Treatment of Enlarged Heart and Pulmonary Congestion
Immediate treatment requires intravenous loop diuretics (furosemide) to reduce pulmonary congestion, combined with oxygen therapy and vasodilators (nitroglycerin) if blood pressure permits (systolic BP ≥90 mmHg), while simultaneously initiating long-term heart failure therapy with ACE inhibitors and beta-blockers once stabilized. 1, 2
Acute Management of Pulmonary Congestion
Immediate Interventions
- Administer oxygen therapy immediately to maintain oxygen saturation >90%, as arterial oxygen saturation is typically <90% on room air in acute pulmonary edema 1
- Give intravenous loop diuretics (furosemide) promptly as the cornerstone treatment for pulmonary congestion, with dosing titrated to resolve clinical evidence of fluid overload 1, 2
- Administer intravenous nitroglycerin as a first-line vasodilator to reduce preload and improve symptoms, unless systolic blood pressure is <90 mmHg 1
Clinical Monitoring
- Perform serial lung examinations to assess resolution of rales (crackles), which are the hallmark lung sounds indicating pulmonary congestion 1
- Monitor natriuretic peptides (BNP or NT-proBNP), with a decrease >30% by day 5 and discharge value <1500 pg/mL indicating good prognosis 1
- Consider bedside lung ultrasound if expertise is available, as it has superior sensitivity compared to chest X-ray for detecting interstitial syndrome and quantifying B-lines to assess treatment response 1
Diagnostic Workup
Essential Initial Tests
- Obtain 12-lead electrocardiogram to exclude ST-elevation myocardial infarction, identify arrhythmias, and assess for prior infarction or left ventricular hypertrophy 3, 4
- Perform two-dimensional echocardiography with Doppler during initial evaluation to assess left ventricular ejection fraction, chamber size, wall thickness, valve function, and diastolic parameters 3, 4
- Measure natriuretic peptides (BNP or NT-proBNP) using point-of-care assay to confirm heart failure diagnosis, with NT-proBNP >2000 pg/mL or BNP >400 pg/mL making chronic heart failure highly likely 1, 4
Laboratory Assessment
- Order complete blood count, serum electrolytes (including calcium and magnesium), blood urea nitrogen, serum creatinine, fasting glucose, lipid profile, liver function tests, and thyroid-stimulating hormone 3, 4
- Check troponin levels to assess for acute coronary syndrome as a precipitating factor 1
Imaging Studies
- Review chest radiograph for cardiomegaly, pulmonary venous congestion, interstitial edema (Kerley B lines), and pleural effusions 3, 1
- A normal chest X-ray makes pulmonary congestion unlikely but does not completely rule out heart failure, especially in early or well-compensated cases 1
Long-Term Pharmacological Management
First-Line Therapy
- Initiate ACE inhibitors as first-line therapy in patients with reduced left ventricular systolic function, starting with low doses and building up to maintenance dosages shown effective in large trials 3
- Start beta-adrenoceptor antagonists once the patient is stabilized, as they are recommended in appropriate patients with heart failure 3
- Continue diuretics in combination with ACE inhibitors for ongoing symptom management when fluid overload is present 3
ACE Inhibitor Initiation Protocol
- Review and potentially reduce diuretic doses 24 hours before starting ACE inhibitors to avoid excessive diuresis 3
- Start with low doses, preferably in the evening when supine to minimize blood pressure effects 3
- Check blood pressure, renal function, and electrolytes 1-2 weeks after each dose increment, at 3 months, and subsequently at 6-monthly intervals 3
- Avoid potassium-sparing diuretics during initiation and avoid NSAIDs 3
Diuretic Management
- Use loop diuretics or thiazides initially, always in addition to an ACE inhibitor 3
- If glomerular filtration rate <30 mL/min, do not use thiazides except synergistically with loop diuretics 3
- For insufficient response, increase diuretic dose, combine loop diuretics and thiazides, or administer loop diuretics twice daily 3
- In severe chronic heart failure with persistent fluid retention, add metolazone with frequent measurement of creatinine and electrolytes 3
Critical Diagnostic Considerations
Exclude Cardiac Mimics
- Do not presume all patients with congestion and preserved ejection fraction have typical heart failure - consider infiltrative cardiomyopathy (especially cardiac amyloidosis in men >50 years), hypertrophic cardiomyopathy, pericardial disease, and valvular heart disease 3, 5
- Screen for cardiac amyloidosis with technetium pyrophosphate scan and serum/urine protein electrophoresis if clinical features suggest restrictive cardiomyopathy (biatrial enlargement disproportionate to ventricular size, increased wall thickness, preserved ejection fraction) 3, 5
- Consider cardiac MRI to differentiate restrictive cardiomyopathy from constrictive pericarditis and identify infiltrative processes 5
Exclude Non-Cardiac Causes
- Evaluate for non-cardiac mimics including kidney disease, liver disease, and chronic venous insufficiency that can cause congestion without primary cardiac dysfunction 3
- Assess for chronic kidney disease, which is present in approximately 25% of heart failure cases and creates a vicious cycle where each condition exacerbates the other 6, 7
Common Pitfalls to Avoid
- Do not assume absence of rales rules out heart failure - some patients present with predominantly peripheral edema with minimal lung findings, or exercise intolerance without evidence of fluid retention 1
- Do not withhold ACE inhibitors and beta-blockers in patients with renal disease - these medications are often under-used in patients with chronic kidney disease and heart failure despite proven benefits 6, 8
- Avoid NSAIDs, as they double the rate of hospitalization in patients with congestive heart failure 7
- Do not overlook anemia, which is found in one-third to half of heart failure cases and may be caused by chronic kidney disease or the heart failure itself, contributing to worsening cardiac and renal status 7
Special Populations
Patients with Chronic Kidney Disease
- Heart failure prevalence increases dramatically as renal function deteriorates, reaching 65-70% at end-stage renal disease 7
- Uncontrolled heart failure is associated with rapid decline in renal function, while adequate heart failure control can prevent this progression 7
- Treatment of chronic kidney disease can prevent heart failure, and vice versa - aggressive treatment of both conditions may markedly slow progression of both diseases 7
Hypertensive Heart Disease
- Longstanding hypertension leads to diastolic dysfunction and concentric left ventricular hypertrophy initially, progressing to heart failure with preserved ejection fraction 9
- The end stage results in dilated cardiomyopathy with both diastolic dysfunction and reduced ejection fraction 9
- "Decapitated hypertension" describes the decrease in blood pressure resulting from reduced pump function in advanced heart failure 9