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Cardiology > Heart Failure > Flashcards

Heart Failure Flashcards

1
Q

What are the 4 basic mechanisms of heart failure?

A
  1. Increased blood volume/preload
  2. Increased resistance to blood flow/afterload
  3. Decreased contractility
  4. Decreased filling
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2
Q

Causes of increased volume/predload

A

Mitral regurg

Aortic regurg

Volume overload

L to R shunts

Chronic kidney disease

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3
Q

What can cause increased afterload?

A

Aortic stenosis or coarctation

Htn

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4
Q

What can cause decreased contractility?

A

Ischemic cardiomyopathy (MI)

Myocarditis

Toxins (anthracycline, alcohol, cocaine)

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5
Q

What can cause decreased filling?

A

mitral stenosis

constriction

restrictive cardiomyopathy

hypertrophic cardiomyopathy

infiltrative cardiomyopathy

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6
Q

What’s the difference between systolic/diastolic HF?

A

Systolic: impaired filling, concentric hypertrophy (thick walled heart), usually in older patients due to htn

Diastolic: impaired contraction, eccentric hypertrophy, all ages, related to coronary artery disease

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7
Q

What is the difference between compensated and decompensated heart failure?

A

Compensated: body counteracts heart failure

Decompensated: compensation ends –> congestion (orthopnea, ascites, edema, abdominojugular reflex), low perfusion (narrow pulse pressure, cool extremities)

Can be warm/cold or wet/dry

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8
Q

What’s the difference between high output failure/low output failure?

A

High output: decreased vascular resistance (anemia, obseity, preg, etc)

Low output: decreased CO (low CO)

Both ultimately cause decreased fullness of the arterial vasculature

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9
Q

What are the 3 types of diuretics?

A

Loop diuretics: impair generation of hypertonic interstitium –> less ater reabsorption in collecting duct
**these are most effective***
- furosemide, bumetanide, torsemide

  • *Thiazide**: act on distal convuluting tubule & potentiate sodium and water excretion in the setting of loop diuretics
  • hydrochlorothiazide

K+ sparing: spironolactone, eplerenone

All are given IV

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10
Q

When do you use diuretics? SE?

A

Treat excessive volume (preload)

Symptomatic relief

SE= dehydration, hypoalkemia, contraction alkalosis, ototoxicity

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11
Q

What is the mechanism of nitrates?

A

Vascular smooth muscle vasodilation via producing NO in ET cells

Mostly venodilator, at low dose

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12
Q

When do you give nitrates?

A

Relive pulmonary congestion

Relieves chest pain if related to coronary artery vasoconstriction

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13
Q

What are the SE of nitrates?

A

HA, tachyphylaxis

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14
Q

What is the mechanism of action of hydralazine?

A

Arterial vasodilator

Treats htn by reducing afterload

SE=reflex tachycardia, lupus-like syndrome

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15
Q

What’s the mechanism of action of ACEI? SE?

A

Inhibits angiotensin converting enzyme, blocking conversion of angiotensin I to II

Blocks the action of angiotensin II wich includes vasoconstriction, Na/H2O reabsorption, release of aldosterone, myocardial fibrosis (remodeling)

Effect is to promote vasodilation –> decrease BP & decrease afterload, facilitate natriuresis, reverse remodel the heart
** improves survival ***

SE: hypotension, renal insufficiency, hyperalkemia, cough, angioedema

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16
Q

Which meds improve survival?

A

Beta blockers

ACEI

Angiotensin receptor blockers

Aldosterone antagonists

Nitrates/hydralazine

17
Q

What is the mechanism of angiotensin receptor blockers?

A

ARBs block AT1 receptor– effectively same as ACEI

ARBs more effective bc angiotensin II can be generated via ACE escape pathway

Anti-hypertensives

SE=same as ACEI except cough (bc don’t inhibit bradykinin pathway)

18
Q

When are ARBs indicated?

A

In hypertensive patients

Heart failure pt’s who can’t tolerate ACEI

You can also administer ARBs with ACEI

Don’t use in combination with aldosterone antagonists!!

19
Q

What is the mechanism of action of beta blockers?

A

Block deleterious effect of catecholamines on the myocardium: negative inotrope via SNS blockade

Chronic beta receptor stimulation during heart failure –> downregulation and desensitization of beta receptors

Beta blockade allows for gradual re-upregulation of beta receptors (increased receptor density) while blocking the incessant catecholamine toxic effects on the myocardium

20
Q

What are the effects and SE of beta blockers?

A

Negative inotrope

Morbidity and mortality benefit

SE: heart block, hypotension, fatigue, elevated TG’s, decreased HDL, masks hypoglycemia

21
Q

When should you not use beta blockers?

A

Don’t give to pt’s with decompensated CHF

22
Q

What is the mechanism of aldosterone antagonists?

A

Modest diuretic: blocks Na reabsorption and K excretion of collecting duct

Reduced mortality when used in heart failure patients after best medical therapy

SE=hyperalkemia

Gynecomastia with spironolactone (not eplerenone)

Cardiology (13 decks)

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