Mod 6 part 1 quiz Flashcards
what is heart failure
progressive disorder r/t ventricular dysfunction, reduced CO, volume overload, and insufficient tissue perfusion
Symptoms of HF
fatigue
weakness
sob, orthopnea, PND
early satiety
increased JVP
edema
ascites
Natriuretic peptides
ANP and BNP hormones released in response to stretch of atria and dilation of ventricles
-promote arteriole and veins dilation
-promote loss of Na and water by kidneys
-helps balance vasoconstriction by SNS and angiotensin II caused by RAAS, but eventually becomes overwhelmed as CHF progresses
-BNP are key indicators for CHF status
lower BNP=better outcomes
HF treatment
-focus on increasing forward flow and decreasing backup of flow
-decreasing afterload
What medications increase forward flow by increase force of contractions
Inotropes- digoxin, milrinone, dobutamine
Beta blockers: decrease rate allowing increase filling time
Decrease backward flow/preload
vasodilators/nitrates-slow return from veins to heart
diuretics to decrease intravascular volume
Decrease afterload
-ace inhibitors and hydralazine
Prototype diuretics
Loop diuretics: furosemide (most effective)
Thiazide diuretics: E.g. Hydrochlorothiazide (moderate diuresis)-only used with minimal edema
Potassium sparing diuretics: Spironolactone
Furosemide (indications, MOA)
Indications: Pulmonary edema, CHF, hepatic congestion, resistant HTN that does not respond to other diuretics
MOA: acts in loop of Henle to block reabsorption of Na and Cl to prevent passive reabsorption of water
Diuretic complications
Severe dehydration or hypovolemia: may present as excessive weight loss, dry mouth, tenting skin, increase thirst
-acid base imbalance
-hypotension
-renal impairement
-electrolyte abnormlaities (hypokalemia)
-ototoxicity (increased risk with use of aminoglycoside)
Potassium sparing diuretics
-moderately increase urine production and decrease K excretion
2 subcategories of Potassium sparing diuretics
aldosterone antagonist: spironolactone
non-aldosterone antagonist: triamterene and amiloride
spironolactone
MOA,inications, complication
blocks action of aldosterone in the distal nephron, causes retention of K and increased excretion of Na
indication: blood pressure management, edema (not indicated for monotherapy), and CHF
Major complication: Hyperkalemia
Agents affecting volume and ion contents
Na and Chloride are influenced by diuretics
-loop and thiazides may cause hypokalemia, hypomangensmia
potassium sparing diuretics-helpful for hypokalemia
Monitor: BMP, Mg, phos closely w/ diuretic use
Prototype drugs acting on RAAS
ACEI: lisinopril
ARB:losartan
DRI: aliskiren
Aldosterone antagonist: eplernone
Drugs acting on RAAS
activated by low perfusion from the heart that causes release of renin
-arterial BP decreases causes decrease GFR
-effects results in vasoconstriction and renal retention of Na and water–>elevates BP
-ACEI blocks conversion of angiotensin I to angiotensin II
-ARBS block angiotensin II receptor to prevent effects
-both medications result in less vasoconstrictive effects–> lower bp
ACEI
angiotensin II regulates arterial bp through vasoconstriction and stimulation of aldosterone release
-MOA: 1. reduces angiotensin II levels–>dilate blood vessels, reduce blood volume, prevent pathological changes to the heart and blood vessels
2. increases level of bradykinin–> vasodilation
ACEI indications
-essential HTN
-HF-part of GDMT for SHF (EF<40%)
-MI
diabetic and nondiabetic nephropathy-renoprotective, can help slow progression of renal disease
ACEI adverse effects
-First dose hypotension-precipitous drop in BP after first dose
-increase levels of bradykinin may result in cough and/or angioedema
-hyperkalemia
-neutropenia
-renal failure-espeically in those with bilateral renal artery stenosis
-Do not use in 2nd or 3rd trimester of pregnancy
ARBs
indications: similiar to those of ACEIs (CHF, HTN, Post MI, stroke prevention, diabetic nephropathy/retinopathy)
MOA:blocking actions of Angiotensin II
1. dilate arteries and veins–>prevent pathologic changes in cardiac structure
2. decrease aldosterone release
-generally used when ACEIs are intolerable
Adverse effects: renal failure (especially in those with bilateral renal artery stenosis)
-compared to ACEIs less likely to develop hyperkalemia and/or angioedema
Used in place of an ACEI/ARB
Entresto (ARNI) angiotensin receptor neprilysin inhibitor
-newer med for stage II-IV HF
-found to be superior to enalapril
Adverse effects: angioedema, hyperkalemia, hypotension
Vasodilators
differ based on blood vessels they effect
hydralazine and manoxidile-cause selective dilation of arterioles
nitroprusside: cause dilation of arteriols and veins
Hydralazine
indications: Essential HTN and CHF (isosorbide dinitrate can reduce afterload)
-MOA: dilation of arterioles (little to no effect on veins)
Adverse effects: reflex tachycardia, increased blood volume, systemic lupus erythematosus-like syndrome
Low risk for postural hypotension, but when used with additional anti-hypertensive initiate at low doses
Inotropes
Oral: Digoxin
IV: sympathomimetic: dopamine and dobutamine
phosphodiesterase: milrinone
Digoxin
-cardiac glycoside
-indications: positive inotrope, second line CHF
-increased myocardial contractile force, increase CO, neurohormonal benefits
MOA: inhibits enzyme sodium-potassium adenosine triphosphatase–>calcium accumulation within myocytes causing contractile force
Adverse effect: dysrhythmias, anorhexia, N,V, fatigue, visual disturbances (yellow tinge, halos around dark objects)
Goal range .5-.8 ng/ml
Inotrope given for decompensated heart failure for short term therapy
phosphodiesterase inhibitirs: IV milrinone
milrinone
-used for severe decrease cardiac output and decrease organ perfusion
moa: increases myocardial contractility and promotes vasodilation
adverse effect: induce dysrhythmias, myocardial ischemia from increased metabolic demand
no identifiable cause, chronic and progressive
primary HTN
primary htn
Atreatment: lifestyle modifications–>exercise, dietary changes, weight loss, low Na diet
pharm treatment:
diuretics: decrease blood volume
vasodilators: decrease arterial resistance
CCB: block ca activated smooth muscle contraction
Aldosterone antagonist: block aldosterone
ACE/ARB: block RAAS
elevated BP d/t an identifiable primary cause
secondary HTN
secondary hypertension
common secondary causes relate to procceses that increase arterial resistance, blood volume, and/or co
common causes of secondary HTN
renal artery stenosis, cushings, hyperaldosteronism, hyperthyroidism, vasculitis, increase epi/norepi r/t pheochromocytoma
HTN guideline care
-refer to journal of american college of cardiology guidelines
-1st rec lifestyle modification
-if no improvement start single drug
-if inadequate response or poorly tolerated, then, add or transition to second agent
-assess reason for failure prior to making changes
-drugs must come from diff classes
-using 2 different drugs allows bp effects through diff mechanisms, allow for lower doses–>less risk for side effects, agents can offset adverse effects of the other
CCB
verapamil-nondihydropyridine- affects heart and blood vessles
nifedipine-dyhydropyridine, affects blood vessels
Verapamil indications
angina pectoris, essential HTN, cardiac dysrhymthimas
Verapamil MOA
MOA: block Ca channels in blood vessels and heart
Blockade at: 1. peripheral arterioles causing dilation and decrease arterial pressure 2. arteries and arterioles of heart to cause increase coronary perfusion 3. SA node reducing HR 4. AV node decreasing AV nodual conduction 5. Myocardium causes decreased force of contraction
Verapamil adverse effects
Adverse Effects: constipation, dizziness, facial flushing, headache, and ankle/feet edema
Diltiazem indications
CCB
Indications: same as verapamil (angina pectoris, essential HTN, cardiac dysrhythmias)
Diltizem MOA
blocks Ca channel blockers in the heart and blood vessels
Diltiazem adverse effects
less constipation than verapamil, dizziness, facial flushing, headache, ankle/feet edema
-exacerbate cardiac dysfunction with bradycardia, SSS, CHF, and heart blocks
What med causes chronic examoatous rash in the elderly
Diltiazem
How to improve non-adherence
-Patient education
-minimize side effects
-establish collaborative relationship
-simplify regimen by minimizing frequency and utilizing combo drugs
-cost effective regimen
-involve family
-schedule appointments at convenient times for patients
-Optimal diuretic for patients with renal impairment or decreased GFR
-Able to promote diuresis even with low renal blood flow
Loop diuretics- E.g. Furosemide, Torsemide, Bumetanide, Etha crynic
First line CHF
-beta blockers
