CAD And HF Flashcards

1
Q

Angina can lead to

A

MI, CHF, arrhythmias

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2
Q

At rest
Coronary BF
% CO
%02 extracted from myocardial tissue beds

A

70 ml/min/100g
5% co
70%

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3
Q

Coronary bf at exercise
Coronary bf alteration
CO demand increase, what also increases

A

2-4x
4-7x
Preload, hr, contractility

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4
Q

When coronary arteries fill

What perfusion pressure to LV is

A

Diastole

DBP-LVEDP

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5
Q

Factors that increase myocardial 02 demand 4

A

Tachycardia, high afterload, high preload, increased contractility

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6
Q

What increases myocardial 02 supply

6

A

Hgb conc, 02 sat, bradycardia, inc DBP, low normal preload, decreased contractility

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7
Q

CAD

Hr goal, indicated, contra/cautious use

A

Slow
BB and CCB
Isoproterenol, dobutamine, ketamine, pancuronium

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8
Q

CAD goals
Preload goal
Indicated
Contraindicated

A

Low normal
Ntg and diuretics
Volume overload

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9
Q

CAD goals
Afterload goal
Indicated
Contra/caution

A

High normal
Phenylephrine
Nitroprusside, high dose volatile agent

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10
Q

CAD
Contractility goal
Indicated
Contra

A

Normal to decreased
BB, CCB, high dose volatile
Contra: epi, dopamine

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11
Q

Stable angina tx

A
A- ASA, antianginals (nitrates, Ccb, bb)
B- BP control 
C- cholesterol, no cigs 
D- diet, dm 
E- edu, exercise
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12
Q

Organic nitrates
What they do
3 ex

A

Inc conc NO in smooth muscle

Ntg, isordil, imdur

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13
Q

Organic nitrates
What they do to veins and arteries, cv fx
Isordil DOA

A

Relax venous capacitance vessels and large coronary arteries to decrease preload and ventricular wall tension. Decrease demand, inc supply
6 hrs

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14
Q

Ntg routes

6

A

SL: tab, spray
Oral
Topical: ointment, patch
IV

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15
Q

NO signal pathway through

A

Glutathione and glutathione s transferase to NO

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16
Q

Nitrate MOA

A

Release NO after metab. Activate guanylate cyclase, inc cGMP, inc protein kinase G

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17
Q

Where nitrate signaling cascade ends

A

Dephosphorylation of myosin light chains, sequesters intracellular Ca, vessel relaxes

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18
Q

Anti angina actions of nitrates

A

Reduces 02 consump (dec preload thru vasodilation, dec afterload thru arterial dilation)
Dilates collateral vessels serving ischemic areas, attentuates spasms, inc rate of relaxation like NO

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19
Q

NTG
Metabolism
1/2t

A

90% degraded by liver to inactive metabolites.
E 1/2 1.5 min IV
SL and transdermal bypasses 1st pass and liver

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20
Q

Ntg

SE

A

HA
Postural hypotension
Methomoglobinemia (high iv dose and liver disease)

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21
Q

Nitrate tolerance

About, do what

A

Limits efficacy. Tolerance to AE.

Have intervals w no use, remove path at night. Oral siorbine: long t 1/2 w low levels

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22
Q

Nitrate drug interac
3
What happens
Tx

A

Viagra, cialis, levitra
Inhib phosphodiesterase, breaks down cGMP
Additive effect. Tx phenylephrine

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23
Q

Beta adrenergic antag
Overall effect
Indic

A

Favorable 02 supply and demand balance

Prevents unstable and stable angina

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24
Q

Beta adrenergic antag

What it does to heart itself

A

Dec 02 demand by dec CO. Dec catechol inc in SA ndode and AV node- HR dec. Improves diastolic filling time to inc supply, CO drop more dramatic w activity than rest

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25
Q
BB 
Use primarily what 
Improves survival in who 
Dont do what 
Avoid in what
A

B1 selective, metoprolol and atenolol
CAD
D/c suddenly
Variant angina

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26
Q

BB

SE 6

A

Depression, insomnia, masks hypoglycemia signs in DM, exercise intolerance, bronchospasm asthmatics

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27
Q

CCB L type

Action (MOA)

A

Bind to A1 subunit of l type channel in mode 0 when channel wont respond to depolarization stimula

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28
Q
CCB 
Effect at 
SA 
AV
Muscle 
Coronary vasculature
A

Dec hr,
Dec conductivity and hr
Dec contractility
Dilates vessels and arterioles

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29
Q

CCB

AE 5

A

AV block, cardiac failure, HA, constipation, hypotension

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30
Q

Dihydropyridines
3 ex
What they are
May cause what

A

Amlodipine, nifedipine, nicardipine
More selec for ca ch than vasculature than non-dihydropyridines
Reflex tachycardia

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31
Q

Non dihydropyridines
2 ex
More selec for
More at risk for, avoid what

A

Verapamil and dilt
Ca ch in heart
Heart block, avoid use of BB

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32
Q

Asa

Role, MOA

A

Plt activation contributes to thrombus formation

Antiplatelet activity imp CAD

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33
Q

ASA
Inhib what
Duration
Dose

A

Irreversible inhibited TxA2, lifespan of plt 10 days, 80 mg

34
Q

Unstable angina

4 drugs you would use

A

Antianginals, heparin or asa, hpIIb/a agonists like integrillin, plavix

35
Q

STEMI tx

A

Surgery, streptokinase, tPA

36
Q

Plavix
MOA
Indic

A

Irreversible plt ADP receptor a antag
All ACS pts w ASA allergy
Reduces recurrent coronary events

37
Q

Plavix

Caution w what

A

Combo w ASA/GPIIb/a inc risks of major bleeding. May still usein some pts

38
Q

GP IIb/IIIa inhib
3 ex
Indic

A

Reapro, integrillin, aggrastat

Reduce risk mi in unstable angina and urgent revasc w nstemi

39
Q

Tx acute angina

A

Nitrates, bb, Ccb

40
Q

Tx unstable angina

A

Nitrate, bb, Ccb, aspirin or plavix, hepatic or thrombolytics, glyco II/III inhib

41
Q

Tx variant angina

A

Nitrates and Ccb

42
Q

Systolic dysfunc
EF < ___%
Causes

A

40
CAD
NICM: htn, valvular disease, etoh, thyroid disease, cardiotoxic drugs

43
Q

Diastolic dysfunc
Impaired ___
2 causes

A

Filling
Cardiomyopathies
Incomplete relaxation of LV during ischemia (myocytes need ATP to relax)

44
Q

HF manifestations

A

Dyspnea: DOE, orthopnea, PND

Fatigue, fluid retention

45
Q

NYHA
Class I
Class II

A

No symp w ordinary activity

Symp w ordinary activity, slight limitation

46
Q

NYHA classification
Class III
Class IV

A

Symp w less than ordinary activity, marked limit

Symp w any activity, also at rest

47
Q

Physio drug goals
Reduce ___: 3
Reduce ___:3

A

Preload: diretics, aldosterone antag, venodilators
Afterload: ACEi, BB, vasodilator

48
Q

Physio drug goals

Increase ___: 3

A

Inotropy: cardiac glycosides, sympathomimetic amines, phosphodiesterase inhib

49
Q

CHF goals
HR: __ to ___
Drugs:
Contra:

A

Normal to elevated
Dopamine and dobutamine
BB (high doses)

50
Q

CHF goals
Preload
goal: ___, indicated, contra

A

Normal
IVF if decreased
NTG (if now preload), thiopental

51
Q

CHF goals Afterload

Goal, indic, contra

A

Low
ACE, ntp, amrinone
Phenylephrine

52
Q

CHF goals contractility

Goal, indic, contra

A

Increased
Dopamine, dobutamine, epi, amrinone
C: high dose inhaled agents and high dose BB

53
Q

Diuretics
Consider __ before giving
No evidence of __ benefit w __ or __ diuretics

A

Preload

Mortality, thiazide, loop

54
Q

Diuretics
__ ones most commonly used
3 ex. Inhibit what. Inc excretion of what

A

Loop
Furosemide, bumetanide, torsemide
Inhib na k 2 cl cotransporter in loop of henle. Excrete na, k, water

55
Q
Diuretics 
Distal tubule: 5-10% \_\_ excretion 
2 drugs 
2 that spare k 
Lose effectiveness when what
A

Na
Thiazides, zaroxolyn
Spironolactone, eplerenone
Creat <30 ml/min

56
Q

Diuretics

Loop: 20-25% __ excretion

A

Na

57
Q

Spironolactone

How it acts

A

K sparing, competitive antagonist at aldosterone receptor

Dec k/na exchange in distal tubule and collecting duct of nephron

58
Q

Spironolactone
Inc mortality or not
Monitor what w ACE

A

Decreases mortality

Monitor k, both decrease k excretion

59
Q

Aldactone SE

A

Gynecomastia and impotence from inhibiting androgen and mineralcorticoid receptors

60
Q

Inspa

What is is comp to aldactone

A

Also an aldosterone antagonist. More selective- less SE

61
Q

NTG

CV effects

A

Inc venous capacitance, reduces venous return to heart. Dec myocardial o2 demand. Alleviates ischemia, improves diastolic relaxation and improves LV compliance

62
Q

Ntg

Caution in these pts

A

Dont decrease preload too much

63
Q

ACEi

Actions

A

Reverses RAA vasoconstriction and vol retention. Reduces afterload which increases SV, inc GFR , inc natiuresis/diuresis. Dec preload. Mortality benefit

64
Q

ARB

Comparison to ACE

A

Similar hemodynamics, no bradykinin related vasodilation so less preload reduction. Mortality benefit. May be additive when used w ACEI

65
Q

B blockers

Benefits r/t

A

Inhib renin release. Attenuates signaling from catecholamines and prevents ACS.

66
Q

B blockers
Dont use in who
Benefit

A

Acute decompensated HF

Mortality benefit

67
Q

Hydralazine and isorbide initiate
Action
Use when
Benefit

A

Vasodilator.
When pt doesnt tolerate ACEi
Mortality dec only in African Americans

68
Q

What is bidil, why its useful

A

Hydralazine (arterial dilator) and isorbide dinitrate (venodilator).

69
Q

Digoxin

Action

A

Na k adenosine triphosphate inhib. Dec SNS outflow, inc PNS outflow. Dec conduction, inc av refractory period. Dec hr/preload/afterload. Inc ca. Dec na abs

70
Q

Digoxin
Therap level
Onset
Half life

A

0.5-1.2
30-60 min
36 hrs, takes 7 days to reach steady state serum conc

71
Q

Digoxin
Excretion
AE
Antidote

A

90% really excreted
Hypokalemia, av block, ventricular ectopy
Digibind/fab

72
Q

Digoxin

Pharm interactions

A

Inc risk av block w bb
Bb and ccb decrease contractility
Abx inc absorption

73
Q

Digoxin

Drugs that inc levels and how

A

Verapamil, quinidine, amio. Affect Vd and/or renal clearance

74
Q

Dobutamine

Action

A

Stim B1, inc contractility. Stim B2- arterial vasodilation, dec afterload. Short term tx acute HF

75
Q

Phosphodiesterase inhib

Do what on cell level

A

Inhib degradation of cAMP and cGMP in cardiac myocytes and vascular smooth muscle

76
Q

Phosphodiesterase inhib

Cardiac effects

A

Inc contractility w little inc in 02 demand. Arterial and venous dilation dec after and preload. Mild bronchodilation. Improved diastolic relaxation.

77
Q

Pde inhib

Good in OD of what

A

Beta blocker

78
Q

Amrinone

Cv effects

A

Inc CO and LV EF
Dec LVEDP and wedge pressures.
HR inc slightly, BP dec slightly

79
Q

Amrinone
1/2 life
Excretion
AE

A

6 HRS
Renal, unchanged
Hypotension and thrombocytopenia. May cause arrhythmias from inc ca

80
Q

Milrinone
Comp to amrinone
E 1/2
Excretion

A

Less tachycardia and thrombocytopenia
2.7 hrs
80% excreted unchanged in kidneys

81
Q

Milrinone

Long term use shows what

A

No improvement of M and M. May increase it. More helpful for pulm htn management