User:Ferozemide/Bradycardia/Bibliography

Notes on big sources:
==== Notes on Braunwald's Heart Disease, 12e. Chapter 68: Bradyarrhthmias and Atrioventricular Block ====
 * Large population studies suggest a lower limit of normal of 50 BPM.
 * Frequently accompanied by arrythmias
 * Can be normal in well trained atheletes or adolescents and young adults during sleep.
 * Typically categorized by the level of interruption of the normal cardiac conduction system.
 * Sinus Bradycardia: Sinus node firing at < 50 bpm
 * Normal P waves before each QRS complex, with constant PR interval > 120 msec
 * Etiology: Excess vagal tone; decreased sympathetic tone, anatomic disruption of the sinus node.
 * Sinus Arrhythmia
 * Variation in a sinus cycle length in excess of 120 msec.
 * Most common arrythmia
 * Typically physiologically normal
 * Common in the young, especially in atheletes, and after administration of morphine or digitalis
 * Two basic forms: respiratory and non respiratory
 * Respiratory: Heart rate varies with breathing, increasing as the vagal tone drops in inspiration, and slowing during expiration
 * Non respiratory sinus arrhythmia can include sinus pause or sinus arrest, which both involve slowing or arrest of automatic impulse generation from the sinus node. This can lead to ventricular asystole if ventricular escape rhythms do not activate.
 * Sinoatrial exit block is a similar nonrespratory phenomenon of temporarily lost SA node impulses. However, in contrast to sinus pause, the impulse is generated at the SA node, but either unable to leave or delayed from leaving the node, delaying or preventing atrial depolariziation. Therefore, the length of the pause is usually a multiple of the P-P interval as seen on electrocardiography. Like sinus pause, sinoatrial exit block can be symptomatic, especially with prolonged pauses length.
 * Sinus Node Dysfunction
 * Encompasses several sinus node dysfunctions, including:
 * persistent sinus bradycardia or chronotropic incompetence
 * Sinus arrest or exit block
 * Combinations of SA/AV node conduction disturbances
 * Alternating periods of tachyarrythmias and bradicardias (Tachy-brady syndrome)
 * Intrinsic disease vs autonomic abnormalities, or some combination
 * Most causes of symptomatic sinus brady are caused or exacerbated by medications
 * Destruction of the sinus node
 * Can occur in the absence of underlying cardiac disease due to age related fibrosis and fatty infiltration of the SA node, or as a side effect of acute MI, stroke, or excessive vagal tone.
 * Occlusion of the sinus node artery can also lead to this condition.
 * AV Block
 * Normal sinus node impulse not conudcted or delayed passage through AV node when not in a refractory state due to preceeding impulse.
 * From AV node or in the His-Purkinje system. Equal conduction delays in the left and right bundle branches simultaneously can create PR prolongation without QRS complex widening. Occasionally, PR prolongation can be due to intra-atrial conduction delays.
 * There is some spectrum of disease presentations, as 2nd degree type 1 AV block can revert to 1st degree block with elevated sinus rates, and type 1 AV blocks can progress to type 1 2nd degree blocks with excess vagal tone, from carotid sinus massage.
 * 1st degree: delayed, but no missed conductions
 * 2nd degree: some dropped impulses, split into two categories. The dropped P wave phenomenon can be intermittent or regularly occurring.
 * Type 1: progressive lengthening of PR interval until successive ventricular beat is dropped. Location of block can usually be determined from surface ECG, with normal QRS complexes implying damage to the AV node without implication of the His-Purkinje system.
 * Type 2: sudden dropped beat without noticeable change in prior PR interval or conduction time
 * 3rd degree: no impulses from above the ventricles are transmitted through the AV node.

==== AHA/ACC 2018 guidelines on the evaluation and management of bradyarrythmias. ====


 * Slow heart rate and changes in intercellular conduction: normal in aging AND disease progression
 * Bradyarrythmias often dx in elderly
 * Classifications involve lesions of the SA node, atrial tissue, AV nodal tissue, conduction system
 * In patients with age related sinus node dysfunction (SND) who require atrial pacing; the development of heart block is common, suggesting that a similar fibrotic process that affects patients in SND can also affect the AV node.
 * SND: Most common in elderyly 70s-80s. Concomitant heart disease common: ischemic, HF, valvular disease, cerebrovascular disease, AF
 * Intrinsic causes of SA/AV nodal disease: Ischemia/infarction, infiltrative disease, collagen vascular disease, surgical trauma, endocrine,

==== Normal values of the electrocardiogram for ages 16-90 years ====


 * Normal ECG values from age 16-90
 * 4 Dutch studies collated, n = 13,354 healthy individuals with 12 lead ECG
 * Normal limits taken as 2nd-98th percentiles

Harrison's chapter 243, Principles of Clinical Cardiac Electrophysiology


 * Cardiac impulses generated at SA node, located between SVC and RA.
 * SA node demonstrates "automaticity" which generates regular impulses
 * Impulse at the SA node travels across the RA/LA via specialized conduction tissue, causing atrial contraction, notably creating the P wave on a surface ECG.
 * Once the impulse reaches AV node, conduction slows, demonstrated by the PR interval on a surface ECG. The AV node is, in anatomically normal hearts, the only electrical connection path between the atria and ventricles
 * This pause of conduction at the AV node is necessary for improved pump function as a delay in ventricular contraction allows for filling of blood by the atria
 * SA and AV node are regulated chiefly by the autonomic fibers of the central nervous system, which allow for increased heart rates during periods of metabolic stress and exercise.
 * After the AV node, the electrical impulse originally generated by the SA node travels down the His-Purkinje system, which allows for synchronized contraction of the left and right ventricles. This is because conductions travel faster along this specialized conduction tissue than they do between adjacent cardiomyocytes (cells of the heart muscle).
 * Depolarization of the ventricular myocytes creates the QRS complex seen on surface ECGs.
 * Cardiac repolarization occurs shortly after ventricular contraction, creating T waves seen on the ECG.

Harrison's Chapter 237: Basic Biology of the Cardiovascular system

Harrison's Chapter 245: The Bradyarrhythmias: Disorders of the Atrioventricular Node


 * Different connexons/gap junction in AV nodal tissue reduce electrical coupling, slowing conduction of action potentials
 * Capable of pacemaker activity, slow, 20-60 BPM
 * Compromised AV node can lead to bradycardia manifested by slow ventricular rates.
 * Transient AV conduction block can be normal in young adults, due to high resting vagal tone
 * Estimated incidence of 1 in 5000 per population per year
 * AV node disease much more common in those with structural heart disease, myocardial ischemia, age related fibrosis
 * 1st degree AV Block
 * Defined by ECG appearance
 * PR interval > 200 msec on EKG
 * Impulse is not blocked, but delayed.
 * Typically due to AV node damage, but can also be due to damage of the his-purkinje system
 * 2nd degree, Mobitz type 1
 * PR interval elongation, RR interval shortening
 * Difference between PR just before dropped beat and PR just after dropped beat will have the largest discrepancy, helping with diagnosis of type 1 2nd degree block. (The PR interval is usually consistent in the normal heart).

Outline of proposed changes
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 * Need a section outlining the basics of the normal cardiac conduction system, with sources
 * Lyme disease and infiltrative cardiomyopathy as a cuase of bradycardia -- where to put these rarer causes?
 * Sinus node dysfunction vs chronotropic incompetence