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