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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
Isosorbide dinitrate side effects:
Tachycardia (reflexive), HA SAME AS HYDRALAZINE
26
Nesiritide mechanism of action:
It's a recombinant hBMP, so binds BMP receptor and activates cGMP (vasodilator)
27
Nesiritide side effects:
Hypotension, renal damage
28
Digoxin is a(n) (X) agent with which mechanism of action?
X = inotropic Inhibits Na/K ATPase, increasing intracellular Na and Ca by decreasing Ca exit (increase contractility)
29
Digoxin side effects:
N/V, diarrhea, arrhythmia
30
(X) drug is given to treat both chronic HF and atrial fibrillation.
X = Digoxin
31
List the agents that inhibit cardiac remodeling.
1. Beta-blockers (metroprolol) 2. ACE-I (lisinopril) 3. K-sparing diuretic/mineralocorticoid antagonist (Spironolactone)
32
ACE-I/ARB for chronic HF treatment decrease all-cause mortality by (X)%.
X = 25
33
Beta-blockers for chronic HF treatment decrease all-cause mortality by (X)%.
X = 35 (most value are metroprolol and carvedilol)
34
Digoxin for chronic HF treatment decrease all-cause mortality by (X)%.
X = 0
35
Hallmark feature of hypertrophic cardiomyopathy is (systolic/diastolic) function.
Diastolic (filling), though both impaired
36
Pulsus Bisferiens is seen in (dilated/hypertrophic/restrictive) cardiomyopathy. Describe this phenomenon.
Hypertrophic; Spike and dome waveform from initial rapid (unimpeded) ejection and then mid-systolic obstruction of LV outflow
37
Harsh crescendo-decrescendo murmur heart best at mid-left sternal border is characteristic of (X) abnormality, especially if (S3/S4) present.
X = hypertrophic cardiomyopathy S4
38
Hypertrophic cardiomyopathy murmur gets (softer/louder) with valsalva and (softer/louder) with squatting.
Louder (decreased VR and EDV, so smaller LV and greater obstruction); Softer (increased VR)
39
Low voltage ECG should make you think of (X) cardiomyopathy.
X = restrictive
40
List the categories of etiologies for restrictive cardiomyopathy.
1. Non-infiltrative 2. Infiltrative 3. Storage diseases 4. Fibrotic/inflammatory
41
Your patient undergoing radiation therapy is at risk for (dilated/hypertrophic/restrictive) cardiomyopathy.
Restrictive (fibrotic/inflammatory etiology)
42
Non-infiltrative causes of restrictive cardiomyopathy include:
Scleroderma
43
Infiltrative causes of restrictive cardiomyopathy include:
Amyloidosis, sarcoidosis
44
(X) are examples of glycogen storage diseases that put patient at risk for (dilated/hypertrophic/restrictive) cardiomyopathy.
X = Pompe's Restrictive
45
(X) are examples of lysosomal storage diseases that put patient at risk for (dilated/hypertrophic/restrictive) cardiomyopathy.
X = Hurler's and Fabry's Restrictive
46
Which ECG changes are common in patients with cardiac sarcoidosis, a (dilated/hypertrophic/restrictive) cardiomyopathy.
Restrictive; Ventricular tachyarrhythmia and complete heart blocks
47
Aside from sarcoidosis, (X) deposits are another infiltrative etiology of (dilated/hypertrophic/restrictive) cardiomyopathy.
X = amyloid fibrils Restrictive
48
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.
Restrictive; X = amyloidosis
49
AL amyloidosis caused by excess (X) fragments. More common in (men/women) around (5/6/7/8) decade of life.
X = immune-globulin light chain AL Men; 6
50
AL amyloidosis involves cardiac tissue (X)% of time. With the development of heart failure, the median survival is (Y) months/years.
``` X = 60 Y = 4 months ```
51
Hereditary form of amyloidosis that mainly affects (X) population.
X = AA (over 60 y.o.) TTR (Transthyretin-related) amyloidosis
52
When suspecting restrictive cardiomyopathy, it is important to rule of (X) disease on your differential because (X) may respond to (Y) stripping therapy.
``` X = constrictive pericarditis Y = pericardial ```
53
Vasodilators are not indicated for (dilated/hypertrophic/restrictive) cardiomyopathy. Why?
Hypertrophic and restrictive (decrease preload not good for either of these diseases)
54
Your 75 y.o. patient has restrictive cardiomyopathy secondary to amyloidosis. He experiences palpitations. Should you prescribe CCB to control his arrhythmias?
NO! DETRIMENTAL
55
Hypertrophic cardiomyopathy. Most common genetic mutations are in which proteins?
Sarcomere proteins: 1. Myosin-binding protein C3 (49%) 2. Myosin heavy chain (39%)
56
Digoxin administration will (increase/decrease) outflow obstruction in hypertrophic cardiomyopathy.
Increase (increases contractility)
57
Hand-grip will (increase/decrease) outflow obstruction in hypertrophic cardiomyopathy.
Decrease
58
Beta (agonists/antagonists) and alpha (agonists/antagonists) will decrease outflow obstruction in hypertrophic cardiomyopathy.
Antagonists; agonists (ex: phenylephrine)

CVD (8 decks)

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