What are the signs and treatment options for congestion in patients with and without a history of cardiovascular disease?

Signs of Congestion in Heart Failure

Cardinal Clinical Signs

The primary clinical signs of congestion include dyspnea/orthopnea, jugular venous distension (JVD), pulmonary rales, and peripheral edema—these are the key manifestations that drive hospitalization and predict mortality in heart failure patients. 1

Symptoms of Congestion

• Dyspnea and orthopnea are the most common presenting symptoms, representing pulmonary congestion from elevated left ventricular diastolic pressure 1
• Paroxysmal nocturnal dyspnea indicates significant pulmonary venous congestion 2
• Weight gain often accompanies fluid accumulation, though many patients are discharged without losing body weight despite persistent congestion 1

Physical Examination Findings

• Jugular venous distension (JVD): JVP <8 cm indicates no congestion, 8-10 cm mild, 11-15 cm moderate, and >16 cm severe congestion often with massive tender hepatomegaly 1, 3
• Hepatojugular reflux can be elicited even when static JVP appears normal and serves as a marker for occult congestion 1, 3
• Pulmonary rales (fine crackles) indicate alveolar edema from elevated pulmonary capillary pressure 1, 2
• Peripheral edema: graded as 1+ (mild), 2+ (moderate), to 3+/4+ (severe/pitting) 1
• Hepatomegaly: ranges from liver edge enlargement to massive tender enlargement extending to midline in severe cases 1, 3

Important Caveat About Physical Signs

Physical examination has only 58% sensitivity for detecting elevated pulmonary capillary wedge pressure ≥22 mmHg—signs and symptoms are late manifestations that only detect moderate to high levels of congestion. 1, 3 Hemodynamic congestion precedes clinical congestion by days or even weeks. 1, 3

Signs of Peripheral Hypoperfusion ("Cold and Wet" Profile)

When congestion occurs with reduced cardiac output, patients present with the "cold and wet" profile: 2

• Cold and clammy skin from peripheral vasoconstriction 2
• Dry mucous membranes despite pulmonary volume overload—this paradoxical finding results from peripheral hypoperfusion 2
• Normal or low blood pressure 2
• Oliguria from reduced renal perfusion 2

Prognostic Significance

Patients with dyspnea, edema, and JVD on admission have a 2-3 fold increase in 60-day mortality compared to those without these features. 1 Those with ≥3 residual signs of congestion at discharge have only 41% two-year survival compared to 87% in those with no residual congestion. 1

Grading Congestion Severity

The European Society of Cardiology proposes a systematic scoring system combining: 1

Bedside Assessment:

• Orthopnea: none (0), mild/one pillow, moderate/multiple pillows, severe/sleeps seated
• JVP: <8 cm (0), 8-10 cm or hepatojugular reflux, 11-15 cm, >16 cm
• Hepatomegaly: absent, liver edge enlargement, moderate pulsatile, massive tender
• Edema: none, 1+, 2+, 3+/4+

Laboratory:

• BNP: <100 (0), 100-299,300-500, >500 pg/mL 1
• NT-proBNP: <400 (0), 400-1500-3000, >3000 pg/mL 1

Dynamic Maneuvers:

• 6-minute walk test: >400 m (0), 300-400 m, 200-300 m, 100-200 m, <100 m 1
• Valsalva maneuver: normal response vs absent overshoot vs square wave pattern 1

Total score: <1 = none, 1-7 = mild, 8-14 = moderate, 15-20 = severe congestion 1

Differential Diagnosis: Cardiac vs Non-Cardiac Congestion

Before presuming all patients with congestion and preserved ejection fraction have HFpEF, exclude non-cardiac mimics and specific cardiomyopathies. 1

Non-Cardiac Causes of Congestion:

• Kidney disease causing fluid retention 1
• Liver disease with ascites and hypoalbuminemia 1
• Chronic venous insufficiency causing peripheral edema 1

Cardiac Mimics Requiring Specific Workup:

• Infiltrative cardiomyopathy (especially transthyretin cardiac amyloidosis)—suspect with increased LV wall thickness, carpal tunnel syndrome, lumbar spinal stenosis 1
• Hypertrophic cardiomyopathy 1
• Pericardial disease (constrictive pericarditis, tamponade) 1
• Valvular heart disease (especially mitral regurgitation, which may have minimal murmur in acute severe cases) 1, 2
• High-output heart failure 1

Treatment Approach

Acute Decongestion Strategy

Loop diuretics are essential first-line agents for rapid symptom relief, with torsemide having the longest duration and highest bioavailability. 4 However, diuretic-based strategies improve symptoms but have no impact on mortality or rehospitalization rates. 4

The critical shift must occur from a "diuretic-centric" approach to early initiation and rapid up-titration of neurohormonal blockade and SGLT-2 inhibitors. 4

Specific Recommendations:

• SGLT-2 inhibitors should be initiated immediately in hospital after initial stabilization—they address sodium avidity at the nephron level while providing mortality and hospitalization benefits 4
• Once excess fluid is removed, focus on implementation and fast up-titration of guideline-directed medical therapy rather than increasing diuretic doses 4
• Do not discharge patients with residual congestion—this is the strongest predictor of early rehospitalization and death 4

For "Cold and Wet" Profile:

• Normotensive patients: nitroprusside increases anterograde output and reduces mitral regurgitation 2
• Hypotensive patients: combine nitroprusside with inotropic agent (dobutamine)—never give nitroprusside alone 2

Monitoring Response:

• A decrease >30% in natriuretic peptides at day 5 predicts better outcomes 4
• Accept minor creatinine increases if the patient is decongesting and clinically improving—this often represents beneficial hemodynamic changes rather than true kidney injury 4