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Pharmacology > Drugs for Heart Failure > Flashcards

Drugs for Heart Failure Flashcards

1
Q

AT1 Receptors

A

Vasoconstriction decreases afterload
NE release
LV remodeling
aldosterone/vasopressin secretion

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2
Q

AT2 receptors

A

Vasodilation
Apoptosis
Regression of hypertrophy
Stimulate NO production

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3
Q

ANP and BNP

A

released from specialized cells in atrial (ANP) and ventricular (BNP) muscle in response to stretching of myocytes
Results in direct arterial vasodilation, increased GFR and diuresis

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4
Q

High output failure

A

high metabolic demands due to underlying medical conditions (hyperthyroid, anemia) –> healthy heart, pumps normal to high volume of blood –> heart becomes exhausted and unable to meet demand.
tx underlying condition

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5
Q

Low output failure

A

diminished volume of blood pumped by a weakened heart in patients who have otherwise normal metabolic needs

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6
Q

Low output, systolic dysfunction

A 
dilated cardiomyopathy
60-70%
< ejection fraction
reduces muscle contractility
increases afterload
enlarged heart
S3 heart sound heard
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7
Q

Low output diastolic dysfunction

A 
30-40%
Normal EF
Normal contractalitiy 
normal heart size, thickened left ventricle 
increase preload 
stiff left ventricle
impaired left vent filling and relaxing
exagerated S4 sound
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8
Q

Diuretics use in HF

A

Loop for systlic and diastolic for sx fluid overload.

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9
Q

ACE I / ARBs use in HF

A

reduce preload and afterload. Decreases mortality in systolic. Also used in diastolic

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10
Q

B-Blockers use in HF

A

systolic to increase sympathetic tone, reduces mortality. Used in diastolic to slow HR and allow improved diastolic filling

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11
Q

Digitalis glycosides use in HF

A

Moderate–improves sx in severe systolic not responding to vasodilators

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12
Q

Other inotropic agents use in HF

A

short-term use for severe systolic dysfunction, sx improvement

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13
Q

Vasodilators use in HF

A

hydralazine and nitrates for systolic. combo first tx shown to improve survivial in severe systloic. good for AA

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14
Q

CCB use in HF

A

relatively contraindicated in systolic HF–negative inotrope. Verapamil may be indicated for diastolic HF to slow heart rate and enhance filling

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15
Q

Spironolactone use in HF

A

Aldosterone antagonist. Less myocardial and vascular fibrosis, improve ortho hotn. renal effects.
Use in mod-severe HF and recent decompensation or early post-MI LV dysfunction
Avoid in SCR > 2 and K > 5
ADE: hyperkalemia, gynecomastia, GI

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16
Q

Eplerenon

A

HTN and HF
More specific aldosterone antagonist–less steroid effect
ADE: hyperkalemia

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17
Q

ACE I MOA

A

Leads to decrease vasoconstriction and decreased Na/water retention (aldosterone)
ACE structurally similar to kinase II–may also inhibit breakdown of bradykinin
Improved HF sx and functional status, decrease hospitalizations and reduce mortality

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18
Q

ACE I agents

A 
Benazapril
Captopril (food affects absorption)
Enalapril
Fosinopril (hepatic/renal elim)
Lisinopril
Moexipril (hepatic elim)
Perindopril
Quinapril
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19
Q

ACE I uses

A

CHF, HTN, diabetic nephropathy

Reduce both preload and afterload

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20
Q

ACE I ADRs

A

Kinin related: cough (due to reduces metabolism of prostaglandins/bradykinin); angioedema, rash, loss of taste (dysgeusia)
CONTRAINDICATED IN PREG
HYPERKALEMIA

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21
Q

ACEI and Renal blood flow

A

decreases efferent pressure to decrease glomerular pressure by blocking angiotensin II

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22
Q

ACEI monitoring

A

BP, renal function, potassium w/in 1-2 weeks

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23
Q

ACEI D/Is

A

K sparing diuretics (added hyperkalemia)
NSAIDs
Lithium
Antacids

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24
Q

Captopril dose

A

Short-acting

6.25-12.5 mg tid

25
Q

Enalapril dose

A

2.5-5 mg qd

26
Q

Fosinopril dose

A

5-10mg qd

27
Q

Lisinopril dose

A

2.5-5 mg qd

28
Q

Angiotensin II receptor blockers

A

Selectively block angiotensin II type 1 receptor. does not affect bradykinin
USE: HTN, HF, diabetic nephropathy
2nd line after ACE if cough not tolerated

29
Q

ARB agents

A

Candesartan, Irbesartan, Losartan, telmisartan, valsartan, eprosartan, olmesartan

30
Q

ARB ADR

A

Well tolerated. no cough
HoTN, renal fxn and hyperkalemia, angioedema
Contraindicated in preg
Maybe increased risk of CA

31
Q

ARB D/Is

A

Cimetidine, fluconazole, phenobarbital, digoxin, aliskiren

32
Q

Candesartan dose

A

8-32mg/d

33
Q

Irbesartan dose

A

75-300mg /d

34
Q

Losartan

A

25-100 mg/d

35
Q

Valsartan

A

80-320 mg / d

36
Q

Azilasartan

A

New ARB to tx HTN

40-80mg qd

37
Q

B-blockers

A

Activation of sympathetic nervous system–> beta receptor down regulation, LVH, cardiotoxic effects and arrhythmia
Negative inotropic effects
MUST START SLOW AND TITRATE!!

38
Q

Beta-blocker agents

A

Bisoprolol, metoprolol (selective B1-adrenergic blockers)
Carvedilol (non selective BB with alpha adrenergic ((causes more HoTN d/t vasodilation)) blocking and antioxidant effects)
ACE I and BB are synergistic and should be used together whenever possible

39
Q

Metoprolol XL dose

A

initial 12.5-25mg qd, double dose q2w to target dose 200mg qd

40
Q

Carvedilol dose

A

Initial dose 3.125 mg bid, titrate at min q2w to target 25-50 mg bid
Give with food to decrease HoTN

41
Q

BiDil

A

Fixed combo hydralazine 37.5mg (vasodilator) and isosorbide dinitrate 20 mg
Reduces mortality

42
Q

Digitalis glycosides

A

Sources: white and purple foxglove, mediterranean sea onion, oleander, lily of the valley, milkweed
MOA: inhibits Na/K ATPase–> increased intracellular Na, –> increased Na so decreased Na/Ca exchanger activity –> increased intraceullular Ca –> increased intensity of interaction of actin and myosin filaments; shortenin gof action potentional duration
Net results: increased contractility and positive inotropic effect. Parasympathetic effects

43
Q

Digitalis uses

A

HF: reduce sx and hosp for systolic heart failure, stage 3 with pts already on BB and ACEI
Arrhythmias: rate control AF

44
Q

Digitalis agents

A

Digoxin

Digitoxin (higher protein binding)

45
Q

Digitalis ADRs

A

Prolonged PR interval (AV block), junctional rhythms, multifocal atrial tachy, afib, PVCs, bigeminy, trigeminiy, vtach, vfib
INCREASE RISK OF CARD EVENTS WITH HYPOKALEMIA
causes hyperkalemia in accute OD
GI
Psych disturbances, fatigue
VISUAL DISTURBANCES–yellow green vision
Gynecomastia

46
Q

Digitalis: factors predisposing to toxicity

A

Hypokalemia
Hypomagnesemia
Hypercalcemia
Increased age

47
Q

Digoxin levels

A

0.5-1.2 ng/ml
DELAYED DISTRIBUTION: OBTAIN LEVELS at least 4 HOURS after IV, 6-8 hours after ORAL DOSE!
Toxic levels: >2, >6 is deadly
Loading dose: 0.5-1.5mg in divided doses

48
Q

Digoxin DIs

A

Antacids, bile acid sequestreants, erythro, tetracycl, cylcosporin, laxatives
DIURETICS–reduce serum potassium, increase risk of digoxic tox
Spironolactone–reduce renal excretion of digoxin

49
Q

Digoxin-specific antibodies (Digibind)

A

Produced in immunized sheep
High binding affinity for digoxin, renders digoxin inactive
Complex renally eliminated–t1/2 16-20hr
Reversal of digitalis tox in 30-60min, complete in 4 hrs
Used in life-threatening arrhythmias and in select pts w/ renal insuff and cardiomyopathy

50
Q

Drugs for acutely dcompensated HF

A

diuretics–loop +/- HCTZ or metolazone
Vasodilator: nbitroprusside or nitrate
Nesiritide
Inotropes

51
Q

Nitroprusside

A

MOA: potent vasodilator, increases cGMP, reduces preload and afterload
Given IV only, t1/2 - 2minutres
Use: rapid BP control
ADE: accumulation of cyanide, metabolic acidocis, arrhythmias

52
Q

Phosphodiesterases inhibitors

A

Selectively inhibit phosphodiesterase, increase cAMP, increased Calcium flux, increased contractility
Vasodilator: both preload and afterload reducers
Incresed mortaility long term, use short-term only

53
Q

Inamrinone

A

PO Failed to gain FDA d/t dose-dependant reversible thrombocytopenia, drug fever, n/v, lft issues, arrhythmias
Used IV only in severe stage D HF

54
Q

Milrinone

A

similar to inamrinone; both inotropic and vasodilating

ADRs: arrhythmias, HoTN, h/a, ches pain

55
Q

Dobutamine

A

B1-selective synthetic catecholamine which also activates A1 receptors
Increased myocardial contractility, HR and CO, but also increased myocardial o2 demand
Long-term infusion w/ pts w/ refractory HF or awaiting transplant
May be cardiotoxic w/ long-term use

56
Q

Dopamine

A

Immediate metabolic precursor or NE
Activates D1 receptors, leading to vasodilation. Activates B1 receptors in heart
At low doses (1-3 mcg/kg/min)–decreased peripheral resistance, vasoconstriction at higher rates of infusion (>10mcg/kg/min).

57
Q

Nesiritide

A

Indication: IV tx of pts with acutely decompensated HF with dyspnea at rest
Natural diuretic from atrium and ventricles
Binds to vascular smooth muscle and endothelial cells, increases cGMP and smooth muscle relaxation
ADR: hypotension, hypersens, renal fx, increased mortality

58
Q

HF inducing drugs

A

Negative inotropic drugs: Beta blockers, calcium antagonists, anti-arrhythmics
Direct cardiotoxin: cocaine, amphetamines, anthracyclines chemotx
Anti-TNF agents: etanercept and infliamab
Plasma volume expansion: NSAIDs, steroids, black licorice, high Na drugs, antihypertensive vasodilators

Pharmacology (10 decks)

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