Cardio 7.13 Flashcards
second degree heart block
P wave is not always followed by QRS
describe mobitz type I
a second degree heart block
PR interval gets progressively longer and then QRS will drop
describe motbitz type II
randomly dropped QRS
PR interval the same and then random drop of QRS
mobitz type II thought to reflect damage to
specialized conduction system
which is worse mobitz type I or II
II
what happens to AP with hyperkalemia
it shortens - it promotes potassium conductance so increased potassium current
what happens to rate of rise with yperkalemia
slowed - this is the sodium current
what happens to AP with hyperkalemia
shortens AP duration
as you depol cell you switch from what for sodium channels
to inactivated state
how do you get from inactivated state to closed state
negative resting membrane potential again
QRS you don’t want bigger than
2 little boxes (80)
peaked t wave
cells really sensitive to high potassium (hyperkalemia) so they repol fast and you get peak t wave (pg 205)
causes of conduction block
closure of gap junctions
what could cause closure of gap junctions
ischemia
low pHi
high Cai
what happens to pH during ischemia
low
why is pH low in ischemia
CO2 increases
what happens to calcium in ischemia
increases - can close gap junctions
lidocaine does what
blocks sodium channels
cocaine does what
blocks sodium channels
sodium channel blockers used to block pain and also as
antiarthmia
sodium current (INa) produces upstroke of
everything but SA and AV, so atrial ventricular, Hi-spurkinje myocytes
inhibition of Ica by medications
decreases upstroke of AV and SA nodes, would think it would also decrease AP duration
Ica produces
upstroke of SA and AV nodal cells
Ach blocks
calcium current
Ach affects
conduction velocity through AV nodes and contractability of atria
what is most common caues of tachycardia
re-entry
how can you get unidirectional conduction
dead cells that can’t fire AP - you end up with one cell trying to activate a bunch and i isn’t ble to do that (pg 210)
what is reentry
AP is re-entering in spacial area (like dog chasing its tail)
when wave fronts come through ventricles what normall yhappens
collide come togther, activate, and extinguish (but in re-entry it doesn’t extinguish)
re-entry in AV node would cause
ventricles to fire at fast rate
micro-rentry you would see in
ventricular fibrulation
two broad types of reentry and reentrant arrhytmias
anatomical & functional (spiral waves)
what do you need for re-entry to proceed
excitable gap
put a premature beat in and what happens
anatomical reentry (ppt 210) there is video
look at anatomical reentry
pg 215
describe reentrant ventricular tachycardia
very fast HR lower CO
QRS wider than normal and no distinguishable P or T waves
pg 216
if there is bypass track what syndrome can develop
wolff-parkinson white syndrome
what is bypass track
band of muscle tat connects atria directly to ventricle
describe wolff parkinson white syndrome
fast AP conduction via accessory pathway (bypass track_ - short PR interval. pre-excitation with delta waves
What does WPW stand for
wolff-parkinson-white syndrome
what is delta wave
ramp like start to R wave, no Q wave
Look at WPW
pg 217
pt with WPW pre-disposed to what
pre-disposed to re-entrant ventricular tachycardia
what does AVRT stand for
atrioventricular reentrant ventricular tachycardia
how might you treat WPW
can identify the bypass track and put catheter and apply frequency nd destroy the accessory pathway
can also reduce calcium current, so it slows AV node, so can give pt calcium channel blockers
adenosine is
fast channel calcium blocker
atrial flutter characterized by
“saw-tooth”atrial activity
atrial flutter describe
crazy re-entry through the atria every time it fires - goingso fast it’s not contributing to ventricle filling
how to identify atrial flutter
the saw tooth pattern of p waves
atrial flutter can degrade into
atrial fibrulation
Ventricular fibrillation can be caused easily by
even small hit to tet
or electrecutted
VF stands for
ventricular fibrillation
SCA stands for
sudden cardiac arrest
who is at risk for SCA
pts with coronary artery disease
pts with heart failure
pts with inherited channelopathies causing ventricular arrhythmia
most widespread sustained arthymia
atrial fibrillation
AF stands for
atrial fibrillation
describe AF
no visible P waves
ventricular firing often fast and irregular
look at AF
pg 225
what is missing in ECG in AF
p wave
why isn’t there P wave in AF
P wave is b/c of normal coordinated propegation of AP through atria - so you might get little squiggle but no discernible p wave.
how do you treat arrhythmia
Electrical Cardioversion
Antiarrhythmic Drugs
Catheter Ablation
Implanted Rhythm Devices
defibrilation
- put electrodes on chest (v fib)
cardioversion
apply shock and convert to normal sinus
ccardioversion vs. defibrillation
cardioversion apply shock during QRS
