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Cardio > Heart Failure > Flashcards

Heart Failure Flashcards

1
Q

What causes PND and orthopnea?

A

Left sided heart failure

When you lie back, you are increasing venous return into an already congested cardipulmonary circulation, exacerbating HF

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2
Q

What causes pulmonary crackles?

A

elevated pulmonary capillary hydrostatic pressure

there is more pressure in the pulmonary veins from left-sided heart failure

more fluid is in the interstitium

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3
Q

What secondary heart sound can dilated heart failure produce?

A

mitral regurgitation secondary to dilatation of the LV and mitral annulus

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4
Q

How does PV curvechange in HFrEF?

A

reduction in contractility causes a decrease in slope of the ESPVR

correspondingly, a decrease in contractility pushes the ESV to the right (greater ESV)

also have a decrease in stroke volume (width) and EDV also increases

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5
Q

Can viral myocarditis lead to heart failure?

A

yes

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6
Q

What are 2 things to check to rule out restrictive cardiomyopathy?

A

congo red stain (amyloid) and iron stains

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7
Q

is dilated cardiomyopathy HFpEF and HFrEF?

A

HFrEF due to systolic dysfunction

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8
Q

What is most common etiology of dilated CM?

A

idiopathic

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9
Q

Increased venous return leads to …

A

worse pulmonary edema

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10
Q

If you have increased volume, what type of hypertrophy do you get?

A

eccentric hypertrophy

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11
Q

What 3 processes are activated with heart failure? What do they do?

A

1) adrenergic system results in tachycardia (CO = SV * HR)

2) RAAS (causes vasoconstriction with decreased renal perfusion)

3) Increased secretion of ADH and aldosterone (retention of Na/H20)

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12
Q

When someone has acute heart failure, what is the first treatment decision you need to make?

A

if they are cold and wet, use an IV inotrope to increase CO before diuresis

if warn and wet, proceed directly to diuresis

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13
Q

What do you give for IV inotropic therapy?

A

1) beta agonist like dobutamine

2) Phosphodiesterase inhibitors like milrinone

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14
Q

What is the MOA of milrinone?

A

inhibits PDE inhibitor

this prevents conversion of cAMP to AMP and increases contractility

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15
Q

What drugs can you give to chronically manage HFrEF? (4)

A

B-blocker

aldosterone antagonist

ACE/ARB

SGLT-2 inhibitor

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16
Q

How does nitroglycerin change at different doses?

A

lower dose venous dilator decreases preload

higher dose arterial dilator decreases afterload

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17
Q

When is digoxin not indicated?

A

if you don’t have a problem with contractility, you don’t need digoxin

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18
Q

Why do you not see peripheral edema and hepatomegaly when someone acutely goes into heart failure?

A

there is not enough time (<24hr) to see full effects of Na/H2O retention

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19
Q

Which cardiac biomarker decreases first?

A

CK-MB

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20
Q

What do we call it when an MI prompts heart failure?

A

ischemic cardiomyopathy

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21
Q

How can diuretics help with supply-sided ischemia?

A

decrease intravascular volume

decreases preload which leads to a reduction in LV wall tension and O2 needed

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22
Q

Are lipid values during an MI accurate?

A

no

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23
Q

What are two other causes of right-sided HF besides left-sided HF?

A

Primary pulmonary arterial hypertension

Cor pulmonale

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24
Q

What is cor pulmonale?

A

enlarged right ventricle due to a pulmonary condition

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25
Q

What does the presystolic impulse on palpation indicate?

A

Non-compliant, stiff left ventricle

similar to S4

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26
Q

What type of heart failure can longstanding HTN cause?

A

diastolic dysfunction due to stiff, hypertrophied left ventricle

diastolic dysfunction = HFpEF

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27
Q

How will PV curve change in HFpEF? How does the PV curve remain the same?

A

shift upward and to the left

EDV goes down (left, decreased filling) and pressure goes up

stroke volume decreases

contractility has no change

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28
Q

What 4 factors can lead to an increase in wall tension of ventricle?

A

1) volume overload

2) increase in radius

3) increase in pressure

4) decrease in wall thickness

29
Q

How do you treat HFpEF?

A

really only can give spironolactone and maybe SGLT-2 inhibitors long term

30
Q

What patients tend to be older? HFpEF or HFrEF?

A

HFpEF

31
Q

What is a difference in side effects between ACE inhibitors and ARBs why?

A

ACE normally breaks down bradykinin

if you inhibit ACE, you increase levels of bradykinin which can lead to cough and angioedema

32
Q

What type of drug is spironolactone?

A

Aldosterone receptor anatogonist

prevents aldosterone from reabsorbing Na+

33
Q

Is calcific AS a passive process?

A

No! Many studies have shown that it is associated with active inflammation

34
Q

What does a soft aortic component of S2 indicate?

A

severe AS

the leaflets are not closing as well, leading to a reduction in sound

35
Q

What does carotid pulse look like in aortic stenosis?

A

pulsation that is low in amplitude with a delayed upstroke

delayed upstroke is due to it taking longer for blood to get through the AV

pulsus parvus et tarvus

36
Q

summation gallop

A

can occur when someone is tachycardiac

hard to distinguish between S3 and S4

37
Q

What type of heart failure can aortic stenosis lead to?

A

Increased afterload leads to increased pressure

increased pressure = concentric hypertrophy

HFpEF as most of problem is from a stiff ventricle

38
Q

Should you use verapamil / diltiazem in heart failure?

A

No! It has negative ionotropic and chrontropic effects which can lead to decreased CO

39
Q

Aortic area of severe AS

A

< 1 cm2

40
Q

What does a laterally displaced PMI tell you?

A

LVH (left ventricular hypertrophy) / cardiomegaly

41
Q

How can you have decreased EF but still strong functional capacity?

A

some individuals are able to compensate better than others

42
Q

When should you consider an ICD? (general rule)

A

EF < 30%

you are at a higher risk of sudden cardiac death in this scenario

43
Q

4 levels of NY heart failure

A

1) cardiac disease but no symptoms and no limitations in ordinary physical activity

2) Mild symptoms and slight limitation during ordinary activity

3) Significant limitation in activity due to symptoms

4) Severe limitation. Symptoms even at rest

44
Q

If you think a patient’s CM is idiopathic, what other testing should you do?

A

r/o ischemia, toxicity, or infiltrative causes of CM

45
Q

What are 3 mainstay treatments in HFrEF?

A

ACE/ARB

B-blocket

aldosterone antagonist

46
Q

2 aldosterone antagonists

A

Eplerenone

Spirinolactone

47
Q

What is the hallmark of HF, even if EF is okay?

A

decreased CO

48
Q

What is always high in left heart failure?

A

LVEDP

49
Q

What does RAAS activation lead to?

A

increased TPR

50
Q

How can BP stay normal in HF if CO is decreased?

A

the RAAS system vasoconstricts

BP = CO * TPR

51
Q

What counteracts RAAS?

A

ANP / BNP

52
Q

What does ANP signal?

A

tries to increase secretion of Na/H2O and increase urine output

53
Q

What type of heart failure has reduced EF?

A

systolic since there is a problem with contraction in systole

54
Q

Is dilated CM systolic or diastolic?

A

Systolic

cannot contract well

55
Q

is dilated cardiomyopathy eccentric or concentric?

A

eccentric from increased fluid

56
Q

What 2 scenarios really result in concentric hypertrophy?

A

aortic stenosis

htn

57
Q

Concentric hypertrophy is normally systolic or diastolic dysfunction?

A

diastolic

58
Q

What is the most common form of systolic HF?

A

MI / ischemic

59
Q

What drug class can lead to acute HF?

A

NSAIDs

inhibit COX = decrease prostaglandins = increase Na/H2O

60
Q

MOA of loop diuretics

A

inhibit Na-K-Cl pump in ascending loop of Henle

61
Q

ACE inhibitors MOA

A

prevent conversion of angiotension I to angiotension II

angiotension II is main effector of RAAS system. So by decreasing angiotension II you prevent vasoconstriction

62
Q

What is the only oral inotrope?

A

digoxin

63
Q

What are digoxin’s 2 MOAs?

A

1) inhibit Na-K-ATPase pump which causes more Na and more Ca2+, therefore more contractility

2) suppress AV node / activate parasympathetic

64
Q

ARB MOA

A

directly blocks the angiotension receptor

65
Q

What do aldosterone antagonists do?

A

prevent Na+ reabsorption

66
Q

Sacubitral MOA

A

inhibits neprilysin

neprilysin normally breaks down ANP / BNP

more ANP / BNP can counteract the RAAS system

67
Q

Entresto MOA

A

combines sacubitral with ARB

68
Q

How can Coxsackie cause heart failure? And what type?

A

can cause myocarditis which then can cause dilated CM

Cardio (8 decks)

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