Heart Failure Flashcards
1
Q
discuss the body’s short term response to heart failure & what its consequences are.
A
- chronic HR
- due to systolic dysfunction
- inability of heart to pump sufficiently.
- intitially - BP drops & the body is inadequately perfused.
- body’s response is to: activate:
- baroreceptor reflex is activated: HR, contractility, vasoconstriction
- RAAS: promotes fluid retention, increasing afterload/preload
- body’s response is to: activate:
- due to systolic dysfunction
temporarily - cardiac output & blood pressure are restored
2
Q
discuss the long term effects of the body’s response to heart failure & its consequences.
A
continuous SNS activation puts extreme workload on an already weak heart.
- ultimately, there will be back up in pulmonary & systemic cirulcation
- –> pulmonary & systemic congestion
- decreased cardiac ouput
3
Q
describe the activity of natruiretic peptides in chronic heart failure
A
- although ANP/BNP release is high during CHF due to persistent SNS activity creating a hypertensive streat, their metabolizer, neprilysin, is also expressed high levels, and they don’t have an effect
4
Q
what is the MOA & clinical uses of ACE inhibitors/ARBs in the treatment of heart failure?
A
“-sartans” and “-prils”
- overall MOA:
- reduce preload & afterload
- inhibit cardiac remodeling
- clinical uses:
- both: top choice drug for HR
- can reduce mortality in patients with reduced ejection fraction (HFrEF)
- ARBS: indicated especially in patients with persistent dry cough/angioedema (those are AEs of ACE inhibitors)
- both: top choice drug for HR
5
Q
what are the MOA & clinical uses of aldosterone receptor blockers in the treatment of heart failure?
A
= spironoloactone, epleronone
- clinical uses: can be administered at a lower dose to reduce morbidity/mortality in patients with
- symptomatic HFrEF not corrected by standard therapy (ACE inhibitor + B-blocker)
- symptomatic of HFrEF that:
- just had an MI
- have an hx of diabetes
6
Q
adverse effects and contraindications of of aldosterone receptor antagonists?
A
spironolactone, eplerenone
adverse effects:
- hyperkalemia
- spironolactone specifically:
- gynecomastia
- menstrual irregularities
- decreased libido
contraindications:
- renal insufficiency
- serum [K+] > 5 mmol/L
- combination w/other K+ sparing diuretics (amiloride, triamterine)
7
Q
what is ARNI?
- what is its MOA /clinical use in the treatment of heart failure?
- what are its AEs/contraindications?
A
= sacutratibril + valsartan
- MOA:
- sacutribril: enhance action (vasodilation) of natruiretic peptides (NPs) by inhibiting their metabolizer, valsartan
- valsartan: is an ACE inhibitor
- clinical uses:
- patients with chronic symptomatic HF with preserved ejection fraction (HFreF) who can tolerate but don’t prefer ACE inhibitors/ARBS
- AEs:
- similar to ACEs/ARBS:
- hypotension
- hypokalemia
- angioedema
- similar to ACEs/ARBS:
- contraindications:
- co-administration with ARB: leads to angioedema
8
Q
what are the beta blockers used to treat HF and what are their indications?
A
- indications:
- are a part of a standard therapy (in combo w/ ACE inhibitors) - along with diuretics as needed - in the treatment of HFreF as long as pts are hemodynamically stable
- drugs:
- selective B1 antagonists:
- bisoprolol
- metoprolol
- nonselective antagonists:
-
carvedilol: blocks a1, B1 and B2
- also has anti-oxidant and anti-proliferative properties
- due to B2 blockage, is C/I in pts with:
- COPD
- asthma
-
carvedilol: blocks a1, B1 and B2
- selective B1 antagonists:
9
Q
- what are the vasodilators used to treat chronic heart failure?
- what are their specific indications?
- AEs?
- contraindications?
A
- types of vasodilators:
- arteriolar dilators: relax arteriole smooth muscle
- hydralazine
- venodilators: relax venous smooth muscle
- isorbiside dinitrates
- arteriolar dilators: relax arteriole smooth muscle
- clinical uses:
- for pts with HFrEF intoleant to standard therapy (ARBs/ACE inhibitors)
- eg: African Americans
- for pts with HFrEF intoleant to standard therapy (ARBs/ACE inhibitors)
- AEs:
- headache, flushing, postural hypotension, reflex tachycardia
- contraindications:
- hypotension due to PDE Inhibitors
10
Q
- what are the SGLT inhibitors?
- what is their MOA and indications in the treatment of heart failure?
A
- “-glifozin”
- MOA: inhibit Na+/glucose reabsorption
- increased Na+ reabsorption induces natriuresis diruesis –> reducing circulating blood volume –> reducing preload/afterload
- indications: added to standard therapy (B-blocker + ACE/ARB) in patients with HFrEF w/out diabetes.
- reduces hospitalization
- decreases mortality
- protect renal function
11
Q
AEs, drug drug interaction, and contraindications of SGLT2 inhibitors
A
- AEs
- urogenital: UTIs, yeast infections, increased urine output
- DKA
- hypotension
- major drug-drug interactions: hypoglycemic drugs
- contraindications:
- end stage renal disease
- dialysis
- hypersensitivity
12
Q
vericiguat
- MOA and indications in the treatment of heart failure?
A
- MOA: is a soluble gaunylate cyclase stimulator –> induces vasodilation while serving as an anti-fibrotic
- clinical uses: combined with standard therapy for HFreF to r_educe mortality/hospitalizatio_n time in patients who
- have recently been hospitalized
- received IV diuretic therapy
13
Q
- veriguat - AEs, contraindications and drug drug interactions
A
- AEs
- hypotension
- anemia
- contraindications: pregnant women - potential fetal toxicity
- drug drug interactions: NO donors, PDE inhibitors
14
Q
loop diuretics
- MOA and clinical uses in treatment of heart failure
A
= furosemide
- MOA: promote renal loss of sodium and water
- clinical uses: first choice for the rapid relief of pulmonary/peripheral congestive symptoms
- often combined with other agents to increase effectiveness
15
Q
adverse effects of loop diuretics
what cautions should be taken when giving loop diuretics?
A
- AEs
- dizziness
- headache
- hyponatremia
- hypokalemia
- alkalosis
- hyperglycemia, hyperlipidemia, hyperuricemia
- caution: start off patient at a low dose to avoid over diuresis/electrolyte imbalance
16
Q
digoxin
- what type of drug
- what is its MOA and
- cardiac effects?
- extra-cardiac effects?
A
- digoxin is a cardiac glycoside
- MOA: it is an ionotropic drug
- inhibits N/K ATPase (pumps K+ in & Na+ out)
- this makes Na+ influx less favorable, slowing down the an Na/Ca++ exchanger (pumps Na+ in and Ca+ out), which slows down Ca+ removal from cell, increasing intracellular [Ca++]
- inhibits N/K ATPase (pumps K+ in & Na+ out)
- cardiac effects:
- increases cardiac contractility
- but slows HR and AV node conduction at therapuetic dose by inducing PNS activity (?)
- extra-cardiac effects:
- renal diuresis (since it increases contractility and CO)
- GI: PNS activity can stimulate CTZ (chemoreceptor trigger zone) on gut smooth muscle cause –> nausea
- MOA: it is an ionotropic drug
