Heart Failure Basics & Treatment Goals
Cardiac Glycosides (Digoxin)
PDE3 Inhibitors (Milrinone)
HCN Channel Blockers (Ivabradine)
ARNI (Sacubitril/Valsartan)
100

This HF stage includes structural heart disease but no symptoms.

What is Stage B?

Stage B = heart structure changes already happened, but the patient doesn’t feel symptoms yet.

100

Digoxin increases this ion inside heart cells to improve contraction.

Digoxin slows conduction through this cardiac structure.

What is calcium?
Rationale: More calcium = stronger squeeze. Stronger squeeze = better cardiac output.

What is the AV node?
Rationale: That’s why it helps control certain arrhythmias. it slows down signal transmission.

100

Milrinone increases contractility by increasing this intracellular signaling molecule.

What is cAMP?
Rationale: More cAMP leads to more calcium = stronger heart contractility.

100

Ivabradine reduces heart rate by acting on this pacemaker structure.

What is the SA node?
Rationale: It slows the natural pacemaker without messing with contraction strength.


100

This component increases natriuretic peptides by blocking neprilysin.

This ARB component blocks angiotensin II receptors.

What is sacubitril?
Rationale: More natriuretic peptides, the more fluid removal and less pressure.

What is valsartan?
Rationale: Blocking angiotensin II reduces vasoconstriction and fluid retention.


200

his NYHA class means symptoms occur with marked activity limitation.

What is Class III?
Rationale: Class III patients feel fatigue or dyspnea with normal activities.

200

These vision disturbances are a neurological sign of digoxin toxicity.

What is blurred or yellow vision?

200

A major cardiovascular adverse effect is this abnormal heart rhythm risk.

What are ventricular arrhythmias?
Rationale: Stronger contraction can push the heart into dangerous rhythms.

200

Ivabradine is indicated when patients remain in this rhythm.

What is sinus rhythm?
Rationale: It only works when the SA node is actually in charge.

200

A required safety step is waiting this long after stopping ACE inhibitors.

What is 36 hours?
Rationale: Without that washout, angioedema risk gets dangerously high.

300

This stage involves refractory HF needing specialized interventions.

What is Stage D?
Rationale: Stage D is severe, advanced HF. These patients need advanced therapies or hospital level care.

300

A classic GI sign of digoxin toxicity is this loss of appetite symptom.

What is anorexia?
Rationale: If a patient suddenly hates eating and feels nauseous, think digoxin toxicity.

300

Milrinone should not be mixed in the same IV line with this diuretic.

What is furosemide?
Rationale: They precipitate together, meaning they form crystals. This is not ideal for veins.


300

Ivabradine is metabolized through this enzyme system and patients taking other medications that are strong inhibitors of this metabolic pathway are contraindicated.

What is CYP3A4?

Rationale: If another drug messes with CYP3A4, ivabradine levels can spike or crash. If metabolism stops, drug levels shoot up and bradycardia risk skyrockets.

300

A contraindication includes use during this physiologic condition.

What is pregnancy?
Rationale: RAAS blockers can seriously harm fetal development.

400

This NYHA class has symptoms even at rest.

What is Class IV?

400

Digoxin is mainly eliminated through this organ system.

What are the kidneys?
Rationale: A patient having bad kidneys means digoxin sticks around in their system longer (toxicity risk increases).

400

This vital sign requires close monitoring because vasodilation may cause drops.

What is blood pressure?
Rationale: Vasodilation can lower BP  

400

A dangerous rhythm complication that must be monitored for is this atrial arrhythmia.

What is atrial fibrillation?
Rationale: The drug slows HR, but sometimes rhythm problems may occur.

400

This organ function must be monitored due to risk of impairment.

What is renal function?
Rationale: Kidneys take a hit if perfusion drops, so labs help catch problems early.

500

One treatment strategy is interrupting this hormonal system that worsens HF progression.

What is neurohormonal activation (RAAS)?
Rationale: HF meds try to calm down the body’s stress response that keeps making the heart work harder.

500

This electrolyte imbalance increases digoxin toxicity risk.

What is low potassium?

500

This drug is used in severe, hospitalized HF patients and can only be used for this level of treatment.

Milrinone is administered using this route only.

What is short-term treatment?

Rationale: It’s not for home use due to it being an ICU-level helper drug.

What is IV?
Rationale: fast action, controlled setting, not a take-home med.

500

A unique visual adverse effect causes brief flashes of light called this.

What are phosphenes?
Rationale: Patients might see bright spots, but it’s expected.


500

Sacubitril/valsartan is eliminated through these two routes.

What are renal and fecal elimination?
Rationale: Dual elimination means you still monitor kidneys but consider overall metabolism.


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