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Cardiovascular > SM 144 Heart Failure Treatment > Flashcards

SM 144 Heart Failure Treatment Flashcards

1
Q

What is Heart Failure?

A

Heart Failure is a syndrome where the heart cannot produce enough cardiac output or can only do so at the cost of increased filling pressures

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2
Q

What causes HFrEF?

A

Impaired contractility + Increased afterload

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3
Q

What causes HFpEF?

A

Impaired diastolic filling

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4
Q

What are the Stages of HF and are they unidirectional or bidirectional?

A

The stages span A - D and represent the extent of damage a patient has endured; A = high risk, B = damage but asymptomatic, C = HFrEF or HFpEF and symptomatic, D = HFrEF end stage; they are unidirectional because damage cannot be undone

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5
Q

What are the Classes of HF and are they unidirectional or bidirectional?

A

The Classes span I - IV and represent the symptoms experienced by a patient; I = none while IV = symptoms at rest; they are bidirectional because symptoms can be improved

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6
Q

What is the first step in managing HF?

A

Prevent it to begin with! Control BP, DM, Lipids, Smoking, and Weight

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7
Q

How does Hypertension relate to HF?

A

Hypertension can directly lead to HFrEF or cause HFpEF which can then worsen to HFrEF

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8
Q

What are symptoms of HF?

A

Low exercise capacity, dyspnea, orthopnea, nocturia

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9
Q

What are signs of HF?

A

Elevated JVP, rales, edema, hepatomegaly

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10
Q

What is BNP?

A

A biomarker elevated in HF

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11
Q

What tests can be used to diagnose HF?

A

BNP, EKG, CXR, Swan-Ganz catheterization

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12
Q

What drugs are always indicated in chronic treatment of HFrEF?

A

ACE-I or ARB or Sacubutril + ARB; Beta Blockers

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13
Q

What Beta Blockers are approved for HF?

A

Metropolol Succinate, Bisoprolol, Carvedilol

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14
Q

What are the pure venodilators?

A

Nitrates = reduce preload

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15
Q

What are mixed vasodilators?

A

Nitroprusside, ACE-I/ARBs, a-agonists, central a2 agonists = reduce afterload + preload

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16
Q

What are the arteriolar dilators?

A

Hydralazine, Minoxidil, CCB’s = reduce afterload

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17
Q

How does spironolactone affect the RAAS system?

A

Normally AngII binds the AT1 receptor to produce Aldosterone, which increases Na/Water reabsorption; Spironolactone prevents Aldosterone from binding it’s receptor, decreasing Na/Water reabsorption

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18
Q

How does Sacubutril work?

A

Sacubutril inhibits Neprilysin, potentiating Bradykinin and causing vasodilation

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19
Q

What are ACE-I’s and ARBs indicated for?

A

ACE-I and ARB’s are indicated for HF and HTN

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20
Q

How does Sacubutril compare to ACE-I/ARB’s?

A

Sacubutril is better but more expensive, while ACE-I’s and ARB’s are equivalent

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21
Q

How do Beta agonists work?

A

Beta blockers bind to an adrenergic receptor to increase inotropy and heart rate, leading to shorter diastole and lower coronary O2 supply

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22
Q

How do Beta blockers treat HF if they reduce inotropy?

A

Is the short run, Beta Blockers make HF worse due to decreased inotropy lowering CO; however, over time, more Beta receptors are expressed on myocytes increasing sensitivity to adrenergic signaling and contractility

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23
Q

How are Beta1 adrenergic receptors internalized?

A

B-ARK phosphorylated Beta receptors that are active, allowing B-Arrestin to bind and internalize the receptor, decreasing sensitivity to adrenergic signaling

24
Q

When is Metropolol Succinate the right Beta Blocker to use?

A

Purely B1 cardioselective, good choice for asthma

25
Q

When is Bisoprolol the right Beta Blocker to use?

A

Purely B1 cardioselective

26
Q

When is Carvedilol the right Beta Blocker to use?

A

Combined A1/B2 effects allows for additional vasodilation

27
Q

How do Mineralocorticoid/Aldosterone Antagonists work?

A

Spironolactone prevents the binding of Aldosterone to the internal Mineralocorticoid receptor in the Principal Cell, causing diuresis as well as protection against fibrosis

28
Q

Compare Spironolactone to Eplerenone?

A

Spironolactone is cheap/generic, relatively nonselective, and is a prodrug with many metabolites; Eplerenone is highly selective for the Mineralocorticoid Receptor; both cause hyperkalemia

29
Q

How do Nitrates work?

A

Primarily venodilators that decrease Preload, have minor arteriolar dilation effects that can decrease afterload in high doses

30
Q

What is Hydralazine and how does it work?

A

Mechanism unknown, causes smooth muscle relaxation to vasodilate arterioles

31
Q

What is the evidence based Nitrate of choice for HF?

A

Isosorbide Dinitrate

32
Q

What are side effects of Nitrates?

A

Headache, hypotension

33
Q

What is Ivabradine?

A

Selective sinus node inhibitor that alters pacemaker Phase 4 to lower HR; not used often clinically

34
Q

What is the only evidence based treatment for HFpEF?

A

Blood pressure control

35
Q

What drug is most useful for HFpEF?

A

Spironolactone

36
Q

How should HFpEF be managed?

A

Volume control, BP control, Spironolactone, weight + exercise

37
Q

What causes HF to worsen?

A

Decompensation events

38
Q

What are the proarrhtymic effects of Digoxin?

A

Digoxin can cause almost any arrythmia

39
Q

How does Digoxin improve HF?

A

Digoxin is a positive inotrope via Ca/Na potentiation

40
Q

What can decompensate HF?

A

Medication non-adherence, high salt diet, increased metabolic demands, increased afterload, decreased contractility

41
Q

What are signs of congestion?

A

Orthopnea, elevated JVP, edema, pulmonary rales = “wet”

42
Q

What are signs of poor perfusion?

A

Cool extremities, decreased BP, decreased pulse pressure = “cool” + give Nitroprusside

43
Q

What should be done when a HF patient is “warm and dry”?

A

Warm = well perfused + dry = no congestion, so reconsider HF diagnosis

44
Q

What should be done when a HF patient is “warm and wet”?

A

Warm = well perfused + wet = congested, so diurese the patient and uptitrate HF meds

45
Q

What should be done when a HF patient is “cool and dry”?

A

Cool = poor perfusion + dry = no congestion, treat with inotropes + vasodilators (Nitroprusside) + LVAD/Heart Transplant to increase cardiac output/perfusion

46
Q

What should be done when a HF patient is “cool and wet”?

A

Cool = poor perfusion and wet = congestion, treat with vasodilators (Nitroprusside) first to increase perfusion and allow for diuresis later, inotropes can improve perfusion but raise mortality

47
Q

What drugs can be given to treat acute pulmonary edema?

A

LMNOP; Loop diuretics, Morphine, Nitrates, Oxygen, Positve Pressure Ventilation (BiPap); treat underlying problem later

48
Q

What do loop diuretics do when treating pulmonary edema?

A

Loop diuretics acutely venodilate than natriuresis occurs

49
Q

What does Morphine do when treating pulmonary edema?

A

Venodilator + lowers sensation of dyspnea

50
Q

What do nitrates do when treating pulmonary edema?

A

Venodilator + increase pulmonary venous capacitance

51
Q

What does oxygen do when treating pulmonary edema?

A

Increase Oxygen supply during a period of high demand

52
Q

What does positive pressure ventilation do when treating pulmonary edema?

A

Improve oxygenation

53
Q

What can cause acute pulmonary edema?

A

Elevated BP, ACS, Increased Dietary Na

54
Q

When should Inotropes be used in HF?

A

Sparingly because they cause higher mortality, use in Class IV patients (symptomatic at rest)

55
Q

What are the two types of Inotropes?

A

B1 agonists + Phosphodiesterase 3 Inhibitors

56
Q

When B1 agonist is used to treat HF and why?

A

Dobutamine, which binds B1 and B2 equally; results in increased HR, SV, and vasodilation

57
Q

How do phosphodiesterase inhibitors work in HF and name one?

A

Milrinone bypasses the Beta1 receptor to increase cAMP directly to increase contractility

Cardiovascular (25 decks)

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