Brainscape's Knowledge GenomeTM

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


See full index

MOD 2 > Arrhythmia and Pharmacotherapy > Flashcards

Arrhythmia and Pharmacotherapy Flashcards

1
Q

phase 2 “plateau” of ventricular depolarization

A

L-type calcium channel, predominant channel in heart

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

conduction velocity is the function of ____

A

Na channel (function of the inward current magnitude and related to the rate in rise in phase 0 of AP)

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

Note how SA and AV nodal cells’ AP differ than ventricular action potentials (5)

A
  • relatively depolarized (-60), due to l ack of IK1 channel (ventricular AP rests at -85)
  • T-type calcium channel
  • If channel: pacemaker current
  • L-type calcium channel current mediates the AP upstroke (in ventricle its the fast Na channel)
  • rich autonomic innervation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Two examples of bradyarrhythmias

A
  1. sinus node arrest or exit block
    - usually due to fibrosis from idiopathic degerantion, inflammmation, infiltration, drugs, autonimc influences
  2. AV conduction problems
    - first, second, third AV block
    - level of AV node: first degree and Mobitz I second degree(wnekebach)
    - level of His-bundle: Second degree Mobitz II or third degree
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

describe the EKG in sinoatrial exit block

A

sinus rate is regular before and after, and the pause is exactly twice the sinue cycle length

see a little blip-sinus P wave failed to get out of the SA nodal area, so no conduction to the AV node, to the ventricle, and thus no QRS

next interval still comes on time

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

describe EKG in a sinus pause

A

sinus activation = P wave

in EKG< you would see no initiation of sinus activity at all

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

third degree block

A

no atrial impulse is propagated to the ventricle

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

Tachycardia-bradycardia syndrome: describe EKG

A

supraventricular tachycardia, HR is very fast, followed by 6-sec pause that causes dizziness (bradycardia <60), then normalizes

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

two principle mechanisms of tachyarrhythmias

A
  1. disorder of impulse propgation: reentry
  2. disorder of impulse formation: enhanced automaticity and triggered activity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Explain the 4 features of reentry in tachyarrhythmias

A
  1. difference in conduction or refractoriness in two or more regions connected by a closed loop
  2. unidirectional block in one pathway
  3. slow conduction over the other pathway
  4. re-excitation of the first, blocked path
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe enhanced automaticity and triggered activity

A

automaticity typically arises from SA node or AV junction, specialized atrial fibers and purkinje fibers

triggered activity may be early (from prolonged AP), or delayed (digitalis toxicity, VT induced by exercise or reperfusion) after depolarization

due to increased calcium inside cell

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

What’s the difference between Early After Depolarization (EAD) and Delayed After Deplarization (DAD)?

A

EAD: reactivation of L-type Ca current

DAD: intracellular calcium overload

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

Explain what’s going on at each dot in this EKG

and interpret the bottom EKG

A
  • no real P wave
  • wider QRS –appears to come earlier than when it should = Ventricular Premature Complex (VPC)
  • inverted-some coming from RV, some from LV
  • two VPCs in a row = couplet

VPC = automatic focus (abnormal pacemaker that has an If current or T channel) comes from the ventricle

bottom EKG: 8 wide complexes in a row, tachycardia

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

This type of tachycardia is a secondary arrhythmia, ie, secondary to stress or high catecholamines

A

Sinus tachycardia (when you see this, always think of underlying cause: too much thyroid, fever, sepsis, dehydration, blood loos, hypovolemia)

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

Atrial flutter is due to ____

A

atrial reentry in the right atrium

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

Paroxysmal supraventricular tachycardia (PSVT) is usually due to _____

2 common examples

A

reentry

examples: AV nodal reentry tachycardia and AV reentry tachycardia

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

AV reentrant tachycardia involves _____

A

bypass tract (different path from ventricles to atria)

usually presents as a delta wave on QRS

WPW results when pre-excitation of the ventricles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Susatained V tach is usually associated with ____

Sustained uniform VT is due to ____

____ is a terminal rhythm, requiring immediate defibrillation

A
  • decreased BP
  • due to rentry around an old infarct
  • V flutter and/or fibrillation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

K channel mutatione ffect on QRS

A
  • less K coming out of cell, less repolarization, longer AP, longer QT interval
  • these mutations are most common cause of congenital QT elongation (long QT = LQT)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What can cause an elevated ST segment, that can mimic an MI on EKG?

A

mutation with a short QT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What’s wrong with this pt

A

Patient in complete heart block - depolarization initiated by the AV node or bundle, pace at a very slow HR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the three mechanisms for arrhythmia

A
  1. abnormal automaticity
  2. triggered activity
  3. reentry
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Abnormal Automaticity and 3 clinical examples

A
  • cells outside conduction system acquire automaticity
  • injury causes membranes to “leak” ions
  • creation of ectopic beats
  • myocyte depolarization on its own (when they’re sick)
  1. premature atrial contractions (PAC)
  2. atrial tachycardia
  3. some forms of ventricular tachycardia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Triggered activity and 5 clinical examples

A
  • abnormal conditions cause afterdepolarizations
  • can become self-perpetuating
  • early vs. late (EAD vs. LAD)
  1. digitalis toxic rhythms
  2. torsades de points (long QT)
  3. some forms of ventricular tachycardia
  4. electrolyte arrhythmias
  5. drug-related arrhythmias: antiarrhytmic agents, tri-cyclic antidepressants
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Re-entry and 3 clinical examples

A
  • injury –> mosaic of conducting cells (occurs after people have had an MI) = abnormal impulse conduction
  • need two things:
    • unidirectional block
    • slow retrograde conduction
  1. ventricular tachycardia
  2. AV nodal reentry tachycardia (AVNRT)
  3. AV reentry tachycardia (AVRT)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Describe the EKG

A
  • no P waves before QRS
  • narrow QRS
  • fast rhythm: 150 bpm
  • bumps in ST segment = retrograde p waves

= AV nodal reentrant tachycardia (AVNRT)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Describe AVNRT

A
  • dual pathways in the AV node
  • 2 roadways: 1 conducts slowly, 1 conducts fast
  • you HAVE to have dual pathways present AND a premature atrial contraction to start the arrhythmia (PAC will send electricity down slow pathway since it has a short refractory pathway, and when it reaches bottom, fast pathway has recovered and it can go up the fast, and then down the slow etc.
  • if you have a sinus rhythm, you wont notice it
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what causes the retrograde P wave in an AVNRT?

A
  • there are no P waves because the rhythm is being generated by the AV node, which will send electricity down to the His Bundle and generate the QRS
  • when electrical activity comes back to the AV node, it sends a retrograde signal up to the atria from the AV node, creating this retrograde P wave
  • circle goes again, sends another heartbeat down to His bundle, then another retrograde P wave
  • still normal QRS because still using His bundle system
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

common symptom in PTs with AVNRT

A

recurrent episodes of palpitations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

How do you break the arrhythmia in AVNRT?

A
  • decrease conduction slow pathway
  • carotid massage (massage on neck stretches fibers, tricks carotid sinus into thinking theres high BP, brain increases PNS and slows conduction through the heart and AV node, usually blocks the AVNRT)
  • vagal manuevers (hold breath)
  • adenosine (vasodilator, medicin that slows conduction through AV node)
31
Q

AVNRT chronic treatment

A
  • many pt need no therapy
  • beta blockers, verapamil/diltiazem (slows conduction in slow pathway + AV node)
  • surgical ablation of slow pathway
32
Q

If you had to develop an antiarrhythmic drug, what do you think would make the drug ideal?

A
  • drug works on selective ion channels only in specific pathophsyiologic states (i.e. tachycardia)
  • converting **unidrectional block **into birdirectional block to get rid of reentrant teachycardias

-suppression of abnormal automaticity

33
Q

What are some of the main ideas behind the mechanism of lidocaine as use of an antiarrhythmic drug

A

Modulated Receptor hypothesis:

  • voltage, time, and use dependence of receptor occupancy by the drug
  • effect on the channel kinetics including channel availability, effects on the action potential
34
Q

Antiarrhythmic drugs that prolong the AP duration

  • side effects
  • exception
A
  • class III and some class IA drugs
  • can cause torsades de pointes tachycardias
  • exception: amiodarone: likely related to this form of arrhythmia due to blocking action on multiple channels blockade (ICaL, and Ina, and K channel)
35
Q

use and side effects of amiodarone

A
  • atrial fibrillation - only works in 60% of cases
  • pulmonary fibrosis, liver and thyroid toxicity
36
Q

use of internal cardioverter-defibrillator (ICD) use

A

patients after myocardial infarction whose heart function remains depressed significantly. Created after failure of flecanide to reduce high risk of ventricular arrhythmias and sudden cardiac death.

37
Q

Antiarrhythmic Drugs:

Class I - drugs and action

A

Ia - disopiramide, quinidine, procainamide

Ib - lidocaine, mexiletine, tocainamide

Ic - flecainide, propafenone

all block Na channels in the heart in phase 0

38
Q

Class II antiarrhythmic drugs mechanism

A

beta blockers

39
Q

Class III aniarrhythmic drugs: drug list and mechanism

A
  • amiodarone, sotalol, dofetilide, ibutilide
  • K channel blockers (slows rate at which K leaves during phase 3)
40
Q

Class IV antiarrhythmic drugs: drugs and mechanism

A
  • verapamil/diltiazem
  • Ca-channel blockers
41
Q

Class II and IV antiarrhythmic drugs work on which types of cell?

A
  • beta blockers and calcium channel blockers work on pacemaker cells
  • they don’t affect APs of atria or ventricular cells
42
Q

Review the phases of the atrial/ventricular action potential

A

see figure

43
Q

effect on QRS, QT, AP and effective refractory period (ERP) for class Ia, Ib, and Ic drugs

A

see figure

(blue line is Ib)

44
Q

effect on QRS, QT, AP, and ERP with Class III drugs

A

see figure

45
Q

When do you see torsade de pointes occur? What is the result? Which drugs cause this?

A
  • possible outcome when QT gets prolonged
  • results in cardiac arrest

-Class IA and III drugs prolong QT

46
Q

what do beta blockers (class II drugs) affect? Describe what they do to: HR, conduction velocity, phase 4 of AP, and PR interval

A
  • beta blockers affect pacemaker AP, not myocytes
  • decrease HR, decrease conduction velocity, decrease slope of phase 4, and increase PR interval
47
Q

recall the AP phases for SA-AV nodal cells

A

If = nonselective cation channel

48
Q

explain effects of Class IV CCB on HR, conduction veloctiy, and PR interval

A

decreaes HR, decrease conduction velocity, and increase PR interval

-decreases slope, so you see a slower rise

49
Q

Amiodarone

  • drug type, target, effect
  • other effects
  • what is it good for
  • potential side effects? who is at greatest risk?
A
  • class III drug- K channel blocker, prolongs QT
  • also has effects on the other class drugs (I, II, IV) - prolongs QRS
  • suppresses atrial fib and ventricular tachycardia

-lots of potential side effects: less likely at lower dosages, risk accumulates over time, young patients on indefinite therapy at greater risk

50
Q

What are the specific side effects with amiodarone (4)

A
  • hyper and hypo thyroidism
  • pulmonary fibrosis
  • skin sensitivity to sun
  • increased liver function tests
  • note: when starting amiodarone: check CXR, PFT< TFT (thyroid), annd LFT*
51
Q

Lidocaine

  • class, target,
  • preferential impact
  • oral version
A
  • class Ib- Na channel blocker
  • preferentially impacts ischemic tissue
    i. e. ventricular tachycardiia in ischemia, pateient having MI develops VT and cardiac arrest
  • mexilitine = oral lidocaine
52
Q

Propafenone/Flecainide:

  • class drug, target
  • use
  • action
  • alarm
A
  • class Ic - Na channel blocker
  • suppresses paroxysmal atrial fibrillation
  • prolongs refractory period in AV node which is a special property since most drugs affect atria or ventricile
  • must have structurally normal hearts (no LVH, Heart failure history, coronary disease)
53
Q

Propafenone/Flecainide

“use dependent”

A
  • more effect at faster heart rates - good for tachyarrhthmia suppression
  • normal QRS at rest –> prolonged QRS during exercise
  • more risk of arrhythmia at lower heart rates
    note: class III drugs have “reverse use dependence”
54
Q

Drugs that cause drug-induced lupus (3) and key finding

A
  • procainamide (class Ia), hydralazine (blood pressure pill), izoniazide
  • anti-histone antibodies
55
Q

procainamide use

A
  • A fib with WPW
  • suppresses conduction over the bypass tract

(class Ia drug, Na channel blocker)

56
Q

adenosine

  • mechanism of action
  • effects (2 main ones)
A
  • drives K+ out of cells
  • hyperpolarizes cells (makes it harder to depolarize)
  • slows down conduction through AV node
  • vasodilator: flushing, hypotension (body thinks there’s increased metabolic activity so it will dilate)
  • supraventricular tach will break or reveal etiology
57
Q

An acute management of torsades. What is its mechanism of action and effect

A
  • magnesium
  • blocks influx of Ca into cells

(recall Ca influx leads to early afterdepoliarzations)

58
Q

Atropine

  • what is it
  • what does it do
  • what’s it used for
A
  • muscarinic receptor antagonist
  • BLOCKS parasympathetic system
  • speeds conduction through AV node
  • used for bradycardia
59
Q

Digoxin

  • what does it do
  • what is it used for
  • its effects are similar to what other drugs?
A
  • suppresses AV node conduction, increases contractility, activates parasympathetic
  • can be used to slow heart rate in rapid A fib
  • effects similar to BB and CCB in AV node: prolong refractory period, increases PR interval
60
Q

Digoxin toxicity

  • what does it target,
  • effect
A
  • blocks Na-K-ATPase in ventricular cells
  • raises resting potential atrial/vent cells
  • increasd automaticity/afterdepolarizations
  • dig toxic rhythms: atrial, junctional, vent tach (often with evidence of AV node block)
  • watch for PACs, PVCs, or Heart block

see figure: dashed line is someone on dig-resting potential has gone up, phase 3 is not so flat anymore

61
Q

for class 1 drugs, compare how each affects the action potential duration (APD) and type of kinetics required to dissociate from the channel

A

Ia- prolongs APD, dissociates with intermediate kinetics

Ib- shortens APD in some heart tissues; dissociates with rapid kinetics

Ic - minimal effects on APD, dissociate from channel with slow kinetics

62
Q

The resting potential is mainly determined by ____

The resting potential greatly influences the ____ channel availability, with more channels at (less/more) negative potentials

A

Potassium

Na channel; more channels at less negative potentials

63
Q

relatively minor changes in K+ concentration can have major effects on resting potential:

hyperkalemia leads to _____ potentials

hypokalemia leads to _____

A

hyperkalemia = less negative potentials

hypokalemia = hyperpolarization

(hyperpolarization occurs when K leaves the cell, so if theres low K outside cell, you will be more likely to hyperpolarize)

64
Q

What happens when you have fewer available Na channels?

A

Leads to slower conduction and conduction block

65
Q

sodium channels are dependent on these two factors

A
  • voltage dependent (activated when membrane gets depolarized, Na further depolarizes the cell and rushes in)
  • time dependent (gets inactivated very quickly)
66
Q

When myocytes due to ischemia, what is one important thing they release that has a big domino effect?

A

Myocytes release K+ when they die –> local hyperkalemia –> decreased AP and less negative resting membrane potential –> results in partially inactivated Na+ channel with conduction slowing and unidirectional block

67
Q

lidocaine binds preferentially in the ____ state with ____ kinetics

lidocaine has bigger effect in _____ cells

lidocaine works wel in ventricular ____ caused by ____ by converting ____ into _____

A
  • inactivated or open state with rapid kinetics
  • bigger effect in partially depolarized cells (less Na channels available and cells with long AP [purkinje fibers])
  • ventricular tachycardia, ischemia, converts unidirectional block into bi-directional block
68
Q
  • flecanide effect on ventricular arryhthmias and mortality
  • amiodarone effects on arrhythmias and mortaility
  • ICD therapy effect on sudden death
A
  • flecanide: does NOT prevent ventricular arrhythmias after MI, increases mortality
  • amiodarone prevents arrhythmias after MI, no effect on mortality
  • ICD therapy prevents suddent deaths after pts with MI
69
Q

what causes EAD, what causes DAD

A

EAD:

  • occurs at slow heart rates
  • cells with long APs more susceptible
  • due to Ca-influx during phase 2 and 3
  • LQT, Class II antiarrhythmias

DAD:

  • occurs at fast heart rates
  • associated with digoxin intoxication
  • Ca release and membrane oscillation from SR (comes from INSIDE, not outside)
70
Q

Rate of automaticity can be changed by the following 3

A
  • changing slope of diastolic depolarization
  • changing the threshold
  • changing the resting potential

(If and Ica channels)

71
Q

Some antiarrhythmics can change the voltage threshold such as ____ and ____ to more positive levels

A

Quinidine and procainamide (class Ia)

72
Q
  • which type of myocytes have a very low tendency to develop automaticity?
  • which type of myocytes have the potential to show normal AND abnormal automaticity?
  • abnormal automaticity of ___ can occur when the ___ is reduced
A
  • normal atrial and ventricular myocytes
  • purkinje fibers
  • purkinje fibers can show abnormal automaticity when the diastolic potential is reduced
73
Q

when do you consider ablation of atrial fibrillation?

A

symptomatic patients who failed antiarrhythmic therapy

MOD 2 (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions