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Oral Medicine and Diagnosis > Caring for Patients with Atrial Fibrillation > Flashcards

Caring for Patients with Atrial Fibrillation Flashcards

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1
Q

cardiac arrhythmias occur in up to _____ of patients treated with digoxin

A

25%

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2
Q

cardiac arrhythmias occur in up to _____ of anesthetized patients

A

50%

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3
Q

cardiac arrhythmias occur in up to _____ of patients with acute MI

A

over 80%

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4
Q

rythms that are _________ can reduced cardiac output

A

too rapid, too slow, or asynchronous

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5
Q

early premature ventricular depolarizations can:

A

precipitate ventricular fibrillation

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6
Q

what is one of the dangers of antiarrhythmics

A

can precipitate lethal arrythmias in some patients

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7
Q

treatment of asymptomatic of minimally symptomatic arrhythmias should be:

A

avoided

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8
Q

premature ventricular contractions are ___ in pts recovering from MI

A

common

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9
Q

increased numbers of PVCs are associated with:

A

an increased risk of sudden death

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10
Q

flecainide and encainide treated patients had significantly increased:

A

mortality compared to untreated patients

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11
Q

is encainide still used

A

no it is no longer available for use

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12
Q

what non pharmacologic therapies are used to treat arrhythmias

A
  • pace makers
  • cardioversion
  • catheter ablation
  • surgery
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13
Q

what arrhythmias should not be treated

A

CAST

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14
Q

what needs to be done to minimize risk of antiarrhythmic therapies

A
  • monitor plasma concentrations
  • drug interactions
  • patient specific contraindications such as heart failure and dronedarone, and amiodarone can cause interstitial lung disease and pulmonary fibrosis
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15
Q

describe the electrophysiology of normal cardiac rhythm

A
  • the electrical impulse that triggers a normal cardiac contraction at regular intervals in the SA node
  • this impulse spreads rapidly through the atria and enters the AV node
  • conduction through the AV node is slow, requiring about 0.15 sec
  • the impulse then propogates through the His-Purkinje system and invades all parts of the ventricles
  • ventricular activation is complete in less than 0.1 sec
  • contraction of all the ventricular muscle is synchronous and hemodynamically effective
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16
Q

what happens in the SA node

A
  • pacemaker cells spontaneously depolarize at a frequency of 60-100 beats per minute
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17
Q

describe the AV node impulse

A

the AV node is normally the only conduction pathway between the atria and ventricles

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18
Q

why is the slowness of the AV node important

A

this delay provides time for atrial contraction to propel blood into the ventricles

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19
Q

describe signal propagation through the heart on the electrocardiogram- PR interval, QRS, and QT

A
  • the PR interval is a measure of conduction time from atrium to ventricle
  • the QRS duration indicates the time required for all of the ventricular cells to be activated
  • the QT interval reflects the duration of the ventricular action potential
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20
Q

arrhythmias consist of cardiac depolarization where there is an abnormality in:

A

the site of origin of the impulse, its rate or regularity, or its conduction

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21
Q

what happens in each phase of excitation contraction coupling

A
  • phase 4: resting
  • phase 0: Na+ in
  • Phase 1: Ca++ in; Na+ channel closed; K+ out
  • Phase 2: Ca++ in
  • Phase 3: K+ out
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22
Q

what happens in each portion of the P, QRS and T graph

A
  • P: atrial depolarization
  • QRS: ventricular depolarization
  • T: ventricular repolarization
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23
Q

what can precipitate or exacerbate arrhythmias

A
  • ischemia
  • hypoxia
  • acidosis
  • alkalosis
  • electrolyte abnormalities
  • excessive catecholamine exposure
  • autonomic influences
  • drug toxicity
  • overstretching of cardiac fibers
  • presence of scarred or otherwise diseased tissue
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24
Q

all arrhythmias result from:

A
  • disturbances in impulse formation
  • disturbances in impulse conduction
  • or both
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25
what are the types of arrhythmias
- normal rhythm - bradycardia - heart block - supraventricular arrhythimas: atrial tachycardia, atrial fibrillation , wolff- parkinson- white - ventricular tachycardia - ventricular fibrillation
26
what is atrial fibrillation characterized by
disorganized, rapid and irregular atrial activation with loss of atrial contraction and with an irregular ventricular rate that is determined by AV nodal conduction
27
describe the ventricular rate in Afib
- tends to be rapid and variable, between 120 and 160 BPM but in some patients it may exceed 200 beats per min
28
patients with _____ or ____ may have slow ventricular rates
high vagal tone or AV nodal conduction
29
what are the types of AFib
- paroxysmal AFib - persistent AFib
30
what does paroxysm mean
sudden attack or worsening
31
descirbe paroxysmal afib and what it is initiated by
- episodes that start spontaneously and stop within 7 days of onset - often initiated by small reentrant or rapidly firing foci in sleeves of atrial muscle that extend into the pulmonary veins
32
what stops paroxysmal AF
catheter ablation that isolates these foci, although some pts also have initiating foci in other locations
33
some patients progress over years from paroxysmal to______
persistent AFib
34
what is persistent AFib facilitated by
structural and electrophysiological atrial abnormalities, particularly fibrosis that uncouples atrial fibers promoting reentry and focal automaticity
35
how long is long standing persistent AFib and what are the complications from it
- greater than one year - signficiant fibrosis is usually present and it is difficult to restore and maintain sinus rhythm
36
what is the most common sustained arrhythmia
AFib
37
____ of AFid patients are over 60 years of age
greater than 95%
38
prevelance of AFib by age 80 is ____
about 10%
39
lifetime risk of developing AFib for men 40 years old is _____
about 25%
40
lifetime risk of developing AFib for women 40 years old is ____
about 23%
41
what are the risk factors for atrial fibrillation
- age - prior heart attack or heart disease - hypertension - diabetes mellitus - obesity - sleep apnea - excessive alcohol - smoking
42
Afib is also associated with a risk of:
developing heart failure and vice versa
43
AFib increases the risk of stroke by ____ and is estimated to be the cause of ____ of strokes
fivefold; 25%
44
Afib increases the risk of _______ detected by MRI
dementia and silent strokes
45
what are the signs and symptoms of Afib
- irregular and rapid heartbeat - heart palpitations or rapid thumping inside the chest - dizziness, sweating and chest pain or pressure - shortness of breath or anxiety - tiring more easily when exercising - fainting
46
what are the sequelae of AFib
- dizziness/falls - stroke - 5x increase in risk - chronic fatigue - additional arrhythmias - heart failure
47
what are the treatments for AFib
- pharmacotherapy - electrical cardioversion - surgery
48
what is the pharmacotherapy for Afib
- beta blockers, digoxin, calcium channel blockers or amiodarone: slows heart rate - anticoagulants: prevents stroke
49
what does electrical cardioversion do
return heart to sinus rhythm
50
what surgical procedures are done for AFib
- catheter ablation - pacemaker
51
what are the antiarrhythmic drugs
- singh/Vaughan- Williams Classification - L: Na+ channel blockage (Class 1A-C)- lidocaine - E: blockade of sympathetic autonomic effects on the heart (class 2)- esmolol - A: prolongation of action potential duration and the effective refractory period (Class 3) - amiodarone - D: Ca++ channel blockade (Class 4) - dilitiazem
52
describe the class 1 agents
- sodium channel blockers: lidocaine, flecainide, propafenone, disopyramide - flecainide sometimes used for chemical cardioversion - options for subjects without significant structural heart disease - but negative ionotropic and pro arrhythmic effects warrant avoidance in patients with coronary artery disease or heart failure
53
describe class 2 agents
- Beta adrenergic blockers: esmolol, atenolol, metoprolol, propranolol, sotalol
54
describe class 4 agents
Ca++ channel blockers: diltiazem, verapamil
55
what do class 2 and class 4 agents do
- help control ventricular rate by slowing AV nodal conduction - improve symptoms - possess a low risk profile - but have low efficacy for preventing AFib episodes
56
describe class 3 agents
- potassium channel blockers prolonging action potential duration: amiodarone, dofetilide, sotalol
57
dofetilide and sotalol should be initiated only:
in a hospital with ECG monitoring
58
what is the downfall of dronedarone
increases mortality in patients with heart failure
59
class 3 agents have modest efficacy in:
patients with paroxysmal AFib - 30-50% will benefit
60
describe amiodarone as a class 3 agent
- more effective, maintaining sinus rhythm in approximately two thirds of patients - can be administered to patients with heart failure and CAD - but over 40% of patients experience amiodarone related toxicities during long term therapy - sometimes used in chemical cardioversion - prolonged action potential duration (QTc) and risk of torsades de pointes polymorphic ventricular tachycardia - lower risk with amiodarone due to beta blocking and calcium channel blocking effects
61
what are the side effects of diltiazem
- bradycardia - hypotension - constipation - gingival hyperplasia
62
describe sotalol
- prolonged action potential during (QTc) and risk of torsades de pointes polymorphic ventricular tachycardia - lower risk with sotalol due to beta blocking effects - bradycardia, heart block
63
what are the side effects of amiodarone
- bradycardia, heart block - pulmonary fibrosis - hepatotoxicity - optic neuritis and visual disturbances - altered thyroid function
64
what does dofetilide do
- prolonged action potential during (QTc) and risk of torsades de pointes polymorphic ventricular tachycardia
65
describe pacemakers
- modern pacemakers are more resistant to elecromagnetic interferences - but caution is required when using electrical devices
66
what are the drug interactions with antiarrhythmic drugs
- cytochrome P450 mediated (GI tract, liver) - substrates/inhibitors: amiodarone, diltiazem, verapamil -subtractes/inhibitors: macrolide antibiotics (erythromycin, azithromycin, clarithromycin) - organic cation transporter (kidney) - subtrate: dofetilide eliminated by renal OCT2 - inhibitor: trimethoprim (sulfamethoxazole- trimethoprim)
67
what other drugs might be used to treat arryhtmias
- anxiolytics - analgesics - antibiotics
68
what can anxiolytics be used for and which ones
- can be used to lessen stress and anxiety that may come from anticipation of a dental procedure - perhaps prevent/reduce increased release of catecholamines that can exacerbate AFib or other arrhythmias - diazepam, alprazolam, lorazepam, midazolam
69
what can analgesics do and which ones are used
- NSAIDs and aspirin - interfere with anticoagulants that are highly bound to plasma proteins - warfarin
70
what antibiotics might be used
- macrolide antibiotics (erythromycin, azithromycin, clarithromycin) - trimethoprim (sulfamethoxazole- trimethoprim) - fluoroquinolones (ciprofolxacin, ofloxacin, levofloxacin)
71
what do macrolide antibiotics do
can significantly inhibit cytochrome P-450 in liver and GI tract
72
what can trimethoprim do
can inhibit the organic cation transporter in the kidney and inhibit renal elimination of some drugs
73
what can fluoroquinolones do
- many potential adverse effects - can inhibit cytochromes P450 and some can affect cardiac ion currents
74

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