antiarrhythmics clinical cases

Question 1

Atrial fibrillation clinical consequences and treatment

Answer 1

Clinical consequences: ventricular response rates may be rapid and lead to symptoms, hypotension, or heart failure

Rapid atrial activation results in absence of organized atrial contraction- blood stasis in atrium (thrombus) in left atrial appendage with risk of embolization and stroke

Treatment: anticoagulation (acute -cardioversion, chronic- CHADSVasc score)

Rate control: AV nodal blockade (beta blocker, CCB, digoxin)
Restoration sinus rhythm: cardioversion then 3 weeks of anticoagulation or TEE, Antiarrhythmics, catheter ablation

Question 2

Stroke in Atrial fibrillation

Answer 2

5x increase risk of stroke,
Anticoagulation therapy
Left atrial thrombus in AF 90% localized to left atrial appendage
Blood stasis from rapid electrical activation of atrium (loss of atrial contractility–> thrombi w/ larger fibrin than platelet (anticoagulation over antiplatelet drugs for stroke risk reduction in atrial fibrillation)

Question 3

AF: oral anticoagulants

Answer 3

Warfarin- inhibits hepatic vit K epoxide to recycle vit k –> decreased carboxylation of vitk clotting factors (279 10), metabolism CYP2C9, reduced stroke risk by 61%, monitor INR, REversal via Vit k FFP

Dabigatran- prodrug, direct thrombin inhibitor, renal elimination of Pgp, reversal via Idarucizumab

Rivaroxaban- Xa inhibitor (prevents thrombin activation), elimination 3a4 (1/3rd unchanged, reversal via Adexanet alfa

Apixaban: Xa inhibitor, sape as rivaroxaban

Question 4

Direct oral anticoagulants vs Warfarin

Answer 4

DOACs shorter t.5 than warfarin, contraindicated in valvular atrial fibrillation (moderate to severe mitral stenosis or mechanical artificial heart plus atrial fibrillation)

Question 5

Triggered Activity

Answer 5

Early Afterdepolarizations (EADs): Membrane oscillations which occur within the AP either in plateau (phase2) or During repolarization (phase 3), Promoted by conditions which prolong the AP (QT prolongation), related to inward Ca current in phase2 or reactivation of fast Na current in phase 3, clinical mechanism of TdP VT, precipitated by Qt prolonging drugs

Question 6

Reentry

Answer 6

Most common cause of SVT in young adults

reentry–>abnormal endless loop myocardial propagation, not cellular in nature, but many myocytes working in sequence

Normal propagation is constrained to a single activation of each myocyte due to a wall of refractory tissue preventing the wavefront from looping back on itself

REQUIREMENTS: 2 distinct paths, Slowed conduction in one path, unidirectional block (tissue capable of conduction in one but not the opposite directional)

Question 7

svt: av nodal reentrant tachycardia

Answer 7

Most common cause SVT, Reentry utilizing 2 AV nodal paths, a fast (rapid conduction and long refractory period) and Slow (slow conduction and short refractory period)

RElies on transient unidirectional block in one pathway due to long refractory period and relatively slow conduction in the other

Typically antegrade from A to V occus over slow and retrograde limg of reentrant over fast pathway

Question 8

SVT: Atrioventricular Reentrant Tachy cardias

Answer 8

reentry utilizing an accessory pathway (an abnormal band) connects the A and the V

can be antegrade or retrograde

If tract is only retrograde can promote SVT tachycardia (CONCEALED)

If tract conducts antegrade produces WPW syndrome, preexcitation

Question 9

WPW syndrome

Answer 9

Delta wave, conduction over AP beats AVN, short PR
Slurred QRS
No delta wave in orthodromic tachycardia

Question 10

Monomorphic vs Polymorphic VT

Answer 10

Monomorphic: QRS identical, reentry due to slowed conduction thru surviving myocardial cells within areas of myocardial scar

Polymorphic: QRS changes–> could cause TdP