Congestive Heart Failure

Introduction: -
 Congestive Heart Failure is older term for heart Failure.
 It is still used interchangeably by some to indicate heart failure in general.
 The newer term heart failure is preferred because volume overload or congestion either in
the lungs or periphery is not present in everyone with heart failure all the time.

Definition: -
 Heart failure is a condition characterized by unable to pump blood by heart (Left
ventricle) according to body demand evidence by vasoconstriction, fluid retention and
edema.
 Cardiac failure is a physiological state in which the heart cannot pump enough blood to
meet metabolic needs of the body.
 Cardiac failure occurs when the cardiac output is inadequate to provide the oxygen need
of the body.
 The term heart failure indicates myocardial disease in which there is a problem with
contraction of the heart (systolic dysfunction) or filling of the heart (diastolic dysfunction)
that may or may not cause pulmonary or systemic congestion.
 It is a progressive and lifelong condition that is manage with life style changes and
medication to prevent acute decompensated heart failure. These episodes are
characterized by an increase in symptoms, decrease co2 and low perfusion.

Etiology: -

 Dehydration
 Hypovolemia
 Hypervolemia
 Hypertension
 Pulmonary valve stenosis
 Aortic Valve stenosis
 Mitral valve stenosis
 Tricuspid valve stenosis
 Valve regurgitation
 Valvular prolapse
 Neurotic heart Failure
 Shock
 CAD
 Cardiomyopathy
 Renal Dysfunction
Precipitating Cause of Heart Failure
Anemia- ↓ O2-carrying capacity of the blood stimulating↑ in CO to meet tissue demands,
leading to increase in cardiac workload and increase in size of LV
Infection- ↑ O2 demand of tissues, stimulating ↑ CO
Thyrotoxicosis- Changes the tissue metabolic rate, ↑ HR and workload of the heart
Hypothyroidism -Indirectly predisposes to ↑ atherosclerosis; severe hypothyroidism
decreases myocardial contractility
Dysrhythmias- May ↓ CO and ↑ workload and O2 requirements of myocardial tissue
Bacterial Endocarditis-Infection: ↑ metabolic demands and O2requirements
Valvular dysfunction: causes stenosis and regurgitation
Pulmonary embolism-↑ Pulmonary pressure resulting from obstruction leads to pulmonary
hypertension, ↓ CO
Paget’s disease- ↑ Workload of the heart by ↑ vascular bed in the skeletal muscle
Nutritional Deficiencies-May ↓ cardiac function by ↑ myocardial muscle mass and
myocardial contractility
Hypervolemia -↑ Preload causing volume overload on the RV

Classification Criteria Patient Characteristics Treatment

Recommendation for
appropriate patients

Stage -A Patients at high-risk for Heart healthy lifestyle

developing left ventricular
dysfunction but without
structure heart disease
or symptoms of HF
Patient with left ventricle
dysfunction or structural
Stage -B heart disease who have not
developed symptoms
of HF
Hypertension
Atherosclerotic disease
Diabetes
Metabolic Syndrome
History of myocardial
infarction
Left ventricular hypertrophy
Low ejection Fraction
Risk factor control of
hypertension, lipid,
diabetes,
obesity
Implement stage -A
recommendations plus
 ACE inhibitor or
ARB for low EF or
History of MI
 Beta blocker
 Statin
 Stage -C Patient with left ventricular Shortness of breath Implement stage A & B
dysfunction or Fatigue recommendation
structural heart disease with Decreased exercise tolerance  Diuretics
current or prior  Aldosterone
symptoms of heart disease antagonist
 Sodium restrictions
 Implantable
defibrillator
 Cardiac
resynchronization
therapy
Stage -D Patient with refractory end- Symptoms despite maximal Implement Stage A, B &
stage HF requiring medical therapy C recommendation
specialized interventions Recurrent hospitalization  Fluid restriction
 End of life care
 Inotropes
 Cardiac
transplantation
 Mechanical Support

Classification of Heart Failure: -

AMERICAN COLLEGE OF CARDIOLOGY AND AMERICAN HEART ASSOCIATION
CLASSIFICATION OF HEART FAILURE

According to Location of the heart failure: -

HF is usually manifested by biventricular failure, although one ventricle may precede the
other in dysfunction. Normally the pumping actions of the left and right sides of the heart are
synchronized, producing a continuous flow of blood. However, as a result of pathologic
conditions, one side may fail while the other side continues to function normally for a time.
Because of the prolonged strain, both sides of the heart eventually fail, resulting in
biventricular failure.

 Left sided Heart Failure: -

. The most common form of HF is left-sided HF. Left-sided HF results from left
ventricular dysfunction. This prevents normal, forward blood flow and causes blood to back
up into the left atrium and pulmonary veins. The increased pulmonary pressure causes fluid
leakage from the pulmonary capillary bed into the interstitium and then the alveoli. This
manifests as pulmonary congestion and edema.
 Right-Sided Heart Failure. - Right-sided HF occurs when the right ventricle (RV)
fails to contract effectively. Right-sided HF causes a backup of blood into the right atrium
and venous circulation. Venous congestion in the systemic circulation results in jugular
venous distention, hepatomegaly, splenomegaly, vascular congestion of the
gastrointestinal tract, and peripheral edema. Right-sided HF may result from an acute
condition such as right ventricular infarction or pulmonary embolism. Cor pulmonale
(right ventricular dilation and hypertrophy caused by pulmonary disease) can also cause
right-sided HF.

Pathophysiology: -

Clinical Manifestation: -
Classic symptoms of heart failure include dyspnea with exertion, orthopnea, nocturnal
dyspnea, a dry, hacking cough, and unexplained fatigue. When volume overload contributes
to pathology, the following additional symptoms occur: rales, a third heart sound, peripheral
edema, unexplained weight gain, jugular venous distention, hepatic engorgements, ascites
and worsening dyspnea. Compensatory mechanism accounts for many of the clinical signs
and symptoms of heart failure.
The more common symptoms as well as symptoms encountered with progressive heart failure
are as follows:

• Respiratory symptoms
– Dyspnea.
– Orthopnea.
– Paroxysmal nocturnal dyspnea.
– Persistent hacking cough.
– Alternating periods of apnea and hyper apnea.
– Rales (Crackles).
• Cardiovascular symptoms
– Angina.
– Jugular venous distention.
– Tachycardia.
– Decrease in systolic blood pressure with
increase in diastolic pressure.
– S3 and S4 heart sounds.
• Gastrointestinal symptoms
– Enlargement and tenderness in the right upper quadrant of abdomen.
– Ascites.
– Nausea.
– Vomiting.
– Bloating.
– Anorexia.
– Epigastric pain.
• Cerebral symptoms
– Altered mental status (confusion, restlessness).
• Generalized symptoms
– Fatigue.
– Decrease in activity intolerance.
– Edema (Peripheral pitting).
– Weight gain.

• Psychosocial
– Anxiety.
The clinical manifestations specific to right-sided
and left-sided heart failure are as follows:

• Right-sided heart failure.

Signs
– Right ventricle heaves.
– Murmurs.
– Peripheral edema.
– Weight gain.
– Edema of dependent body part (sacrum, anterior tibias, pedal edema)
– Ascitis.
– Anasarea (Massive generalized body edema).
– Jugular venous distension.
– Hepatomegaly (Liver engorgement).
– Right-sided pleural effusion.
Symptoms
– Fatigue.
– Dependent edema.
– Right upper quadrant pain.
– Anorexia and GI bloating.
– Nausea.
• Left-sided heart failure
Signs
– Left ventricle heaves.
– Cheyne-Stokes respirations.
– Pulsus alternans (alternating pulses: strong, weak).
– Increased heart rate.
– PMI displaced inferiorly and posteriorly (LV hypertrophy).
– Decreased PaO2, slight increased PaCO2 (poor oxygen exchange).
– Crackles (Pulmonary edema).
– S3 and S4 heart sounds.
Symptoms
– Fatigue.
– Dyspnea (Shallow respiration up to 32-40/m).
– Orthopnea (Shortness of breath in recumbent position).
– Dry, hacking cough.
– Pulmonary edema.
• Nocturia.
• Paroxysmal nocturnal dyspnea
The

Epidemiology: -
 lifetime risk of developing HF is 20% for Americans ≥40 years of age. In
the United States, HF incidence has largely remained stable over the
past several decades, with >650 000 new HF cases diagnosed annually.
 HF incidence increases with age, rising from approximately 20 per
1000 individuals 65 to 69 years of age to >80 per 1000 individuals
among those ≥85 years of age Approximately 5.1 million persons in the
United States have clinically manifest HF, and the prevalence
continues to rise
 In the Medicare-eligible population, HF prevalence increased from 90
to 121 per 1000 beneficiaries from 1994 to 2003. HFrEF and HFpEF
each make up about half of the overall HF burden. One in 5 Americans
 will be >65 years of age by 2050. Because HF prevalence is highest in
this group, the number of Americans with HF is expected to
significantly worsen in the future.
 Disparities in the epidemiology of HF have been identified. Blacks have
the highest risk for HF. In the ARIC (Atherosclerosis Risk in
Communities) study, incidence rate per 1000 person-years was lowest
among white women and highest among black men, with blacks
having a greater 5-year mortality rate than whites. HF 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.

Diagnostic Evaluation: -

 History collection:
 The diagnosis and classification of HF are primarily based on the presence and severity
of symptoms and physical exam findings. It is imperative to obtain a detailed history of
symptoms, underlying medical conditions, and functional capacity to treat the patient
adequately.
 Acute CHF presents primarily with signs of congestion and may also present with organ
hypo perfusion or cardiogenic shock The most commonly reported symptom is shortness
of breath. This must be further classified as exertional, positional (orthopnea), and
whether acute or chronic.
 Other commonly reported symptoms of CHF include chest pain, anorexia, and exertional
fatigue. Anorexia is due to hepatic congestion, bowel edema, and reduced blood flow to
splanchnic circulation.
 Some patients may present with a recumbent cough due to orthopnoea. Patients may also
experience abdominal discomfort due to hepatic congestion or ascites. Patients with
arrhythmias can present with palpitations, presyncope, or syncope.
 Another symptom that increases morbidity is edema, especially of the lower extremities.
This can limit mobility and balance; total body water and weight increases of > 20 lbs are
not uncommon.
 While patients with acute HF present with overt respiratory distress, orthopnea, and
paroxysmal nocturnal dyspnea, patients with chronic heart failure tend to curtail their
physical activity; hence, symptoms may be obscured. It is essential to identify triggers of
acute decompensation such as recent infection, noncompliance with cardiac medications,
use of NSAIDs, or increased salt intake.

Physical Examination:
The examination findings vary with the stage and acuity of the disease. Patients may have
isolated symptoms of left-sided HF, right-sided HF, or combined.
General physical examination: The general appearance of patients with severe CHF or those
with acutely decompensated HF includes anxiety, diaphoresis, tachycardia, and tachypnea.
Wheezing may be present in acute decompensated heart failure. As the severity of pulmonary
congestion increases, frothy and blood-tinged sputum may be seen. It is important to note that
the absence of rales does not exclude pulmonary congestion. Jugular venous distention is
another classical finding that must be assessed in all patients with HF. In patients with
elevated left-sided filling pressures, hepatojugular reflux (sustained increase in JVP of >4 cm
after applying pressure over the liver with the patient lying at a 45° angle) is often seen .
CBC may suggest anaemia or leukocytosis suggestive of an infection triggering CHF.
A complete renal profile is necessary for all patients with HF. It indicates the degree of
renal injury associated with HF and guides medication choice. It is essential to know baseline
renal function before the patient is started on medications, including renin-angiotensin-
aldosterone (RAAS) inhibitors, sodium-glucose transporter-2 (SGLT-2) inhibitors, or
diuretics. Serum sodium level has prognostic value as a predictor of mortality in patients with
chronic HF. "The Outcomes of a Prospective Trial of Intravenous Milrinone for
Exacerbations of Chronic Heart Failure" (OPTIME-CHF) trial demonstrated a significantly
increased risk of in-hospital mortality as well as 30-day mortality in patients with HF who
presented with hyponatremia.[39]
A liver profile is usually performed. Hepatic congestion secondary to HF may result in
elevated gamma-glutamyl transferase levels, aspartate aminotransferase (AST), and alanine
aminotransferase (ALT).[40]
Urine studies can be useful in diagnosis. If amyloidosis is suspected, urine and serum
electrophoresis and monoclonal light chain assays should be performed. If clinical suspicion
is high despite negative testing for light chains, bone scintigraphy can be performed.[1]
Serum B-type natriuretic peptide (BNP) or N-terminal pro-BNP (NT-ProBNP)
levels can aid in differentiating cardiac from noncardiac causes of dyspnea in patients with
ambiguous presentations. BNP is an independent predictor of increased left ventricular end-
diastolic pressure, and it is used for assessing mortality risk in patients with HF. BNP levels
correlate with NYHA classification, and the utility is primarily used as a marker to assess
treatment efficacy. NT-ProBNP is the chemically inert N-terminal fragment of BNP and has a
longer half-life. The ratio of NT-ProBNP/BNP varies depending on underlying comorbidities
and may be a useful tool in the future.[41] In patients with a clear clinical presentation of HF,
natriuretic peptides should not be used to drive treatment plans. It is important to remember
that BNP and NT-ProBNP levels can be elevated in patients with renal dysfunction, atrial
fibrillation, and older patients. Conversely, BNP levels can be falsely low in patients with
obesity, hypothyroidism, and advanced HF (due to myocardial fibrosis).
Troponin-I or T suggests ongoing myocardial injury when persistently elevated and predicts
adverse outcomes and mortality.
An electrocardiogram may show evidence of prior infarction, chamber enlargement,
intraventricular conduction delay, or arrhythmia. It may also give clues to specific etiologies.
A low voltage and pseudo infarction pattern of ECG is seen in cardiac amyloidosis. An
epsilon wave is seen in ARVC. ECG also suggests the presence of ventricular desynchrony,
with a QRS duration of more than 120 msec, predicting the patient's response to device
therapy for HF.
Chest radiographs are used to assess the degree of pulmonary congestion and cardiac
contour (to determine the presence of cardiomegaly). Findings indicative of CHF on chest
radiographs include enlarged cardiac silhouette, edema at the lung bases, and vascular
congestion. In florid HF, Kerley B lines may be seen on chest radiographs. The absence of
these findings in patients with a suggestive clinical presentation does not rule out CHF.[37]
Echocardiography is the initial choice of modality in patients with suspected HF and is an
easily available bedside tool. Echocardiography quantifies right and left ventricular function,
denotes structural abnormalities in cardiac chambers and valves, and helps visualize the
presence of focal wall motion abnormalities. However, in patients with severe obesity,
pregnancy, or mechanical ventilation, it may be challenging to obtain adequate acoustic
windows. Transesophageal echocardiography (TEE) is an alternative for these patients.
Adequate rate control in patients with tachyarrhythmias is necessary to obtain adequate
echocardiographic images.[37]
Cardiac catheterization is often required for diagnosing ischemic cardiomyopathy and can
be useful for accurately evaluating intracardiac pressures such as left ventricular end-diastolic
pressure or pulmonary artery pressures.
Computed tomography may be used for the assessment of coronary artery disease in a
young patient with ventricular dysfunction (older patients are likely to have baseline
calcifications). It may also be used in patients with congenital heart diseases causing HF.
Cardiac CT may help with the detection of tumours causing HF. CT may also be used for the
evaluation of stent patency and graft evaluation.
SPECT-Myocardial Perfusion Imaging helps define the presence of ischemia in patients
with newly diagnosed left ventricular dysfunction and not undergoing coronary angiography.
It is particularly useful for assessing CAD in patients with no history of ischemia but elevated
troponin. ECG-gated myocardial perfusion imaging is used to evaluate LV EF, regional wall
motion, and regional wall thickening. EF measurement with this study may be affected in
patients with an irregular heart rate, low count density, and extra cardiac radiotracer
uptake. ECG-gated images are also useful in recognizing artifactual defects seen on SPECT
imaging, such as breast tissue and diaphragmatic attenuation
Cardiac magnetic resonance imaging has evolved as an essential tool when a discrepancy
exists between the clinical stage of the disease and echocardiographic findings. It helps with
the precise evaluation of volume, chamber sizes, and ventricular function. It also assesses the
stage of valvular heart disease in detail. Cardiac MRI also helps with the evaluation of
complex congenital heart diseases. The tool can also be used for non-invasive assessment of
conditions such as myocarditis, dilated cardiomyopathy, infiltrative cardiomyopathy, or
arrhythmogenic right ventricular dysplasia
Radionuclide multiple-gated acquisition (MUGA) scan is a reliable imaging technique for
evaluating EF and is used in patients when there is a disparity of EF measurements from
other studies
Noninvasive stress imaging includes stress echocardiography, stress cardiac MRI, and
SPECT imaging. These studies can be used to assess the benefit of coronary revascularization
in patients with ischemic cardiomyopathy.
Genetic testing is indicated for identifying genetic variants causing cardiomyopathies, such
as Titin, laminin A or C, myosin heavy chain, and cardiac Troponin-T mutations
Management:
Pharmacological Management -
Diuretics. - Diuretics are the mainstay of treatment in patients with volume overload.
Diuretics act to decrease sodium reabsorption at various sites within the nephrons, thereby
enhancing sodium and water loss. Decreasing intravascular volume with the use of diuretics
reduces venous return (preload) and subsequently the volume returning to the LV. It allows to
contract more efficiently. CO is increased, pulmonary vascular pressures are decreased, and
gas exchange is improved. Loop diuretics (e.g., furosemide [Lasix], bumetanide [Bumex])
can be administered by IV push and act rapidly in the kidneys.
Vasodilators-. IV nitroglycerin is a vasodilator that reduces circulating blood volume. It also
improves coronary artery circulation by dilating the coronary arteries. Therefore,
nitroglycerin reduces preload, slightly reduces afterload (in high doses), and increases
myocardial oxygen supply. When titrating IV nitroglycerin, monitor BP frequently (every 5
to 10 minutes) to avoid symptomatic hypotension.
Sodium nitroprusside (Nipride) is a potent IV vasodilator that reduces both preload and
afterload, thus improving myocardial contraction, increasing CO, and reducing pulmonary
congestion.
Morphine. Morphine sulfate reduces preload and afterload. It is frequently used in the
treatment of acute coronary syndrome and HF. It dilates both the pulmonary and systemic
blood vessels. Results include a decrease in pulmonary pressures and myocardial oxygen
needs, and an improvement in gas exchange. When morphine is used, the patient often
experiences relief from dyspnea and, consequently, the anxiety that often is associated with
dyspnea
Positive Inotropes. - Inotropic therapy increases myocardial contractility. Drugs include β-
adrenergic agonists (e.g., dopamine [Intropin], dobutamine [Dobutrex], epinephrine,
norepinephrine [Levophed]), the phosphodiesterase inhibitor milrinone (Primacor), and
digitalis. Dopamine dilates the renal blood vessels and enhances urine output.
NON-PHARMACOLOGICAL
Compliance:
Give careful advice about disease, treatment, and self help strategies
Diet: Ensure adequate general nutrition and, in obese patients, weight reduction. Salt:
Advise patients to avoid high salt content foods and not to add salt (particularly in severe
cases of congestive heart
failure).
Fluid: Urge overloaded patients and those with severe congestive heart failure to restrict their
fluid intake
Alcohol: Advise moderate alcohol consumption (abstinence in alcohol related
cardiomyopathy)
Smoking: Avoid smoking (adverse effects on coronary disease, adverse haemodynamic
effects)
Exercise: Regular exercise should be encouraged
Vaccination: Patients should consider influenza and pneumococcal vaccinations
Physical rest: In acute phase, absolute bed rest is advised. Early ambulatory is advocated to
avoid deep vein thrombosis. Prophylactic low dose heparin 5,000 units SC/IV BD can be
given. Degree of activity can be decided depending on the cardiac status.
Mental rest: Diazepam 2-5mg twice or thrice daily is given for several
days.
Oxygen: It improves oxygen delivery and relieves dyspnoea.
Diet: Sodium Restriction: In severe cases sodium is restricted to 500 mg/day and
subsequently it can be increased to 2-3g/day with usage of diuretics.
Water Restriction: 1-1.5 L/day is permitted. Fluid intake Fluid restriction (1.5-2 litres
daily) should be considered in patients with severe symptoms, those requiring high dose
diuretics, and those with a tendency towards excessive fluid intake. High fluid intake negates
the positive effects of diuretics and induces hyponatraemia.
Role of Nurses in Medication
-Nurses are also responsible for educating the patient as well as family regarding the care of
the person with heart failure which include:
1. Monitor for signs and symptoms of recurring heart failure and report these signs and
symptoms to the primary provider. • Weight gain of 1 to 1.5 kg (2 to 3 lb). • Loss of appetite.
• Shortness of breath. • Orthopnea. • Swelling of ankles, feet or abdomen • Persistent cough. •
Frequent night-time urination.
2. Avoid fatigue and plan activity to allow for rest periods. Incorporate ADL, occupational
activity and sexual activity into daily routine by pacing activities
. 3. Plan and eat meals within sodium restrictions. • Avoid salty foods. • Avoid drugs with
high sodium content (e.g. some laxatives and antacids, Alee-seltser)- read the labels. • Eat
several small meals rather than three large meals per day.
4. Take prescribed medications. • If several medications are prescribed, develop a method to
facilitate accurate administration. • Digitalis: Check own pulse rate daily; report a rate of less
than 50/min to primary provider and signs and symptoms of toxicity. • Diuretics: – Weigh
self-daily at same time of day. – Eat foods high in potassium and low in sodium (such as
oranges, bananas) if on potassium-depleting diuretics. • Vasodilators: – Report signs of
hypotension (light-headedness, rapid pulse, syncope) to physician. – Avoid alcohol when
taking vasodilators.
5. Adopt healthy lifestyle choices; daily routines; develop support groups; smoking
cessation; alcohol intake limited to not more than one drink per day and minimize risk of
infections.
6. Comply with follow-up appointment. Thorough evaluation also needed for follow-up
scheme. CARDIAC DYSRHYTHMIA