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Drugs for Heart Failure Flashcards

1
Q

Principal symptoms of HF

A

Dyspnea and fatigue
Exercise intolerance
Fluid retention
Some present primarily with exercise intolerance, others fluid overload

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2
Q

People w/ HTN have a ___ increased risk of HF

A

6x

need to manage HTN

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3
Q

Several complex compensatory mechanisms to maintain cardiac output and oxygenation of vital organs

(4)

A

Increased sympathetic tone
Activation of renin-angiotensin-aldosterone system: Sodium and water retention

Cardiac remodeling (ventricular dilation and hypertrophy)
(we don't have meds that affect this)

Other neurohormonal adaptations – endothelial hormones, vasopressin, natriuretic peptide

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4
Q

Sympathetic Autonomic Nervous System as it pertains to HF

A

Initially NE causes increased inotropic and chronotropic effects –> maintain near-normal CO and preserve perfusion of vital organs (CNS, heart)

Vasoconstriction in skin, GI, renal circulation decreases perfusion to these organs, and increases cardiac work load via –> SVR

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5
Q

in response to NE

beta1 receptors-G protein effector system ____ and with
beta 2 _______

A

beta1 receptors-G protein effector system downregulation

beta 2 not affected

this is why we give BB even though we see a further decrease in HR initially

but if we block the beta receptor you can re-sensitize the body to the NE that is there

w/ first dose sxs can worsen

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6
Q

ANP is the bodies

A

natural diuretic

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

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7
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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8
Q

High output failure

A

high metabolic demands due to underlying medical conditions (hyperthyroidism, anemia) –>healthy heart, pumps normal to high volume of blood; –> heart becomes exhausted fromincrease work load and unable to meet demand

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9
Q

High output failure tx

A

need to tx underlying condition

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10
Q 
Ejection fraction (EF) < 40%
Reduced myocardial muscle contractility
Enlarged heart (dilated left ventricle)
A

HFrEF – systolic heart failure

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11
Q

Normal EF (>50%), decrease SV & CO
Normal left ventricular contractility
Stiff left ventricle with impaired left ventricular filling

A

HFpEF – diastolic heart failure

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12
Q

Heart Failure Etiology

A

Hypertension  Valvular disease
Amyloidosis, sarcoidosis Coronary ischemia
Pericarditis
Drug Induced
Alcoholism Scarring post-MI
Enlarged left ventricular septum (hypertrophic cardiomyopathy)

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13
Q

Symptoms of heart failure

A 
SOB
Cough
Orthopnea
PND (paroxysmal nocturnal dyspnea)
DOE (dyspnea on exertion)
Reduced exercise tolerance
Fatigue
Weight gain
Edema
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14
Q

Physical findings in HF

A 
Tachycardia
Increasing weight
JVD or hepatojugular reflex
Presence of S3
Laterally displaced apical impulse
Fluid retention 
        Pulmonary crackles or 
        wheezes
        Peripheral edema
Hepatomegaly
Objective test to measure EF (2-D echocardiogram with Doppler flow studies or cardiac catheterization)
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15
Q

Non-pharmacologic Interventions To reduce risk of new cardiac injury

A

Attain or maintain normal weight
Smoking cessation
Alcohol consumption discouraged
Manage co-morbities (HTN, DM, HLP)

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16
Q

Interventions To reduce risk of new cardiac injury Maintain fluid balance

A

Na restriction, daily weight, fluid restriction

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17
Q

what is structural heart dz (stage B)

A

vascular dz
remodeling
valve issues

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18
Q

stage A of heart failure

A

pts without strucutral heart diease but with

htn
dm
atherosclerotic dz
obesity
metabolic syndrome

or using cardiotoxins or with Fhx

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19
Q

1st line TX for HF

A

ACEI and BB

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20
Q

staging A B C D of HF

A

doesn’t move back and forth

A. no structural abnormalities but high risk
B structural disease but without sxs
C. structural disease with prior sxs
D, refractory HF

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21
Q

RAAS drugs

A

ACE and ARB
BB
not CCB

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22
Q

Diuretics provide what kind of control in HF

A

sx

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23
Q

two kinds of K sparing diuretics

A

aldosterone antagonists: spironalactonin and eplerenone

inhibitions of Na/k pump: triamterene and amiloride

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24
Q

two types of aldosterone antagonists

A

spironlactone and

eplerenone has less hormonal effects and is more specific for receptors in the kidney and less overall steroid effect

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25
which diuretics are used in HF
loop
26
how often do you dose loop diuretics in HF
once a day | 2x daily for HTN
27
what labs do you want to monitor on a loop
K creatinin to monitor their renal function
28
why do we worry about kidney function in loop diuretics?
decreased renal profusion through hypotension and decreased renal sufficiency don't want too dramatic of a diuresis takes a while for interstitial fluid to redistribute back into the blood stream Hypokalemic metabolic acidosis
29
name the loop diuretics (4) | which one can be used with a sulfa allergy
``` Furosemide Bumetanide Torsemide Ethacrynic acid " --->Only one that can be used w/ sulfa allergy ```
30
why do we loose Mg with loops
normally you get excess K seeping back into the tubule net positive charge results in the absorption of Ca and Mg if you're blocking this you loose Mg wut? look into this later
31
what is the mechanism (if you have renal artery stenosis ) by which you will see renal failure with ARB and ACEI
blocking angiotensin and dialating efferent you are blocking efferent but if you have stenosis in the afferent arteriole won't have as much back pressure and wont' have sufficient filtration will lead to a dramatic rise in creatinine
32
what do we need to monitor in a pt taking ARB
" Monitor BP, renal fxn, for hyperkalemia since increase serum Cr and worsen renal function w/in 1-2 wks
33
ACEI names and dosages
Benazapril Captopril -6.25- 12.5mg tid Enalapril -2.5-5mg qd (20mg) Fosinopril -5-10mg qd (20mg) Lisinopril -2.5-5mg (20mg) Moexipril
34
name ARBS
``` Candesartan -8-32mg qd Irbesartan -75-300mg qd Losartan -25-100mg qd Telmisartan Valsartan -80-320mg qd Azilasartan ```
35
Mechanism by which loop diuretics work that interferes with NSAIDS
giving a non steroidal blocks the production of prostaglandins through the COX pathway and negates HTN effect
36
angioedema with ACEI is there cross reactivity with ARBs?
no, it looks like you should wait 6 weeks after stopping the ACEI though
37
3 BB for cardio protection
Metoprolol XL Carvedilol Bisoprolol
38
Sacubitril and Valsartran (Entresto) indication
patients with optimal dosing ACE/ARB and beta-blockers and MRA CI with ACEI
39
MOA w/ BB in HF
Deactivation of SNS --> leads to B-receptor down-regulation, LVH, arrhythmia, cardiotoxic effects they reduce mortality AS LONG AS they are dose appropriately
40
which BB for HF is non selective and is associated with alpha adrenergic blocking and antioxidant effects
carvedilol (coreg)
41
If pt has borderline BP and HF which BB would you be most likely to use
alpha blocking gives you unopposed beta 2 alpha blocking is vasodialating metroprolol is more selective and is usually used in pts with lower blood pressure however as long as you use appropriate dosing you could in theory use both
42
Metoprolol XL initial dosing for HF | and target
12.5-25mg 1xday | most people are 25 2x daily
43
Carvedilol (Coreg, generiic) initial dosing for HF | and target
initial dose 3.125mg bid, titrate at minimum q2 wks to target 25 – 50 mg bid people will often see worsening of HF sxs initially because of up regulation initially
44
Bisoprolol (Zebeta) initial dosing for HF | and target
not used as frequently as carved or meto initial dose 1.25mg qd; increase by 1.25mg q wk until 5mg qd, then increase by 2.5mg q4 wks to target dose 10mg qd
45
why do we give carvedilol with food?
Carvedilol should be given with food to reduce incidence of orthostatic hypotension
46
why should you not abruptly stop a BB
because you would have sns surge (rebound)
47
Ivabradine (Corlanor) MOA
slow heart rate through a different mechanism than bb | : inhibits f-channels in the SA node, prolonging diastole, reducing heart rate
48
Ivabradine (Corlanor) indicated for pts who...
on target dose of BB but still have HR over 77
49
BiDil is a combination of what two drugs
combination hydralazine 37.5mg (vasodilator) and isosorbide dinitrate 20mg
50
when is BiDil indicated
shown to further reduce mortality in AA population
51
hydralazine reduces.... ISDN reduces..... MOA of BiDil
" Vasodilator " Mixed Hydralazine: ↓afterload ISDN: ↓preload similar to an ACE because it addresses both
52
how do ACEI reduce preload and afterload
reduce vasoconstriction (afterload) and release of aldosterone (preload)
53
MOA of digoxin
Blocks Na-K-ATPase pump and therefore Na-Ca exchanger --> ↑Ca (intracellular) ---> ↑contractility and have positive anotropic effect
54
two effects of digoxin
direct on AP duration and PSNS effects (slower) can block conduction in supraventricular arrhythmias
55
why does digoxin not reduce mortality? what is it doing?
does not actually save lives because of pro arrhythmic effect just decreases sxs and hospitalizations
56
indications of digoxin
in stage III on pts already on ACEI and BB to minimize hospitalizations maybe for afib too
57
1/2 life of digoxin
1.5-2 days x 4-5 to get to a steady state = week to a week and a half
58
ADE of digoxin
" AV block /arrhythmias (Prolonged PR interval) " --->Junctional rhythms, MAT w/ block, PAT, AF, PVCs, VT, VF " High risk hypokalemia we see hypokalemia though with diuretics so this is an issue...
59
hallmark of digoxin toxicity
visual disturbances and halos around lights
60
digoxin levels at trough
.5-.9 ng/ml make sure this is NOT during post distribution phase have pt withhold meds in morning if you are running dig levels takes 4 hours to distribute with IV 6-8 hours with PO
61
besides AV blocks and arrhythmias what side effects are we looking for that indicate toxicity
" Anorexia, N/D " Gynecomastia in chronic therapy " CNS: fatigue, weakness, psychic & visual disturbances (hazy, yellow-green vision)
62
digitilization
give loading dose over 24 hr period to allow time for distribution
63
what are we concerned about in a pt on Erythromycin or tetracyclines
knocks out bacteria in the gut and decreases absorbtion
64
DID with digoxin
Antacids, cholestyramine, colestipol, kaolin-pectin: reduced absorption due to adsorption Erythromycin, tetracyclines Erythromycin, tetracyclines Laxatives, metoclopramide: reduced absorption due to increased gut motility
65
what can we do for a pt with an arrhythmia who we suspect has a dig overdose
Digibind
66
Drugs for Acutely Decompensated HF
Diuretics: loop +/- HCTZ or metolazone metaolzaone o Vasodilator: Nitroprusside or nitrate. Used in fluid overload to decrease preload o Inotropes stimulate contraction; only used in people w/ low BP
67
why do we use Diuretics: loop +/- HCTZ in Acutely Decompensated HF
blocks sequential parts of the loop and dramatically increases diuresis
68
Nitroprusside
only given IV potent vasodilator; activates guanyl cyclace leads to increase cGMP --> smooth muscle relaxation Dilates both venous and arterial vessels – reduces preload and afterload 2 minute half life used in immediate short term for rapid bp control has both preload and afterload reduction for the mngmt of HF
69
Milrinone
only used short term for decomp in HF awaiting heart transplant Both inotropic and vasodilating Selectively inhibit phosphodiesterase F –III (cardiac and vascular cyclic-AMP-specific)   cAMP  Ca++ flux  enhanced contractility only used short term because it causes arrhythmias
70
b1-selective synthetic catecholamine which also activates b1 receptors Increased myocardial contractility, HR and CO, but also increases myocardial oxygen demand Given as long term infusion for 48-72 hours in patients with refractory HF or awaiting transplant
Dobutamine
71
Immediate metabolic precursor of NE Activates D1 receptors in several vascular beds --> vasodilation (effect on renal vasculature may be of clinical importance; better than dobutamine); also activates B 1 receptors in heart
Dopamine
72
Drugs that INDUCE heart failure:
Negative inotropic drugs: BB, CCB, antiarrhythmics (disopyramide, quinidine) Direct cardiotoxins: cocaine, amphetamines, anthracyclines (doxorubicin, daunorubicin) Anti-TNF agents: etanercept, infliximab Drugs that cause plasma volume expansion: NSAIDs, glucocorticoids, estrogens, androgens, black licorice, antihypertensive vasodilators (hydralazine, methyldopa, prazosin, minoxidil --> decrease RBF and activate RAAS), drugs high in Na
73
Drugs that cause plasma volume expansion
NSAIDs, glucocorticoids, estrogens, androgens, black licorice, antihypertensive vasodilators (hydralazine, methyldopa, prazosin, minoxidil --> decrease RBF and activate RAAS), drugs high in Na

Pharm II (16 decks)

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