CARDIO TSU HEART FAILURE

HF

• definition

• causes

• defintion

  • inability of ehart to pump enough blood to meet demands of body

• causes

  • systolic dysfunction (HFrEF)

  • diastolic dysfunction (HFpEF)

HF risk factors

• major

• HFrEF

• HFpEF

• major

  • Age > 65 years old

  • Hypertension

  • Myocardial infarction (MI)

  • History of heart murmurs

  • Enlarged heart

  • Diabetes

  • Family history of an enlarged heart

• HFrEF

  • Males

  • post-myocardial infarction

  • coronary artery disease

  • smokers

• HFpEF

  • Females

  • hypertension (long-standing)

  • older age

  • atrial fibrillation

  • diabetes.

S/Sx of HF: Congestion

• Respiratory

  • Dyspnea (on exertion)

  • Orthopnea (difficulty breathing lying flat, "pillow orthopnea"), Paroxysmal Nocturnal Dyspnea (PND)

  • Tachypnea (rapid breathing)

  • Rales/Crackles (abnormal lung sounds)

  • Cough (due to fluid in lungs)

  • Pulmonary edema

  • Pleural effusion.

• Systemic: Elevated

  • Jugular Venous Distention (JVD)

  • Hepatojugular reflux

  • Hepatomegaly (enlarged liver)

  • Peripheral edema (pitting edema).

• GI

  • GI discomfort (swollen/tender abdomen, poor appetite).

S/Sx of HF: hypoperfusion

• Cold extremities.

• Fatigue.

• Poor appetite.

• Worsening renal function.

• Altered mental status.

HF Work-Up

• History & Physical Examination.

• Complete Metabolic Panel (CMP)

• Echocardiogram:

  • Evaluates abnormalities in pericardium, myocardium, heart valves.

  • CRUCIAL for classifying HF as HFrEF or HFpEF (by measuring Ejection Fraction - EF).

• Cardiac Troponins:

  • Commonly slightly elevated in ADHF, usually due to "demand ischemia" (stress on heart) not true plaque rupture.

  • Renal dysfunction can lead to troponin accumulation.

• BNP (B-type Natriuretic Peptide) or NT-proBNP:

  • Synthesized and secreted by ventricular myocardium in response to increased wall stress, hypertrophy, volume overload.

  • Usually elevated in HF, helps support clinical diagnosis, useful for prognosis.

  • Should NOT be used in isolation to confirm or exclude HF diagnosis.

• ECG/EKG: May show ST-T wave changes (due to MI), Atrial Fibrillation, Bradycardia, Left Ventricular Hypertrophy (LVH).

Ejection Fraction (EF) - Functional Classification

• formula

• normal EF

• rEF

• pEF

• mEF

• Ejection Fraction (EF) = Stroke Volume (SV) / End-Diastolic Volume (EDV).

• Normal EF: 55-70%.

• HFrEF (Heart Failure with reduced EF / "Systolic Dysfunction"):

  • EF < 40%.

  • Heart muscle is thin and weak, struggles to pump. Ventricles are often enlarged.

  • SV is small because pump function is impaired, even though EDV may be large.

• HFpEF (Heart Failure with preserved EF / "Diastolic Dysfunction"):

  • EF ≥ 50%.

  • Heart muscle is thick and stiff, struggles to fill. Ventricular volumes are smaller.

  • SV is small because filling is impaired, even though EF may be normal. More likely due to long-standing hypertension.

• HFmrEF (Heart Failure with mildly-reduced EF):

  • EF 40-50%. Represents an intermediate group.

NYHA (New York Heart Association) Functional Classification

• Class I (Mild): No limitation of physical activity.

• Class II (Mild): Slight limitation of physical activity; comfortable at rest, but ordinary activity results in symptoms.

• Class III (Moderate): Marked limitation of physical activity; comfortable at rest, but less than ordinary activity causes symptoms.

• Class IV (Severe): Unable to carry out any physical activity without discomfort; symptoms present at rest; any physical activity increases discomfort.

ACC/AHA (American College of Cardiology/American Heart Association) Staging

• Stage A (At-Risk for HF): High risk for HF, but without structural changes or symptoms.

• Stage B (Pre-HF): Structural heart disease, but without signs or symptoms of HF.

• Stage C (Symptomatic HF): Structural heart disease with prior or current symptoms of HF.

• Stage D (Advanced HF): Refractory HF requiring specialized interventions.

Goals of Therapy for ADHF

• Relieve signs and symptoms of congestion and hypoperfusion.

• Prevent worsening of underlying cardiac function.

• Education of patient and family to prevent re-hospitalization.

Who Should Be Hospitalized?

• Evidence of severely decompensated HF: Hypotension, worsening renal function, altered mental status, significant pulmonary/systemic congestion.

• Dyspnea at rest.

• Hemodynamically unstable arrhythmia.

• Acute coronary syndrome (ACS).

Forrester Classification (Hemodynamic Subsets)

• Cardiac Index (CI) on Y-axis: Measured by cardiac output / BSA.

  • CI > 2.2: Well-perfused (Warm).

  • CI < 2.2: Hypoperfused (Cold).

• Pulmonary Capillary Wedge Pressure (PCWP) on X-axis: Indirect measure of preload.

  • PCWP > 18: Pulmonary congestion (Wet).

  • PCWP < 18: No pulmonary congestion (Dry).

. Non-Pharmacological Management

• Sodium Restriction: < 2 grams daily for most. Stricter if recurrent/refractory volume overload.

• Fluid Restriction: < 2 liters daily for moderate hyponatremia or fluid overload. Stricter if severe/worsening hyponatremia.

• Education: Regarding sodium and fluids upon discharge.

Pharmacological Management

• diuretics

• vasodilators

• inotropes

Diuretics

• most common

• goal

• effects

• monitoring

• hospitalized pts

• Loop Diuretics are most common

• Goal

  • Relieve symptoms and adequate urine output without intravascular depletion.

• Effects

  • Improves pulmonary congestion, decreases body weight. No effect on mortality or rehospitalization.

• Monitoring

  • Scr, I/O, K⁺/Mg²⁺, BP.

• Hospitalized Patients

  • Administer IV, give dose greater than home dose. Titrate to effect.

Strategies for Diuresis

• Increase Bolus Dose

  • Double dose until adequate urine output (e.g., Furosemide 20mg IV → 40mg IV).

• Continuous Infusion

  • Constant delivery. No difference in patient symptoms/renal function vs. bolus (DOSE trial). High levels linked to ototoxicity/nephrotoxicity.

• Sequential Nephron Blockade (Add Diuretic of Different Class):

  • Thiazide/Thiazide-like: Metolazone PO, HCTZ PO, Chlorothiazide IV.

  • Acetazolamide.

Ethacrynic acid

Option for patients with sulfa allergy

Vasodilators

• preferred…

• use

• effects

• agents

• Preferred first-line over routine IV Inotropes

• Use

  • Only if no symptomatic hypotension (SBP > 90 mmHg).

• Effects

  • Decrease preload, afterload, or both (↓BP, PCWP, SVR).

• agents

  • NTG

  • nitroprusside

  • nesiritide (d/c in US)

NTG

• MOA

• monitoring

• administration

• MOA: NO-mediated smooth muscle vasodilation. Primarily venous vasodilation at lower doses; arterial vasodilation at higher doses. Coronary vasodilation.

• Monitoring: Tachyphylaxis (if >24h infusion), headache, hypotension.

• Administration: Short half-life, easily titratable. Dispense in glass bottle, special tubing.

nitroprusside

• MOA

• risk of toxicity

• administration

• monitoring

• MOA

  • NO-mediated smooth muscle vasodilation. Causes both venous and arterial vasodilation.

• Risk of Toxicity

  • Hepatic dysfunction → cyanide toxicity. Renal dysfunction → thiocyanide toxicity.

• Administration

  • Protect IV bag from light (opaque sleeve).

• Monitoring

  • Hypotension (requires invasive hemodynamic monitoring, arterial line), hepatic/renal dysfunction, mental status changes, metabolic/lactic acidosis.

inotropes

• place in therapy

• ADE

• indications

• agents

• Not first-line due to increased mortality with routine use

• Adverse Effects

  • Arrhythmias, hypotension, myocardial ischemia.

• Indications (to improve end-organ function):

  • SBP < 90 mmHg.

  • Symptomatic hypotension despite adequate filling pressures.

  • Unresponsive or intolerant to vasodilators

• agents

  • Dobutamine

  • Milrinone

Dobutamine

• MOA

• effects

• monitoring

• half life

• MOA

  • Primarily Beta-1 adrenergic agonist.

• Effects

  • Increases CO, slight decrease in SVR. Effects attenuated by BB.

• Monitoring

  • Tachyphylaxis, hypotension, arrhythmias.

• Half-life

  • 2 minutes. No caution in organ dysfunction.

Milrinone

• MOA

• effects

• monitoring

• half life

• MOA

  • Phosphodiesterase (PDE) type-3 inhibitor ("Inodilator").

• Effects

  • Venous/arterial vasodilation, decrease systemic/pulmonary vascular resistance, increased CO

• Monitoring

  • Hypotension, pulmonary vasodilation, arrhythmias. Longer duration of action.

• Half-life

  • 60 minutes (180 minutes in HF). Renal adjustment needed (↓ dose if CrCl < 50 mL/min, omit bolus dosing).

Chronic HF Management & Discharge: Non-Pharmacological Considerations

• HF Modifiable Risk Factor Treatment

  • Hypertension, Diabetes, Hyperlipidemia, Inactivity, Obesity, Alcohol, Smoking, Dietary Sodium.

• Exercise Training

  • For chronic, stable HF.

• Sodium Restriction

  • Minimizes volume retention, allows lower diuretic dose. Restrict to < 1500 mg/day if hypertension exists. Educate on reading labels, avoiding added salt/high-sodium foods, caution with K⁺ salt substitutes.

• Water Restriction

  • May be needed for hyponatremia or persistent volume retention despite diuretics/sodium restriction. Limit to 2 L/day.

• Smoking Cessation

• Self-awareness and monitoring by patient

ARNI (Angiotensin Receptor-Neprilysin Inhibitor) - Sacubitril/Valsartan (Entresto®)

• Preferred over ACEI/ARB.

• MOA

  • Inhibits RAAS via ARB, inhibits neprilysin (↑ beneficial natriuretic peptides). Attenuates myocardial remodeling.

• Benefits

  • ↓ Symptoms, ↓ hospitalizations, improved survival (↓ mortality).

• Recommendations

  • Substitute for ACEI/ARB in NYHA Class II/III. DO NOT use concomitantly with ACEI (or within 36 hours of last dose of ACEI) due to angioedema risk

  • Do not use in patients with history of angioedema.

• Adverse Effects

  • Hypotension, hyperkalemia, cough, renal failure.

ACE Inhibitors: (e.g., Captopril, Enalapril, Lisinopril, Ramipril)

• MOA

• benefits

• titration

• substitutions

• MOA

  • ↓ Angiotensin II/Aldosterone. Prevents ventricular remodeling, myocardial fibrosis, myocyte apoptosis, cardiac hypertrophy, vasoconstriction, sodium/water retention.

• Benefits

  • Improved exercise tolerance, ↓ symptoms, ↓ hospitalizations, slowed progression, improved survival (↓ mortality).

• Titration

  • Titrate to target doses used in clinical trials, as tolerated, during BB uptitration.

• Substitutions

  • ARBs if cough/angioedema. Hydralazine/oral nitrate combo if ARB intolerant (hyperkalemia/renal insufficiency with ACEI likely same with ARBs).

ARBs: (e.g., Candesartan, Losartan, Valsartan).

• MOA

• Benefits

• Titration

• MOA

  • Blocks AT₁ receptors.

• Benefits

  • Less incidence of angioedema/cough vs. ACEI. No proven benefit over ACEI.

• Titration

  • To target doses used in clinical trials, as tolerated, during BB uptitration.

Beta-blockers (BBs): (Selected: Bisoprolol, Carvedilol, Metoprolol Succinate)

• MOA

• benefits

• initiation

• MOA

  • ↓ Ventricular remodeling, ↓ systolic/diastolic volumes, attenuates SNS activation, ↓ HR/MVO₂, inhibits plasma renin release.

• Benefits

  • ↓ Symptoms, ↓ hospitalizations, slow progression, improved survival (↓ mortality)

  • Recommended for LVEF ≤ 40%, patients with prior MI.

• Initiation

  • Start low doses, uptitrate gradually (q2-week intervals for reduced LVEF; q3-10 days after newly diagnosed MI)

  • Initiate in hospital at low dose prior to discharge in stable patients (after volume status optimization).

Mineralocorticoid Receptor Antagonists (MRAs): (e.g., Spironolactone, Eplerenone)

• MOA

• benefits

• recommendations

• MOA

  • Inhibits cardiac extracellular matrix/collagen deposition → reduces cardiac fibrosis/ventricular remodeling. Minimal diuretic effects.

• Benefits

  • ↓ Symptoms, ↓ hospitalizations, slow progression, improved survival (↓ mortality).

• Recommendations

  • For patients already receiving standard therapy (including diuretics) who have NYHA Class III/IV HF (LVEF ≤ 35%)

  • Closely monitor Scr and K⁺.

SGLT2 Inhibitors: (e.g., Dapagliflozin, Empagliflozin, Sotagliflozin)

• MOA

• benefits

• MOA

  • Diuretic, glucuretic, natriuretic effects. Reduces volume burden/ventricular stress, BP, weight. Prevents cardiac remodeling, improves energy metabolism, reduces inflammation/oxidative stress.

• Benefits

  • Approved to decrease mortality and hospitalizations in both HFrEF and HFpEF patients (with or without diabetes)

Digoxin

• MOA:

• Benefits

• Target Serum Conc.

• Consideration

• MOA

  • Minimizes excessive SNS activation, provides beneficial effects on quality of life.

• Benefits

  • ↓ hospitalizations. Does NOT improve mortality.

• Target Serum Conc.

  • 0.5 – 0.8 ng/mL (concentrations >1.0 ng/mL linked to ↑ adverse effects/mortality).

• Consideration

  • For HFrEF with symptoms despite standard therapy. Benefits in HFpEF for additional rate control.

Hydralazine/Isosorbide Dinitrate: (BiDil®)

• MOA

• benefits

• drawback

• MOA

  • ISDN ↑ NO bioavailability, Hydralazine ↓ oxidative stress → attenuates myocardial remodeling.

• Benefits

  • Approved for use in African American patients in addition to standard therapy.

• Drawback

  • TID dosing.

Ivabradine (Corlanor®)

• MOA

• benefits

• MOA

  • Selectively inhibits I_f ("funny" current) in SA node → reduces HR without affecting cardiac contractility.

• Benefits

  • Can reduce HF hospitalizations in symptomatic HFrEF (NYHA II-III) already on max tolerated BB with resting HR > 70 bpm.

Vericiguat

• MOA

  • Novel oral soluble guanylate cyclase stimulator.

• Benefits

  • Adjunctive therapy in HFrEF patients symptomatic despite optimal standard regimen

• Adverse Effects

  • Most common AE is hypotension. Avoid with long-acting nitrates and PDE-5 inhibitors.

HFpEF (EF ≥ 50%): Most medications are similar to HFrEF, but evidence for beneficial clinical outcomes is lower.

• Diuretics: As needed for volume control.

• SGLT2 inhibitors: Benefit seen in lower range of HFpEF (EF 50-60%), improve clinical outcomes.

• ARNI, MRAs, ARBs: Some evidence for clinical benefits (especially for HFmrEF).

• Non-DHP CCBs: Can be used in HFpEF (but harmful in HFrEF) for symptom control (HR, BP).

• Treatment aimed at etiology and disease progression: Control HTN, DM, obesity, HR, treat CAD.

Discharge Criteria & Preventing Re-admissions

• Before Discharge

  • Initiation/optimization of chronic therapy, address causes/barriers to care, volume/BP status, renal function/electrolytes, manage comorbidities, HF education (self-care, emergency plans, adherence), palliative care needs.

• Follow-Up

  • Visit within 7-14 days and/or telephone call within 3 days of discharge.

• National Hospital Inpatient Quality Measures:

  • Discharge instructions (activity, diet, follow-up, meds, symptoms, weight monitoring).

  • LVEF assessment.

  • ACEI or ARB (or ARNI) at discharge if LVEF < 40%.

  • MRA at discharge if LVEF < 40%.

  • BB at discharge if LVEF < 40%.