bradyarrhythmias Flashcards
ECG correlation
right before P wave- sinus node P wave- atria downslope of p wave- AVnode right after P wave- hisbundle right before qrs- bundle branches qrs- ventricular muscle
hierarchy cardiac pacemaker cells/regions
Sinus node- highest intrinsic rate, SN rates and acceleration decline with age (60-180 bpm)
Atrial foci- subordinate rates to the SN in the normal heart, p wave morphology on the ECG differs from the SN, Rates (60-680 bpm)
Junctional foci- may occur as isolated escape complexes or as a sustained rhythm, the QRS is generally narrow and is not preceded by p waves. (40-60)
Sustained ventricular escape rhythms are a sign of a sick heart, all of the dominant pacemakers must fail before this ryhtm kicks in, the QRS is wide and bizarre and without preceding P waves. Rates (20-40 bpms)
sinus node
heterogenous anatomical structure composed of multiple different cell types interacting with each other If current (voltage clock) and rhythmic release of Ca ions from the sarcoplasmic reticulum (Ca clock) of specialized non contractile atrial cells
Superior portion the dominants
sinus node dysfunction
aka sick sinus syndrome
1/600 adults over the age of 65 yrs (highest prevalence in very elderly>75), disorder of impulse generation
Sick sinus syndrome-23.1 % of pacemaker implants
Clinically presents as: sinus bradycardia, sinus pauses/ sinus arrest, tachycardia-bradycardia syndrome
sinus node dysfunction causes
intrinstic cardiac causes: SN dysfunction and atrial arrhythmias primarily result from degenerative age related atrial fibrosis, infiltartive diseases (amyloidosis, hemochromatosis, sarcoidosis) and ion channel dysfunction associated with (age, HTN, DM, renal disease, MI, valvular disease, heart failure)
Extracardiac causes: meds targeting rhythm control of atrial fibrilation AF, (antiarrhyrthimic meds- amidarone, flecainide, sotalol), rate control (B blockers, Ca channel blockers, digoxin) – exacerbate subclinical SN dysfunction and –> sinus bradycardia or post AF conversion pauses–> presyncope-syncope
Off target effects of non cardiac meds (lithium, and timolol for glaucoma
Long pauses upon conversion of AF to sinus rythm and periods of sustained brady cardia, may warrent permanent pacemaker if continuation of the casual med is deemed medically necessary. or autonomic insufficiency (parkinsons) and pertuburations of autonomic function (neurallymediated syncope, carotid sinus HS, obstructive sleep apnea
Sinus node dysfunctiion therapies
rate control therapies to treat rapid ventricular rates in AF or AFL (flutter) – beta (adrenergic blockers) metaprolol and or non dihydropyridine CA channel blocker (diltazemor verapamil
Pauses<3 s are common and asymptomatic, Pauses > 3 s during wake–lightheadedness or presyncope symptoms
sinus brady cardia- under 60 bpm (could be due to meds, increased vagal tone via GIT, or abnormalities of SAn fibrosis or MI)
Node pauses and exit blocks
Sinus node pauses- abrupt slowing of the sinus rate on ECg with a period of atrial asystole >3 s
Sinoatrial ext block: the pause is an exact multiple of the preceding sinus rate, P cells in SN generate an impulse that does not propagate to atrial myocardium, next P wave is on time
sinus node arrest
primary failure of impluse generation - prolonged atrial asystole
tachybrady syndrome
paroxysmal, persistent pr permanent AF AFL atrial tachycardia (AT) with rapid ventricular rates alternating with periods of junctional bradycardia or sinus arrest/brady cardia
Junctional escape rhythm- when theres a QRS without a p wave,,
AV block
1st degree- atrioventricular conduction delay with PR interval >.2 sec (1:1 conduction is maintained)
2nd degree: Type 1- conduction failure is predictable on the ECG and ussually occurs in the AV node (skip a beat every 3rd time). Type 2- conduction failure unpredictable, occurs without preceding PR prolongation common in patients with advanced HD and wide QRS, conduction block is infranodal
3rd degree AV block: the atrium and ventricles are 100% electrically dissociated from each other (#P> #QRS), p waves and QRS complexes occur completely independnety from one another, when the escape rhythm has a wide QRS, the level of clock is distal to the AV node (infranoda)
Right bundle branch block (RBBB)
QRS duration >120 msec, S wave slurrring in leads 1 and V6, rabit ears (RSR in lead V1)
complete Left bundle branch block
QRS>120 msec, QS or Rs in lead V1, monophasic R wave in leads 1 and V6
Broad notched or slurred R waves in leads 1 AVL V5 and V6
ECG criteria for left anterior fascicular block
left axis deviation between -45 and -90 Leads 1 and AVL qr Leads 2 3 avf rs QRS could be prolonged Prolong3ed R wave peak time in AVL >45 msce
left posterior fascicular block
RAD: 90-+120
Lead 1 and avl rs
Leads 2 3 AVF qr
Prolonged r wave peak time
no right ventricular hypertrophy not other cause of right axis deviation (COPD, pulm HTN)
