arrythmias Flashcards
gradual onset/termination, P wave identical to NSR
sinus tach
HR <55-60bpm
brady
- inappropriate sinus bradycardia
- Alternating bradycardia & atrial tachyarrhythmias (tachy-brady syndrome)
- Sinus pause/arrest: sinus pause >3s = sinus arrest (+/- escape rhythm)
- SA nodal exit block
SND
Block occurs IN the AV node:
▪︎first-degree
▪︎second-degree Mobitz type I (Wenckebach)
prolonged PR interval (>200ms)
first-degree AV block
Block occurs BELOW the AV node:
▪︎second-degree Mobitz type II
▪︎third-degree (complete heart block)
progressively longer interval followed by non-conducted P
Second-degree, Mobitz I (Wenckebach):
NO atrial impulses reach ventricles; complete dissociation between P waves & QRS complexes
▪︎third-degree (complete heart block)
random dropped QRS, stable PR
Second-degree, Mobitz II
*ONE irritable atrial focus causing atrial depolarization
– sudden onset/termination
*circuit usually initiated by PAC
a flutter
atrial rate ~300bpm, ventricular rate ~150bpm
a flutter
absence of discrete P waves ⇢ replaced by small, rapid, continuously varying
fibrillatory waves oscillating at 350-600bpm
a fib
narrow QRS, retrograde P wave after QRS, ⊖delta wave
Orthodromic AVRT
wide QRS, ⊕ delta wave, P wave rarely visible
antidromic AVRT
fast & slow pathways in AV node; often trigged by PAC
AVNRT
reentry mechanism via bypass tract between atria/ventricles,
AVRT
premature beat followed by a normal QRS, P wave has different morphology from sinus P wave
PAC
premature wide QRS w/o preceding P wave followed by full compensatory pause
PVC
≥3 PVCs =
nonsustained VTACH
*regular, broad complex tachycardia
*uniform QRS complexes within each lead (i.e., each QRS is identical)
monomorphic VT
hereditary, characterized by structurally normal heart
*associated w/ ventricular dysrhythmias ⇢ syncope & sudden cardiac death
– d/t mutation in cardiac Na gene channel (“sodium channelopathy”)
brugada
pseudo-RBBB + persistent ST segment ⇡ (coved) in V1-V2
brugada
*total disorganized ventricular depolarization
*ventricle impulse rates up to 500bpm
*total loss of synchronized ventricular contraction, complete loss of CO
vfib
chaotic irregular zigzag pattern of varying amplitude
▪︎no identifiable P waves or QRS complexes, rates varying between 150-500bpm
▪︎as times passes, amplitude typically decreases (coarse ⇢ fine)
vfib
broad, notched, or slurred R waves (rR’/RR’) in leads I, aVL, V5/V6
▪︎dominant S wave in lead V1
LBBB
terminal R wave in V1/V2 (rSR’) w/ discordant ST/T waves
RBBB
