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IPC Cardiology 2 > Heart Failure(HFmrEF/HFpEF) Treatment > Flashcards

Heart Failure(HFmrEF/HFpEF) Treatment Flashcards

1
Q

What is HFpEF?

A
  • “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%
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2
Q

What casuses HFpEF?

Heart failure with preserved ejection fraction

A

Long standing hypertension leading to myocyte hypertrophy in the LV

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3
Q

Treatment approach in patients with symptomatic HF and an EF >/- 50%

A
  • 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
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4
Q

Fluid management in HFpEF

A
  • Primary agents are loop diuretics
  • Primary goal is to increase excretion of NaCl and H2O
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5
Q

Concerns of fluid management in HFpEF patients

A
  • Patients already have trouble filling enough blood to pump adequately
  • Removal of an excess amount of fluid can lead to even less profusion
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6
Q

What is HFmrEF?

Heart failure with mildly reduced ejection fraction

A
  • HFpEF getting worse, or HFrEF getting better
  • EF 40-50%
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7
Q

Treatment patients with symptomatic HF and ejection fraction 40-50%

A
  • 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.
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8
Q

What if patients are on home GDMT?

A
  • 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
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9
Q

What if a patient is on SGLTi?

Keep on if at all possible

A
  • 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
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10
Q

Treatment for warm and dry patients(Class I)

A

DO NOTHING….. this is the goal!!

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11
Q

Treatment for warm and wet(Class II)

A

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

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12
Q

Treatment for cold and dry(Class III)

A

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

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13
Q

Contraindications for Nitroglycerin

A
  • Concurrent use with PDE-5 inhibitors(avanfil,sildenafil,tadalafil,or varendafil)
  • Concurrent use with soluble guanylate cyclase stimulators(vericiguat,riociguat)
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14
Q

Monitoring for Nitroprusside

A
  • BP,cyanide and thiocyanate toxicity(particularly if on for >3days at >3mcg/kg/min)
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15
Q

MOA for Dobutamine

A
  • Stimulates myocardial Beta1-adrenergic receptors, resulting in increased contractility and HR
  • Stimulates both b2 and a1 receptors in the vasculature
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16
Q

Drug interactions of Dobutamine

A
  • Increases arrhytmogenic potential in combination with other pro-arrhythmic agents
17
Q

MOA of Milrinone

A

Selective phosphodiesterase-3 inhibitor in cardiac and vascular tisssue, resulting in vasodilation and inotropic effects

18
Q

Drug interactions for Milrinone

A

Anagrelide:Category X
* incrases arrhythmogenic potential in combination with other pro-arrhythmic agents

19
Q

Clinical Pearls of Milrinone

A

Moderate risk of arrhythmia, high risk of hypotension, renally eliminated(more renal dysfunction)–>more drug exposure and hypotension

20
Q

Treatment of cold and wet(Class IV)

A

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

21
Q

Vasopressors used in Class IV treatment

A

Norepinephrine,epinephrine,dopamine

22
Q

Three main causes of drug induced HF

A
  1. Sodium and volume retention
  2. Direct cardiotoxicity->cardiomyopathy
  3. Negative ionotropy
23
Q

Drugs that induce HF due to sodium and fluid retention

A
  • NSAIDs
  • Steroids
  • Thiazolidinediones(TZDs)
24
Q

Drugs that induce HF due to cardiomyopathy

A
  • Chemotherapeutic agents
  • Biologic Agents
  • Alcohol
25
Q

Drugs that induce HF due to Negative ionotropy

A
  • Non-dihydropyridine calcium channel blockers
  • Beta-blockers
26
Q

BBW of TZDs

A

Avoid in patients with NYHA III-IV HF

27
Q

Examples of chemotherapeutic agents

A
  • Anthracyclines(doxorubicin,daunorubicin)
  • Alkylating agents
28
Q

Biological agent

A

Trastuzumab

29
Q

Risk factors for anthracycline toxicity

A

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?

30
Q

Risk factor for developing cardiomyopathy using trastuzumab

A
  1. Advanced age
  2. Presence of CV comorbidities
  3. Previous treament with anthracyclines
31
Q

Inhibition of HER2 receptors lead to HF via—>

A
  • Increased reactive oxygen species(ROS)
  • Reduced NOS expression
  • Reduced NO bioavailabilty
  • Increased angiotensin II
32
Q

Treatment: Trastuzumab induced cardiomyopathy

A
  • 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

IPC Cardiology 2 (6 decks)

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