Arrhythmias Flashcards
conduct
transmit electrical charges
cardiac conductive system
electrical signalizing system that causes the atria and ventricles to contract
auscultation
listening to heart with stethoscope
arrhythmia
abnormal heart rhythm
can result in bradycardia (slow) or tachycardia (fast)zz
symptoms of arrythmia
heart “fluttering” or “skipping a beat”
dizziness
SOB
fatigue
diagnosis of arrhythmia
`ECG
Holter monitor
ambulatory ECG
detects intermittent arrythmias
normal sinus rhythm (NSR)
starts at SA node = pacemaker
60-100 BPM
conduction pathway
SA node
R and L atrium
AV node
Bundle of His
R bundle branch and R ventricle
L bundle branch and L ventricle
Purkinje fibers
source of arrhythmias
SA node firing abnormal rate/rhythm
scar tissue from past heart attack blocks/diverts signals
another part of the heart is acting as pacemaker
action potential
movement of ions through channels in myocytes that cause electrical impulses in the cardiac conduction pathway
give electricity to power heart
SA
pacemaker that has automaticity in cells = initiate own action potentials
Phase 0
heartbeat initiated
rapid ventricular depolarization = influx of Na = ventricular contraction
QRS complex
Phase 2
plateau response to influx of Ca and efflux of K
Phase 3
rapid ventricular repolarization bc efflux of K = ventricular relaxation
T wave
most common cause of arrhythmias
myocardial ischemia or infarction
non-cardiac conditions that can cause arrhythmias
electrolyte imbalances - K, Mg, Na, Ca
high sympathetic state - hyperthyroidism, infection, drugs (illicit drugs, antiarrhythmics, drugs that inc QT
origins of arrhythmias
supraventricular (above AV node)
ventricular (below AV node)
most common type of arrhythmia
atrial fibrillation
irregular/usually rapid ventricular response
inc risk of clot = stroke risk = may need anticoagulation
ventricular arrhythmias
premature ventricular contractions = skipped heartbeat; related to stress or too much caffeine
if in series = HR >100 = ventricular tachycardia
untreated VT can degenerate into ventricular fibrillation = completely disorganized electrical activation of ventricles = medical emergency
prolongation of QT interval
risk for Tosade de Pointes = can cause sudden cardiac death
QT prolongation risk factors
high dose of drug
multiple drugs
reduced drug clearance (drug interaction)
electrolytes: hypokalemia, hypomagnesemia
other cardiac conditions
drugs that inc or prolong QT interval
antiarrhythmics: !a, !c, III
hydroxychloroquine
azoles (except isavuconazaonium)
macrolies
quinolones
Lefamulin
SSRIs (worst w citalopram and escitalopram)
TCAs
mirtazapine
trazodone
venlafaxine
setrons
droperidol
metopclopramide
promethazine
First generation antipsychotics (haloperidol,
chlorpromazine, thioridazine)
Second generation antipsychotics (ziprasidone worst)
androgen deprivation therapy (leuprolide)
TKIs (nilotinib)
oxaliplatin
other: cilostazol, donepezil, fingolimod, hydrozyzine, loperamide, methadone, ranolazine, solifenacin, tacrolimus
what to do before starting drug from non-life-threatening arrythmia
check electrolytes/tox screen for reversible cause
Vaughan Williams classification
categorizes antiarrhymic drugs based on dominant electrophysiological effect
Double Quarter Pounds, Lettuce, Mayo, Fries Please
Because Dieting During Stress Is Always Very Difficult
Class I drugs
Na-channel blockers
proarrhythmic; caution with cardiac disease
Ia: disopyramide, quinidine, procainamide
Ib: lidocaine, mexiletine
Ic: flecainide, propafenone
Class II drugs
Beta-blockers
slow ventricular rates
Class III drugs
K-channel blockers
Dronedarone
Dofetilide
Sotalol
Ibutilide
Amiodarone
Class IV
Ca-channel blockers, non-DHP
verapamil
diltiazem
amiodarone and dofetilide preferable for AF in pts with HF
Sotalol
low ventricular rate
digoxin
Na-K-ATPase blocker