creation date: 2025-05-01 18:50
tags: Pathologies
Congestive Heart Failure
Background
Definitions
Heart failure is a complex clinical syndrome that is characterized by a structural or functional impairment of ventricular filling and/or ejection of blood.
Terminology
Congestive HF: refers to HF with signs of fluid overload
Left HF: impairment of left heart resulting in tissue hypoperfusion and/or increased pulmonary capillary pressure (more common than right)
Right HF: impairment of right heart resulting in impaired blood flow to pulmonary circulation and/or elevated venous pressure
Biventricular (global) HF: both left and right ventricles affected
Chronic compensated HF: symptoms are stable
Acute decompensated HF: acute HF due to decompensation of preexisting disease and/or cardiomyopathy
Systolic dysfunction: reduced ventricular contractility resulting in ventricular enlargement and reduced ejection fraction
Diastolic dysfunction: reduced ventricular compliance characterized by elevated filling pressures, abnormal relaxation, and increased ventricular stiffness
Note, classification of HF is discussed under diagnostic criteria.
Etiology
Heart failure can be caused by a number of conditions which includes:
- Ischemic heart disease (eg. Coronary Artery Disease, myocardial infarction)
- Hypertension
- Valvular heart disease
- Cardiomyopathy, including inflammatory, infiltrative, Takotsubo, or peripartum cardiomyopathy - results in LV or RV dysfunction
- Tachycardia and arrhythmia
Pathogenesis
Heart failure is a progressive disease that is often initiated by some damage or alteration of the cardiac structure. The alteration causes compensatory mechanisms and then, once exhausted, maladaptation.
In early stages of CHF, the heart attempts to maintain cardiac output to meet systemic needs by activation of the sympathetic nervous system. This has several downstream effects:
- Reduced beta-receptor responsiveness
- Changes in myocyte regeneration
- Myocardial hypertrophy
- Myocardial hypercontractility
- Activation of RAAS system causing systemic vasoconstriction and sodium retention
The decrease in CO stimulates the release of epinephrine, norepinephrine, endothelin-1, and vasopressin. This causes further vasoconstriction and thus increasing afterload. In addition to hypercontractility which increases myocyte oxygen demands, a greater cardiac output is needed - creating a positive feedback spiral leading to myocardial cell death.
BNP from ventricular myocytes are also secreted as a response to increased ventricular filling and stretching. In cases of decompensated CHF, natriuretic peptides are no longer effective. Neprilysin breaks down hormones such as BNP, ANP, and bradykinin.
As demand continues to increase and cardiac output decrease, maladaptive responses occur. Loss of myocytes (eg. due to MI) and thus contractility results in decreased ejection fraction. If instead, ventricular compliance is decreased (eg. due to ventricular wall hypertrophy), ejection fraction may be preserved but filling is decreased.
Left-sided failure occurs first more often and usually results in upstream congestion and failure as disease progresses.
Clinical Presentation
Signs & Symptoms
Symptoms of HF consist of those relating to fluid accumulation:
- Dyspnea
- Orthopnea (and paroxysmal nocturnal dyspnea)
- Edema
- Pain from hepatic congestion
- Abdominal discomfort due to ascities
and those relating to cardiac output reduction: - Fatigue and weakness, especially with exertion
Symptoms may also differ based on the acuity. In acute and subacute cases, dyspnea may be more pronounced. RUQ pain may be present due to hepatic congestion.
In chronic presentations (months), fatigue, anorexia, and fluid retention symptoms may be more prominant than dyspnea. Dyspnea may not be noticed as it is often exertional and many patients will withdraw from physical activity.
History & Physical Exam
Detailed history should elucidate extent of symptoms.
Physical exam findings can be specific but insensitive. Absence of these findings should not exclude HF:
- Laterally displaced apical heart beat
- Distal extremity pallor/coolness (hypoperfusion)
- Pulsus alternans (alternating strong weak peripheral pulse) - pathognomonic of severe LV systolic dysfunction
- Bilateral basilar crackles on asucultation
- Elevated JVP
- Peripheral edema (legs → abdomen → arms)
Risk factors
Factors that contribute to developing CHF include unhealthy lifestyle factors common with cardiovascular diseases:
- Smoking
- Diet
- Lack of physical activity
- Alcohol consumption
These contribute to health conditions that predispose an individual to developing CHF such as:
- Coronary artery disease
- Diabetes
- Hypertension
- Cardiac ischemia
Diagnosis
Criteria
Diagnosis is made using clinical evaluation and an echocardiogram. HF is confirmed if a patient has clinical features attributable to structural or functional cardiac abnormalities and either:
- Elevated natriuretic peptides
- Evidence of cardiogenic pulmonary or systemic congestion
Diagnostic tests done during the workup will support the diagnosis as well as assess for etiology and severity.
Classification by LV ejection fraction
Heart failure with preserved ejection fraction (HFpEF):
- Reduced stroke volume, due to reduced compliance of LV
- Normal or reduced end-diastolic volume
- Preserved LVEF (≥50%)
- Evidence of increased LV filling pressures (eg. natriuretic peptides, hemodynamic measurements)
Heart failure with reduced ejection fraction (HFrEF): - Reduced stroke volume
- Reduced LVEF (≤40%)
Heart failure with improved ejection fraction (HFimpEF): - Previously HFrEF
- Follow-up LVEF measurement >40%
Heart failure with mildly reduced ejection fraction (HFmrEF): - Mildly reduced LVEF (41-49%)
- Evidence of increased LV filling pressures
ACC/AHA classification stages
Stage A (at risk):
- Asymptomatic
- No structural heart disease
- Has risk factors for HF
Stage B (pre-HF): - Asymptomatic
- Has evidence of at least one of the following:
- Structural heart disease
- Increased filling pressures
- Risk factors for HF and increased BNP or troponin with no alternative diagnosis
Stage C (symptomatic):
- Signs and symptoms of HF
- Structural heart disease
- Once patient is classified as C, remains as such even if treatment eliminates symptoms
Stage D (advanced HF): - Symptoms of HF that disrupt daily life
- Frequent hospitalization despite optimized management
NYHA functional classification
Used for assessment of limitations in physical activity and symptoms.
Class I:
- No limitations in physical activity
- No HF symptoms
Class II: - Mild symptoms and slight limitations during ordinary physical activity
- Asymptomatic at rest
Class III: - Marked limitations in physical activity
- Symptoms with less than ordinary activity
- Comfortable only at rest
Class IV: - Severe limitations
- Symptom with any exertion and at rest
Work-up
The workup begins when a clinical suspicion of HF is established from history or physical examination and symptoms cannot be attributed to a noncardiac condition.
Initial testing typically consist of:
- ECG - high Sn, limited Sp for HFrEF; low Sp for HFpEF
- Blood tests:
-
Troponin
-
CBC - for differential or exacerbating factors
-
Serum electrolytes, blood urea, creatinine, TSH, lipids - for related conditions that contribute to exacerbation
-
Liver function tests - for hepatic congestion
-
A1C / fasting blood glucose - for underlying DM
-
BNP/NT-proBNP - regularly now (previously was not covered)
- NT-probNP > 125 pg/mL
- BNP > 50 pg/mL
-
- Chest radiograph - findings include:
- Cardiomegaly
- Pleural effusion
- Alveolar edema
- Kerley B lines
- Bronchiolar-alveolar cuffing
While chest radiographs are not used for diagnosis, a number of findings are frequently seen:
- Alveolar and/or interstitial edema (eg. “Kerley B” lines, peribronchial cuffing)
- Cephalization of blood vessels
- Vascular congestion
An echocardiogram should be performed which will evaluate:
- LV systolic and/or diastolic dysfunction
- Quantitative measure of LVEF
- Atrial and ventricular size and thickness
- Evidence of complications
- Underlying causes (eg. LVH)
If HF is suspected to coexist with other causes, pulmonary function studies and cardiopulmonary exercise tests can be used.
Differential
As many signs and symptoms of HF are nonspecific, it is important to consider alternative diagnoses. Some examples of alternative or overlapping conditions are listed below.
Symptoms of dyspnea:
- Myocardial ischemia
- Pulmonary disease
Fatigue: - Deconditioning
- Sleep apnea
- Depression
Fluid retention: - Venous thrombosis or insufficiency
- Renal sodium retention
- Drug side effects
- Cirrhosis
Red Flags / Complications
A number of complications exist:
- Reduced quality of life
- Arrhythmia and sudden cardiac death
- Cardiac cachexia
- Cardiorenal disease
- Liver dysfunction
- Functional valvular insufficiency (eg. mitral or tricuspid regurgitation)
- Mural thrombi and risk of thromboembolism
- Recurrent hospitalizations and associated risk of hospitalization
CHF is associated with high mortality:
- ~80-90% one year survival
- ~50-60% 5 year survival
- ~30% 10 year survival
Management
Lifestyle / Social
Non-pharmacological management primarily revolves around managing risk factors:
- Controlling hypertension and diabetes
- Smoking cessation
- Weight loss
- Routine immunization
Monitoring should include:
- Blood pressure
- Daily weight measurement (sign of fluid overload)
- Signs of decompensation
Sodium restriction may be considered (2-3g/day).
Pharmacological / Interventional
Standard pharmacological management of HF consist of the “quadruple therapy”. The 4 medications and some examples of each are as follows:
- Angiotensin receptor-neprilysin inhbitor (ARNI)
- Sacubitril-valsartan 24mg/26mg PO BID initially, titrate to target 97mg/103mg BID as tolerated
- ACEi or ARB can be used in place and substituted later on; substitution requires 36 hr wash-out period to avoid angioedema
- Rationale: reduces RAAS which reduces afterload, BP, and ventricular remodelling
- Beta-blocker
- Carvedilol 3.125mg PO BID, titrate to target 25mg BID
- Bisoprolol 1.25mg PO daily, titrate to target 10mg daily
- Metoprolol succinate XR 12.5-25mg PO daily, titrate to target 200mg PO daily
- Rationale: inhibits adrenergic stimulation that causes tachycardia, arrhythmias, and myocardial oxygen demand
- Mineralocorticoid receptor antagonist (MRA)
- Spironolactone 12.5-25mg PO daily initially, titrate to target 25-50mg daily
- Eplerenone 25mg PO daily initially, titrate to target 50mg daily
- Rationale: suppresses aldosterone-mediated sodium retention and myocardial fibrosis
- SGLT2 inhibitor
- Dapagliflozin 10mg PO daily
- Empagliflozin 10mg PO daily
- Rationale: provides osmotic diuresis which reduces preload and afterload, improving cardiac efficiency and renal hemodynamics
Depending on comorbidities and if control is adequate, therapy can be individualized with sinus node inhibitors, sGC stimulators, vasodilators, and digoxin.
For patients with symptoms of fluid overload, diuretics can be used. The first-lane medications are loop diuretics:
- Bumetanide 0.5-1mg PO daily or BID, titrate up to max 10mg daily prn
- Furosemide (Lasix) 20-40mg PO daily or BID, titrate up to max 600mg daily prn
- Torsemide 10-20mg PO daily, titrate to max 200mg daily prn
Thiazide diuretics may be added if loop diuretics are insufficient.
It should be noted that the quadruple therapy has only been shown to reduce mortality and morbidity in HFrEF. In patients with HFpEF, treatment primarily focuses on symptom relief and comorbidity control.
Long-term monitoring
Due to the high risk of mortality, CHF must be closely monitored. CHF specific appointments should occur at least 1-2 times annually. Assessment should also be made 3 months following initiation of treatment and with symptomatic presentation.
Blood work to follow include:
- CBC
- Iron studies
References
Tools / Guidelines
CCS - Heart Failure Guidelines 2021