Brainscape's Knowledge GenomeTM

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


See full index

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

Caring for Patients with Atrial Fibrillation Flashcards

1
Q

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

A

25%

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

cardiac arrhythmias occur in up to _____ of anesthetized patients

A

50%

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

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

A

over 80%

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

rythms that are _________ can reduced cardiac output

A

too rapid, too slow, or asynchronous

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

early premature ventricular depolarizations can:

A

precipitate ventricular fibrillation

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

what is one of the dangers of antiarrhythmics

A

can precipitate lethal arrythmias in some patients

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

treatment of asymptomatic of minimally symptomatic arrhythmias should be:

A

avoided

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

premature ventricular contractions are ___ in pts recovering from MI

A

common

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

increased numbers of PVCs are associated with:

A

an increased risk of sudden death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

flecainide and encainide treated patients had significantly increased:

A

mortality compared to untreated patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

is encainide still used

A

no it is no longer available for use

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

what non pharmacologic therapies are used to treat arrhythmias

A
  • pace makers
  • cardioversion
  • catheter ablation
  • surgery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what arrhythmias should not be treated

A

CAST

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

what happens in the SA node

A
  • pacemaker cells spontaneously depolarize at a frequency of 60-100 beats per minute
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

describe the AV node impulse

A

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

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

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

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

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

A
  • P: atrial depolarization
  • QRS: ventricular depolarization
  • T: ventricular repolarization
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

all arrhythmias result from:

A
  • disturbances in impulse formation
  • disturbances in impulse conduction
  • or both
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what are the types of arrhythmias

A
  • normal rhythm
  • bradycardia
  • heart block
  • supraventricular arrhythimas: atrial tachycardia, atrial fibrillation , wolff- parkinson- white
  • ventricular tachycardia
  • ventricular fibrillation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what is atrial fibrillation characterized by

A

disorganized, rapid and irregular atrial activation with loss of atrial contraction and with an irregular ventricular rate that is determined by AV nodal conduction

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

describe the ventricular rate in Afib

A
  • tends to be rapid and variable, between 120 and 160 BPM but in some patients it may exceed 200 beats per min
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

patients with _____ or ____ may have slow ventricular rates

A

high vagal tone or AV nodal conduction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what are the types of AFib

A
  • paroxysmal AFib
  • persistent AFib
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what does paroxysm mean

A

sudden attack or worsening

31
Q

descirbe paroxysmal afib and what it is initiated by

A
  • 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
Q

what stops paroxysmal AF

A

catheter ablation that isolates these foci, although some pts also have initiating foci in other locations

33
Q

some patients progress over years from paroxysmal to______

A

persistent AFib

34
Q

what is persistent AFib facilitated by

A

structural and electrophysiological atrial abnormalities, particularly fibrosis that uncouples atrial fibers promoting reentry and focal automaticity

35
Q

how long is long standing persistent AFib and what are the complications from it

A
  • greater than one year
  • signficiant fibrosis is usually present and it is difficult to restore and maintain sinus rhythm
36
Q

what is the most common sustained arrhythmia

A

AFib

37
Q

____ of AFid patients are over 60 years of age

A

greater than 95%

38
Q

prevelance of AFib by age 80 is ____

A

about 10%

39
Q

lifetime risk of developing AFib for men 40 years old is _____

A

about 25%

40
Q

lifetime risk of developing AFib for women 40 years old is ____

A

about 23%

41
Q

what are the risk factors for atrial fibrillation

A
  • age
  • prior heart attack or heart disease
  • hypertension
  • diabetes mellitus
  • obesity
  • sleep apnea
  • excessive alcohol
  • smoking
42
Q

Afib is also associated with a risk of:

A

developing heart failure and vice versa

43
Q

AFib increases the risk of stroke by ____ and is estimated to be the cause of ____ of strokes

A

fivefold; 25%

44
Q

Afib increases the risk of _______ detected by MRI

A

dementia and silent strokes

45
Q

what are the signs and symptoms of Afib

A
  • 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
Q

what are the sequelae of AFib

A
  • dizziness/falls
  • stroke - 5x increase in risk
  • chronic fatigue
  • additional arrhythmias
  • heart failure
47
Q

what are the treatments for AFib

A
  • pharmacotherapy
  • electrical cardioversion
  • surgery
48
Q

what is the pharmacotherapy for Afib

A
  • beta blockers, digoxin, calcium channel blockers or amiodarone: slows heart rate
  • anticoagulants: prevents stroke
49
Q

what does electrical cardioversion do

A

return heart to sinus rhythm

50
Q

what surgical procedures are done for AFib

A
  • catheter ablation
  • pacemaker
51
Q

what are the antiarrhythmic drugs

A
  • 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
Q

describe the class 1 agents

A
  • 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
Q

describe class 2 agents

A
  • Beta adrenergic blockers: esmolol, atenolol, metoprolol, propranolol, sotalol
54
Q

describe class 4 agents

A

Ca++ channel blockers: diltiazem, verapamil

55
Q

what do class 2 and class 4 agents do

A
  • 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
Q

describe class 3 agents

A
  • potassium channel blockers prolonging action potential duration: amiodarone, dofetilide, sotalol
57
Q

dofetilide and sotalol should be initiated only:

A

in a hospital with ECG monitoring

58
Q

what is the downfall of dronedarone

A

increases mortality in patients with heart failure

59
Q

class 3 agents have modest efficacy in:

A

patients with paroxysmal AFib
- 30-50% will benefit

60
Q

describe amiodarone as a class 3 agent

A
  • 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
Q

what are the side effects of diltiazem

A
  • bradycardia
  • hypotension
  • constipation
  • gingival hyperplasia
62
Q

describe sotalol

A
  • 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
Q

what are the side effects of amiodarone

A
  • bradycardia, heart block
  • pulmonary fibrosis
  • hepatotoxicity
  • optic neuritis and visual disturbances
  • altered thyroid function
64
Q

what does dofetilide do

A
  • prolonged action potential during (QTc) and risk of torsades de pointes polymorphic ventricular tachycardia
65
Q

describe pacemakers

A
  • modern pacemakers are more resistant to elecromagnetic interferences
  • but caution is required when using electrical devices
66
Q

what are the drug interactions with antiarrhythmic drugs

A
  • 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
Q

what other drugs might be used to treat arryhtmias

A
  • anxiolytics
  • analgesics
  • antibiotics
68
Q

what can anxiolytics be used for and which ones

A
  • 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
Q

what can analgesics do and which ones are used

A
  • NSAIDs and aspirin
  • interfere with anticoagulants that are highly bound to plasma proteins - warfarin
70
Q

what antibiotics might be used

A
  • macrolide antibiotics (erythromycin, azithromycin, clarithromycin)
  • trimethoprim (sulfamethoxazole- trimethoprim)
  • fluoroquinolones (ciprofolxacin, ofloxacin, levofloxacin)
71
Q

what do macrolide antibiotics do

A

can significantly inhibit cytochrome P-450 in liver and GI tract

72
Q

what can trimethoprim do

A

can inhibit the organic cation transporter in the kidney and inhibit renal elimination of some drugs

73
Q

what can fluoroquinolones do

A
  • many potential adverse effects
  • can inhibit cytochromes P450 and some can affect cardiac ion currents
74
Q
A

Oral Medicine and Diagnosis (12 decks)

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