S2: Ch1 Cv 2-0

Front 1

275. What should you do if Vfib persists after first 3 shocks?

Back 1

a. Continue CPR
b. Intubation may be indicated.
c. Epi 1 mg bolus initially, and then every 3-5 minutes. This increases myocardial and cerebral blood flow and decreases the defibrillation threshold.
d. Attempt to defibrillate again 30 to 60 seconds after the first epi dose.

Front 2

275. What should you do if Vfib persists after first 3 shocks?

Back 2

a. Continue CPR
b. Intubation may be indicated.
c. Epi 1 mg bolus initially, and then every 3-5 minutes. This increases myocardial and cerebral blood flow and decreases the defibrillation threshold.
d. Attempt to defibrillate again 30 to 60 seconds after the first epi dose.

Front 3

276. Other options if the above procedures fail (refractory Vfib)?

Back 3

a. IV amiodarone followed by a shock- New ACLS guidelines recommend the use of amiodarone over other antiarrhythmic agents in refractory Vfib.
b. Lidocaine, bretylium and procainamide are alternative second-line txs.
c. Sodium bicarb is no longer recommended.

Front 4

276. Other options if the above procedures fail (refractory Vfib)?

Back 4

a. IV amiodarone followed by a shock- New ACLS guidelines recommend the use of amiodarone over other antiarrhythmic agents in refractory Vfib.
b. Lidocaine, bretylium and procainamide are alternative second-line txs.
c. Sodium bicarb is no longer recommended.

Front 5

277. What should you then do if cardioversion is successful for Vfib?

Back 5

a. Maintain continuous IV infusion of the effective antiarrhythmic agent.
b. IV amiodarone has been shown to be the most effective.
c. Implantable defibrillators have become the mainstay of chronic therapy in pts at continued risk for VFF. Long-term amiodarone therapy is an alternative.

Front 6

277. What should you then do if cardioversion is successful for Vfib?

Back 6

a. Maintain continuous IV infusion of the effective antiarrhythmic agent.
b. IV amiodarone has been shown to be the most effective.
c. Implantable defibrillators have become the mainstay of chronic therapy in pts at continued risk for VFF. Long-term amiodarone therapy is an alternative.

Front 7

278. Why is the presence of ventricular irritability (frequent PVCs, VT) especially worrisome in pts w/underlying heart disease and left ventricular dysfunction?

Back 7

a. These pts are at high risk for sudden cardiac death.

Front 8

278. Why is the presence of ventricular irritability (frequent PVCs, VT) especially worrisome in pts w/underlying heart disease and left ventricular dysfunction?

Back 8

a. These pts are at high risk for sudden cardiac death.

Front 9

279. What should you always suspect in a pt w/wide QRS (>0.12s)?

Back 9

a. VT.

Front 10

279. What should you always suspect in a pt w/wide QRS (>0.12s)?

Back 10

a. VT.

Front 11

280. What is wide complex tach in adults w/a hx of structural heart disease much more likely to be due to?

Back 11

a. VT than SVT w/aberrancy.
b. It is important to distinguish monomorphic VT from SVT w/aberrant conduction.

Front 12

280. What is wide complex tach in adults w/a hx of structural heart disease much more likely to be due to?

Back 12

a. VT than SVT w/aberrancy.
b. It is important to distinguish monomorphic VT from SVT w/aberrant conduction.

Front 13

281. Cardiac arrest vs. sudden cardiac death?

Back 13

a. Cardiac arrest is sudden loss of cardiac output; potentially reversible if circulation and oxygen delivery are promptly restored.
b. Sudden cardiac death is unexpected death w/in 1 hr of sx onset secondary to a cardiac cause.

Front 14

282. Where do narrow complex tachycardias originate?

Back 14

a. Above ventricles.

Front 15

281. Cardiac arrest vs. sudden cardiac death?

Back 15

a. Cardiac arrest is sudden loss of cardiac output; potentially reversible if circulation and oxygen delivery are promptly restored.
b. Sudden cardiac death is unexpected death w/in 1 hr of sx onset secondary to a cardiac cause.

Front 16

283. Where do wide complex tachs originate?

Back 16

a. W/in ventricles and are more ominous bc they are more likely to progress to Vfib.

Front 17

282. Where do narrow complex tachycardias originate?

Back 17

a. Above ventricles.

Front 18

284. Can drugs convert Vfib by themselves?

Back 18

a. No, defibrillation is key.

Front 19

283. Where do wide complex tachs originate?

Back 19

a. W/in ventricles and are more ominous bc they are more likely to progress to Vfib.

Front 20

284. Can drugs convert Vfib by themselves?

Back 20

a. No, defibrillation is key.

Front 21

285. Does defibrillation work for asystole?

Back 21

a. No, it generally does not work for asystole.
b. Try transcutaneous pacing instead.

Front 22

286. Pulseless Electrical Activity (PEA)?

Back 22

a. Occurs when electrical activity is on the monitor but there are no pulses (even w/Doppler), and carries a grim prognosis.
b. Tx possible causes: Hypoxia, hypovolemia, hypotension, hyperkalemia, tamponade, tension pneumothorax, Massive PE, and so on.

Front 23

287. Sinus Bradycardia?

Back 23

a. < 60 BPM: Clinically significant when rate is persistently < 45 bpm.
b. Causes include ischaemia, increased vagal tone, antiarrythmics drugs. Normal findings in trained athletes.
c. Can be asymptomatic; pts may complain of fatigue, inability to exercise, angina, or syncope.

Front 24

288. Tx of Sinus Bradycardia?

Back 24

a. Atropine can elevate the sinus rate by blocking vagal stimulation to the SA node.
b. A cardiac pacemaker may be required if bradycardia persists.

Front 25

289. Sick Sinus Syndrome?

Back 25

a. Sinus node dysfunction characterized by spontaneous sinus bradycardia.
b. Sx:
1. Dizziness
2. Confusion
3. Syncope
4. Fatigue
5. CHF.

Front 26

290. Tx of Sick Sinus Syndrome?

Back 26

a. Pacemaker implantation may be required.

Front 27

291. First-degree AV block?

Back 27

1. PR interval is prolonged (>0.20s)
2. A QRS complex follows each P wave.
3. Delay is usually in the AV node.
4. Benign condition that does not require tx.

Front 28

292. Second-degree AV block: Mobitz type I (Wenckebach)?

Back 28

a. Characterized by progressive prolongation of PR interval until a P wave fails to conduct.
b. Benign condition that usually does not require tx.

Front 29

293. Where is the block usually located w/ Second-degree AV block: Mobitz type I (Wenckebach)?

Back 29

a. Site of block is usually w/in the AV node.

Front 30

294. Mobitz II heart block?

Back 30

a. P wave fails to conduct suddenly, w/o a preceding PR interval prolongation; therefore, the QRS drops suddenly.
b. Often progresses to complete heart block.