Congestive Heart Failure: Definition and Management in Older Adults
What is Congestive Heart Failure?
Congestive heart failure is a complex clinical syndrome resulting from structural or functional impairment of ventricular filling or ejection of blood, manifesting primarily as dyspnea, fatigue, and fluid retention. 1 The condition represents a progressive disorder where the heart cannot pump enough blood to meet the body's metabolic needs. 2
Pathophysiology and Progression
The disease begins with injury or stress to the myocardium and progresses through a process called cardiac remodeling, where the left ventricle dilates, hypertrophies, and becomes more spherical. 1 This structural change increases hemodynamic stress on the heart walls, depresses mechanical performance, and may worsen mitral regurgitation—all of which perpetuate the remodeling cycle. 1
Neurohormonal activation plays a central role in disease progression, with elevated levels of norepinephrine, angiotensin II, aldosterone, endothelin, vasopressin, and cytokines adversely affecting cardiac structure and function. 1 Importantly, cardiac remodeling precedes symptoms by months or years and continues despite treatment, contributing to clinical deterioration. 1
Clinical Presentation
The hallmark pulmonary finding is rales (crackles), typically heard at the lung bases first and extending throughout both lung fields as severity increases. 3 However, a critical caveat: not all heart failure patients present with classic pulmonary rales—some have predominantly peripheral edema with minimal lung findings, and absence of rales does not rule out heart failure. 3
Additional signs include orthopnea, jugular venous distension, hepatojugular reflux, S3 gallop rhythm, and cardiomegaly. 3 Chest radiography may demonstrate pulmonary venous congestion, interstitial edema, pleural effusions, and Kerley B lines. 3
Staging System for Heart Failure
The ACC/AHA guidelines use a four-stage classification system that recognizes heart failure as a progressive disease: 1
Stage A: High risk for heart failure but no structural heart disease or symptoms (patients with hypertension, atherosclerotic disease, diabetes, obesity, metabolic syndrome, or family history of cardiomyopathy) 1
Stage B: Structural heart disease present but no signs or symptoms (includes left ventricular hypertrophy, reduced ejection fraction, asymptomatic valvular disease, or previous myocardial infarction) 1
Stage C: Structural heart disease with prior or current symptoms of heart failure 1
Stage D: Refractory heart failure requiring specialized interventions, with marked symptoms at rest despite maximal medical therapy 1
Treatment Approach in Older Adults with Risk Factors
Stage A: Prevention is Primary
For patients with hypertension, diabetes, coronary artery disease, or previous myocardial infarction who have not yet developed structural heart disease, prevention of heart failure should be the primary objective. 1 The development of ventricular dysfunction and heart failure may be delayed or prevented by treating these underlying conditions. 1
ACE inhibitors or ARBs should be initiated in appropriate patients at this stage to prevent progression to structural heart disease. 1 Beta-blockers are also recommended in appropriate patients. 1
Stage B: Preventing Symptom Development
Patients with structural heart disease but no symptoms should receive ACE inhibitors or ARBs at high doses unless contraindicated. 1 Beta-blockers should be added in appropriate patients. 1 This aggressive approach aims to prevent progression to symptomatic heart failure.
Stage C: Symptomatic Management
For symptomatic patients, the cornerstone of therapy includes ACE inhibitors (or ARBs if ACE inhibitors are not tolerated), beta-blockers, and diuretics for fluid retention. 1 Aldosterone antagonists should be added in selected patients. 1
Diuretics are essential for managing fluid overload, with loop diuretics being the cornerstone for treating pulmonary congestion, with dosing titrated to resolve clinical evidence of congestion. 3 However, in elderly patients, thiazides are often ineffective due to reduced glomerular filtration rate. 1
Digoxin remains useful for symptom management and may reduce hospitalizations, though it does not improve survival. 1 In elderly patients, low initial dosages are recommended due to increased susceptibility to adverse effects and delayed excretion. 1
For patients who cannot tolerate ACE inhibitors, the combination of hydralazine and nitrates may offer prognostic benefit. 4
Special Considerations for Elderly Patients
The therapeutic approach in elderly patients should be principally identical to younger patients, but applied more cautiously due to altered pharmacokinetics and pharmacodynamics. 1
ACE inhibitors and ARBs are effective and well-tolerated in elderly patients, but low-dose titration is advisable due to greater likelihood of hypotension and delayed excretion. 1 Initiation should include monitoring of supine and standing blood pressure, renal function, and serum potassium levels. 1
Beta-blockers are surprisingly well tolerated in the elderly if patients with contraindications such as sick sinus node, AV-block, and obstructive lung disease are excluded. 1 Beta-blockade should not be withheld because of increasing age alone. 1
In elderly patients, hyperkalaemia is more frequently seen with combinations of aldosterone antagonists and ACE inhibitors or NSAIDs. 1 Careful monitoring is essential.
Drugs to Avoid
NSAIDs and COX-2 inhibitors should be avoided or used with extreme caution as they can worsen heart failure and interact dangerously with other heart failure medications. 1 Class I antiarrhythmic agents should also be avoided. 1
Monitoring and Follow-up
Serial lung examinations should be performed to assess resolution of rales, and natriuretic peptides (BNP or NT-proBNP) should be monitored, with a decrease >30% by day 5 indicating good prognosis. 3 Echocardiography is essential to assess cardiac function and should be performed during initial evaluation to assess left ventricular ejection fraction, chamber size, wall thickness, and valve function. 1
Acute Decompensation
When acute pulmonary edema develops, immediate treatment includes oxygen therapy, intravenous loop diuretics (e.g., furosemide), and intravenous nitroglycerin unless the patient is hypotensive (systolic BP <90 mmHg). 3