Heart Failure Flashcards
How does your body compensate for HFrEF?
1) ↑ preload by retaining fluid
2) ↑ SNS
3) Cardiac remodeling
1) Who gets and ACEi?
2) Why?
3) What else can be added?
1) All pts with HF d/t LV systolic dysfunction or any HF w/ low EF
2) start early to stop remodeling
3) diuretic only if fluid retention, can add beta blockers or Dig
What are the two pathways affected by ACEi and what results?
- ANG I to ANG II is shut off by ACEi –> ↓ vasocxn, ↓ SNS stimulation, and ↓ aldosterone production
- Breakdown of bradykinins are blocked –> ↑ [bradykinin]
1) Who should be on a diuretic?
2) Why should diuretics not be used as monotherapy?
1) All pts with HF and Fluid Retention
2) ↑ u/o –> ↓ perfusion –> ↑ RAAS = remodeling
What 3 important things does Angiotensin do?
- Vasoconstrictor
- Activates SNS
- Causes increased Aldosterone
What is Diuretic Resistance?
What are somethings you can do?
What should you never do?
Best indicator of diuretic efficacy?
Def:
- Prolonged rate of absorption resulting in diminished [peak] d/t ↑ tubular Na resorption @ another location
Can do:
- bigger oral or IV doses
- gang up on nephron using combos but use small doses d/t possible pronounced diuresis (use smaller doses)
- ↑ renal blood flow (hard to do)
Not Do:
- NEVER give NSAIDS –> ↓ renal blood flow to nephron
Best Indicator:
- Peak LVLs = diuretic ability in blood
1) What is the goal of HF Diuresis?
2) How much fluid loss should occur?
3) What tells us we’re still within a safe margin?
- Diuresis should not be faster than the movement of fluid from interstitial to intravascular –> HoTN
- 1 kg of fluid/day; faster than this = Acute Renal Failure
- < 20:1 BUN:Cr is prerenal azotemia aggressive zone
1) How does HF –> Hypokalemia?
↓CO –> HoTN –> ↓ renal perfusion –> ↑ RAAS –> hyperaldosteronism –> hypokalemia
MoA of Thiazides in HF?
When to use?
When to not use?
MoA: block Na and Cl reabsorb in DCT - ↓ Na by 5-8% To use: - use early in HF as weak diuretic Not use: - ineffective if GFR <30 - longer use --> ineffective b/c PCT ↑ absorption
How do diuretics treat HF?
What happens if we do this in Pts w/o HF?
- In HF, diuretics ↓ preload w/o compromising CO. In HF, SV not changed much b/c Frank-Starling curve less steep
- In nml Pts, the same drop in preload –> a large drop in CO which –> symptoms
4 ways you control HF?
1) maintain fluid balance
- decrease sodium,
- add a diuretic
2) improve physical conditioning
3) Rate control in select Pts (A-fib)
4) Avoid CCBs, NSAIDs, and in some cases anti-disrrhythmics
HF –> ↓CO –> Hypotension –> ? (2 branches)
1) ↑ Sympathetic tone –> ↑ catecholamines, ↑ vasopressin (ADH)
2) ↓ renal perfusion -->
↑ RAAS
--> ↑ Angiotensin II --> ↑ aldosterone
and
--> ↑ EPI --> ↑HR
(Both) –> vol overload, edema (↑ PCWP), and cardiac remodeling
3 Therapeutic Strategies for HFrEF
1) Remove underlying cause/drives (structural/medical)
2) Remove precipitating cause (infection, arrhythmia, Rx)
3) Control HF State (↑ pump performance, ↓ workload, control excess Na/H2O)
How to improve performance in HF Pts
1) symptom mgmt (improve QoL)
2) Prolong Survival (manage cardiac remodeling)
What are the 3 ways to prevent HF?
1) Prevent initial injury
2) Prevent further injury
3) Prevent post-injury deterioration
Staging System of HF
- Definition and Key Point
- Where is the Pt in the progress of their HF. Can’t go back up like NYHA
Stage A Heart Failure
- No Sx, no structural changes, but risk of HF
- Risk of HF
Stage B Heart Failure
- Fully compensated, asymptomatic, some dmg
Stage C Heart Failure
- Current or prior Sx w/ structural changes
- “C” for “Classic CHF Pt”
- No longer fully compensated
Stage D Heart Failure
- Refractory HF w/ special interventions
- Decompensated
- Marked Sx @ rest despite med therapy
1) Most valuable quantitative measure of HF?
2) Most valuable diagnostic test? - what can it show?
3) What other tests can you do?
1) Ejection Fraction
2) Echocardiogram; shows systolic failure from other processes, shows were remodeling occurring, geometric measures
3) Rt heart cath, EEP, BNP
What are the qualitative evaluations of HF Pts?
Functional Testing:
- Exercise testing, QoL survey, peak O2 consumption
Fluid Status:
- BODY WEIGHT, JVD, edema, lung/liver congestion
NYHA Heart Failure Classes
- Definition and 4 key points
system based on functional capabilities
- measure of when we give meds and how we’re doing
- can go up and down
- Sx based
- Slice in time
Class I-IV
I - No Sx w/ nml activity
II - Nml activity –> Sx
III - Ok @ rest, ANY activity –> Sx
IV - Sx @ rest, ↑ discomfort
Two Big Goals in HF Mgmt?
1) Fix Sx now
2) Prevent HF Later
Mechanism to Improve HF Performance?
- ↑ contractility w/ (+) inotropes
- ↓ impedence
- slow/prevent cardiac remodeling
1) What are the ACEi/ARB Contraindications
2) Relative contraindications that we could still attempt use of ACEi/ARBs with
1) previous life threatening rxn and pregnancy
2) SBP < 80 mmHg, Scr > 3mg/dL, Bilat renal artery stenosis, serum K > 5.5
1) How to Start ACEi/ARB and Dosing?
When to reassess?
What drug to start out on?
1) Assess fluid status - If vol depleted, w/hold diuretic 24-48 hrs
Start low –> titrate up
- if risk of hypoTN (LV dysfxn, SBP <100, Na <135) = 6.25mg monitor for 2 hr, then titrate up to starting
- Elderly (>75 yo) = 12.5 mg q day –> titrate PRN
- Nml Dose = 12.5 mg TID
- HTN = 25 mg TID
2) Reassess in 48 hr by phone; back off if dizz/weakness
- Office visit weekly until titrated to target dose
3) Captopril d/t most rapid acting and shortest acting (2hr)
What to reassess weekly during ACEi/ARB titration?
If any of these are present:
- Scr ↑ 0.5 mg or more
- K > 5.5
- Symptomatic hypoTN
What is GDMT stand for?
What drugs is GDMT referring to?
1) Guideline Directed Medical Therapy
2) 4 ACEi/3 ARBs
4 ACEi and 3 ARBs for HF
Captopril
Enalapril
Ramipril
Lisinopril
Candesartan
Losartan
Valsartan
Loop Diuretics:
1) MoA
2) Who gets them?
3) Other effects on kidneys
1) blocks Na and Cl reabsorption in ascending limb of loop (20-25%)
2) Moderate - severe HF
3) PTG - mediated ↑ in renal blood flow; works in renal insufficiency but may need to ↑ dose
What causes angioedema in ACEi reactions?
blocks deactivation of bradykinins that –> inflammation
1) What’s common if Pt at risk of HoTN and RAAS is activated?
2) What do you do?
1) hyponatremia and rapid diuresis
2) Hold diuretics for 1-2 days
What are the risks of treatment for ACEi/ARBs
1) HypoTN
2) Worsening Renal Fxn
3) K Retention
1) What can K retention cause when ACEi are used?
2) What factors ↑ risk of this occurring?
3) How do we manage this?
1) can cause heart dysfxn
2) ↓ renal fxn, K supplement, DM
3) equillibriate with diuretic
1) What do Beta Blockers do?
1) (-) inotrope and (-) chronotrope b/c they block SNS by binding to Beta 1 receptors (some bind alpha receptors)
1) Who gets Digoxin?
2) What are the risks?
1) HF Pts that are symptomatic (Stage C, Class II/III) and have A-Fib where ALL other therapies maxed
2) Arrhythmias
Which HF Pts get Beta Blockers?
What can BBs get added to?
1) STABLE class II/III and stage B/C d/t LV systolic dysfxn (EF <35%-40)
2) Preexisting ACEi + Diuretic combo
When are Beta Blockers contraindicated?
- bronchospastic dz (asthma)
- Sx bradycardia (HR < 50)
- Adv heart block (caution in 2, no in 3)
- acute decompensated HF
What are the 3 Beta Blockers used in HF?
Which BB is different from the others and why?
1) carvedilol, bisprolol, metoprolol succinate (SR)
2) carvedilol; the “i” says it’s also an alpha blocker
Who gets Bidil?
HF adjunct therapy in self-identified black Pts
1) Who gets aldosterone antagonists?
2) How do you spell them?
3) What is always a risk with AAs?
1) Class IV HF add-on in low doses
2) spironolactone and eplerenone
3) hyperkalemia
How to titrate Beta Blockers?
What should you monitor for and do after?
1) Double dose q 2-4 weeks if tolerate present dose –> titrate to highest dose
2) bradycardia, hypoTN, fluid retention, worsening HF –> back dose off but do everything to keep them on BB
1) When does HoTN typically occur with beta blockers
2) What do you do?
3) What do you not do? Why?
1) common w/ carvedilol and in first dose
2) may require temp dose reduction in ACEi, once BP ↑ then ↑ ACEi again
3) Do not ↓ diuretic b/c if you do –> BB will cause fluid retention & worsening HF
“Recommended” Means?
Thou Shalt
Why should calcium antagonists (CCBs) not be used in HF?
- Lack of evidence of efficacy
- (-) inotrope –> safety issues (verapamil = most dangerous CCB)
Who gets Hydralazine + Nitrate Combo?
Why typically not used?
Why not used as single drugs?
1) HF Pt if ACE/ARB not tolerated and self-identified African American
2) HF Pts cant handle SE
3) Little evidence to suggest benefit when not used in combo
Aldosterone Anatagonist Contraindications
- K > 5.5
- DM 2 with microalbuminuria
- CrCl < 50
- Concurrent K-sparring diuretic
What is synthetic natruretic peptide (Nesiritide) indicated for?
acute decompensated HF
(Diagram) Volume Overload leads to?
↑ atrial pressure --> ANP release
and
↑ LV filling --> BNP release
both lead to
Vasodilation, ↓ sympathetic tone, natruresis and diuresis
all lead to
↓ blood volume and ↓ arterial pressure
that ultimately -->
improved hemodynamicsWhat are the goals when trying to control HF?
1) Reduce workload
2) Improve pump performance
3) Reduce Na/H2O Intake
When to you actually use (in real life) Thiazides in HF?
1) Don’t use in HF
2) Loses effectiveness
How to manage Loop Diuretics?
- Titrate to effect, then adjust as needed
- Avoid NSAIDS
What are the side effects of Diuretics?
- Hypokalemia
- Prerenal azotemia
- HypoTN
When do ACEi/ARB show benefit in HF?
At target dose –> captopril 50 mg TID
What chemicals effect blood flow through the Glomerular apparatus?
PTGs –> Afferent Dilation
NSAIDs –> block PTGs –> Afferent Cxn
ANG II –> Efferent Cxn (decreases peritubular pressure –> increased fluid shift back into blood)
1) How does aldosterone affect electrolyte balance?
2) What stimulates and decreases aldosterone production?
1) Na absorption and H2O retention and elim of K, Mg, and H and simultaneous K uptake by cells
2) Aldosterone release stimulated by hyperkalemia but ↓ by dopamine and ANP
What are the two Digoxin doses/parameters?
1) Nml dose = 0.25 mg
2) >70 y.o., hepatic/renal dysfxn = 0.125 mg
What is important to know about Digoxin monitoring parameters?
- no data suggests an optimal dose or optimal [serum]
- routine monitoring not required
- just avoid toxicity
What are the ADRs for sprironolactone?
What do you do if Pt reporting hormonal SE?
1) HA, dizzy, angina, MI, ↑ GGT
2) Switch to eplerenone
1) How do you switch a Pt from an ARB to an ARNI?
2) How do you switch a Pt from an ACEi to an ARNI?
1) Stop the ARB, then you can immediately start the ANRI
2) Stop the ACEi, wait for 36 hours, then start the ARNI
1) What is an ARNI and what’s in it?
2) Who gets an ARNI?
1) ANG-II and Neprilysin Inhibitor, valsartan and sacubitril
2) Class II or III HFrEF that can tolerate an ACEi or ARB
What are the ANRI SE?
angioedema (valsartan), HoTN/dizzy, impaired renal fxn, hyperkalemia
1) What is ivabradine?
2) What drug therapy can it be added to?
1) selective SA node inhibitor
2) Beta blockers
What are the 5 criteria that must be met to start ivabradine?
- symptomatic chronic stable HF
- EF < 35%
- In NSR
- Resting HR > 70 bpm, despite optimal BB
- On max tolerated dose of BB
What are the contraindications to ivabradine?
- BP sucks
- Can’t maintain HR
- Liver doesn’t work
ACC/AHA/HFSA Recommendations for Stage A
3 things
- ↓ risk factors
- Stop doing unhealthy shit
- Get an echo if needed
- Start on ACEi/ARB if possible
ACC/AHA/HFSA Recommendations for Stage B
4 things
- Treat for remodeling
- ACEi/ARB/ARNI + BB
- ARNI for Class II/III
- No Sx = No Digoxin
ACC/AHA/HFSA Recommendations for Stage C
5 things
- Same as A and B recommendations
- RAAS blocker + Beta blocker
- Hydralazine + Nitrate OK problems with ACEi/ARB
- AAs OK with careful monitoring
- NEVER ACEi + ARB + AA, only 2 of 3
Principle 1
Target dose = best outcomes
Principle 2 - What do you do if you can’t reach target doses?
1) Address factors limiting GDMT
If can’t get to target doses then drop AA (if GFR <30 or K > 5.5)
2) Symptomatic HoTN probably d/t overdiuresis or vasoactive Rx
Principle 3
- best single drug = BB
- ↓ RAAS blockers if needed
Principle 4
- Rate control > 70
- Optimize BB, then add Ivabridine (Corlanor)
Principle 5
Af Am with Class III –> Hydralazine + ISDN
Principle 6
Use diuretics to relieve congestion
Principle 7
Start therapy early, titrate doses
