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03b: HF Flashcards

1
Q

T/F: All drugs given parenterally for treatment of acute HF.

A

True

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2
Q

Which drugs should cross your mind for treatment of acute HF?

A

(ALL IV)

  1. Diuretics (furosemide)
  2. Nitrovasodilators
  3. Inoroptes (dobutamine)
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3
Q

What are drawbacks/complications of using diuretics in acute HF?

A
  1. Electrolyte issues
  2. RAAS activation
  3. Overdiuresis
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4
Q

Treating patient with acute HF: taking someone who is (warm/cold) and (wet/dry) and making them the opposite.

A

Cold and wet;

Making them warm and dry

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5
Q

T/F: Furosemide/lasix is given for acute HF at a fixed dose.

A

False - threshold for effective diuresis is individualized (titrate)

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6
Q

Which electrolytes may be depleted upon administration of furosemide?

A

K, Mg, and Ca

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7
Q

Most common inotropes used in acute HF:

A
  1. Dobutamine (beta-agonist)

2. Milrinone (PDE Inhibitor)

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8
Q

List the most common nitrovasodilators used in acute HF.

A
  1. Nesiritide (hBNP)
  2. Nitroprusside
  3. Nitroglycerin
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9
Q

(Nesiritide/nitroprusside) acts as a NO donor. It is (more/less) potent and (more/less) safe to use as (Nesiritide/nitroprusside).

A

Nitroprusside;
More; less safe (cyanide toxicity on liver/kidneys)
Nesiritide

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10
Q

Nitrates, like nitroglycerin, are given to treat acute HF and primarily cause (venodilation/arterial dilation). What’s its mechanism of action?

A

Venodilation (as well as arterial at higher doses);

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11
Q

Acute HF: mechanism of action of milrinone.

A

PDE inhibitor; increases cAMP (inhibits its breakdown)
Heart tissue: this increases Ca and contractility
SM: cAMP causes vasodilation

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12
Q

Acute HF: adverse effects of dobutamine

A

Cardiac arrhythmia

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13
Q

Acute HF: adverse effects of milrinone

A

Cardiac arrhythmia (plus hypotension)

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14
Q

In acute HF, CO is gonna be (low/high) and PCWP is gonna be (low/high) in nearly all cases, so (X) level is the guide to therapy.

A

Low; high

X = SVR

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15
Q

Which drugs should cross your mind for treatment of chronic HF?

A

(ALL ORAL)

  1. Diuretics (hydrochlorothiazide)
  2. ACE-I
  3. Beta-blockers
  4. Digoxin (glycoside)
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16
Q

Hydrochlorothiazide mechanism of action.

A

Blocks Na/Cl transporter at DCT

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17
Q

Hydrochlorothiazide side effects.

A
  1. Hyperglycemia, hyperlipidemia, hyperuricemia

2. Hypokalemia

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18
Q

T/F: Both ACE-I and ARBs reduce cardiac remodeling

A

True

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19
Q

Spironolactone is (X) drug used to treat (acute/chronic) HF. What is the mechanism of action?

A

X = K-sparing diuretic
Chronic;

Blocks aldosterone receptor in collecting tubule

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20
Q

Spironolactone side effects.

A

Hyperkalemia, gynecomastia

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21
Q

(X) drugs are second-line for chronic HF, behind (Y) drugs, except in african americans and some other disease states.

A 
X = nitrates (nitrovasodilators) PLUS hydralazine
Y = ACEI/ARBs
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22
Q

Pt with both chronic heart and renal failure. What’s first-line agent to treat his HF?

A

Isosorbide dinitrate (nitrovasodilator) and hydralazine

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23
Q

Hydralazine is a(n) (X) agent that has which mechanism of action

A

X = (direct acting) vasodilator

Increases NO release from endothelial cells

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24
Q

Hydralazine side effects:

A

Tachycardia (reflexive), HA

SAME AS ISOSORBIDE

25
Q

Isosorbide dinitrate side effects:

A

Tachycardia (reflexive), HA

SAME AS HYDRALAZINE

26
Q

Nesiritide mechanism of action:

A

It’s a recombinant hBMP, so binds BMP receptor and activates cGMP (vasodilator)

27
Q

Nesiritide side effects:

A

Hypotension, renal damage

28
Q

Digoxin is a(n) (X) agent with which mechanism of action?

A

X = inotropic

Inhibits Na/K ATPase, increasing intracellular Na and Ca by decreasing Ca exit (increase contractility)

29
Q

Digoxin side effects:

A

N/V, diarrhea, arrhythmia

30
Q

(X) drug is given to treat both chronic HF and atrial fibrillation.

A

X = Digoxin

31
Q

List the agents that inhibit cardiac remodeling.

A
  1. Beta-blockers (metroprolol)
  2. ACE-I (lisinopril)
  3. K-sparing diuretic/mineralocorticoid antagonist (Spironolactone)
32
Q

ACE-I/ARB for chronic HF treatment decrease all-cause mortality by (X)%.

33
Q

Beta-blockers for chronic HF treatment decrease all-cause mortality by (X)%.

A

X = 35 (most value are metroprolol and carvedilol)

34
Q

Digoxin for chronic HF treatment decrease all-cause mortality by (X)%.

35
Q

Hallmark feature of hypertrophic cardiomyopathy is (systolic/diastolic) function.

A

Diastolic (filling), though both impaired

36
Q

Pulsus Bisferiens is seen in (dilated/hypertrophic/restrictive) cardiomyopathy. Describe this phenomenon.

A

Hypertrophic;

Spike and dome waveform from initial rapid (unimpeded) ejection and then mid-systolic obstruction of LV outflow

37
Q

Harsh crescendo-decrescendo murmur heart best at mid-left sternal border is characteristic of (X) abnormality, especially if (S3/S4) present.

A

X = hypertrophic cardiomyopathy

S4

38
Q

Hypertrophic cardiomyopathy murmur gets (softer/louder) with valsalva and (softer/louder) with squatting.

A

Louder (decreased VR and EDV, so smaller LV and greater obstruction);

Softer (increased VR)

39
Q

Low voltage ECG should make you think of (X) cardiomyopathy.

A

X = restrictive

40
Q

List the categories of etiologies for restrictive cardiomyopathy.

A
  1. Non-infiltrative
  2. Infiltrative
  3. Storage diseases
  4. Fibrotic/inflammatory
41
Q

Your patient undergoing radiation therapy is at risk for (dilated/hypertrophic/restrictive) cardiomyopathy.

A

Restrictive (fibrotic/inflammatory etiology)

42
Q

Non-infiltrative causes of restrictive cardiomyopathy include:

A

Scleroderma

43
Q

Infiltrative causes of restrictive cardiomyopathy include:

A

Amyloidosis, sarcoidosis

44
Q

(X) are examples of glycogen storage diseases that put patient at risk for (dilated/hypertrophic/restrictive) cardiomyopathy.

A

X = Pompe’s

Restrictive

45
Q

(X) are examples of lysosomal storage diseases that put patient at risk for (dilated/hypertrophic/restrictive) cardiomyopathy.

A

X = Hurler’s and Fabry’s

Restrictive

46
Q

Which ECG changes are common in patients with cardiac sarcoidosis, a (dilated/hypertrophic/restrictive) cardiomyopathy.

A

Restrictive;

Ventricular tachyarrhythmia and complete heart blocks

47
Q

Aside from sarcoidosis, (X) deposits are another infiltrative etiology of (dilated/hypertrophic/restrictive) cardiomyopathy.

A

X = amyloid fibrils

Restrictive

48
Q

Abdominal fat biopsy shows apple-green birefringence under polarized light when stained with congo red stain. Patient likely has (dilated/hypertrophic/restrictive) cardiomyopathy, secondary to (X) etiology.

A

Restrictive;

X = amyloidosis

49
Q

AL amyloidosis caused by excess (X) fragments. More common in (men/women) around (5/6/7/8) decade of life.

A

X = immune-globulin light chain AL

Men; 6

50
Q

AL amyloidosis involves cardiac tissue (X)% of time. With the development of heart failure, the median survival is (Y) months/years.

A 
X = 60
Y = 4 months
51
Q

Hereditary form of amyloidosis that mainly affects (X) population.

A

X = AA (over 60 y.o.)

TTR (Transthyretin-related) amyloidosis

52
Q

When suspecting restrictive cardiomyopathy, it is important to rule of (X) disease on your differential because (X) may respond to (Y) stripping therapy.

A 
X = constrictive pericarditis
Y = pericardial
53
Q

Vasodilators are not indicated for (dilated/hypertrophic/restrictive) cardiomyopathy. Why?

A

Hypertrophic and restrictive (decrease preload not good for either of these diseases)

54
Q

Your 75 y.o. patient has restrictive cardiomyopathy secondary to amyloidosis. He experiences palpitations. Should you prescribe CCB to control his arrhythmias?

A

NO! DETRIMENTAL

55
Q

Hypertrophic cardiomyopathy. Most common genetic mutations are in which proteins?

A

Sarcomere proteins:

  1. Myosin-binding protein C3 (49%)
  2. Myosin heavy chain (39%)
56
Q

Digoxin administration will (increase/decrease) outflow obstruction in hypertrophic cardiomyopathy.

A

Increase (increases contractility)

57
Q

Hand-grip will (increase/decrease) outflow obstruction in hypertrophic cardiomyopathy.

58
Q

Beta (agonists/antagonists) and alpha (agonists/antagonists) will decrease outflow obstruction in hypertrophic cardiomyopathy.

A

Antagonists; agonists (ex: phenylephrine)

CVD (8 decks)

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