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Pathophysiology - Cardiovascular > Pharmacology of Heart Failure > Flashcards

Pharmacology of Heart Failure Flashcards

1
Q

What are the Class I-IV grades for heart failure?

A

Class I - no limitation on physical activity
Class II - dyspnea on exertion
Class III - symptoms appear on less than normal activity
Class IV - bedridden, unable to carry out physical activity

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2
Q

What effects does Angiotensin II have on the vasculature and cardiac muscle by binding the AT1 receptor? What drugs block this?

A

Induction of vasoconstriction
Causes cardiac and vascular remodelling
Of course stimulates Aldosterone secretion

-> these effects are blocked by ACE inhibitors indirectly or AT1 receptor blockers (ARBs) directly

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3
Q

Why are ACE inhibitors / ARBs preferred in heart failure? When are they used?

A

Decreased mortality by preventing Angiotensin II induced remodeling of heart, and also lower blood pressure, preventing RAA activation

Used in early HF for blood pressure control, and later stages of both systolic heart failure to reduce mortality. Okay in diastolic too.

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4
Q

What are the adverse effects of ACE inhibitors which may be less severe in ARBs?

A

Angioedema and dry cough (since bradykinin is thought to also be broken down by ACE)

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5
Q

What are other side effects of concern with ACE inhibitors?

A

Hypotension
Hyperkalemia (K+ sparing diabetic, and blocks aldosterone)
Increase in serum creatinine by lowering GFR (creatinine credit card in sketchy)

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6
Q

Why are ACE inhibitors thought to cause kidney dysfunction when used in heart failure / bilateral RA stenosis but PREVENT kidney dysfunction in diabetic nephropathy / HTN?

A

HF / bilateral renal artery stenosis -> low volume states, where little blood is reaching the kidney in the first place. AT1-receptor mediated efferent arteriole vasoconstriction is needed to maintain GFR

Diabetes / HTN -> nephropathies caused by too high of a GFR -> removal of AT1-receptor mediated vasoconstriction -> less kidney problems

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7
Q

What is the drug which can inhibit neprilysin and what is it given with? What does neprilysin do?

A

Sacubitril, given with valsartan, an ARB

-> approved for heart failure

Neprilysin is a nephro-lysin, lyses natriuretic peptides which work in the kidney, important for reducing volume in heart failure.

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8
Q

What are the potential side effects of sacubitril / valsartan? What should be discontinued for use?

A

Same side effects as ARBs, except increased risk of hypotension

Must have discontinued ACE inhibitor or ARB which was previously taking for at least 36 hours before starting

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9
Q

What is the primary therapeutic role of sacubitril / valsartan, and why is it used?

A

Used in Stage C systolic heart failure (HFrEF) because it has been show to reduce morbidity / mortality, replacing ACE inhibitor or ARB alone.

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10
Q

What are the major side effects of furosemide?

A

Hypokalemia (due to increased reabsorption of Na+ via ENaC)
Hypomagnesia (due to lack of Mg+2 reabsorption)
Dehydration
Hyperuricemia (uric acid reabsorption is increased in hypovolemia) -> gout
**Deafness - think of the gong in sketchy

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11
Q

What are the major drug interactions of concern with diuretics?

A

NSAIDs -> cause fluid retention by constricting afferent arteriole

Digoxin -> hypokalemia increases activity, as K+ stops binding of K+ to Na/K+ ATPase

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12
Q

What metabolic ion dysfunction can diuretics cause and why?

A

Hypokalemic metabolic alkalosis
-> Increased K+ in the collecting duct leads to increased H+ / K+ exchange in the alpha intercalated cells, losing H+ into the urine -> increased bicarbonate in the blood

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13
Q

What is the primary type of diuretics used in heat failure and what is the purpose?

A

Loop diuretics -> controls symptoms of fluid retention / volume overload in Stage C and D

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14
Q

Do diuretics have a mortality benefit? How should you monitor the patient who is on them? Why are they monitored?

A

No -> just control symptom

Monitor intake and output of fluids closely. Below a certain cc/kg/hour urine output, step back the diuretics to prevent causing acute renal failure

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15
Q

What is spironolactone used for and why? What drug is similar?

A

Severe CHF -> aldosterone mediates myocardial fibrosis, and spironolactone antagonizes this effect of cardiac remodeling

  • > improves overall SURVIVAL in Stage C/D heart failure
  • > similar drug = eplerenone (apple)
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16
Q

What are the side effects of concern with spironolactone and what is the cutoff for not using?

A
  1. Hyperkalemia -> less aldosterone = less ENaC / ROMK channels running, retain K+ (K+-sparing diuretic)
  2. Increased serum creatinine
  3. Gynecomastia - blocks androgen receptor as well

Cutoffs - SCr must by <2.5 in men or 2.0 in women, with <5 mEq/L of K+.

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17
Q

What are the drug interactions of spironolactone?

A

Digoxin - competes for secretion (despite hyperkalemia being good to prevent toxicity)
ACE/ARBs / Cyclosporine / Tacrolimus - addative hyperkalemia

18
Q

What is digoxin used for in heart failure?

A

Increases LVEF and contractility / exercise capacity in systolic heart failure -> reduces hospitalizations but not mortality

19
Q

What are the adverse effects of digoxin toxicity?

A
  1. Hyperkalemia - due to K+ not being able to be taken into cells acutely
  2. Nausea, vomiting, diarrhea - first manifestations are GI
  3. Bradycardia / AV block - vagal
  4. Arrhythmias such as PVCs / PACs
  5. Vision disturbances - seeing yellow like van Gogh
20
Q

What is safe Digoxin range, and what must be watched closely? How does its administration differ from other medications?

A

<2 ng/mL
Must watch kidney function -> declining kidney function can increase serum halflife
Does not require a full loading dose, unlikely other drugs

21
Q

What beta blockers have shown a reduction in mortality in heart failure? In what stages should they be used?

A

Carvedilol, Metoprolol, and Bisprolol

Used in Stages B-D, even if no history of MI

Okay to control blood pressure in Stage A or HFpEF

22
Q

What are the mechanisms of acting of hydralazine and nitrates?

A

HydrAlAzine - reduce afterload by inducing arteriolar vasodilation

Nitrates - reduce preload via causing venodilation

23
Q

What are the side effects of hydralazine and nitrates?

A

Hydralazine - Hypotension, reflex tachycardia (Give with beta blocker), drug-induced lupus

Nitrates - Flushing, hypotension, headache

24
Q

What is the role in heart failure therapy of hydralazine + nitrate combination?

A

Stage C only

  • Improves mortality if added to ACE / Beta blocker regimen in AFRICAN AMERICANs
  • Improves mortality in rest of patients if used when ACE / ARBs are contraindicated
25
Q

What is the mechanism of action of Ivabradine and its role in therapy? What is its primary side effect?

A

Blocks the Ifunny channel in pacemakers to slow heart rate

Role - Stage C heart failure with STABLE patients only to reduce hospitalization

Side effect - Bradycardia exacerbated by CYP3A4 inhibitors

26
Q

Describe what it means to be in all of the following groups of acute decompensated heart failure:

  1. Normal cardiac index but increased pulmonary capillary wedge pressure
  2. Normal pulmonary capillary wedge pressure but decreased cardiac index
  3. Decreased cardiac index with increased pulmonary capillary wedge pressure
A
  1. Normal cardiac index but increased pulmonary capillary wedge pressure
    - > pulmonary congestion
  2. Normal pulmonary capillary wedge pressure but decreased cardiac index
    - > hypoperfusion
  3. Decreased cardiac index with increased pulmonary capillary wedge pressure
    - > pulmonary congestion and hypoperfusion

1/3 are typical decompensation scenarios

27
Q

What are the three inotropic agents typically used in the management of acute decompensated heart failure?

A
  1. Dopamine
  2. Dobutamine
  3. Milrinone - one in a million!
28
Q

What is the mechanism of action of dobutamine and why is it typically not used in decompensated heart failure?

A

B1-agonist, increasing contractility, with slight beta-2 agonist activity to decrease blood pressure

Not used because its effects are partially blocked by normal beta-blocker regimens

29
Q

What is the mechanism of action of milrinone on HF?

A

Phosphodiesterase inhibitor

  • > prevents breakdown of cAMP in cardiac myocyte
  • > increases muscle contraction from increased cAMP levels
30
Q

What is a major side effect of concern with milrinone and why? Why would it be used over dobutamine?

A

Hypotension - more than dobutamine
Due to cAMP levels increasing in arteries, causing relaxation (beta-2-like effect)

Used because beta blockers don’t interfere

31
Q

What are other indications for positive inotropes in HF other than acute decompensation?

A

Used periodically for better quality of life despite increased mortality -> palliative care

Bridge therapy until heart becomes available for transplant or LVAD is put in

32
Q

What is the mechanism of action of Sodium nitroprusside and why is it not used for long periods?

A

Think of the lady in the nitroprusside boat in sketchy

Causes BOTH preload AND afterload reduction via vasodilatory effects.

Not used for long periods because it is metabolized to cyanide, which becomes toxic

33
Q

How can liver and kidney problems predipose to nitroprusside toxicity?

A

Liver - Unable to metabolize cyanide quickly to thiocyanate

Kidney - cannot expel thiocyanate quickly

34
Q

What are the symptoms of cyanide and thiocyanate toxicity?

A

Cyanide - drug will look like it stops working, CO drops off and patient goes into lactic acidosis

Thiocyanate - CNS symptoms, abdominal pain, convulsions
-> from renal insufficiency or too much infusion quickly

35
Q

What does it mean when you find yourself in all of the following states / what do you need to do to get out of this?

  1. Normal cardiac index but increased pulmonary capillary wedge pressure
    - > pulmonary congestion
  2. Normal pulmonary capillary wedge pressure but decreased cardiac index
    - > hypoperfusion
  3. Decreased cardiac index with increased pulmonary capillary wedge pressure
    - > pulmonary congestion and hypoperfusion
A
  1. Pulmonary congestion -> volume overload despite adequate cardiac output
    Give diuretics / vasodilators
    -i.e. furosemide + nitroprusside
  2. Hypoperfusion -> stop giving diuretics!! CO is okay but fluids are low. Need IV fluids.
  3. Pulmonary congestion and hypoperfusion systemically -> need inotropes!
    - i.e. dobutamine, milrinone, dopamine
36
Q

What is the theoretical action of low, medium, and high doses of dopamine?

A

D>b>a
Dopamine, beta, alpha

D1 receptors - maintain renal and mesenteric perfusion in hypertension

Beta1 - increased contractility and heart rate
-> main use in heart failure as an inotrope

Alpha1 - highest dose, increases afterload, blood pressure, and systemic vascular resistance.

37
Q

What are the two other major pressor drugs other than dopamine and their mechanism?

A

Epinephrine -> beta1/2 > alpha1
increases CO and SVR

Norepinephrine -> alpha1 > beta1, no beta2
increases SVR

38
Q

What are the indications to use a pressor agent?

A

Systolic BP <90 mmHg WITHOUT hypovolemia

-> cardiogenic or septic shock

39
Q

What are the side effects of concern with pressors?

A

Increased arrhythmogenesis due to increased HR, increased myocardial oxygen demand

40
Q

What drugs are typically used to treat diastolic heart failure, but are actually harmful in systolic heart failure?

A

Non-DHP calcium channel blockers: Verapamil and diltazem

Pathophysiology - Cardiovascular (24 decks)

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