CHF

Question 1

neurohumoral impact

Answer 1

• PTs with HF have elevated levels of NE, Angio II, Aldo, endothelin, vasopressin, cytokines

Question 2

ACE In

Answer 2

• 1st line tx
• arteriovenous vasodilation –> increase CO
• no change in HR/contractility
• decrease MVO2
• in contrast to other vasodilators, no neurohumoral activation or reflex tachy
• “-pril”

Question 3

ARBs

Answer 3

• can be used in place of ACEI when cough is an issue
• can also be used in tandem with ACEI
• “sartans”

Question 4

Diuretics

Answer 4

• decrease volume and preload
• no direct effect on CO (bc PT is operating on flat part of curve) but if you unload too much volume you can decrease CO
• less flow to kidneys –> neurohormonal activation
• mostly furosemide is used (but only use them when you need them)

Question 5

aldosterone antagonists

Answer 5

• lower mortality but have to be used at low doses
• only use low doses bc it can cause hyperkalemia –> cardiac probs
• add to class C if creat and K+ ok

Question 6

beta blockers

Answer 6

• 2nd line tx
• inhibit adverse effects of sympa NS
• can only use Bisoprolol, metoprolol, carvedilol
• start at very low doses and increase gradually bc then are negative inotropes

Question 7

Digoxin

Answer 7

• inhibit Na/K ATPase –> intracellular Na builds up and drives the Na/Ca exchanger –> high intracellular Ca –> increases contractility
• also increases vagal efferent activity to heart –> decreased neurohormonal activation
• 2nd line tx because it improves quality of life but doesn’t prolong life
• narrow therapeutic-toxic window –> cardiac arrhythmias (increased Ca2+ –> DAD)
• kidney metabolism –> careful in kidney failure
• add to class C if frequent rehospitalizations

Question 8

dobutamine

Answer 8

• acute decompensated HF
• inotrope (front door approach)
• stimulates b1 receptors –> positive inotrope and chronotrope
• some beta2 and alpha receptor effects too
• continuous IV infusion (quick onset of action and t1/2)
• can develop tolerance after 24-48 hrs of same dose

Question 9

Milrinone

Answer 9

• acute decompensated HF
• inotrope (back door approach)
• inhibit phosphodiesterase IIIa: increased levels of cAMP –> increased contractility, HR and relaxation + vasodilation
• continuous IV infusion
• no development of tolerance
• short-term use only

Question 10

Nesiritide

Answer 10

• acute decompensated HF
• recombinant form of BNP –> natriuresis and diuresis
• vasodilation
• IV continuous infusion

Question 11

NYHA functional classifications

Answer 11

• Class I: disease but no limitations of physical activity
• Class II: slight limitations of physical activity (symptomatic with ordinary physical activity)
• Class III: symptomatic with less than ordinary physical activity
• Clas IV: symptomatic at rest

Question 12

compensatory mechs in HF

Answer 12

ANS

• increased HR, contractility, relaxation
• arteriovenous vasoconstriction

Kidney

• activation of RAAS –> arteriovenous vascoconstriction, Na and water retention

Other

• endothelin 1, vasopressin, BNPs, PGEs, FS mechanism, hypertrophy, altered peripheral O2 delivery, anaerobic metabolism

Question 13

JACC HF stages and recommended tx

Answer 13

• stage A: at high risk for HF (ie: have HTN atherosclerosis) but w/o structural HD or sx of HF –> ACEI
• Stage B: structural HD disease but w/o symptoms (prior MI, LV remodeling, low EF) –> ACEI and BB
• Stage C: disease and symptomatic –> ACEI, BB and diuretics/hydralazine/aldo antag
• Stage D: refractory HF –> hospice
• **can add digoxin in stage C or D and aldosterone antag

Question 14

hydralazine and nitrates

Answer 14

• use in place of ACEI/ARBs if they can’t be tolerated
• add as adjunct in class C if persistently symptomatic

Question 15

Acute decompensated HF hemodynamic profile and tx

Answer 15

1. wet –> elevated filling pressures –> diuretic/vasodilator
2. cold –> poor perfusion –> inotrope

Question 16

ADHF tx options

Answer 16

• diuretics to decrease volume/preload
• inotropes to improve contractility (dobutamine, milrinone)
• vasodilators and natriuretic peptide to decrease preload and afterload (nitroglycerin, nitroprusside, nesiritide)

Question 17

mortality benefit systolic HF vs symptom relief

Answer 17

• ACEi/ARBs, BB, ASA (mortality benefit)
• diuretic and digoxin (sx relieft)

Question 18

diastolic HF

Answer 18

• LV thickening
• don’t want to give diuretics, nitrates or CCB because a thick, stiff wall relies on high preload to fill enough