Acute Decompensated Heart Failure (ADHF)

1️⃣ What is ADHF?

Acute Decompensated Heart Failure (ADHF) is the rapid onset or worsening of signs and symptoms of heart failure requiring urgent therapy and often hospitalization.

It may occur as:

  • De novo HF (newly diagnosed)
  • Acute decompensation of chronic HF
  • Progression to cardiogenic shock

Major guidelines:

  • American Heart Association (AHA)
  • European Society of Cardiology (ESC)


2️⃣ Pathophysiology of ADHF

Core Mechanisms

  1. Elevated LV filling pressure Pulmonary congestion
  2. Reduced cardiac output Hypoperfusion
  3. Neurohormonal activation
    • SNS activation
    • RAAS activation
    • Vasopressin
  1. Endothelial dysfunction
  2. Renal congestion Cardiorenal syndrome


Hemodynamic Profiles 

Profile

Congestion

Perfusion

Clinical Type

Warm & Wet

Yes

Adequate

Most common

Cold & Wet

Yes

Poor

High mortality

Cold & Dry

No

Poor

Hypovolemic / overdiuresed

Warm & Dry

No

Adequate

Compensated


3️⃣ Precipitating Factors 

Remember: “CHAMP”

  • C – Acute Coronary Syndrome
  • H – Hypertensive crisis
  • A – Arrhythmia (AF common)
  • M – Mechanical cause (MR, VSD)
  • P – Pulmonary embolism

Others:

  • Infection
  • Anemia
  • Thyroid disorders
  • Non-compliance
  • Renal failure
  • NSAIDs


 Symptoms in ADHF

Symptom

Mechanism (Why it happens)

Dyspnea on exertion

LV filling pressure pulmonary venous congestion lung compliance

Orthopnea

Supine position venous return pulmonary capillary pressure

Paroxysmal nocturnal dyspnea (PND)

Nocturnal fluid redistribution + reduced adrenergic tone

Acute breathlessness at rest

Sudden alveolar flooding (acute pulmonary edema)

Pink frothy sputum

RBC transudation into alveoli due to high capillary pressure

Cough (worse at night)

Pulmonary interstitial edema stimulating cough receptors

Wheezing (“cardiac asthma”)

Peribronchial edema causing airway narrowing

Fatigue

Reduced cardiac output skeletal muscle hypoperfusion

Reduced exercise tolerance

Impaired oxygen delivery to tissues

Palpitations

AF or sinus tachycardia secondary to SNS activation

Chest pain

Demand ischemia / ACS precipitating ADHF

Rapid weight gain

Fluid retention (RAAS activation)

Abdominal fullness

Hepatic congestion / ascites

Early satiety

Congested liver + gut edema

Nausea / vomiting

Splanchnic congestion

Confusion / altered sensorium

Cerebral hypoperfusion

Reduced urine output

Renal hypoperfusion + venous congestion

Nocturia (early HF)

Improved renal perfusion in supine position

Cold intolerance

Peripheral vasoconstriction

Anxiety / air hunger

Severe hypoxia in pulmonary edema


Signs of Left-Sided Congestion

Sign

Mechanism

Tachypnea

Hypoxia + J receptor stimulation

Use of accessory muscles

Increased work of breathing

Basal crackles (crepitations)

Alveolar/interstitial fluid

Widespread crackles

Severe pulmonary edema

Wheezing

Bronchial wall edema

Hypoxia (SpO₂)

V/Q mismatch

Cyanosis

Severe hypoxemia

S3 gallop

Rapid ventricular filling into dilated LV

S4 gallop (HFpEF)

Stiff ventricle with atrial contraction

Displaced apex beat

Dilated LV

Mitral regurgitation murmur

LV dilation annular dilation


 Signs of Right-Sided Congestion

Sign

Mechanism

Raised JVP

Elevated right atrial pressure

Hepatojugular reflux

Inability of RV to handle venous return

Peripheral pitting edema

Venous hypertension

Sacral edema (bedridden)

Dependent venous pooling

Ascites

Chronic hepatic congestion

Tender hepatomegaly

Passive venous congestion

Splenomegaly (chronic)

Long-standing portal congestion

Anasarca

Severe systemic congestion


  Signs of Hypoperfusion (Low Output State)

Sign

Mechanism

Cool clammy extremities

SNS-mediated vasoconstriction

Delayed capillary refill

Poor peripheral perfusion

Hypotension

Reduced stroke volume

Narrow pulse pressure

Low forward flow

Tachycardia

Compensatory SNS activation

Weak peripheral pulses

Low cardiac output

Oliguria (<0.5 mL/kg/hr)

Renal hypoperfusion

Lactic acidosis

Tissue hypoxia

Altered mental status

Cerebral hypoperfusion


 Severe / Advanced ADHF (Cardiogenic Shock)

Feature

Mechanism

SBP < 90 mmHg

Severe LV dysfunction

Lactate > 2 mmol/L

Anaerobic metabolism

Multi-organ dysfunction

Sustained hypoperfusion

Pulmonary edema + shock

Combined congestion + low output

Arrhythmias

Ischemia / electrolyte imbalance


 Atypical Presentation

Scenario

Why It Occurs

Elderly without dyspnea

Blunted symptom perception

Isolated confusion

Low CO state

GI symptoms dominant

Right HF predominance

Flash pulmonary edema

Sudden afterload increase (hypertensive crisis)

Normal EF with severe symptoms

HFpEF (diastolic dysfunction)



 Laboratory Investigations

A. Natriuretic Peptides (Cornerstone Biomarker)

Test

What It Reflects

What to Expect

BNP

Ventricular wall stretch

Elevated (>100 pg/mL in ER supports HF)

NT-proBNP

Prohormone fragment

>300 pg/mL (acute setting supports HF)

  • False high: CKD, elderly, sepsis
  • False low: Obesity


B. Cardiac Biomarkers (Troponin)

Why Order?

What to Expect

Rule out ACS

Mild elevation common

Risk stratification

Higher levels = worse prognosis

 Troponin elevation ≠ always MI


C. Renal Function

Parameter

Expected Finding

Mechanism

Creatinine

Elevated

Renal hypoperfusion + venous congestion

BUN

Elevated

Reduced renal flow

BUN/Cr ratio

>20

Prerenal physiology

This may indicate cardiorenal syndrome.


D. Electrolytes

Electrolyte

Expected Finding

Why?

Sodium

Hyponatremia

RAAS + ADH activation

Potassium

Hyper/hypokalemia

Diuretics or renal dysfunction

Magnesium

Low

Diuretics

Hyponatremia = Poor prognostic marker.


E. Liver Function Tests

Finding

Mechanism

Elevated AST/ALT

Hypoperfusion (“shock liver”)

Elevated bilirubin

Congestive hepatopathy

Elevated ALP

Cholestasis from congestion


F. Lactate

Elevated in:

  • Cardiogenic shock
  • Severe hypoperfusion

Lactate > 2 mmol/L = tissue hypoxia


G. Complete Blood Count

Finding

Why?

Anemia

Precipitating factor

Leukocytosis

Infection trigger

Hemoconcentration

Aggressive diuresis


 2️⃣ ECG (Mandatory in All)

What to look for:

Finding

Interpretation

Sinus tachycardia

Compensatory

Atrial fibrillation

Common precipitant

ST changes

ACS

LVH

Chronic hypertension

LBBB

Structural disease


3️⃣ Chest X-Ray

Finding

Mechanism

Cardiomegaly

Dilated LV

Kerley B lines

Interstitial edema

Bat-wing pattern

Alveolar edema

Pleural effusion

Elevated hydrostatic pressure

Upper lobe diversion

Pulmonary venous hypertension

 Early ADHF may have normal CXR.


 4️⃣ Echocardiography (Essential)

Should be done early in all new ADHF.

What to Assess:

1. LVEF

  • <40% HFrEF
  • 41–49% HFmrEF
  • ≥50% HFpEF

2. Regional Wall Motion Abnormality

Suggests ischemia

3. Diastolic Dysfunction

  • E/e′ > 15
  • LA enlargement

4. RV Function

  • TAPSE in RV failure

5. Valvular Disease

  • Acute MR
  • AS
  • TR

6. IVC Size

  • Plethoric, non-collapsible high RA pressure


5️⃣ Lung Ultrasound 

Finding

Meaning

B-lines

Interstitial edema

Pleural effusion

Congestion

Rapid reduction with therapy

Response to diuresis

More sensitive than CXR for early congestion.


6️⃣ Hemodynamic Monitoring (Advanced Cases)

Used in:

  • Cardiogenic shock
  • Uncertain diagnosis
  • Refractory cases

Using Pulmonary Artery Catheter:

Parameter

Expected in ADHF

PCWP

>15 mmHg

Cardiac Index

<2.2 L/min/m² (if shock)

SVR

Elevated (compensatory)


 7️⃣ Coronary Evaluation

Indicated if:

  • Suspected ACS
  • High-risk ECG changes
  • Elevated troponin

May require:

  • Coronary angiography


 8️⃣ Additional Tests (Based on Clinical Suspicion)

Test

When to Order

Thyroid function

New AF

D-dimer

Suspected PE

Procalcitonin

Suspected infection

ABG

Severe respiratory distress



Diagnostic Criteria (ESC Approach)

According to ESC, ADHF diagnosis requires:

A. Symptoms ± Signs of HF

AND

B. Elevated natriuretic peptides

AND/OR

C. Objective evidence of structural/functional cardiac abnormality

BNP Cutoffs (ESC Emergency Setting)

Test

Rule-Out Value

BNP

< 100 pg/mL

NT-proBNP

< 300 pg/mL

If below these HF unlikely.

Elevated values support diagnosis but are not specific.

Management

1️⃣ Oxygen Therapy

  • Target SpO₂ > 92%
  • Avoid routine oxygen if saturation normal

2️⃣ Non-Invasive Ventilation 

CPAP/BiPAP

Benefits:

  • Preload
  • Afterload
  • Improves oxygenation
  • Reduces intubation rate

Indicated in:

  • Acute pulmonary edema
  • Severe dyspnea

3️⃣ Intubation (If Required)

Indications:

  • Altered sensorium
  • Severe hypoxia
  • Exhaustion
  • Cardiogenic shock

 Use caution: Positive pressure can reduce preload in hypotensive patients.


 Decongestion 

 IV Loop Diuretics (First-Line)

Drug:

Furosemide IV

Dosing Strategy:

  • If chronic user: ≥ home oral dose IV equivalent

Expected Response:

  • Urine output within 1–2 hours
  • Relief of dyspnea


 Diuretic Resistance

If inadequate response:

  1. Double dose
  2. Switch to continuous infusion
  3. Add thiazide (metolazone)
  4. Consider ultrafiltration (selected cases)


Vasodilators (If BP > 110 mmHg)

IV Nitroglycerin

Best in:

  • Hypertensive pulmonary edema
  • Flash pulmonary edema

Mechanism:

  • Venodilation preload
  • At higher dose afterload

Contraindicated in:

  • Hypotension
  • Severe aortic stenosis


Sodium Nitroprusside

Powerful arterial + venous dilator
Used in:

  • Severe afterload excess

Requires:

  • ICU monitoring
  • Watch for cyanide toxicity


Inotropes 

Indicated in:

  • Cold profile
  • Cardiogenic shock
  • Low cardiac output with hypotension


Dobutamine

  • β1 agonist
  • contractility
  • Mild vasodilation

Best for:

  • Low CO with normal BP


Milrinone

  • PDE-3 inhibitor
  • Inotrope + vasodilator
  • Good in pulmonary hypertension

Avoid in:

  • Hypotension


Norepinephrine (Preferred Vasopressor)

Used in:

  • Cardiogenic shock with hypotension

Mechanism:

  • SVR
  • Maintains perfusion pressure


 Cardiogenic Shock Protocol

If SBP < 90 + hypoperfusion:

  1. Norepinephrine first-line
  2. Add dobutamine if low CO persists(If pressure improves but perfusion does not Cardiac output is still low.)
  3. Consider mechanical support


  Mechanical Circulatory Support

Used when:

  • Refractory shock
  • Persistent hypoperfusion despite drugs

Options:

Device

Role

IABP

Afterload, coronary perfusion

Impella

Direct LV unloading

VA-ECMO

Full circulatory support

Bridge to:

  • Recovery
  • LVAD
  • Transplant



 GDMT During Hospitalization

Continue unless contraindicated:

Drug

Continue?

ACEi/ARB/ARNI

Hold if hypotension/AKI

Beta-blocker

Continue unless shock

MRA

Usually continue

SGLT2 inhibitor

Can continue/start once stable

Important principle:
Do NOT abruptly stop beta-blockers unless shock present.


 Fluid & Sodium Management

  • Sodium restriction (≤2 g/day)
  • Fluid restriction (1.5–2 L/day if hyponatremia)
  • Strict I/O monitoring
  • Daily weights