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Dysrhythmias
Cardiology
Question | Answer |
---|---|
PVC: tx | beta blocker, amiodarone, possibly ablation |
Tachyarrhythmia pathophysiology | narrow complex (QRS <.12) or wide (usu VT); either by abnormal impulse formation (enhanced automaticity) or abnormal impulse propagation (reentry) |
Most common cause of tachyarrhythmia | reentry; >1 pathway |
SVT risk factors | hyperthyroid, HTN, MV dz; VT: prior MI, ischemia, long QT, antiarrhythmics, low Mg |
AVRT/AVNRT tx | nodal blockers |
AV block Pathophysiology: 1st degree: | AV node most common site; SA impulse is delayed thru AV. PR >.20 (long but consistent). All beats conducted to ventricle. |
Wenckebach usually due to: | normal pt w/heightened vagal tone, or drugs (digitalis, CCB, beta blocker) |
2nd degree Mobitz type II is usually due to lesion located: | at bundle of His |
3rd degree AV block is usually due to lesion located: | distal to bundle of His; bilateral BBB |
3rd degree AV block: Sx/Sx: | wide QRS & V-rate <50; wide pulse pressure, cannon venous neck pulses; syncope |
AV block Tx | Mobitz II or 3d degree: need ventricular pacing |
2nd degree AV block Type I (Wenckebach) is characterized by: | progressively lengthening PR interval, until QRS is dropped |
2nd degree AV block Type II (Mobitz) is characterized by: | intermittent dropped QRS with uniform PR interval; atrial > V-rate; often a 2:1 or 3:1 pattern |
3rd degree AV block is characterized by: | complete disassociation between atria and ventricles; no atrial impulses reaching ventricles. If ectopic pacemaker is ventricular, QRS is wide |
Wolff Parkinson White (WPW) is characterized by: | delta wave / slurred upstroke of QRS; wide WRS >0.10; short PR <0.12 |
Abrupt onset of HR 200-250bpm, from atrial or junctional foci; common presentation of WPW or reentry phenomenon = | Paroxysmal SVT |
HR in atrial flutter: | 250-300 bpm; often with AV block causing 2:1 or 3:1 ratio of atrial to V-rate |
Atrial flutter mgmt | Rate control (BB/sotalol, CCB, or digoxin); cardioversion (50-100 J) (use with anticoag if >48h). If chronic: amiodarone, ibutilide/dofetilide, or EPS with ablation |
A-fib with RVR mgmt (if stable): | Rate control (firstline: diltiazem, verapamil; secondline: Lopressor/atenolol, digoxin); consider cardioversion with amiodarone |
A-fib mgmt (if unstable): | Synchronized electrical cardioversion with / without ibutilide. If in AF >48h & stable, do TEE first to look for atrial thrombus |
A-fib mgmt: if atrial thrombus is present: | anticoagulate x4 weeks prior to cardioversion & 4 weeks after |
Rhythm control agents used in A-fib: | Firstline: dronedarone (Maltaq); secondline: amiodarone, propafenone, flecainide, dofetilide |
V-tach is characterized by: | HR 150-250 bpm, originating from ectopic ventricular focus; wide & regular |
V-tach mgmt: | Firstline: amiodarone (2: procainamide; 3: sotalol). Unstable: defibrillate. Stable: sync cardioversion +/- IV lidocaine |
Premature junctional contractions = | ectopic premature beats originating from AV node or junction; retrograde P waves (may be inverted or buried in QRS, or appear after narrow QRS) |
Drugs that prolong QT interval: | TCAs (amitriptyline, desipramine, doxepin, imipramine, nortriptyline); macrolides, FQs, imidazole, antimalarials; Haldol; pentamidine |
Risk for thromboembolic event is greatest when A-fib has been present for: | >48 hours |
In A-fib, anticoagulation (warfarin) reduced stroke risk by: | 50-80% |
In WPW, what is the drug of choice for converting A-fib? | procainamide (2nd: flecainide) |
DO NOT use rhythm control agents (for A-fib) along with: | dabigatran (Pradaxa) |
A-fib: high risk factors = | prior CVA, TIA, systemic VTE |
A-fib: moderate risk factors = | >75 y.o., HTN, HF, LVEF <35%, DM |
A-fib: warfarin is superior to: | Plavix and aspirin |
A-fib: digoxin is indicated in patients with: | HF and reduced LV function |
Treat pulseless V-tach the same as: | V-fib (1st: defib 120-200J; 2nd: epi or vasopressin; 3rd: amiodarone 300mg x1 then maybe 150; 4th: lidocaine) |
V-fib mgmt: | Tx of choice: defib 120-200J -> CPR 5 cycles (30:2) -> repeat defib, etc. |
V-fib medications: | 1st: Epi / vasopressin; 2nd: amiodarone 300mg x1 then maybe 150; 3rd: lidocaine (maybe) 1-1.5mg/kg, then 0.5-0.75mg/kg IV |
SVT mgmt: | 1st: vagal maneuvers, then adenosine (6mg/12mg/12mg = 30mg total); 2nd: diltiazem; 3rd: electrical cardioversion; 4th (outpatient): flecainide |
Flecainide mechanism of action | regulates flow of Na in heart -> prolongation of cardiac cycle -> slows tachy or arrhythmia |
Meds contraindicated in AV block: | CCBs (interfere with SA conduction) |
CHAD2-VASC = | CHF, HTN, Age 65-74, >75), DM, Stroke; vaxcular disease (MI, PVD), female |
Class I antiarrhythmic agent MOA | Na channel blockade. A: procainamide, quinidine. B: lidocaine. C: flecainide, propafenone. |
Class II antiarrhythmic agent MOA | beta blockade. Propranolol, sotalol |
Class III antiarrhythmic agent MOA | Action potential prolongation. Amiodarone, dofetilide (Tikosyn). |
Class IV antiarrhythmic agent MOA | CCB. Verapamil, adenosine |
Order this lab in new-onset A-fib patients | TSH |
In a patient with Graves disease and irregular HR (160-175), what is tx of choice? | Atenolol (beta blocker) |
What is most important med to give to a pt with A-fib? | Anticoagulant agent (eg, warfarin) |
Pt with WPW cannot be given: | adenosine or CCBs |