Acute Decompensated Heart Failure

Acute Decompensated Heart Failure (ADHF)

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)

Pathophysiology of ADHF

Core Mechanisms

Elevated LV filling pressure → Pulmonary congestion
Reduced cardiac output → Hypoperfusion
Neurohormonal activation
Renal congestion → Cardiorenal syndrome

In most cases, hospitalization in heart failure is driven by volume overload with pulmonary and/or venous congestion, reflected by elevated right- and left-sided filling pressures.

Sympathetic activation reduces venous capacitance, shifting blood from reservoirs (like the splanchnic circulation) to the heart, thereby increasing filling pressures without increasing total body volume.

Although weight gain is a simple marker of worsening heart failure, it is not a sensitive indicator in all patients.

Hemodynamic Profiles

Profile	Congestion	Perfusion	Clinical Type
Warm & Wet	Yes	Adequate	Most common(80%)
Cold & Wet	Yes	Poor	High mortality
Cold & Dry	No	Poor	Hypovolemic / overdiuresed
Warm & Dry	No	Adequate	Compensated

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
Dyspnea on exertion(most common symptom of hypervolemic ADHF,	↑ 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 cardiac 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

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

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

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

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.

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

6. IVC Size-Plethoric, non-collapsible → high RA pressure

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.

Hemodynamic Monitoring-Pilmonary artery catheter (Not routinely recommended )-indications are

Respiratory distress or impaired systemic perfusion with inadequate clinical

assessment

Persistent HF symptoms and Unclear fluid status (wet or dry) and/or perfusion status (warm or cold)
Uncertain systemic or pulmonary vascular resistance
Worsening kidney function
To guide IV vasodilator or inotropic therapy
To guide potential mechanical cardiac support or heart transplant decisionsUsing Pulmonary Artery Catheter:

Hemodynamic Goals in ADHF

Parameter	Target (Goal)
Right Atrial Pressure (RAP)	< 8 mmHg
Pulmonary Capillary Wedge Pressure (PCWP)	< 15 mmHg
Systemic Vascular Resistance (SVR)	1000–1200 dynes-sec/cm⁵
Cardiac Index (CI)	≥ 2.2 L/min/m²
If CI remains low	—

Coronary Evaluation

Indicated if:

Suspected ACS,High-risk ECG changes,Elevated troponin

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.