) is the most common arrhythmia in clinical practice. It is
estimated to currently affect over 6 million patients in Europe and
approximately 3.0 million in the United States, and this number is
projected to at least double in the next 25 years because of the increasing
proportion of the ageing population.5,6
Coffee contains several hundred different substances including lipids,
carbohydrates, minerals, vitamins, alkaloids and phenolic compounds.
Nevertheless effects of coffee on cardiovascular system have been mainly
related to caffeine. Caffeine is an alkaloid present in coffee beans, in
humans come from a number of dietary sources i.e. tea, coffee, cocoa
beverages, chocolate bars and soft drinks and recently energy drinks. (ED).
The content of caffeine of these items ranges from 4 to 180 mg/150 ml for
coffee, 15 to 29 mg/180 ml for cola, 24 to 50 mg/150 ml for tea, 2 to 7
mg/150 ml for cocoa and 1 to 36 mg/28 mg for chocolate, 100 to 286 mg
for common ED, however some brands of ED contain 550 mg caffeine per
can or bottle.5,6

The clinical effect of intakes of caffeine from coffee, tea, caffeinated soda
and energy drinks on AF remain inconclusive. The patho-physiology of
the arrhythmias have been described in detail, however the mechanism
underlying electrical changes and the possible triggering factors remain
largely unknown. Several studies evaluated the acute effects of caffeine on
heart rate and found controversial results.6

Studies on human atrial myocytes from patients with AF suggests that an

adenosine mediated signaling pathways could lead to increased
spontaneous sarcoplasmic reticulum calcium release and could contribute
to the initiation of AF. Caffeine may mediate AF by resulting in
neurohormonal stimulation and sympathetic activation and the effects
could be enhanced in nonhabitual coffee drinkers. Caffeine toxicity
produces supraventricular tachycardia, atrial fibrillation and ventricular
fibrillation.6

The risk of cardiac arrhythmias associated with daily consumption of

caffeine does not seem to be increased at ventricular level, but more
information is needed about supraventricular level. The Framingham
Heart study and a Danish study showed no association between daily
caffeine intake and incident AF. Similarly in the Women Health study,
caffeine consumption was not associated with an increased risk of incident
AF in a selected population of initially healthy middle-aged women.
Other studies identified moderate coffee consumption (1–4 cups coffee/d)
as a contributor to AF risk, whereas another study showed that caffeine
was associated with less successful cardioversion in hypertensive patients.
It is plausible that the effects of caffeine varies in habitual versus non-
habitual consumers and also depends on the dose, on the modality of
preparation and on the modality of intake, i.e. coffee after meals. Further
studies are necessary to clarify the relation of caffeine exposure to risk of
 incident and recurrent AF in healthy individuals and patients with a
predisposition for AF.6
CAFFEINE AND RISK OF ARRHYTHMIA

A 1994 survey of several hundred physicians from Minnesota and Vermont

found that 94 percent of those surveyed recommended reducing or stopping
caffeine for patients complaining of palpitations (Hughes et al., 1988).
Jeffrey Goldberger described the finding as “remarkable” and considered it
his task for the workshop to examine whether the evidence supports that
recommendation. In his experience, it is not often that 94 percent of
physicians agree on something even when its benefits have been
demonstrated in randomized clinical trials, such as the use of beta-blockers
after myocardial infarction or anticoagulants for atrial fibrillation. It is
difficult to get that kind of consensus and interesting to consider where it
comes from.4

There are many data sources on the effects of caffeine on arrhythmias,

including case reports, animal studies, human physiologic studies, human
small-case series, and human observational trials. The predominant focus of
Goldberger's presentation was on human observational trials. He noted that
most of the data comes from coffee-intake studies and emphasized the need
to keep in mind, while reviewing these studies, the variation in the amount
of caffeine in different coffee drinks.4

There are also many end points to consider when evaluating the effects of
caffeine on the heart, including physiologic surrogates (i.e.,
electrophysiological effects such as QRS duration, which is the time
required to depolarize the ventricles), specific arrhythmias, and
epidemiological outcomes. He focused on three types of specific
arrhythmias: (1) atrial fibrillation, a common arrhythmia in middle-aged and
older individuals; (2) premature ventricular complexes, which are extra
beats that arise from the ventricles and are common at all ages and in people
 either with or without heart disease; and (3) arrhythmias that can lead to
sudden cardiac death, which include ventricular fibrillation and very rapid
ventricular tachycardia.4

3. What is classification of aritmia?

Based on the mechanism, arrhythmias are divided into tachyarrhythmias
and bradyarrhythmias, whereas based on their location arrhythmias are
divided into7
supraventricular arrhythmias and ventricular arrhythmias.
Tachyarrhythmias are a form of nonsustained tachycardia (lasting <30
seconds), and (sustained> 30 seconds) originating from the focus of the
myocardium or reentran circuit. The standard definition of tachycardia is a
rhythm that produces ventricular velocity of> 100 beats / minute
Bradyarrhythmias are all abnormal disturbances in heart rhythms,
bradyarrhythmias are bradycardia (heart rate is less than 60 times per
minute)7
accompanied by symptoms of synopsy or almost syncope, congestive heart
failure exercise intolerance, fatigue, or improved mental status with
improvement bradycardia.
Based on the location of arrhythmias divided into supraventricular
arrhythmias and ventricular arrhythmias, Supraventricular ventricular
arrhythmias7
Supraventricular aritmia ventricular
1 Sinus tachyarrhythmia Nonsustaine
(physiological tachycardia sinus,
d VT
inappropriateness tachycardia,
orthostatic postural tachycardia
syndrome, sinus node Re-entry
tachycardia (SNRT)

2 Atriovenricular Nodal reciprocating Sustained

tachycardia (AVNRT) VT
 3 Focal dan nonparoxysmal junction Bundle
tachycardia(focaljunctional branch re-
tachycardia,nonparoxysmaljunction entrant
al tachycardia tachycardia
4 Atrioventricular reciprocating Bidirectional
tachycardia VT
5 Focal atrial tachycardias Torsades de
pointes

4. What are the factor that influence cardiac conduction that can make heart
palpitation?
Factors that can cause heart palpitations
1. Hypoxia: all diseases that cause oxygen deficiency in the myocardium
such as lung disease, cardiomyopathy, or coronary heart disease can
cause arrhythmias
2. Myocardial ischemia: Myocardial ischemic causes are the trigger
factors for arrhythmias.
3. Stimulation of the autonomic nervous system: excessive stimulation
of the sympathetic and parasympathetic nerves can cause arrhythmias.
4. Medications: all antiarrhythms affect the cardiac depolarization and
repolarization phase, so they have an arrhythmogenic effect. In addition,
drugs such as caffeine, aminophylline, tricyclic antidepressants, and
digitalis also have arithmogenic effects.
5. Disorders of electrolyte balance and blood gas: this is easily
understood because the phase of depolarization and repolarization of the
heart muscle is caused by the transfer of various electrolyte ions through
the cell membrane.
6. Stretching of the heart muscle wall: a stretched heart wall such as atrial
or ventricular dilatation due to heart failure, cardiomyopathy or valve
diseases can cause arrhythmias
 7. Conduction system structural abnormalities: patients who have fatal
depression on the av node and fasciculo-ventricular connection, or who
have an accessory pathway such as Wolf-Parkinson-white syndrome are
very susceptible to arrhythmias through a pre-excitatory mechanism.
8. Past medical history: such as thyroidism where T3 stimulates a)
transcription of hc-β myosin and inhibits myosin hc-β, resulting in
increased myocardial muscle contraction. b) transcription of Ca2 +
ATPase in the sarcoplasmic reticulum increases diastolic tone. c) change
the concentration of G protein adrenergic receptors. So that finally this
thyroid hormone has a positive yonotropic effect. Clinically seen as an
increase in cardiac output and tachycardia.8,9

5. What is regular and irregular ECG ??

Heart Rhythm Disorders

 Definition of heart rhythm disorders

The term arrhythmia refers to a change in the mechanism of propagating

the heart's electrical impulses which causes a disturbance in heart rhythm. 2
basic forms of arrhythmia are:
 Tachycardia, if the heart rate> 100x / minute
 Bradycardia, if the heart rate is <60x / minute

Some arrhythmias occur briefly so that the overall heart rate is not too
affected. But if the arrhythmia lasts long enough it can cause the heart rate
to be too slow or too fast so that the heart's ability to pump blood becomes
less effective. 8 Tachycardia reduces cardiac output by shortening
ventricular filling time and stroke volume, while bradycardia reduces
cardiac output by reducing the frequency of ventricular ejection.

Arrhythmia can occur if:

1. Pacemaker (SA node) produces an abnormal rhythm
 2. There is interference with the normal conduction pathway
3. The heart part other than the SA node takes over as a pacemaker

Classification of heart rhythm disorders

Based on the mechanism, arrhythmias are divided into tachyarrhythmias
and bradyarrhythmias, whereas based on their location arrhythmias are
divided into supraventricular arrhythmias and ventricular arrhythmias.
The following are some types of heart rhythm disorders:
a. Supraventricular Tachycardia (SVT)
Supraventricular tachycardia is the whole form of tachycardia that
emerges from the HIS file or above the HF bifurcation.11 In general, the
symptoms that arise are palpitations, lightheadedness, dizziness, loss of
consciousness, chest pain, and shortness of breath12. These symptoms
appear suddenly (sudden onset) and stop suddenly (abrupt onset)

Figure 1. Supraventricular classification of tachycardia

1. Sinus Tachycardia
Sinus tachycardia is a sinus rhythm with a heart rate> 100x / minute.
There are 2 types of sinus tachycardia, namely physiological and non
physiological. Physiological sinus tachycardia describes the normal state or
is physiological stress response (physical activity, anxiety), pathological
conditions (fever, thyrotoxicosis, anemia, hypovolemia), or
pharmacological stress to keep the cardiac output stable. Whereas non-
physiological sinus tachycardia occurs due to disorders of the vagal system,
sympathetic, or on the SA node itself.

Figure 2. ECG Interpretation of Sinus Tachycardia

2. Atrial Fibrillation
 Atrial fibrillation is the most common form of arrhythmia. In atrial
fibrillation, electrical impulses do not start from the SA node, but from other
parts of the atrium or near v. Pelmonalis. This will cause impulses that are
fast and irregular so that the atrium will beat correctly and irregularly as
well. When an electrical impulse reaches the AV node, the AV node will
continue the impulse even though it is not as fast as the initial impulse so
the ventricle will also beat fast but not as fast as the atrium. Therefore, the
atria and ventricles no longer beat together. This causes the blood in the
atrium not to pump into the ventricles as they should.
The risk of atrial fibrillation will increase in conditions of hypertension,
coronary heart disease, heart failure, rheumatic heart disease, heart structure
defects (eg Mitral Valve Prolapse), pericarditis, congenital heart disease,
hyperthyroidism, obesity, diabetes, and lung disease.
Complications that can be caused are strokes and heart failure. Stroke
results from the release of a blood clot (thrombus) in the atrium which then
clogs the blood vessels of the brain. Heart failure occurs if the heart cannot
pump blood sufficiently according to the needs of the body. On an ECG
there are irregular wave images, narrow QRS complexes, and speeds> 300x
/ minute.
 Figure 3. ECG Interpretation of Atrial Fibrillation
3. Atrial Flutter
Atrial flutter can be caused due to injury to the heart due to heart disease
or heart surgery procedures. But atrial flutter can also occur in patients
without heart problems. This condition is referred to as Lone Atrial Flutter.
In atrial flutter the electrical impulse does not start from the SA node but
from the right atrium and involves a large circuit that covers the area near
the tricuspid valve. This will cause the atrium to beat quickly and spur the
ventricles to beat fast too. Atrial flutter generally occurs in people with heart
disease, such as congestive heart disease, rheumatic valve disease,
congenital heart disease or other medical conditions, such as pulmonary
emphysema and hypertension. The risk of atrial flutter will increase in post-
cardiac surgery patients due to the formation of injury to the atrium.

Figure 4. Interpretation of ECG on Atrial Flutter

4. Atrial Extrasystole
Atrial extrasystoles often appear in the normal heart, but are generally
associated with structural heart disease and their frequency increases with
age. On the ECG picture is characterized by the presence of P waves that
arise before the P wave in normal sinuses appears. In APC that occurs too
early can cause prolongation of the PR interval and some can also not be
conditioned into the ventricles so that the pulse becomes irregular.
 Figure 5. Interpretation of ECG on Atrial Extrasystole

b. Ventricel Tachycardia
The ventricel tachycardia is ≥ 4x consecutive ventricular arising. Is one
of the lethal arrhythmias (dangerous) because it easily develops into
ventricular fibrillation and can cause cardiac arrest (cardiac arrest).
Ventricel tachycardia is caused by a condition that interferes with the
cardiac conduction system, such as a lack of supply of O2 due to
interference with coronary arteries, cardiomyopathy, sarcoidosis, heart
failure, and digitalis poisoning. Diagnosis is established if a heart rate of
150-210x / minute is found symptoms of headache, lightheadedness, loss of
consciousness, and sudden and unprecedented cardiac arrest. ECG
examination shows the presence of wide QRS complexes which occur
continuously and continuously at> 150x / minute

Figure 6. Interpretation of ECG in Ventricular Tachycardia

c. Ventricular Fibrillation
Ventricular fibrillation is the most dangerous type of arrhythmia. The
heart no longer pulses but only vibrates so that the heart cannot pump blood
effectively. This can cause cardiac arrest (cardiac arrest). Symptoms that
arise in the form of a reduced patient response, the patient is not breathing
or just gasping, cardiac arrest that appears suddenly (Sudden Cardiac
Arrest).
 Figure 7. Interpretation of ECG in Ventricular Fibrillation

d. Ventricular Extrasystole
Ventricular Extrasystole is a rhythm disorder in the form of a premature
heartbeat that originates from 1 or more focus in the ventricles. It is the most
common heart rhythm disorder. Extracystic ventricles can be caused by
myocardial ischemia, acute myocardial infarction, heart failure, prolonged
QT syndrome, mitral valve prolapse, cerebrovascular accident, digitalis
poisoning, hypokalemia, myocarditis, cardiomyopathy. But it can also arise
in the normal heart. ECG images show wide and bizzare QRS complexes
and are not preceded by wave P.
 Figure 8. Interpretation of ECG in Ventricular Extrasystole
Source: Kowalak, Jennifer Lynn

Figure 8. Interpretation of ECG in Ventricular Extrasystole

Figure 8. Interpretation of ECG in Ventricular Extrasystole

e. Bradikardi
Bradycardia is a heart rhythm disorder in which the heart beats slower
than normal, which is 60x / minute. Bradycardia is caused by a disturbance
in the SA node, cardiac conduction system disorders, metabolic disorders
(hypothyroidism), and damage to the heart due to a heart attack or heart
disease. 28 Symptoms that arise vary from asymptomatic to symptoms of
syncope / almost syncope, dyspnea, pain chest, weakness, and dizziness

Figure 9. ECG Interpretation of Bradikardi Sinus

6. how to diagnose based on the scenario

I. Anamnesis
The spectrum of clinical presentation atrial fibrillation varies greatly,
starting fromasymptomatic to cardiogenic shock or cerebrovascular
events weight. Nearly 50% of FA episodes do not cause symptoms
(silent atrial fibrillation).
Some mild symptoms that patients may complain about among
others:
 Palpitations. Generally expressed by patients as:
drum punch, thunder thunder, or fish on in the chest
• Easily tired or low tolerance for physical activity
• Presinkop or syncope
• General weakness, dizziness
In addition, FA can also cause hemodynamic disorders,
cardiomyopathy induced by tachycardia and thromboembolism
systemic. Initial assessment of patients with the FA for the first time
diagnosed must focus on the hemodynamic stability of the patient. 33
In addition to looking for the symptoms mentioned above, history
from
every patient suspected of having an FA must include relevant
questions, such as: 34
• Assessment of FA classification based on presentation time,
duration,
and frequency of symptoms.
• Assessment of precipitation factors (eg activity, sleep,
alcohol). The role of caffeine as a trigger factor is still
contradictory.35
• Assessment of ways of termination (eg vagal maneuvers).
• History of antiarrhythmic drug use and rate control
previous.
• Assessment is the underlying structural heart disease.
• History of surgical FA ablation procedures (Maze surgery)
or percutaneous (with a catheter).
• Evaluation of potential comorbidities
to contribute to FA initiation (eg hypertension,
coronary heart disease, diabetes mellitus, hyperthyroidism, disease
valvular heart, and COPD).

Relevant questions to be asked of patients suspected or known to the

FA
n question
o
1 . Does the heart rhythm when the attack episode feels regular or not
 regular?
2 Are there precipitating factors such as physical activity, emotions or
alcohol intake?
3 Do symptoms during episodes feel moderate or severe - degrees
severity can be expressed using EHRA scores
4 Are episodes that are felt often or rarely, and are brief
or long enough?
5 Is there a history of comorbidities such as: hypertension, disease
coronary heart disease, heart failure, peripheral vascular disease, disease
cerebrovascular, stroke, diabetes or chronic pulmonary disease?
6 Is there a history of alcohol abuse?
7. Is there a family history with the FA?

Klasifikasi simtom terkait FA (skor EHRA )

EHRA Explanation
class
EHRA I Without symptoms
EHRA Mild symptoms, normal daily activity is not
II affected

EHRA Severe symptoms, disturbed daily

III activities

EHRA Symptoms are crippling, daily

IV activity stops
FA = atrial fibrillation, EHRA = European Heart Rhythm
Association
II. Physical examination
Physical examination always starts with a road check breath (airway),
breathing (Breathing) and circulation (Circulation) and vital signs, to
direct follow-up towards the FA. Physical examination can also
provide information about the basics causes and sequelae of FA.
Vital Signs
Measurement of pulse rate, blood pressure, breathing speed and
Oxygen saturation is very important in evaluating hemodynamic
stability and adequate rate control in the FA. On physical examination,
pulse the pulse is generally irregular and fast, around 110-140x /
minute, but rarely exceed 160-170x / minute. Patients with
hypothermia or with the toxicity of heart drugs (digitalis) can
experience bradycardia.
Head and Neck
Head and neck examination can show exophthalmus, thyroid
enlargement, increased jugular venous pressure or cyanosis.Bruits in
the carotid artery indicate peripheral arterial disease and the
possibility of comorbidities of coronary heart disease.

Lungs
Lung examinations can reveal signs of failure heart (eg ronki, pleural
effusion). Wheezing or lengthening Expiration indicates a possible
chronic lung disease underlying the occurrence of FA (eg COPD,
asthma)
Heart
Cardiac examination is very important in the examination physical in
FA patients. Complete palpation and auscultation very important for
evaluating valvular heart disease or cardiomyopathy. Shift from
maximum punctum or sound additional heart (S3) indicates
ventricular enlargement and increased left ventricular pressure. The
hardened II (P2) sound can indicates the presence of pulmonary
hypertension.
Pulsus deficit, where there is a difference in the amount of pulse that
is palpable by auscultation the heart rate can be found in FA patients.
Abdomen
 Presence of ascites, hepatomegaly or palpable liver capsules
tightening may indicate right heart failure or intrinsic liver disease.
Upper left quadrant pain, maybe caused splenic infarction due to
peripheral embolization.
Lower limb
On examination the lower extremities can be found cyanosis, clubbing
or edema. Cold and without limbs pulse may indicate peripheral
embolization. Weakening of pulse peripheral can indicate peripheral
or bulk arterial disease decreased heart.
Neurological
Transient Ischemic Attack (TIA) signs or events Cerebrovascular can
sometimes be found in FA patients. Increased reflexes can be found
in hyperthyroidism.

III. Laboratory examination

Laboratory examinations are intended to seek interference / hidden
disease, especially if the ventricular rate is difficult controlled. One
study showed that mild elevation of troponin I when admitted to
hospital related to mortality and cardiac events higher, and may be
useful for risk stratification
Laboratory tests that can be examined include:
• Complete blood (anemia, infection)
• Electrolytes, urea, serum creatinine (electrolyte disorders or kidney
failure)
• Cardiac enzymes such as CKMB and or troponin (myocardial
infarction as the originator of the FA)
• Natriuretic peptides (BNP, N-terminal pro-BNP and ANP) have
association with the FA. Plasma level of natriuretic peptides this is
 increased in patients with paroxysmal FAand persistent, and dropped
back quickly after restoration of sinus rhythm.
• D-dimer (if the patient has a risk of pulmonary embolism)
• Thyroid function (thyrotoxicosis)
• Digoxin levels (evaluation of subterapeutic levels and / or toxicity)
IV. Electrocardiogram (ECG)
ECG findings can usually confirm the FA diagnosis and usually
includes the irregular ventricular rate and is not present a clear P wave,
replaced by an irregular F wave and random, followed by irregular
QRS complexes. Other ECG manifestations that can accompany the
FA include:
• Heart rate generally ranges from 110-140x / minute, but rarely
exceed 160-170x
/ minute.
• Pulse can be found with aberrant conduction (wide QRS) after a
long, short interval R-R cycle (the Ashman phenomenon)
• Pre-excitement
• Left ventricular hypertrophy
• Block branch files
• Sign of acute / old infarction
An electrocardiogram is also needed to monitor intervals
QT and QRS from patients receiving antiarrhythmic therapy for FA
V. Chest X-ray
Chest X-ray examination is usually normal, but sometimes evidence
of heart failure or signs of pathology can be found
pulmonary parenchyma or vascular (eg pulmonary embolism,
pneumonia).
VI. Training test or six-minute walking test
A training test or a six-minute walking test can help assess whether
the rate control strategy is adequate or not (pulse target <110x / minute
after walking 6-minutes). Training tests can get rid of ischemia before
 giving class 1C antiarrhythmic drugs and can also used to reproduce
FA triggered by activity physical
VII. Echocardiography
Transthoracic echocardiography has a sensitivity low in detecting
thrombus in the left atrium, and echocardiograph transesophageal is
the chosen modality for this purpose.
Transthoracic echocardiography (ETT) is especially useful for:
• Evaluation of valve heart disease
• Evaluate the size of the atria, ventricles and wall dimensions
• Estimated ventricular function and evaluation of ventricular
thrombus
• Estimated pulmonary systolic pressure (pulmonary hypertension)
• Evaluation of pericardial disease
VIII. Computed tomography (CT) scans and magnetic resonance imaging
(MRI)
In patients with positive D-dimer results, CT angiography may be
needed to rule out pulmonary embolism. Technology 3 dimensions
such as CT scans or MRI are often useful for evaluating atrial anatomy
if FA ablation is planned. Data
imaging can be processed to create anatomical maps from left atrium
and VP.14

7. what is the differential diagnosis?

Premature atrial contraction

Premature atrial contractions (PACs), also known as atrial
premature complexes (APC) or atrial premature beats (APB), are a
common cardiac dysrhythmia characterized by premature heartbeats
originating in the atria. While the sinoatrial node typically regulates the
heartbeat during normal sinus rhythm, PACs occur when another region
of the atria depolarizes before the sinoatrial node and thus triggers a
 premature heartbeat. The exact cause of PACs is unclear; while several
predisposing conditions exist, PACs commonly occur in healthy young
and elderly people. Elderly people that get PACs usually don't need any
further attention besides follow ups due to unclear evidence. PACs are
often completely asymptomatic and may be noted only with Holter
monitoring, but occasionally they can be perceived as a skipped beat or a
jolt in the chest. In most cases, no treatment other than reassurance is
needed for PACs, although medications such as beta blockers can reduce
the frequency of symptomatic PACs.13

Risk factors
Hypertension, or abnormally high blood pressure, often signifies
an elevated level of both psychological and physiological stress. Often,
hypertension goes hand in hand with various atrial fibrillations including
premature atrial contractions (PACs). Additional factors that may
contribute to spontaneous premature atrial contractions could be:

 Increased age
 Abnormal body height
 History of cardiovascular disease (CV)
 Abnormal ANP levels
 Elevated cholesterol

o When have a PAC, might notice:

A flutter in your chest
Fatigue after exercise
Shortness of breath or chest pain
Lightheadedness or dizziness
o Causes things can make PACs more likely:
Pregnancy
High blood pressure, heart disease, or hyperthyroidism
 Stress or fatigue
Caffeine
Alcohol
Smoking
Cold or hay fever medicine
Asthma medicine
Dehydration

Diagnosis
Premature atrial contractions are typically diagnosed with an
electrocardiogram, Holter monitor, or cardiac event monitor.

Electrocardiogram

On an electrocardiogram (ECG), PACs are characterized by an abnormally

shaped P wave. Since the premature beat initiates outside the sinoatrial
node, the associated P wave appears different from those seen in normal
sinus rhythm. Typically, the atrial impulse propagates normally through
the atrioventricular node and into the cardiac ventricles, resulting in a
normal, narrow QRS complex. However, if the atrial beat is premature
enough, it may reach the atrioventricular node during its refractory period,
in which case it will not be conducted to the ventricle and there will be no
QRS complex following the P wave.

Treatment
Premature atrial contractions are often benign, requiring no treatment.
Occasionally, the patient having the PAC will find these symptoms
bothersome, in which case the doctor may treat the PACs. Sometimes the
PACs can indicate heart disease or an increased risk for other cardiac
arrhythmias. In this case the underlying cause is treated. Often a beta
blocker will be prescribed for symptomatic PACs.
 Prognosis
In otherwise healthy patients, occasional premature atrial contractions are
a common and normal finding and do not indicate any particular health
risk. Rarely, in patients with other underlying structural heart problems,
PACs can trigger a more serious arrhythmia such as atrial flutter or atrial
fibrillation. In otherwise healthy people, PACs usually disappear with
adolescence.15,16

Premature Ventricular Contraction

 Epidemiology

PVCs are one of the most common arrhythmias and can occur in patients
with or without heart disease. Their prevalence varies greatly, with estimates
ranging from less than 3% to more than 60% in asymptomatic individuals.
Data from large, population-based studies indicate that the prevalence
ranges from less than 3% for young white women without heart disease to
almost 20% for older African American individuals with hypertension.

 Etiology

Cardiac causes of premature ventricular contractions include the

following:

 Acute MI or myocardial ischemia

 Myocarditis
 Cardiomyopathy, dilated or hypertrophic - Two consistent predictors of of
PVC-induced cardiomyopathy are PVC burden and PVC QRS duration
 Myocardial contusion
 Mitral valve prolapse
 Other causes of PVCs include the following:

 Hypoxia and/or hypercapnia

 Medications (eg, digoxin, sympathomimetics, tricyclic antidepressants,
aminophylline, caffeine)
 Illicit substances (eg, cocaine, amphetamines, alcohol, tobacco)
 Hypomagnesemia, hypokalemia, hypercalcemia

 Pathophysiology

PVCs reflect activation of the ventricles from a site below the

atrioventricular node (AVN). Suggested mechanisms for PVCs are reentry,
triggered activity, and enhanced automaticity. Reentry occurs when an area
of one-way block in the Purkinje fibers and a second area of slow
conduction are present. This condition is frequently seen in patients with
underlying heart disease that creates areas of differential conduction and
recovery due to myocardial scarring or ischemia. During ventricular
activation, the area of slow conduction activates the blocked part of the
system after the rest of the ventricle has recovered, resulting in an extra beat.
Reentry can produce single ectopic beats, or it can trigger paroxysmal
tachycardia.

Triggered beats are considered to be due to after-depolarizations triggered

by the preceding action potential. These are often seen in patients with
ventricular arrhythmias due to digoxin toxicity and reperfusion therapy after
myocardial infarction (MI).

Enhanced automaticity suggests an ectopic focus of pacemaker cells in the

ventricle that has a subthreshold potential for firing. The basic rhythm of the
heart raises these cells to threshold, which precipitates an ectopic beat. This
process is the underlying mechanism for arrhythmias due to excess
 catecholamines and some electrolyte deficiencies, particularly
hyperkalemia.

Ventricular ectopy associated with a structurally normal heart most

commonly occurs from the right ventricular outflow tract beneath the
pulmonic valve. The mechanism is thought to be enhanced automaticity
versus triggered activity. These arrhythmias are often induced by exercise,
isoproterenol (in the electrophysiology laboratory), the recovery phase of
exercise, or hormonal changes in female patients (pregnancy, menses,
menopause).

 Physical Examination

Important findings on the physical examination are those that provide clues
to the underlying cause of the ventricular ectopy, including the following:

 Blood pressure - Frequent PVCs may result in hemodynamic compromise;

frank hypotension is rare, but relative hypotension is not uncommon,
particularly in patients with underlying cardiac disease
 Pulse - The ectopic beat may produce a diminished or absent pulse,
depending on the force of the ventricular contraction
 Pulse oximetry - Hypoxia may precipitate PVCs
 Cardiac findings - Cannon A waves may be observed in the jugular venous
pulse if the timing of the PVC causes an atrial contraction against a closed
tricuspid valve
 Cardiopulmonary findings - Findings in conjunction with longstanding
hypertension (elevated BP and an S 4 ) or congestive heart failure (S 3 and
rales) are important clues to the cause and clinical significance of PVCs
 Neurologic findings - Agitation and findings of sympathetic activation (eg,
dilated pupils, warm and dry skin, tremor, tachycardia, hypertension)
suggest that catecholamines may be the cause of the ectopy

 Laboratory Studies

In young, healthy patients without concerning concomitant symptoms,

laboratory tests are not typically necessary. The following diagnostic
measures may be necessary, depending on the patient's history and
underlying illness(es):

 Obtain serum electrolyte levels, in particular potassium levels; consider

checking the magnesium level, especially in patients with low potassium
levels
 In selected patients, a drug screen may be helpful
 For patients taking medication with known proarrhythmic effects (eg,
digoxin, theophylline), drug levels may be useful

Echocardiography

Echocardiography is useful not only in evaluating the ejection fraction,

which is important in determining the prognosis and also in identifying
valvular disease or ventricular hypertrophy.

Electrocardiography

Electrocardiography (ECG) allows characterization of the ventricular

ectopy and determination of the cause. In addition to the standard 12-lead
ECG, a 2-minute rhythm strip may help in determining the frequency of the
ectopy and capturing infrequent premature ventricular contractions (PVCs).
Findings may include the following:

 Left ventricular hypertrophy

 Active cardiac ischemia (ST-segment depression or elevation and or T-wave
inversion)
 In patients with previous MI - Q waves or loss of R waves, bundle-branch
block
 Electrolyte abnormalities (hyperacute T waves, QT prolongation)
 Drug effects (QRS widening, QT prolongation)

On ECG, PVCs may be premature in relation to the next expected beat of

the basic rhythm. The pause after the premature beat is usually a fully
compensatory one. The R-R interval surrounding the premature beat is equal
to double the basic R-R interval, showing that the ectopic beat did not reset
the sinus node. PVCs may appear in a pattern of bigeminy, trigeminy, or
quadrigeminy (ie, may occur every other beat, every third beat, or every
fourth beat). PVCs with identical morphologies on a tracing are called
monomorphic or unifocal.

 Treatment
Medical Care

The optimal indications for therapy for premature ventricular contractions

(PVCs) have not yet been elucidated. Involvement of a cardiologist may be
indicated if the patient's condition is refractory to standard therapy.

Prehospital care

Perform telemetry, and secure intravenous (IV) access. Administer oxygen,

if any hypoxia exists. Complex ectopy in the setting of myocardial ischemia
or causing hemodynamic instability should be suppressed. Use lidocaine for
patients with myocardial ischemia.

Emergency department care

The decision to treat PVCs in the emergency or outpatient settings depends

on the clinical scenario. In the absence of cardiac disease, isolated,
asymptomatic ventricular ectopy, regardless of configuration or frequency,
requires no treatment. With cardiac disease, certain toxic effects, and
electrolyte imbalances, treatment may be required. Establish telemetry and
 IV access, initiate oxygen, and obtain a 12-lead electrocardiogram (ECG).
Note the following:

 Hypoxia - Treat the underlying cause; secure the ABCs and provide oxygen.
 Drug toxicity - Specific therapy is indicated for certain toxic effects—for
example, digoxin (Fab antibodies), tricyclics (bicarbonate), and
aminophylline (gastrointestinal decontamination and possibly
hemodialysis)
 Correct electrolyte imbalances, particularly those of magnesium, calcium,
and potassium

Prognosis

In asymptomatic patients without underlying heart disease, the long-term

prognosis is similar to that of the general population. Asymptomatic patients
with ejection fractions greater than 40% have a 3.5% incidence of sustained
ventricular tachycardia or cardiac arrest. Therefore, in patients with no
evidence of heart disease on noninvasive workup, reassurance is
appropriate.

In asymptomatic patients without underlying heart disease, the long-term

prognosis is similar to that of the general population. Asymptomatic patients
with ejection fractions greater than 40% have a 3.5% incidence of sustained
ventricular tachycardia or cardiac arrest. Therefore, in patients with no
evidence of heart disease on noninvasive workup, reassurance is
appropriate.17
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