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===Medical Therapy===
===Medical Therapy===
Medical therapy is divided into urgent and chronic management. Drug treatment of sinus bradycardia is usually not indicated for asymptomatic patients. In symptomatic patients, underlying [[electrolyte]] or [[acid-base disorders]] or [[hypoxia]] should be corrected. Intravenous [[atropine]] may provide temporary improvement in symptomatic patients. Persistently severe [[bradycardia]] is considered an absolute contraindication to the use of the medications such as [[Acebutolol]], [[Atenolol]], [[Carvedilol]], [[Metoprolol]] and [[Nebivolol]].
Medical treatment is categorized into emergent and permanent. Usually, [[sinus bradycardia]] treatment is not recommended for [[asymptomatic]] patients. Correcting underlying [[electrolyte]] or acid-base deficiencies or [[hypoxia]] in symptomatic patients. Intravenous [[atropine]] can temporarily help symptomatic patients. Persistently severe [[bradycardia]] is considered an absolute contraindication to the use of the medications such as [[Acebutolol]], [[Atenolol]], [[Carvedilol]], [[Metoprolol]] and [[Nebivolol]].


===Surgery===
===Surgery===

Revision as of 21:34, 7 September 2020

Bradycardia Microchapters

Home

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Bradycardia from other Conditions

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

Chest X Ray

CT

Echocardiography

MRI

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ibtisam Ashraf, M.B.B.S.[2]

Overview

Bradycardia is generally characterized as a heart rhythm of less than 60 beats per minute. It can be a significant problem if the heart doesn't pumps enough oxygen-rich blood into the bloodstream. When symptomatic, fatigue, weakness, dizziness, nausea and fainting will result. Numerous factors influence it, differing in part with age and conditioning. Sinus arrhythmia, variation in sinus rate due to respiratory processes, also causes sinus bradycardia. It is graded by impulse origin i.e. atria, AV junction, ventricles, and infantile. There are numerous pathophysiological disorders that can contribute to bradycardia such as acute myocardial infarction, obstructive sleep apnea, elevated vagal activity, heightened intracranial pressure, and infectious diseases such as Lyme disease, rocky mountain spotted fever, Chagas disease, psittacosis, Q fever and typhoid fever but the most common are sinus node and AV node dysfunction.

Historical Perspective

Jan Evangelista Purkinje found a net of gelatinous fibers in the subendocardium of the heart in 1839. Later on, in the 1880s, Walter Gaskell found that the region where the cardiac impulse generated was near the sinus venosus. The conduction bundle which links the sinus node and AV node was found by Wilhelm His Jr in 1893. In 1906, Sunao tawara assumed that a tissue present at the proximal end of the his bundle was the beginning of an electrical conducting system, which proceeded from the AV node through the bundle of His, separated into the bundle branches, and ended up as the Purkinje fibers. In the same year, Flack and Keith made the first observation of the mammalian sinoatrial node (SAN).

Classification

Bradycardia is a decrease in the heart rate due to abnormalities in the atria, AV node or ventricles. Atrial is further divided into Respiratory Sinus Arrhythmia, Sinus Bradycardia, and Sick Sinus Syndrome. The atrioventricular nodal bradycardia or junctional escape rhythm is usually caused by the absence of the electrical impulse from the sinus node. 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 a lack of electrical impulses or stimuli from the atrium. 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.

Pathophysiology

The underlying mechanism is not clinically relevant to treatment, which is the same in both cases of sick sinus syndrome: a permanent pacemaker. There are generally two types of problems that result in bradycardia: Sinus node dysfunction and AV node dysfunction. Sinus bradycardia can also be seen in Acute myocardial infarction, obstructive sleep apnea, exaggerated vagal activity, increased intracranial pressure and Infectious causes such as Lyme disease, Chagas disease, legionella, psittacosis, Q fever, typhoid fever, typhus, babesiosis, malaria, leptospirosis, yellow fever, dengue fever, viral hemorrhagic fevers, trichinosis, and Rocky Mountain Spotted fever.

Causes

Pathologic bradycardias are caused by disorders of impulse generation (impaired automaticity at SA node), impulse conduction (heart block) or escape pacemakers and rhythms. Bradycardia can be underlain by several causes, which are best divided into cardiac and non-cardiac causes or based on the location of the abnormality. Many drugs causes bradycardia such as Calcium gluconate, Ceritinib,Cosyntropin, Crizotinib, Dolasetron mesylate, Fosphenytoin sodium, Fosaprepitant, Lanreotide and Lorcaserin. Some Life-threatening causes include conditions such as acute myocardial infarction, Acute renal failure, Respiratory failure, Acute respiratory failure, Acute rheumatic fever, Bacterial endocarditis, Beta blocker overdose, Carbamate poisoning, Cervical spine injury.

Bradycardia differential diagnosis

Bradycardia must be differentiated from Sinoatrial Block, Atrioventricular heart block or dissociation, Wandering atrial pacemaker, Junctional (AV nodal) escape rhythms and Ventricular escape (idioventricular) rhythms.

Epidemiology and Demographics

Incidence is One in 600 adults over the age of 65 has sinus node dysfunction. The frequency of sick sinus syndrome is unknown in the general population, while in cardiac patients it has been estimated to be 3 in 5000. Bradycardia is more common in older patients, over the age of 65 years. There is no racial predilection to bradycardia. Bradycardia affects men and women equally.

Risk Factors

Common risk factors in the development of bradycardia include Congenital heart disease, Infection of the heart tissue, Heart surgery, Hypothyroidism or other metabolic condition, Damage caused by a heart attack or heart disease, electrolyte imbalance in the blood, Obstructive sleep apnea, Inflammatory diseases (rheumatic fever or lupus).

Screening

There is insufficient evidence to recommend routine screening for bradycardia.

Natural History, Complications and Prognosis

Natural History

Sinus bradycardia occurs in healthy patients as an adaptive response, particularly in well-conditioned persons or while sleeping, but it can also occur as a pathologic response in a variety of conditions. Sinus bradycardia itself does not cause symptoms directly, although a patient with comorbid conditions that may be exacerbated by decreased cardiac output (e.g. angina, heart failure) may have worsening symptoms related to comorbidity. Slower sinus rates are often very well tolerated. Asymptomatic resting bradycardias, particularly in trained athletes and young individuals are not pathological and don't require treatment.

Complications

Common complications of bradycardia include Heart failure, Syncope, Angina pectoris, hypotension and hypertension.

Prognosis

The prognosis is good when the rhythm is quickly identified by the healthcare provider. Nevertheless, people with sick sinus syndrome who have bradycardia appear to have a poor 5-year survival prognosis of 45-70 percent.

Diagnosis

History and Symptoms

Most patients with sinus bradycardia do not have symptoms. Individuals with symptoms can experience fatigue, exercise intolerance, lightheadedness, dizziness, syncope or presyncope, worsening of anginal symptoms, worsening of heart failure, or cognitive delay.

Physical Examination

Common physical examination findings of bradycardia include decreased level of consciousness, cyanosis, peripheral edema, pulmonary vascular congestion, dyspnea, poor perfusion and syncope.

Laboratory Findings

Laboratory findings pointing towards the diagnosis of bradycardia include electrolyte levels, glucose level, calcium level, magnesium level, thyroid function tests, toxicologic screen and troponin.

Electrocardiogram

An ECG may be helpful in the diagnosis of bradycardia. An upright P wave in leads I, II, and aVL, and a negative P wave in lead aVR, indicates a sinus origin of the bradycardia. It is vital to exclude other causes of bradyarrhythmias such as AV block.

X-ray

There are no x-ray findings associated with bradycardia.

Echocardiography and Ultrasound

There are no echocardiography/ultrasound findings associated with bradycardia.

CT scan

There are no CT scan findings associated with bradycardia.

Other Imaging Findings

There are no other imaging findings associated with bradycardia.

Other Diagnostic Studies

There are no other diagnostic studies associated with bradycardia.

Treatment

Medical Therapy

Medical treatment is categorized into emergent and permanent. Usually, sinus bradycardia treatment is not recommended for asymptomatic patients. Correcting underlying electrolyte or acid-base deficiencies or hypoxia in symptomatic patients. Intravenous atropine can temporarily help symptomatic patients. Persistently severe bradycardia is considered an absolute contraindication to the use of the medications such as Acebutolol, Atenolol, Carvedilol, Metoprolol and Nebivolol.

Surgery

Surgery is not the first-line treatment option for patients with bradycardia. However, temporary pacemaker followed by permanent pacemaker therapy may be required in some conditions.

Primary Prevention

There are no established measures for the primary prevention of bradycardia.

Secondary Prevention

There are no established measures for the secondary prevention of bradycardia.

References

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