Bradycardia & Tachycardia

Hendri Saputra
 Regulation of heart rate
• Adjustments in heart rate are important in the short
term control of cardiac output and blood pressure.
• Tissues require different volumes of blood flow under
different conditions.
• Stroke volume may fall if the ventricular myocardium is
damaged or if blood volume is reduced by bleeding =>
homeostatic mechanisms maintain adequate cardiac
output by increasing the heart rate and contractility.
• Among the several factors that contribute to regulation
of heart rate, the most important are the autonomic
nervous system and hormones released by the adrenal
medullae (epinephrine and norepinephrine).
 Autonomic regulation of heart rate

A continually shifting balance exists between sympathetic

and parasympathetic stimulation of the heart.
 Chemical regulation of heart rate
• Hormones. Epinephrine and norepinephrine (from the
adrenal medullae) enhance the heart’s pumping
effectiveness.
– Thyroid hormones also enhance cardiac contractility and
increase heart rate.
• Cations. Concentrations of three cations—K, Ca2, and
Na—have a large effect on cardiac function.
– Elevated blood levels of K or Na decrease heart rate and
contractility.
– Excess Na blocks Ca2 inflow during cardiac action potentials,
thereby decreasing the force of contraction, whereas excess
K blocks generation of action potentials.
– Moderate increase in interstitial (and thus intracellular) Ca2
level speeds heart rate and strengthens the heartbeat.
 Other Factors in Heart Rate Regulation
• Age, gender, physical fitness, and body temperature
• Newborn baby is likely to have a resting heart rate over 120
beats/min
• Adult females often have slightly higher resting heart rates than
adult males
• Increased body temperature causes the SA node to discharge
impulses more quickly -> increasing heart rate.
• Decreased body temperature decreases heart rate and strength
of contraction.
• Well-trained athlete can achieve a cardiac output double that of a
sedentary person during strenuous activity, in part because
training causes hypertrophy of the heart. In resting state, resting
cardiac output is about the same as in a healthy untrained person
-> decrease HR.
 Bradikardi

• Bradikardi adalah frekuensi nadi kurang dari

60x/menit
• Frekuensi nadi yang lambat secara fisiologis bisa
tidak menjadi masalah bagi sebagian orang, tetapi
dapat juga menimbulkan gejala klinis yang buruk
bagi sebagian orang lain.
• Pada bradikardi yang disertai tanda dan gejala
gangguan perfusi seperti hipotensi, gangguan
kesadaran yang akut, nyeri dada, gagal jantung
kongesti, kejang, sinkop, atau tanda-tanda syok yang
lain, harus diatasi dengan pemberian tindakan atau
obat-obatan berikut:
– Atropin, pilihan pertama pada bradikardi yang disertai gejala
klinis yang buruk. Dosis 0,5 mg secara bolus IV tiap 3-5 menit
sampai dosis max 3 mg.
– Pacu jantung transkutan harus segera dipasang pada
bradikardi tidak stabil (AV blok derajat II mobitz II atau
derajat III) atau jika pemberian atropine tidak efektif.
– Epinefrin dan dopamin dapat diberikan apabila pemberian
atropine tidak efektif atau jika pacu jantung belum
terpasang/jika pacu jantung tidak efektif. Dosis epinefrin 2-
10 µg/menit, titrasi. Dosis dopamin 2-10 µg/kgBB/menit,
titrasi.
 Takikardi
• An elevated resting heart rate (> 100 beats/min)
• Takikardi diklasifikasikan berdasar tampilan gel. QRS
atau berdasarkan keteraturan iramanya.
• Takikardi QRS sempit: Supra Ventrikel Takikardi (SVT) ->
gel. QRS < 0,12 s
– Sinus takikardi
– Atrial fibrilasi
– Atrial flutter
– AV nodal reentry
– Accessory pathway mediated tachycardia
– Atrial tachycardia
– Multifocal atrial tachycardia (MAT)
– Junctional tachycardia
• Takikardi QRS lebar:
– Ventrikel takikardi
– SVT dengan aberansi (sindrom WPW)
– Pre excited tachycardia
• Berdasarkan keteraturan irama
– Takikardi dengan irama yang tidak teratur: Atrial fibrilasi,
atrial flutter
– Takikardi dengan irama teratur
Terima kasih