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
