bradyarrhythmia

徐脈性不整脈

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2013/04/09 15:59:20」(JST)

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Bradycardia

Sinus bradycardia seen in lead II with a heart rate of about 50.
ICD-10	R00.1
ICD-9	427.81, 659.7, 785.9, 779.81
MeSH	D001919

Bradycardia (pron.: /ˌbrædɪˈkɑrdiə/; Greek βραδυκαρδία, bradykardía, "heart slowness"), in the context of adult medicine, is the resting heart rate of under 60 beats per minute bpm, though it is seldom symptomatic until the rate drops below 50 beats/min. It sometimes results in fatigue, weakness, dizziness and at very lower rates fainting. During sleep the heart normally beats slower than 60 beats/min, this is because the body at rest requires less oxygen. A heart rate of 40-50 bpm is not unusual while a person is asleep.

Trained athletes may also have a very slow resting heart rate as sport adaptation, which prevents tachycardia during training. (e.g. professional cyclist Miguel Indurain had a resting heart rate of 28 beats per minute). Whilst Martin Brady achieved the world record for the slowest heartbeat in a healthy human with a heart rate of just 27 bpm in 2005 (a record that still stands)

The term relative bradycardia is used in explaining a heart rate which, although not actually below 60 beats per minute, is still considered too slow for the individual's current medical condition.

Definition

Bradycardia in an adult is any heart rate less than 60 beats per minute (bpm), although symptoms usually manifest only for heart rates less than 50.

Classification

Atrial

See also: Sinus bradycardia and Sick sinus syndrome

Atrial bradycardias are divided into three different types. The first, respiratory sinus arrhythmia, is usually found in young and healthy adults. Heart rate increases during inhalation and decreases during exhalation. This is thought to be caused by changes in the vagal tone during respiration. If the decrease during exhalation drops the heart rate below 60 bpm on each breath, this type of bradycardia is usually deemed benign and a sign of good autonomic tone.

The second, sinus bradycardia, is a sinus rhythm of less than 60 bpm. It is a common condition found in both healthy individuals and those who are considered well-conditioned athletes. Studies have found 50-85% of conditioned athletes have benign sinus bradycardia, as compared to 23% of the general population studied. The heart muscle of athletes has become conditioned to have a higher stroke volume, so requires fewer contractions to circulate the same volume of blood.

The third, Sick sinus syndrome, covers conditions that include severe sinus bradycardia, sinoatrial block, sinus arrest, and bradycardia-tachycardia syndrome (atrial fibillation, flutter, and paroxysmal supraventricular tachycardia).

Atrioventricular nodal

See also: Junctional rhythm

An atrioventricular nodal bradycardia or AV junction rhythm is usually caused by the absence of the electrical impulse from the sinus node. This usually appears on an EKG with a normal QRS complex accompanied with an inverted P wave either before, during, or after the QRS complex.

An AV junctional escape is a delayed heartbeat originating from an ectopic focus somewhere in the AV junction. It occurs when the rate of depolarization of the SA node falls below the rate of the AV node. This dysrhythmia also may occur when the electrical impulses from the SA node fail to reach the AV node because of SA or AV block. This is a protective mechanism for the heart, to compensate for an SA node that is no longer handling the pacemaking activity, and is one of a series of backup sites that can take over pacemaker function when the SA node fails to do so. This would present with a longer PR interval. A junctional escape complex is a normal response that may result from excessive vagal tone on the SA node. Pathological causes include sinus bradycardia, sinus arrest, sinus exit block, or AV block.

Ventricular

See also: Atrioventricular block

A ventricular bradycardia, also known as ventricular escape rhythm or idioventricular rhythm, is a heart rate of less than 50 bpm. This is a safety mechanism when there is lack of electrical impulse or stimuli from the atrium. Impulses originating from or below the His bundle, also known as ventricular, will produce a wide QRS complex with heart rates between 20 and 40 bpm. Those above the His bundle, also known as junctional, will typically range between 40 and 60 bpm with a narrow QRS complex. In a third degree heart block, approximately 61% take place at the bundle branch-Purkinje system, 21% at the AV node, and 15% at the His bundle. AV block may be ruled out with an EKG indicating "a 1:1 relationship between P waves and QRS complexes." Ventricular bradycardias occurs with sinus bradycardia, sinus arrest, and AV block. Treatment often consists of the administration of atropine and cardiac pacing.

Infantile

For infants, bradycardia is defined as a heart rate of less than 100 bpm (normal is around 120-160). Premature babies are more likely than full-term babies to have apnea and bradycardia spells; their cause is not clearly understood. Some researchers think the spells are related to centers inside the brain, that regulate breathing, which may not be fully developed. Touching the baby gently or rocking the incubator slightly will almost always get the baby to start breathing again, which increases the heart rate. Medications (theophylline or caffeine) can be used to treat these spells in babies if necessary. NICU standard practice is to electronically monitor the heart and lungs for this reason.

Causes

This cardiac arrhythmia can be underlain by several causes, which are best divided into cardiac and noncardiac causes. Noncardiac causes are usually secondary, and can involve recreational drug use or abuse; metabolic or endocrine issues, especially in the thyroid; an electrolyte imbalance; neurologic factors; autonomic reflexes; situational factors such as prolonged bed rest; and autoimmunity. Cardiac causes include acute or chronic ischemic heart disease, vascular heart disease, valvular heart disease, or degenerative primary electrical disease. Ultimately, the causes act by three mechanisms: depressed automaticity of the heart, conduction block, or escape pacemakers and rhythms.

Generally, two types of problems result in bradycardias: disorders of the sinoatrial node (SA node), and disorders of the atrioventricular node (AV node).

With sinus node dysfunction (sometimes called sick sinus syndrome), there may be disordered automaticity or impaired conduction of the impulse from the sinus node into the surrounding atrial tissue (an "exit block"). Second degree sinoatrial blocks can only be detected by use of a 12-lead EKG. It is difficult and sometimes impossible to assign a mechanism to any particular bradycardia, but the underlying mechanism is not clinically relevant to treatment, which is the same in both cases of sick sinus syndrome: a permanent pacemaker.

Atrioventricular conduction disturbances (aka: AV block; 1^o AV block, 2^o type I AV block, 2^o type II AV block, 3^o AV block) may result from impaired conduction in the AV node, or anywhere below it, such as in the Bundle of His. The clinical relevance pertaining to AV blocks is greater than that of sinoatrial blocks.

Patients with bradycardia have likely acquired it, as opposed to having it congenitally. Bradycardia is more common in older patients.

Beta-blocker medicines also can slow the heart rate and decrease how forcefully the heart contracts. Beta blockers may slow the heart rate to a dangerous level if prescribed together with calcium channel blocker type medications.

Diagnosis

A diagnosis of bradycardia in adults is based on a heart rate less than 60 bpm. This is determined usually either via palpation or an EKG.

If symptoms occur, a determination of electrolytes may be helpful in determining the underlying cause.

Management

The treatment of bradycardia is dependent on whether or not the person is stable or unstable. If oxygen saturations are low, supplemental oxygen should be provided.

Stable

Emergent treatment is not needed if the person is asymptomatic or minimally symptomatic.

Unstable

If a person is unstable the initial recommended treatment is intravenous atropine. Doses less than 0.5 mg should not be used as this may further decrease the rate. If this is not effective intravenous inotrope infusion (dopamine, epinephrine) or transcutaneous pacing should be used. Transvenous pacing may be required if the cause of the bradycardia is not rapidly reversible.

References

UpToDate Contents

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• 1. 洞徐脈 sinus bradycardia
• 2. 小児における徐脈 bradycardia in children
• 3. Permanent cardiac pacing: Overview of devices and indications
• 4. 胎児不整脈の診断および治療に対する一般的アプローチの概要 overview of the general approach to diagnosis and treatment of fetal arrhythmias
• 5. 成人における確定診断を得られていない低血圧やショックの評価および初期アプローチ evaluation of and initial approach to the adult patient with undifferentiated hypotension and shock

English Journal

• Effect of propranolol on the treatment of infantile hemangiomas: a single tertiary center 3-year experience.

• Park YW1, Yeom KB, Choi JW, Kim DY, Shin H, Kim KH.Author information 1Department of Dermatology, Seoul National University College of Medicine.AbstractBACKGROUND: Propranolol has recently become a successful first-line therapy in the treatment of infantile hemangiomas (IHs).
• The Journal of dermatological treatment.J Dermatolog Treat.2014 Oct;25(5):391-5. doi: 10.3109/09546634.2012.761667. Epub 2013 Feb 24.
• BACKGROUND: Propranolol has recently become a successful first-line therapy in the treatment of infantile hemangiomas (IHs).OBJECTIVE: To evaluate and analyze the authors' experience of propranolol treatment for IHs.METHODS: A retrospective, observational study was conducted. Medical records were re
• PMID 23273264

• Cardiorespiratory effects induced by 2-nitrate-1,3-dibuthoxypropan are reduced by nitric oxide scavenger in rats.

• Queiroz TM1, Mendes-Júnior LG1, Guimarães DD1, França-Silva MS1, Nalivaiko E2, Braga VA1.Author information 1Biotechnology Center, Federal University of Paraiba, João Pessoa, PB, Brazil.2School of Biomedical Sciences and Pharmacy, University of Newcastle, NSW, Australia. Electronic address: Eugene.nalivaiko@newcastle.edu.au.AbstractThe search for new nitric oxide donors is warranted by the limitations of organic nitrates currently used in cardiology. The new organic nitrate 2-nitrate-1,3-dibuthoxypropan (NDBP) exhibited promising cardiovascular activities in previous studies. The aim of this study was to investigate the cardiorespiratory responses evoked by NDBP and to compare them to the clinically used organic nitrate nitroglycerine (NTG). Arterial pressure, heart rate and respiration were recorded in conscious adult male Wistar rats. Bolus i.v. injection of NDBP (1 to 15mg/kg; n=8) and NTG (0.1 to 5mg/kg; n=8) produced hypotension. NDBP induced bradycardia at all doses, while NTG induced tachycardia at three lower doses but bradycardia at higher doses. Hydroxocobalamin (20mg/kg; HDX), a NO scavenger, blunted hypotension induced by NDBP (15mg/kg), and its bradycardic effect (n=6). In addition, HDX blunted both hypotension and bradycardia induced by a single dose of NTG (2.5mg/kg; n=6). Both NDBP and NTG altered respiratory rate, inducing a biphasic effect with a bradypnea followed by a tachypnea; HDX attenuated these responses. Our data indicate that NDBP and NTG induce hypotension, bradycardia and bradypnea, which are mediated by nitric oxide release.
• Autonomic neuroscience : basic & clinical.Auton Neurosci.2014 Apr;181:31-6. doi: 10.1016/j.autneu.2013.12.012. Epub 2013 Dec 24.
• The search for new nitric oxide donors is warranted by the limitations of organic nitrates currently used in cardiology. The new organic nitrate 2-nitrate-1,3-dibuthoxypropan (NDBP) exhibited promising cardiovascular activities in previous studies. The aim of this study was to investigate the cardio
• PMID 24418115

• Sympathetic nerve activity and simulated diving in healthy humans.

• Shamsuzzaman A1, Ackerman MJ2, Kuniyoshi FS2, Accurso V2, Davison D2, Amin RS3, Somers VK2.Author information 1Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA; Mayo Clinic, Rochester, MN, USA. Electronic address: Abu.Shamsuzzaman@cchmc.org.2Mayo Clinic, Rochester, MN, USA.3Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.AbstractThe goal of our study was to develop a simple and practical method for simulating diving in humans using facial cold exposure and apnea stimuli to measure neural and circulatory responses during the stimulated diving reflex. We hypothesized that responses to simultaneous facial cold exposure and apnea (simulated diving) would be synergistic, exceeding the sum of responses to individual stimuli. We studied 56 volunteers (24 female and 32 male), average age of 39years. All subjects were healthy, free of cardiovascular and other diseases, and on no medications. Although muscle sympathetic nerve activity (MSNA), blood pressure, and vascular resistance increased markedly during both early and late phases of simulated diving, significant reductions in heart rate were observed only during the late phase. Total MSNA during simulated diving was greater than combined MSNA responses to the individual stimuli. We found that simulated diving is a powerful stimulus to sympathetic nerve traffic with significant bradycardia evident in the late phase of diving and eliciting synergistic sympathetic and parasympathetic responses. Our data provide insight into autonomic triggers that could help explain catastrophic cardiovascular events that may occur during asphyxia or swimming, such as in patients with obstructive sleep apnea or congenital long QT syndrome.
• Autonomic neuroscience : basic & clinical.Auton Neurosci.2014 Apr;181:74-8. doi: 10.1016/j.autneu.2013.12.001. Epub 2013 Dec 12.
• The goal of our study was to develop a simple and practical method for simulating diving in humans using facial cold exposure and apnea stimuli to measure neural and circulatory responses during the stimulated diving reflex. We hypothesized that responses to simultaneous facial cold exposure and apn
• PMID 24368150

Japanese Journal

• 心電図の読み方レッスン : 基本を学ぶ (東邦医学会雑誌) -- (教授特別講演(第145回東邦医学会例会))

• 池田 隆徳
• Toho journal of medicine 1(2), 104-110, 2015-06
• NAID 40020526581

• 徐脈性疾患と分子遺伝学 (特集 循環器疾患と分子遺伝学)

• 石川 泰輔,蒔田 直昌
• 循環器内科 77(4), 360-365, 2015-04
• NAID 40020456002

• Fetal Bradyarrhythmia Associated With Congenital Heart Defects : Nationwide Survey in Japan

• Miyoshi Takekazu,Maeno Yasuki,Sago Haruhiko [他]
• Circulation journal : official journal of the Japanese Circulation Society 79(4), 854-861, 2015-04
• NAID 40020412405

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bradyarrhythmia /brady·ar·rhyth·mia/ (brad″e-ah-rith´me-ah) any disturbance in the heart rhythm in which the heart rate is abnormally slowed. brad·y·ar·rhyth·mi·a (brăd′ē-ə-rĭth′mē-ə) n. A disturbance of the heart's rhythm resulting in a ...

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★リンクテーブル★

リンク元

「徐脈性不整脈」

「徐脈性不整脈」

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bradyarrhythmia, bradyarrhythmias

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徐拍性不整脈

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