Heart failure is a dysfunction of either the right or left ventricle, which is diagnosed clinically and supported with imaging and plasma natriuretic peptide levels. It is treated with goal-directed medical therapy (GDMT).
Pathophysiology
- Heart is unable to provide adequate perfusion to meet metabolic needs
- Pulmonary and/or venous pressure increases, causing organ congestion
Left Ventricle Failure
- Cardiac output decreases
- Pulmonary venous pressure increases
- Pulmonary capillary pressure > oncotic pressure = fluid extravasation into interstitial space/ alveoli (pulmonary edema)
- Reduces pulmonary compliance
- Increases work of breathing
- Pulmonary edema decreases systemic arterial oxygenation (PaO2) -> dyspnea
Severe Left Ventricle Failure
- Pleural effusion -> even worse dyspnea
- Minute ventilation increases -> PaCO2 decreases, blood pH increases (respiratory alkalosis)
- Interstitial edema of small airways eventually elevates PaCO2, indicating inability to compensate -> respiratory failure
Right Ventricle Failure
- Systemic venous pressure increases -> fluid extravasation and edema
- Particularly affects feet and ankles, abdominal visceera
- Liver mostly affected: moderate hepatic dysfunction
- Increased conjugated and unconjugated bilirubin, PT, and hepatic enzymes (alkaline phosphatase, gamma-glutamyl transpeptidase)
- Inability to break down aldosterone causes more fluid accumulation
- Stomach and intestine can become congested
- Anorexia
- Malabsorption
- Protein losing enteropathy (diarrhea, marked hypoalbuminemia)
- Chronic GI blood loss
- Ischemic bowel infarction
- Ascites: fluid in peritoneal cavity
Heart Failure with Reduced Ejection Fraction (HFrEF)
- Left ventricular systolic dysfunction due to:
- Poor contraction
- Decreased ejection fraction
- Inadequate emptying
- Increased diastolic volume and pressure
- Increased diastolic volume and pressure from LV failure can lead to RV failure
Compensatory Responses
Cardiovascular
- Ventricular remodeling: both ventricles dilate and hypertrophy
- LV also changes from ovoid to spherical
- Dilation can cause mitral or tricuspid valve regurgitation due to annular dilation -> increases end-diastolic volume
- Increases diastolic stiffness and wall tension -> diastolic dysfunction
- Compromised cardiac performance, exacerbated by physical stress
- Increased oxygen demand and myocardial cell apoptosis
- Increased O2 extraction from blood by shifting oxyhemoglobin dissociation curve to the right
- Arterial baroreflex activation -> increased sympathetic tone, decreased parasympathetic tone
- Increased HR and myocardial contractility
- Arteriole and venous constriction
- Sodium and water retention
Renal
- Activation of renin-angiotensin-aldosterone system (RAAS) in response to decreased renal perfusion
- Increases sodium and water retention
- Increases renal and peripheral vascular tone
- Works in tandem with arterial baroreflex activation
- Increased angiotensin II causes a few problems:
- Vasoconstriction including efferent renal vasoconstriction (increases end-diastolic volume)
- Increases aldosterone production -> myocardial and vascular collagen deposition/ fibrosis
- Contributes to aldosterone that is already produced by the heart
- Increases norepinephrine release -> stimulates vasopressin release and apoptosis
- Contributes to heart remodeling
Neurohumoral
- Goal is to increase heart function, maintain blood pressure, and maintain organ perfusion
- Beta-1 receptor downregulation as response to intense sympathetic activation
- Impaired myocyte contractility -> decreases oxygen demand
- Increased heart rate -> increases cardiac output
- Vasopressin release in response to blood pressure decrease
- Decreases renal excretion of free water -> hyponatremia
- Atrial natriuretic peptide and brain natriuretic peptide (BNP) release in response to ventricular stretching
- Increases renal sodium excretion
- Not as effective due to decreased renal perfusion pressure
- TNF alpha release -> catabolism and cardiac cachexia
- Increased free fatty acid utilisation and decreased glucose utilisation
Heart Failure with Preserved Ejection Fraction (HFpEF)
- Impaired LV filling resulting in increased LV end-diastolic pressure
- Pressure backs up into the left atrium, causing pulmonary hypertension and congestion
- Normal LV end-diastolic volume
- Normal contractility means that a normal percent of the filled ventricle is ejected
Contextual Factors
- Increased cardiac output demand: anemia, hyperthyroidism, Paget disease
- Arrhythmia
- Conduct defects: AV node block, left bundle branch block
- Infiltrative or matrix disorders: amyloidosis, chronic fibrosis, hemochromatosis
Systolic Dysfunction
- Myocardial infarction
- Myocarditis
- Dilated cardiomyopathy
Diastolic Dysfunction
- Impaired ventricular relaxation
- Increased ventricular stiffness
- Old age
- Obesity
- Hypertension
- Diabetes
- Chronic kidney disease
- Valvular disease
- Aortic stenosis
- Mitral regurgitation
- Tricuspid regurgitation
- Constrictive pericarditis
- Acute myocardial ischemia
- Hypertrophic cardiomyopathy
Clinical Manifestation
- Fatigue
- Cool peripheries
- Postrual lightheadedness
- Nocturia
- Decreased daytime micturition
LV Failure
- Dyspnea, sometimes with nocturnal cough
- Paroxysmal nocturnal dyspnea (PND): dyspnea that awakens patient after several hours, requiring sitting up for relief
- Sleep apnea
- Cheyne-Stokes respiration: periodic/ cyclic breathing consisting of apnea -> faster and deeper breathing -> slower and shallower breathing
- Tachycardia
- Tachypnea
- Cyanosis (lips, fingers, toes)
RV Failure
- Ankle swelling
- Abdominal/ neck fullness
- RUQ discomfort
- Early satiety, anorexia, abdominal bloating
Geriatric Atypical Presentations
- Confusion
- Delirium
- Falls
- Sudden functional decline
Cardiac Exam
- Pansystolic murmur from mitral regurgitation at apex
HFrEF
- Diffuse, sustained, laterally displaced apical impulse
- Audible S3, S4 heart sounds
- Accentuated pulmonic component of S2
RV Failure
- Jugular venous pressure elevation with a or v waves
- Lower extremity nontender peripheral pitting edema
Pulmonary Exam
- Early inspiratory basilar crackles that do not clear with coughing
- Signs of pleural effusion: dullness to percussion and diminished breath sounds at lung bases
Abdominal Exam
- Abdominal swelling and ascites
- Enlarged/ pulsatile liver palpable below the right costal margin
New York Heart Association (NYHA) Classification
- Based on clinical presentation
| Class | Definition | Limitation | MET Activity Level |
|---|
| I | “Ordinary physical activity does not cause undue fatigue, dyspnea, or palpitations.” | None | <= 7 (snow shoveling) |
| II | “Ordinary physical activity causes fatigue, dyspnea, palpitations, or angina.” | Mild | <= 5 (1 flight of stairs) |
| III | “Comfortable at rest; less than ordinary physical activity causes fatigue, dyspnea, palpitations, or angina.” | Moderate | <= 2 (showering) |
| IV | “Symptoms occur at rest; any physical activity increases discomfort.” | Severe | < 2 |
Complications
- Fluid congestion
- Hypokalemia
- Cardiomyocyte necrosis
- Arrhythmia
- Pulmonary edema
- Cardiogenic shock
Diagnosis
Clinical
- Can be clinically diagnosed
- Might be confused with COPD symptoms early on
- High suspicion if history of MI, hypertension, or valvular disease
Labs
Imaging
- ECG
- Chest x-ray
- Echocardiography
- Expensive: Cardiac radionuclide scan and/or MRI
Ejection Fraction
| Type | Ejection Fraction |
|---|
| HFrEF | < 40% |
| HFmrEF | Between 40% and 50% |
| HFpEF | >= 50% |
Treatment
- Diet and lifestyle changes
- Sodium restriction
- Weight and fitness level modification
- Treatment of cause
- Goal directed medical therapy
- Beta-blocker
- ACEi/ ARB/ ARNi
- MRA
- SGLT-2
- Device thereapy
- Implantable cardioverter-defibrillator
- Cardiac resynchronization therapy
- Mechanical circulatory support
- Heart transplant
Arrhythmia
- Normalise electrolytes
- Control atrical and ventricular rate
- Antiarrhythmics