Congestive Heart Failure - Causes, Symptoms, and Treatments

Last updated date: 05-Feb-2022


13 mins read

Congestive Heart Failure

Heart failure is a complicated clinical condition that occurs when the heart is unable to pump enough blood to satisfy the body's needs. It is caused by any functional or anatomical cardiac disease that impairs ventricular filling or blood ejection to the systemic circulation to fulfill systemic demands.

The majority of individuals with heart failure have symptoms as a result of decreased left ventricular myocardial function. Patients often report with dyspnea, reduced exercise tolerance, and fluid retention, as seen by pulmonary and peripheral edema.

Heart failure caused by left ventricular dysfunction is classified as heart failure with decreased ejection fraction based on the left ventricular ejection fraction (LVEF) (usually considered LVEF 40 percent or less)

Due to a varied cut off for systolic dysfunction employed by different research, individuals with an ejection fraction ranging from 40% to 50% have been regarded to constitute an intermediate group of patients. These individuals should be treated frequently for underlying risk factors and comorbidities, as well as with appropriate guideline-directed treatment.

When heart failure occurs, compensatory systems try to raise cardiac filling pressure, muscle mass, and heart rate. However, in many situations, there is a gradual decrease in cardiac function.


Heart failure risk factors

Heart failure can be caused by a variety of conditions, including illnesses of the pericardium, myocardium, endocardium, cardiac valves, vasculature, or metabolism.

Idiopathic dilated cardiomyopathy (DCM), coronary heart disease (ischemic), hypertension, and valve disease are the most prevalent causes of systolic dysfunction.

Hypertension, obesity, coronary artery disease, diabetes mellitus, atrial fibrillation, and hyperlipidemia are highly prevalent in patients with Heart failure with preserved ejection fraction (HFpEF). Hypertension by far is the most important cause of HFpEF. Furthermore, diseases such as hypertrophic obstructive cardiomyopathy and restrictive cardiomyopathy are linked to substantial diastolic dysfunction, which leads to HFpEF.


Causes of high-output failure include:

  • Anemia
  • Hyperthyroidism
  • AV fistulas
  • Beri-beri
  • Multiple myeloma
  • Pregnancy
  • Paget disease of bone
  • Carcinoid syndrome
  • Polycythemia vera

Very common causes of decompensation in a stable patient with HF include:

  • Excessive sodium consumption in the diet Inappropriate medication decrease
  • insufficient physical activity
  • Medication noncompliance
  • Extensive physical activity
  • Emotional breakdown
  • Weather changes that occur unexpectedly Excessive water use


Heart failure classification

Based on the location of the deficiency, heart failure can be categorized as mainly left ventricular, predominantly right ventricular, or predominantly biventricular. HF is categorized as acute or chronic based on the time of onset. Clinically, it is divided into two kinds based on the functional condition of the heart: heart failure with preserved ejection fraction (HFpEF) and heart failure with reduced ejection fraction (HFrEF) (HFrEF).

EF is frequently greater than 50% in patients with HFpEF, who are primarily females and older individuals; the volume of the left-ventricular (LV) cavity is normally normal, but the LV wall is thickened and stiff; hence, the ratio of LV mass/end-diastolic volume is high. HFpEF is further classified as borderline HF if the EF remains between 41 and 49 percent and improved HF if the EF is more than 40 %.

  • Heart failure reduced ejection fraction

In individuals with HFrEF, however, the LV cavity is generally dilated, and the LV mass/end-diastolic volume ratio is either normal or decreased. At the cellular level, both cardiomyocyte diameter and myofibril volume are greater in HFpEF than in HFrEF. In terms of therapy and result, individuals with HFrEF respond favorably to conventional pharmacological treatment regimens and have a better prognosis. 

Patients with HFpEF, on the other hand, have not been proven to react to typical pharmacological therapies, with the exception of nitrates, and hence have a poor prognosis, particularly during the decompensated phase of HF. Furthermore, HF is categorized as high-output failure or low-output failure depending on cardiac output. High-output failure is a rare disease defined by a resting cardiac index of more than 2.5–4.0 L/min/m2 and low systemic vascular resistance.

Severe anemia, vascular shunting, hyperthyroidism, and vitamin B1 insufficiency are the most prevalent reasons of high output failure. This occurs as a result of ineffective blood volume and pressure, which stimulate the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS), resulting in the release of antidiuretic hormone (ADH), all of which lead to ventricular enlargement, negative ventricular remodeling, and HF.

Low-output failure is far more prevalent than high-output failure and is characterized by inadequate forward cardiac output, especially during periods of elevated metabolic demand. Low output failure is caused by left ventricular dysfunction caused by a massive MI, right ventricular dysfunction caused by an abrupt pulmonary embolus, and biventricular dysfunction.

Recently, it has been hypothesized that exercise intolerance in HFpEF is caused by a reduction in oxygen supply to or reduced oxygen consumption by the exercising skeletal muscles.

Given the slowed oxygen uptake kinetics in HF, as well as the impairment of peripheral muscle function, exercise rehabilitation appears to be a logical and necessary factor in improving the inflammatory imbalance, relieving elevated cardiac filling pressures, restoring exercise capacity, quality of life, and reducing morbidity and mortality associated with HF. As a result, in HFpEF patients, high-intensity exercise training, as compared to moderate-intensity exercise training, has been found to dramatically enhance rate of oxygen consumption or VO2 without impairing endothelial function.


Genetics of cardiomyopathy

In both dilated cardiomyopathy and arrhythmic right ventricular cardiomyopathy, autosomal dominant inheritance has been established. Restrictive cardiomyopathies are generally sporadic and linked to the cardiac troponin I gene. Cardiomyopathies can be tested genetically at large genetic institutes.

The at-risk patient should be evaluated and monitored in families where a first-degree relative has been diagnosed with cardiomyopathy leading to heart failure. An ECG and an echocardiography are the recommended screenings. Asymptomatic LV dysfunction should be recorded and addressed if it exists in the patient.



In the United States, approximately 5.1 million people have clinically evident heart failure, and the prevalence is increasing. Heart failure incidence has been constant over the last decades, with more than 650,000 new instances of heart failure identified each year, particularly among people over the age of 65.

Because the prevalence of heart failure is higher in this age range, the situation is anticipated to deteriorate in the near future. There are epidemiological disparities. When compared to whites, black males had the highest incidence rate (1000 person-years) of heart failure and the highest five-year death rate.

White women have the lowest prevalence. Heart failure affects 4.5 percent of non-Hispanic black men and 3.8 percent of non-Hispanic white males and females, compared to 2.7 % and 1.8 % of non-Hispanic white males and females, respectively.

Despite improvements in survival, the absolute death rate for people with heart failure remains over 50% within five years of diagnosis. The survival rate is inversely related to the severity of heart failure staging. 


Heart failure pathophysiology

When trying to maintain appropriate cardiac performance, the adaptive mechanisms that may be enough to maintain the overall contractile function of the heart at generally normal levels become maladaptive. Myocyte hypertrophy, apoptosis, and regeneration are the major cardiac responses to chronically increasing wall stress. This process eventually leads to remodeling, generally of the eccentric type, and decreased cardiac output, resulting in a neurohumoral and vascular cascade.

When carotid baroreceptor stimulation and renal perfusion are reduced, the sympathetic nervous system and the Renin-Angiotensin-Aldosterone system are activated.

The stimulation of the sympathetic nervous system causes a rise in heart rate and inotropy, which leads to myocardial toxicity. The activation of the Renin-Angiotensin-Aldosterone pathway causes vasoconstriction, raising afterload (angiotensin II), and hemodynamic changes, increasing preload (aldosterone).

BNP and ANP are both peptides that are produced from the atria and ventricles in response to heart chamber pressure/volume increase. These peptides increase natriuresis and vasodilation. Furthermore. BNP reduces sodium reabsorption in the proximal convoluted tubule. It also inhibits the secretion of renin and aldosterone.

There is poor relaxation and increased ventricular stiffness in individuals with HFpEF, resulting in dysfunction in diastolic filling of the left ventricle. Patients with concentrcleft ventricular hypertrophy exhibit a shift to the left in the diastolic pressure volume curve, resulting in an increase in diastolic pressures, increased energy expenditure, oxygen demand, and myocardial ischemia.

All of these processes will promote negative remodeling and decrease left ventricular function, resulting in heart failure symptoms.


Systolic and diastolic failure

Systolic and diastolic failure

Stroke volume decreases as a result of both systolic and diastolic heart failure. This activates peripheral and central baroreflexes and chemoreflexes, which can cause significant increases in sympathetic nerve traffic.

Although there are similarities in the neurohormonal responses to reduced stroke volume, the neurohormone-mediated processes that follow have been well understood in those with systolic heart failure. The subsequent increase in plasma norepinephrine corresponds directly with the degree of myocardial dysfunction and has important prognostic consequences.

While norepinephrine is directly harmful to cardiac myocytes, it also causes a number of signal-transduction problems, including downregulation of beta1-adrenergic receptors, uncoupling of beta2-adrenergic receptors, and increased activity of inhibitory G-protein. Overexpression of beta1-adrenergic receptors occurs as a result of beta1-adrenergic receptor changes, which promotes cardiac hypertrophy.


Atrial natriuretic peptide and B-type natriuretic peptide

ANP and BNP are endogenously produced peptides that are triggered in response to atrial and ventricular volume/pressure expansion, respectively. The atria and ventricles produce ANP and BNP, which both induce vasodilation and natriuresis.

Their hemodynamic effects are mediated by reductions in ventricular filling pressures caused by decreases in cardiac preload and afterload. BNP, in particular, causes selective afferent arteriolar vasodilation while inhibiting sodium reabsorption in the proximal convoluted tubule.

It also suppresses the release of renin and aldosterone, and therefore adrenergic activity. In chronic heart failure, ANP and BNP levels are high. BNP, in particular, has significant diagnostic, therapeutic, and prognostic consequences.


Heart failure symptoms

Heart failure symptoms include those caused by excess fluid buildup (dyspnea, orthopnea, edema, discomfort from hepatic congestion, and abdominal distention from ascites) as well as those caused by a decrease in cardiac output (fatigue, weakness) that is most noticeable with physical activity.

Shortness of breath at rest and/or with activity, orthopnea, paroxysmal nocturnal dyspnea, and right upper quadrant pain owing to acute hepatic congestion define acute and subacute presentations (days to weeks) (right heart failure). If the patient develops atrial or ventricular tachyarrhythmias, palpitations with or without lightheadedness may ensue.

Fatigue, anorexia, abdominal distension, and peripheral edema may be more severe than dyspnea in chronic presentations (months). Anorexia is caused by a number of causes, including inadequate splanchnic circulation perfusion, intestinal edema, and nausea caused by hepatic congestion.

Characteristic features:

  • Pulsus alternans: characterized by alternating strong and weak peripheral pulses.
  • Apical impulse: laterally displaced past the midclavicular line, indicative of left ventricular enlargement.
  • S3 gallop: a low-frequency, brief vibration occurring in early diastole. It is the most sensitive indicator of ventricular dysfunction.


Heart failure edema

Congestive heart failure occurs when one or both of your heart's bottom chambers lose their capacity to efficiently pump blood. As a result, blood can pool in your legs, ankles, and feet, resulting in edema. Swelling in your abdomen can also be caused by congestive heart failure. 




Physical examination to determine the presence of clinical symptoms and signs, blood tests, including complete blood count, urinalysis, complete metabolic profile for levels of serum electrolytes (including calcium and magnesium), blood urea nitrogen, serum creatinine, glucose, fasting lipid profile, liver function tests, and thyroid-stimulating hormone.

Tests include:

  • Electrocardiogram (ECG): for identifying acute or prior myocardial infarction or acute ischemia, also for rhythm abnormalities, such as atrial fibrillation. 
  • Chest x-ray: characteristic findings are cardiac-to-thoracic width ratio above 50%, cephalization of the pulmonary vessels, and pleural effusions.
  • Blood test: Cardiac troponin (T or I), complete blood count, serum electrolytes, blood urea nitrogen, creatinine, liver function test and brain natriuretic peptide (BNP). The level of BNP (or NT-proBNP) provides more diagnostic value to the history and physical examination than the other first tests listed above.
  • Transthoracic Echocardiogram: to determine ventricular function and hemodynamics.


Heart failure vs heart attack

Heart attacks and cardiac failure are both kinds of heart disease, however they are not the same thing. Heart attacks occur when the heart loses blood flow, whereas heart failure occurs when the heart is unable to properly pump blood around the body.


Heart failure treatment

The major goals of treatment in heart failure are

  1. to improve prognosis and reduce mortality and
  2. to decrease morbidity and symptoms by correcting or decreasing cardiac and peripheral dysfunction.

For in-hospital patients, in addition to the above goals, other goals of therapy are 

  1. to reduce the length of stay and subsequent readmission
  2. to prevent organ system damage and
  3. to manage the co-morbidities that may contribute to poor prognosis 

Despite advances in science, healthcare practitioners have found it difficult to manage heart failure (HF), which often manifests as a clinical syndrome. This is evident in the significantly greater readmission rate, as well as the increased mortality and morbidity associated with HF.

Diuretics, beta-blockers, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, angiotensin receptor neprilysin inhibitor, hydralazine with nitrate, digoxin, and aldosterone antagonists can all help to alleviate symptoms.

  • Heart failure beta blockers

Beta blockers, angiotensin-converting enzyme inhibitors, angiotensin receptor neprilysin inhibitor, hydralazine with nitrate, and aldosterone antagonists have all been shown to improve patient survival. Diuretic treatment has more limited evidence of survival benefit.

In chronic symptomatic patients with CHF NYHA class II-III who have sufficient blood pressure and are tolerating an optimum dosage of these medicines, replace angiotensin converting enzyme inhibitors or angiotensin receptor blockers with angiotensin receptor neprilysin inhibitors. Angiotensin receptor neprilysin inhibitors should not be administered within 36 hours of angiotensin-converting enzyme inhibitors.


Device therapy: 

An implanted cardioverter-defibrillator (ICD) is used to prevent sudden cardiac death as a main or secondary measure. Cardiac resynchronization treatment using biventricular pacing can improve symptoms and survival in patients with sinus rhythm, a low left ventricular ejection fraction, and a lengthy QRS duration. The vast majority of patients who meet the criteria for cardiac resynchronization therapy implantation are also candidates for an implanted cardioverter-defibrillator and are given a combination device.

A ventricular assist device (as a bridge to transplant or as a destination therapy) or cardiac transplant are reserved for individuals with severe illness who have failed all other treatment options.

Patient treatment in acute heart failure consists of stabilizing the patient's clinical condition, determining the diagnosis, etiology, and triggering events, and beginning therapy to offer fast symptom alleviation and survival benefit,

Surgical options for heart failure include:

  • Revascularization procedures,
  • Electrophysiologic intervention,
  • Cardiac resynchronization therapy (CRT),
  • Implantable cardioverter-defibrillators (ICDs), 
  • Valve replacement or repair, 
  • Ventricular restoration, 
  • Heart transplantation, and 
  • Ventricular assist devices (VADs)


Differential Diagnosis

  • Acute Kidney Injury
  • Acute Respiratory Distress Syndrome (ARDS)
  • Bacterial Pneumonia
  • Cirrhosis
  • Community-Acquired Pneumonia (CAP)
  • Emphysema
  • Interstitial (Nonidiopathic) Pulmonary Fibrosis
  • Myocardial Infarction
  • Nephrotic Syndrome
  • Pneumothorax Imaging
  • Pulmonary Embolism (PE)
  • Respiratory Failure
  • Venous Insufficiency
  • Viral Pneumonia



NYHA Classification of Heart failure

  • Class 1: No limitations in physical activity
  • Class 2: Mild limitations in physical activity
  • Class 3: Moderate limitations in physical activity
  • Class 4: Symptoms occur at rest and any physical activity is not possible without symptoms



Heart failure is a severe medical condition with a high death rate. At one year and five years, mortality rates are 22% and 43%, respectively. Patients with advanced NYHA class had the greatest death rate. Furthermore, cardiac failure linked with a MI has a mortality rate of 30-40%. Over a 5-year period, heart failure linked with systolic dysfunction has a 50% death rate. Furthermore, individuals with heart failure require several hospitalizations over the course of their lives.

Numerous demographic, clinical and biochemical variables have been reported to provide important prognostic value in patients with heart failure, and several predictive models have been developed.

To help prevent recurrence of heart failure in patients in whom heart failure was caused by dietary factors or medication noncompliance, counsel and educate such patients about the importance of proper diet and the necessity of medication compliance.



Heart failure is a frequent clinical condition characterized by dyspnea, tiredness, and indications of volume overload, such as peripheral edema and pulmonary rales. Diseases affecting the endocardium, myocardium, pericardium, heart valves, arteries, or metabolic problems can all lead to heart failure.

The majority of individuals with heart failure have symptoms as a result of decreased left ventricular myocardial function. Patients often report with dyspnea, reduced exercise tolerance, and fluid retention, as seen by pulmonary and peripheral edema.

Many diseases, including coronary artery disease, hypertension, valvular heart disease, and diabetes mellitus, can cause or contribute to chronic heart failure decompensation. Diastolic heart failure with maintained left ventricular function affects up to 40% to 50% of individuals with heart failure, and the overall mortality rate is similar to that of systolic heart failure. 

To detect causes or precipitating factors, the first evaluation involves a history and physical examination, chest radiography, electrocardiography, and laboratory testing. Heart failure can be identified by a shifted cardiac apex, a third heart sound, and chest radiography indications of venous congestion or interstitial edema. When the Framingham criteria are not satisfied or when the B-type natriuretic peptide level is normal, systolic heart failure is improbable.

Echocardiography is the gold standard for confirming systolic or diastolic heart failure by measuring the left ventricular ejection fraction. Given that coronary artery disease is the most prevalent cause of heart failure, individuals with heart failure should be evaluated for ischemic heart disease, especially if angina is present.

Heart failure is a severe condition that requires the collaboration of a multidisciplinary team that includes the primary care physician, emergency department physician, cardiologist, radiologist, cardiac nurses, internist, and a cardiac surgeon. It is critical to address the underlying cause of heart failure.

Nurses and other healthcare personnel who care for these individuals must be informed with current treatment recommendations. Heart disease risk factors must be addressed, and the pharmacist should educate the patient on the significance of drug adherence.

The dietician should educate the patient on the benefits of eating a low-salt diet and reducing fluid consumption. The nurse should educate the patient on the significance of exercise, stress reduction, and maintaining contact with the cardiologist. The pharmacist should ensure that the patient knows the significance of medication adherence, which is frequently the single most critical factor contributing to decompensation.

Patients must be taught on the significance of keeping a healthy body weight, quitting smoking, managing blood pressure, and maintaining normoglycemia. These individuals should be followed and monitored by a cardiac nurse. 


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