W12 Arrhythmias And Atrial Fibrillation Flashcards
the autonomic nervous system:
PNS NT on effector organ?
SNS NT on effector organ? And via the blood stream
What does parasympatholytic mean
What does sympathomimetic mean
🔑thus, to increase HR (treat bradycardia), give:
● parasympatholytic (↓parasympathetic activity), and/or
● sympathomimetic (↑sympathetic activity)
What is the parasympatholytic drug of choice?
what’s going to get the HR up?
Route?
3 other examples
What can they cause? ADR
🔑ATROPINE IV
● The prototype anticholinergic (aka antimuscarinic or parasympatholytic) b/c ACh acts on these receptors
● Naturally occuring, tertiary amine alkaloid ester of tropic acid, found in the plant Atropa belladonna (deadly
nightshade)
○ other anticholinergics that share a similar name - tiotropium, benztropine, tropicamide
● All anticholinergic drugs (and drugs w/ anticholinergic properties) can potentially cause tachycardia
○ conversely, cholinergic agents can potentially cause bradycardia
● less cholinergic innervation of the ventricles = less utility for heart blocks below the AV node (eg, Mobitz II and 3rd
deg)
sympathomimetic drugs
4
Route?
Which pharm agents are recommended in the ACLS algorithm for bradycardia?
Agents w/ β1 agonism (all of these are given IV)
● ⭐️ epinephrine
—B1 agonism, increases inotropy and chronotropy
—also provides ɑ1 agonism (vasoconstriction)
● ⭐️ dopamine
—given at moderate-high doses provides ɑ1 agonism (vasoconstriction)
—low doses = vasodilation
● dobutamine
—mainly B1 agonist: increases ino/chronotropy (HF)
—also used in cardiac stress test
● isoproterenol
Agents recommended in the ACLS algorithm for bradycardia, along with pacing:
—atropine
—epinephrine
—dopamine
Vaughan Williams classification of antiarrhythmics
(an oversimplification; some drugs have multiple targets)
See notebook to test p8
Know all the Class Ia,b,c, II, III anti-arrhythmic drugs
Know these inside and out because could be asked which class, which target, what MOA, what effect etc
SoBe PoCa
for channel/receptor target
1. Sodium
2. Beta
3. Potassium
4. Calcium
MBA Class
for clinical effect
1. Membrane stabilization
2. Beta blockade
3. Action potential, repolarization,
refractory period delay
4. Calcium channel blockade
What are the class I anti-arrhythmic agents?
What type?
What is the effect?
Na+ channel blockers
Effect = membrane stabilisation
🔑 Amiodarone
MOA
Uses — two groups
Precautions/things to know about the drug — 2
CIs — 3
MOA:
—categorized as class III (K+ block)
—but actually blocks all four targets
—sodium, potassium channels, as well as calcium channels and beta receptor
—hence utility for most types of arrhythmias
Uses:
—supraventricular (AF, aflutter, AVNRT, focal atrial tachycardia)
—and ventricular tachycardias
Precautions
—large Vd and very long and variable half-life (1.5-2 months)
—numerous DDIs
CI’s:
—hypersensitivity to iodine
—sick sinus syndrome or any heart block
—cardiogenic shock
dronedarone (Multaq)
—related to amiodarone but non-iodinated;
—fewer non-cardiac toxicities and
—promising use for afib,
—but later trials revealed risk of cardiovascular events and death in patients with NYHA class III-IV HF, recent decompensated HF, or permanent AF
→ FDA warnings → less use
🔑 Amiodarone toxicities [know well]
● CNS - gait, ataxia, dizziness, fatigue, sleep
disturbance, paresthesias
● Ocular - neuritis, epithelial keratopathy
● Thyroid (related to amio’s iodine content) - hyperthyroidism or hypothyroidism
● Pulmonary (BBW) - pneumonitis, fibrosis, acute respiratory distress syndrome (ARDS)
● Cardiovascular - prolonged QTc and arrhythmia (BBW); hypotension, bradycardia
● Hepatic (BBW) - hepatitis, injury
● Dermatologic - blue-colored hyperpigmentation, photosensitivity, solar dermatitis
CXR baseline before starting amiodarone, check lungs, LFTs, thyroid function, pulmonary function
🔑Agent for PSVT?
MOA?
Diagnostic for what?
Additional use?
C/I — 4 (ABBB)
S/Es — 4
Food interaction?
Half life? Route
🔑Adenosine —adenosine
Paroxysmal supraventricular tachycardia (PSVT) : AVNRT (remember AVRT treatment is procainamide, WPW)
—usually d/t reentry in/around the AV node;
—agonism of adenosine receptors in the AV node results in:
—interruption of re-entry pathways in AV node (think: adeNODEsine)
— slowed conduction time and therefore heart rate
diagnostic
— can reveal flutter if you slow the HR down
● additional use
—cardiac stress test:
—vasodilation of healthy coronary arteries (and little effect on stenosed
arteries); decreased thallium uptake = diseased vessels
● contraindications:
—🔑bronchospastic lung dz including asthma
—WPW (procainamide) and afib/flutter
—bradycardia
—heart block
● SEs:
—chest pain/discomfort
—facial flushing
—hypotension
—bronchospasm
● drug/food interactions:
—caffeine and theophylline (adenosine receptor blockers)
● fun factoid:
—half-life is <10 seconds
—must be given as rapid IV push
Adenosine alternatives - other things that block the AV node
● IV diltiazem/verapamil
● IV metoprolol
● catheter ablation
digoxin (a cardiac glycoside)
What is the MOA — 2
Uses — 2
What is the goal trough level ? (Lowest concentration in system)
What are the S/S for toxicity? (cv, CNS, renal)
Antidote?
—cardiac glycosides - organic compounds
—inhibit Na-K ATPase pumps
—resulting in increased inotropy
—and negative chronotropy (dec HR); found in Lily of the Valley, oleander, foxglove
🔑uses:
● atrial fibrillation (digoxin slows HR)
● heart failure (digoxin increases contractility)
🔑goal trough levels
—is typically 0.5-1 ng/mL
—know that this must be checked regularly
narrow therapeutic index, so know s/sxs of toxicity:
● 🔑 cardiac: bradycardia, AV block
● 🔑 CNS: headache, confusion, abnormal vision
● s/sxs of toxicity is exacerbated by hypokalemia and hypomagnesemia
● 🔑 renally cleared, builds up VERY easily in acute renal dysfunction
Antidote for toxicity:
—digoxin immune Fab (Digibind)
Torsades de Pointe (TdP)
Aka
Drug of choice
= polymorphic VTach
Just know drug of choice = IV magnesium
AAD for:
Afib/flutter
SVT (AVNRT)
Torsades
Afib/flutter
—CCBs or BBs
—amiodarone
—flecainide
—consider cardioversion
other supraventricular tachycardias
—adenosine
—CCBs, BBs,
—consider cardioversion and/or ablation.
verapamil with asthma!
Torsades
—magnesium sulfate, pacing (drug or electric)
QTc prolongation
Risk factors that are non-preventable
risk factors that are preventable
Risk factors that are non-preventable
● demographics (older age, females)
● channelopathies (LQTS, LQT2)
● cardiac disease - bradycardia, conduction dz,
structural heart dz
risk factors that are preventable
● 🔑 electrolytes: hypoCa, hypoK, hypoMg
● medications that prolong the QT or contribute to
electrolyte imbalance; drug accumulation - importance of close monitoring (and dose adjustment or avoidance) in hepatic and renal impairment
Medications: ABCDEF
QTc prolonging med classes
treatment of drug-induced EKG changes
Wide QRS: two agents
Long QTc: 1 agent
Wide QRS (>120 msec)
● oftentimes indicative of sodium blockade - many agents have this effect, including local anesthetics, antipsychotics, antidepressants…
● treatment: sodium!
—sodium bicarbonate or hypertonic sodium chloride
Long QTc (>470 msec in women, >450 msec in men)
● 🔑treatment: magnesium sulfate
Afib remodeling changes
What is paroxysmal afib
What is long-standing afib
What is permanent afib?
paroxysmal: resolves in < 7d
persistant: >7d
long-standing persistant: >12m
What are the 4 pillars of afib management?
- Lifestyle and risk management (obesity, physical activity, sleep, DM, HTN…)
- Anti-coagulation
- Rhythm control
- Rate control
Afib — lifestyle modifications — just be familiar
Afib relationship w/ HF
FYI
Assessing stroke risk — i.e need for anticoagulation
🔑 must be able to calculate score for the exam
What does CHA2DS2VASc stand for?
How many points for each criteria?
How many points for no, preferred and recommended DOAC for M/F?
Your score correlates to your risk per year, roughly
So a score of 2 is 2% risk per year
Scoring for anticipating major bleed on anticoagulation
HAS-BLED score
What are the scores?
Over which score requires frequent monitoring and f/u? but doesn’t necessarily mean don’t anti-coagulate
‘major’ bleed = intracranial, requiring hospitalization or transfusion, ↓Hgb by ≥2 g/dL
—a high HAS-BLED score (≥3) = patient needs regular review and f/u;
—a high score does not necessarily mean don’t anticoagulate
- What does CHADS2VASC not apply to? 2
- What treatment is not recommended for afib?
- What treatment should mechanical valve patients be on, regardless of Afib status?
- Patients w/ mechanical valves or mitral stenosis
- Anti-platelets are not recommended
- Mechanical valve = always Warfarin
Summary of DOACs or NOACs. Takeaways:
—all used for non-valvular AF
—know reversal agent for rivaroxaban, apixaban and dabigatran
—all really cleared, so renally dosed
—edoxaban is the only one with minimal hepatic metabolism
—always check for drug interactions b/c some are CYP/PgP substrates
What do you do if a patient needs a DOAC for afib but also DAPT post PCI?
—do it for one month or less
When is anticoagulation not possible or repeatedly fails, what treatment option?
LAA occlusion, usually WATCHMAN™ implant
● consider in patients w/ nonvalvular AF at increased stroke risk and contraindications to long-term anticoagulation (eg, major bleed while on anticoagulation, condition or occupation or lifestyle that makes patient prone to trauma)
● in trials compared w/ warfarin, this procedure has non-inferior efficacy for stroke prevention, and fewer major bleeding events**
Review BBs vs CCBs vs Digoxin
Uses/benefits vs ADRs/drawbacks
Review therapies for afib.
Key takeaways:
NO CCB for LV failure, HFrEF
Amiodarone is last line
3 ways to control rhythm
Antiarrhythmics used in AF — 3
- Anti-arrhythmic medication
—flecanide PO (class Ic membrane stabilisation, pts w/ normal heart structure)
—propafenone PO (class Ic membrane stabilisation, pts w/ normal heart structure)
—amiodarone PO/IV (class III K+ channel blocker) - Cardioversion
- Ablation
Pharmacologic cardioversion in the guidelines. Which meds should you know for afib?
afib, meds for no structural HD and w/ structure HD
—when is ablation 1st line for afib?
—what is an ADR for class III AAD?
—what are the “pill in a pocket” meds?
—when should they NOT be given?
—what should they be combined with?
—ablation is 1st for afib if paroxysmal
—QT prolongation, so caution of torsades de pointes
—pill in a pocket: propafenone †, flecanide †
†do not give if structural heart dz, give amiodarone
—combine with nodal blocking agent i.e BB, CCB
—amiodarone and catheter ablation is an option for both w/ w/o structural HD
🔑 anticoagulation timing relative to pharmacologic or
electric cardioversion (slide 1/2)
How do you prevent a thromboembolism:
—W/ afib/flutter ≥48h
—W/ afib/flutter >48h + immediate need
—W/ afib/flutter <48h + high stroke risk
—how long to form a thrombus?
—how long to dissolve existing thrombus while on anti-coags?
—how long for atria to recover after cardioversion?
🔑thrombus timing considerations
● 24-48h for a thrombus to form
● 3 weeks to dissolve an existing thrombus w/anticoagulation
● 4 weeks for atrial function to recover post-cardioversion (ie, no more risk of clot formation)
anticoagulation timing relative to pharmacologic or
electric cardioversion (slide 2/2)
—W/ afib/flutter ≥48h BUT no 3w prior anti-coag therapy, what do you do?
—start anti-coag therapy
—perform TEE before cardioversion
—make sure no thrombus identified
—anti-coag for 4w post cardioversion
