Congestive Heart Failure: Symptoms, Stages & Treatment
Congestive Heart Failure (CHF): This lecture reviews heart failure definition, signs, symptoms, causes, stages, diagnosis, treatment, pathophysiology, and more!
Guest Author
Guest Author: Prof. (Dr.) K.V. Sahasranam, MD, DM (Cardio), FACC, FCSI and Retired Senior Consultant Cardiologist
The lecture below was written by guest author Dr. Sahasranam, who is a retired senior consultant cardiologist.
Medical illustrations were created and provided by EZmed.
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What is Congestive Heart Failure?
Let’s begin by defining congestive heart failure.
Do the terms congestive heart failure vs heart failure mean the same?
Definition
Congestive heart failure (CHF) is a clinical syndrome where the heart is unable to pump enough blood to meet the body’s requirements.
CHF is due to a functional or structural disorder of the heart.
Put simply, it means the heart is unable to maintain an adequate cardiac output.
The cardiac output is the amount of blood the heart pumps in a minute.
The cardiac output is determined by heart rate and stroke volume, which is the volume of blood pumped out of the left ventricle with each contraction.
The term “congestive heart failure” denotes the clinical condition characterized by systemic and venous congestion due to heart failure (HF).
Both “congestive heart failure” and “heart failure” are used synonymously.
Congestive Heart Failure (CHF) Definition: A condition in which the heart is unable to pump enough blood to meet the body’s needs.
Pathophysiology and Pathogenesis
As previously mentioned, cardiac output is determined by 2 factors:
Heart Rate
Stroke Volume
Heart rate is the number of times the heart beats in a minute, and stroke volume is the volume of blood pumped out of the left ventricle with each cardiac contraction.
Three factors determine the stroke volume in a normal heart. They are:
Preload = The amount of ventricular stretch prior to cardiac contraction determined by the pressure and volume of blood in the ventricle at the end of diastole.
Afterload = The pressure and volume of blood in the ventricle during systole; The amount of resistance or the pressure against which the heart must overcome to pump blood during systole.
Myocardial Contractility = The inherent ability of the myocardial cells to contract and denotes the pumping capacity of the heart muscle.
Cardiac Output Equation: Cardiac output is determined by heart rate and stroke volume; 3 factors influence stroke volume: Preload, afterload, and contractility.
Ventricular dysfunction can negatively affect the stroke volume.
Ventricular dysfunction can be due to two reasons:
Impaired Systolic Contraction (Systolic Dysfunction) = The ventricles, particularly the left ventricle, are unable to contract well during systole.
Due to myocardial disease or damage as occurs in myocardial infarction and cardiomyopathies.
Impaired Diastolic Relaxation (Diastolic Dysfunction) = The ventricles do not relax properly during diastole.
Due to abnormal relaxation or stiffness of the myocardium as occurs in ventricular hypertrophy or restrictive cardiomyopathies.
Systolic or diastolic dysfunction can negatively impact the above factors that determine stroke volume, which can lead to impaired cardiac output and heart failure as a result.
Congestive Heart Failure Pathophysiology: Systolic or diastolic dysfunction of the heart can affect stroke volume and cardiac output, which can lead to heart failure.
Compensatory Mechanisms in CHF
In most patients with heart failure, both systolic and diastolic dysfunction exist together to a variable extent.
The decrease in ventricular function triggers a cascade of changes which are the hallmark of heart failure.
At the onset of heart failure, compensatory mechanisms are activated which help to sustain the cardiac output at normal levels.
However, later these compensatory mechanisms are overwhelmed and lead to the clinical syndrome of overt heart failure.
Below lists the compensatory mechanisms and the cascade of changes that occur in heart failure:
The initial change in heart failure is a reduction in cardiac output.
Because of reduced cardiac output, the sympathetic nervous system gets stimulated. This is the earliest change.
This causes peripheral arteriolar constriction, increase in the force of myocardial contraction, and increase in heart rate which compensate for the decrease in cardiac output.
Next the Renin Angiotensin Aldosterone System (RAAS) is activated. This is due to the relative ischemia of the kidneys combined with sympathetic stimulation of the kidneys.
Renin is released from the juxtaglomerular apparatus of the kidneys. This converts Angiotensinogen produced by the liver to Angiotensin I.
Angiotensin I is converted to Angiotensin II by the enzyme Angiotensin Converting Enzyme (ACE) which is present in tissues like the lungs, heart, and blood vessel walls.
Angiotensin II acts on the Angiotensin II type 1 receptors (AT1) present in the heart, kidneys, and blood vessels.
Stimulation of the AT1 receptors cause vasoconstriction, release of aldosterone from the adrenal glands and release of catecholamines.
Aldosterone causes salt and water retention by its action on the kidneys to retain sodium in exchange for potassium.
Angiotensin II also stimulates the release of vasopressin or antidiuretic hormone (ADH) from the posterior pituitary gland, which plays a role in vasoconstriction as well as water reabsorption in the kidneys.
The long-term effects of Angiotensin II and Aldosterone are also detrimental. Angiotensin can cause fibrosis in the heart, kidneys, and other organs of the body. Aldosterone can cause hypertrophy and fibrosis in the ventricular myocardium and the blood vessels. This causes increased stiffness of the blood vessels and the ventricular muscle.
All these long-term changes in the heart due to heart failure lead to Ventricular Remodeling which is defined as the change in size, shape, and function of the ventricles due to injury or increased load. These changes are brought about by myocardial hypertrophy and fibrosis. These cause changes to the shape and size of the ventricles. The ventricles become enlarged and more spherical in shape.
Congestive Heart Failure: Compensatory mechanism include activating the sympathetic nervous system and renin-angiotensin-aldosterone system (RAAS).
Causes of Heart Failure
A physiological classification can be used to organize the causes of heart failure:
Causes due to Myocardial Dysfunction:
Myocardial Infarction
Cardiomyopathies
Causes due to increased Ventricular Afterload:
Systemic Hypertension
Aortic Valve Stenosis
Coarctation of Aorta
Pulmonary Valve Stenosis
Pulmonary Hypertension
Causes due to increased Ventricular Preload:
Mitral & Aortic valve regurgitation
Ventricular Septal Defect
Atrial Septal Defect
High Output failures like Anemia, Thyrotoxicosis
Congestive Heart Failure Causes: The etiology of heart failure can be from conditions that cause increased ventricular preload, myocardial dysfunction, or increased ventricular afterload.
Staging & Classification of Heart Failure
Heart failure can be staged and classified.
Stages of Heart Failure
The American College of Cardiology/American Heart Association (ACC/AHA) developed 4 stages of heart failure as described:
Stage A (At Risk) – At high risk of HF but with no structural heart disease or symptoms of HF.
Stage B (Pre-HF) – Structural heart disease is present. But no symptoms of HF.
Stage C (HF) - Structural heart disease is present. Symptoms of HF are also present.
Stage D (Advanced HF) – Severe refractory heart failure.
Congestive Heart Failure Stages: The classification and stages of CHF based on severity and their definitions
Classifications of Heart Failure
**The New York Heart Association (NYHA) functional classification system will be discussed in the next section below under “Symptoms of Heart Failure”.
Heart failure can be classified based on which side of the heart is predominantly affected:
Left Heart Failure – The left ventricular output decreases and the left atrial and pulmonary venous pressure increase as in:
Myocardial infarction
Aortic valve disease
Mitral stenosis
Right Heat Failure – The right ventricular output is reduced, and the right atrial and systemic venous pressure increase as in:
Pulmonary stenosis
Pulmonary hypertension
Chronic lung disease
Pulmonary embolism
Biventricular Heart Failure – The left and right ventricles are affected and fail as in:
Cardiomyopathies
When right ventricular failure follows left ventricular failure due to development of pulmonary hypertension.
Heart failure can also be classified as acute and chronic:
Acute Heart Failure – Indicates an acute left ventricular dysfunction leading to acute pulmonary edema as occurs in:
Acute myocardial infarction
Severe hypertension
Acute myocarditis
Similarly, acute failure of the right ventricle occurs in acute pulmonary embolism
Chronic Heart Failure – Occurs in all types of heart diseases and indicates:
Recurrent attacks of heart failure and persistent symptoms
Chronic heart failure is often referred as “Congestive Heart Failure”.
**Congestive Heart Failure (CHF) is discussed in detail in this lecture.
Another classification of heart failure is based on the ejection fraction which is calculated using echocardiography.
Heart Failure with Reduced Ejection Fraction (HFrEF) – When the EF is below 40%.
Heart Failure with Preserved Ejection Fraction (HFpEF) – When the EF is above 50%.
Heart Failure with Mid-Range Ejection Fraction (HFmrEF) – Denotes the gray zone of ejection fractions between 40-50%.
The ejection fraction (EF) is the percentage of the End Diastolic Volume (EDV) that is ejected out of the ventricle with each ventricular contraction (systole).
The EF is expressed as a percentage.
Ejection Fraction = (Stroke Volume/End Diastolic Volume) x 100
The Stroke Volume (SV) is the difference between the End Diastolic Volume (EDV) and the End Systolic Volume (ESV).
**This lecture will discuss HFrEF only.
Congestive Heart Failure Classification: Based on left vs right, acute vs chronic, and by ejection fraction (EF).
Symptoms of Heart Failure
There are various symptoms of heart failure. The most important symptoms are provided below:
Dyspnea on exertion is the most common symptom. Dyspnea is the medical term for shortness of breath, difficulty breathing, or labored breathing. Dyspnea on exertion (DOE) is shortness of breath or trouble breathing with physical activity.
DOE can be graded into four functional classes according to the New York Heart Association (NYHA) classification as follows:
Class I – No limitation of physical activity and no symptoms
Class II – Slight limitation of physical activity and mild symptoms
Class III – Marked limitation of physical activity due to symptoms
Class IV - Unable to carry out any physical activity, symptoms at rest
An easily remembered practical classification would be:
Class I - No limitation of physical activity
Class II - Symptoms with unaccustomed activity
Class III - Symptoms with accustomed activity
Class IV - Symptoms at rest
Congestive Heart Failure Symptoms: The New York Heart Association (NYHA) classification system for stages of shortness of breath and dyspnea on exertion.
Dyspnea when lying down is shortness of breath in the recumbent position, typically relieved by sitting up or standing. This may be present in CHF.
The medical term for dyspnea when lying down is Orthopnea.
Dyspnea when bending forward (i.e. tying shoelaces, praying while kneeling and bending forward, etc.) is called Bendopnea.
Dyspnea when lying to the left side is called Trepopnea.
Severe fatigue is often an important symptom of CHF.
Paroxysmal nocturnal dyspnea (PND) is a common symptom. PND is sudden shortness of breath during sleep.
The patient is awakened at night by sudden onset dyspnea and must sit up to breathe normally.
This is due to the extracellular fluid getting absorbed from the tissues leading to an increase in blood volume causing pulmonary congestion.
Nocturnal cough is also a frequent symptom due to the pulmonary congestion.
Weight gain is noticed by the patient in CHF due to the edema in extracellular tissues.
The patient may notice pedal edema (swelling to the feet and legs) and ascites (swelling and abnormal fluid buildup in the abdomen).
Cardiac cachexia may be seen in severe CHF.
Cardiac cachexia is unintentional severe weight loss caused by severe heart failure.
The patient may be emaciated and lose a large amount of body fat and muscle.
Right upper quadrant pain of the abdomen is often present due to the hepatic congestion.
Decreased appetite is often due to the gastric congestion.
Oliguria may be present due to associated renal failure.
Oliguria is the medical term for decreased urine output.
Somnolence is the state of being drowsy or sleepy.
Somnolence can be caused by the decreased cerebral blood flow in CHF.
The patient may exhibit Cheyne-Stokes breathing at night.
A cyclical pattern of breathing at night characterized by progressively deeper and faster breathing (hyperventilation) followed by a gradual slowing of breathing that potentially leads to a temporary stop (apnea).
Congestive Heart Failure Symptoms: List of common symptoms seen in heart failure.
Signs of Heart Failure
The signs of congestive heart failure are elicited on physical examination of the patient:
Tachycardia or fast heart rate is noticed on examination of the pulse.
The pulse is often of low volume.
Occasionally irregularity of the pulse is detected in the presence of atrial fibrillation.
Peripheral cyanosis or bluish discoloration of the distal extremities (hands, feet, fingers, toes, etc.) may be noted.
The extremities may be cold to touch.
Jugular venous pressure is raised and is determined with the patient reclining at a 45-degree angle.
Dependent pitting edema is seen around the ankles and feet in those who are ambulant.
In bedridden patients, the edema is seen in the thighs and over the sacrum.
Ascites or swelling/fluid buildup in the abdomen may be appreciated on abdominal examination
Hepatomegaly or enlarged liver may also be noticed on abdominal examination
Splenomegaly may rarely be detected in chronic CHF.
The hepatojugular reflux may be elicited by applying pressure over the liver in the right upper quadrant causing the neck veins to distend.
Abnormal heart sounds may be present on auscultation of the heart
A third heart sound may be present on auscultation of the heart, which indicates increased filling of the left ventricle.
A fourth heart sound may be heard on auscultation of the heart, which indicates a stiff left ventricle.
In addition, murmurs may be detected.
A soft murmur of mitral regurgitation indicates dilation of the mitral annulus leading to the regurgitation.
Presence of other murmurs may point to the cause of the heart failure.
Abnormal lung sounds may be present on auscultation of the chest
Rhonchi, crackles, and crepitations may be present on auscultation of the chest, which indicate pulmonary congestion.
A pleural effusion or fluid buildup around the lung may be detected and may be bilateral.
In addition to the findings of CHF, clinical examination may reveal other signs indicating the etiology of the heart failure such as valve lesions, systemic hypertension, hyperthyroidism, anemia, etc.
Congestive Heart Failure Signs: List of common signs of heart failure on physical examination.
Precipitating Factors for Heart Failure
There are many factors which may precipitate, trigger, or cause a sudden exacerbation of a patient’s heart failure, potentially necessitating hospitalization.
Some of the important factors are:
Any Infection or Illness (i.e. influenza, respiratory infections, etc.)
Infective Endocarditis (infection of the inner lining of the heart) is a serious condition which can precipitate resistant heart failure
Acute Mitral Valvular Regurgitation which may occur due to rupture of chordae tendineae
Myocardial Ischemia (decreased blood flow to the heart)
Myocardial Infarction (heart attack)
Cardiac Arrhythmias – Atrial and Ventricular (abnormal heart rate or rhythm)
Pulmonary Embolism (blood clot in the arteries of the lung)
Anemia (decreased red blood cells or hemoglobin)
Thyrotoxicosis (excess thyroid hormone activity)
Pregnancy
Administration of Medications like NSAIDS and steroids (which may have a negative inotropic action). Calcium antagonists and antiarrhythmic medications can also precipitate heart failure.
Inadvertent Reduction or Discontinuation of Medication by the patient
Alcohol Consumption by the patient
Congestive Heart Failure Precipitating Factors: List of triggers or causes to heart failure or an acute exacerbation of heart failure.
Diagnosis of Heart Failure
There are several diagnostic methods to diagnose congestive heart failure:
Chest X-Ray. This is the simplest and most important test to be done when CHF is suspected. It may reveal cardiomegaly (enlarged heart), pulmonary venous congestion seen in the upper lobe pulmonary veins, interstitial edema in the lungs, and pleural effusion. Interstitial pulmonary edema may be seen as thin, horizontal opacities in the lower lobe called Kerley B lines.
Congestive Heart Failure: Chest x-ray of congestive heart failure showing cardiomegaly and pulmonary edema.
Electrocardiogram (ECG). Various changes in the ECG such as ventricular hypertrophy (LVH, RVH), myocardial ischemia or infarction, arrhythmias, and low voltage QRS complexes as in certain cardiomyopathies may be present.
Echocardiography (ECHO). Echocardiography provides valuable information regarding the structural and functional abnormalities of the heart. Various measurements help in determining the ejection fraction, LVH, RVH, intracardiac pressures, chamber sizes, and blood flow velocities.
Blood Tests. Blood is tested for various routine laboratory parameters like blood sugar (glucose), serum creatinine, serum electrolytes, blood urea nitrogen (BUN), complete blood count, liver enzyme estimation and routine urinalysis. Other tests like thyroid function test, troponin, serum uric acid, lipid profile, serum transferrin saturation, etc., are done in appropriate circumstances.
Biomarkers. Serum biomarkers are used in the differential diagnosis and in assessing prognosis of the CHF. The most common biomarkers tested are B-type Natriuretic Peptide (BNP) and N-terminal-Pro B type natriuretic peptide (NT-proBNP). These are interpreted considering the clinical findings. Both are elevated in heart failure and their reduction is an indication of improvement. The more severe the heart failure, the higher the values of these biomarkers.
Other Imaging Modalities. Other imaging modalities like cardiac computed tomography (Cardiac CT), cardiac magnetic resonance imaging (Cardiac MRI) and nuclear imaging are also used to determine the morphology, chamber sizes, and cardiac function.
Congestive Heart Failure Diagnosis: List of common tests to diagnose heart failure.
Treatment of Heart Failure
The treatment of CHF can be organized into the following categories that will be discussed below:
General Measures
Reduction of Excess Volume Overload (Preload Reduction)
Improvement of Ventricular Function (Afterload Reduction)
Device Therapy
Surgical and Revascularization Measures
Congestive Heart Failure Treatment: Overview of treatment and medication options for heart failure.
1. General Measures
Any precipitating factors for CHF as discussed earlier must be identified and removed.
The primary cause for CHF like myocardial infarction, valvular diseases, thyrotoxicosis, anemia, systemic hypertension, cardiomyopathy, etc., should be identified and appropriately treated.
The diet of the patient should be nutritious and sodium restriction of 2-3 grams of sodium per day is advised.
Fluid restriction is not necessary when diuretics are administered, but if the patient is in resistant heart failure with fluid overload, fluid intake should be restricted to 1 – 1.5 liters per day. Hyponatremia (low blood sodium levels) is another indication for fluid restriction.
Adequate rest is needed. The head end of the bed may be elevated if the patient feels orthopneic (see orthopnea above under symptoms).
Mild exercises like walking indoors should be encouraged. Temperature extremes in the patient’s room should be avoided.
Alcohol and smoking are forbidden. Administration of NSAIDs and steroids are avoided as much as possible.
When there is a fall of oxygen saturation, oxygen may be administered by nasal cannula or a non-rebreather mask.
Pneumococcal, influenza, and COVID vaccinations should be administered to the patient with CHF.
2. Reduction of excess volume overload (Preload Reduction)
The excess retention of salt and water increases the extracellular fluid and the blood volume.
Removing this is needed to reduce the preload on the heart.
Various types of diuretics are available for reduction of the excess fluid in the body.
Different classes of diuretics are available including (See Table Below):
Loop Diuretics: Act on the ascending loop of Henle and prevent salt and water reabsorption.
The commonly available loop diuretics are Furosemide, Torsemide and Bumetanide.
Thiazide and Thiazide-Like Diuretics: Act on the tubules to lose excess sodium and water.
Chlorthalidone, Hydrochlorothiazide and Metolazone are examples of this class of diuretics.
Mineralocorticoid Receptor Antagonists (MRA Antagonist): They increase the excretion of salt and water and retain potassium.
Spironolactone and Eplerenone belong to this group of diuretics.
Potassium Sparing Diuretics: They promote sodium excretion and potassium retention.
Triamterene and Amiloride belong to this category.
Ultrafiltration: In extreme cases of fluid overload, the fluid may be removed by ultrafiltration where the excess fluid and salt is removed using equipment, through which the patient’s blood is passed and the blood returned to the patient after ultrafiltration.
Diuretics are always started in the smallest dose and titrated upwards.
The minimum dose giving the maximum benefit to the patient is used.
Combination of diuretics like the thiazide or loop diuretics with the MRA antagonists may be used for optimum diuretic effect.
Intravenous (IV) administration of diuretics may be needed initially in severe water retention.
The major side effects of diuretic use are hypotension due to salt and water loss, electrolyte disturbances like hypokalemia, hyperkalemia, hyponatremia, and hypomagnesemia.
Diuretics may also lead to renal dysfunction.
Electrolytes should be monitored while administering diuretics.
Serum potassium should be maintained between 4–5 mmol/L.
Hyperkalemia is a complication when aldosterone antagonists are given along with ACE inhibitors or ARBs.
Hyponatremia may accompany loop diuretic use.
Congestive Heart Failure Treatment: Diuretic medication options for heart failure; Table of class, mechanism of action, examples, dose, and side effects.
3. Improvement of ventricular function (Afterload Reduction)
Medications that antagonize the sympathetic nervous system and renin angiotensin aldosterone system are helpful in improving the ejection fraction in patients with HFrEF.
These medications act by promoting vasodilation which decreases systemic vascular resistance and afterload.
They thus prevent disease progression.
These medications include (See Table Below):
Angiotensin Converting Enzyme Inhibitors (ACEIs): Started in small doses, ACEIs are very effective in improving EF. The dose of drug is doubled every 4-5 days. Hyperkalemia, hypotension, renal dysfunction, non-productive cough, and angioedema are potential side effects. Captopril, Enalapril, Lisinopril, and Ramipril are some of the ACEI available.
Angiotensin Receptor Blockers (ARBs): The clinical effects of ARBs are like that of ACEIs. They lack the side effect of cough and can be used when ACEIs cannot be given. Other side effects are like ACEIs. Losartan, Valsartan and Candesartan are available.
Beta Blockers (BBs): Beta blockers reverse the detrimental effects of the sympathetic nervous system by antagonizing their adrenergic effects. They reduce symptoms and improve ventricular remodeling. They can be given in combination with the ACEIs or ARBs. The commonly used BBs are Sustained release Metoprolol, Bisoprolol and Carvedilol. Bradycardia, heart blocks, fatigue and aggravation of asthma are potential side effects.
Ivabradine: This is a drug which reduces heart rate in patients in sinus rhythm. It is found to be effective when used in HFrEF patients and can be used in combination with ACEIs or ARBs. Caution is needed when it is combined with BBs. It is useful only in patients in sinus rhythm.
Digoxin: Digoxin is a time-tested drug. But is seldom used in heart failure now owing to its side effects. It is indicated for ventricular rate control in atrial fibrillation.
Hydralazine + Isosorbide Dinitrate: This combination is used in patients who cannot take ACEIs or ARBs due to side effects or renal dysfunction. The effect of this combination is to reduce afterload, thereby reducing the work of the ventricle due to their vasodilator effect.
Congestive Heart Failure Treatment: Medications options to treat heart failure; Table of medication class, mechanism of action, medications, dose, and side effects.
Newer medications. Newer medications have been added to the armamentarium of HFrEF management. These are discussed below:
Angiotensin Receptor Neprilysin Inhibitors (ARNI): This is a combination of two medications – Valsartan and Sacubitril. Valsartan is an ARB. Sacubitril is a drug which inhibits the enzyme Neprilysin which breaks down Natriuretic peptides (NP). Natriuretic peptides are responsible for sodium and water clearance from the body and hence Sacubitril makes more NP available in the body hence leading to sodium and water excretion. This drug is started in a small dose and increased gradually. Side effects are hypotension, hyperkalemia, renal failure, and allergic reactions. It may be combined with BBs but never with ACEIs or ARBs.
Sodium Glucose Cotransporter 2 Inhibitors. (SGLT2 Inhibitor): These are oral anti-diabetic drugs which increase the clearance of glucose by the kidneys. These drugs are found to be effective in heart failure to improve the EF and prevent ventricular remodeling, thereby reducing hospitalization and mortality in HFrEF. They act by reducing preload due to their osmotic diuretic effect. The drugs available are Dapagliflozin and Empagliflozin.
Vericiguat: This is a soluble guanylate cyclase stimulator found to be very effective in heart failure owing to its smooth muscle relaxing effect leading to vasodilatation. It also inhibits ventricular hypertrophy, inflammation, and fibrosis. All these factors reduce ventricular remodeling and improve the ventricular function leading to reduction in hospitalization and mortality in heart failure.
4. Device Therapy
Cardiac Resynchronization (CRT): Biventricular pacing is resorted for resynchronization of the heart when the patient has a low ejection fraction <35% along with LBBB and a QRS duration more than 150 msec. Resynchronization causes the ventricles to beat in synchrony leading to better cardiac output and improvement in EF. It also improves the quality of life and reverses ventricular remodeling.
Implantable Cardioverter Defibrillator (ICD): ICDs are implanted in patients with an EF less than 35%, and who are on optimal medical therapy, in order to reduce the incidence of sudden cardiac death seen.
Ventricular Assist Devices (VAD): These devices are often used as a bridge to improve circulation in patients awaiting cardiac transplantation. Various types of devices are available.
5. Surgical and Revascularization Measures
In patients who have viable myocardium, revascularization procedures like angioplasty or coronary artery bypass graft (CABG) are done.
Valve repair surgery or valve replacement is considered in patients with valve diseases as the cause of their CHF.
Transcutaneous Aortic Valve Replacement (TAVR) is now available for patient’s at high risk due to diseases of the aortic valve.
Ventricular restoration surgery is available for improving ventricular muscle function.
Complications of Heart Failure
The following complications may occur in congestive heart failure:
Renal Failure. Poor renal perfusion caused by the low cardiac output in CHF leads to renal failure. Drugs used in the treatment of CHF may also contribute to the renal dysfunction.
Liver Dysfunction. Poor hepatic perfusion and congestion secondary to raised systemic venous pressure may lead to mild jaundice and liver dysfunction seen as raised liver enzymes and derangement of coagulation.
Electrolyte Disturbances. Hypokalemia (low blood potassium levels) may follow the use of loop diuretics. Hyperkalemia (high blood potassium levels) on the other hand can follow treatment with mineralocorticoid receptor antagonists combined with ACE inhibitors or angiotensin receptor blockers (ARBs). Hyponatremia (low blood sodium levels) is a complication which follows use of diuretics which flush out salt and water from the body. The presence of hypokalemia may be serious as it can precipitate arrhythmias in the already compromised heart.
Atrial and Ventricular Arrhythmias. Many different types of tachyarrhythmias can occur in CHF. But the most common is atrial fibrillation which can cause harm to the patient, as it can lead to thromboembolism and is a common cause of stroke in heart failure.
Thromboembolism. Prolonged bed rest and venous pooling in the lower limbs can lead to deep vein thrombosis (DVT) and pulmonary embolism (PE). Likewise, systemic embolism can occur due to embolism from the atrial appendage in a patient with atrial fibrillation. A left ventricular thrombus as in myocardial infarction or ventricular aneurysm can also cause thromboembolism.
Sudden Cardiac Death is not an uncommon complication and is seen in almost half of the patients with CHF. Ventricular fibrillation is usually the terminal event.
Infections. Recurrent respiratory infections especially pneumonia are a frequent complication of CHF. When valvular lesions are present, the risk of infective endocarditis is high and may lead to resistant heart failure and death.
Cardiac Cachexia. This denotes extreme weight loss with fatigue which may occur in CCF due to muscle wasting.
Congestive Heart Failure Complications: List of complications that can result from heart failure.
Prognosis of Heart Failure
The prognosis of heart failure depends on the presence of various factors.
Some of the factors causing adverse prognosis are:
Persistent hyponatremia
Markedly elevated BNP
Hypotension – Systolic BP < 120 mm Hg.
Presence of a third heart sound
Severe uncontrolled diabetes
Severe anemia
Cardiac cachexia
Need for frequent hospitalizations
The one-year survival in NYHA class II and III heart failure is approximately 85% whereas it is only 35% for NYHA class IV heart failure.
Congestive Heart Failure Prognosis: List of factors that contribute to the prognosis and life expectancy of heart failure.
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