Exam 2: Arrhythmias Flashcards
Class 1 Medications are _______ and act on phase _________
Sodium channel blockers, 0
Class 2 Medication are __________
and act on phase ________
propranolol and metoprolol, 4
Class 3 Medications are _______ and act on phase _________
Potassium channel blockers (amiodarone, sotalol), 3
Class 4 Medications are _______ and act on phase __________
Calcium channel blockers, 2
Electrical Conduction in the Heart Steps
- SA node fires
- Excitation spreads through atrial myocardium
- AV node fires
- Excitation spreads down AV bundle
5: Purkinjie fibers distribute excitation though ventricular myocardium
What influences nodal firing?
Pacemakers have automaticity
+
input from SNS and PSNS
Important Ion Channels in the Heart
sodium channels
calcium channels
potassium channels
HCN channels
hERG channel
Significance of hERG channels
an important channel to avoid being targeted when developing new drugs
Membrane Potential Outside of Cell
0 mV
Electrolyte Concentrations Outside of Cell
K = 5 mM
Na = 142 mM
Ca= 5 mM
Cl = 103 mM
Membrane Potential Inside of Cell
-70 mV
Electrolyte Concentrations Inside of Cell
K = 148 mM
Na = 10 mM
Ca= < 1 uM
Cl = 4 mM
Concentration Gradient: Sodium
flows inside of cell (142 -> 10)
Electrical Gradient: Sodium
flows inside of cell (+ to -)
Concentration Gradient: Potassium
flows outside of cell (5 <- 148)
Electrical Gradient: Potassium
inside of cell (+ to -)
Pacemaker Cells
calcium dependent spikes
non contractile cells
depolarized
high automaticity
Ventricular Myocytes
sodium dependent spikes
contractile cells
hyperpolarized
Currents for pacemaker APs: iCa
carries AP upstroke (phase 0)
Currents for pacemaker APs: iK
repolarizing K+ current (phase 3)
Currents for pacemaker APs: if
diastolic pacemaker current (phase 4)
HCN channel
Currents for pacemaker APs: iK(ACh)
K+ current activated by vagus (phase 4)
Acetylcholine
decreased HCN and calcium current
hyper-polarization (GIRK)
Atrium and SA/AV nodes
Myocyte AP Currents: iNa
carries ap upstroke (phase 0)
Myocyte AP Currents: iKto
transient outward repolarizing current (phase 1)
Myocyte AP Currents: iCa(L)
plateau Ca2+ current critical for muscle contraction (phase 2)
Myocyte AP Currents: iK
repolarizing K+ current (phase 3)
Myocyte AP Currents: if
pacemaker current (phase 4, very minimal)
No _______ channel involved in myocytes
calcium channels
neuronal action potential
The Refractory Period
result of a 2nd stimulus on ability to elicit an AP is greater as you progress through the RRP (relative refractory period)
Re-entry requirements
multiple parallel pathways
unidirectional block
conduction time greater than ERP (effective refractory period)
Class 2 Drugs
beta AR blockade
shifts the timing of the peak
HCN channel slows down the pacemaker cell, longer phase 4
useful for arrhythmias involving catecholamines (epi, norepi, etc)
increases refractoriness of SA, AV node
Class 4 Drugs
calcium channel blockades
lower the mV of the peak
frequency dependent block
protect ventricular rate from atrial tachycardia
increases refractoriness of AV node and PR interval
Class 2 Change in EKG
increases PR interval
beta blockers used in antiarrhythmics: esmolol
cardioselective B1
very short half life ~9 min due to plasma esterase hydrolysis
given iv
beta blockers used in antiarrhythmics: acebutolol
cardioselective
weak partial agonist at B1AR (sympathomimetic)
weak sodium channel blockade
beta blockers used in antiarrhythmics: propranolol
non selective
weak sodium channel blockade
clinical uses of bAR blockers
arrhythmias involving catecholamines
atrial arrhythmias
post mi prevention of ventricular arrhythmias
prophylaxis in long QT syndrome
Calcium channel blockers in arrhythmias: MOA
frequency dependent block of calcium channels
selective block for channels opening more frequently
accumulation of blockade in rapidly depolarizing tissue
clinical uses of CCBs in arrhythmias
block re-entrant involving AV node
protect ventricular rate in aflutter and afib
Class 1A effect on AP
prolonged qt interval
Class 1B effect on AP
no clinically significant effect on ECG
Class 1C effect on AP
strong sodium channel block
widens QRS
Class 1A Drug
quinidine
Class 1B Drug
lidocaine
mexiletine
Class 1C
flecainide
ventricular and supra-ventricular
orally available
Class 3 MOA
block IKr
prolong action potential duration and QT interval
increases effective refractory period
increased ERP above conduction time around circuit will terminate re-entry
Class 3 Drugs
Amiodarone
blocks IKr the most
top choice prevention of afib
suppresses emergency ventricular and atrial arrhythmias
Adverse Effects: Amiodarone
hypothyroidism
pulmonary fibrosis
photosensitization
Digoxin
inhibition of AV node
also increase intropy, used for CHF
Adenosine
leads a brief but potent slowing of the heart
Questions to ask when looking at an EKG?
P wave in front of every QRS?
QRS after P wave?
Intervals are the same?
What is the rate?
PR interval normal
0.12-0.20 seconds (120-200 ms)
QTc interval in men
360-450 ms
QTc interval in women
360-460 ms
Torsades de Pointes
QTc interval ≥ 500 ms, there is an increased risk of the drug-induced arrhythmia known as TDP
can cause sudden cardiac death
Sinus bradycardia
heart rate < 60 bpm
sinus bradycardia moa
decreased automaticity of the SA node
drugs that cause sinus bradycardia
digoxin
beta blockers
ccbs
amiodarone!
dronedarone
ivabrandine
symptoms of bradycaria
hypotension
dizziness
syncope
treatment of sinus bradycardia is only necessary when________
if patient is symptomatic
first line treatment of sinus bradycardia
atropine 0.5-1mg IV, repeat every 5 minutes
max: 3 mg
if unresponsive to first line sinus bradycardia treatment
transcutaneous pacing
dopamine
epi
isoproterenol
atropine adverse effects
tachycardia
urinary retention
blurred vision
dry mouth
mydriasis
treatment of sinus bradycardia after heart transplant or spinal cord injury
Aminophylline
IV then oral of theophylline in HT
Oral of theophylline in SCI
Long term treatment of Sinus Bradycardia
permanent pacemaker
if unwilling to have pacemaker, theophylline oral
afib: atrial activity
chaotic and disorganized, no atrial depolarizations
afib: ventricular rate
120-180 bpm
afib: rhythm
irregularly irregular
afib: p waves
absent
stage 1 afib
presence of modifiable and nonmodifiable risk factors associated with AF
stage 2 afib
pre-atrial fibrillation
evidence of structural or electrical findings that further predispose patients to AF
- atrial enlargement
- frequent atrial premature beats
- atrial flutter
Stage 3a afib
paroxysmal AF
AF that is intermittent and terminates within ≤ 7 days of onset
Stage 3b afib
persistent AF
af that is continuous and sustains for > 7 days and requires intervention
stage 3c afib
long standing persistent AF
af that is is continuous for > 12 months in duration
stage 3d afib
successful af ablation
freedom form af after percutaneous or surgical intervention to eliminate AF
stage 4 afib
permanent trial fibrillation
no further attempts at rhythm control after discussion between the patient and clinician
mechanisms of afib
abnormal atrial/pulmonary vein automaticity
atrial reentry
Risk factors/etiologies of AFib
socioeconomic status
thoracic surgery
hyperthyroidism
alcohol
heart failure
idiopathic
symptoms of afib
may be asymptomatic
palpitations
dizziness
fatigue
lightheadedness
sob
hypotension
syncope
angina
exacerbation of hf symptoms
CHADSVAsc
CH x 1
HTN x1
Age ≥ 75 x 2
DM x1
Stroke x 2
Vascular Disease (PAD,aortic plaque, MI) x 2
Age 65-74 x1
Oral AC recommended for pts with afib and ______
chadsvasc score
≥ 2 in men
≥ 3 in women
oral ac reasonable for pts with afib and _______
chadsvasc score
1 in men
2 in women
prevention of stroke/systemic embolism treatments
doacs preferred overwarfarin in most patients
warfarin preferred over doacs
Mechanical Heart Valve (INR 2.5-3.5)
Heart Valve Disease (iNR 2.0-3.0)
warfarin or apixaban preferred
ESCD (CrCl < 15 mL/min)
hemodialysis
antidote for dabigatran
idarucizumaba
antidote for xa factors
adexanet alfa
drugs for ventricular rate control
diltiazem
verapamil
esmolol
propranolol
metoprolol
digoxin
amiodarone
adverse effects: nonDHP CCBs
hypotension
bradycardia
HF exacerbation
AV block
adverse effects: BBs
hypotension
bradycardia
HF exacerbation (if dose too high or increased too aggressively)
AV block
adverse effects: digoxin
nausea
vomiting
ventricular arrhythmias
adverse effects: amiodarone
hypotension (IV)
bradycardia
blue-grey skin
photosensitivity
corneal microdepositis
pulmonary fibrosis
hepatotoxicity
hypothyroidism
hyperthyroidism
qt prolongation
conversion to sinus rhythm is safe when
if af has been present for ≤ 48 hours
if af has been present for > 48 hours
conversion to SR should not be preformed
until
pt AC’d for 3 weeks or TEE has been preformed to rule out clot in atrium
DCC risks
general anesthesia (aspiration)
ibutilide mechanism
class III
ibutilide aes
torsades de pointes
procainamide class
class 1a
procainamide aes
qt prolongation
torsades de pointes
hypotension
HFrEF exacerbation
agranulocytosis
neutropenia
flecainide class
class 1c
propafenone class
class 1c
flecainaide and propafenone aes
dizziness
blurred vision
HFrEF exacerbation
Drugs for Conversion to SR
DCC
Amiodarone
Ibutilide
Procainamide
Flecainide
Propafenone
Drugs for Maintenance of SR
amiodarone
dofetilide
dronedarone
sotalol
propafenone
flecainide
dofetilide aes
torsades de pointes
dronedarone aes
bradycardia
diarrhea
nausea
asthenia
rash
sotalol aes
beta blockade
torsades de pointes
Dofetilide dose
CrCl based
> 60: 500 mcg orally bid
40-60: 250 mcg orally bid
20-39: 125 mcg orally bid
< 20: CI
proceed for dofetilide use if QTc is
≤440 ms
proceed with sotalol use if QTC is
≤450 ms
catheter ablation place in therapy
antiarrhythmic drugs have been ineffective, contraindicated, not tolerated or not preferred
can be 1st line
supraventricular tachycardia
regular rhythm
narrow QRS
HR 110 to >250 bpm
spontaneous initiation and termination
paroxysmal SVT
intermittent episodes of SVT that start sudddenly and spontaneously, lasts for minutes to hours, and terminate suddenly and spontaneously
mechanism of SVT
premature impulses
symptoms of SVT
neck pounding
palpitations
dizziness
weakness
lightheadedness
near syncope
syncope
polyuria
goals of svt
terminate SVT, restore sinus rhythm
prevent recurrence
drugs for termination of SVT
adenosine
BBlockers
Diltiazem
Verapamil
adenosine aes
chest pain
flushing
shortness of breath
sinus pauses
bronchospasm
adenosine dosing
6 mg IV rapid bolus
if no response in 1-2 minutes, 12 mg IV rapid bolus
can repeat the 12 mg IV dose once
contraindicated in pts with cad
flecainide
propafenone
frequent PVC
at least one PVC on a 12 lead ECG
> 30 PVCs per hour
mechanism of premature ventricular complexes
increased automaticity of ventricular muscle cells/purkinje fibers
symptoms of PVCs
usually asymptomatic
palpitations
dizziness
lightheadedness
treatment of PVCs not appropriate when
if asymptomatic
treatment of PVCs in pts who do not have CAD OR HF or have CAD
BB, non DHP CCBs
if unresponsive, antiarrhythmic
treatment of frequent symptomatic PVCs unresponsive to BB, non DHP CCBs or antiarrhythmic
catheter ablation
treatment of symptomatic PVCs in pts who have HF
beta blockers
ventricular tachycardia
regular rhythms
wide qrs complexes
≥ 3 consequtive VPDs at a rate of > 100 bpm
non-sustained VT
≥ 3 consecutive VPDs, terminates spontaneously
sustained
VT lasting > 30 seconds
requires termiantion because of hemodynamic instability in < 30 seconds
sustained monomorphic VT in pts with no structural heat disease is known as
idiopathic vt
mechanisms of vtach
increased ventricular automaticity
reentry
drugs that cause vtach
flecainide
propafenone
digoxin
symptoms of vtach
may be asymptomatic (nonsustained)
palpitations
hypotension
dizziness
lightheadedness
syncope
angina
goals of therapy: vtach
terminate VT, restore SR
prevent recurrence of VT
reduce the risk of sudden Cardiac death
Drugs for termiantion of ventricular tachycardia
procainamide
amiodarone
sotalol
verapamil
beta blockers (es,meto,prop)
prevention of recurrence and sudden cardiac death
icd
amiodarone
sotalol
catheter ablation
treatment of ventricular fibrillation
defibriillation
epinephrine
amiodarone
lidocaine