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Clinical Pharmacy 2 > Arrhythmias > Flashcards

Arrhythmias Flashcards

1
Q

What 2 heart conditions are typically caused by medication?

A
  • heart block

- torsades de pointes

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2
Q

What does the p wave correspond to?

A
  • first depolarization
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3
Q

What does the QRS complex correspond to?

A
  • larger ventricle depolarizing
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4
Q

What does the T wave correspond to?

A
  • ventricle is repolarizing
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5
Q

What are the main pathological reasons for a tachyarrhythmia?

A
  1. automaticity: abnormality in impulse generation
    - often starts the arrhythmia
  2. re-entry: abnormality in pulse conduction
    - often maintains the arrhythmia
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6
Q

What are considered to be escape pacemakers of the heart?

A
  • AV node
  • bundle of His
  • bundle branches
  • Purkinje network
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7
Q

What is the role of the AV node?

A
  • the AV node is the gatekeeper

- other cells are between the ventricles and the atria do not have enough capacity to conduct an electrical current

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8
Q

If the AV node or the bundle of His become the main pacemakers, what will the heart rate be?

A

40-50 bpm

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9
Q

If the bundle branches or the purkinje network become the main pacemakers, what will the heart rate be?

A

20-40 bpm

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10
Q

What is the pathology of a re-entry arrhythmia?

A
  • if side of the heart (or the SA node) is still refractory when an electrical current is trying to pass through, then the electrical current will back up and loop through the heart the other way (the AV node or bundle of His will become the pacemaker) and when it gets back to the refractory section it can pass through now since it is non-refractory. The heartbeat will continue on to be the same this way
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11
Q

What is a class 1 AAD?

A

Na channel blocker

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12
Q

What is a class 2 AAD?

A

beta blockers

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13
Q

What is a class 3 AAD?

A

K channel blockers (these are the most common in terms of rhythm control)

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14
Q

What is a class 4 AAD?

A

calcium channel blockers

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15
Q

What does reducing automaticity do?

A
  • prevents and slows arrhythmias
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16
Q

What is the effect of beta blockers on the heart during an arrhythmia?

A
  • reduced adrenergic stimulation of the SA/AV nodes

- decreased stimulation of myocardial contractility

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17
Q

What is the effect of non-DBP Calcium channel blockers on an arrhythmia?

A
  • reduced calcium current and recover in the SA/AV nodes

decreased calcium influx in myocytes, decreased myocardial contractility

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18
Q

What is the effect of digoxin on an arrhythmia?

A
  • increased myocyte Na/Ca, decreased K, increased AV node refractory period
  • increased vagal tone, decreased SA/AV node activity
    (increased intracellular Na, exchanged for Ca, increased contractility)
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19
Q

What ion channels do digoxin block?

A

Na/K ATPase

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20
Q

What do sodium channel blockers do to the heart?

A
  • decrease in conduction velocity

- re-entry loop loses “steam”, SA node takes over

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21
Q

What do potassium channel blockers do to the heart in an arrhythmia case?

A
  • they cause a prolonged refractory period

- re-entry loop “catches its tail”, SA node takes over

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22
Q

Are more agent pure rhythm control agents or have multiple activity on the heart?

A
  • few are pure rhythm control agents
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23
Q

What is quinidine?

A
  • class 1a and K blocker
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24
Q

What is sotalol?

A
  • class 3 and beta blocker
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25
Q

What is amiodarone?

A
  • class 3 and Na, Ca, and beta blocker
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26
Q

What is propafenone?

A

class 1c and beta blockers

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27
Q

What is flecainide?

A
  • pure class 1c, but high risk for VT in CAD
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28
Q

What is ibutilide/dofetilide?

A
  • pure class 3, but high risk here for tornadoes de points
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29
Q

Heart rates of what are considered tachyarrythmic?

A

> 100 bpm

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30
Q

Heart rates under what are considered bradyarrhythmic?

A

<60 bpm

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31
Q

What is atrial fibrillation?

A
  • very fast atrial rate and a disorganized atrial rhythm that is irregularly irregular
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32
Q

What happens when there is a loss of the atrial kick?

A
  • the heart is not filled up as efficiently
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33
Q

What does an extremely fast atrial rhythm result in?

A
  • a fast ventricular rate
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34
Q

How much of the pumping to the heart do you lose upon atrial fibrillation?

A

10-20% of the extra flow that fills the heart comes from the atria

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35
Q

What action does a rate controlling agent have?

A
  • slows doen the rate of the ventricles
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36
Q

What action does a rhythm controlling agent have?

A
  • tries to normalize the rhythm of the atria
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37
Q

What are the categories of atrial fibrillation?

A
  • acute
  • paroxysmal
  • persistent
  • permanent
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38
Q

What is acute atrial fibrillation?

A

atrial fibrillation that lasts 48 hours

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39
Q

What is paroxysmal atrial fibrillation?

A

this terminates spontaneously within 7 days - can come back multiple times

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40
Q

What is persistent atrial fibrillation?

A

-continues for greater than 7 days

41
Q

What is permanent atrial fibrillation?

A
  • does not terminate even with cardioversion attempts
42
Q

What are some of the temporary factors that may precipitate a. fib?
(things that cause HIGH ADRENERGIC TONE)

A
  • alcohol withdrawal
  • sepsis
  • post surgery
  • excessive physical exertion
  • sympathomimetic
  • theophylline
  • digoxin toxicity
43
Q

What are some of the permanent factors that may precipitate a. fib? (things that cause ATRIAL DISTENSION)

A
  • ischemia
  • hypertension (increases the size of the atria)
  • valvular disorder
  • congenital abnormalities
  • cardiomyopathy
  • pulmonary embolism
  • pulmonary hypertension
  • obesity
44
Q

What are the signs of atrial fibrillation?

A
  • irregular pulse
  • HR >100 bpm
  • hypotension
  • EKG
45
Q

What are the symptoms of atrial fibrillation?

A
  • asymptomatic
  • palpitations
  • dizziness
  • syncope
  • angina
  • heart failure
46
Q

What are the serious complications associated with atrial fibrillations?

A
  • tachycardia induced heart failure
  • severe hypotension/heart failure
  • embolic stroke (blood flow through the atrium is not normal, can cause clots to form)
47
Q

What are the major goals of therapy in treating an arrhythmia?

A
  • control of rapid ventricular response = ventricular rate control
  • restoration of normal sinus rhythm = atrial rhythm control
  • prevention of thromboembolic complications
48
Q

What drugs control rate of the heart?

A
  • beta blocker

- calcium channel blocker

49
Q

What is an example of why you would go straight to rhythm control rater than trying to get symptom control from rate controlling agents?

A
  • heart failure
50
Q

When would it be appropriate to use a pill in pocket therapy? (giving medication only when AF occurs)

A
  • when there is a low recurrence of paroxysmal atrial fibrillation
51
Q

What is the rate controlling drug choices when the person has heart failure?

A
  • beta blocker potentially with digoxin
52
Q

What is the rate controlling drug choice when a person has CAD?

A

beta blocker
CCB
or combination therapy

53
Q

What can be used as a rate controlling agent when a person has had neither heart failure or CAD?

A
  • beta blocker
  • calcium channel blocker
  • digoxin
  • combination therapy
54
Q

What are the end goals that we want with rate controlling agents?

A
  • heart rate <100 bpm

- minimize symptoms: palpitations, dizziness, SOB

55
Q

What are the AE associated with diltiazem/verapamil?

A
  • BP <100/60

- <hr>

56
Q

What are the interactions with diltiazem and verapamil?

A

3A4 and P-GP inhibitor

- watch out with 3A4 substrates (statins) or P-GP substrates (digoxin)

57
Q

What are the AE associated with metoprolol/atenolol?

A
  • bp <100/60
  • HR <60
  • CHF
  • asthma
  • diabetes
  • weakness
  • fatigue
  • PVD
  • abrupt d/c
58
Q

What are the AE associated with digoxin?

A
  • GI: anorexia, N/V, diarrhea
  • neurological: headache, fatigue, confusion
  • visual: blurred vision, disturbed color vision, halos (yellow/green) around bright objects
  • cardiac: arrythmias
59
Q

What should the digoxin trough levels be?

A

1-2 mcg/L

60
Q

What should K levels be while on digoxin? Why?

A

< 3.5 mmol/L

they should be lower because they will exacerbate the Na/K channel blocking and can lead to toxicity of the digoxin

61
Q

What are the drug interactions that are associated with digoxin?

A
  1. amiodarone/dronedarone, propafenone, quinidine/quinine, verapamil, itraconazole
    - inhibition of both P-GP and P450
    - reduce digoxin dose by 50%
  2. macrolide: increased levels via P-GP/ P450 plus kill eubacterium
  3. cholestyramine, Al-Mg antacids, kaolin-pectin, dietary fibre, sucralfate
  4. beta blockers, non-DHP CCPs
  5. calcium, rapid IVs: arrhythmias
  6. diuretics, amphotericin B, laxatives(indirect via hypokalemia)
62
Q

What is catheter ablation?

A
  • putting the catheter into the atrium and find the beat that is firing abnormally- you can find the disabled rhythm from here
63
Q

Restoration of the normal sinus rhythm is used to stop what?

A
  • to stop atrial fibrillation
64
Q

What is the medication that is used for new onset a. fib in hospital?

A
  • amiodarone
65
Q

To use the pill in the pocket method of treating arrhythmias, the patient must be ____ controlled first?

A

rate

66
Q

What are options to use in RHYTHM control in patients where there is no history of CHF?

A
  • dronedarone
  • flecainide
  • propafenone
  • sotalol
  • amiodarone
67
Q

What are options to use in RHYTHM control in patients that have a history of CHF or left ventricular systolic dysfunction?

A
  • amiodarone

- sotalol

68
Q

When is the ONLY case that you would want to use amiodarone as a rhythm controlling agent?

A
  • when a person has a EF <35% because it is the only agent that does not cause an increase in death vs the placebo
  • HOWEVER it has the most systemic toxicity so it is important to be aware of this
69
Q

What are the rhythm control endpoint goals that we want to meet?

A
  • want to maintain normal sinus rhythm

- no palpitations, dizziness, SOB

70
Q

What are the main AE associated with sotalol?

A
  • BB SE
  • plus N/V
  • diarrhea
  • QTc>500 msec
  • torsades de pointes
  • CrCl <60 mL/min
71
Q

What is the main AE associated with propafenone?

A
  • BB SE
  • plus headache
  • taste disturbances
  • N/V
  • lupus
  • ventricular arrhythmias (high risk with CAD)
72
Q

What are the main AE associated with flecainide?

A
  • blurred vision
  • dizziness
  • dyspnea
  • headache
  • tremor
  • nausea
  • worsening HF
  • conduction disturbances
  • QTc > 500 msec
  • ventricular arrhythmias (high risk with CAD)
  • CrCl < 50 mL/min
73
Q

What are the main drug interactions associated with sotalol?

A
  • QT prolonging medications
74
Q

What are the main drug interactions associated with propafenone?

A

CYP45- 2D6 substrate

- inhibits digoxin elimination

75
Q

What are the main drug interactions associated with flecainide?

A
  • QT prolonging medications

- CYP450 2D6 substrate

76
Q

What are the main SE associated with strong CYP 2D6 inhibitors?

A
  • buproprion
  • paroxetine
  • quinidine
  • cinacalcet
77
Q

What are the main serious SE associated with amiodarone?

A
  • pulmonary fibrosis
  • hypothyroidism
  • hyperthyroidism
  • optic neuropathy
  • corneal microdeposits
  • hepatotoxicity
  • bradycardia/heart block
  • tremor, ataxia, peripheral neuropathy
  • photosensitivity/blue-grey skin discoloration
78
Q

Why does amiodarone have such major interactions with the thyroid?

A

it is 1/3 iodine molecules- these will interact with the thyroid gland

79
Q

What are some of the medications with a recommended dosage decrease when starting up amiodarone ?

A
  • digoxin
  • warfarin
  • flecainide
  • quinidine
  • atorvastatin
  • simvastatin
    (max dose here is 20 mg/day)
80
Q

What other medications will amiodarone have an additive effect with?

A
  • rate controlling agents: HR < 60 bpm

- QT prolonging agents: QTc > 500 msec

81
Q

What enzymes does amiodarone inhibit?

A

CYP450 1A4, 2C9, 2D6, 3A4, and P-glycoprotein

82
Q

What oral anticoagulants can be used in rate control?

A
  • warfarin
  • dabigatran
  • rivaroxaban
  • apixaban
83
Q

If a person is >65 and has a fib, what anticoagulation therapy should they be on?

A

OAC

84
Q

If a person as had a prior stroke, hypertension, HF, or diabetes and has a fib, what anticoagulation therapy should they be on?

A

OAC

85
Q

If a person has CAD or arterial vascular disease and has a fib, what anticoagulation therapy should they be on?

A

ASA

86
Q

If a fib is less than 48 hours, is anticoagulation therapy needed?

A

no

87
Q

If a fib is over 48 hours, is anticoagulation therapy needed?

A
  • yes. needed for 3 weeks pre-cardioversion and at least 4 weeks post
88
Q

Given the possibility of paroxysmal a fib, consider long term anticoagulation if what?

A
  • if CHADS >= 1
89
Q

What are the toxicity endpoints with warfarin?

A
  • when the INR is over 3
90
Q

What are the interactions associated with warfarin?

A
  • lots of interactions - substrate CYP 450 2C9 - interacts with fluconazole and septra
  • caution with all antibiotics
  • kills of vitamin K producing bacteria in gut
91
Q

What is the toxicity endpoints associated with the new oral anticoagulants?

A
  • CrCl < 30 mL/min
92
Q

What are the interactions that are associated with the new oral anticoagulants?

A
  • amiodarone/dronedarone, propafenone, quinidine/quinine, verapamil, itraconazole, ketoconazole
93
Q

What would you recommend for a patient with acute CHF that is hemodynamically unstable?

A
  • SBP <90 – recommend electrical cardioversion
94
Q

What would you recommend to a patients with acute CHF that is hemodynamically stable with a HR >100 bpm?

A
  • rate control with digoxin
  • consider electrical cardioversion given the severity of his symptoms with a fib
  • anticoagulation for 3 weeks pre cardioversion (unless TEE rules out atrial thrombus)
  • anticoagulation at least 4 weeks post cardioversion
95
Q

In ALL patients with acute CHF, you should consider long term what to prevent the recurrence of a fib?

A
  • long term amiodarone
96
Q

What are the efficacy endpoints associated with rate controlling agents?

A
  • HR <100 bpm

- minimize palpitations, dizziness, SOB

97
Q

What are the efficacy endpoints associated with rhythm controlling agents?

A
  • maintain NSR

- no palpitations, dizziness, SOB

98
Q

What are the efficacy endpoints associated with OACs?

A
  • no focal neurological deficits, headache, sudden change in vision, one sided weakness, slurred speech, loss of balance
  • INR should be 2-3 for warfarin

Clinical Pharmacy 2 (18 decks)

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