Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Julie Pharm > drugs used in heart failure > Flashcards

drugs used in heart failure Flashcards

1
Q

equation for CO

A

SV*HR = CO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

equation for bp

A

BP= CO*TPR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

response to decreased cardiac output

A

increase sympathetic nervous tone -> Increase HR, Stroke volume and renin release -> vasoconstriction
-Frank -starling compensation-> increased filling to increase wall tension and thus force results in increased preload
-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

three interventions for chronic HF

A

increase inotropy (inotropes)

  • reduce afterload ( ace inhibitors, vasodilators)
  • reduce preload ( diuretics and vasodilators)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

inotropic agents - MOA

A

increase contractility

  1. increasing resting Ca++ levels
  2. increase Ca++ entry during an action potential
  3. increasing Ca++ sensitivity of the contractile apparatus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Digoxin ( digitalis drugs)

A

MOA: inhibits Na/K ATPase -> which reduces the Na/Ca transporter and this increase the resting Ca++ levels and thus have a stronger condtraction when the AP is induced- strong CO

  • increase parasympathetic effects on the heart
  • reduces HR - better filling
  • blocks sympathetic effects on the heart - some vasodilation
  • no decrease in mortality
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

digoxin - toxicity

A

TOXICTIY: blocks Na/K ATpase is found in all tissues! so it gets blocked everywhere
30% show toxicity

cardiac: depressed AV function-> Premature ventricular depolarization
- av blockade

extras :
anorexia, nausea, diarrhea, color vision abnormality, disorientation, yellow vision, gynecomastia ( in males)

long half life( 40 hr for digoxin and 170 digitoxin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

digoxin- drug interactions

A

metabolized in the kidney and kidney function decreases with age -> increase of toxicity

  • agents that alter renal clearance can lead to elevation- quinidine
  • diuretics-> induce hypokalemia( thiazides and loop diuretics) and increase risk for toxicity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

sympathomimetic inotropes

A

increase Ca++ entry

- not used for Chronic HF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

diuretics

A

reduction in salt and water retention
- reduce ventricular preload -> reduces edema and reduction in cardiac size which increases pumping efficiency

  • thiazides -low ceiling ( med edema)
    -loop diuretics - high ceiling (bad edema)
    both can induce K+ loss -> exacerbate digoxin
  • **( reduce mortality) - spironolactone/ eplerenone -> aldosterone antagonist - K sparing diuretics
    - blocks aldosterone effects ( so we will reduce myocardial fibrosis,increase NO)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

vasodilators

A

reduce afterload ( hydralazine )
reduce preload ( nitrates)
verapamil and diltiazem DHP -> NO - inotropes
B.Dil - hydralazine/ isosnbide dinitrate - in African Americans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Beta Blockers

A 
LOW DOSES - reduce mortality 
MOA? : better filling 
- protects against arrhythmias 
-antiapoptotic 
-reducing renin release

carvedilol, metoprolol, bisprolol
M+B= beta 1 selective
C= non selective B1,B2 A1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

ACE inhibitors and angiotensin receptor blockers

A

DECREASE MORTALITY

reduce peripheral resistance -> afterload
by reducing aldosterone secretion -> reduce preload via reduction of salt and water retention.
- reduce long-term remodeling of the heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Dobutamine

A
  • Beta 1 selective agonist with high inotropic and low chronotropic activity
  • MOA - increase cAMP levels -> B1-> heart B2- > periperharl vasodilation

ACUTE USE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Amrinone and Milrinone

A

phosphodiesterase (PDE) inhibitor -> elevation of cAMP

  • orally active agents -> selective for cardiac isoform PDE3
  • decrease mortality
  • ACUTE IV treatment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Dopamine

A

low doses -> release NE at the heart-> leads to B1 adrenergic stim
- activation of dopamine receptors in periphery leads to inhibiition of NE release and vasodilation and enhanced renal and cerebral perfusion.

Higher doses-> direct alpha 1 adrenergic activit-> vasoconstrition.

ACUTE IV

17
Q

norepinephrince

A

ACUTE HF - when systolic pressure needs to be increased due to cardiogenic shock

18
Q

Nesiritide

A

recombinant version of the human B-type natriuretic peptide. Activates guanylate cyclase and leads to vasodilation, especially reducing right atrial pressure and pulmonary capillary wedge pressure. maybe a short-term mortality increase with it-> usefulness not proven yet

19
Q

standard step therapy for chronic HF

A
  1. reduce workload of the heart thru weight reduction, limiting activity
  2. restrict NA intake to help reduce fluid retention
  3. diuretics to reduce blood volume
  4. ace inhibitors
  5. b-blockers
  6. digitalis compounds
  7. vasodilators
20
Q

ACE inhibitors
MOA
hemodynamic effect
clinical notes

A

MORTALITY REDUCTION
inhibits AT II generation
-> decrease AT1 receptor activation

decrease afterload and preload

may cause hyperkalemia

21
Q

B-antagonist
MOA
hemodynamic effect
clinical notes

A

MORTALITY REDUCTION
competitive antagonist at B-adrenergic receptor -> decrease renin release

decrease afterload and preload

may be relatively contraindicated in severely decompensated heart failure

22
Q

spironolactone
MOA
hemodynamic effect
clinical notes

A

MORTALITY REDUCTION
competitive antagonist at aldosterone receptor

decrease preload

mortality benefit may be independent of hemodynamic effects ; may cause hyperkalemia

23
Q

Na+/ H20 resitriction
MOA
hemodynamic effect
clinical notes

A

decrease intravascular volume
decrease preload
may help limit edema formation

24
Q

diuretics
MOA
hemodynamic effect
clinical notes

A

inhibit renal Na+ reabsorption
decrease preload
furosemide most effective

25
Q

aquaretics
MOA
hemodynamic effect
clinical notes

A

competitive antagonist at vasopressin
->V2 receptor- decrease renal aquaporin expression and membrane trafficking , decrease free water reabsorption

decrease preload

increase solute-free urine output; increased serum sodium

26
Q

digoxin
MOA
hemodynamic effect
clinical notes

A

inhibits Na/K aTPAse - increase intracellular Ca2+ and contractility

increased contractility

delays atrioventricular nodal conduction

27
Q

organic nitrates
MOA
hemodynamic effect
clinical notes

A

increase NO -> venous smooth muscle relaxation
-> increase venous capacitance

decreased preload

reduces myocardial 02 demand

28
Q

dobutamine
MOA
hemodynamic effect
clinical notes

A

stimulates B- adrenergic receptors

increased contractility (b1) 
decreased afterload (b2)

ACUTE setting only

29
Q

inamrinone , milrinone
MOA
hemodynamic effect
clinical notes

A

inhibit phosphodiesterase
-> increase B-adrenergic effect

increase contractility
decreased afterload
decrease preload

used in the acute setting only

30
Q

increase contractility

A

inotropes; digoxin and beta agonist

31
Q

reduce afterload

A

Ace inhibitors and arterio vasodilators

32
Q

reduce preload

A

diuretics, ace inhibitors venodilators

Julie Pharm (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions