Arrhythmias Flashcards
(98 cards)
1
Q
What 2 heart conditions are typically caused by medication?
A
- heart block
- torsades de pointes
2
Q
What does the p wave correspond to?
A
- first depolarization
3
Q
What does the QRS complex correspond to?
A
- larger ventricle depolarizing
4
Q
What does the T wave correspond to?
A
- ventricle is repolarizing
5
Q
What are the main pathological reasons for a tachyarrhythmia?
A
- automaticity: abnormality in impulse generation
- often starts the arrhythmia - re-entry: abnormality in pulse conduction
- often maintains the arrhythmia
6
Q
What are considered to be escape pacemakers of the heart?
A
- AV node
- bundle of His
- bundle branches
- Purkinje network
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
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
9
Q
If the bundle branches or the purkinje network become the main pacemakers, what will the heart rate be?
A
20-40 bpm
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
11
Q
What is a class 1 AAD?
A
Na channel blocker
12
Q
What is a class 2 AAD?
A
beta blockers
13
Q
What is a class 3 AAD?
A
K channel blockers (these are the most common in terms of rhythm control)
14
Q
What is a class 4 AAD?
A
calcium channel blockers
15
Q
What does reducing automaticity do?
A
- prevents and slows arrhythmias
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
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
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)
19
Q
What ion channels do digoxin block?
A
Na/K ATPase
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
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
22
Q
Are more agent pure rhythm control agents or have multiple activity on the heart?
A
- few are pure rhythm control agents
23
Q
What is quinidine?
A
- class 1a and K blocker
24
Q
What is sotalol?
A
- class 3 and beta blocker
25
What is amiodarone?
- class 3 and Na, Ca, and beta blocker
26
What is propafenone?
class 1c and beta blockers
27
What is flecainide?
- pure class 1c, but high risk for VT in CAD
28
What is ibutilide/dofetilide?
- pure class 3, but high risk here for tornadoes de points
29
Heart rates of what are considered tachyarrythmic?
>100 bpm
30
Heart rates under what are considered bradyarrhythmic?
<60 bpm
31
What is atrial fibrillation?
- very fast atrial rate and a disorganized atrial rhythm that is irregularly irregular
32
What happens when there is a loss of the atrial kick?
- the heart is not filled up as efficiently
33
What does an extremely fast atrial rhythm result in?
- a fast ventricular rate
34
How much of the pumping to the heart do you lose upon atrial fibrillation?
10-20% of the extra flow that fills the heart comes from the atria
35
What action does a rate controlling agent have?
- slows doen the rate of the ventricles
36
What action does a rhythm controlling agent have?
- tries to normalize the rhythm of the atria
37
What are the categories of atrial fibrillation?
- acute
- paroxysmal
- persistent
- permanent
38
What is acute atrial fibrillation?
atrial fibrillation that lasts 48 hours
39
What is paroxysmal atrial fibrillation?
this terminates spontaneously within 7 days - can come back multiple times
40
What is persistent atrial fibrillation?
-continues for greater than 7 days
41
What is permanent atrial fibrillation?
- does not terminate even with cardioversion attempts
42
What are some of the temporary factors that may precipitate a. fib?
(things that cause HIGH ADRENERGIC TONE)
- alcohol withdrawal
- sepsis
- post surgery
- excessive physical exertion
- sympathomimetic
- theophylline
- digoxin toxicity
43
What are some of the permanent factors that may precipitate a. fib? (things that cause ATRIAL DISTENSION)
- ischemia
- hypertension (increases the size of the atria)
- valvular disorder
- congenital abnormalities
- cardiomyopathy
- pulmonary embolism
- pulmonary hypertension
- obesity
44
What are the signs of atrial fibrillation?
- irregular pulse
- HR >100 bpm
- hypotension
- EKG
45
What are the symptoms of atrial fibrillation?
- asymptomatic
- palpitations
- dizziness
- syncope
- angina
- heart failure
46
What are the serious complications associated with atrial fibrillations?
- tachycardia induced heart failure
- severe hypotension/heart failure
- embolic stroke (blood flow through the atrium is not normal, can cause clots to form)
47
What are the major goals of therapy in treating an arrhythmia?
- control of rapid ventricular response = ventricular rate control
- restoration of normal sinus rhythm = atrial rhythm control
- prevention of thromboembolic complications
48
What drugs control rate of the heart?
- beta blocker
| - calcium channel blocker
49
What is an example of why you would go straight to rhythm control rater than trying to get symptom control from rate controlling agents?
- heart failure
50
When would it be appropriate to use a pill in pocket therapy? (giving medication only when AF occurs)
- when there is a low recurrence of paroxysmal atrial fibrillation
51
What is the rate controlling drug choices when the person has heart failure?
- beta blocker potentially with digoxin
52
What is the rate controlling drug choice when a person has CAD?
beta blocker
CCB
or combination therapy
53
What can be used as a rate controlling agent when a person has had neither heart failure or CAD?
- beta blocker
- calcium channel blocker
- digoxin
- combination therapy
54
What are the end goals that we want with rate controlling agents?
- heart rate <100 bpm
| - minimize symptoms: palpitations, dizziness, SOB
55
What are the AE associated with diltiazem/verapamil?
- BP <100/60
| -
56
What are the interactions with diltiazem and verapamil?
3A4 and P-GP inhibitor
| - watch out with 3A4 substrates (statins) or P-GP substrates (digoxin)
57
What are the AE associated with metoprolol/atenolol?
- bp <100/60
- HR <60
- CHF
- asthma
- diabetes
- weakness
- fatigue
- PVD
- abrupt d/c
58
What are the AE associated with digoxin?
- GI: anorexia, N/V, diarrhea
- neurological: headache, fatigue, confusion
- visual: blurred vision, disturbed color vision, halos (yellow/green) around bright objects
- cardiac: arrythmias
59
What should the digoxin trough levels be?
1-2 mcg/L
60
What should K levels be while on digoxin? Why?
< 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
What are the drug interactions that are associated with digoxin?
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
What is catheter ablation?
- putting the catheter into the atrium and find the beat that is firing abnormally- you can find the disabled rhythm from here
63
Restoration of the normal sinus rhythm is used to stop what?
- to stop atrial fibrillation
64
What is the medication that is used for new onset a. fib in hospital?
- amiodarone
65
To use the pill in the pocket method of treating arrhythmias, the patient must be ____ controlled first?
rate
66
What are options to use in RHYTHM control in patients where there is no history of CHF?
- dronedarone
- flecainide
- propafenone
- sotalol
- amiodarone
67
What are options to use in RHYTHM control in patients that have a history of CHF or left ventricular systolic dysfunction?
- amiodarone
| - sotalol
68
When is the ONLY case that you would want to use amiodarone as a rhythm controlling agent?
- 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
What are the rhythm control endpoint goals that we want to meet?
- want to maintain normal sinus rhythm
| - no palpitations, dizziness, SOB
70
What are the main AE associated with sotalol?
- BB SE
- plus N/V
- diarrhea
- QTc>500 msec
- torsades de pointes
- CrCl <60 mL/min
71
What is the main AE associated with propafenone?
- BB SE
- plus headache
- taste disturbances
- N/V
- lupus
- ventricular arrhythmias (high risk with CAD)
72
What are the main AE associated with flecainide?
- 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
What are the main drug interactions associated with sotalol?
- QT prolonging medications
74
What are the main drug interactions associated with propafenone?
CYP45- 2D6 substrate
| - inhibits digoxin elimination
75
What are the main drug interactions associated with flecainide?
- QT prolonging medications
| - CYP450 2D6 substrate
76
What are the main SE associated with strong CYP 2D6 inhibitors?
- buproprion
- paroxetine
- quinidine
- cinacalcet
77
What are the main serious SE associated with amiodarone?
- pulmonary fibrosis
- hypothyroidism
- hyperthyroidism
- optic neuropathy
- corneal microdeposits
- hepatotoxicity
- bradycardia/heart block
- tremor, ataxia, peripheral neuropathy
- photosensitivity/blue-grey skin discoloration
78
Why does amiodarone have such major interactions with the thyroid?
it is 1/3 iodine molecules- these will interact with the thyroid gland
79
What are some of the medications with a recommended dosage decrease when starting up amiodarone ?
- digoxin
- warfarin
- flecainide
- quinidine
- atorvastatin
- simvastatin
(max dose here is 20 mg/day)
80
What other medications will amiodarone have an additive effect with?
- rate controlling agents: HR < 60 bpm
| - QT prolonging agents: QTc > 500 msec
81
What enzymes does amiodarone inhibit?
CYP450 1A4, 2C9, 2D6, 3A4, and P-glycoprotein
82
What oral anticoagulants can be used in rate control?
- warfarin
- dabigatran
- rivaroxaban
- apixaban
83
If a person is >65 and has a fib, what anticoagulation therapy should they be on?
OAC
84
If a person as had a prior stroke, hypertension, HF, or diabetes and has a fib, what anticoagulation therapy should they be on?
OAC
85
If a person has CAD or arterial vascular disease and has a fib, what anticoagulation therapy should they be on?
ASA
86
If a fib is less than 48 hours, is anticoagulation therapy needed?
no
87
If a fib is over 48 hours, is anticoagulation therapy needed?
- yes. needed for 3 weeks pre-cardioversion and at least 4 weeks post
88
Given the possibility of paroxysmal a fib, consider long term anticoagulation if what?
- if CHADS >= 1
89
What are the toxicity endpoints with warfarin?
- when the INR is over 3
90
What are the interactions associated with warfarin?
- 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
What is the toxicity endpoints associated with the new oral anticoagulants?
- CrCl < 30 mL/min
92
What are the interactions that are associated with the new oral anticoagulants?
- amiodarone/dronedarone, propafenone, quinidine/quinine, verapamil, itraconazole, ketoconazole
93
What would you recommend for a patient with acute CHF that is hemodynamically unstable?
- SBP <90 -- recommend electrical cardioversion
94
What would you recommend to a patients with acute CHF that is hemodynamically stable with a HR >100 bpm?
- 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
In ALL patients with acute CHF, you should consider long term what to prevent the recurrence of a fib?
- long term amiodarone
96
What are the efficacy endpoints associated with rate controlling agents?
- HR <100 bpm
| - minimize palpitations, dizziness, SOB
97
What are the efficacy endpoints associated with rhythm controlling agents?
- maintain NSR
| - no palpitations, dizziness, SOB
98
What are the efficacy endpoints associated with OACs?
- no focal neurological deficits, headache, sudden change in vision, one sided weakness, slurred speech, loss of balance
- INR should be 2-3 for warfarin
