readings Flashcards
(27 cards)
bradycardia cause
failure of sinus node function of AV conduction disturbances
some causes of bradycardia
autonomic disturbances, drugs, chronic intrinsic conduction system disease, acute cardiac damage (endocarditis, infarction, etc.)
sick sinus syndrome/sinus node dysfunction
increasing prevalence with age
accounts for 50% of pacemaker patients
failure of intrinsic automaticity and failure of propagation of sinus node impulses to the surrounding atrial tissue
referred to as sinus node block
clinical presentation of sick sinus syndrome
persistent or episodic brady
inability to augment HR with exercise (chronotropic incompetence)
sinus pauses
or a comination
escape mechanisms
competent “escape mechanisms” allow a way around the sinus node dysfunction
these patients can be asymptomatic, clinically well tolerated, and require no treatment
sx of brady
fatigue, listlessness, or dyspnea
LH, pre-syncope, or syncope
exacerbates CHF
sinus node arrest/pause on EKG
pause in atrial activity –> absence of P waves
pauses greater than 3 seconds = pathologic
indications for pacemaker therapy
sinus pauses lasting >3 seconds
associated sx
history of sx related to bradycardia
sinoatrial exit block
sinus node dysfunction –> often accompanied by significant atrial fibrosis –> impeded propagation to the atrial tissue
EKG finding for sinoatrial exit block
abrupt halving of the P wave rate followed by an abrupt return to baseline sinus rate
bradycardia-tachycardia
tachyarrythmia
intermittent atrial arrythmias, often with intermittent Afib, with concomitant sinud node dysfunction resulting in long pauses or symptomatic bradycardia
typical manifestation: period of asystole with after termination of Afib due to recovery of automaticity
pacemaker indication
PR interval
AV conduction
first portion-start of P wave (sinus node) to the AV node (not clinically important, first portion does not change over time much with each patient)
second portion-propagation time through the AV node
last component-propagation through the bundle of His bundle and bundle branches (clinically important)
first degree AV block
PR interval exceeding 0.2 s in the setting of otherwise preserved AV conduction
implies a delay in AV conduction, usually at the level of AV node or His-Purkinje system
usually asymptomatic
second degree AV block
may be seen normally during sleep or in athletes
may be asymptomatic or be associated with palpitations, LH, syncope, fatigue
second degree AV in the subnodal system (His bundle and bundle branches)
malignant with a tendency to progress abruptly to greater degrees of AV block with unstable or absent escape mechanisms
can progress to complete heart block/sudden death
Mobitz Type I second degree AV block vs. Mobitz Type 2 second degree AV block
Type 1 - at the level of the AV node
Type 2 - below the AV node (His + bundles)
Mobitz Type 2
always a reason for concern
usually preceded by the development of a fixed bundle branch block
good clinical rule: these patients will also exhibit a full bundle branch block during periods of conduction in between episodes of 2nd degree AV block
AV nodal function improves with activity!
infranodal blocks do not improve with exercise
therefore, worsen with exercise or stress (increased HR)
2:1 AV block
failure of conduction every other P wave
high degree AV block
second degree AV block with conduction failure of 2 or more consecutive P waves
third degree AV block (complete heart block)
complete failure of the AV conduction system
atrial rate that is faster than the ventricular rate with AV dissociation
Afib always presents as an irregular ventricular response. therefore, the finding of a slow and regular response during Afib implies that the person also has an associated complete heart block.
supraventricular tachycardias
SVTs –> PSVT (paroxsymal), focal atrial tachycardia, atrial flutter, organized reentrant atrial tachycardias, Afib
