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CPR Exam 1 > Drugs for HF > Flashcards

Drugs for HF Flashcards

1
Q

ACE Inhibitor suffix and prototype

A

-prils

Captopril and Lisonopril

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2
Q

Angiotensin Receptor Blocker (ARB) suffix

A

-sartans

Losartan and Valsartan

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3
Q

Briefly describe the symptoms of Left-sided HF

A 
Pulmonary edema
Right-sided HF
Ascites
Edema
Orthopnea and PND
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4
Q

Systolic vs. Diastolic Dysfunction

A

Systolic (HFref): dilated chambers and weak musculature

Diastolic (HFpef): hypertrophied chambers with decreased filling ability

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5
Q

Ischemia in the presence of Diastolic HF that raises LA pressure can lead to what?

A

“Flash” pulmonary edema

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6
Q

LaPlace’s Law in a nutshell

A
  1. Increased wall Thickness decreases wall stress (seen in HFpef)
  2. Increased radius of the chamber (HFref) decreases pressure but increases wall stress.
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7
Q

What happens when an MI causes fibrosis?

A

Spherical ventricular dilation and increased interstitial collagen deposition between myocytes.

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8
Q

Why does remodeling of the heart in response to low CO not solve the issue?

A

It can never keep up, so the cycle repeats which causes more damage than good

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9
Q

3 pharmacological ways to prevent deterioration of Cardiac function

A
  1. ACEi/ARBs
  2. BB
  3. Aldosterone Antagonist (Spironolactone)
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10
Q

Summary of the RAAS

A
  1. JG cells sense drop in BP and secrete Renin (or Macula Densa sense drop in salt content)
  2. Renin activates Angiotensin I
  3. Angio I converted to Angio II by ACE in lungs
  4. Angio II promotes Aldosterone release, vasoconstriction, and cardiac remodeling
  5. Aldosterone causes resorption of Na+ and secretion of K+
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11
Q

Name the drug classes that block each sequential step of the RAAS

A
  1. Aliskiren blocks Renin
  2. ACEi block Angio I to Angio II
  3. ARBs block Angio II at AT1 receptors
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12
Q

Why is a side effect of ACEi a cough?

A

ACE is used to deactivate bradykinin.

Bradykinin causes Vasodilation, Decreased GFR, and Cough

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13
Q

Main results from ACEi

A
  1. Decreased after load (vasodilation)
  2. Decreased preload secondary to decreased Aldosterone (decreased volume)
  3. Decreased Mitogen activity in the heart
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14
Q

What would you find on blood test of a person taking Captopril (renin, angiotensin, aldosterone)

A
  1. Increased Renin (feedback)
  2. Decreased Aldosterone (downstream)
  3. Increased Angio I
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15
Q

Captopril profile

A

ACEi
Lowers BP in HFref
Also used in Diabetic Nephropathy
Side effects: Cough and angioedema

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16
Q

2 additional ACEi that are widely used because of a long half life

A
  1. Benazepril

2. Lisonopril

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17
Q

Losartan Profile

A

ARB (AT1 1000x greater affinity)
NO increased bradykinin (no cough)
Treats HTN alone or in combo with AntiHypertensives
Treats CKD as well

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18
Q

Why use Valsartan over Losartan?

A

Valsartan is not a prodrug, so does not need to be activated.
Excreted in the poo so no need for good liver or kidney function

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19
Q

Patient presents with LV systolic failure (aka HFref) what do you prescribe?

A

ACEi or ARB

Beta blocker

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20
Q

5 contraindications for ACEi or ARB

A
  1. Intolerant
  2. Pregnancy
  3. Hypotension
  4. Increased Creatinine
  5. Hyperkalemia
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21
Q

Action of ANP and BNP

A

Increase GFR
decrease renin, aldosterone, and ADH.
Promotes diuresis and natriuresis

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22
Q

Sacubitril

A

Endopeptidase Inhibitor

prevents the breakdown of BNP and ANP

23
Q

3 Beta blockers that are beneficial in HF

A

Metoprolol
Bisoprolol
Carvedilol

24
Q

Carvedilol profile

A

Nonselective a/B blocker (B>a)
Treats previous MI or ACS and HFref
Side effects: SOB, weight gain, pain, swelling

Prevents down-regulation of B1 receptors due to increased sympathetic tone. Keeps heart responsive

25
Q

When is labetalol used?

A

Hypertensive emergencies

26
Q

What is the number one black box warning with Beta blockers?

A

Do NOT abruptly withdraw because the body will be sensitized to SNS stimulation

27
Q

Ivabradine

A

Inhibits funny Na+ channels in nodal tissue to prolong diastole and slow HR (increase filling time)

Treat HFref with a HR>70bpm who are:

  1. maximally dosed beta blockers
  2. contraindicated for beta blockers
28
Q

Spironolactone profile

A

Competitive Aldosterone Antagonist
HFref
K+ sparing diuretic that acts at the collecting duct (counteracts K+ losing diuretics)
Reduces aldosterone-mediated fibrosis

29
Q

Common reasons for diuretics

A
  1. Primary HTN

2. Edema: CHF, Liver failure, Kidney Failure

30
Q

2 classes of Diuretics

A
  1. K+ sparing: Collecting duct
    - Triamterene
    - Amiloride
    - Spironolactone
  2. K+ losing: Proximal to CD
    - Thiazides
    - Loop Diuretics
    - CAi
    - Osmotic diuretics
31
Q

Cardiac abnormalities caused by Hyperkalemia

A
  1. Increased membrane potential closer to threshold
  2. Arrhythmias (tall T’s, prolonged PR, Widened QRS)
  3. In nodal tissue, hyperkalemia increases activity of K+ channels and actually causes HYPERpolarization leading to Bradycardia

Just remember: wanna stop the heart? Give K+!

32
Q

Cardiac abnormalities caused by hypokalemia

A
  1. Hyperpolarization
  2. prolonged QT
  3. Tall U waves
  4. VT and VF
33
Q

Which diuretic is the cannon and causes the most diuresis?

A

Loop Diuretics- Furosemide (Lasix)

34
Q

Furosemide profile

A

Blocks Na/K/2Cl cotransporter in the thick ascending loop.
Used to manage volume overload in HF (decreases preload)
Side effects: Ototoxicity, hypocalcemia, hypomagnesemia, hypochloremic alkalosis

35
Q

What loop diuretic can be given in place of Furosemide in a person with a sulfa allergy?

A

Ethacrynic Acid

36
Q

What other ions does Furosemide also cause to be lost in the urine?

A

Ca2+ and Mg2+

Without a negative potential across the membrane caused by K+ resorption, there is no drive for Ca or Mg absorption

37
Q

Order of diuretic usage in HF

A
  1. Loop Diuretic
  2. K+ sparing if needed
  3. Thiazide last
38
Q

HCTZ profile

A

K+ losing diuretic that inhibits the NaCl cotransporter in the distal convoluted tubule.
Treats HTN

39
Q

Vasodilators used in chronic HF

A
  1. Isosorbide Dinitrate (venous)

2. Hydralazine (arterial)

40
Q

Hydralazine profile

A

Directly vasodilators arterioles (decreased TPR)
Treats HTN, hypertensive emergency in pregnancy
Off-label use: HFref
Side effects: Pruritus, rash, urticaria

41
Q

Nitroglycerin profile

A

NO producer that increases cGMP and dephosphorylates MLC to cause vasodilation (mainly venous)

Uses: Angina Pectoris, acute decompensated HF

42
Q

Digoxin

A

Inhibits Na-K ATPase in myocardium
Increases contractility by promoting Ca2+ influx
Suppresses nodal tissue to prolong AP

Uses: Controls Ventricular rate in Afib and treats HF

43
Q

Hemodynamic effects of Digoxin

A

Decreased SNS tone
Increased Urine
Decreased Renin

44
Q

Electrophysiologic effects of Digoxin

A
  1. Increased automaticity of Purkinje’s
  2. Increased AV refractory period (decreased conduction velocity)
  3. Decreased Ventricular refractory

Can cause a form of 3rd degreee HB where atria are uncoupled from Ventricles

45
Q

Noncardiac side effects of Digoxin

A

Visual disturbances (halos, yellow/green tinge)

46
Q

Main drug interaction with Digoxin

A

K+ losing diuretics can cause hypokalemia and enhance effects of Digoxin to a toxic amount

47
Q

ACC/AHA Stages of HF

A

A- At risk without structural disease or symptoms
B- Structural disease without symptoms
C- Structural Dz with symptoms
D- Advanced structural Dz with marked symptoms

48
Q

Stage A HF Therapy

A

Lifestyle mods

ACEi or ARB +/- Statins

49
Q

Stage B HF Therapy

A

ACEi/ARB

Beta Blockers

50
Q

Guidelines for treatment of HFref Stage C

A

ACEi/ARB or ARNI (Sacubitril + Valsartan)
Beta Blockers
Aldosterone Antagonist

51
Q

Guidelines for treatment of HFpef

A

Direct therapy at symptoms and associated conditions

Edema- Loop diuretics
B blockers, ACEi/ARBs, CCB’s as needed

NO evidence for: Nitrates, PDE5i, digoxin

52
Q

Studies to obtain in Acute Decompensated HF

A

ECG
CXR
CBC with Troponins
ECHO

53
Q

ADHF patients are all volume overloaded. What is the correct therapy to initiate?

A

Diuretics. Get out the urine cannons

Can also give Nitrates to decrease preload if not hypotensive

54
Q

Patient presents to ED with decompensated HF and hypotension with evidence of end-organ damage. In addition to diuretics, what else could be warranted?

A

Sympathomimetics- Dobutamine and Dopamine
Make sure you discontinue any Beta blockers slowly

Also PDEIII inhibitor (Milrinone) which increases cAMP

CPR Exam 1 (19 decks)

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