S2: Ch1 Cv 1-9

Front 1

245. Wolf-Parkinson-White Syndrome General characteristics?

Back 1

a. An accessory conduction pw from atria to ventricles causes premature ventricular excitation bc it lacks the delay seen in the AV node.
b. May lead to a paroxysmal tachycardia, which can be produced by 2 possible mechanisms:
1. Orthodromic reciprocating tachycardia
2. Supraventricular tachycardia (Afib or atrial flutter).

Front 2

246. Orthodromic reciprocating tachycardia (Wolf-Parkinson-White syndrome)?

Back 2

a. The impulse travels through the AV node (anterograde limb) and depolarizes the ventricles. Then it travels back through the accessory pathway (the retrograde limb) and redepolarizes the atria, creating a reentry loop.
b. No delta waves because conduction occurs retrograde over the accessory pathway.

Front 3

247. Supraventricular tachycardias (Afib or atrial flutter) (Wolf-Parkinson-White syndrome)?

Back 3

a. Usually, AV node only allows certain impulses to get to ventricles.
b. With an accessory pathway, all or most of the impulses may pass to the ventricles.
c. A fast ventricular rate may occur and cause hemodynamic compromise.

Front 4

248. Diagnosis of Wolf-Parkinson-White syndrome?

Back 4

a. ECG: Narrow complex tachycardia, a short P-R interval, and a delta wave (upward deflection seen before the QRS complex)

Front 5

249. Tx for WPW?

Back 5

a. Radiofrequency catheter ablation of one arm of the reentrant loop (i.e., of the accessory pathway) is an effective tx.
b. Avoid drugs active on the AV node (e.g. digoxin) because they may accelerate conduction through the accessory pathway:
c. Type IA or IC antiarrhythmics are better choices.

Front 6

250. Diagnosis of WPW?

Back 6

a. ECG: Narrow complex tachy
b. Short P-R interval
c. Delta wave (upward deflection seen before the QRS complex.

Front 7

251. General characteristics of Ventricular Tachycardia?

Back 7

a. Defined as rapid and repetitive firing of 3 or more PVCs in a row, at a rate of between 100-250 bpm.
b. AV disassociation is present (i.e., sinus P wave continue w/their cycle, unaffected by the tachycardia.
c. Originates below the Bundle of His.

Front 8

252. Causes of Ventricular Tachycardia?

Back 8

a. CAD w/prior MI is most common cause.
b. Active ischaemia, hypotension
c. Cardiomyopathies
d. Congenital defects
e. Prolonged QT syndrome
f. Drug toxicity.

Front 9

253. Sustained vs. nonsustained VT in Ventricular Tachycardia- Sustained?

Back 9

a. Sustained VT:
1. Lasts longer than 30 seconds and is almost always symptomatic!!!
2. Often associated w/marked hemodynamic compromise (i.e., hypotension) and/or development of myocardial ischaemia.
3. A life-threatening arrhythmia.
4. Can progress to Vfib if untreated.

Front 10

254. Nonsustained VT in ventricular tachycardia?

Back 10

a. Brief, self-limited runs of VT.
b. Usually, asymptomatic.
c. When CAD and LV dysfunction are present, it is independent risk factor for sudden death.
d. Therefore, pts w/nonsustained VT should be thoroughly evaluated for underlying heart disease and LV dysfunction.

Front 11

255. Prognosis for Ventricular tachycardia?

Back 11

a. Depends on the presence of heart disease and on whether VT is sustained or nonsustained.
b. VT after an MI usually has poor prognosis, especially if it is sustained.
c. In pts w/no underlying heart condition, the prognosis is good.

Front 12

256. Clinical features of VT?

Back 12

1. Palpitations
2. Dyspnea
3. Light-headedness
4. Angina
5. Impaired consciousness (syncope or near-syncope).
b. May present w/sudden cardiac death.
c. Signs of cardiogenic shock may be present.
d. May be asymptomatic if rate is slow.

Front 13

257. Physical findings w/VT?

Back 13

a. Cannon a waves in the neck (secondary to AV dissociation which results in atrial contraction during ventricular contraction) and an S1 that varies in intensity.

Front 14

258. Diagnosis of VT?

Back 14

a. ECG: Wide and Bizarre complexes
b. QRS complexes may be monomorphic or polymorphic.
i. In monomorphic VT, all QRS complexes are identical.
ii. In polymorphic VT, the QRS complexes are different.
c. Unlike PSVT, VT does not respond to vagal maneuvers or adenosine.

Front 15

259. Tx of VT in general?

Back 15

a. Identify and treat reversible causes.

Front 16

260. Tx of sustained VT?

Back 16

a. Hemodynamically stable pts w/mild sx and systolic BP > 90: pharmacotherapy.
i. New ACLS guidelines recommend IV amiodarone, IV procainamide, or IV sotalol over IV lidocaine or IV Bretylium.
b. Hemodynamically unstable pts or pts w/severe sx:
i. Immediated synchronous DC cardioversion.
ii. Follow w/iV amiodarone to maintain sinus rhythm.
c. Ideally, all pts w/sustained VT should undergo placement of an ICD, unless EF is normal (then consider amiodarone).

Front 17

261. Tx of nonsustained VT?

Back 17

a. If no underlying heart disease and asymptomatic, do not treat.
b. These pts are NOT at increased risk of sudden cardiac death.

Front 18

262. What should you do for nonsustained VT if the pt has underlying heart disease, a recent MI, evidence of left ventricular dysfunction, or is symptomatic?

Back 18

a recent MI, evidence of left ventricular dysfunction, or is symptomatic?
a. Order an electrophysiologic study: If it shows inducible, sustained VT, ICD placement is appropriate.

Front 19

263. Pharmacologic therapy for nonsustained VT?

Back 19

a. Second-line tx.
b. However, amiodarone has the best results of all antiarrhythmic agents.

Front 20

264. Side effects of Adenosine?

Back 20

a. HA
b. Flushing
c. Shortness of breath
d. Chest Pressure
e. Nausea

Front 21

265. What 2 conditions cause 75% of episodes of cardiac arrest?

Back 21

a. VT or VFIB.

Front 22

266. Ventricular fibrillation general characteristics?

Back 22

a. Multiple foci in the ventricles fire rapidly, leading to a chaotic quivering of the ventricles and no cardiac output.
b. Most episodes of VFib begin w/VT (except in the setting of acute ischaemia/infarction.

Front 23

267. Likelihood of VFib recurrence when not associated w/acute MI?

Back 23

a. High (up to 30% w/in the first year). These pts require chronic therapy: either prophylactic antiarrhythmic therapy (amiodarone) or implantation of an automatic defibrillator

Front 24

268. Likelihood of VFib recurrence if associated w/acute MI?

Back 24

a. If it develops w/in 48 hours of an acute MI, long-term prognosis is favourable and the recurrence rate is low (2% at 1 yr).
b. Chronic therapy is not required in these pts.

Front 25

269. Most effective tx in a pt w/underlying heart disease who is found to have nonsustained VT?

Back 25

a. Implantable defibrillator.

Front 26

270. Most common cause of VFib?

Back 26

a. Ischaemic heart disease is the most common cause

Front 27

271. Other causes of Vfib?

Back 27

a. Antiarrhythmic drugs, esp those that cause torsades de pointes (prolonged QT intervals).
b. AFib w/a a very rapid ventricular rate in pts w/Wolff-Parkinson-White syndrome.

Front 28

272. Clinical features of Vfib?

Back 28

a. Cannot measure BP; absent heart sounds and pulse.
b. Pt is unconscious.
c. If untreated, lead to eventual sudden cardiac death.

Front 29

273. Dx of Vfib on ECG/

Back 29

a. No trial P waves can be identified
b. No QRS complexes can be identified.
c. In sum, no waves can be identified; there is a very high irregular rhythm.

Front 30

274. Tx of Vfib?

Back 30

a. Immediate defibrillation and CPR are indicated.
b. Initiate unsynchronized DC cardioversion immediately. If the equipment is not ready, start CPR until it is.
c. Give up to 3 sequential shocks to establish another rhythm; assess the rhythm between each.