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3 PHARM SELF > 43-44 Mech of HF and Drugs > Flashcards

43-44 Mech of HF and Drugs Flashcards

1
Q

What are the three cardinal manifestations of HF?

A

dyspnea, fatigue, fluid retention

[not all patients have fluid overload and thats why they don’t call it congestive HF anymore]

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2
Q

T-F– heart failure can occur when CO is high or low?

A

True

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3
Q

What are the 4 causes mentioned of HF when CO is high?

A

hyperthyroidism
beriberi
anemia
major AV shunts

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4
Q

Increased force of contraction is produced when?

A

increased sarcomere length during diastole- closely related to end diastolic filling pressure (pre-load)

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5
Q

What is the inotropic state of the heart-

A

contractile state of the heart determined by its contractile properties and influence of autonomic nerves and circulating catecholamine which can also influence HR

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6
Q

What protein pumps CA into the sarcoplasmic reticulum? out of the SR?

A

SERCA

RyR2

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7
Q

What proteins pump CA out of the cell?

A

Ca ATPase

NCX polarized

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8
Q

What pumps Ca into the myocyte during the depolarized state.

A

L-type Ca channel

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9
Q

What happens to the NCX Na/Ca exchanger during depolarization ?

A

breifly reverses so Ca goes into the cell

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10
Q

In heart failure what is systolic dysfunction? diastolic dysfunction?

A
  1. abnormally weak contraction during systole
  2. abnormal relaxation during diastole
    [remember they can be individual or in combination]
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11
Q

T-F– energy delivery, production and storage and energy utilization are thought to be heavily involved in pathogenesis of failure?

A

False-not involved

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12
Q

What are 5 signs and symptoms of HF?

A
  1. numerous hemodynamic abnormalities
  2. dysregulation of Ca homeostasis- impair contraction and relaxation
  3. dysreg of contractile proteins and interferes with cross bridge recycling
  4. densensitized b adrenergic pathway–> reduced Ca uptake in SR.
  5. myocytes lost by cell death–>fibrosis
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13
Q

Reduction in CO does what?

A

activates SNA and RAS and increases venous volume

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14
Q

Increases in intravascular and ventricular volumes leads to what?

A

increased diastolic and systolic wall stress, leading to hypertrophic remodeling of the hear and impaired contraction

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15
Q

Neurohumoral mediated increases in arterial and venous constriction increase what?

A

ventricular after load and preload respectively

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16
Q

Neurohumoral activation (SNA, ANGII, and aldosterone) act directly on the myocardium to promote what?

A

Unfavorable remodeling via myocyte apoptosis and changes in gene expression and EM composition

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17
Q

Reduced function of both arterial and venous baroreceptors leads to what?

A

increased activity of SNA, RAS, and vasopressin

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18
Q

T-F–hypertrophied heart operates at a higher inotropic state?

A

False- lower

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19
Q

What happens in renal function due to sympathetic- induced vasoconstriction ?

A

Shunts blood from glomeruli, stimulates renin, –>NA retention, increased blood volume, edema

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20
Q

SNS RAS and vasopressin all react to sustain arterial pressure with low cardiac out put by what? good or bad?

A
  1. increasing peripheral resistance

2. Not beneficial

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21
Q

What is the first thing we must do in the pharmacological treatment of HF?

A

correct any reversible causative factors

[arrythmias, hypertension, valve defects, anemia, thyrotoxicosis etc.]

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22
Q

AHA stage A and B include who? C and D?

A

at risk for heart failure

with heart failure

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23
Q

What is stage A? Drugs usually used?

A
  1. at risk but w/out structural heart disease or symptoms

2. ACEI or ARBS

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24
Q

What is stage B? Drugs typically used?

A
  1. Structural heart disease but without signs or symptoms

2. ACEI or ARB and Beta blockers

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25
Q

What is stage C? What drugs typically used/

A
  1. structural heart disease with prior or current symptoms

2. diuretics, ACEI and beta blockers

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26
Q

What is stage D HF? Tx?

A
  1. refractory HF requiring specialized interventions
  2. drugs from classes A,B,C, end of life care, and extraordinary measures (transplant, inotropes, mechanical support, experimentals)
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27
Q

What drugs do we use for after load reduction?

A

ACEI, ARBs, isosorbide dinitrite or hydalazine

28
Q

What diuresis drugs do we use for HF?

A

loop diuretics and thiazides, spironolactone

29
Q

What drugs do we use for positive isotropy?

A

adrenergic agoinsts
cAMP phosphodiesterase inhibitors
digitalis glycosides

30
Q

What are the only drugs to date that have reduced mortality when used alone?

A

ACEI
ARB
beta blockers

31
Q

How do beta blockers effect renin?

A

block renin release

32
Q

What molecules do ACEI suppress?

A

Ang II, Ang III, and aldosterone

33
Q

What do ACEIs prevent degradation of?

A

bradykinin [potent vasodilator]

34
Q

Are ACEIs more potent arterial or venous dilators?

A

Arterial- effects after load and CO

35
Q

ACEI are often first line therapy and should be prescribed to all patients with what?

A

reduced LVEF

[often used in combination with beta-blocker]

36
Q

T-F– survival benefit in patients with mild-moderate and moderate-severe HF in patients taking enalapril compared to isosorbide dinitrite/hydralizine?

A

True

37
Q

T-F–ACEI prevent progression of HF in patients after MI?

A

True

38
Q

T-F–ARBs allow for residual AT2 receptor stimulation by AngII and AngIII to promote vasoconstriction and diuresis?

A

False- vasodilation and natriuresis

39
Q

Is there incremental benefit of combining ARBs and ACEIs?

A

No

40
Q

T-F– in HF the kidney retains Na and water allowing the heart to operate at higher EDV to maintain LV stroke volume? what does this lead to?

A

True- increase end diastolic filling pressure leading to ventricular remodeling, pulmonary venous congestion and edema

41
Q

Because patients with HF operate on a plateau phase on the starling curve, pre-load reduction can occur without what?

A

decreases in cardiac output

42
Q

How do diuretics improve symptoms of congestive hear t failure?

A

moving patients to lower cardiac filling pressures along the same ventricular function curve

43
Q

When might thiazides be preferred over loop diuretics in HF?

A

in hypertensive patients

44
Q

T-F–diuretics produce symptomatic benefits more rapidly than any other drug for heart failure?

A

Yes- hrs or days vs weeks to months for ACEIs and Bblockers

45
Q

When should diuretics not be used alone?

A

in patients with stage C heart failure

46
Q

Do diuretics have a strong mortality benefit in heart failure?

A

No

47
Q

Is heart failure characterized by sympathetic hypo activation?

A

No hyperactivity

48
Q

Do beta blockers benefit inotropic performance?

A

No they impair it, but they improve symptoms, exercise tolerance, and increase LVEF in HF over months

49
Q

Improvement of abnormal Ca2+ handling may occur with beta antagonists how?

A

possibly by preventing hyperphosphorylation of the Ryanodine receptor which causes diastolic leak of Ca2+ from SR

50
Q

Beta blockers should be given to all patients with HF due to reduced LVEF unless what?

A

they are contraindicated (bradycardia or reactive airway disease)

51
Q

Has carvedilol been associated with a significantly reduced mortality compared with metoprolol?

A

Yes

52
Q

How does digoxin increase the force of cardiac contraction ? What does this do to renal perfusion?

A
  1. increasing intracellular free Ca2+

2. up CO–> decr SNA and increases renal perfusion

53
Q

Where do cardiac glycoside binding occur?

A

Na/K ATPase

54
Q

What are dioxins two main effects in non-cardiac tissues?

A
  1. sensitizes cardiac barorecepotrs –> decr. sympathetics and increase para
  2. Inhibit Na/K pump in kidney–> reduces renin release
55
Q

Is digoxin a first line therapy?

A

NO NO NO!! maybe with patients in atrial fibrillation, or those with persistent symptoms despite therapy with diuretics, ACEI and beta blocker

56
Q

Can digoxin toxicity be treated ?

A

yes with digoxin immunotherapy

57
Q

Does digoxin show a strong effect of increased survival in HF?

A

No- actually increased risk of death due to arrythmias or MI

58
Q

can aldosterone exert adverse effects on the heart independently and in addition to deleterious effects produced by AngII?

A

YEs

59
Q

Addition of aldosterone antagonist should be considered when in HF?

A

moderately severe HF with left ventricular dysfunction after MI- need to use concomitant diuretic therapy

60
Q

Do arteriodilators decrease systemic vascular resistance and increases renal perfusion/diuresis?

A

Yes

61
Q

Is isosorbide dinitrite usually used in combination with something?

A

Yes- hydralazine– because it is not as effective as an arteriodilator

62
Q

Can hydrazine reduce renal vascular resistance and increase renal blood flow?

A

yes

63
Q

How is sodium nitroprusside and nitroglycerin given in HF?

A

usually acute setting by IV [parenteral]

64
Q

Are inotropic agents used long term?

A

No- acute use only

65
Q

Does dobutamine activate dopamine receptors?

A

No

66
Q

Do cAMP phosphodiesterase inhibitors stimulate just venous dilation?

A

No- both arterial and venous

3 PHARM SELF (13 decks)

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