EKG things Flashcards
What is the normal transition point for the precordial leads?
V3-V4
this is where the isoelectric point will be
What are some causes of a counterclockwise rotation? What does this look like?
Posterior MI and RVH (right ventricular hypertrophy) or pre-excitation
will have the transition point at V1-V2, will show tall R waves in V1.
What is “tachy-brady” syndrome?
seen in old people with a sick sinus node and a fib
can get long pause and syncope when switch out of a fib and the sick sinus node does not take over–> long pause in CO –> pass out
What class of drug is diltiazem (used to treat A. fib)? what does it better control, rate or rhythm?
Class IV
Ca2+ channel blocker (block L-type)
rate control because the pacemaker APs are dependent on Ca2+ channels (phase 0)
*will block the AV node (SA node too but the SA node is NOT functioning in a fib)
How does Digoxin work?
inhibit NA/K ATPase==>increase intracellular Ca2+—> less Na+/Ca2+ exchange–> less intracellular Ca2+–> increase vagal tone
What phase of the pacemaker AP do beta blockers work on?
slow the rate of phase 4 depolarization (rate control)
target nodal»_space; mm cells
If a pt has A.fib for > 48 hours, they have an increased risk of _______. Why? Where does this problem most likely originate?
Stroke
don’t have organized atrial contraction and can get blood stasis –> spontaneous coagulation
Left atrial Appendage***
Which part of the EKG is most affected by sotoalol? Why? What class of drug is Sotalol?
QT interval
class III: K+ channel blocker –> decrease the time of re-polarization (in mm cells) –> increase QT
What class of drug is Propafenone? What does this medication do?
class I c Na+ channel
phase 0 of the AP –> affects the QRS (ventricular depolarization)
What are the possible forms of SVT?
- AV nodal reentry
- atrioventricular reentrant
- atrial tachycardia
What is the physiological effect of the carotid sinus massage on AVNRT or AVRT?
reflex to increase vagal output
(1) reduces If and Ca++ channel opening
(2) increases acetylcholine-sensitive K channel => drives K out => MDP (resting potential) more negative
will slow sinus and slow AV rate so much that the circuit breaks –> return to sinus rhythm
AV node is necessary for either of these reentry loops
If an SVT responds to carotid sinus massage, what could it be?
Reentrant SVT
AVNRT or atrioventricular reentrant
What is the most likely cause of paroxysmal SVT in adults? Does this respond to vagal maneuvers?
AVNRT *****
(assume this if 30 yo without any other info)
should respond to vagal maneuvers
What is the most common sustained arrhythmia in adults?
Atrial fibrillation
How does AVNRT work? What is the idea behind the treatment of AVNRT?
2 pathways:
1 path=conduction slow with short refractory
2nd path=fast conduction with long refractory
Treat: slow conduction in retrograde or prolong refractory of the other tissue so the retrograde will not depolarize it
What is Wolff-Parkinson-White?
AVRT (atrioventricular reentrant)
1 part of pathway through the AV node and another pathway “accessory pathway” that goes around the AV node
can have a retrograde P wave visible –> longer loop so less likely to be hidden
What are some other vagal maneuvers?*** what effect will these have on reentrant tachycardias?
Carotid sinus
massage
Coughing
Valsalva maneuver (bear down)
Gagging
Immersing your face in ice-cold water
will all cause the AVNRT and AVRT to return to sinus rhythm
Which medication can used to block the AV node? How? What is this used to treat?
adenosine =an endogenous purine nucleoside –> binds aloha1 receptor –> inhibits adenylyl cyclase–> K+ out –> cell hyperpolarizes
rapid onset, potent and short duration
treat AVNRT or AVRT
What EKG abnormality is seen in WPW? What is the cause of this abnormality?
delta wave –> loss of the PR segment
due to the accessory pathway –> conduction can go either through this accessory path or through the AV node
Kent bundle spreads the depolarization through the ventricular myocardium before the normal conduction gets there–> delta wave when meet up
Where is the conduction from the atria to the ventricle typically seen on an EKG?
PR segment
In a young person with atrial fibrillation, what should you consider? (regularly irregular, sometimes wide and sometimes narrow QRS) **
WPW!!
–> pre-excited atrial fibrillation
regularly irregular
What should you NOT treat pre-excited atrial fibrillation (seen in WPW) with? WHY??
AV nodal blockers (beta blockers, Ca2+ channel blockers, digoxin) (“ABCD” -AV node blockers=BCD)
if block AV node conduction –> go down the accessory pathway
Lose the slowing due to the AV node when goes down the accessory path and the rate will go 350 (same as atria)
some of these can even shorten the accessory pathway refractory period–> can kill them
What should you give to a pt in pre-excited atrial fibrillation?
Procainamide
Amiodarone
Both slow conduction and prolong refractory period of accessory pathway and AV node
What is a capture beat? What rhythm can this be seen in?
The atria contracts sometimes randomly and sometimes catches the ventricle and causes a depolarization of the ventricle
can be a clue in V tach
