Afib, AntiCoag, & NOAC reversal Flashcards
intervals and rate of Afib
PR interval < 0.20 sec
atrial rate > 300bpm
What is the most common arrhythmia in clinical practice?
A.Fib
increases with advancing age
⅓ of hospitalizations are caused by Afib
Define Paroxysmal Afib
AF terminates spontaneously or with intervention within 7 days of onset
Define Persistent Afib
AF lasts > 7 days
requires meds or electrocardioversion
-
Subcategory:
- long standing persistent: AF > 12 months
Define Permanent Afib
Persistent AF + Pt & provider have made the decision to no longer try to have rhythm control
Clinical Implications of AFib
- decreased diastolic filling → decreased cardiac output
- tachycardia -→ cardiomyopathy → decreased cardiac output
- blood stasis & atrial clot formation → thromboembolism → increased stroke risk
- ALL lead to INCREASED MORBIDITY & MORTALITY
Indications for Cardioversion in AFib
- hemodynamic instability
- acutely altered mental status
- SBP <90 mmHG or s/sxs of shock
- ischemic chest discomfort
- acute HF
- 1st episode:
- symptomatic only (<65yo)
- NOT for asymptomatic elderly (>80 yo) + comorbidities
- Long-Term rhythm control
- Symptomatic Persistent AFib
- Failure of Rate control
- d/t persistent symptoms despite adequate rate control
- or inability to attain rate control
Atrial Fibrillation Treatment Algorithm
No HF → PAID Fees: Propafenone, Amiodarone, Ibutilide, Dofetilide
HF → AID: Amiodarone, Ibutilide, Dofetilide
Class II Vaughan-Williams Antiarrhythmic Agents
- Beta-adrenoreceptor antagonists: Esmolol, metoprolol, propanolol
- MOA: predominant action on the sinus node →affect Rate & Rhythm
Class III Vaughan-Williams Antiarrhythmic Agents
Potassium blockers → widen the duration of the action potential
Rhythm
amiodarone, ibutilide, sotalol
Class IV Vaughan-Williams Antiarrhythmic Agents
non-dihydropyridine CCBs → diltiazem, verapamil
predominant action on the AV node → affect Rate & rhythm
Class Ia Vaughan-Williams Classification Antiarrhythmic Drugs and MOA
- Drugs: procainamide, quinidine, disopyramide
- MOA: Na+ channel blockade, prolonged repolarization → anti-arrhythmic not affecting rate
Class Ib Vaughan-Williams Classification Antiarrhythmic Drugs and MOA
- Drugs: lidocaine, phenytoin
- MOA: Na+ channel blockade, shorten repolarization → antiarrhythmic that does not affect rate
Class Ic Vaughan-Williams Classification Antiarrhythmic Drugs and MOA
- Drugs: Flecainide, Propafenone
- MOA: Na+ channel blockade, repolarization unchanged → antiarrhythmic that does not affect rate
Procainamide (Pronestyl)
Class Ia antiarrhythmic→ Na channel blockade, prolong repolarization
- Indications: atrial & ventricular tachydysrhythmias
-
SEs:
- ventricular dysrhythmia
- agranulocytosis
- Systemic-Lupus erythematosus (SLE) -like syndrome
- Leukopenia, Maculopapular rash, flushing
- Torsades from QT prolongation
-
Contraindications:
- known hypersensitivity, heart block and SLE
Quinidine (Quinidex)
Class 1a Antiarrhythmic→ Na+ channel blockade, prolong repolarization
- Indications: A.fib/flutter, life-threatening Ventricular arrhythmia, malaria
- Quinidine gluconate (IV or PO) and Quinidine Sulfate (PO/Tab only)
-
SEs:
- QT prolongation → torsades, AV block
- tremor, nervousness, photosensitivity
Black Box Warning: increased mortality in tx of non-life threatening arrhythmias; increase risk of structural heart disease
- DDI: lots of DDIs, will interact with drugs causing bradycardia or QT prolongation
Disopyramide (Norpace)
Class 1a antiarrhythmic→ Na+ channel blockade, prolong repolarization
-
Indications: 1. Ventricular arrhythmias
- 2.A.fib conversion or prevention
-
SEs:
- Torsades, CHF,
- Agranulocytosis → just like procainamide
- Hypokalemia
Black Box Warning: increased mortality
- DDI: hypoglycemia, anticholinergic effects, 3A4 substrate
Phenytoin
Class 1b antiarrhythmic → Na+ channel blockade, faster repolarization
-
Indications: atrial and ventricular tachhycysrhtymias caused by digitalis toxicity or long QT syndrome
- also seizure disorders
-
SEs:
- bradycardia, pancytopenia, hepatotoxicity, SJS
Lidocaine
Class 1b antiarrhythmic → Na+ channel blockade, faster repolarization
-
Indications: used for ventricular arrhythmias only
- → raises the ventricular fibrillation threshold
-
SEs:
- twitching, convulsions, confusion, Respiratory arrest/depression
-
Contraindications:
- hypersensitivity
- Heart block
- Stokes-Adams Syndrome (fainting spell d/t arrhythmias)
- Wolff-Parkinson-White → tachycardia
Flecainide (Tambocor)
Class 1c antiarrhythmics→ sodium channel blockade, no change in repolarization
-
Indications: used for SEVERE ventricular dysrhythmias
- can be used in afib, a.flutter, Wolff-Parkinson White, & SVT
- analogue of Procainamide
- Negative inotropic effects and depresses left ventricular function
-
SEs:
- QT prolongation, CHF, dyspnea etc
-
Contraindications:
- hypersensitivity, cardiogenic shock
- second or 3rd degree AV block
- dysrhythmias
Beta-Blockers as Antiarrhythmics
reduce or block sympathetic NS stimulation → reducing transmission of impulses in the heart’s conduction system
affect Rate and Rhythm
-
Indication: myocardial depressant for both supraventricular dysrhythmias and ventricular dysrhythmias
- antianginal
- antihypertensive
- Drugs: esmolol, metoprolol, propranolol
Amiodarone
Class III antiarrhythmic → K+ channel blockers, increase action potential duration
- MOA: blocks both the alpha and beta adrenergic receptors
-
indications: sustain V.tach, V.fib
- drug of choice for V. dysrhythmias according to ACLS
-
SEs:
- corneal deposits → visual halps
- photophobia, and dry eyes
- phototoxicity (uv light)
- pulmonary toxicity → pulmonary fibrosis
-
DDI:
- digoxin & warfarin (may have a delayed reaction)
-
Contraindication:
- hypersensitivity, severe sinus brady, Heart Block
Diltiazem & Verapamil as Antiarrhythmics
- Class IV antiarrhythmics→ depress phase 4 of depolarization → affect RATE & rhythm
-
indications:
- paroxysmal supraventricular tachycardia
- rate control for atrial fib and flutter
-
Contraindications:
- Acute MI
- Pulmonary congestion
- Wolff-Parkinson white
- Severe Hypotension, cardiogenic shock
- sick sinus syndrome
- Heart Block
General Antiarrhythmic SEs
- All antidysrhythmic can cause dysrhythmias
- hypersensitivity rxns
- N/V/D
- dizziness
- headache & blurred vision
- prolongation of the QT interval
-
DDI:
- warfarin (Coumadin): monitor INR
- Grapefruit Juice:
- amiodarone (III), disopyramide (1a), and quinidine (1a)
CHA2DS2-VASc
- Congestive HF/LV dysfunction +1
- Hypertension +1
- Age 65-74 +1
- Diabetes Mellitus +1
- Stroke/TIA +2
- Vascular disease ( previous MI, PAD, aortic plaque): +1
- Age ≥ 75 +2
- Sex category (female): +1
- +Recommendations:
- ≥ 2 for men = anticoag
- ≥ 3 for women = anticoag
General Anticoagulants
inhibit the clotting cascade, decrease fibrin formation
- Vitamin K antagonists
- Direct Thrombin Inhibitors
- Factor Xa inhibitors
When are Dabigatran (Direct thrombin inhibitor), Rivaroxaban (inhibit factor Xa), apixaban (inhibit factor Xa), or edoxaban (inhibit factor xa) preferred over warfarin?
for nonvalvular & non-cancer patients
When is low molecular weight heparin preferred over vitamin K antagonists, dabigatran, rivaroxaban, apixaban, or edoxaban?
for pts with cancer-associated thrombosis
When is aspirin recommended to prevent recurrent venous thromboembolism (VTE)?
for pts who stop anticoagulation therapy and do not have a contraindication to aspirin
Thrombolytic Therapy and pulmonary embolism
- generally not recommended in pts with acute PE
- it is preferred in selected patients with acute PE who have no hypotension and a low bleeding risk (grade 2c)
Warfarin (Coumadin): MOA, metabolism, & monitoring
vitamin K antagonist → affects factor II, VII, IX, X, and protein C & S → takes 48-72 hours for this med to take effect
- R & S enantiomers primarily metabolized by CYP2C9
- Excretion: primarily renal
-
Monitoring therapy:
- narrow therapeutic window → use INR (monitors PT- prothrombin time)
Warfarin (Coumadin) Dosing
Recommended patient admin time is every evening
*
Warfarin and Disease State Interactions
What common food group can increase vitamin K and affect Warfarin?
Green leafy vegetables
→ counsel patients on the importance of a CONSISTENT diet
Warfarin SEs
BLEEDING→ nosebleed, gum bleed, unexplained brusing, etc
- warfarin-induced skin necrosis
- Purple-toe syndrome
- Teratogen (pregnancy category X)
Dabigatran (Pradaxa)
- MOA: direct thrombin inhibitor (Prodrug)
- NOT recommended in severe ESRD or those on hemodialysis
- Do not require drug level monitoring but EXPENSIVE!
-
SEs:
- GI sxs
- bleeding
- GI sxs
- Monitoring: renal funx prior to initiation & at least annually
-
Important Pt info:
-
do NOT open, chew, or break the capsule
- ***store in the original package to protect from moisture***
-
do NOT open, chew, or break the capsule
- better than warfarin for stroke or systemic embolism prevention
- AVOID in pts with Mechanical Heart Valves
Rivaroxaban (Xarelto)
- MOA: inhibits Factor Xa
- metabolism: by the liver
- monitoring: renal funx prior to initiation & at least annually
- Not better than warfarin for stroke or systemic embolism prevention
- AVOID in pts with Prosthetic Heart Valves
Apixaban (Eliquis)
- MOA: factor Xa inhibitor
- metabolism: liver
- monitoring: Renal funx prior to initiation & at least annually
- Better than warfarin for stroke or systemic embolism prevention
- CAN be used in ESRD patients on hemodialysis
- CYP3A4 substrate → monitor for DDIs
AVOID in pts with Prosthetic Heart Valves
Edoxaban (Savaysa)
- MOA: factor Xa inhibitor
-
Dosing: CrCl 50 - 95 mL/min
- Pts with CrCl > 95 mL/min: AVOID use – drug level too low
- AVOID in pts with Prosthetic Heart Valves
Black box warning for all NOAC agents
Dabigatran, Rivaroxaban, apixaban, edoxaban, betrixaban
Premature d/c increases risk of thrombosis; spinal/epidural hematomas
What is the reversal agent for Dabigatran (Pradaxa) overdose?
- Activated charcoal if used within 1-2 hours of ingestion
- dialysis: removes 62% at 2 hours; 68% at 4 hours
-
idarucizumab (Praxbind) -
- humanized monoclonal antibody fragment
What is the reversal agent for factor Xa inhibitors
Andexanet alfa (Andexanet)/(Andexxa)
reverses both Rivaroxaban & Apixaban
during life threatening or uncontrolled bleeding
What is the reversal agent for warfarin?
Vitamin K
Andexxa Dosing (general), SEs, and Black box warning
- Dose based on rivaroxaban or apixaban dose
-
SEs:
- infusion related rxns
- thromboembolic events
- bleeding
- cardiogenic shock, sudden death, CHF, acute respiratory failure
- Black Box Warning: Arterial & Venous thromboembolic events; ischemic events including MI and stroke; Cardiac Arrest; sudden death
Heparin vs LMWH
Fibrin Specific Thrombolytics
decrease systemic activation of plasminogen → prevent degradation of circulating fibrinogen
- do not have significant lytic action when exposed to fibrinogen with plasminogen
- tissue plasminogen activator (t-PA) = Alteplase (recombinant t-PA)
- Reteplase (Retevase)
- Tenecteplase (TNKase)
Non-Fibrin Specific Thrombolytics
cause both fibrinolysis and fibrinogenolysis
Streptokinase
urokinase
Alteplase (Activase)
Fibrin specific thrombolytics
-
indications;
- acute MI, acute ischemic stroke, Acute PE
-
SEs:
- Bleeding (severe), thromboembolism, cholesterol embolism, hypersensitivity rxn
Reteplase (Retavase)
2nd gen recombinant t-PA from E.coli
- does not bind to fibrin as tightly as t-PA
- penetrates clots better
- dissolve clots faster
- indications: STEMI
-
Contraindications:
- active bleeding
- recent stroke
- intracranial/spinal surgery within 3 months
- severe uncontrolled HTN
-
SEs:
- bleeding, hypersensitivity (less than t-PA), cholesterol embolism
Tenecteplase (TNKase)
fibrin specific thrombolytics
- recombinant with modification of alteplase (from hamster ovary cells)
- indication: Acute MI
-
SEs:
- bleeding, choelsterol embolism, arrhythmias (brady or tachy) → antiarrhythmic tx be ready during TNKase tx
- Anaphylaxis
-
Contraindications:
- active internal bleeding
- hx of cerebrovascular accident
- intracranial/spinal surgery or trauma within 2 months
- severe uncontrolled HTN
