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Block 3 > MMT: treating arrhythmia > Flashcards

MMT: treating arrhythmia Flashcards

1
Q

What are sinus arrhythmias?

A

Arrhythmia originating in the SA node; all the elements of the EKG are present, just at an altered rate.

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2
Q

What is a major way to alter sinus arrhythmia?

A

Modifying phase 4 via decreasing its slope, modifying threshold potential, increasing maximum diastolic potential, or increasing AP duration/prolonging the refractory period.

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3
Q

Decreasing camp will…

A

Flatten phase 4 and slow HR.

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4
Q

How can we increase maximum diastolic potential? What is the significance of this?

A

Making the membrane potential more negative; this means the cell has further to go to reach AP. This can be done via PSNS.

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5
Q

What do we do to treat sinus bradycardia?

A

Correct the precipitating event or atropine.

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6
Q

What do we do to treat sinus tachycardia?

A

Correct precipitating event or beta blockers.

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7
Q

What does a premature ventricular contraction look like on EKG?

A

Wide QRS with no preceding p wave.

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8
Q

How do we treat PVC?

A

Generally, we don’t. Can reduce the stimulus such as caffeine, stress, sympathomimetic drugs.

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9
Q

Where do atrial arrhythmias originate?

A

Above the bundle of His.

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10
Q

Give examples of supraventricular arrhythmias.

A

Afib, atrial flutter, AVNRT, AP mediated reentrant tachycardia.

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11
Q

Describe afib.

A

Typically caused by reentry and appears as irregular firing on EKG. They can be a result of structural heart diseases such as HTN, MI, ischemia, etc.

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12
Q

How does hypertension lead to afib?

A

Hypertension causes left ventricular hypertrophy, resulting in increased LA pressure. This increased pressure can cause increased LA stretch, causing afib.

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13
Q

Afib causes a loss of what?

A

Atrial kick, leading to a small loss of CO. Can also show a loss of p waves on EKG.

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14
Q

What is a significant consequence of afib?

A

Risk of stroke. The atrial stasis makes thromboembolism a major concern, often leading them to take aspirin.

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15
Q

what kind of drugs do we use for rate control in afib?

A

drugs that can control rate in the ventricles by slowing conduction from the AV node. these are typically beta blockers or CCB

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16
Q

what do do for acute rhythm control in afib?

A

drugs to restore sinus rhythm in the SA node (cardioversion). this is typically DC cardioversion, but drugs like ibutilide, dofetilde, and amiodarone can be used.

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17
Q

What drug should we not use for rate control in afib?

A

Digoxin.

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18
Q

What is the recent data regarding rhythm vs rate control in afib?

A

Early rhythm control has a lower risk of adverse cardiovascular events.

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19
Q

What is necessary before cardioversion?

A

Assessment for clot risk.

20
Q

Between DC cardioversion and pharmacologic cardioversion, which is preferred?

A

DC cardioversion.

21
Q

What are drug options for
pharmacologic cardioversion?

A

Ibutilide, dofetilide, amiodarone.

22
Q

What drugs are used for chronic maintenance of sinus rhythm in patients with afib?

A

Amiodarone, sotalol, and flecainide (avoid in pts with SHD).

23
Q

a patient with long-tern afib cannot get control of it with drugs. what is another option?

A

catheter ablation or AV node ablation

24
Q

Describe AVNRT.

A

Normally, there is a fast and a slow channel in the AV node. A premature impulse can block the fast pathway, and the impulse will go to the slow pathway. The slow pathway can send the impulse to both the bundle of His as well as back to the fast pathway. This results in a loop in the AV node between fast and slow channels. The SA node loses control, and the AV node gains control.

25
Q

How do we treat AVNRT?

A

It can be managed by Valsalva maneuver or carotid massage to stimulate PSNS to help the SA node regain control. If this doesn’t work, use adenosine.

26
Q

What are the drugs of choice for chronic treatment of AVNRT?

A

Verapamil, beta blockers, or diltiazem.

27
Q

What is AVRT?

A

A reentrant loop across an accessory pathway that allows the impulse to bypass the AV node. This creates a pre-excitation delta wave in the QRS.

28
Q

What is a common example of AVRT?

A

WPW.

29
Q

What is orthodromic AVRT?

A

Impulse from a rogue myocyte (not SA node) travels through AV node and the accessory pathway.

30
Q

How do we treat AVRT?

A

Ablation of the accessory pathway

31
Q

If you want to treat AVRT with drugs, what can you use?

A

Adenosine, verapamil, beta blockers, class 1A or 1C.

32
Q

In what instance do we not want to block the AV node?

A

WPW and afib; gives the accessory pathway a chance to go wild.

33
Q

how do we treat Afib + WPW

A

procainamide and ablation of the accessory pathway

34
Q

how do we treat 2nd and 3rd AV block

A

pacemaker

35
Q

A patient is hemodynamically unstable and has AV block. What drug can we use?

A

Atropine

36
Q

What is monomorphic V tach?

A

Reentrant loop in the ventricles that causes the ventricle to depolarize independent of the typical electrical system. Results in wide QRS.

37
Q

How do we treat vtach?

A

Direct current cardioversion. Drug options are amiodarone, lidocaine, procainamide in that order.

38
Q

What is used for recurrent vtach?

A

An ICD device, and sometimes amiodarone or sotalol. these drugs can decrease VT or VF

39
Q

how do we treat someone at risk for vtach

A

beta blockers or amiodarone

40
Q

what is thought to be associated with torsades

A

early after depolarizations caused by prolonged QT, hypokalemia, hypomagnesemia, cell damage

41
Q

What is the treatment for torsades de pointes?

A

Magnesium.

42
Q

How do we treat vfib?

A

Defibrillator!!

43
Q

After defibrillation, what drugs can we add for vfib?

A

Amiodarone, lidocaine, procainamide.

44
Q

We use ___ for vtach and ___ for vfib.

A

Cardioversion; defibrillator.

45
Q

What drug can be used in asystole?

A

Epi and atropine.

Block 3 (29 decks)

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