Pharm - HF Flashcards
(12 cards)
ACE-I, ARB, Sacubutril/Valsartan
Who, Effect, Side Effects, Type
For Everyone with chronic HFrEF
ACE-i: “-prils”; suppress AII formation - lower VC, less Na retention, less symp stim, more bradykinin production; SE: Cough, angioedema, hypotension, hyperkalemia, TERATOGENIC
ARB: “-artan”; block AT1 receptor - less VC, less Na retention, less symp stim; SE: hypotension, hyperkalemia, TERATOGENIC
Sacubutril: Neprilysin Inhibitor = increased bradykinin = more VD; used in combination drug with valsartan - better outcomes but more expensive
Beta-Blockers
Who, Mechanism, Types, Side Effects
for EVERYONE with chronic HFrEF
M: blocks B-adrenergic signaling = less contractility = anti-anginal/anti-HTN ALSO: during HF - toxic neurohormonal milieu (overproduces EPI, overactivates receptor, activates B-ARK, phosphorylates receptor, B-arrestin binds, receptor internalized, heart desensitized to EPI); B-blockers RESTORE SENSITIVITY to EPI (need to gradually add drug to avoid dropping CO too much)
T: Metoprolol Succinate (long-acting, once daily drug, pure B-1 blocking - better choice for asthma/COPD patients)
Bisoprolol: pure B-1 blocking
Carvediol: B-1, B-2, A-1 antagonist (A-1: extra VD)
SE: Fatigue, Cognitive Impairment, Bronchospasm, Sexual Dysfunction, Hypotension
Other Indications: HTN, post-MI, arrhythmia
Mineralocorticoid Receptor Antagonist (MRA)
Who, Mechanism, Types, Side Effects, Other Indications
for Class II/III Sx pt’s with EF < 35%
M: in collecting duct, block aldo-R = less Na retention (diuretic) PLUS complex blocking of fibrosis/cardiohypertrophy
Spironolactone: cheap/generic; prodrug - active metabolites w/ long half-life = long time to steady state; SE: hyperkalemia, nonselective (sex steroid hormone - gynecomastia, irregular menses)
Eplerenone: very selective for aldo-R (no cross-reactivity), SE: hyperkalemia
OI: HTN, HFpEF!
Isosorbide Dinitrate (Nitrates) + Hydralazine (Mechanism, Dosing, Side Effects, who)
ID: mostly venodilation = decrease preload (help heart dilatation); some arteriodilation in coronary beds/face (anti-angina + flushing); TID (3x/day) DOSE; SE: headache, hypotension, tachyphylaxis (effect wanes over time)
H: arteriolar vasodilation (unknown mech - SMC relaxation = decrease afterload); TID DOSE; 3rd/4th line agent for HTN; SE: headache, tachycardia
Who: all pt’s particular african americans, use for pt’s who can’t tolerate ACE-I/ARBs; adherence is a challenge
Ivabradine
Mechanism, Side Effects
M: selective SAN inhibitor, acts on If in Phase IV - lower slope = slow HR
SE: bradycardia, visual disturbances
(Not often used clinically)
Digoxin
Mechanism, Use, Side Effects
M: Increase Contractility; Vagomimetic (slow phase IV depolarization)
U: dwindling in HF, but can improve sx and decrease hospitalizations
SE: toxicity (nausea, vomiting, yellow vision, pro-arrythmic) - tx with anti-digoxin Fab fragments
Diurectics
Mechanism, Purpose, Types
Purpose: as needed for volume control
Thiazides (HCTZ): block Na resorption in DCT - more common
Furosemide: block Na resorption in TALH - more effective
Life Saving Shock - Defibrillator
Type, Purpose
CRT-D: Cardiac Resynchronization Therapy-Defibrillator
helps heart walls contract in sync
Tx of Chronic HFpEF (5 types)
- Volume Control
- BP Control
- Spironolactone: evidence-based therapy
- Weight Management: Decrease inflammatory adipokines
- Exercise
3 Types of Acute Decompensated HF & Their Tx
- Warm + Wet (Congested + Perfused): most common type (high filling pressures, okay CO) - Tx: Diuretics + up-titrate HF meds
- Cold + Dry (Malperfused): least common type (fine filling pressures, low CO) - Tx: Inotropes, Vasodilators, LVAD or Heart Transplant - depends on pt wishes
- Cold + Wet (Malperfused + Congested): middle common (high filling pressure, low CO) - Tx: Vasodilators if high SVR, Inotropes, Diuretics
Signs of Congestion vs. Signs of Malperfusion
C: Orthopnea, high JVP, rales, ascities, leg swelling
MP: cool extremities, hypotension, low pulse pressure, sleepy, worsening renal fx, low urine output
Inotropes
Indications, Mechanism, Types, Side Effects, Use
I: only Class IV pts (Sx at rest)
B-1 agonists: dobutamine (B1+B2 agonist), dopamine (B1»A agonist), norepinephrine (B1=A agonist)
Phosphodiesterase-3 Inhibitors: Milrinone (bypass B receptor, directly increases cAMP, SE: Hypotension)
Use: palliation for end stage HF, may increase mortality but alleviates sx
