Cardiac 2 Flashcards
(39 cards)
Therapeutic goals for HF
Correct sodium and water retention and volume overload (diuretics)
block negative compensatory mechanisms (RAAS - ACEi, ARBs, DRIs, ARNIs)
Reduce inotopic, chronotropic, dromotropic workload of heart (BB, CCB)
Control precipitating and complicating factors -> lifestyle
Furosemide
Loop diuretic
SOA: ascending limb of the Loop of Henle -> potent and rapid
ADRs: all diuretics ADRs (Hypovolemia, hypotension, change in pH-Acid Base Imbalance, electrolyte imbalances, sleep disturbances, Hyperglycemia, Cholesterol levels: ↑ LDL ↓ HDL, Hyperuricemia (gout)) + OTOTOXICITY
Indic.: rapid or continued mobilization of fluid, IV for emergent or urgent diuretic needs (significant edema, HTN)
Interactions: all diuretics inter. + ototoxic drugs
Nursing Implications: K+ rich foods, changes to hearing/balance, orthostatics, daily weights, insulin, take in the morning
Hydrochlorothiazide (HCTZ)
Thiazide diuretic
**dependent on GFR (renal function is necessary)
SOA: early distal tube of nephron (moderate reabsorption, less than loop)
ADRs: all diuretics ADRs (Hypovolemia, hypotension, change in pH-Acid Base Imbalance, electrolyte imbalances, sleep disturbances, Hyperglycemia, Cholesterol levels: ↑ LDL ↓ HDL, Hyperuricemia (gout)) + HYPERCALCEMIA
Indic.: mild/mod. HTN, edema, postmenopausal osteoporosis (reabsorb Ca+)
Contras: hypersensitivity (SJS), renal disease
Nursing Implications: K+ rich foods, orthostatics, daily weights, insulin, take in the morning
Spironolactone/eplerenone
Potassium sparing diuretic (aldosterone antagonist -> also included in RAAS agents)
MOA: blocks action of aldosterone in the distal tubule; K+ retention
SOA: late distal tube of nephron (weak diuretic)
ADRs: HYPERKALEMIA + ENDOCRINE EFFECTS
Indic.: HTN, edema, HF, hyperaldosteronism, hormonal acne/PCOS, hypokalemia (used with other antihypertensives to counteract K+ loss)
Contras: hypersensitivity, hyperkalemia, anuria, AKI
Nursing Implications: monitor for K+ (salt substitutes and no supplements)
Captopril/lisinopril/enalapril
-pril
MOA: angiotensin converting enzyme inhibitors (ACEis) -> block vasoconstriction and fluid retention
ADRs: persistent cough, first dose hypotension, angioedema, hyperkalemia, fetal harm
Indic.: HTN, HF, diabetic & non- DM nephropathy, MI (reduce rate of cardiac remodeling)
Contras: renal failure
Interactions: other HTN, lithium, NSAIDs, ^K+ drugs
Nursing Implications: monitor first dose, hyperkalemia warnings and diet restrictions
Losartan
-sartan
MOA: Angiotensin II Receptor Blockers (ARBs) -> similar to ACEis
ADRs: first dose hypotension, angioedema, fetal harm
Indic.: HTN, HF, diabetic & non- DM nephropathy, MI
Contras: renal failure
Nursing Implications: monitor first dose
Sacubitril/valsartan
Angiotensin Receptor Neprilysin Inhibitor (ARNI)
(Entresto)
MOA:
Sacubitril - increase release of natriuretic peptides
Valsartan - ARB -> suppress neg effects from RAAS
ADRs: angioedema, hypotension, and some hyperkalemia, decreased GFR, fetal harm (all related to ARB)
Risks: low BP issues and renal stenosis
Aliskiren
MOA: direct renin inhibitor -> blocks entire RAAS
ADRs: less hyperkalemia, cough, and angioedema, BUT same fetal danger and some GI upset
Contras: pt w/ DM also taking ACEis or ARBs -> cause renal impairment
Carvedilol/Bisoprolol/SR metoprolol
guidelines just indicate these over the other BB specifically for HF
MOA: improve CO by reduce workload from SNS stim (dec. HR & BP, dec. dsyrythmias)
Start low and slow, not used alone (w/ACEi, ARB, ARNI, or diuretic)
ADRs: Fluid retention worsening HF(?), CNS fatigue, hypotension, bradycardia or heart block, may worsen HF in acute decompensated situation
Dapagliflozin/empaglifozin
(Jardiance)
SGLT-2 Inhibitors -> “-aglifozin”
MOA: blocks SLGT2 to increase glucose excretion via urine. More glucose in nephron -> H2O follows higher concentration to increase diuresis
not first line, but would add on later
typically used in DM but also now in HF (pt doesn’t have to be diabetic)
ADRs: more UTIs and genital infections, increased UOP, orthostatic hypotension, hypoglycemia (dizzy, lightheaded)
ADD PIC FROM SLIDES
Ivabradine
MOA: Blocks channels responsible for cardiac pacemaking (i.e.: SA Node) (dec. conduction, but not contractility)
Useful for patients who need additional beta blockade (on BBlkrs and HR is still >70) or those who have a contraindication to a beta blocker
ADRs: cardiac changes, hypotension, fetal danger
BiDil
Isosorbide Dinitrate plus Hydralazine
MOA: venous and direct acting arteriole vasodilation
BiDil is indicated as an alternative to ACEis and ARBs (contras or GFR too low) and in black pts w/HF
ADR: Hypotension, reflex tachycardia
Digoxin
used only as a 2nd line for HF when exhausted all other options and sometimes when there is a dysrythmia too
MOA: inhibits the enzyme Na+K+-ATPase to increase intracellular calcium in myocytes
positive inotrope -> increase contractility to improve CO
Toxic - direct relationship to potassium levels (hypokalemia** = increased risk for dig tox)
Narrow Therapeutic Range (0.5-0.8 ng/mL)
ADRs: GI upset and yellow/green visual disturbances (early warning signs) -> later: arrhythmias, bradycardia, ECG changes, AV/SV blocks, anorexia, N/V/D, fatigue
Implications: teach pt early signs, check apical 1 min and need recent K+ value, be very careful with diuretics, corticosteroids and other K+ lowering drugs
Digoxin interactions
Diuretics - hypokalemia
ACEis - increases likelihood of dig tox
Sympathomimetics (dobutamine) - increase risk of dysrythmias
Dobutamine
sympathomimetic - acts on beta1 only in heart
Used: HF & Shock
IV dobutamine - rescue med for severe, acute HF, short action
catecholamine
improves LVEF and improves kidney function through improved perfusion
Dopamine
sympathomimetic
Used: HF & Shock
activates beta1 and dopamine receptors (alpha1 at high doses)
catecholamine
continuous IV for short-term rescue of severe, acute HF
ADR: DYSRHYTHMIAS!!!
Milrinone
PDE3 Inhibitor
MOA: ^cAMP -> increases contractility and leads to vasodilation (“ino-dilator”)
continuous IV and only short-term for severe HF
Drugs to avoid in HF
Antidysrhythmics -> Can cause worsening of HF
Amiodarone: has been shown not to decrease survival
Calcium Channel Blockers: most increase risk of CV events
NSAIDS: promote Na+ and peripheral vasoconstriction
Nitroglycerin
MOA: vasodilates the arteries and veins -> decreases venous return (preload) and less volume in ventricles (workload)
**does not dilate atherosclerotic coronary arteries - instead pain relief comes from venous dilation
ADR: orthostatic hypotension, HA, tachy, flushing
Interactions: PDE5 Inhibitor (viagra) * look at safety alert life-threatening vasodilation
short term - sublingual or transligual spray (acute anginal attacks)
Isosobide dinitrate
long acting nitrate - SR oral
high dose due to first pass effect and admin on fixed schedule
may be instructed to have “drug-free” time by removing for 8 -12 hours
Metoprolol/atenolol/propanolol
1st line for prevention of angina by decreasing O2 demand of myocardium
Nifedipine/amlodipine
Dihydropyridines - CCB
MOA: selective to calcium block in arterioles **can relax coronary vasospasm
ADRs: severe reflex tachy
Indic.: angina, HTN, Prophylaxis for vascular headaches
Nursing Implications: assess HR before dose
Diltiazem/verapamil
Non-dihydropyridines
MOA: blocks calcium channels in heart and arterioles **can relax coronary vasospasm
Indic.: angina, HTN, supraventricular dysrhythmias (fib/flutter, SV tach)
Contras: use w/ caution w/ pts bradycardia, HF or AV block
Nursing Implications: no grapefruit**, interacts with Digoxin (toxicity)
Ranolazine
newest class of antianginal agents…preventative for angina
Clinical trials showed a reduction in anginal episodes and an increase in activity tolerance
+inotrope, vasodilator
MOA: Reduces accumulation of sodium and calcium in myocardial cells -> heart uses energy more efficiently
(exact mechanism is not understood)
ADRs: Prolonged QT interval, multiple drug interactions
Combined with other agents for angina – nitrates, BBlkrs, etc.
