Atrial Fibrillation (A Fib) Overview

Atrial fibrillation (A fib) is an irregular and often rapid heart rhythm. The
irregular rhythm, or arrhythmia, results from abnormal electrical impulses
in the upper chambers (atria, singular=atrium) of the heart that cause the
heartbeat (ventricle contraction) to be irregular and usually fast. The
irregularity can be continuous, or it can come and go. Some individuals,
especially patients on medications, may have atrial fibrillation constantly
but not have a rapid (>100 heartbeats per minute) rate at rest. Variations
of A fib may be termed paroxysmal, persistent, or permanent (these are
further described below). A fib is the most common heart arrhythmia.
Normal heart contractions begin as an electrical impulse in the right
atrium. This impulse comes from an area of the atrium called the
sinoatrial (SA) or sinus node, the "natural pacemaker" that causes the
normal range of regular heartbeats. Normal heartbeats proceed as
follows:

The electrical impulse originates in the SA node of the right atrium.

As the impulse travels through the atrium, it produces a wave of
muscle contractions. This causes the atria to contract.
The impulse reaches the atrioventricular (AV) node in the muscle wall
between the two ventricles. There, it pauses, giving blood from the
atria time to enter the ventricles.
The impulse then continues into the ventricles, causing ventricular
contraction that pushes the blood out of the heart, completing a single
heartbeat.

Figure 1. Picture of
electrical pathways
of the heart

In an adult person with a normal heart rate and rhythm the heart beats
50-100 times per minute at rest (not under stress or exercising).

If the heart beats more than 100 times per minute, the heart rate is
considered fast (tachycardia).
If the heart beats less than 50 times per minute, the heart rate is
considered slow (bradycardia).

In atrial fibrillation, multiple sources of impulses other than only from the
SA node travel through the atria at the same time. The reason that these
sources develop are not completely understood, but cardiac muscles in
the pulmonary veins have electrical generating properties and may be
one source of these extra impulses.

Instead of a coordinated contraction, the atrial contractions are

irregular, disorganized, chaotic, and very rapid. The atria may
contract at a rate of 400-600 beats per minute. The blood flow from
the atria to the ventricles is often disrupted.
These irregular impulses reach the AV node in rapid succession, but
not all of them make it past the AV node. Therefore, the ventricles
beat more slowly than the atria, often at fairly fast rates of 110-180
beats per minute in an irregular rhythm.
The resulting rapid, irregular heartbeat causes an irregular pulse and
sometimes a sensation of fluttering in the chest.

Atrial fibrillation can occur in several different patterns.

Intermittent (paroxysmal): The heart develops atrial fibrillation and

typically converts back again spontaneously to normal (sinus) rhythm.
The episodes may last anywhere from seconds to days.
Persistent: Atrial fibrillation occurs in episodes, but the arrhythmia
does not convert back to sinus rhythm spontaneously. Medical

treatment or cardioversion (electrical treatment) is required to end the

episode.
Permanent: The heart is always in atrial fibrillation. Conversion back
to sinus rhythm either is not possible or is deemed not appropriate for
medical reasons. In most cases, the rate is reduced by medications
and the patients are placed on anticlotting medication for their
lifetime.

Atrial fibrillation, often called A Fib, atrial tachyarrhythmia, or atrial

tachycardia, is one of the very common heart rhythm disorders.

It affects about 4% of the population, mostly people older than 60

years. This amounts to more than 2.6 million people in the U.S.
People older than 40 have about a 25% chance of developing A fib in
their lifetime.
The risk of developing atrial fibrillation increases as we get older.
About 10% of people older than 80 years have atrial fibrillation.

For many people, atrial fibrillation may cause symptoms but does no
harm.

Complications like blood clot formation, strokes, and heart failure can
arise, but appropriate treatment reduces the chances that such
complications will develop.
If treated properly, atrial fibrillation infrequently causes serious or lifethreatening problems.

Atrial Fibrillation (A Fib) Diagnosis

The doctor will often begin by asking the patient about their medical
history to help determine the severity of symptoms. The doctor will
assess if any associated factors (for example, alcohol or caffeine intake)
may be contributing to the patient's symptoms. The doctor will also listen

to the patient's heartbeat and lungs. The evaluation may include the
following tests:
Electrocardiogram (ECG or EKG): This is the primary test to determine
when an arrhythmia is atrial fibrillation. The ECG can help the doctor
distinguish A fib from other arrhythmias that may have similar symptoms
(atrial flutter, supraventricular tachycardia, or runs of ventricular
tachycardia). The test can also sometimes reveal damage (ischemia) to
the heart, if there is any.
The following illustrations show the usual ECG tracing from a patient
with A fib; the second figure shows the different appearance between a
normal (single lead) ECG tracing and the irregular appearance of an
atrial fibrillation (single lead) ECG tracing. The atrial tracing for the A fib
tracing shows a slowed irregular heartbeat of A fib, where the irregular
waves are easily seen before the heartbeat (Figure 2). These waves can
be seen if the heartbeat is slowed; they are difficult to see in patients
with a rapid heartbeat shown in Figure 3.

Figure 2. Rapid heart rate ECG of a patient with

atrial fibrillation. SOURCE: Image reprinted with
permission

from Medscape.com, 2012.

Lab tests: There is no blood test that can confirm that a person has
atrial fibrillation. However, blood tests may be done to check for certain
underlying causes of atrial fibrillation and to rule out heart damage, as
from a heart attack. People already taking medication for atrial fibrillation
may need blood tests to make sure there is enough of the drug
(usually digoxin) in their system to work effectively. Blood tests that may
be done to rule out other conditions include:

Complete blood cell count (CBC)

Markers for heart injury or stress (enzymes such as troponins
and creatinekinase [CK] and BNP)
Digoxin drug level (in patients taking this medication)
Prothrombin time (PT) and international normalized ratio (INR) (For
those taking warfarin [Coumadin] to prevent blood clotting, these
tests show how well the drug is working to lower the risk of a blood
clot forming in the heart or elsewhere.)
Serum electrolytes to evaluate sodium and potassium levels
Thyroid function tests for hyperthyroidism

Atrial Fibrillation (A Fib) Prognosis

In general, the outlook for most individuals with A fib is good to fair,
depending on the cause of the disease and how well the patient
responds to treatment. The most dangerous complication of atrial
fibrillation is stroke.

Someone with atrial fibrillation is about 3-5 times more likely to have
a stroke than someone who does not have atrial fibrillation.

The risk of stroke from atrial fibrillation for people aged 50-59 years is
about 1.5%. For those aged 80-89 years, the risk is about 30%.
Warfarin (Coumadin), when taken in appropriate doses and
monitored carefully, reduces this risk of stroke by over two-thirds.
It is important to know that clinical trial data have shown that
individuals can live just as long with atrial fibrillation with a controlled
heart rate -- for example, with medications plus Coumadin -- as other
people in normal sinus rhythm (AFFIRM trial).

Another complication of atrial fibrillation is heart failure.

In heart failure, the heart no longer contracts and pumps as strongly

as it should.
The very rapid contraction of the ventricles in atrial fibrillation can
gradually weaken the muscle walls of the ventricles.
This is uncommon, however, because most people seek treatment for
atrial fibrillation before the heart begins to fail.

Patients with complications of stroke or heart failure have a more

guarded outcome than those without complications. However, for most
people with atrial fibrillation, relatively simple treatment dramatically
lowers the risk of serious outcomes. Those who have infrequent and
brief episodes of atrial fibrillation may need no further treatment other
than learning to avoid the triggers of their episodes, such as caffeine,
alcohol, or overeating.

Chest x-ray: This imaging test is used to evaluate for complications

such as fluid in the lungs or to estimate heart size.

Echocardiogram or transesophageal echocardiogram: This is

an ultrasoundtest that uses sound waves to make a picture of the heart
while it is beating.

This test is done to identify problems in heart valves or ventricular

function or to look for blood clots in the atria.
This very safe test uses the same technique used to check a fetus
inpregnancy.

Ambulatory electrocardiogram (Holter monitor): This test involves

wearing a monitor similar to that used for an ECG for a period of time
(usually 24-48 hours) to try to document the arrhythmia while people go
about their everyday activities.

The device is worn for 24-48 hours and is named a Holter monitor.
An event monitor is a device that can be worn for 1-2 weeks and
records the heart rhythm when it is activated by the patient; it is
similar to a Holter monitor but only records heart rhythms when
activated by the patient.
These tests may be used if symptoms come and go and ECGs do not
reveal the arrhythmia or other problems that could lead to similar
symptoms of A fib.

SHOCK KARDIOGENIK
Shock
kardiogenik disebabkan
oleh
kegagalan
fungsi
pompa jantung yang mengakibatkan curah jantung menjadi berkurang atau
berhenti sama sekali untuk memenuhi kebutuhan metabolisme. Shock
kardiogenik ditandai
oleh
gangguan
fungsi
ventrikel,
yang
mengakibatkan gangguan berat pada perfusi jaringan dan penghantaran
oksigen ke jaringan.
Ventrikel kiri gagal bekerja sebagai pompa dan tidak mampu menyediakan
curah jantung yang memadai untuk mempertahankan perfusi
jaringan. Shock kardiogenikdapat didiagnosa dengan mengetahui adanya
tanda-tanda shock dan dijumpai adanya penyakit jantung, seperti infark

miokard yang luas, gangguan irama jantung, rasa nyeri daerah torak, atau
adanya emboli paru, tamponade jantung, kelainan katub atau sekat
jantung.
Masalah yang ada adalah kurangnya kemampuan jantung untuk
berkontraksi. Tujuan utama pengobatan adalah meningkatkan curah
jantung.
Etiologi Shock Kardiogenik
1.
Gangguan kontraktilitas miokardium.
2.
Disfungsi ventrikel kiri yang berat yang memicu terjadinya
kongesti paru dan/atau hipoperfusi iskemik.
3.
Infark miokard akut ( AMI),
4.
Komplikasi dari infark miokard akut, seperti: ruptur otot
papillary, ruptur septum, atau infark ventrikel kanan, dapat
mempresipitasi (menimbulkan/mempercepat) syok kardiogenik pada
pasien dengan infark-infark yang lebih kecil.
5.
Valvular stenosis.
6.
Myocarditis ( inflamasi miokardium, peradangan otot jantung).
7.
Cardiomyopathy ( myocardiopathy, gangguan otot jantung
yang tidak diketahui penyebabnya ).
8.
Acute mitral regurgitation.
9.
Valvular heart disease.
10. Hypertrophic obstructive cardiomyopathy.
Patofisiologi Shock Kardiogenik
Tanda dan gejala shock kardiogenik mencerminkan sifat sirkulasi
patofisiologi gagal jantung. Kerusakan jantung mengakibatkan penurunan
curah jantung, yang pada gilirannya menurunkan tekanan darah arteri ke
organ-organ vital. Aliran darah ke arteri koroner berkurang, sehingga
asupan oksigen ke jantung menurun, yang pada gilirannya meningkatkan
iskemia dan penurunan lebih lanjut kemampuan jantung untuk memompa,
akhirnya terjadilah lingkaran setan.
Tanda klasik shock kardiogenik adalah tekanan darah rendah, nadi cepat
dan lemah, hipoksia otak yang termanifestasi dengan adanya konfusi dan
agitasi, penurunan haluaran urin, serta kulit yang dingin dan lembab.
Disritmia sering terjadi akibat penurunan oksigen ke jantung.seperti pada
gagal jantung, penggunaan kateter arteri pulmonal untuk mengukur

tekanan ventrikel kiri dan curah jantung sangat penting untuk mengkaji
beratnya masalah dan mengevaluasi penatalaksanaan yang telah dilakukan.
Peningkatan tekanan akhir diastolik ventrikel kiri yang berkelanjutan
(LVEDP = Left Ventrikel End Diastolik Pressure) menunjukkan bahwa
jantung gagal untuk berfungsi sebagai pompa yang efektif.
Menurut Mubin (2008), diagnosis syok kardiogenik adalah berdasarkan:
A. Keluhan Utama Syok Kardiogenik
1. Oliguri (urin < 20 mL/jam).
2. Mungkin ada hubungan dengan IMA (infark miokard akut).
3. Nyeri substernal seperti IMA.
B. Tanda Penting Shock Kardiogenik
1. Tensi turun < 80-90 mmHg.
2. Takipneu dan dalam.
3. Takikardi.
4. Nadi cepat, kecuali ada blok A-V.
5. Tanda-tanda bendungan paru: ronki basah di kedua basal paru.
6. Bunyi jantung sangat lemah, bunyi jantung III sering terdengar.
7. Sianosis.
8. Diaforesis (mandi keringat).
9. Ekstremitas dingin.
10. Perubahan mental.
Komplikasi Shock Kardiogenik
1. Cardiopulmonary arrest
2. Disritmi
3. Gagal multisistem organ
4. Stroke
5. Tromboemboli
Penatalaksanaan Medis Shock Kardiogenik :
1.
Patikan jalan nafas tetap adekuat, bila tidak sadar sebaiknya
dilakukan intubasi.
2.
Berikan oksigen 8 - 15 liter/menit dengan menggunakan
masker untuk mempertahankan PO2 70 - 120 mmHg
3.
Rasa nyeri akibat infark akut yang dapat memperbesar syok
yang ada harus diatasi dengan pemberian morfin.

4.
Koreksi hipoksia, gangguan elektrolit, dan keseimbangan asam
basa yang terjadi.
5.
Bila mungkin pasang CVP.
6.
Pemasangan kateter Swans Ganz untuk meneliti hemodinamik.
Medikamentosa :
1.
Morfin sulfat 4-8 mg IV, bila nyeri.
2.
Anti ansietas, bila cemas.
3.
Digitalis, bila takiaritmi dan atrium fibrilasi.
4.
Sulfas atropin, bila frekuensi jantung < 50x/menit.
5.
Dopamin dan dobutamin (inotropik dan kronotropik), bila
perfusi jantung tidak adekuat. Dosis dopamin 2-15 mikrogram/kg/m.
6.
Dobutamin 2,5-10 mikrogram/kg/m: bila ada dapat juga
diberikan amrinon IV.
7.
Norepinefrin 2-20 mikrogram/kg/m.
8.
Diuretik/furosemid 40-80 mg untuk kongesti paru dan
oksigenasi jaringan.
9.
Digitalis bila ada fibrilasi atrial atau takikardi supraventrikel.
Obat alternatif:
Menurut Dean AJ, Beaver KM (2007):
1. Emergent therapy
Terapi ini bertujuan untuk menstabilkan hemodinamik pasien dengan
oksigen, pengaturan jalan nafas (airway control), dan akses intravena.
Diperlukan usaha untuk memaksimalkan fungsi ventrikel kiri.
2. Volume expansion
Jika tidak ada tanda volume overload atau edema paru, volume expansion
dengan 100mL bolus dari normal saline setiap 3 menit sebaiknya dicoba;
hingga, baik perfusi yang cukup maupun terjadi kongesti paru. Pasien
dengan infark ventrikel kanan memerlukan peningkatan tekanan untuk
mempertahankan atau menjaga kardiak output.
3. Inotropic support

Pasien dengan hipotensi ringan (tekanan darah sistolik 80-90

mmHg) dan kongesti pulmoner, untuk hasil terbaik dirawat dengan
dobutamine (2,5 mikrogram/kg berat badan/menit, pada interval 10 menit).
Dobutamine menyediakan dukungan inotropik saat permintaan oksigen
miokardium meningkat secara minimal.

Pasien dengan hipotensi berat (tekanan darah sistolik kurang dari 7580 mmHg) sebaiknya dirawat dengan dopamine.
Pada dosis lebih besar dari 5,0 mikrogram/kg berat badan/menit, stimulasi
alfa-adrenergik secara bertahap meningkat, menyebabkan vasokonstriksi
perifer. Pada dosis lebih besar dari 20 mikrogram/kg berat badan/menit,
dopamine meningkatkan ventricular irritability tanpa keuntungan
tambahan.

Kombinasi dopamine dan dobutamine merupakan strategi terapeutik

yang efektif untuk syok kardiogenik, meminimalkan berbagai efek
samping dopamine dosis tinggi yang tidak diinginkan dan menyediakan
bantuan/dukungan inotropik.

Jika dukungan tambahan untuk tekanan darah diperlukan, maka

dapat dicoba norepinephrine, yang berefek alfa-adrenergik yang lebih
kuat. Dosis awal : 0,5-1 mikrogram/menit.
4. Terapi reperfusi
Reperfusi miokardium iskemik merupakan terapi yang efektif untuk pasien
dengan infark miokard akut dan syok kardiogenik.