Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Cardio Exam 1 > EKG things > Flashcards

EKG things Flashcards

1
Q

What is the normal transition point for the precordial leads?

A

V3-V4

this is where the isoelectric point will be

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are some causes of a counterclockwise rotation? What does this look like?

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is “tachy-brady” syndrome?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What class of drug is diltiazem (used to treat A. fib)? what does it better control, rate or rhythm?

A

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 well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How does Digoxin work?

A

inhibit NA/K ATPase==>increase intracellular Ca2+—> less Na+/Ca2+ exchange–> less intracellular Ca2+–> increase vagal tone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What phase of the pacemaker AP do beta blockers work on?

A

slow the rate of phase 4 depolarization (rate control)

target nodal&raquo_space; mm cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

If a pt has A.fib for > 48 hours, they have an increased risk of _______. Why? Where does this problem most likely originate?

A

Stroke

don’t have organized atrial contraction and can get blood stasis –> spontaneous coagulation

Left atrial Appendage***

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Which part of the EKG is most affected by sotoalol? Why? What class of drug is Sotalol?

A

QT interval

class III: K+ channel blocker –> decrease the time of re-polarization (in mm cells) –> increase QT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What class of drug is Propafenone? What does this medication do?

A 
class I c 
Na+ channel

phase 0 of the AP –> affects the QRS (ventricular depolarization)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the possible forms of SVT?

A
  1. AV nodal reentry
  2. atrioventricular reentrant
  3. atrial tachycardia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the physiological effect of the carotid sinus massage on AVNRT or AVRT?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

If an SVT responds to carotid sinus massage, what could it be?

A

Reentrant SVT

AVNRT or atrioventricular reentrant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the most likely cause of paroxysmal SVT in adults? Does this respond to vagal maneuvers?

A

AVNRT *****

(assume this if 30 yo without any other info)

should respond to vagal maneuvers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the most common sustained arrhythmia in adults?

A

Atrial fibrillation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How does AVNRT work? What is the idea behind the treatment of AVNRT?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is Wolff-Parkinson-White?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are some other vagal maneuvers?*** what effect will these have on reentrant tachycardias?

A

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

18
Q

Which medication can used to block the AV node? How? What is this used to treat?

A

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

19
Q

What EKG abnormality is seen in WPW? What is the cause of this abnormality?

A

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

20
Q

Where is the conduction from the atria to the ventricle typically seen on an EKG?

A

PR segment

21
Q

In a young person with atrial fibrillation, what should you consider? (regularly irregular, sometimes wide and sometimes narrow QRS) **

A

WPW!!

–> pre-excited atrial fibrillation
regularly irregular

22
Q

What should you NOT treat pre-excited atrial fibrillation (seen in WPW) with? WHY??

A

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

23
Q

What should you give to a pt in pre-excited atrial fibrillation?

A

Procainamide

Amiodarone

Both slow conduction and prolong refractory period of accessory pathway and AV node

24
Q

What is a capture beat? What rhythm can this be seen in?

A

The atria contracts sometimes randomly and sometimes catches the ventricle and causes a depolarization of the ventricle

can be a clue in V tach

25
Q

What can cause ventricular tachycardia (RVOT VT)?

A

Delayed after depolarization

small depolarization after the depolarization can trigger another AP

due to high intracellular Ca2+

26
Q

how can digitalis cause RVOT VT? how can stress?

A

Digitalis blocks Na+/K+ ATPase

causes an increase in intracellular Na+–> less Ca2+ out–> increase intracellular Ca2+

stress (catecholamines) stimulates beta receptors –> increase cAMP–> increase SERCA to increase in Ca2+

27
Q

What medication(s) can be used to treat RVOT VT?

A

class II and class IV

IV=Ca2+ channel blocker

II=block the beta stimulation ===> block intracellular Ca2+

28
Q

what is likely the cause of monomorphic VT in an older person? what is the mechanism?

A

previous heart injury/infarction

Reentry over a fixed anatomic circuit (related to scar tissue)

following one specific pathway

29
Q

What is the mechanism of torsades de pointes? What should you not treat this pt with?

A

prolonged QT

class III anti-arrhythmic –> will further prolong QT

30
Q

What is a common electrolyte imbalance that can lead to sinus bradycardia?

A

hyperkalemia

31
Q

How does hypothyroidism contribute to heart rate?

A

can cause bradycardia because thyroid hormone normally increases Beta 1 receptors

without thyroid hormone–> decrease in beta 1–> less SNS activity

32
Q

What is the treatment for an asymptomatic bradycardia pt?

A

NOTHING

don’t treat if not symptomatic

33
Q

What is the typical cause of sinus tahcycardia? What is the treatment?

A

NOT an intrinsic cardiac problem

autonomic dysfunction

tx=treat underlying cause

34
Q

How can you treat abnormal automaticity?

A

Reduced If (voltage gated Na) current makes phase 4 less steep

Maximum diastolic potential (resting potential) more negative

Increased threshold potential

35
Q

What is the normal atrial rate seen in A. flutter? Where is the reentry path commonly found?

A

atrial rate 180-350

reentry along cavotricuspid isthmus

36
Q

How is A. flutter normally treated?

A

ablation

37
Q

What 2 things does reentry require? How is it treated pharmacologically?

A

unidirectional block and slowed conduction

treatment: decrease conduction in circuit–> increase refractory period

38
Q

What will happen if you give adenosine to a pt in A flutter?

A

the AV node will be blocked

will continue to see sawtooth conduction from the atria

39
Q

What is the atrial rate in A. fib? what are some causes? How is it treated?

A

350-600

high LA pressure (HTN, heart failure), thyrotoxicosis, alcohol

treated pharmacologically

40
Q

What are likely causes of MAT and WAP?

A

intracellular Ca2+ overload in hypoxemia (pulmonary problems!!)

41
Q

If there are more ventricular beats than atrial beats, what do you think the rhythm is?

A

ventricular tachycardia or accelerated ventricular rhythm

not being controlled by atria–> ventricular rhythm

42
Q

How does vagal output affect the conduction system?

A

(1) reduces If and Ca++ channel opening
(2) increases acetylcholine-sensitive K channel => drives K out => MDP more negative

sensitivity: SA and AV node> atrial >ventricular

Cardio Exam 1 (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions