Caring for Patients with Atrial Fibrillation Flashcards
cardiac arrhythmias are a frequent problem in clinical
practice
— occurring in up to –% of patients treated with digoxin
— –% of anesthetized patients
— over –% of patients with acute myocardial infarction (MI)
25
50
80
arrhythmias may require treatment
— rhythms that are too rapid, too slow, or asynchronous can
reduce cardiac output
some arrhythmias can precipitate more serious or even
lethal rhythm disturbances
— e.g. early premature ventricular depolarizations can
precipitate —
— in such patients, — drugs can be life saving
ventricular fibrillation
antiarrhythmic
Dangers of Antiarrhythmics
— the hazards of antiarrhythmic drugs has led
to a continual reevaluation of their relative
risks and benefits
* in particular the fact that they can precipitate
lethal — in some patients
— in general, treatment of asymptomatic or
minimally symptomatic arrhythmias should
be …
arrhythmias
avoided
— are
common in patients recovering from MI
premature ventricular contractions (PVCs)
- increased numbers of PVCs are associated with an
increased risk of
sudden death
» therefore, treat PVCs?
— Cardiac Arrhythmia Suppression Trial (CAST)
* premature ventricular contractions (PVCs) are
common in patients recovering from MI
* increased numbers of PVCs are associated with an
increased risk of sudden death
» therefore, treat PVCs?
- (2) treated patients had
significantly increased mortality compared to
untreated patients
flecainide and encainide
- therefore, the decision to initiate any form of
— drug therapy should be predicated on
the knowledge (or strong assumption) that benefits
outweigh the risks - — is no longer available for use
antiarrhythmic
encainide
Treatments
— arrhythmias can be treated with drugs or
non-pharmacologic therapies
(4)
- pacemakers
- cardioversion
- catheter ablation
- surgery
some arrhythmias should not be treated
(e.g. —)
CAST
symptoms due to arrhythmias
(2)
- asymptomatic (benefit vs. risk?)
- palpitations (nothing to one person, debilitating
to other)
choose therapeutic approaches
* e.g. atrial fibrillation:
* to use drugs or not?
(3)
decrease ventricular rate,
restore sinus rhythm,
anticoagulated
Principles of Antiarrhythmic Therapy
* Minimize Risk
— anti-arrhythmic drugs can cause —
— monitor — concentrations
— – interactions
— patient-specific contraindications
arrhythmias
plasma
drug
patient-specific contraindications
* heart failure and —
* amiodarone can cause (2)
dronedarone
interstitial lung disease
and pulmonary fibrosis (what about COPD?)
Signal Propagation through the Heart
— the electrical impulse that triggers a normal cardiac
contraction at regular intervals is in the —
* pacemaker cells spontaneously depolarize at a frequency of – beats per minute
— this impulse spreads rapidly through the atria and enters the —
* the AV node is normally the only conduction pathway between
the —
— conduction through the AV node is slow, requiring about —
* this delay provides time for atrial contraction to …
sinoatrial (SA) node
60-100
atrioventricular (AV) node
atria and ventricles
0.15 sec
propel blood into the ventricles
Electrophysiology of Normal Cardiac
Rhythm
* Signal Propagation through the Heart
— the impulse then propagates through the
— system and invades all parts of
the —
— ventricular activation is complete in less
than —
— contraction of all of the ventricular muscle is
— and — effective
His-Purkinje
ventricles
0.1 sec
synchronous, hemodynamically
Signal Propagation through the Heart
— on the electrocardiogram
* the PR interval is a measure of …
* the QRS duration indicates the …
» i.e. the — conduction time
* the QT interval reflects the …
conduction time from atrium to
ventricle
time required for all of the ventricular cells to be activated
intraventricular
duration of the ventricular action potential
arrhythmias consist of cardiac depolarizations that deviate
from this normal propagation in one or more aspects
* there is an abnormality in (3)
the site of origin of the impulse,
its rate or regularity,
or its conduction
skipped
many factors can precipitate or exacerbate
arrhythmias
(lots)
- ischemia, hypoxia, acidosis or alkalosis,
electrolyte abnormalities, excessive
catecholamine exposure, autonomic influences,
drug toxicity (e.g. digoxin or antiarrhythmic
drugs), overstretching of cardiac fibers, and the
presence of scarred or otherwise diseased tissue
all arrhythmias result from
(3)
- (1) disturbances in impulse formation
- (2) disturbances in impulse conduction
- or (3) both
ARRHYTHMIA RESOURCES
(7)
▪ Normal Rhythm
▪ Bradycardia
▪ Heart Block
▪ Atrial Tachycardia
▪ Atrial Fibrillation
▪ Ventricular Tachycardia
▪ Ventricular Fibrillation
Atrial fibrillation (AFib)
* 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
AFib
the ventricular rate tends to be rapid and
variable, between — beats/min, but
in some patients, it may exceed — beats/min
120 and 160
200
AFib
patients with high vagal tone or AV nodal
conduction disease may have
slow ventricular
rates
Types of AFib
* Paroxysmal AFib
— “paroxysm” =
— episodes that start spontaneously and stop
within – days of onset
— often initiated by
— catheter ablation that isolates these foci usually
abolishes —, although some
patients also have initiating foci in other
locations.
ATRIAL FIB
sudden attack or worsening
7
small reentrant or rapidly
firing foci in sleeves of atrial muscle that extend
into the pulmonary veins (PV)
paroxysmal AF
Persistent AFib
— some patients progress over — from
paroxysmal to persistent AFib
— persistence of the AFib is likely facilitated by (2) atrial
abnormalities, particularly — that (2)
— long-standing persistent AFib (>1 year),
significant fibrosis is usually present and it is
difficult to restore and maintain —
years
structural and electrophysiologic
fibrosis,
uncouples atrial fibers promoting reentry and focal automaticity
sinus rhythm
Epidemiology
* AFib is a major — problem
* AFib is the most common —
* Prevalence increases with —
public health
sustained
arrhythmia
age
Prevalence increases with age
— >95% of AFib patients are >– years of age
— prevalence by age 80 is ~–%
— lifetime risk of developing AFib for men 40
years old is ~–%
— lifetime risk of developing AFib for women
40 years old is ~–%
60
10
25
23
ATRIAL FIBRILLATION
▪ Risk Factors
(8)
- age
- prior heart attack or heart disease
- hypertension
- diabetes mellitus
- obesity
- sleep apnea
- excessive alcohol
- smoking
Risk of Sequela
* AFib is also associated with a risk of
developing — and vice-versa
— patients with — have an increased
risk of developing AF
* AFib increases the risk of stroke by
fivefold and is estimated to be the cause
of —% of strokes
* AFib increases the risk of — and
silent strokes detected by MRI
heart failure
25
dementia
ATRIAL FIBRILLATION
▪ Signs & Symptoms
(6)
- irregular and rapid heartbeat
— wearables helping to identify - 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 (syncope)
Sequela
(5)
- dizziness/falls
- stroke
— 5X increase in risk - chronic fatigue
- additional arrhythmias
- heart failure
ATRIAL FIBRILLATION
▪ Treatments
* Pharmacotherapy
(5)
— beta blockers, digoxin, calcium channel blockers
or amiodarone
* slow heart rate
— anticoagulants (covered elsewhere in course)
* prevent stroke
ATRIAL FIBRILLATION
▪ Treatments
Electrical Cardioversion
— return heart to sinus rhythm
ATRIAL FIBRILLATION
▪ Treatments
Surgery
(2)
— catheter ablation
— pacemaker
Singh/Vaughan-Williams (MechanismBased) Classification
LEAD
L * Na+ channel blockade (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)
— diltiazem
Antiarrhythmic Therapy for AFib
* Class 1 agents
— sodium channel–blockers
*(4)
— options for subjects without significant
—
— but (2)
effects warrant avoidance in patients with
coronary artery disease or heart failure
lidocaine, flecainide, propafenone, disopyramide
structural heart disease
negative inotropic and proarrhythmic
ANTIARRHYTHMIC DRUGS
▪ Antiarrhythmic Therapy for AFib
* Class 2 (β-adrenergic blockers) and Class 4
(calcium channel blockers) Agents
— Class 2 b-blockers: (5)
— Class 4 Ca++ channel blockers: (2)
— help control ventricular rate by —
— improve symptoms
— possess a low-risk profile
— but have low efficacy for preventing AFib
episodes
esmolol, atenolol,
metoprolol, propranolol, sotalol
diltiazem,
verapamil
slowing AVnodal conduction
Antiarrhythmic Therapy for AFib
* Class 3 Agents
— potassium channel blockers prolonging action
potential duration
* (4)
— — should be initiated only in a hospital with ECG monitoring
* — worthy of same approach
— dronedarone increases mortality in patients
with —
— all of these agents have modest efficacy in
patients with —
* ~—% will benefit
amiodarone, dronedarone, dofetilide, sotalol
dofetilide
sotalol
heart failure
paroxysmal AFib
30–50
Antiarrhythmic Therapy for AFib
* Class 3 Agents
— amiodarone is more effective, maintaining
sinus rhythm in approximately two-thirds of
patients
* it can be administered to patients with (2)
* but, over –% of patients experience
amiodarone-related toxicities during long-term
therapy
heart
failure and coronary artery disease
40
Antiarrhythmic Treatments
* Pacemakers
— modern pacemakers are more resistant to
—
— but, caution is required when using —
electromagnetic interferences
electrical
devices (e.g., ultrasound and electric scalpels)
Antiarrhythmic Treatments
Drug Interactions
— cytochrome P450-mediated (GI tract, liver)
(2)
— organic cation transporter (kidney)
(2)
- amiodarone, diltiazem, verapamil
- macrolide antibiotics (erythromycin, azithromycin,
clarithromycin) - dofetilide
- trimethoprim (e.g. sulfamethoxazole-trimethoprim)
Other Drugs That Might Be Used
* anxiolytics:
— can be useful to lessen — that
may come from anticipation of a dental
procedure
* perhaps prevent/reduce increased release of
— that can exacerbate AFib or other
arrhythmias
— (3)
* analgesics
— (2)
— interfere with — that are highly
bound to —
stress and anxiety
catecholamines
diazepam, alprazolam, lorazepam, etc
non-steroidal anti-inflammatory drugs (NSAIDs) and aspirin
anticoagulants
plasma proteins (e.g. warfarin)
Other Drugs That Might Be Used
* antibiotics
(3)
— macrolide antibiotics (e.g. erythromycin,
azithromycin, clarithromycin)
— trimethoprim (e.g. sulfamethoxazoletrimethoprim)
— fluoroquinolones (e.g. ciprofloxacin, ofloxacin,
levofloxacin)
— trimethoprim (e.g. sulfamethoxazoletrimethoprim)
(1)
- can inhibit the organic cation transporter in the
kidney to inhibit renal elimination of some drugs
— macrolide antibiotics (e.g. erythromycin,
azithromycin, clarithromycin)
(1)
- can significantly inhibit cytochromes P-450 in liver
and GI tract
— fluoroquinolones (e.g. ciprofloxacin, ofloxacin,
levofloxacin)
(2)
- many potential adverse effects
- can inhibit cytochromes P-450 and some can affect
cardiac ion currents
