3- Mechanisms of Dysrhythmias Flashcards
what phases correspond to the absolute refractory period?
phase 0,1, and2
time that the cell is unable to respond to another incoming impulse
absolute refractory period
relative refractory period phase
phase 3
sustained inability to respond to an incoming impulse under normal conditions
relative refractory period
why doesn’t the heart tetanize like skeletal muscle?
extended absolute refractory period due to calcium channels
AND
no recruting
*everything is all or none
define calcium spark
calcium-induced(voltage) calcium release(SR calcium channels)
name of calcium release channels
ryanodine receptors
increased activity of SERCA by SNS =
calcium taken away to increase relaxation faster ALSO SNS increases rate of calcium release from ryanodine.
Together = increased contractions
classify: abnormal or enhanced automaticity
active arrhytmia
classify: triggered activity
active arrhythmia
classify: reentrant circuits
active arrhythmias
slower than normal
sinus bradycardia
faster (>100) would be sinus tachycardia
effect of hypokalemia
decreases phase 4 K availabale –> easier depolarization and less time between AP
effect of mild hyperkalemia
increased AP
effect of severe hyperkalemia
unexcitable, no AP
“triggered activity”
delayed or early afterdepolarization
arrhythmia is generated at a time when the cell is fully repolarized
DAD
arrhythmia generated during phase 2 or phase 3 depending
EAD
characteristically extended action potential duration indicates…
EAD
reduced potassium current –>
repolarization takes longer than normal –> prolonged APD
increased intracellular calcium –>
extended plateau phase and extra calcium can activate an additonal sodium current –> prolonged APD
mutation of NCX to increase current during the end of phase 2 –>
prolonged APD
when can EADs be accentuated..
at lower heart rates due to the physiologically natural longer APDs at this point
exacerbated by higher HR…
DADs
because ther is not sufficient time to reduce intracellular calcium between successive beats
a fixed pathway exists which connects atrial tissue to ventricular tissue and in doing so, bypasses the AV node
wolff-parkinson-white syndrome
how does wolff parkinson white syndrome manifest on ECG
shortened PR interval (because the bypass impulse travels faster to ventricles than normally conducted signal)
core of inexciteable tissue would be..
functional reentract obstacle
associated with spiral wae
anatomical-define reentrant circuit
stable spiral wave originating from one position within the ventricular mass
monomorphic ventricular tachycardia
meandering or drifting spiral waves throughout the ventricular mass
polymorphic tachycardia
rely on the principles of electrical anisotropy and spatial inhomogeneities
reentrant circuits
conduction abnormality as a result of tissue structure
passive arrhythmia
“source sink”
a smaller sink will increase APD and a larger sink will reduce APD and conduction velocity
contributes to anisotropy and inhomogeneity in the propogating wavefront
true or false: changing the AP duration will change the refractory period
true
vagal stimulation would have what effect on HR
vagal is parasympathetic so it would derease automaticity and decrease HR –> sinus brady cardia
sympathetic would be the opposite: sinus tachyccardia
if both para and symp are stimulate who will win for HR?
para
how does Ach change automaticity
slower
by increasing potassium current
how does NE change automaticity
faster by increasing calcium and funny current
how do hypokalemia and ischemia change automaticity
faster becasue of a decreased potassium current
what 4 things could cause a prolonged APD?
- reduced potassium current
- increased calcium
- increased sodium-calcium exchanger activity
- increased late sodium current
true or false: only anatomically defined reentrant circuits rely on electrical anisotropy and tissue inhomogeneiteies
FALSE
both anatomical and cuntionally defined reentrant ircuits rely on electrical anisotropy and tissue inhomogeneiteies
spiral wave
functioanlly defined reentrant circuit
fixed pathway with excitable gap
anatomically defined reentrant circuit
