Brainscape's Knowledge GenomeTM

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


See full index

Humber Cardio FINAL > Arrythmias 1 > Flashcards

Arrythmias 1 Flashcards

1
Q

Normal Electrocardiogram (ECG)
PQRST

  1. Normal PR interval
  2. Normal QRS complex
  3. Normal QT interval
A
  1. 0.12-0.2 sec
  2. 0.04 - 0.14 sec
  3. < 0.42 sec
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Ventricular AP : WHats the influx, whats the efflux?

Nodal Tissue : Whats influx, whats efflux?

A
  1. Sodium influx, Potassium Efflux
  2. Calcium influx, Potassium Efflux
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Abnormal Impulse Generation –Automatic Tachycardias

  1. What can cause this?
  2. If the rate of impulse generation from “latent” pacemaker cells is > rate of SA node, what starts?
  3. What are some causes of Incr Phase 4 Slope?
A
  1. Incr in phase 4 slope causing heightened automaticity of “latent” pacemaker cells
  2. An arrhythmia
  3. Digitalis, or catecholamines
    Hypoxemia
    Electrolyte imbalance (hypokalemia)
    Fiber stretch (Cardiac dilation)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Abnormal Impulse Generation - Triggered Automaticity

Occur prior to phase 4 :
1) During repolarization (Early after depol , EADS)
-Caused by ? (3)

2) After repolarization (Delayed after depolarization , DADs)
-Caused by ? (2)

A
  1. hypokalemia
    class 3 and 1a AAD’s
    -Slow stimulation rates
  2. Digitalis or catecholamines
    -can be suppressed by Calc Channel Antags
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Name 4 ways that AAD’s can slow automatic Rhythms ?

A
  1. Altering phase 4 slope
  2. increasing threshold potential
  3. Incr maximum diastolic potential
  4. incr AP duration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Class 1 AAD (1A, 1B, 1C)
1. Predom effect is to ?
2. Slows ___
3. How does each class affect the ventricular AP?

A
  1. block the fast inward Na+ channels leading to a decr in the depolarization rate of phase 0
  2. intra-cardiac conduction
  3. 1a has moderate Na channel block, and prolonged repolarization
    -1b has mild Na channel block, and shortened repolarization
    -1c has MARKED Na channel block, and no change in repolarization
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Which drugs are in class 1A, 1 B and 1C?

A

1A : Disopyramide, Quinidine, Procainamide
1B : Lidocaine, Mexiletine
1C: Flecainide, Propafenone

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

Class 1 A
1. Broad spectrum AAD meaning it can help with which 2 Arrhythmias ?
2. CLass Electrophys effects ?
-Widen ___
-Lengthen ____
-Lengthen ____
-No or slightly lengthen ___
3. Part of EP effects can be attributed to ?
4. ALL are effective in suppressing ?
5. In re-entrant tachycardias, they produce ?

A
  1. Supraventricular and ventricular
  2. QRS
    -QT interval (may induces TdP)
    -Refractory period
    - PR interval
  3. K+ channel blockade
  4. Automatic tachycardias
  5. bidirectional block (by depressing conduction and prolonging refractoriness)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Disopyramide :
1. Used to maintain ___ in ___ or __
2. Used to prevent recurrence of ___ or ___
3. Prolongs __ and ___
4.Prominent ___ action = AE’s
5. Signif AE’s ? (6)

A
  1. Sinus rhythm, atrial flutter, fibrillation
  2. ventricular tachycardias , fibrillation
  3. QRS and QT interval
  4. anticholinergic action
  5. HYPOTENSION
    -ANTICHOLINERGIC SYNDROME (Dry mouth, constipation, urinary retention, precip glaucoma)
    -Gi upset
    -Hypoglycemia
    -PROARRHYTHMIAS (TdP )
    -HF (Depression of cardiac contracility)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Quinidine
1. Maintains ___ in Afib or flutter and prevents recurrence of ?
2. Blocks ___ and multiple __
3. Prolongs ___, due to ?
4. Produces ___ and ___ **
5. AE’s (7)

A
  1. sinus rhythm , ventricular tach or fibrillation
  2. Na+ current, K+ currents
  3. Cardiac AP duration, K+ blocking
  4. Beta receptor blockade and vagal inhibition
  5. Cinchonism (D/N/Tinnitus, Visual changes, dizzi, HA)
    -HYPOTENSION
    -THROMBOCYTOPENIA
    -Hemolytic anemia
    -QT INTERVAL PROLONG AND TDP
    -Proarrhythmia
    -DIARRHEA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Procainamide
1. Used to treat ?
2. FOr acute tx? WHats no longer commerically available?
3. Procainamide (PA) and its Metab (NAPA)
-PA decreases ___, increases ___, slows __, and prolongs __ and ___
-NAPA lacks ___ but is equally potent in blocking ___

  1. Why must you use in caution with HF pt’s with reduced EF?
  2. Monitor PA and NAPA levels… wat are those levels?
A
  1. SUPRA and ventricular arrhythmias
  2. IV, PO version
  3. automaticity
    -refractory periods
    -conduction
    -QRS and QT intervals
    -NA+ blockade, outward K+
  4. Negative Inotrope
  5. PA = 4-8 mcg/mL
    NAPA = 4-10 mcg/mL
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Procainamide :
1. Eliminated rapidly by ?
2. AE’s ? (7)

A
  1. renal excretion , hepatic metabolism
  2. HYPOTENSION (IV USE)
    -Nausea
    -TDP! Particularly with NAPA accum
    -LUPUS LIKE SYNDROME!!!!! (Test question) , this occurs more often and earlier during tx in “Slow acetylators”
    -Bone marrow aplasia
    -QT prolongation (less than quinidine)
    -Fever
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Class 1B : Lidocaine and Mexiletine

  1. COnsiderably more effective for ?
  2. Class EP effects
    -No effect on __ and ___
    -Decr in ___
    -No effect on ___
  3. WHat accentuates its effects?
    -Changes in pH alter time that lidocaine is bound to ?
  4. Attractive for which pt’s?
A
  1. Ventricular arrhythmias
  2. QRS, QT length
    - refractory period
    - PR interval
  3. Acidosis
    - Na+ channel
  4. Post -MI pt’s
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Lidocaine
1. Reduces ___ and alters ___
2. It’s not really effective as ___ only 15-20% effective in pt’s with ___
3. Minimal effects on __ or __

PK
1. How is it metabolized ?
2. What affects Vd and CL?
3. WHat causes reduced CL?
4. Therapeutic levels?

A
  1. slope of Phase 4, threshold for excitability
  2. monotherapy. Monomorphic VT
  3. CO or BP
  4. Liver metabolized
  5. Heart failure
  6. Hepatic disease
  7. 1.5-5 mcg/mL
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Lidocaine AE’s

  1. Levels > 5 mcg/mL
    C,S,D,D,V,M,P,N,T
  2. Levels > 9mcg/mL
    P,S,R,S,B,C
A
  1. Confusion
    slurred speech
    dizziness
    drowsiness
    vertigo
    muscle twitching
    perioral numbness
    Nausea
    tinnitus
  2. Psychosis
    seizures
    respiratory suppression
    sinus arrest
    bradycardia
    complete heart block
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Mexiletine
1. oral analog of ?
2. Modifed to reduce __ allowing for ?
3. EP effects are?
4. Approved for treating ?
5. NOT EFFECTIVE FOR ?
6. Often used in combo with other AAD’s such as ?
7. AE’s (4) or 2 major ones

A
  1. lidocaine
  2. first pass metab, chronic oral therapy (F = 90%)
  3. Similar to lidocaine
  4. Ventric arrhythmias
  5. atrial arrhythmias
  6. Sotalol or quinidine to incr efficacy while limiting ae’s
  7. CNS (Dizzi, tremor, ataxia, slurred speech, blurred vision , mem impairment, rarely psychosis or seizures)
    -Pro arrhythmia
    -GI upset
    -Thrombocytopenia (rare)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Class 1C : Flecainide, Propafenone

  1. Class EP effects?
    -Widen ___
    -Lengthens?
    -Decr?
    -Lengthens?
  2. Profoundly slows __
  3. Cannot be used in pt’s with ?!!!
A
  1. QRS interval
    -QT interval (primarily via qrs widening)
    -Conduction velocity
    -PR interval
  2. conduction velocity because of Slow association and dissociation with Na+ Channel
  3. Structural heart disease (LVH, CHF, CAD , s/p MI and to a lesser extent heart valvular lesions)
18
Q

Flecainide (Tambocor)
1. Derivative of procainamide that does what?
2. Negative ___
3. effective for ?
4. CAUTION WHEN?
5. Currently used in ?
6. It profoundly slows ___
7. It blocks 3 currents (what r they)
8. In atrial tissue, What’s prolonged?
9. EP effects : Prolongs duration of ? (3)

A
  1. Na+ channel blocker
  2. Inotrope
  3. BOTH supra and ventric arrhythmias
  4. used for life threatening venrtric arrhythmias (Pro arrhytmic)
  5. in absence of structural hd, for maintenance of sinus rhythm in supraventric arrhythmias (AFIB)
  6. conduction velocity
  7. Na+current, Delayed rectifier K+ current, and Ca2+ currents
  8. AP duration prolonged at fast rates
  9. PR, QRS, and QT
19
Q

Flecainide AE’s
1. P
2. B, D, L
3.n/v
4. Exacerbates ___ in pt’s with ___
5. __ in pt’s with pre existing conduction disease

A
  1. Proarrhythmic
  2. blurred vission , drowsiness, lightheadedness
  3. heart failure, depressed LEFT ventric function
  4. Heart block
20
Q

Propafenone

  1. What channel blocker? some ___
  2. Structurally similar to ? but has weaker ___
    -CI in ?
  3. EP effects?
  4. ECG effects?
  5. Used primarily to maintain ??
  6. How is it eliminated ?
A
  1. Na+ channel blocker (Slow recovery)
    -Some K+ channel blocker
  2. Beta blockers
    -Beta blocker activity
    -COPD or Asthma
  3. Slows conduction in fast response tissues
  4. prolongs PR and QRS duration
  5. Sinus rhythm in pt’s with SUPRAventricular arrhythmias (AFIB)
  6. Renal and hepatic (CYP2D6)
21
Q

Propafenone AE’s
-P
-Worsening ___
-B
-C
-G
-M
Propafenone would better charlie’s general mind

A

Proarrhythmia
-CHF
-Bronchospasm
-CNS effects (blurred vision, dizzi , pre syncope)
- GI upset
-Metallic bitter taste

22
Q

Class 2 AAD’s
1. Beta ADrenergic blocking agents like ?
2. Reduces inflow of ?
3. Increases AV nodal __ and prolongs AV nodal ___

  1. ____ in AFIB or flutter
  2. Class EP effects
    -No effect on ?
    -Incr ___On atrial and AV nodal tissues
    -Decr __
    -WIdened ___
A
  1. Propanolol , esmolol, metoprolol, carvedilol, acebutolol
  2. ca2+ into cell
  3. conduction time, refractoriness
  4. Ventricular RATE control
  5. QRS or QT interval
    -Refractory period
    -Conduction velocity
    -PR interval
23
Q

Esmolol
1. Selective ?
2. What admin method?
3. Used primarily to ?
4. Dosing ? LD, MD, Rebolus

A
  1. Beta 1 blocker
  2. IV only
  3. control ventric response in AFIB (rate control)
  4. Loading dose 500 mcg/kg IV over 1 minute

– maintenance dose 50 mcg/kg/min to start and may increase by 50 mcg/kg/min every 4 minutes until a maximum of 300 mcg/kg/min

– may rebolus w/ 500 mcg/kg before each dose increase

24
Q

Class 3 : Name the 5 drugs

  1. Delays repolarization by ?
  2. Lengthens ___
    -Increases ___
    -Prolongs ____
A

Amiod, Dronedarone, Ibutilide, Dofetilide, Sotalol

  1. blocking k+ channels
  2. QT interval!!!
    -refractory period
    -cardiac AP
25
Q

Amiodarone
1. Metab where? via?
2. Elimination half life?
3. Inactivated ____
-Non selective ___
Blocks ___
Small degree of ?

  1. Treats what ?
  2. Maintains __ in AFIB
  3. IV formulation good for ?
A
  1. Liver, CYP3A4
  2. 15-100 days
  3. Na channel blocker (Fast on and off kinetics)
    - Beta blocking properties
    - K+ channels
    -Ca2+ antagonism decr Ca2+ current
  4. Recurrent ventric Tachycardia or fibrillation resistant to other drugs
  5. sinus rhythm
  6. acute termination of ventric tachycardia and fibrillation
26
Q

Amiodarone :
1. THE GOOD
- WHat kind of arrhythmias?
-Efficacy?
-May cause less ___ than sotalol
-Ok for which pt’s ?

  1. The BAD
    -Oral amio has ?
    -Requires ___
    -many potentially serious __
    -Caution with what kind of allergy?
  2. See chart for dose
A
  1. Supra and ventric
    - > than other AADs
    -TDP
    -Post MI pt’s or CHF pt’s with LOW EF
  2. SLOW ONSET OF ACTION
    - large total LD ( ~10 grams)
    -AE’s
    -Iodine
  3. See chart
27
Q

Amiodarone AE’s
1. H
2. B
3. T
4. P
5. Hypo and Hyper ___
6. Incr __ but rarely hepatitis
7. C
8. Dermatological rxns like (2)

Her brother takes her puppy into college dorms

A
  1. Hypotension (solvent used in IV )
  2. Bradycardia
  3. TDP (optimize electrolytes)
  4. Pulm FIBROSIS!!!
  5. Thyroidism
  6. LFTS
  7. Corneal microdeposits
  8. Photosensitivity
    -skin discoloration or blue grey skin
28
Q

Dronedarone
1. What form of amio?
2. Tx of Atrial Fib and Flutter
-Maintains ___
3. Less __ than amio
4. Less ___ than amio
5. What channels does it block?
6. COmmon ae’s?

A
  1. Non -iodinated
  2. sinus rhythm
  3. AE’s
  4. Effective
  5. K, Na, and Ca2+
  6. V/D/N, Abd pain, ASthenia, prolonged QTC, acute liver injury
29
Q

Dronedarone
1. Metab by ?
2. Moderate inhib of ?
3. DOnt use in ?
4. Dont use in ?
5 Increased mortality in ? Severe
-CI in ?? (2)

A
  1. CYP 3a4
  2. CYP3A, CYP2D6, AND PGP
  3. PERM ATRIAL FIB OR FLUTTER
  4. BRADYCARDIC PT”S (HR < 50 bpm, QTC > 500 ms, 2nd or 3rd degree Heart block)
  5. Severe HF (CI in NYHA CLass IV, recent hospitalization within 30 days for decomp HF)
30
Q

Ibutilide
1. Blocks ?
2. Used to convert pt’s from aflutter or afib to ?
3. Greater efficacy in ?
4. Effiacy is greater with ?
5. AE”s (5)

A
  1. Delayed rect K+ current and inward Na+ current in some systems
  2. Sinus rhythm
  3. Aflutter
  4. recent onset (days) vs prolonged presence (weeks)
  5. AV and bundle branch blocks
    every kind of arrhythmia
    HA
    hypotension
    n/V
31
Q
  1. Ibutilide DOSING ?
  2. Terminate infusion at signs of?
  3. Optimize __ and ___ prior to infusion
  4. May cause ___ for up to 4 hrs post dose
  5. Avoid which drugs 6 hrs after ?
A

-0.01 mg/kg IV over 10 minutes (weight < 60-kg)
– 1 mg IV over 10 minutes (weight > 60-kg)
– may repeat 10 minutes after END of the first infusion w/ additional equal dose

Toxicity or success
Potass and Magnesium
TDP
Class 1A or Class 3

32
Q

Dofetilide
1. Blocks ?
2. Used for maintenance of ___ in some1 who has undergone recent cardioversion and in pharm conversion of Afib or Aflutter to normal sinus rhythm

  1. What closely correlates to serum conc?
  2. Initiated in ?
  3. DDi’s ? (6) (very cool kids take piano music)
A
  1. Delayed K+ rectifier current
  2. SINUS RHYTHM
  3. QT prolongation
  4. hospital
  5. verapamil, cimetidine, trimethoprim, ketoconazole,prochlorperazine, megestrol
33
Q

Dofetilide DOsing ? Requires?

AE’s? (7)

A

500 mcg PO twice daily (normal starting dose)
-Renal and QTc interval dose adjust

-headache
– chest pain
– dizziness
– dyspnea
– QT prolongation (and torsades de pointes (1-3%)) !!!!!!
– AV and bundle branch block
– ventricular tachycardia and fibrillation

34
Q

Sotalol
1. Non specific ___
2. Primary action is prolonging cardiac AP by ?
3. Secondary action is ?
4. Used for both ?
5. QT interval ?
6. Monitor QT interval when ?
7. AE’s ? (7)

A
  1. Beta blocker
  2. inhibiting delayed rect K+ channels
  3. Non select B Blocker
  4. Ventric tachyarrhythmias and AFIB or AFLUTTER
  5. prolonged
  6. 2-3 hrs after each dose during initiation or dose incr (3 day hospitalization for initiation)
  7. increased QT interval
    – torsades de pointes (1.5-2%) – seems dose / concentration dependent
    – Bradycardia, fatigue, depression, bronchospasm, impotence!!!!!!!
35
Q

Sotalol Dosing See chart

A

See chart

36
Q

Channel IV AAD’s

  1. What do they block? WHat drugs
  2. Useful in terminating ?
  3. Class EP
    -Incr ___
    -Decr __
    -INCR __
    -No effect on ___
  4. DOSING SEE CHART
A
  1. CA2+ channel , NON DHP Verap and Diltiazem
  2. re-entrant arrhythmias that involve the AV node and controlling the ventricular rate in atrial fibrillation or flutter
  3. refractory period
    -conduction velocity
    -PR interval
    -QT or QRS intervals
  4. See chart for dosing
37
Q

Misc Drugs : Adenosine

  1. Activates ACetylcholine sensitive ___ in atrium and sinus and AV nodes resulting in ? (3)
  2. 1st line agent for? (3)
  3. It can unmask ___
  4. Can help differentiate between ?
  5. AE”s?
A
  1. K+ current
    -shortening of the AP
    – hyperpolarization
    – slowing of normal automaticity
  2. terminating narrow complex PSVT
    – AV nodal reentry or AV reentry (such as WPW)
    – treating patients w/ a concealed accessory pathway
  3. Atrial activity (AF or AFl)
  4. VT or SVT
  5. flushing, dyspnea, chest pain, ASYSTOLE,
    bronchospasms, abdominal discomfort
38
Q

Adenosine
1. Half life?

  1. Dosing ?
    -What must be given immed after to ensure drug delivery to AV node prior to degradation ?
  2. May repeat with ____ if No response
  3. total acceptable dose is?
A
  1. 10-30 secs !
  2. 6 mg IV push rapidly over 1-3 secs
    - 20-30 mL saline flush
  3. 12 mg IV push in 1-2 mins –> if no response, can repeat AGAIN
  4. 30 mg
39
Q

Digoxin

  1. 2 primary uses?
  2. ECG effects –> what does it lengthen? what does it do to ST seg?
A
  1. inotropic effects in heart failure
    - vagotonic actions, yielding inhibition of
    Ca2+ currents in AV node and activation of
    acetylcholine mediated K + currents in
    atrium
  2. PR lengthening
    - depression
40
Q

Digoxin

  1. DDI’s?
  2. Serum conc in HF and in rate control -AFIB AFL ?
  3. Managing toxicity includes ? (3)
  4. DOsing see chart
A
  1. PGP
  2. 0.5-0.9 ng/mL
    0.5-1.2 ng/mL
  3. Atropine (minor), Magnesium, and or Digoxin immune fab (Ovine)
41
Q

Digoxin :

  1. AE’s
    -Arrhythmias … What are the risk factors?
    -What are the 5 types of arrhythmias?
    -N
    -Disturbances of ?
    -Blurred or ___
A
  1. Elevated digoxin levels, hypoxia, hypokalemia
  • DAD related tachycardias
  • sinus bradycardia
  • heart block
  • atrial tachycardia with AV block
  • ventricular bigeminy

-Nausea
-COgnitive function
-yellow vision

Humber Cardio FINAL (13 decks)

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