Bradycardia overview: Difference between revisions
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[[Bradycardia]] is a condition typically described as a resting [[heart rate]] of under 60 beats per minute. It usually does not cause symptoms until the rate drops below 50 BPM. Once symptomatic, it can induce [[fatigue]], [[weakness]], [[dizziness]], [[nausea]], and [[fainting]] at very low rates. Numerous factors affect it and vary in part with age and physical conditioning. [[Sinus arrhythmia]], changes in sinus rate due to respiratory cycles, often accompanies [[sinus bradycardia]]. It is classified according to the origins of the impulse i.e. [[atria]], [[AV junction]] and [[Ventricles]]. There are several pathophysiologic conditions that can result in bradycardia such as [[Acute Myocardial infarction]], [[Obstructive sleep apnea]], Exaggerated vagal activity, [[Increased intracranial pressure]] and infectious diseases such as [[Lyme disease]], [[Rocky Mountain spotted fever|rocky mountain spotted fever]], [[Chagas disease]], [[psittacosis]], [[Q fever]] and [[typhoid fever]] but the most common are sinus node and [[AV node]] dysfunction. | [[Bradycardia]] is a condition typically described as a resting [[heart rate]] of under 60 beats per minute. It usually does not cause symptoms until the rate drops below 50 BPM. Once symptomatic, it can induce [[fatigue]], [[weakness]], [[dizziness]], [[nausea]], and [[fainting]] at very low rates. Numerous factors affect it and vary in part with age and physical conditioning. [[Sinus arrhythmia]], changes in sinus rate due to respiratory cycles, often accompanies [[sinus bradycardia]]. It is classified according to the origins of the impulse i.e. [[atria]], [[AV junction]] and [[Ventricles]]. There are several pathophysiologic conditions that can result in bradycardia such as [[Acute Myocardial infarction]], [[Obstructive sleep apnea]], Exaggerated vagal activity, [[Increased intracranial pressure]] and infectious diseases such as [[Lyme disease]], [[Rocky Mountain spotted fever|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 == | ==Historical Perspective== | ||
In 1839, Jan Evangelista Purkinje discovered a net of gelatinous fibres in the subendocardium of the heart. Walter Gaskell in the 1880s observed that the impulse of the heart began in the sinus venosus, and that this region had the most rhythmic ability. A conducting bundle between the atrium and the ventricle was found by Wilhelm His, Jr in 1893. In 1906, Sunao Tawara found a “complex Knoten” of tissue at the proximal end of the His bundle. He concluded that this was the inception of an electrical conducting system that continued from the AV node through the bundle of His, divided into the bundle branches, and terminated as the Purkinje fibres. In 1906, Martin Flack, a medical student, reported to Keith the first observation of the mammalian sinoatrial node (SAN). | In 1839, Jan Evangelista [[Purkinje fibers|Purkinje]] discovered a net of [[gelatinous]] fibres in the [[Endocardium|subendocardium]] of the heart. Walter Gaskell in the 1880s observed that the impulse of the heart began in the [[sinus venosus]], and that this region had the most rhythmic ability. A conducting bundle between the [[atrium]] and the [[ventricle]] was found by Wilhelm His, Jr in 1893. In 1906, Sunao Tawara found a “complex Knoten” of tissue at the proximal end of the [[His bundle|His bundle.]] He concluded that this was the inception of an electrical conducting system that continued from the [[AV node]] through the [[bundle of His]], divided into the bundle branches, and terminated as the Purkinje fibres. In 1906, Martin Flack, a medical student, reported to Keith the first observation of the mammalian [[Sinoatrial node|sinoatrial node (SAN)]]. | ||
==Classification== | ==Classification== | ||
Revision as of 02:46, 27 August 2020
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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 a condition typically described as a resting heart rate of under 60 beats per minute. It usually does not cause symptoms until the rate drops below 50 BPM. Once symptomatic, it can induce fatigue, weakness, dizziness, nausea, and fainting at very low rates. Numerous factors affect it and vary in part with age and physical conditioning. Sinus arrhythmia, changes in sinus rate due to respiratory cycles, often accompanies sinus bradycardia. It is classified according to the origins of the impulse i.e. atria, AV junction and Ventricles. There are several pathophysiologic conditions that can result in bradycardia such as Acute Myocardial infarction, Obstructive sleep apnea, Exaggerated vagal activity, Increased 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
In 1839, Jan Evangelista Purkinje discovered a net of gelatinous fibres in the subendocardium of the heart. Walter Gaskell in the 1880s observed that the impulse of the heart began in the sinus venosus, and that this region had the most rhythmic ability. A conducting bundle between the atrium and the ventricle was found by Wilhelm His, Jr in 1893. In 1906, Sunao Tawara found a “complex Knoten” of tissue at the proximal end of the His bundle. He concluded that this was the inception of an electrical conducting system that continued from the AV node through the bundle of His, divided into the bundle branches, and terminated as the Purkinje fibres. In 1906, Martin Flack, a medical student, reported to Keith 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 impulse 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
It is difficult and sometimes impossible to assign a mechanism to any particular bradycardia. However, 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 doesn'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 per cent.
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 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.
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.