Drugs for Heart Failure Flashcards
What used to be the main treatment for heart failure?
Digitalis
Characteristics of diastolic heart failure
Prevalence approx 40-60%
More common in women
Concentric remodeling
Preserved EF
What makes DHF distinct from SHF?
DHF has poor tolerance of AFib
DHF has poor tolerance of tachycardia
DHF worsened by increased MAP
Can cause “flash” pulmonary edema
What does chronic compensatory remodeling include?
Aortic stenosis
Chronic HTN
Valvular regurgitation
ARB =
Angiotensin II receptor blockers
Aliskiren inhibits:
Conversion Angiotensinogen –> Angiotensin I
Renin
ACE inhibitors inhibits which conversion?
Angiotensin I –> Angiotensin II
What does Spironolactone inhibit?
Aldosterone’s action at the kidneys
What suffixes are associated with ACE inhibitors?
- prils
- sartans
Less Angiotensin II leads to:
Less vasoconstriction - decreased afterload
Less aldosterone secretion and lass sodium/water retention - decerased preload
Decreased cell proliferation and remodeling
Captopril MOA:
PKs (1/2 life):
Toxicities:
Competitively inhibit ACE
1.7 hrs.
Cough, angioedema
Losartan MOA:
Non-peptide angiotensin II receptor antagonist (ARB)
Valsartan 1/2 life
Candesartan 1/2 life
6-10 hrs, not a pro-drug
5-9 hrs, irreversible binding
Which ACE inhibitors have a long half-life and allow for 1x/day dosing?
Benazepril
Lisinopril
Valsartan/Sacubitril MOAs
Clinical applications:
S/E:
Valsartan antagonizes Angiotensin I receptors (ARB). Sacubitril inhibits neprilysin (NEP), which delays degredation of ANP.
HF, can be substituted for ACEI or ARB.
HypoTN, hyperkalemia, increased serum creatinine.
What drug class is recommended for first-line treatment of HF?
Which patients should get these drugs?
What are containdications?
ACEI
All pts. w/ LV systolic failure or LV dysfunction w/o HF.
Unable to tolerate Pregnant HypoTN Elevated serum creatinine Hyperkalemia
Carvedilol MOA
Effect:
Who should get it?
Used in tandem with?
Prevents down-regulation of beta-1 receptors and make them more sensitive to SNS activation.
Protects from arryhthmias, lower [renin], lower myocardial consumption, limits remodeling.
Patients who are STABLE w/ symptomatic CHF and LVEF < 40%.
ACEI
Ivabradine MOA
Clinical applications:
Disrupts funny current to prolong diastole and slow HR.
Pts. w/ resting HR > 70 bpm w/ LVEF < 35% (elevated HR and low EF).
Sprinolactone MOA
Benefits of Spironolactone:
Why is it often under-utilized?
Competitively inhibit Aldosterone by increasing plasma K+ and decreasing Na+ and volume.
Decrease myocardial fibrosis
Reduce morning rise in HR
Reduce mortality/morbidity
There is a fear of hyperkalemia.
Damaged heart vasculature can synthesize what?
Aldosterone post MI
Recommended restriction of salt/day
< 3 gm salt/day
What does Furosemide inhibit?
What is the major toxicity?
Na+/K+/2Cl- cotransporter
Sulfonamide
What diuretic is used for patients with a sulfa allergy?
Ethacrynic acid
What is the 2-drug combo given to only AAs?
Isosorbide dinitrate (to dilate vv. and lower pre-load) and hydralazine (dilate aa. and lower afterload)
Major toxicity of Hydralazine?
Drug-induce lupus
Digoxin MOA
Benefits:
Competes w/ Na+/K+ ATPase to increase inotropic effect.
Increased CO
- less SNS activity
- increased urination
- reduced renin
ECG changes w/ Digoxin at therapeutic levels:
Toxic levels:
Depression of ST segment and increased PR interval
AV dissociation - no relationship between P and QRS
