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cardio:heart_failure:start

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Module 6 – Heart Failure

Heart failure is a clinical syndrome of impaired forward flow and maladaptive neurohormonal activation.

It is not primarily a pump failure problem — it is a neurohormonal disease.


Hemodynamic Foundation

Core equation:

CO = HR × SV

Stroke Volume depends on:

• Preload • Afterload • Contractility

In heart failure:

• ↓ Contractility (HFrEF) • ↑ Afterload • ↑ Preload • ↑ Neurohormonal activation (RAAS + SNS)


Classification

HFrEF (Reduced EF)

• EF ≤ 40% • Systolic dysfunction • Proven mortality-reducing therapies exist


HFpEF (Preserved EF)

• EF ≥ 50% • Diastolic dysfunction • Limited mortality-reducing therapies


HFmrEF

• EF 41–49% • Treated similar to HFrEF


The Neurohormonal Model

Compensatory systems become maladaptive:

1. Sympathetic activation

2. RAAS activation

3. Aldosterone excess

4. Ventricular remodeling

Modern therapy blocks these pathways.


**HFrEF – Guideline Directed Medical Therapy (GDMT)**

The Four Pillars of HFrEF Therapy

All patients with HFrEF should receive:

1. ARNI (preferred) OR ACE Inhibitor OR ARB 2. Evidence-Based Beta-Blocker 3. Mineralocorticoid Receptor Antagonist 4. SGLT2 Inhibitor

These therapies reduce mortality and hospitalization.


RAAS Inhibition

Preferred:

Sacubitril/Valsartan (ARNI)

Alternative:

ACE InhibitorARB

Effects:

• ↓ Afterload • ↓ Aldosterone • ↓ Remodeling • ↓ Mortality


Evidence-Based Beta-Blockers

Only three reduce mortality:

Carvedilol

Metoprolol Succinate

Bisoprolol

Effects:

• ↓ Sympathetic drive • ↓ Remodeling • ↓ Sudden cardiac death


Mineralocorticoid Receptor Antagonists (MRAs)

Spironolactone

Eplerenone

Effects:

• ↓ Aldosterone-mediated fibrosis • ↓ Remodeling • ↓ Mortality

Monitor potassium closely.


SGLT2 Inhibitors

Dapagliflozin

Empagliflozin

Effects:

• ↓ HF hospitalization • ↓ Mortality • Benefit independent of diabetes status


Secondary / Add-On Therapies

Hydralazine + Isosorbide Dinitrate

• Particularly beneficial in Black patients

Ivabradine

• If HR ≥70 on maximally tolerated beta-blocker

Vericiguat

• Soluble guanylate cyclase stimulator


Diuretics (Symptom Control)

Diuretics DO NOT reduce mortality.

Used for congestion relief:

FurosemideTorsemide

Effect:

• ↓ Preload • ↓ Pulmonary edema • Symptom improvement only


**HFpEF**

No strong mortality-reducing therapies except:

SGLT2 Inhibitors

Management focuses on:

• Blood pressure control • Diuretics for congestion • Treating atrial fibrillation • Managing ischemia


**Acute Decompensated Heart Failure**

Pulmonary Edema

IV Loop Diuretics

Nitroglycerin

• Oxygen

• Positive pressure ventilation if needed


Cardiogenic Shock

Dobutamine

Dopamine

Short-term hemodynamic support only.


Remodeling Prevention

Chronic neurohormonal activation causes:

• LV dilation • Fibrosis • Progressive decline in EF

GDMT prevents remodeling.


Clinical Pearls

✔ Heart failure is a neurohormonal disease ✔ Diuretics improve symptoms, not survival ✔ Four pillars reduce mortality ✔ Only specific beta-blockers reduce mortality ✔ SGLT2 inhibitors benefit even non-diabetics ✔ Start low, titrate slowly


Related:

Hypertension ModuleDysrhythmias ModuleReturn to Cardiovascular Modules

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