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.
