S2: Ch1 Cv 1-7

Front 1

188. How common are PACs?

Back 1

a. PACs are found in >50% of normal adults who undergo Holter monitoring and are of no significance in a normal heart, but may be a precursor of ischaemia in a diseased heart.

Front 2

189. Significance of PACs?

Back 2

a. May cause palpitations or give rise to PSVTs.

Front 3

190. Sx of PACs?

Back 3

a. Usually asymptomatic and do not require tx.
b. Monitor for increased frequency.
c. If symptomatic (e.g., palpitations), β-blockers may be helpful.

Front 4

191. Systolic vs. diastolic dysfunction CHF- ejection fraction?

Back 4

a. EF < 45%
b. EF >45%

Front 5

192. Premature ventricular complexes (PVCs)?

Back 5

a. This early bear fires on its own from a focus in the ventricle and then spreads to the other ventricle.

Front 6

193. Causes of PVCs?

Back 6

a. Hypoxia
b. Electrolyte abnormalities
c. Stimulants
d. Caffeine
e. Meds

Front 7

194. How is the QRS affected by PVCs?

Back 7

a. Wide QRS. Bc conduction is not through normal conduction pathways, but rather through ventricular muscle, it is slower than normal, causing a wide QRS.
b. Wide, bizarre QRS complexes followed by a compensatory pause are seen; a P wave is not usually seen because it is “buried” w/in the wide QRS complex.

Front 8

195. How common are PVCs?

Back 8

a. Appear in > 50% of men who undergo Holter monitoring.
b. Most pts are asymptomatic.

Front 9

196. Tx of PVCs if symptomatic?

Back 9

a. β-blockers may be used.

Front 10

197. What are pts w/frequent repetitive PVCs and underlying heart disease at increased risk for?

Back 10

a. Sudden cardiac death due to cardiac arrhythmias (especially Vfib).
b. Order an electrophysiologic study bc pts may benefit from implantable cardioverter defibrillator (ICD).

Front 11

198. What did the cardiac arrhythmia suppression trial CAST I and CAST II show regarding the use of antiarrhythmic drugs to suppress PVCs after MI?

Back 11

a. Increases the risk of death.

Front 12

199. Couplet?

Back 12

a. 2 successive PVCs.

Front 13

200. Bigeminy?

Back 13

a. Sinus beat followed by PVC

Front 14

201. Trigeminy?

Back 14

a. Sinus beat followed by 2 PVCs.

Front 15

202. What do pts w/underlying heart disease have an especially high risk of?

Back 15

a. Embolization and hemodynamic compromise.

Front 16

203. General characteristics of AFib?

Back 16

a. Multiple foci in the atria fire continuously in a chaotic pattern, causing a totally irregular, rapid ventricular rate. Instead of intermittently contracting, the atria quiver continuously.
b. Atrial rate is over 400 bpm, but most impulses are blocked at the AV node so ventricular rate ranges between 75-175.

Front 17

204. What are pts w/Afib and underlying heart disease at a markedly increased risk for?

Back 17

a. Adverse events, such as thromboembolism and hemodynamic compromise.

Front 18

205. 9 Causes of Afib?

Back 18

1. Heart Disease: CAD, MI, HTN, Mitral Valve disease.
2. Pericarditis and pericardial trauma (e.g., surgery)
3. Pulmonary disease, including PE
4. Hyperthyroidism/hypothyroidism.
5. Systemic illness (e.g., sepsis, malignancy, DM)
6. Stress (e.g., postoperative)
7. Excessive alcohol intake (“holiday heart syndrome”)
8. Sick Sinus Syndrome
9. Pheochromocytoma

Front 19

206. Clinical features of Afib?

Back 19

a. Fatigue and exertional dyspnea
b. Palpitations, dizziness, angina, or syncope may be seen.
c. An irregularly irregular pulse
d. Blood stasis (secondary to ineffective contraction) leads to formation of intramural thrombi, which can embolize to the brain.

Front 20

207. Diagnosis of Afib?

Back 20

a. ECG findings: Irregularly irregular rhythm (irregular RR intervals and excessively rapid series of tiny, erratic spikes on ECG w/a wavy baseline and no identifiable P waves).

Front 21

208. Tx of Acute Afib in a hemodynamically UNSTABLE pt?

Back 21

a. Immediate electrical cardioversion to sinus rhythm.

Front 22

209. Tx of Acute Afib in a hemodynamically Stable pt?

Back 22

a. Rate control
b. Cardioversion to sinus rhythm (after rate control is achieved)
c. Anticoagulation to prevent embolic CVA.

Front 23

210. How is rate control elicited in AFib?

Back 23

a. Determine pulse in a pt w/Afib. If it is too rapid, it must be treated- Target rate is 60-100 bpm.
b. Ca-channel blockers are preferred. β-blockers are an alternative.
c. If left ventricular systolic dysfunction is present, consider digoxin or amiodarone.

Front 24

211. Cardioversion for Afib?

Back 24

a. Electrical cardioversion is preferred to pharm.
b. Use pharmacologic cardioversion only if electrical fails or is not feasible.

Front 25

212. What drugs are used for pharm cardioversion of Afib?

Back 25

a. Paternal ibutilide
b. Procainamide
c. Flecainide
d. Sotalol
e. Amiodarone.

Front 26

213. Anticoag to prevent CVA in Afib?

Back 26

a. If Afib present > 48 hours (or unknown period of time), risk of embolization during cardioversion is significant (2-5%).
b. Anticoagulate pts for 3 wks before and 4 wks after cardioversion.
c. To avoid waiting 3 wks for anticoagulation, obtain a transesophageal echo (TEE) to image the L. atrium.
i. If no thrombus is present, start IV heparin and perform cardioversion w/in 24 hrs.
ii. Pts still require 4 wks of anticoag after cardioversion.

Front 27

214. INR goal range for pt w/Afib?

Back 27

a. 2-3

Front 28

215. Chronic Afib tx?

Back 28

a. Rate control w/β-blocker or calcium channel blocler.
b. Anticoag: Pts w/ “lone Afib (I.e., Afib in the absence of underlying heart disease or other cardiovascular risk factors) under age 60 do not require anticoagulation bc they are at low risk for embolization (aspirin may be appropriate)
c. Tx all other pts w/chronic anticoag (warfarin).

Front 29

216. Cardioversion?

Back 29

a. Delivery of a shock that is in synchrony w/the QRS complex: Purpose is to terminate certain dysrhythmias such as PSVT or VT.
b. An electric shock during T wave can cause Vfib, so the shock is timed not to hit the T wave.

Front 30

217. 4 Indications for Cardioversion?

Back 30

1. Afib
2. Atrial flutter
3. VT w/pulse
4. SVT