pharm exam 3 arrhythmias Flashcards
Conduction velocity is determined by regulation of the action potential, specifically the slope of phase ___ depolarization
0
The ____/____ refractory period is the time during which cardiac cells cannot conduct nor propagate an action potential
effective/absolute
The ___ refractory period is the time during which cardiac cells may conduct and propagate action potentials secondary to strong electrical stimuli
relative
resting membrane potential
in the ventricle =
AV node =
SA node =
- 75 mv
- 70 mv
- 60 mv
Upon depolarization, an influx of ___ raises the gradient from a negative value towards a positive value, allowing for conduction of the electrical current
During repolarization, the gradient returns back to baseline as ___ effluxes
cations (Na+ and/or Ca2+)
K+
Mechanisms responsible for cardiac arrhythmias are generally divided into 2 major categories:
1)
2)
1) abnormal impulse formation
- abnormal automaticity
- triggered activity
2) abnormal conduction
- conduction delay
- re-entry
During triggered activity, heart cells contract ___
example = torsades
twice
____ produces no cardiac output and causes most cases of sudden cardiac arrest
v fib
Arrhythmias are defined by location and rate
____ arrhythmias arise from abnormalities in the SA node, atrial tissue, AV node, or bundle of His.
____ arrhythmias originate from below the bundle of His.
Supraventricular
Ventricular
T wave =
ventricular repolarization
_____ reflects the duration of the ventricular action potential
QT interval
Mechanism of sinus bradycardia:
what are some causes?
decreased SA node automaticity
MI, hypothyroidism, drug induced, hyperkalemia
consistent prolonged PR interval =
First degree AV block
prolongation of PR interval until a QRS complex is dropped =
Almost always a disease of the AV node
second degree AV block type 1 (wenckebach)
PR interval remains constant and does not increase with each cardiac cycle prior to the ”dropped” QRS complex =
Almost always a disease of His-Purkinje System
second degree AV block type 2 (Mobitz II)
third degree heart block aka
complete heart block
condition in which the nerve impulse generated in the sinoatrial node (SA node) in the atrium of the heart can not propagate to the ventricles =
complete heart block
mechanism of AV block:
what are some causes?
prolonged conduction
MI, drug induced, hyperkalemia, increased vagal tone, myocarditis, AV nodal disease
Atrial Fibrillation and Atrial Flutter are ____ arrhythmias
supraventricular
mechanism of supraventricular arrhythmia =
Enhanced automaticity and reentrant circuits
v tach = 3 or more consecutive ___ at a rate exceeding 100 bpm and a wide QRS interval
PVCs
Specific variety of ventricular tachycardia w/ QRS complexes that appear to twist around the ECG baseline =
torsades
Sodium channel blockers MOA:
blocking the channels leads to a decrease in the slope of phase __. This causes a decrease in ___ velocity in non-nodal tissue (atrial and ventricular muscle, Purkinje system). Ultimately, blocking Na+ channels reduces the __ of action potential transmission w/i the heart. This can serve as an important mechanism of suppressing ___ that are caused by abnormal conduction
0 ; conduction
velocity
tachycardia’s
Na+ Channel Blockers
__ drugs have the greatest decreasing effect on phase 0
__ drugs have the smallest effect on phase 0
__ drugs are intermediate in their effect on phase 0
1C
1B
1A
Na+ Channel Blockers and Effective Refractory period (EFP)
Class __: Increase ERP
Class __: Decrease ERP
Class __: No effect on ERP
Increasing the ERP can interrupt tachycardia caused by reentry mechanisms by prolonging the duration that normal tissue is unexcitable
1A
1B
1C
Disopyramide
what drug class?
restrict use to ___ ventricular arrhythmias
Na+ channel blocker, 1A
life-threatening
Procainamide
what drug class?
Positive ANA may develop drug induced __
extremely short __
50% metabolized to an active metabolite known as __
NAPA may accumulate in patients with __
If you don’t metabolize it quickly enough, it will have anti-arrhythmic effects!
Na+ channel blocker, 1A SLE (Lupus) half life NAPA renal failure
Quinidine
what drug class?
VERY irritating to the __
can also cause __
Quinidine may increase mortality in treatment of __ or __
Na+ channel blocker, 1A
GI tract
Cinchonism
atrial fibrillation or atrial flutter
Cinchonism includes:
Blurred vision Tinnitus Hearing loss Diaphoresis Confusion Psychosis
Lidocaine
contraindication: __ syndrome: Sudden collapse into unconsciousness
Adam-Stokes
Flecainide
what class?
Has ___ effects
Na+ channel blocker, 1C
pro-arrhythmic
All Class __ Antiarrhythmics are PROARRHYTHMIC!
1
β-Blockers: Class II MOA
inhibit ___ influences on cardiac electrical activity, thereby decreasing __ rate, decrease conduction __ (which can block reentry mechanisms), and inhibit aberrant __ activity
Also, BB’s increase action potential duration and the __
sympathetic
sinus ; velocity
pacemaker
effective refractory period (ERP)
Esmolol beta blocker is only used for __ control of arrhythmia
rapid
K+ Channel Blockers: Class III MOA
These drugs bind to and block the K+ channels that are responsible for phase __ repolarization. Blocking these channels slows/delays __, which leads to an increase in action potential duration and an increase in __. these drugs are very useful in suppressing ___ caused by reentry mechanisms
On the ECG, this increases the __
3
repolarization
ERP
tachyarrhythmias
QT-interval
Currently the most effective antiarrhythmic for ventricular arrhythmias; however, it is also the most toxic =
Amiodarone
Amiodarone side effects:
1) Increased liver __ or __ levels (as high as 40-50% in some studies, check at baseline and Q6 months)
2) Pulmonary __ (check PFT at baseline and Q12 months)
3) __ color skin
4) __ deposits
5) Proarrhythmic
6) __tension
7) __thyroidism
8) Abnormal __
9) Impaired ___
10) Involuntary movement
11) __ disturbances
12) __cardia
13) AV block
AST or ALT
fibrosis
Blue-gray
Corneal
Hypo
Hypo
gait/ataxia
memory
Sleep
brady
Amiodarone
half life ranges from __-__ days!!
Initial response is __-__ , peak response takes __-__
PO duration: Up to __ days after D/C of therapy
35-110
2 days to 3 weeks ; 1 week to 5 months
50
AKA: “less toxic Amiodarone”; but not as effective as Amiodarone at maintaining sinus rhythm =
Dronedarone
__ in Class 3 is pregnancy X
Dronedarone
Each of these can cause a substantial \_\_ in Dofetilide plasma concnetrations. (↑ F and ↓ Cl) Verapamil Cimetidine Trimethoprim Ketoconazole Prochlorperazine Megestrol HCTZ
increase
Dofetilide
BBW: Hospitalize minimum of __ days during initiation
3
Ibutilide
BBW: May cause potentially fatal ___
arrhythmias
Sotalol Contraindication: \_\_ Formulations indicated for ventricular and atrial arrhythmias are different: Betapace = \_\_ Betapace AF = \_\_\_
asthma
ventricular
atrial
only the ___ CCB’s are approved as antiarrhythmics
nondihydropyridine
Ca2+ Channel Blockers: Class IV MOA
Decreases conduction velocity and prolongs __, especially at the __. Prolongs phase __ of the AP
repolarization
AV node ; 2
Digoxin MOA in Atrial Fibrillation/Flutter:
Activates __ efferent nerves to the heart (__ effect). Vagal activation can reduce the conduction of electrical impulses w/i the __ to the point where some of the impulses will be blocked. When this occurs, fewer impulses reach the ventricles and ventricular rate falls.
Digoxin also increases ERP within the AV node
vagal ; parasympathomimetic
AV node
Digoxin toxicity
When K+ levels are __, Digoxin can more easily bind to the pump exerting its __ effects
low
inhibitory
Adenosine MOA
POWERFUL __, especially in the coronary circulation; but VERY __ acting
used for the rapid treatment of supraventricular tachycardias
vasodilator
short
