Congestive Heart Failure

Introduction
Heart failure is a complex clinical syndrome that results from any functional or
structural heart disorder, impairing ventricular filling or ejection of blood to the
systemic circulation to meet the systemic needs. Heart failure can be caused by
diseases of the endocardium, myocardium, pericardium, heart valves, vessels or
metabolic disorders. Most patients with Heart failure have symptoms due to impaired
left ventricular myocardial function. Patients usually present with symptoms of
dyspnea, decreased exercise tolerance and fluid retention, characterized by pulmonary
and peripheral edema.
Heart failure due to left ventricular dysfunction is categorized according to left
ventricular ejection fraction (LVEF) into heart failure with reduced ejection fraction
(usually considered LVEF 40% or less), known as HFrEF and heart failure with
preserved ejection fraction; known as HFpEF. The definition of HFrEF has varied
among different studies and guidelines with different left ventricular ejection fraction
(LVEF) cut-offs of ≤35%, <40%, and ≤40%. Randomized controlled trials in patients
with HF have mainly enrolled patients with HFrEF with an EF ≤35% or ≤40%, and it
is only in these patients that efficacious therapies have been demonstrated to date.
According to the most recent ACC/AHA guidelines on heart failure, HFrEF is defined
as the clinical diagnosis of HF with EF ≤40%. In routine clinical practice, many
clinicians would consider EF <45% as significant systolic dysfunction and would
consider it as HFrEF.
Heart failure with preserved ejection fraction (HFpEF) on the other hand has also
been variably classified as EF >40%, >45%, >50%, and/or ≥55%. The term HFpEF
has been used since some of these patients do not have entirely normal EF but also do
not have a major reduction in the systolic function. Patients with an EF between the
range of 40% to 50% have been considered to represent an intermediate group of
patients due to a variable cut off used for systolic dysfunction by the different studies.
These patients should be routinely treated for underlying risk factors and
comorbidities and with optimal guideline-directed therapy, similar to that of HFrEF.
When heart failure develops, compensatory mechanisms attempt to increase the
cardiac filling pressure, muscle mass and heart rate. However, in many cases, there is
usually a progressive decline in heart function.
Etiology
Heart failure is caused by several disorders, including diseases affecting the
pericardium, myocardium, endocardium, cardiac valves, vasculature, or metabolism.
The most common causes of systolic dysfunction (HFrEF) are idiopathic dilated
cardiomyopathy (DCM), coronary heart disease (ischemic), hypertension, and
valvular disease.
Hypertension, obesity, coronary artery disease, diabetes mellitus, atrial fibrillation,
and hyperlipidemia are highly prevalent in HFpEF patients. Hypertension by far is the
most important cause of HFpEF. In addition, conditions like hypertrophic obstructive
cardiomyopathy, and restrictive cardiomyopathy are associated with significant
diastolic dysfunction, leading 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:
 Excess intake of sodium in the diet
 Inappropriate reduction in medications
 Lack of physical activity
 Lack of medication compliance
 Prolonged physical activity
 Emotional crisis
 Sudden changes in weather
 Excess intake of water
Epidemiology
Approximately 5.1 million people in the United States have clinically manifest heart
failure, and the prevalence continues to increase. Heart failure incidence has remained
stable over the past decades, with more than 650,000 new cases of heart failure cases
diagnosed annually, especially for individuals greater than 65 years of age. Because
prevalence is greater in this age group, heart failure prevalence is expected to worsen
in the near future.Epidemiological differences have been noted. Black men have the
highest incidence rate (1000 person-years) for heart failure and the greatest five-year
mortality rate when compared to whites. White women represent the lowest
incidence. Heart failure in non-Hispanic black males and females has a prevalence
of 4.5% and 3.8%, respectively, versus 2.7% and 1.8% in non-Hispanic white males
and females, respectively. Although survival has improved, the absolute mortality
rates for patients with heart failure remain approximately 50% within five years of
diagnosis. The survival rate is inverse proportional to the staging severity of heart
failure. The 5-year survival for stage A, B, C, and D heart failure was found to be
97%, 96%, 75%, and 20%, respectively in a study. By 2013, heart failure costs in the
United States exceeded $30 billion.
Gender differences in heart failure:
1. Between ages 65-85, heart failure incidence doubles in men but at the same time it
triples in women
2. Women are likely to have preserved systolic function compared to men
3. Women, in general, develop heart failure later in life compared to men
4. While the symptoms of heart failure are similar in both genders, they are often
severe in females
5. Women with heart failure tend to have longer survival times compared to men
6. Heart failure in Developing nations
7. The majority of cases of heart failure are from non-ischemic causes
8. Patients generally tend to be young
9. Because of limitations in resources, the outcomes are worse
10. Isolated right heart failure is more common, and may be linked to lung disease,
pollution, pericardial disease, and tuberculosis.
Pathophysiology
The adaptive mechanisms that may be adequate to maintain the overall contractile
performance of the heart at relatively normal levels become maladaptive when trying
to sustain adequate cardiac performance. The primary myocardial response to
chronically increased wall stress is myocyte hypertrophy, death due to apoptosis, and
regeneration. This process eventually leads to remodeling, usually the eccentric type,
and reduced cardiac output, causing a cascade of the neurohumoral and vascular
mechanism.
Decreased carotid baroreceptor stimulation and renal perfusion will activate the
sympathetic nervous system and Renin-Angiotensin-Aldosterone system. 
Sympathetic nervous system activation will cause increased heart rate and inotropy,
leading to myocardial toxicity. Renin-Angiotensin-Aldosterone system activation
leads to vasoconstriction, increasing afterload (angiotensin II) and hemodynamic
alterations, increasing preload (aldosterone).
Both BNP and ANP are peptides released from the atria and ventricles in reposne to
heart chamber pressure/volume expansion. These peptides promote natriuresis and
vasodilatation. In addition. BNP inhibits the reabsorption of sodium in the proximal
convoluted tubule. It also suppresses renin and aldosterone release.
In patients with HFpEF there is impaired  relaxation and increasing ventricle stiffness,
leading to dysfunction in diastolic filling of the left ventricle. Patients with
concentrcleft ventricular hypertrophy have a shift of the diastolic pressure volume
curve to the left, leading to elevation in diastolic pressures, which leads to increased
energy expenditure and oxygen demand and myocardial ischemia.
All of these mechanisms will cause negative remodeling and worsen the left
ventricular function, causing symptoms of heart failure.

History and Physical

Symptoms of heart failure include those due to excess fluid accumulation (dyspnea,
orthopnea, edema, pain from hepatic congestion, and abdominal distention from
ascites) and those due to a reduction in cardiac output (fatigue, weakness) that is most
pronounced with physical exertion.
Acute and subacute presentations (days to weeks) are characterized by shortness of
breath at rest and/or with exertion, orthopnea, paroxysmal nocturnal dyspnea, and
right upper quadrant discomfort due to acute hepatic congestion (right heart failure).
Palpitations, with or without lightheadedness can occur if patient develops atrial or
ventricular tachyarrhythmias
Chronic presentations (months) differ in that fatigue, anorexia, abdominal distension,
and peripheral edema may be more pronounced than dyspnea. The anorexia is
secondary to several factors including a poor perfusion of the splanchnic circulation,
bowel edema, and nausea induced by hepatic congestion. 
Characteristic features:
 Pulsus alternans phenomenon characterized by evenly spaced alternating strong
and weak peripheral pulses.
 Apical impulse: laterally displaced past the midclavicular line, usually indicative
of left ventricular enlargement.
 S3 gallop: a low-frequency, brief vibration occurring in early diastole at the end
of the rapid diastolic filling period of the right or left ventricle. It is the most
sensitive indicator of ventricular dysfunction.

Evaluation
Tests include:
 Electrocardiogram (ECG): important for identifying evidence of acute or prior
myocardial infarction or acute ischemia, also rhythm abnormalities, such as atrial
fibrillation. 
 Chest x-ray: characteristic findings are cardiac-to-thoracic width ratio above
50%, cephalization of the pulmonary vessels, Kerley B-lines, 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). BNP (or NT-proBNP) level adds greater diagnostic value to the history
and physical examination than other initial tests mentioned above.
 Transthoracic Echocardiogram:  to determine ventricular function and
hemodynamics.

Treatment / Management
Diuretics, beta-blockers, angiotensin converting enzyme inhibitors, angiotensin
receptor blockers, angiotensin receptor neprilysin inhibitor, hydralazine plus
nitrate, digoxin, and aldosterone antagonists can produce an improvement in
symptoms
Prolongation of patient survival has been documented with beta blockers, angiotensin-
converting enzyme inhibitors, angiotensin receptor neprilysin
inhibitor, hydralazine plus nitrate, and aldosterone antagonists. More limited evidence
of survival benefit is available for diuretic therapy. Replace an angiotensin converting
enzyme inhibitors or angiotensin receptor blockers by angiotensin receptor neprilysin
inhibitor in chronic symptomatic patients with CHF NYHA class II-III with an
adequate blood pressure who are tolerating an optimal dose of these
medications. Angiotensin receptor neprilysin inhibitor should not be given within 36
hrs of angiotensin converting enzyme inhibitors dose.
In African-Americans, hydralazine plus oral nitrate is indicated in patients with
persistent NYHA class III to IV HF and LVEF less than 40%, despite optimal medical
therapy (beta-blocker, angiotensin converting enzyme inhibitors, ARB, aldosterone
antagonist (if indicated), and diuretics.
Device therapy: implantable cardioverter-defibrillator (ICD) is used for primary or
secondary prevention of sudden cardiac death. Cardiac resynchronization therapy with
biventricular pacing can improve symptoms and survival in selected patients who are
in sinus rhythm and have a reduced left ventricular ejection fraction and a prolonged
QRS duration. Most patients who satisfy criteria for cardiac resynchronization
therapy implantation are also candidates for an implantable cardioverter-
defibrillator and receive a combined device.
A ventricular assist device (bridge to transplant or as a destination therapy) or cardiac
transplant are reserved for those with severe disease despite all other measures.

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

Staging
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

ACC Heart Failure Stages:

 Stage A: Patients at high risk for HF but have no symptoms or structural heart
disease
 Stage B: Patients have structural heart disease but are asymptomatic
 Stage C: Patients have structural heart disease plus symptoms
 Stage D: Patients have refractory HF that requires modified interventions

Prognosis
Heart failure is a serious medical disorder associated with high mortality. Mortality
rates at 1 year and 5 years are 22% and 43%, respectively. The highest mortality is in
patients with advanced NYHA class. In addition, heart failure associated with an MI
carries a mortality of 30-40%. Heart failure that is associated with systolic
dysfunction has a 50% mortality over 5 years. Further, patients with heart failure need
repeated admissions over the years.
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Pearls and Other Issues

To reduce heart failure hospitalizations, it is reasonable (class IIa) to use Ivabradine in
patients with NYHA II-III with guideline-directed medical therapy (including a beta-
blocker) and heart rate of more than 70 bpm.
Heart failure disease management is a complex condition that requires a
multidisciplinary framework for the care of patients, including discharge planning,
patient education, and frequent outpatient assessment.

Enhancing Healthcare Team Outcomes

Heart failure is a serious disorder that is best managed by an interprofessional team
that includes the primary care physician, emergency department physician,
cardiologist, radiologist, cardiac nurses, internist, and a cardiac surgeon. It is
imperative to treat the primary cause of heart failure. Healthcare workers including
nurses who look after these patients must be familiar with current guidelines on
treatment. The risk factors for heart disease must be modified and the pharmacist
should educate the patient on the importance of medication compliance. The dietitian
should educate the patient on the importance of a low salt diet and limiting fluid
intake. The nurse should educate the patient on the importance of exercise, avoiding
stress and ensuring follow up with the cardiologist. The pharmacist should ensure that
the patient understands the importance of medication compliance, which is often the
single most important factor leading to decompensation. Patients need to be educated
on the importance of maintaining a healthy body weight, discontinuation of smoking,
controlling blood pressure and ensuring normoglycemia. A cardiac nurse should
follow these patients and monitor their progress. The only way to lower morbidity and
mortality is through open communication between the team members.
When the condition is not managed appropriately, it is associated with high morbidity
and mortality, including a poor quality of life.
The following are key points to remember from the 2021 European Society of
Cardiology (ESC) Guidelines for the Diagnosis and Treatment of Acute and Chronic
Heart Failure (HF):

1. The nomenclature for HF with left ventricular ejection fraction (LVEF) of 41-
49% has been revised to HF with mildly reduced EF (HFmEF). HF with
LVEF ≤40% remains HF with reduced EF (HFrEF), and HF with LVEF ≥50%
remains HF with preserved EF (HFpEF).
2. All patients with suspected HF should have an electrocardiogm, transthoracic
echocardiogram, chest X-ray, blood tests including cell count, urea and
electrolytes, thyroid function, glycated hemoglobin (HbA1c), lipid, iron
 studies, and B-type natriuretic peptide (BNP/NT-proBNP). Cardiac magnetic
resonance imaging is recommended in those with poor acoustic windows with
an echo or in patients with suspected infiltrative cardiomyopathy,
hemochromatosis, LV noncompaction, or myocarditis.
3. Guideline-directed medical therapy (GDMT) for patients with HFrEF and
New York Heart Association (NYHA) class II symptoms or worse now
includes angiotensin receptor neprilysin inhibitor (ARNI) as a replacement for
angiotensin-converting enzyme (ACE) inhibitors and addition of SGLT-2
inhibitors (dapagliflozin or empagliflozin) as Class I recommendations.
4. Implantable cardioverter-defibrillators (ICDs) are recommended for primary
prevention of sudden cardiac death for symptomatic ischemic or nonischemic
cardiomyopathy with LVEF ≤35% despite 3 months of GDMT if expected
survival is >1 year. ICD is NOT recommended within 40 days of a myocardial
infarction (MI) or for patients with NYHA class IV symptoms who are not
candidates for advanced therapies.
5. Cardiac resynchronization therapy is recommended for symptomatic HFrEF
with EF <35% in sinus rhythm with a left bundle branch block (LBBB) over
150 msec duration despite GDMT. It is also recommended in HFrEF with EF
<35% irrespective of symptoms or QRS duration if there is a high-grade
atrioventricular (AV) block with need for a pacemaker.
6. For HFmEF, diuretics are recommended to relieve congestion. ACE
inhibitors/ angiotensin receptor blockers/ ARNIs/ beta blockers/
mineralocorticoid receptor antagonists may be considered as additional
therapy to reduce mortality and hospitalization (Class IIa recommendation).
7. For HFpEF patients, diagnosis and treatment of contributing factors
(hypertension, kidney disease, etc.) and use of diuretics are recommended. No
specific therapies have been proven to reduce mortality in HFpEF.
8. For all HF patients, enrollment in a multidisciplinary HF program, home, or
clinic-based program and use of self-management strategies are
recommended. Exercise is recommended for all HF patients.
9. For prevention of HF, appropriate treatment of hypertension, use of statins
when indicated, SGLT2 inhibitors in diabetics at high risk for or with
cardiovascular disease and counseling against smoking, alcohol, drug use, and
obesity are all Class I recommendations.
10. For acute decompensated HF, routine use of inotropes is NOT recommended
in the absence of cardiogenic shock and routine use of opioids is NOT
recommended. Routine use of intra-aortic balloon pump in post-MI
cardiogenic shock is NOT recommended.
11. Additional Class I recommendations for hospitalized acute HF patients include
trial of oral GDMT and careful exclusion of volume overload prior to
discharge with early follow-up within 1-2 weeks of discharge.
12. For patients with atrial fibrillation (AF), routine use of anticoagulation for
CHA2DS2-VASc ≥2 in men and ≥3 in women, preferably with direct-acting
oral anticoagulants except in the presence of a prosthetic mechanical valve or
moderate or severe mitral stenosis, is recommended. Urgent cardioversion for
patients in AF with HF and hemodynamic compromise is recommended.
Rhythm control including catheter ablation should be considered for AF
patients with symptoms including HF.
13. For patients with HF and severe aortic stenosis, transcatheter/surgical aortic
valve replacement is recommended using a heart team approach.
14. For HF patients with secondary mitral regurgitation, percutaneous edge-to-
edge mitral valve repair should be considered if severe symptoms persist
despite appropriate GDMT. For patients with secondary mitral regurgitation
and coronary artery disease who need revascularization, coronary artery
bypass grafting and mitral valve surgery should be considered.
15. Cancer patients being considered for cardiotoxic chemotherapeutic agents who
are at risk for cardiotoxicity, should be evaluated ideally by a cardio-
oncologist prior to initiation of therapy.
16. Tafamidis is a Class I recommendation in patients with TTR amyloidosis with
NYHA class I-II symptoms.
17. All HF patients should be periodically screened for iron deficiency anemia.
Ferric carboxymaltose should be considered in symptomatic, ambulatory HF
patients with iron deficiency anemia and EF ≤45% or hospitalized HF patients
with EF ≤50%.

Source:

https://www.ncbi.nlm.nih.gov/books/NBK430873/
https://www.acc.org/latest-in-cardiology/ten-points-to-
remember/2021/08/29/18/05/2021-esc-guidelines-for-hf-esc-2021