Heart Failure

Written By Danial Mirza

Definition

Heart failure (HF) is a clinical syndrome characterized by the heart's inability to pump a sufficient supply of blood to meet the body's metabolic demands, or doing so only at elevated filling pressures. It represents the final common pathway for a multitude of cardiovascular diseases and is defined by symptoms and/or signs resulting from a structural and/or functional cardiac abnormality (15).

Epidemiology

Cardiovascular disease is the leading cause of death in Malaysia, making heart failure a significant and growing public health challenge (5). The prevalence of HF in the Malaysian population is estimated at 6.7% (5). In 2017, Malaysia had one of the highest HF prevalence rates in Southeast Asia, with 721 cases per 100,000 people, a 7.7% increase from 1990 (5). This upward trend is driven by an aging population and a high prevalence of underlying risk factors.

The clinical profile of Malaysian HF patients, as highlighted by the Malaysian Heart Failure (MY-HF) Registry, shows a younger population, with a mean age of approximately 60 years, which is a decade younger than in Western countries (8). The condition predominantly affects males (67%) (9). The primary cause is Ischemic Heart Disease (IHD), accounting for 56-63% of cases (7). This is fueled by a high burden of comorbidities, including hypertension (~72%), diabetes mellitus (~60%), and chronic kidney disease (~31%) (9). Heart Failure with reduced Ejection Fraction (HFrEF) is the most common form, affecting about 65-66% of hospitalized patients (8).

Pathophysiology

The fundamental mechanism of heart failure involves an initial injury or stress to the heart muscle, leading to a decline in cardiac output. This triggers a cascade of compensatory neurohormonal responses, primarily involving the Renin-Angiotensin-Aldosterone System (RAAS) and the Sympathetic Nervous System (SNS). While initially adaptive, chronic activation of these systems leads to detrimental effects, including sodium and water retention, vasoconstriction, myocardial fibrosis, and adverse cardiac remodeling, which further impair cardiac function and lead to the clinical manifestations of congestion and low output (17, 18).

Clinical Presentation

The classic presentation of heart failure arises from fluid retention (congestion) and reduced cardiac output (2).

Common Symptoms (>50%):

  • Dyspnea: Shortness of breath, especially on exertion (2).

  • Orthopnea: Breathlessness when lying flat that is relieved by sitting up (2).

  • Paroxysmal Nocturnal Dyspnea (PND): Sudden, severe shortness of breath that awakens the patient from sleep (2).

  • Reduced Effort Tolerance and Fatigue: A general sense of tiredness or inability to perform usual physical activities (2).

  • Peripheral Leg Swelling: Bilateral ankle or leg edema (2).

⚠️ Red Flag Signs & Symptoms:

  • Elevated Jugular Venous Pressure (JVP): The most reliable clinical sign of fluid overload (2).

  • Third Heart Sound (S3 Gallop): A low-pitched sound in early diastole indicating rapid ventricular filling into a non-compliant ventricle (2).

  • Pulmonary Crepitations (Rales): Crackling sounds on lung auscultation that suggest pulmonary edema (2).

  • Positive Hepatojugular Reflux (HJR): A sustained rise in JVP upon abdominal pressure (2).

Complications

Heart failure can lead to a range of complications affecting multiple organ systems:

  • Cardiovascular: Atrial fibrillation, ventricular arrhythmias and sudden cardiac death, cardiogenic shock (13).

  • Renal: Acute kidney injury, chronic kidney disease, cardiorenal syndrome (9).

  • Hepatic: Congestive hepatopathy.

  • Constitutional: Frailty, sarcopenia, and cachexia (7).

Prognosis

The prognosis for heart failure remains serious, with high rates of hospitalization and mortality. In Malaysia, the 30-day all-cause readmission rate for HF patients is between 13% and 18.1%, and each readmission is associated with a higher risk of mortality (5). The implementation of Guideline-Directed Medical Therapy (GDMT) is critical for improving survival, reducing hospitalizations, and enhancing quality of life (1, 15).

Differential Diagnosis

Chronic Obstructive Pulmonary Disease (COPD): This is a key differential due to the shared symptom of dyspnea. However, COPD is less likely if the patient has a clearly elevated JVP, an S3 gallop, and significant peripheral edema. A natriuretic peptide test can be highly effective in distinguishing between cardiac and pulmonary causes of breathlessness (2).

Pneumonia: Consider this diagnosis, especially if the patient presents with fever, productive cough, and focal chest signs. While both can show opacities on a chest X-ray, the distribution in HF-related pulmonary edema is typically more diffuse and bilateral, often with other signs of fluid overload like pleural effusions and Kerley B lines (13).

Acute Kidney Injury (AKI): AKI can cause fluid overload and peripheral edema, mimicking heart failure. However, in primary renal failure, signs of cardiac dysfunction like an S3 gallop or a highly elevated JVP are usually absent. A thorough clinical examination and urinalysis are key to differentiating the two.

Investigations

Immediate & Bedside Tests

  • A bedside ECG is mandatory to immediately identify potential triggers and underlying pathology. It provides crucial clues such as evidence of a prior myocardial infarction (pathological Q waves), left ventricular hypertrophy, or rhythm abnormalities like atrial fibrillation (13). A completely normal ECG makes a diagnosis of systolic HF highly unlikely (15).

  • A Chest X-ray is essential to assess for cardiomegaly and signs of pulmonary congestion. This helps to confirm fluid overload through findings like pulmonary venous cephalization, interstitial edema (Kerley B lines), and pleural effusions (13).

Diagnostic Workup

  • First-Line Investigations: Natriuretic Peptide (BNP or NT-proBNP) testing is a crucial initial blood test. In a patient with undifferentiated dyspnea, a normal NP level has a high negative predictive value, effectively ruling out acute HF (2). An elevated level strongly supports the diagnosis and justifies further cardiac imaging. This test is critically underutilized in Malaysia, with only 16.5% of hospitalized HF patients receiving it, representing a major gap in care (13).

  • Gold Standard: A transthoracic echocardiogram (ECHO) is the single most important imaging test to confirm the diagnosis. It provides objective evidence of cardiac dysfunction, assesses valvular heart disease, and, most importantly, measures the Left Ventricular Ejection Fraction (LVEF), which is essential for classifying HF and guiding therapy (2, 15).

Monitoring & Staging

  • Serial renal profiles (urea, electrolytes, creatinine) are performed to monitor for cardiorenal syndrome and guide medication dosage. This is vital because many foundational HF therapies can affect renal function and potassium levels (1, 15).

  • A full blood count is necessary to detect anemia, as it is a common comorbidity and a predictor of poor outcomes in heart failure patients (15).

Management

Management Principles

The management of heart failure focuses on relieving symptoms, inhibiting the neurohormonal pathways that drive disease progression, reducing mortality, and preventing hospitalizations through the aggressive implementation of Guideline-Directed Medical Therapy (GDMT) (1, 5).

Acute Stabilisation (The First Hour)

  • Airway/Breathing: Administer high-flow oxygen via a non-rebreather mask to maintain SpO2 >94% (the action), which is crucial to correct hypoxemia and prevent end-organ damage from tissue hypoxia (15).

  • Circulation: Secure IV access and administer an intravenous loop diuretic like IV Furosemide (the action) to urgently relieve the symptoms and signs of congestion (15). The initial dose should be equivalent to or greater than the patient's oral home dose. In hypertensive patients, IV vasodilators (e.g., nitroglycerin) can be added to reduce preload and afterload (15).

Definitive Therapy

The management strategy is dictated by the patient's LVEF classification (1).

Heart Failure with reduced Ejection Fraction (HFrEF; LVEF ≤40%)

The 2023 Malaysian CPG recommends foundational therapy with four "pillar" drug classes (1).

  • First-Line Treatment:

    • Angiotensin Receptor-Neprilysin Inhibitor (ARNI): Sacubitril/valsartan is the preferred agent for RAAS inhibition, shown to be superior to ACE inhibitors in reducing cardiovascular death and HF hospitalizations by 20% (17, 20).

    • Evidence-Based Beta-Blocker: Specific agents like bisoprolol, carvedilol, or metoprolol succinate are essential to counteract sympathetic overactivity, reduce mortality, and improve LV function (1).

    • Mineralocorticoid Receptor Antagonist (MRA): Spironolactone or eplerenone is added to block the harmful effects of aldosterone, reducing mortality and hospitalizations (1).

    • SGLT2 Inhibitor: Dapagliflozin or empagliflozin is recommended for all HFrEF patients, regardless of diabetes status, to significantly reduce cardiovascular death and HF hospitalizations by 25-26% (24, 29).

Heart Failure with preserved Ejection Fraction (HFpEF; LVEF ≥50%)

  • First-Line Treatment: The 2023 Malaysian CPG recommends the use of SGLT2 inhibitors (empagliflozin or dapagliflozin) to reduce the risk of HF hospitalizations by 21%, based on powerful evidence from the EMPEROR-Preserved and DELIVER trials (1, 35, 36).

  • Management also focuses on the meticulous control of comorbidities (especially hypertension and atrial fibrillation) and judicious use of diuretics for congestion (1).

Heart Failure with mildly reduced Ejection Fraction (HFmrEF; LVEF 41-49%)

  • It is advised that the foundational therapies for HFrEF (the four pillars) should be considered for this group, as they have been shown to be beneficial in analyses of this population (1).

Supportive & Symptomatic Care

  • Diuretics: Loop diuretics (e.g., furosemide) are the cornerstone for managing fluid overload and relieving symptoms of congestion in all types of HF (15). The dose should be titrated to the lowest effective level to maintain euvolemia (15).

  • Dietary and Fluid Management: Patients should be counseled on a low-sodium diet (<2 g/day) and, in severe cases, fluid restriction (1.5-2 L/day) (15).

Key Nursing & Monitoring Instructions

  • Strict hourly input/output chart monitoring to assess response to diuretics.

  • Daily weight monitoring to track volume status.

  • Regular monitoring of blood pressure, heart rate, and renal function, especially after initiation or titration of GDMT.

  • Inform the medical officer if urine output is <0.5mL/kg/hr, systolic BP drops below 90 mmHg, or the patient develops worsening shortness of breath or confusion.

Long-Term Plan & Patient Education

The period following a hospitalization for acute HF is a "vulnerable phase" with a high risk of readmission (5). This admission must be treated as a "pit stop" to optimize GDMT (8).

  • Follow-up: Arrange for a clear follow-up plan, ideally in a dedicated multidisciplinary HF clinic within 1-2 weeks of discharge (5, 7).

  • Secondary Prevention: Aggressively manage all cardiovascular risk factors. Encourage smoking cessation and regular, moderate exercise through cardiac rehabilitation programs (15).

  • Patient Education: This is paramount. Educate the patient and family on the importance of medication adherence, daily weight monitoring, dietary restrictions, and recognizing early signs of worsening HF (e.g., increased swelling, weight gain, worsening breathlessness) that warrant seeking medical attention (15).

When to Escalate

Call Your Senior (MO/Specialist) if:

  • The patient presents with signs of cardiogenic shock ("cold and wet" profile), such as hypotension, confusion, or poor urine output (15).

  • The patient develops significant hyperkalemia (K+ >5.0 mmol/L) or a sharp decline in renal function (eGFR <30) after starting RAAS inhibitors or MRAs (1).

  • The patient remains persistently symptomatic or congested despite escalating doses of intravenous diuretics.

  • The patient develops a significant arrhythmia, such as rapid atrial fibrillation or ventricular tachycardia (15).

Referral Criteria

  • Refer to a cardiologist or tertiary center for consideration of device therapy (ICD or CRT) if a patient with HFrEF (LVEF ≤35%) remains symptomatic despite at least 3 months of optimal GDMT (39, 40).

  • Refer to the Nephrology team if acute kidney injury does not resolve or if there is progressive chronic kidney disease.

  • Refer to a multidisciplinary HF clinic for holistic management, especially for patients with high-risk features, multiple comorbidities, or frequent readmissions (5, 7).

References

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Danial Mirza
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