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CVPR Exam I > Dr. French's Review Sesh > Flashcards

Dr. French's Review Sesh Flashcards

1
Q

What does digoxin do to the cardiac AP in a dangerous overdose?

A

too much Ca++ is retained and this causes PVCs, V-tach, and V-fib

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1
Q

*** DON’T CHOOSE ISOPROTERANOL AS AN ANSWER CHOICE***

A

just fyi!

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2
Q

What can high intracellular Ca++ trigger?

A

late delayed afterpolarizations

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2
Q

Digoxin binds to the same site as ____.

A

K+

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3
Q

What is the most commonly used class III antiarrhythmic drug?

A

amiodarone

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4
Q

The Beta-1 receptor normally mediates _____.

A

the HR and inotropy

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5
Q

The alpha-1 thru AT-1 receptors normally mediate ____.

A

the preload and afterload

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6
Q

How do you treat premature ventricular contractions (PVCs)?

A

usually none- but maybe a beta blocker

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6
Q

*** DON’T CHOOSE NITRIDE AS A CHOICE ON THE EXAM***

A

just sayin!

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7
Q

If K+ goes down in someone’s labs, you could blame the ____ drugs. If K+ goes up, you could attribute it to _____ drug.

A

down = loop diuretics or thiazides b/c they’re K+ wasting up = aldosterone antagonists b/c they’re K+ sparing (ACE inhibitors and ARBs)

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8
Q

What does digoxin do to the cardiac AP in a good, safe dose?

A

the Na/K pump is blocked, so Ca++ doesn’t leave the cell as much via the NCX exchanger and this increases contractivity and inotropy

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10
Q

What does amiodarone do?

A

it blocks K+ repolarization and phase 0 Na+

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10
Q

ACE inhibitors end in ____.

A

-pril

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11
Q

What vasodilator is prescribed? To whom?

A

hydralazine PLUS isosorbide dinitrate (nitrates) in black pts

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11
Q

Name 3 inotropes.

A
  1. dobutamine 2. mirinone 3. digoxin
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13
Q

If the tachyarrhythmia is at or above the AV node, use _____ control drugs.

A

rate

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15
Q

Antiarrythmic drugs can either be ____ or ____.

A

rate control; rhythm control

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17
Q

What is the tx for chronic supraventricular tachycardia (SVT)?

A

slow conduction or catheter ablation

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18
Q

In HF, the heart has INCREASED or DECREASED lusitropy?

A

DECREASED - the heart is stiffer in HF

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19
Q

____ is the drug of choice for acute supraventricular tachycardia.

A

Adenosine

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19
Q

What receptor normally mediates the preload?

A

alpha-1 thru AT1

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20
Q

____ (drug) binds to the same site as K+.

A

Digoxin

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22
Q

A long QT interval predisposes you to _____.

A

Torsades de pointes

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23
Q

What does PVC stand for?

A

premature ventricular contractions

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24
Q

What is the most common diuretic?

A

furosemide

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25
Q

When would you add an aldosterone antagonist to therapy?

A

if LVEF

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26
Q

Which RAAS antagonist has antiremodeling effects?

A

the ACE inhibitors (-prils)

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26
Q

What is the maximum K+ level you want your pt to be at?

A

5

27
Q

What is the tx for V-fib?

A

defibrillation followed by epi or vasopressin and amiodarone

28
Q

The ARBs end in ____.

A

sartan

29
Q

What are the 2 types of type 2 AV block?

A

Mobitz I (progressive increased PR interval until blocked beat Mobitz II (disease in His-Purkinje = more unpredictable and urgent to prevent asystole)

29
Q

What receptor normally mediates the afterload?

A

alpha-1 thru AT-1

30
Q

What is the tx for chronic v-tach?

A

ablation and implantable defibrillators

31
Q

What receptor normally mediates the HR?

A

beta-1

32
Q

How is chronic AV block treated?

A

NOT with meds- permanent cardiac pacing

34
Q

Which diuretics have more reliable absorption than furosemide?

A

torsemide and bumetanide

35
Q

Lidocaine is only for _____.

A

ventricular arrhythmias

36
Q

What receptor normally mediates inotropy?

A

Beta-1

37
Q

If your pt is getting digoxin toxic, what should you do?

A
  1. stop the drug 2. monitor serum K+ and give K+ orally 3. if that doesn’t fix it, give IV K+ and antiarrhythmic agents like lidocaine and phenytoin 4. if there’s a serious/suicidal OD (K+ is high already), only give the digoxin antibody, Digibind
38
Q

What is AV block?

A

failure to conduct thru the AV node or below

38
Q

What is sinus tach?

A

SA node firing at a rate of 100-180 (can be normal)

38
Q

The big difference between ARBs and -prils is that only ACE inhibitors prevent the breakdown of ______.

A

bradykinin

40
Q

The big difference between ARBs and -prils is that only ____ prevent the breakdown of bradykinin.

A

ACE inhibitors

41
Q

A pt with _____ is at much greater risk for digoxin toxicity.

A

hypokalemia

42
Q

Atropine is used for ______.

A

vagally mediated bradycardia

44
Q

What is the tx for Torsades de pointes?

A

Potassium chloride and MgSO4 (to correct the electrolyte abnormalities)

45
Q

What is the drug treatment for acute v-tach?

A

class I or III antiarrhythmic (amiodarone)

46
Q

_____ (drug) is unique to the ventricles.

A

Lidocaine

47
Q

How is SA dysfunction treated?

A

a pacemaker- don’t use meds

48
Q

What causes bradyarrhythmias?

A

sinus node dysfunction (failure to initiate)

49
Q

What is triggered automaticity? What are the 2 types?

A

site of initiation is outside the SA node; early and late

49
Q

What are the s/s of digoxin tox?

A

GI disturbances headache visual disturbances

51
Q

The ACE inhibitors and ARBs reduce both ____ and _____.

A

preload; afterload

52
Q

Name 3 beta blockers.

A
  1. carvedilol 2. metroprolol 3. bisprolol
53
Q

What is the only cardiac glycoside we can prescribe?

A

digoxin

54
Q

AV nodal blockers are the _____.

A

beta blockers

56
Q

What is the tx for sinus tach?

A

treat the underlying condition

57
Q

What is the tx for acute supraventricular tachycardia (SVT)?

A

adenosine

59
Q

What is digoxin used for?

A

to increase systolic function (A-fib) and for symptom improvement (HF)

60
Q

When would you used an ARB instead of an ACE inhibitor?

A

when the pt can’t tolerate the ACE inhibitor (usually b/c of the kinin cough)

61
Q

What are the side effects of ACE inhibitors? Why does this happen?

A
  1. increased plasma K+ (lowered aldosterone) 2. hypotension (vasodilation) 3. kidney damage (GFR failure) 4. chronic dry cough (angioedema and irritation) All b/c of increased Bradykinin **** don’t give in pregnancy
62
Q

How can Epi cause arrhythmias?

A

causes Ca++ overload –> prolonged afterdepolarizations–> V tach –> V fib

63
Q

What is enhanced automaticity?

A

abnormal initiation at the SA node

64
Q

What is the preferred aldosterone antagonist?

A

spironolactone (then eplerenone)

65
Q

How is acute AV block treated?

A

***dopamine, epi, atrophine***; also shock and transvenous pacing

66
Q

What class of antiarrhythmics are the rhythm controllers?

A

class I or class III (amiodarone)

67
Q

What is the ECG sign for hyperkalemia?

A

peaked T wave

68
Q

What are the most common triggers of triggered automaticity (early afterdepolarizations)?

A
  1. slow heart rate 2. low K+ 3. drugs that prolong the action potential duration
69
Q

Rhythm control modifies ______ via the _____ current.

A

conduction; sodium

CVPR Exam I (29 decks)

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