Acute Heart fail Drugs (pt 2 HF cases) Flashcards Preview

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Flashcards in Acute Heart fail Drugs (pt 2 HF cases) Deck (40):
1

Dopamine actions

Stimulates release of catecholamines
Always hypothesized to be renal protective, but has never been shown to clinically significant.

2

Dosing of Dopamine changes it's affects at
low doese of 2-5 mcg/kg/min:
doses greater then 6 mcg/kg/min:
doses of 10 mcg/kg/min:

Lower doses 2-5 mcg/kg/min exert effects on dopamine receptors and b receptors.
At doses greater than 6 mcg/kg/min:tachycardia without increased inotropypredominates.
at 10 mcg/kg/min: Afterload increases due to effects on a receptors

3

ACtion of Dobutamine:

Predominant action is a β1 agonist with weak β2 activity.
Increases contractility with mild vasodilator effect.

4

Predominant action is a β1 agonist with weak β2 activity.
Increases contractility with mild vasodilator effect.

Dobutamine

5

Side effect of Dobutamine

1. ARRHYTHMIA
2. ANGINA
3. HYPERTENSION
4. TACHYCARDIA

6

Levosimendan

Calcium sensitizer and Vasodilator
Acts on Troponin C to increase its sensitivity to calcium.
At high concentrations can be a phosphodiesterase III inhibitor

7

Acts on Troponin C to increase its sensitivity to calcium.
At high concentrations can be a phosphodiesterase III inhibitor

Levosimednan

8

Levosimendan effects on:
LVEDP:
Afterload:
SV:

Decrease LVEDP
Decrease Afterload
Increase Stroke Volume

9

What are the issues when using ionotropes in ADHF?

Arrythmias, hypotension, increased troponin release, increases in-hospital stay and 6 month mortality, doesn't decrease hospital stay

10

What do we have to keep in mind when dosing diuretics in Heart fail pts?

dosing needs to be higher to achieve same effect we seen in non-HF pts.

11

What is the Braking phenomenon in regards to diuretic therapy?

“Braking” phenomenon
– Long-term loop diuretic administration results in a reduced natriuretic response
– Relative or absolute contraction of the extracellular fluid volume,
resulting in reduced delivery of solute to the proximal tubule via the RAAS and SNS as well as by enhanced distal nephron solute
reabsorption via adaptive epithelial hypertrophy and hyper function.

12

What is "rebound" phenomenon in regards to diuretics?

“Rebound”
– Infrequent dosing may lead to sodium retention that exceeds natriuresis.
– Divided doses to help with this, but hold off on it as long as possible

13

Why is long term tolerance an issue in Diuretic therapy in HF pts?

Long-term Tolerance
– Tubular hypertrophy to compensate for salt loss

14

Pt comes in with heart fail and your attending stays you will start them on diuretics, which one do you start them on?

Furosemide admin first; in IV as bolus or continous... if it's refractory... switch to bumetadine

15

What type of electrolyte abnormalities do we see in diuretics?

 HYPOKALEMIA
 HYPOMAGNESEMIA
 HYPONATREMIA

16

These drugs cause renal insufficiency when given with digoxin as well as gout exacerbation and cause muscle cramps if given too quickly.

Diuretics

17

You attending had you administered Bumetanide adn mirinone to pt in heart fail. Their saturation went up to 68% but the congestion isn't improving... what do you do next?

re-eval (most likely have Na and fluid restriction)
Increase doses of loop diuretic or do continuous infusion. Additionally, add a second type of diuretic orally (metolazone or spironolactone)or IV chlorothaized

18

74 yo w/ longstanding history of poorly controlled HTN, DM and dyslipidemia; presents saturday AM with shortness of breath and wt gain; went to fish fry, didn't take meds and took ibuprofen for back pain: medications include atenolol 25mg twice daily, HCTZ 25mg
daily, atorvastatin 20mg daily
BP 178/94 mm Hg, HR 90
• PE: Regular, crisp S1, S2, +S3, +S4
• JVP 8cm above clavicle
• Lungs clear with decreased BS at both bases
• 2+ LE edema
• Labs: Normal, except for NT-pro-BNP 4000
Dx?

Warm and Wet
increased JVD is sign of 'wet' as well as the LE edema (or any edema)
Not seeing signs of renal dysfunction or note of cool extremeties and labs aren't showing renal dysnfunction so we think more warm as all those listed are signs of cool

19

Most pts wth acute decompensated HF fall into what category?

Wet and Warm

20

What are our key therapy goals in pts with wet and warm heart fail?

Decrease the filling pressures (LVEDP and PCWP)
Most of the time use IV diuretics and may need vasodialators

21

What vasodialators do we use in ADHF?

Nitroglycerin, nitroprusside, nesiritide

22

Effects of increasing doses of vasodialators:
Afterload:
Stroke Volume:
LVEDP:
Preload:

Afterload decreases
SV increases
LVEDP decreases
Preload decreases

23

IV nitroglycerin hemodynamic effects:

venodialator; arterial vasodilator at high doses
decreases filling pressure at low doses; at high doses, decreases SVR and increases cardiac output
Increased coronary blood flow

24

IV nitroglycerin has several major limitations; what are they?

headache, hypotension (especially if filling pressures are low), prolounged profound hypotension and bradycardia (rare), tachyphylaxsis and 20% don't respond

25

Nitropusside hemodynamic effects

Balanced vasodilator for both veins and arterioles and decreases filling pressure, SVR, PVR, and increases CI

26

venodialator; arterial vasodilator at high doses
decreases filling pressure at low doses; at high doses, decreases SVR and increases cardiac output
Increased coronary blood flow

IV introglycerin

27

Major limitations of nitroprusside:

Cyanide toxicity; manifested by nausea and 'feeling weird' and seen with higher doses
occurs in setting of low hepatic reperfusion d/t low CO
Accumulation of thiocynate: occur over days during chronic use; especially with impaired renal function

28

Pt has Wet and Warm heart fail, what drugs in additoin to diuretics should we give them?

NONE:
ionotropes; ischemia/arrythmias and death
nesiritide: placebo
vasopressin antagonist: no sustained benefit

29

You are trying to decide if you should give IV vasodialtors or ionotropes to pt with heart fail... how do you make your decission?

depends on systemic vascular resistance and BP
If SVR is high, check the SBP!
SBP >/= 85mmHg: use Vasodialtor
SBP< 85mmHg: use Ionotrope + IABP

30

Pt has SBP of 100mmHg, do you use vasodialator or ionotrope +IABP?

over 85mmHg use Vasodialator; if its under use ionotrope

31

When do you give pt nitroprusside if they have acute decompensated heart fail? and does it help overall mortality?

for pts with SBP above 85mmHg and it does help with mortality

32

Mech of ACE inhibitors targeting afterload:

Inhibition of Angiotensin binding of the AT1
receptor to stimulate vasoconstriction
AT1: vasoconstriction, cell growth/prolif/ aldosterone release/ Na and water retention/ CV hypertrophy/ inhibits renin release

33

What does AT2 do?

vasoD, inhibits hypertrophy, antiproliferation, antiproliferation, mediates NO and PGI2, renal Na excreation

34

Not currently approved in the United States. It is sensitizes myofilaments to calcium,
and opens peripheral potassium channels in the vasculature.

Levosimendan:

35

Mixed alpha and beta agonist depending on the dose used.
1-5 mcg/kg/min stimulates
contractility.
Increasing dose > 5mcg/kg/min stimulates heart rate and vasoconstriction.

Dopamine

36

Phosphodiesterase 3 inhibitor acts by preventing the degradation of cAMP thereby
increasing the amount of bioavailable cAMP. Severe hypotension if bolused

milrinone

37

Beta agonist increases heart rate and contractility, but also peripheral vasodilation.

Dobutamine

38

drugs work on increasing myocardial contractility through stimulation of the beta adrenergic
receptor, or through intracellular signaling which results in changes in intracellular calcium

Ionotropes

39

Major issue with ionotropes and what type of heart fail pt gets them?

major complications of all these medications are the increased risk of tachyarrythmias, and most also
cause hypotension. They are reserved for the cold and wet patient who is refractory to other therapies

40

Why is the use of vasodialtors so important at an afterload reducer?

ejection period starts when aortic valve opens, if pressure of aorta can be decreased, the aorta will open earlier and allow more blood to eject per Stroke... ultimately reduces BP