Heart Failure(HFmrEF/HFpEF) Treatment Flashcards
What is HFpEF?
- “Diastolic Heat Failure”
- LV doesn’s fill properly, but does contract, so the same % of blood leaves the ventricle, but from a smaller starting volume
- EF >50%
What casuses HFpEF?
Heart failure with preserved ejection fraction
Long standing hypertension leading to myocyte hypertrophy in the LV
Treatment approach in patients with symptomatic HF and an EF >/- 50%
- Control HTN and Afib in accordance with guidelines
- Diurectics as needed
- SGLT2I: decreased HF hospitilizations and CV mortality
- MRAs: decrease hospitilizations
- ARBs:decrease hospitlizations
- ARNis: decrease hospitilizations
Fluid management in HFpEF
- Primary agents are loop diuretics
- Primary goal is to increase excretion of NaCl and H2O
Concerns of fluid management in HFpEF patients
- Patients already have trouble filling enough blood to pump adequately
- Removal of an excess amount of fluid can lead to even less profusion
What is HFmrEF?
Heart failure with mildly reduced ejection fraction
- HFpEF getting worse, or HFrEF getting better
- EF 40-50%
Treatment patients with symptomatic HF and ejection fraction 40-50%
- Diurectics as needed
- SGLT2i: decreased HF hospitilizationsa and CV mortality
- Patients with current or previous HFmrEF, betablockers,ARNI/ACEI/ARB, and MRA may be considered to reduce HF hospitilizations and CV mortality,especially if EF is on the low end of the spectrum.
What if patients are on home GDMT?
- Discontinuing a BB,ARNI/ACEI/ARB,MRA–>rebound adrenergic output/vasconstriction–>further worsening of HF
Keep on all if possible
- If required, decrease dose instead of discontinuing the medication
- If hemodynamically unstable/requiring vasopressors,stop medications
- If AKI,hold ARNI/ACEI/ARB,MRA
What if a patient is on SGLTi?
Keep on if at all possible
- These may actually help improve diuresis
- Small studies show an improvementin fluid output with these agents
- Do not have to worry about worsening renal function
- Stop if euglycemic ketoacicdosis or pending procedure/surgery
Treatment for warm and dry patients(Class I)
DO NOTHING….. this is the goal!!
Treatment for warm and wet(Class II)
Warm–>Do nothing , this is the goal
Wet–>Dry them out
1. Diuresis:1.5-2.5xhome dose as IV—->No home diuresis? Initiate furosemide 40mg IV or equivalent
2. Give one dose and assess response: Good response–> at least 500mL/hr over first 6 hours
Poor response–> double the dose!
3. Goal urine output: 1-2L negative/day
Treatment for cold and dry(Class III)
Cold
Goal: increase perfusion
Vasodilation–> arterial vasodilation makes it easier to move blood forward from LV(decreases afterload)
* Best for patients who are hemodynamically stable
* Agents:ARNI/ACEI/ARB, hydralazine,IV vasodilators
Ionotropy–> increase squeeze of LV to move blood forward
* Best for patients w/low BP(not in stock)
Agents–> dobutamine, milrinone
Dry
Nothing to do….. dry is the goal
Contraindications for Nitroglycerin
- Concurrent use with PDE-5 inhibitors(avanfil,sildenafil,tadalafil,or varendafil)
- Concurrent use with soluble guanylate cyclase stimulators(vericiguat,riociguat)
Monitoring for Nitroprusside
- BP,cyanide and thiocyanate toxicity(particularly if on for >3days at >3mcg/kg/min)
MOA for Dobutamine
- Stimulates myocardial Beta1-adrenergic receptors, resulting in increased contractility and HR
- Stimulates both b2 and a1 receptors in the vasculature
Drug interactions of Dobutamine
- Increases arrhytmogenic potential in combination with other pro-arrhythmic agents
MOA of Milrinone
Selective phosphodiesterase-3 inhibitor in cardiac and vascular tisssue, resulting in vasodilation and inotropic effects
Drug interactions for Milrinone
Anagrelide:Category X
* incrases arrhythmogenic potential in combination with other pro-arrhythmic agents
Clinical Pearls of Milrinone
Moderate risk of arrhythmia, high risk of hypotension, renally eliminated(more renal dysfunction)–>more drug exposure and hypotension
Treatment of cold and wet(Class IV)
Cold
* Goal–>increase perfusion
* Methods: Vasodilation and ionotropy—>same as before
* Vasopressors:Use if the patient is hemodynamically unstable; Provides increased squeeze of the LV and vasoconstricition to keep BP high
Wet
* Must be warm first ….need to have cardiac output to deliver blood(and drug) to the kidneys
* Loop diuretics: same methods as before
Vasopressors used in Class IV treatment
Norepinephrine,epinephrine,dopamine
Three main causes of drug induced HF
- Sodium and volume retention
- Direct cardiotoxicity->cardiomyopathy
- Negative ionotropy
Drugs that induce HF due to sodium and fluid retention
- NSAIDs
- Steroids
- Thiazolidinediones(TZDs)
Drugs that induce HF due to cardiomyopathy
- Chemotherapeutic agents
- Biologic Agents
- Alcohol
Drugs that induce HF due to Negative ionotropy
- Non-dihydropyridine calcium channel blockers
- Beta-blockers
BBW of TZDs
Avoid in patients with NYHA III-IV HF
Examples of chemotherapeutic agents
- Anthracyclines(doxorubicin,daunorubicin)
- Alkylating agents
Biological agent
Trastuzumab
Risk factors for anthracycline toxicity
Treatment Related
* Cumulative dose of anthracycline(>400mg/m2)
* Dosing schedules
* Previous anthracycline therapy
* Radiation therapy
* Co-administration of potentially cardiotoxic agents
Patient related
* Age
* Pre-exisiting cardiovascular disease or risk factors
* Obesity
* Smoking
* Gender?
Risk factor for developing cardiomyopathy using trastuzumab
- Advanced age
- Presence of CV comorbidities
- Previous treament with anthracyclines
Inhibition of HER2 receptors lead to HF via—>
- Increased reactive oxygen species(ROS)
- Reduced NOS expression
- Reduced NO bioavailabilty
- Increased angiotensin II
Treatment: Trastuzumab induced cardiomyopathy
- Dose adjustments based on LVEF
- Consider dose reduction or discontinuation if HF develops
- Consider using HF medications during treatment if EF declines
-ACEI/ARBS
-Beta-blockers
