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Pharmacology Test #2 > 05 Heart Failure > Flashcards

05 Heart Failure Flashcards

1
Q

what is the major cause of Heart failure?

A

coronary artery disease (main cause, 60-70%)

-in Afro Americans, hypertension is a major cause

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2
Q

what two types of heart failure are there?

A
  • compensated heart failure: fine at rest but not during exercise
  • Congestive heart failure (CHF, decompensated):
  • resting cardiac function inadequate - venous pooling → edema esp. lungs - shortness of breath (dyspnea)
  • ‘neurohumoral storm’
    • ejection fraction of less than 40%
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3
Q

what drug can cause heart failure?

A

adriamycin

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4
Q

what happens to the BP in CHF?

A

BP is well maintained

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5
Q

how is the BP maintained in CHF?

-Sympathetic, parasymp etc

A
  • increased sypathtic tone (tachycardia)
  • decr. parasympathtic tone
  • activation of renin-angiotensin system
  • incr. vasopressin release
  • incr. blood volume
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6
Q

what class of drugs is generally containdicated in the treatment of heart failure?

A

Calcium channel blockers, bc they decrease cardiac function

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7
Q

What is Heart failure?

A

it’s a supply and demand problem, the demand from the body is not met by the CO of the heart

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8
Q

what are the general consequences of cardiac failure?

A

bc CO is less, blood flow is less, renin flow is less, thus the renin agiontensin II system increases, increasing aldosterone, increasing sodium and water retention, leading to edema

  • this decr. force of contraction
  • decr. CO, incr. TPR, decr Stroke volume, =cardiac hypertrophy
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9
Q

what is the “hormonal storm” /cycle of heart failure?

A
  • activation of sympathetic nerve system and of renin-angiotensin-aldosterone axis
  • ->heart tissue reodeling (hypertrophy)
  • ->pumping function disrupted
  • ->additional neuro-humoral activation promoted
  • -> then it starts over again
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10
Q

What do Cardiac Glycosides do to the heart physiology?

A

They inhibit the Na+/K+ ATPase

  • take Na from inside the cell and exchange it for K outside the cell
  • Na out, K in
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11
Q

what is the other “pump” that’s important for ion concentrations inside the heart cells?

A

the Na+/Ca++ exchange, takes Ca inside the cell and exchanges it for Na outside the cell
(Ca out, Na in)

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12
Q

Cardiac glycoside example

A

-Digoxin*** and Digitoxin, they inhibit the Na/K atpase in the heart cells

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13
Q

What do cardiac glycosides bind to, and what is the structure?

A

they bind to a membrane bound transporter (Na/K ATPase)

-it has two alpha and two beta subunits

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14
Q

how can the binding of a cardiac glycoside be stabilized?

A

by phosphorylation of cytosol alpha subunit (on Na/K ATPase)
-this can occur by a DECREASE in extra cellular K, so drug combination with a thiazide would enhance a cardiac glycoside and combination with and ACEI would decrease effectiveness of card. glyc.

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15
Q

Mechanism of cardiac glycosides

A

inhibition of Na/K ATPase leads to:

  • increased intracellular Na
  • causing the Na/Ca exchange to work in reverse (now pumping Na out and Ca in)
  • the increased Ca in the cell is then stored in the sarcoplasmic reticulum
  • this increases contractile force (inotropic effect)
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16
Q

what is the Inotropic effect

A
  • it’s an increase in contractile force

- this is what cardiac glycosides do, increase force=increased CO

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17
Q

what are the toxic effects of cardiac glycosides (Digoxin)

A

tachycardia

  • also it has a very narrow therapeutic index so the toxic effects are close to the effective dose
  • delirium, fatigue, dizziness, VISUAL DISTURBANCES (halo effect, mostly yellow and green)
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18
Q

what is a large contributor to the binding of cardiac glycosides?

A 
potassium concentration (K)
-hypokalemia=increased cardiac glycoside binding=diuretics (thiazide and loop)
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19
Q

what combination drugs would decrease the effectiveness of cardiac glycosides?

A

ACE Inhibitors/ARBs, and K-sparing

20
Q

what heart failure medications work by increasing the cardiac output? (CO)

A

the cardiac glycosides and the catecholamines (Dobutamine and phosphodiesterase III inhibitors)

21
Q

Dobutamine

A

used for acute emergency heart failure (iv)

  • increases cAMP–> incre. in Ca influx–>incre. force of contraction (CO)
  • it is a catecholamine (so are Phosphodiesterase III inhibitors)
22
Q

Milrinone, Amrinone

A
  • Phosphodiesterase III inhibitor
  • this makes it so the cAMP inside the cardiac cell isn’t broken down increasing Ca and thus increasing heart contraction (incr. CO)
  • can be used for chronic heart failure, but not that common bc of increased mortality
23
Q

if a patient has heart failure and diabetes what drug(s) would you give them?

A

the ACE Inhibitors/ARBs/or Renin inhibitor(Alikiren)

24
Q

when are ACE inhibitor contraindicated

A

during pregnancy and renal artery stenosis

25
Q

what drug causes (or has a higher incidence of causing) angioedema and/or glossitis?

A

ACE inhibitors

26
Q

dry cough…

A

adverse effect of ACE inhibitors

27
Q

not generally used for HT, but frontline agents for heart failure

A

loop diuretics

28
Q

what are the classes of Diuretics? (three of them)

A
  • Loop diuretics (Furosemide)
  • Thiazides (Hydrochlorothiazide)
  • K+ sparing (spironolactone)
29
Q

Loop diuretics

A
  • ex: Furosemide
  • inhibit Na-K-2Cl ion cotransporter, decr. Na+, H2O reabsorption: ascending loop of Henle
  • Hypokalemia, hypoagnesemia, hypocalcemia, ototoxicity, most potent, best for edema
30
Q

Thiazides

A
  • ex: Hydrochlorothiazide
  • inhibit Na-Cl cotransporter, decr. Na+, H2O reabsorption in DISTAL CONvoluted tube
  • hypokalemia, hypercalcemia, incr. uric acid–>gout, DM-2
31
Q

K+ Sparing diuretics:

A
  • ex: Spironolactone
  • aldosterone antagonisms at collecting tube
  • hyperkalemia, least potent, adjunct
  • decreases mortality, tissue remoldeling
32
Q

which diuretic (class) causes hypocalcemia, and which causes hypercalcemia

A
  • hypocalcemia: loop

- hypercalcemia: thiazides

33
Q

how do the diuretics work (in general)?

A
  • they decrease plasma volume by increasing sodium and water excretion
  • this decreases the pressure in front of and behind the heart, decreasing edema and symptoms of heart failure
34
Q

vasodilators are another class of drugs used for treatment of HR, what type of vasodilator is contraindicated?

A

Calcium channel blockers

35
Q

which vasodilators open K+ channels?

A

Minoxidil (rogaine) and Diazoxide

36
Q

direct vasodilation

A

hydralazine

37
Q

Nitric oxide (NO) vasodilators

A
  • Beta-natriuretic peptide
  • Nitroprusside
  • Nitrates
38
Q

how do the nitric oxide vasodilators work?

A

They cause the production or release of NO…guanylyl cyclase…leads to the production/elevation of cGMP…causes relaxation

39
Q

SE: lupus syndrome reaction

A

Hydralazine, the lupus will go away when drug is discontinued

40
Q

what is a common side effect of vasodilators?

A

reflex tachycardia

41
Q

Bidil:

A

Isosorbide-dinitrate (ISDN) & Hydralazine

  • HF in Afro-Americans, no effect in caucasion
  • 1st race-based drug, blacks do not respond well to ACEIs/ARBs and beta blockers
  • mechanism same as other Nitric oxide agents (NO–>Guanylyl cyclase–>incr cGMP–> relaxation)
42
Q

which beta-blocker would NEVER be used in heart failure?

A

Propranolol, it would make the situation worse

43
Q

what beta blockers are more commonly used in the treatment of HF?

A

Metoprolol, Carvedilol

44
Q

what is ‘Beta-type Natriuretic peptide?’ and what is the other name for it?

A

Nesiritide (Natrecor)

  • binds to A-type receptor on vascular smooth muscle cell
  • activates (increases) cGMP–>muscle relaxation and vasodilation
  • arterial and venous dialtion–> decr. preload and afterload
  • used in the LATE STAGES of heart failure
  • given by IV, short term admin
45
Q

females are not given what drug for HF?

A

Digoxin

46
Q

what drug is given to a patient with HF that actually decreases survival, but makes the patient more comfortable?

A

Phosphodiesterase III inhibitors (Milrinone), so it’s used in late stages

Pharmacology Test #2 (7 decks)

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