Inotropic Drugs-Limitations in Heart Failure Flashcards Preview

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Flashcards in Inotropic Drugs-Limitations in Heart Failure Deck (26):
1

NE effects

↑ sympathetic outflow → NE effects on β-receptors (1 and 2) and α2 receptors on the myocardium

*downregulate β-1

2

NE Response on:
□ β1, β2, α1 →
□ β1, β2, α1 →
□ β1, β2 →
□ β1, β2 →
□ β1 →

□ β1, β2, α1 → cardiac myocyte response
□ β1, β2, α1 → positive inotropic response
□ β1, β2 → positive chronotropic response
□ β1, β2 → myocyte toxicity
□ β1 → myocyte apoptosis

- too much response can lead to myocyte death/increased arrhythmias

3

Benefits of β-blockers

§ Prevent downregulation of B1 receptor
§ Prevent Apoptosis/Oxidative stress
§ Prevent hypertrophy/fibrosis
§ Prevent increased arrhythmia potential

- b-blockers as shield: upregulate b-1 and prevent negative effects
- reduce mortality and increase EF

4

When should treatment with a beta blocker be started?

1. Tx with a diuretic so that patient has minimal evidence of fluid retention.

2. Tx with an ACE inhibitor for at least 2 weeks.

3. No recent use of IV vasodialators or positive inotropic agents

4. Systolic blood pressure > 90 mmHg

5. Heart rate > 60 beats/min (unless tx with a pacemaker)

6. Absence of end-organ failure

5

Neprilysin inhibitors
example

Valsartan
Sacubitril
L8Q657

6

How does Neprilysin inhibitors work?

when we get additional stretch of atria or ventricles → get release of B-type natriuretic peptide (pro BNP) → converted N-terminal BNP → cleaved to BNP (which has awesome effects)

- well Neprilysin is a dick that degrades BNP. So Neprilysin inhibitors are cock blockers

7

Beneficial Effects of BNP

○ Vasodilator reduces afterload
○ Reduces sympathetic tone
○ Reduces aldosterone
○ Natriuresis, diuresis

8

HFrEF vs HFpEF
what type of dysfunction?

o Heart failure with reduced ejection fraction = HFrEF
- Left ventricular systolic dysfunction = LVSD

o HF with preserved ejection fraction = HFpEF
o Preserved systolic function = PSF
- Diastolic dysfunction

9

Main Mechanism of Digoxin

○ Blocks Na/K ATPase, get accumulation of Na on intracellular side
§ NCX then swaps Na for Ca
§ Increase force of contraction
§ That's why digoxin is thought of as a weak inotrope

○ Other mechanism of digoxin:
§ Neurohormonal modulator via baroreceptors

10

Secondary mech of Digoxin

Neurohormonal modulator via baroreceptors
□ Indiv. can lose sensitivity when heart is overstimulated, symp nervous system is always on and para doesn't respond well

Dig may increase parasymp activity by increasing sensitivity and decreasing symp sensitivity
*remember: digoxin is a weak inotrope that increases F of contraction

11

How is digoxin excreted?
Half life?
Does it have a large or narrow therapeutic window?

Renally
38 hours: takes ~7 days to get to steady state
Narrow

12

Which drugs used in conjunction of Digoxin will double it's [ ]?
(meaning if you are using any of these agents, you have to drop dig levels by 50%)

Quinidine,
varapamil,
amiodarone, draniderone, Propafenone,
itraconazole,
arythromycin,
Erythromycin,
clarithromycin,

13

Digoxin toxicity:

hypokalemia
hypercalcemia
hypomagnesemia

14

How do patients present with Digoxin toxicity? (symptoms)

Neurological: weakness, confusion
Visual: sensitivity to light, yellow halos around eyes, blurred vision
Cardiac: bradycardia, heartblock, arrhythmias
GI: nausea vomiting, ab pain
Electrolyte: hyperkalemia


*recall: hypokalemia
hypercalcemia
hypomagnesemia

15

role of digoxin in patients with HFrEF

Digoxin can be beneficial in patients with HFrEF, unless contraindicated, to decrease hospitalizations for HF

16

Diuretics
- list some
- what do they do

Bumetanide
Furosemide
Torsemide

→ reduced fluid volume

17

Inotropes
- list some
- what do they do

Dobutamine
Milrinone

→ augment contractility

18

Vasodilators
- list some
- what do they do

Nitroglycerin
Nitroprusside
Nesiritide

→ decrease preload and afterload

19

What does it mean when a pt is in :
- subset I "warm and dry"
- subset II "warm and wet"
- subset III "cold and dry"
- subset IV "cold and wet"

- subset I "warm and dry"
Normal
- subset II "warm and wet"
Congestion
- subset III "cold and dry"
Hypoperfusion
- subset IV "cold and wet"
Congestion and hypoperfusion

20

How do you warm up? How do you dry out?

Warm up: use inotrope (dobutamine, milrinone)
Dry out: use diuresis

21

Dobutamine

b-1 agonist to increase contractility,
slight peripheral vasodilation

22

Milrinone

PDE inhibitor, augments myocyte Ca utilization, moderate peripheral vasodilation

- indication: cold and wet

23

Inotropic agents like Dobutamine and milrinone are used specifically to treat patients with:?

1. To relieve symptoms and improve end-organ function
2. Patients with marginal systolic blood pressure (<90 mm Hg)
3. Patients with symptomatic hypotension despite adequate filling pressure
4. Unresponsive to, or intolerant of, intravenous vasodilators.

24

Dopamine MOA

endogenous precursor of norepinephrine-
excerts its effects by directly stimulating adrenergic
receptors, as well as, release norepi from nerve
terminals

25

Dopamine benefits:

RIP!!!
○ R - Renal
§ Dopaminergic, may improve renal output
○ I - Inotrope
§ Beta receptor
○ P - Pressor
§ Alpha receptor

Dopamine acts on different types of receptors

26

Dopamine adverse effects:

Arrythmic
Angina
Increased HR
Increased MAP