Chronic Heart Failure Flashcards
(15 cards)
Definitions
complex clinical syndrome that can result
from any structural or functional cardiac disorder that
impairs the ability of the ventricle to fill with or eject blood
complex clinical syndrome that can result
from any structural or functional cardiac disorder that
impairs the ability of the ventricle to fill with or eject blood
Etiology
Ischemic heart disease -myocardial scar
Myocardial stunning hibernation
Coronary artery disease
Endothelial dysfunction
Toxic damage
-medication heavy metals recreational substance abuse
Radiation
Related to infection
Diverse forms of
Alcohol tacharrhythmias
Bradyarrhythmias infective endocarditis
Valvular disorders
Pathogensisis or pathphysiology
Chronic heart failure (CHF) is a complex clinical syndrome where the heart is unable to pump enough blood to meet the body’s metabolic demands, or it can only do so at elevated filling pressures. This insufficiency can arise from structural or functional impairments of ventricular filling or ejection.
Here’s a breakdown of its pathophysiology and pathogenesis:
1. Initial Cardiac Injury and Dysfunction:
The process often begins with an initial injury or stress to the heart muscle. Common causes include:
* Ischemic heart disease/myocardial infarction (heart attack): Lack of blood flow damages or destroys heart muscle, leading to reduced contractility. This is the most common cause of HF.
* Hypertension (high blood pressure): Chronic high pressure increases the workload on the heart, leading to hypertrophy (thickening) of the heart muscle. Over time, this can lead to stiffness (diastolic dysfunction) or weakening (systolic dysfunction).
* Valvular heart disease: Stenosis (narrowing) or regurgitation (leaky valves) increases the pressure or volume load on the heart, leading to chamber enlargement and dysfunction.
* Cardiomyopathies: Diseases of the heart muscle itself (e.g., dilated, hypertrophic, restrictive cardiomyopathy) can impair its ability to pump or relax. These can be genetic, viral, or due to toxins (e.g., alcohol, certain chemotherapy drugs).
* Arrhythmias: Persistent fast or irregular heartbeats can weaken the heart muscle over time.
* Other systemic diseases: Conditions like diabetes, thyroid disorders, and certain infections can also contribute to heart failure.
This initial injury leads to either:
* Systolic dysfunction: The heart muscle becomes weakened and can’t contract forcefully enough to eject adequate blood (reduced ejection fraction).
* Diastolic dysfunction: The heart muscle becomes stiff and can’t relax properly to fill with enough blood during diastole (preserved ejection fraction). Often, both types of dysfunction are present.
2. Compensatory Mechanisms (Initially Helpful, Later Maladaptive):
When cardiac output falls, the body activates a series of neurohormonal and structural compensatory mechanisms to try and maintain blood pressure and perfusion to vital organs. These include:
* Activation of the Sympathetic Nervous System (SNS):
* Increases heart rate and contractility to boost cardiac output.
* Causes vasoconstriction (narrowing of blood vessels) to maintain blood pressure.
* However, chronic SNS activation leads to increased myocardial oxygen demand, arrhythmias, and direct toxicity to cardiomyocytes (heart muscle cells), contributing to further damage and remodeling.
* Activation of the Renin-Angiotensin-Aldosterone System (RAAS):
* Decreased renal blood flow due to reduced cardiac output triggers renin release.
* Renin leads to the production of Angiotensin II, a potent vasoconstrictor and stimulator of aldosterone release.
* Aldosterone promotes sodium and water retention by the kidneys, increasing blood volume (preload).
* Initially, this increased preload helps maintain stroke volume via the Frank-Starling mechanism (the heart pumps more forcefully when stretched).
* However, chronic activation leads to excessive fluid retention, worsening congestion, increased afterload, and direct deleterious effects on the heart (fibrosis, hypertrophy, and remodeling).
* Ventricular Remodeling:
* In response to chronic stress (e.g., increased preload, afterload, neurohormonal activation), the heart undergoes structural changes.
* Hypertrophy: Heart muscle cells enlarge to generate more force.
* Dilation: The heart chambers stretch and enlarge, initially to accommodate increased blood volume.
* Fibrosis: Increased collagen deposition in the extracellular matrix makes the heart stiffer and less compliant.
* These changes initially help maintain function but eventually become maladaptive, leading to further decline in pumping efficiency, electrical instability, and ultimately, a vicious cycle of worsening heart failure.
* Natriuretic Peptides (BNP, ANP):
* These hormones are released in response to increased cardiac stretch and pressure.
* They act as counter-regulatory mechanisms, promoting vasodilation, natriuresis (sodium excretion), and diuresis (water excretion), which helps to reduce fluid overload and blood pressure.
* While beneficial, their production is often insufficient to fully counteract the effects of the activated SNS and RAAS in chronic heart failure.
3. Progressive Deterioration and End-Organ Damage:
As the compensatory mechanisms become maladaptive, the heart’s pumping ability continues to decline, leading to:
* Reduced cardiac output: Insufficient blood supply to organs.
* Increased systemic and pulmonary venous pressures: Leading to fluid buildup (congestion) in the lungs (dyspnea, orthopnea) and peripheral tissues (edema, ascites).
* Impaired organ perfusion: Affecting the kidneys (leading to renal dysfunction), liver (liver congestion), brain (fatigue, confusion), and skeletal muscles (fatigue, exercise intolerance).
* Cachexia: Severe muscle wasting in advanced stages.
In essence, the pathogenesis of chronic heart failure is a complex interplay of initial cardiac injury, followed by a cascade of compensatory responses that, over time, become detrimental, leading to progressive cardiac remodeling, further dysfunction, and systemic consequences.
Path physiology or pathogensis in my own words
Cardic injury causes decrease of CO
Which causes and activation to the SNS and causes sodium and water retention causes activation of RAAS too
Leads to vasoconstriction increase after load and pre load increase cardiac workload causes cardiac remodeling
Classification
•Heart failure with ‘preserved’ (≥50%) ejection
fraction (HF-PEF)
•Heart failure with reduced (≤40%) ejection fraction
(HF-REF). At least half of patients with HF have a low EF.
•Patients with an EF in the range 41–49% therefore
represent a ‘grey area’ which we now define as
mildly reduced HF.
New York Heart Association (NYHA)
Functional C
New York Heart Association (NYHA)
Functional Classification of HF
• I - No limitation of physical activity. Ordinary physical activity
does not cause undue fatigue, palpitation, dyspnea (shortness
of breath).
• II - Slight limitation of physical activity. Comfortable at rest.
Ordinary physical activity results in fatigue, palpitation,
dyspnea (shortness of breath).
• III - Marked limitation of physical activity. Comfortable at rest.
Less than ordinary activity causes fatigue, palpitation, or
dyspnea.
• IV - Unable to carry on any physical activity without discomfort.
Symptoms of heart failure at rest. If any physical activity is
undertaken, discomfort increases.
The American College of Cardiology
Foundation/American Heart Association (ACCF/AHA
The American College of Cardiology
Foundation/American Heart Association (ACCF/AHA)
classification of heart failure
Stage A- at high risk of HF but without structural heart diseases or symptoms of Hf
Stage B x structural heart sippdisesses but without signs or symptoms of HF
Stage C-structural heard disease with prior or current symptoms of HF
Stage D- refractory hF
The development of structural
abnormalities can have 1 of 3 outcomes:
• 1) patients die before developing symptoms (in Stage A or B)
• 2) patients develop symptoms controlled by treatment
• 3) patients die of progressive HF
Sudden death can interrupt this course at any time
Symptoms
T y p i c a l B r e a t h l e s s n e s s
O r t h o p n o e a
P a r o x y s m a l n o c t u r n a l d y s p n o e a
R e d u c e d e x e r c i s e t o l e r a n c e
F a t i g u e , t i r e d n e s s , i n c r e a s e d t i m e
t o r e c o v e r a f t e r e x e r c i s e
A n k l e s w e l l i n g
L e s s t y p i c a l N o c t u r n a l c o u g h
W h e e z i n g
B l o a t e d f e e l i n g
L o s s o f a p p e t i t e
C o n f u s i o n ( e s p e c i a l l y in t h e
e l d e r l y )
D e p r e s s i o n
P a l p i t a t i o n s
D i z z i n e s s
S y n c o p e
B e n d o p n e a $ 3
Signs
l e v a t e d j u g u l a r v e n o u s p r e s s u r e
H e p a t o j u g u l a r r e f l u x
T h i r d h e a r t s o u n d ( g a l l o p r h y t h m )
L a t e r a l l y d i s p l a c e d a p i c a l i m p u l s e
L e s s s p e c i f i c
W e i g h t g a i n ( > 2 k g / w e e k )
W e i g h t l o s s ( i n a d v a n c e d H F )
T i s s u e w a s t i n g ( c a c h e x i a )
C a r d i a c m u r m u r
P e r i p h e r a l o e d e m a ( a n k l e , s a c r a l ,
s c r o t a l )
P u l m o n a r y c r e p i t a t i o n s
R e d u c e d a i r e n t r y a n d d u l l n e s s t o
p e r c u s s i o n a t l u n g b a s e s ( p l e u r a l
e f f u s i o n )
T a c h y c a r d i a
I r r e g u l a r p u l s e T a c h y p n o e a
C h e y n e S t o k e s r e s p i r a t i o n
H e p a t o m e g a l y
A s c i t e s
C o l d e x t r e m i t i e s
O l i g u r i a
N a r r o w p u l s e p r e s s u r
Left ventricular heart failure
Symptoms,s Dyspnoea,
•Orthopnoea,
•Paroxysmal
nocturnal dyspnoea
•Wheeze (cardiac
‘asthma’),
•Nocturnal cough
•Loud second sound on
A.Pulmon.
•Bibasal
endinspiratory
crackles and rales
Fatigue,
•Cold peripheries,
•Weight loss,
•Muscle wasting
•Temperature↓
•Mental status
abnormalities
•Cardiomegaly
on palpation or
percussion
•Arrhythmias
•Gallop rhythm
on auscultation
•Heart murmur
Right ventricular heart failure
Hepatomegaly
•Ascites
•Fatigue,
•Nausea,
•Anorexia,
•Peripheral
oedema
•Ascites
•Facial
engorgement
Cardiomegaly
on palpation or
percussion
•Arrhythmias
Pulsation in
neck and face
(tricuspid
regurgitation)
•Heart murmurs
•Epigastric
pulsation
Neck-vein
distention
•Abdominal-
jugular neck-
vein reflex
•Pleural
effusions
Fatigue,
•Cold
peripheries,
•Weight loss,
•Muscle
wasting
•Temperature↓
•Mental status
abnormalities
•Cachexi
Diagnostic workout
Echocardiography
•Chest Radiography
•Electrocardiography
•Chest x-ray (Lung disease)
•Pulmonary function (Asthma)
•Blood chemistry (Renal and hepatic disease)
•Blood count (Anaemia)
•Exercise tolerance (if impair
Diagnosing chronic heart failure (CHF) involves a comprehensive workup that includes evaluating a patient’s medical history, conducting a physical examination, and performing various diagnostic tests. These tests help to confirm the diagnosis, determine the underlying cause, assess the severity, and guide treatment.
Here’s a breakdown of the common diagnostic workup for chronic heart failure and what they typically reveal:
1. Medical History and Physical Exam
* Medical History: The doctor will inquire about symptoms like shortness of breath (dyspnea), fatigue, swelling (edema) in the legs, ankles, or abdomen, weight gain, cough, and nocturnal urination. They’ll also ask about risk factors such as coronary artery disease, high blood pressure, diabetes, previous heart attacks, heart valve disease, family history of heart disease, and lifestyle habits (smoking, alcohol use).
* Physical Exam: The examination may reveal signs of heart failure, including:
* Tachycardia: Rapid heart rate.
* Hypotension: Low blood pressure.
* Raised Jugular Venous Pressure (JVP): Distention of neck veins, indicating increased pressure in the right side of the heart.
* Displaced Apex Beat: The strongest pulsation of the heart felt on the chest wall may be shifted, suggesting an enlarged heart.
* Gallop Rhythm (S3): An extra heart sound, often indicative of impaired ventricular filling.
* Murmurs: Abnormal heart sounds that can indicate valvular heart disease.
* Pulmonary crackles/rales: Wet sounds heard in the lungs due to fluid accumulation.
* Peripheral edema: Swelling in the lower extremities.
* Hepatomegaly: Enlarged liver due to fluid congestion.
2. Blood Tests
Blood tests are crucial for diagnosing and monitoring CHF, as well as identifying contributing factors.
* Natriuretic Peptides (BNP and NT-proBNP):
* What they are: Hormones released by the heart in response to increased pressure and stretch.
* What they reveal: Elevated levels of BNP or NT-proBNP are strong indicators of heart failure. The higher the levels, the more severe the heart failure tends to be. A normal level can often rule out heart failure.
* Complete Blood Count (CBC):
* What it reveals: Can identify anemia (low red blood cell count), which can worsen heart failure symptoms.
* Kidney Function Tests (Creatinine, BUN):
* What they reveal: Assess kidney function, as heart failure can affect kidney perfusion and vice versa.
* Liver Function Tests (LFTs):
* What they reveal: Can indicate liver congestion due to right-sided heart failure.
* Electrolytes (Sodium, Potassium):
* What they reveal: Imbalances can occur in heart failure and may be affected by medications.
* Thyroid Function Tests (TSH):
* What they reveal: Both hyperthyroidism and hypothyroidism can affect heart function and mimic or exacerbate heart failure symptoms.
* Cardiac Troponin:
* What it reveals: While primarily used to diagnose acute myocardial infarction (heart attack), elevated troponin can also indicate ongoing myocardial injury in chronic heart failure.
* Lipid Profile (Cholesterol, Triglycerides):
* What it reveals: Assesses risk factors for coronary artery disease, a common cause of heart failure.
* HbA1c:
* What it reveals: Measures long-term blood sugar control, as diabetes is a significant risk factor for heart failure.
3. Electrocardiogram (ECG or EKG)
* What it is: A non-invasive test that records the electrical activity of the heart.
* What it reveals: While a normal ECG does not definitively rule out heart failure, an abnormal ECG is common in CHF patients. It can show:
* Arrhythmias: Irregular heart rhythms like atrial fibrillation.
* Evidence of previous myocardial infarction (heart attack): Q waves.
* Chamber enlargement: Such as left ventricular hypertrophy (thickening of the left ventricle wall) or atrial enlargement.
* Conduction abnormalities: Problems with the heart’s electrical pathways.
* Ischemia: Reduced blood flow to the heart muscle.
4. Echocardiogram (Echo)
* What it is: An ultrasound of the heart that provides real-time images of its structure and function. It is considered the most important diagnostic test for heart failure.
* What it reveals:
* Ejection Fraction (EF): The percentage of blood pumped out of the left ventricle with each beat. This is crucial for classifying heart failure:
* Heart Failure with Reduced Ejection Fraction (HFrEF): EF \le 40\%, indicating a weakened pumping ability.
* Heart Failure with Preserved Ejection Fraction (HFpEF): EF \ge 50\%, where the heart muscle contracts normally but the ventricles don’t relax properly, impairing filling.
* Heart Failure with Mildly Reduced Ejection Fraction (HFmrEF): EF between 41% and 49%.
* Chamber Size and Function: Assesses the size of the heart chambers (atria and ventricles) and their ability to pump blood.
* Wall Thickness: Detects hypertrophy (thickening) or thinning of the heart muscle.
* Valvular Function: Identifies issues like stenosis (narrowing) or regurgitation (leakage) of heart valves, which can cause or worsen heart failure.
* Regional Wall Motion Abnormalities: Areas of the heart muscle that don’t move properly, often indicative of coronary artery disease or previous heart attack.
* Diastolic Dysfunction: Problems with the heart’s relaxation and filling phase, a key feature of HFpEF.
5. Chest X-ray
* What it is: An imaging test that creates pictures of the chest, including the heart and lungs.
* What it reveals: While not diagnostic on its own, it can provide supportive evidence:
* Cardiomegaly: Enlarged heart silhouette (cardiothoracic ratio >50%).
* Pulmonary Edema: Fluid in the lungs, which can appear as:
* Alveolar edema: “Bat-wing” or “butterfly” opacities.
* Interstitial edema: Kerley B lines (short, horizontal lines in the lung periphery).
* Pleural effusions: Fluid accumulation around the lungs.
* Cephalization of pulmonary veins: Increased prominence of blood vessels in the upper lungs due to increased pressure.
6. Other Imaging Tests (if needed)
* Cardiac MRI (Magnetic Resonance Imaging):
* What it reveals: Provides detailed images of heart structure, function, and tissue characteristics (e.g., fibrosis, inflammation), helping to identify specific causes of cardiomyopathy.
* Cardiac CT Scan (Computed Tomography):
* What it reveals: Can provide detailed anatomical information, particularly for evaluating coronary arteries (CT angiography) or assessing the extent of cardiac damage.
* Cardiac Catheterization with Coronary Angiography:
* What it is: An invasive procedure where a catheter is inserted into a blood vessel and guided to the heart. Dye is injected to visualize the coronary arteries.
* What it reveals: Detects blockages or narrowing in the coronary arteries, which are a major cause of heart failure (ischemic cardiomyopathy). It can also measure pressures within the heart chambers.
* Stress Test (Exercise or Pharmacological):
* What it reveals: Assesses how the heart performs under stress. It can uncover underlying coronary artery disease or evaluate the patient’s exercise capacity.
By combining the information from these various diagnostic tests, healthcare providers can accurately diagnose chronic heart failure, determine its specific type and cause, assess its severity, and develop an individualized management plan.
Complications of heart failure
Sudden death !!!!!
• Arrhythmias- Atrial fibrillation; ventricular arrhythmias
(ventricular tachycardia, ventricular fibrillation);
bradyarrhythmias
• Thromboembolism- Stroke; peripheral embolism; deep
venous thrombosis; pulmonary embolism
• Gastrointestinal- Hepatic dysfunction; malabsorption
• Musculoskeletal- Muscle wasting
• Respiratory- respiratory muscle weaknesss
Treatment
The treatment of chronic heart failure (CHF) aims to manage symptoms, slow disease progression, improve quality of life, and prolong survival. It’s a multifaceted approach involving lifestyle modifications, pharmacological therapies, and, in some cases, device therapies or surgical interventions.
1. Lifestyle Modifications
These are foundational for all CHF patients:
* Dietary Changes:
* Sodium Restriction: Limiting salt intake to reduce fluid retention and ease the heart’s workload.
* Fluid Management: For some, fluid intake may need to be restricted to prevent fluid overload.
* Regular Exercise: As tolerated and guided by a healthcare professional, exercise can improve heart function and overall fitness.
* Weight Management: Achieving and maintaining a healthy weight reduces the burden on the heart.
* Smoking Cessation and Alcohol Moderation: Both smoking and excessive alcohol consumption can worsen heart failure.
* Stress Management: Stress can exacerbate heart failure symptoms.
* Monitoring Symptoms: Daily weight checks, monitoring for swelling, and being aware of any worsening symptoms are crucial for early intervention.
* Vaccinations: Annual flu shots and pneumonia vaccines are recommended to prevent respiratory infections that can trigger heart failure exacerbations.
2. Pharmacological Treatments
Medications are the cornerstone of CHF treatment, often used in combination. The “foundational four” drug classes are particularly important for Heart Failure with Reduced Ejection Fraction (HFrEF), and increasingly for Heart Failure with Preserved Ejection Fraction (HFpEF) as well.
A. Foundational Therapies for HFrEF (and increasingly HFpEF):
* Angiotensin-Converting Enzyme (ACE) Inhibitors:
* Mechanism: Block the production of angiotensin II, a powerful vasoconstrictor, leading to vasodilation (widening of blood vessels) and reduced workload on the heart. They also help prevent cardiac remodeling.
* Examples: Lisinopril (Prinivil, Zestril), Ramipril (Altace), Enalapril (Vasotec), Captopril (Capoten).
* What they reveal: Improve survival, reduce hospitalizations, and alleviate symptoms.
* Angiotensin Receptor Blockers (ARBs):
* Mechanism: Block angiotensin II from binding to its receptors, similar effects to ACE inhibitors but often used as an alternative if ACE inhibitors cause a troublesome dry cough.
* Examples: Valsartan (Diovan), Losartan (Cozaar), Candesartan (Atacand).
* What they reveal: Similar benefits to ACE inhibitors in terms of mortality and hospitalization reduction.
* Beta-Blockers:
* Mechanism: Block the effects of adrenaline and noradrenaline on the heart, slowing the heart rate, reducing blood pressure, and improving the heart’s pumping efficiency over time.
* Examples: Carvedilol (Coreg), Bisoprolol (Zebeta), Metoprolol succinate (Toprol XL).
* What they reveal: Improve survival, reduce hospitalizations, and reverse cardiac remodeling. Dosing is crucial; typically started low and gradually increased.
* Mineralocorticoid Receptor Antagonists (MRAs) / Aldosterone Antagonists:
* Mechanism: Block the effects of aldosterone, a hormone that causes sodium and fluid retention and promotes fibrosis in the heart.
* Examples: Spironolactone (Aldactone), Eplerenone (Inspra).
* What they reveal: Improve survival, reduce hospitalizations, and reduce sudden cardiac death risk. Close monitoring of potassium levels and kidney function is required due to risk of hyperkalemia.
* Sodium-Glucose Cotransporter-2 (SGLT2) Inhibitors:
* Mechanism: Originally developed for diabetes, these drugs cause the kidneys to excrete more glucose and sodium in the urine. They have shown remarkable cardiovascular and renal benefits in heart failure patients, regardless of diabetes status.
* Examples: Dapagliflozin (Farxiga), Empagliflozin (Jardiance).
* What they reveal: Significantly reduce hospitalizations for heart failure and cardiovascular mortality, as well as improve renal outcomes.
* Angiotensin Receptor-Neprilysin Inhibitors (ARNIs):
* Mechanism: A combination drug (e.g., sacubitril/valsartan) that combines an ARB with a neprilysin inhibitor. Neprilysin breaks down natriuretic peptides, which have beneficial vasodilatory and natriuretic effects. By inhibiting neprilysin, ARNIs increase the levels of these beneficial peptides while also blocking the renin-angiotensin system.
* Example: Sacubitril/Valsartan (Entresto).
* What they reveal: Often superior to ACE inhibitors in reducing mortality and heart failure hospitalizations in HFrEF.
B. Other Medications for Symptom Management and Specific Conditions:
* Diuretics (“Water Pills”):
* Mechanism: Help the body eliminate excess fluid and sodium, reducing symptoms like swelling and shortness of breath.
* Examples: Furosemide (Lasix), Torsemide (Demadex), Bumetanide (Bumex) (loop diuretics); Hydrochlorothiazide (HCTZ) (thiazide diuretic).
* What they reveal: Relieve congestion and improve symptoms, but do not directly improve survival.
* Digoxin (Lanoxin):
* Mechanism: Strengthens the heart’s contractions and slows the heart rate, especially in patients with atrial fibrillation.
* What it reveals: Improves symptoms and reduces hospitalizations, but generally not shown to improve survival.
* Ivabradine (Corlanor):
* Mechanism: Slows the heart rate by selectively inhibiting the funny current (I_f) in the sinoatrial node.
* What it reveals: Used in select HFrEF patients with a high heart rate despite optimal beta-blocker therapy, it can reduce heart failure hospitalizations.
* Hydralazine/Isosorbide Dinitrate (BiDil):
* Mechanism: A combination of a vasodilator (hydralazine) and a nitrate (isosorbide dinitrate) that relaxes blood vessels.
* What it reveals: Shown to improve survival in self-identified Black patients with HFrEF, particularly if they cannot tolerate ACE inhibitors or ARBs.
3. Device Therapies
* Implantable Cardioverter-Defibrillator (ICD):
* What it is: A small device implanted in the chest that monitors heart rhythm and delivers an electrical shock to correct life-threatening arrhythmias (e.g., ventricular tachycardia, ventricular fibrillation) that can lead to sudden cardiac death.
* When used: Primarily for HFrEF patients at high risk of sudden cardiac death due to very low ejection fraction or history of significant arrhythmias.
* Cardiac Resynchronization Therapy (CRT) / Biventricular Pacemaker:
* What it is: A specialized pacemaker that stimulates both ventricles to contract in a more synchronized manner, improving the heart’s pumping efficiency.
* When used: For HFrEF patients with a significantly reduced ejection fraction and electrical conduction delays (e.g., left bundle branch block), which can lead to asynchronous ventricular contraction.
* Ventricular Assist Devices (VADs):
* What it is: Mechanical pumps implanted in the chest that help the weakened heart pump blood to the body.
* When used: For patients with advanced, end-stage heart failure who are not candidates for heart transplant or are awaiting a transplant (“bridge to transplant” or “destination therapy”). The Left Ventricular Assist Device (LVAD) is the most common type.
4. Surgical Treatments
Surgical options are typically reserved for patients with severe CHF that is not responding to medical therapy or when specific underlying cardiac conditions require intervention.
* Coronary Artery Bypass Grafting (CABG):
* What it is: A procedure to bypass blocked or narrowed coronary arteries using healthy blood vessels from elsewhere in the body.
* When used: When heart failure is primarily caused by severe coronary artery disease (ischemic cardiomyopathy) and significant blockages can be surgically revascularized to improve blood flow to the heart muscle.
* Heart Valve Repair or Replacement:
* What it is: Surgical correction or replacement of diseased heart valves (e.g., aortic stenosis, mitral regurgitation) that are contributing to heart failure.
* When used: When severe valvular heart disease is identified as a primary cause or significant exacerbating factor of heart failure. Procedures can be open-heart or minimally invasive (e.g., Transcatheter Aortic Valve Replacement (TAVR) for aortic stenosis).
* Heart Transplant:
* What it is: Replacement of the diseased heart with a healthy heart from a deceased donor.
* When used: The definitive treatment for end-stage heart failure when all other medical and surgical options have failed and the patient meets strict eligibility criteria. Donor hearts are scarce, leading to long waiting lists.
* Myectomy / Septal Myectomy:
* What it is: Surgical removal of a portion of the thickened heart muscle in the septum (wall between the ventricles).
* When used: Primarily for obstructive hypertrophic cardiomyopathy, where thickened muscle obstructs blood flow from the left ventricle.
The treatment plan for each individual with chronic heart failure is highly personalized, taking into account the type and severity of heart failure, underlying causes, co-existing medical conditions, and patient preferences. Regular monitoring and adjustments to therapy are essential for optimal outcomes.
