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AFN Pharm I > Angina/Arrythmia/HF > Flashcards

Angina/Arrythmia/HF Flashcards

1
Q

Angina denotes chest pain caused by accumulation of ___________ resulting from myocardial ischemia

A

metabolites

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2
Q

What can cause steal syndrome?

A

Nitrates

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3
Q

What is steal syndrome?

A

Occluded vessel naturally dilates to comphensate for occlusion to increase blood flow. By dilating all of the vessels, blood flow is directed to clean vessels that are dilated and less flow is sent through the vessel with the occlusion

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4
Q

You can increase coronary flow by ___% by dilating coronary arteries

A

15%

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5
Q

Whats the equation for CPP

A

AoDP-LVEDP / Coronary vascular resistance

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6
Q

What are the 4 ways to cause myocardial vascular tone relaxation?

A

-decrease Ca++

-Increase cGMP

-Increase cAMP

-Stabilize cell membrane (aka hyperpolarize the cell)

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7
Q

How does cGMP cause relaxation?

A

De-phosphorylates (de-activating) myosin light chain (MLC). Then the myosin light chain combines with actin to cause contraction

*(think actin and myosin interacting in the sarcomere of cardiac muscle)

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8
Q

How does cAMP cause relaxation?

A

It phosphorylates (de-activating) the enzyme myosin light chain kinase, keeping it from activating the myosin light chain

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9
Q

How do B2 agonists cause relaxation in the vasculature?

A

Increase cAMP acting on MLCK

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10
Q

With angina, _______ control is paramount

A

HR control

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11
Q

How do B2 agonists cause myocardial contraction?

A

B2 agonists cause cAMP to activiate PKA, which phosphorylates the L-type Ca++ channel causing increased influx of Ca++

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12
Q

With angina/MI you want HR below ____

A

100

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13
Q

What 3 drugs used to tx angina?

A

-Nitrates

-CCBs

-BBs

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14
Q

How does sildenafil cause smooth muscle relaxation?

A

Its a PDE inhibitor. PDE breaks down cGMP so if we inhibit PDE then we have more cGMP

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15
Q

Why do we give morphine in angina?

A

-Decreases myocardia demand by decreasing pain, which will decrease HR

-vasodilation = decreased preload and decreased workload on heart

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16
Q

(t/f) NTG has a high 1st pass effect

A

Yes

*this is why it’s given sublingual & transdermal patches

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17
Q

Does NTG dilate coronary arteries?

A

Yep

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18
Q

Which CCB is best for angina?

A

Verapamil (almost exclusive cardiac effects)

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19
Q

CCBs (particularly non-dihydropyridines) can be effective in HR control with ______

A

SVT

Afib

*atria arrhythmias that pass through the AV node

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20
Q

What is MOA of class 1 antiarrythmics

A

Na+ channel blockers

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21
Q

What is MOA of class 2 antiarrythmics

A

BBs

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22
Q

What is MOA of class 3 antiarrythmics

A

K+ channel blockers

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23
Q

What is MOA of class 4 antiarrythmics

A

Ca++ channel blockers

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24
Q

What electrolyte depolarizes cardiac nodal cells?

A

Ca++

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25
What electrolyte depolarizes myocardial cells?
Na+
26
In a myocardial cell, what phase is resting membrane potential?
Phase 4
27
In a myocardial cell, what phase is depolarization?
Phase 0
28
In a myocardial cell, what phase is early repolarization?
Phase 1
29
In a myocarial cell what phase is the plateau phase?
Phase 2
30
In a myocardial cell, what phase is repolarization?
Phase 3
31
The plateau phase in a myocardial cell is d/t _____ __flux
Ca++ influx
32
Class ___ antiarrythmics decrease phase 0 of rapid depolarization in myocardial cells
Class I
33
What class antiarrythmic for ventricluar arrthmias
Class I
34
Which local anesthetic is the most caridotoxic?
Bupivicaine
35
Is lidocaine considered highly cardiotoxic?
Nope *one of the least cardiotoxic
36
Procainamide is what drug class?
Class 1A antiarrythmic AKA - Na+ channel blocker
37
What is the purpose of Na+/K+ - ATPase pumps in cardiac nodal cells?
To maintain resting membrane potential in cardiac nodal cells *sets concentration gradient up for another action potential
38
What holds the plateau phase in non-pacemaker cardiac cells and how?
Ca++ influx at the same time as the standard K+ eflux. This holds the cell charge at the same level until the Ca++ channels shut and then there is only an eflux of K+ until resting membrane potential is met.
39
What phases does the pacemaker/nodal cardiac cell not have when compared to non-pacemaker cells?
Doesn't have phases 1 or 2 *no early repolarization or phateau phase because there is no Ca++ channels open during repolarization
40
What ion depolarizes non-pacemaker cardiac cells?
Na+
41
What phase causes contraction in myocardial cells and how?
Phase 2 when the L-type Ca++ channels open. This stimulates the sarcoplasmic reticulum within the cell to release even more stored Ca++ out into the cell and cause contraction.
42
What scenario is digoxin most indicated in?
Pts w/ afib and heart failure w/ low EF
43
Adenosine acts by what 2 mechanisms?
-Via Gi protein activation, it hyperpolarizes nodal cells via K+ channels -Via Gi protein activation, it blocks Ca++ channels (only a mild effect from adenosine)
44
MOA of digoxin
-Stimulates release of Ach from vagus n. acting on M2 receptors, which activate Gi proteins, which inhibit Ca++ channels (slowing depolarization, this is only mild effect similar to adenosine) and stimulate K+ channels to hyperpolarize the cell (most profound effect) -increases contractility by inhibiting Na/K ATPase pump & increasing Ca++ levels by reducing Ca++ expulsion by NCX pumps
45
What class antiarrythmic is lidocaine?
Class 1B
46
Why are class 1 antiarrythmics sublabled with A,B,C subclasses?
These subclasses block Na+ channels to varying degrees Acronym - C.A.B 1C - strongest block (flecainide) 1A - medium block (procainamide) 1B - weakest block (Lidocaine)
47
What is special about class 1A antiarrythmic drugs and their effect on the action potential of myocardial cells?
They block Na+ channels (reduce depolarization slope) and K+ channels (prolong refractory period)
48
Class 1B antiarrythmics (lidocaine) block Na+ channels, but in such a way that does what to the action potential of myocaridal cells?
Shortens the plateau phase *Has a greater affinity for active and inactive Na+ channels (not resting Na+ channels) so this alters the plateau phase
49
Amiodarone is what class antiarrythmic?
Class III (K+ channel blocker)
50
What effect do class III antiarrythmics have on the myocardial action potential?
Prolong refractory period *they block voltage-gated K+ channels
51
What 2 CCBs would be used for rate control?
Verapamil & Diltiazem
52
Amiodarone blocks the conversion of ___ to ___, so monitor ________ function
-T4 to T3 -Thyroid function
53
How long is amiodarone's half-life roughly?
Month *effects can last 1-3 months
54
Amiodarone can cause the accumulation of ______, _______, & ________
-Statins -Digoxin -Warfarin
55
(t/f) you should avoid verapamil in systolic HF pts
True *Ca++ channel blocker, has negative inotropic effects
56
What agent are you gonna give w/ torsades?
Magnesium *Duh
57
What 2 drug classes work well for tachyarrythmias that go through the AV node (aka originate in the atria or at least above the AV node)?
-CCBs (verapamil/diltiazem) -BBs (esmolol/metoprolol)
58
What 2 drugs classes work well for arrhythmias orginating in non-nodal cells and ventricular arrhythmias?
-K+ channel blockers (amio) -Na+ channel blockers (Lido/procainamide)
59
The amount of _____ stored and released from the _______ ________ determines contractility of cariomyocites
-Ca++ -Sarcoplasmic reticulum
60
The ______ receptor is responsible for cardiac nodal cell's automaticity. It pumps out __ Ca++ and __ Na+ in proportionally
-NCX (Na+/Ca++ exchange) receptor -1 Ca++ & 3 Na+
61
What kind of drug is milrinone?
PDEI (PDE3 specifically) *inhibits PDE3, which inactivates cAMP, so increases Ca++ = inotrope *Also vasodilates (especially in the pulmonary vasculature) d/t increase in cAMP in the vasculature inhibits myosin light chain kinase, which activates mysoin light chain to cause smooth muscle contraction.
62
Why does cAMP cause contraction in myocardial cells but relaxation in vascular smooth muscle?
-cAMP in myocardial cells increase Ca++ in cell. -cAMP in vasculature inhibits myosin light chain kinase, preventing the activation of mysosin light chain (MLC causes contraction) ultimately resulting in relaxation/vasodilation
63
Spironolactone, an __________ antagonist, may decrease mortality and morbitity in pt w/ severe HF who is also taking ________
-aldosterone antagonist -ACEI
64
Captopril is an ________
ACEI
65
Whats the name of a fairly new combo drug for HF?
Entresto (sacubitril/valsartan) *Sacubitril is a neprilysin inhibitor. Neprilysin breaks down natriuretic peptides (BNP/ANP/etc.). Therefore it causes natriuresis, reduced sympathetic tone, etc. *Valsartan is an ARB
66
We don't use nesiritide much anymore d/t to a ______ ____ warning
Black box warning
67
Whats the name of the ARNI drug?
Entresto
68
BBs are contraindicated in pts with ________ HF
decompensated HF
69
Which BB is more B1 selective, Metoprolol or carvedilol?
Metoprolol (not much B2 effect) *carvedilol blocks alpha receptors as well so it has vasodilatory effects
70
Which BB has more vasodilatory effects, metoprolol or carvedilol?
Carvedilol (alpha and beta blocker) *metoprolol mainly B1
71
Nebivolol is a b-blocker & a ______ vasodilator
NO vasodilator
72
What AHA stage & NYHA class for HF s/s w/ intense exercise?
-AHA stage B -NYHA class I
73
What AHA stage & NYHA class for HF s/s w/ mild/moderate exercise?
-AHA stage C -NYHA class II/III
74
What AHA stage & NYHA class for HF s/s at rest?
-AHA stage D -NYHA class IV
75
Pt has HF s/s w/ intense exercise only. What meds will they be on?
-ACEI/ARB -BB -Diuretic
76
Pt has HF s/s w/ mild/moderate exercise. What meds will they be on?
-ACEI/ARB -BB -Diuretic -aldosterone blocker, digoxin, vasodilator (no explaination just on power point)
77
What vasodilator drug should be avoided in HF pts?
CCBs

AFN Pharm I (7 decks)

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