Week 2 cardiac and heartfailure Flashcards by India Hofer

what are the four classes of drugs used to treat HTN

ACEI, ARB, CCB, Thiazide diuretics

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what is the suggested initial therapy for hypertension?

thiazide diuretics

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what drug class does captopril, enalapril and lisinopril fall into?

ACEI

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what drug class does candesartan, losartan, valsartan and ibesartan fall into?

ARB

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what drug class does amlodipine and diltiazem fall into?

CCB

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what drug class does indapamide fall into?

thiazide diuretic

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for all patients with CKD what are the drug classes of choice. regardless of race

ACEI and ARB

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what is the mechanism of action for thiazide diuretics

inhibit sodium transport in the distal tubule, and enhanced calcium reabsorption

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what kind of monioring is necessary for thiazide diuretics

BP, sodium & potassium monitoring, calcium monitoring, CrCl

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at a creatinine clearance of <30 what happens with thiazide diuretics

they tend to lose ofptimaleffect

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what kind of dietary problems can negate the effects of thiazides?

high sodium diets

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what drug class should be avoided when taking thiazide diuretics and why?

NSAIDs can lead to sodium retention

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what is the MOA for ACEIs?

inhibit the enzyme that converts angiotensin 1 to angiotensin 2 and prevents bradykinin activation

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what is the overall effect of ACEI drugs

prevent vasoconstriction leading to decreased BP

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what benefits to ACEIs have for diabetics?

prevents kidney damage and slows proteinuria

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what benefit do ACEIs have on heart failure?

decreasing blood volume and slows cardiac remodeling, decreases preload and afterload

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what is the monitoring needed for ACEIs?

potassium: can cause hyperkalemia , BP, respiratory symptoms

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While ACEIs can help with renal failure and diabetic nephropathy, what renal condition are ACEIs contraindicated for?

bilateral renal artery stenosis

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what is the interaction between ACEIs and bilateral renal stenosis?

reduced GFR and renal failure can occurr

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at what point in ACEI treatment can angioedema occur?

anytime in treatment

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what drug can substitute ACEIs when dry cough is bothersome and angioedema occurs?

ARBs can be prescribed due to infrequency of reported effects

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what is the mechanism of action for ARBs?

antagonize angiotensin 1 at the receptor no bradykinin effect

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what condition is ARB drug treatment contraindicated in?

bilateral renal artery stenosis. can lead to decreased GFR and lead to renal failure

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what hypertension drug classes are contraindicated in pregnancy?

ACEI and ARBs.

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why do ACEIs cause dry cough and angioedema?

due to inhibition of bradykinin

what is the MOA for CCBs

inhibit the influx of calcium in arterial smooth muscle causing relaxation and vasodilation

what is the physical effect of CCBs

decrease arterial smooth muscle tone leading to vasodilation, decrease cardiac contractility, decrease HR

what are the two classes of CCBs?

dihydropyridines and non-dihydropyridines

what heart conditions can CCBs in general, treat?

HTN, angina, arrhythmias

while CCBs can treat angina, what subgroup is primarily for HTN not angina or arrhythmias?

the dihydropyridines (amlodipine, nifedipine, isradipine) the -pine drugs

what drug class do the -pine drugs fall into?

dihydropyridine calcium channel blocker antihypertensives

what is a cardiac adverse effect of dihydropiridines?

reflex cardiac stimulation and increase in oxygen demand

which didydropiridine should never be given in its immediate release form for HTN treatment and why?

nifedipine IR should never be administered for HTN due to the risk of reflex tachycardia and sudden drop in BP.

why do dihydropiridines cause reflex tachycardia?

because of vasodilation which is more peripheral. the heart responds by increasing HR

what drug class do Verapamil and diltiazem fall into?

non-dyhydropiridine calcium channel blockers

what is the main diffierence between dihydropyridines and non-dihydropyridines?

the dihydropyridines (pine drugs) are more effective in peripheral smooth muscle (arterial) and the non-dihydropyridines are generally more cardiac specific and cause less reflex cardiac stimulation

why is verapamil less likely to cause reflex cardiac stimulation?

because is is more specific for myocardial calcium channels

which CCB is more commonly indicated for the use of arrhytmias and angina?

verapamil a non-dihydropyridine calcium channel blocker. it tends to decrease myocardial oxygen demand

though diltiazem (cardizem) is still effective on arterial smooth muscle like a dihydropyridine it has less chance of causing WHAT adverse effect?

reflex cardiac excitation/stimulation

what are the ADEs to monitor for in the dihydropiridines?

flushing, Headdache, excessive HoTN, reflex tachycardia

what ADEs should be monitored for in the use of non-dihydropyridines?

excessive bradycardia, AV heart block, decreased cardiac contractility

the non-dihydropyridines should be avoided in what condition

heart failure with ↓ ejection fraction and decreased systolic dysfunction

what are ARNIs? what are they used for

angiotensin-receptor, necrolysin inhibitor, used for heart failure in NYHF classes II and III

what qualifies a patient for ARNI treatment

NYHF classes II and III not well studied in IV, or stage C HF

what is entresto?

an ANRI sacubitril/valsartan

what are the general dosing rules for entresto?

start at low doses for patients who are not on ACEI/ARB in the past double toe doses every 2-4 weeks until target is reached

ARNI drugs should not be administered to what patients

patients with history of angioedema from ACEI drugs. alszeimers patients. may increase the progression of alszeimers pregnant women patients with bilateral renal artery stenosis

when switching from an ACEI/ARB to an ARNI what should providers ensure happens to prevent profound HoTN

give a 36 hour washout period between drugs

what ADEs should you monitor for when initiating entresto/ ARNI drugs

HoTN, angioedema, renal failure, hyperkalemia

what is the mechanism of action for beta blockers

antagnoize beta1 receptors. block epi/norepi

what is the physiologic action of beta blockers

↓ decrease sympathetic effects on the kidneys, heart and vasculatre decreasing water retention, causing vasodilation and decreasing the effects of arrhythmias

are beta blockers symptomatic support or do ehtye decrease mortality in HF

decrease mortality

what are the adverse effects of beta blockers

Hypotension, bradycardia, postural hypotension, fatigue, masking hypoglycemia

in what condition is the use of beta blockers contraindicated

asthma , COPD, reactive airway disease

what is the preferred beta blocker category for patients with COPD

beta1 selective agents.

what should diabetics be counseled on before starting beta blockers

check blood glucose frequently as beta blockers can mask symptoms of hypoglycemia

what is Ivabradine

a medication for heart failure

what are the conditions that must be met before starting ivabradine

symptomatic NYHA class II-III, LVEF /=70bpm

what is the MOA for ivabradine

inhibits electrical current to the SA node slowing the HR. with little to no effect on BP or contractility

what are teh adverse drug effects of ivabradine

bradycardia and visual disturbances.

what drug can be combined with metolazone to treat HF?

loop diuretics

is ivabradine effective for mortality

no, but it leads to less hospitalizations related to heart failure.

at labs should be monitored for the use of loop diuretics

potassium, sodium and chloride due to risks for hyokalemia especially

what is metholaone?

a distal tubule diuretic

what lab should you monitor for when giving an ACEIs/ARBs and aldoseterone antagonist?

potassium, both can cause increased potassium levels.

are potassium sparing diuretics AKA aldosteron antagonists effective in decreasing mortality?

Yes

at a CrCl of 29 would you suggest the use of an aldosterone antagonist such as spironolactone?

no, because there is an increased risk of hyperkalemia if CrCl is <30

does digoxin help with decreasing mortality in heartfailure patients?

no, It is for symptom management and improving quality of life .

what is the mechanism of action for dixoxin:

inhibits sodium pump in heart to increase onctractility, decrease oxygen demand and increase cardiac output.

what are the symptoms of digoxin toxicity

AMS, N/V, halo effect visual changes, bradycardia, arrhythmia