Cardio pharm- heart failure meds

which 4 med classes decrease mortality in heart failure

beta blockers (metoprolol, bisoprolol, carvedilol to be specific)

ACEs

Spironolactone

Hydralazine

T/F: Beta blockers can be used for mild to moderate heart failure and are often used in combo with ACEs

T

T/F: hydralazine can be used in acute heart failure and hypternsion

T- how do we know this?

we know hydralazine is an HTN med (its an arterial dilator) and we know its good for heart failure bc its one of the 4 that decreases mortality in heart failure (beta blockers, ACEs, spironolactone, hydralazine)

Milrinone is a

beta1 agoonist

PDE3 inhibitor

Na+/K+ ATPase inhibitor

PDE3 inhibitor

Dobutamine is an beta1 agonist, meaning

it stimuates Beta1 which we know is in the heart, so it stimulates heart contractility, increasing cardiac output and increasing HR

this is good for emergency situations like acute decompesated heart failure or cardiogenic shock

remember , beta1 receptors are in the heart, not in the blood vesssels!!!! so they have no effect on blood vessel dilation/constriction thats our nonselective betablockers that also target beta2

so when were talking about beta1 were just talking about heart contractility

beta1 receptors increase contractility, so a beta1 agonist, will increase contractility, increasing CO and HR

this med works by inhibiting phosphdiesterase 3, increasing cAMP, thus increasing heart contractility

Miilrinone

Ivabradine ______ heart rate

increases

decreases

DECREASES

think Ivabradine, the I is the first part of the downward arrow, the v is the second, so it DECREASES heart rate

of the RAAS inhibitors, which decrease mortality rate in heart failure

cram the pance BASH mneumonic!! (dif than MONA BASH for MIs be careful)

these decrease mortality in heart failure (specifically reduced EF heart failure)

Beta blockers

Ace inhibitors

Spironolactone

Hydralazine + nitrates

so of the raas inhibitors, that includes the Ace inhibitors and Spironolactone

why are beta blockers (specifically bisoprolol, metoprolol, carvedilol) so great in reducing mortality for heart failure with reduced EF

bc they do all these amazing things

-decrease cardiac remodeling

-decrease mortality rate

-decrease cardiac work

-decrease renin release, decrease preload

-decrease afterload

-decrease peripheral resistance

but how do beta blockers decrease renin if theyre not part of the RAAS system?

beta blockers can decrease renin release even though they are not directly part of the renin-angiotensin-aldosterone system (RAAS), because they work by blocking beta-adrenergic receptors, which are found in the heart and other tissues. In the kidneys, these receptors play a role in regulating renin release. By blocking these receptors, beta blockers reduce the stimulation of renin secretion, thus decreasing the overall renin levels in the body

T/F: someone with heart failure with reduced EF is prob going to be prescribed an ACEinhibitor and beta blocker

T!!

remember the cram the pance BASH mneumonic (dif than MONA BASH for MI be careful)

BASH meds reduce mortality in heart failure

these decrease mortality in heart failure (specifically reduced EF heart failure)

Beta blockers

Ace inhibitors

Spironolactone

Hydralazine + nitrates

someone in ACUTE heart failure who also has hypertension, or who has acute cardiogenic pulmonary edema, what med would we use

hydralazine, isorbide nitrate (ISDN)

T/F: African Americans with heart failure typically respond better to hydralizine-nitrate than ACE inhibitors

T!!

Milrinone is a _______ inhinbitor

PDE3 inhibitor

MOA: Milrinone inhibits PDE3, which decreases cAMP breakdown, thus increasing cAMP levels, which INCREASES HEART CONTRACTILITY, and decreases preload/afterload in vascular smooth muscle

this is used in ACUTE DECOMPENSATED HEART FAILURE, POST HEART TRANSPLANT, ALTERNATIVE IN REFRACTORY CARDIOGENIC SHOCK

think of sending ur kid mail (specifically 3M post it notes) while theyre in summer cAMP

inhibits PDE3, Mirinone, cAMP levels increase (bc we inhibit cAMP breakdown)

ivabradine lowers heart rate by blocking ______ channels

HCN

by doing this it lowers heart raet and decreases SA node automaticity

ACE inhibitors are great at reducing mortality for HFrEF because they decrease _____

cardiac remodeling

this beta1 agonist is used for acute decompensated HF, cardiogenic shock, etc, AKA WHEN WE DESPERATELY NEED TO INCREASE CARDIAC OUTPUT

Dobutamine

think about it, beta1 BLOCKER affect beta1 receptors in the heart and BLOCK their effects aka they lead to decreased contractility, they slow down heart

whereas Dobutamine is not a beta1 blocker, it is a beta1 AGONIST, so it INCREASES heart contractility, when would we need this>? when our cardiac output is super low and we need heart to pump

PDE3 inhibitor Milrinone _____ heart contractility

increases

decreases

INCREASES- this is used for acute decompensated heart failure, aka when we need to get blood to our organs and our CO is low