A.

Definition of CHF (Congestive Heart Failure)

Heart failure (HF) or Congestive Heart Failure (CHF) is a physiologic state in which he
heart cannot pump enough blood to meet the metabolic needs of the body. Heart failure results
from changes in systolic or diastolic function of the left ventricle. The heart fails when, because
of intrinsic disease or structural it cannot handle a normal blood volume or, in absence of
disease, cannot tolerate a sudden expansion in blood volume. Heart failure is not a disease itself;
instead, the term refers to a clinical syndrome characterized by manifestations of volume
overload, inadequate tissue perfusion, and poor exercise tolerance. Whatever the cause, pump
failure results in hypoperfusion of tissues, followed by pulmonary and systemic venous
congestion.

Because heart failure causes vascular congestion, it is often called congestive heart
failure, although most cardiac specialist no longer use this term. Other terms used to denote heart
failure include chronic heart failure, cardiac decompensation, cardiac insufficiency and
ventricular failure.

B. Causes of CHF
Weakness of the left ventricle can be caused by:

 Longstanding uncontrolled hypertension

 Heart attacks — damage to the heart muscle due to coronary artery disease (blocked
arteries)
 Valvular heart disease — longstanding leaking or narrowing of the aortic or mitral valves
 Viral, toxic or metabolic disturbances damaging the heart muscle. Alcohol is the
commonest culprit
 Longstanding rapid heart beating (racing) due to some form of arrhythmia
 Congenital abnormalities e.g. ventricular septal defect (a hole between the left and right
ventricles)

Weakness of the right ventricle may be caused by:

 Failure of the left ventricle

 High blood pressure within the lungs
 Valvular heart disease — pulmonary valve stenosis (narrowing)/tricuspid valve leaking
 Right ventricular infarction (heart attack) due to coronary artery disease
 Congenital abnormalities e.g. atrial septal defect (a hole between the left and right atria)
 Disease affecting the sac surrounding the heart (the pericardium) such as fluid
accumulation (effusion) or abnormal thickening (constriction)
 C. Classification

There are many different ways to categorize heart failure, including:

 the side of the heart involved (left heart failure versus right heart failure). Right heart
failure compromises pulmonary flow to the lungs. Left heart failure compromises aortic
flow to the body and brain. Mixed presentations are common; left heart failure often
leads to right heart failure in the longer term.
 whether the abnormality is due to insufficient contraction (systolic dysfunction), or due to
insufficient relaxation of the heart (diastolic dysfunction), or to both.
 whether the problem is primarily increased venous back pressure (preload), or failure to
supply adequate arterial perfusion (afterload).
 whether the abnormality is due to low cardiac output with high systemic vascular
resistance or high cardiac output with low vascular resistance (low-output heart failure
vs. high-output heart failure).
 the degree of functional impairment conferred by the abnormality (as reflected in the
New York Heart Association Functional Classification
 the degree of coexisting illness: i.e. heart failure/systemic hypertension, heart
failure/pulmonary hypertension, heart failure/diabetes, heart failure/renal failure, etc.

Functional classification generally relies on the New York Heart Association functional
classification. The classes (I-IV) are:

Class Physical Activity Example

I (none) Normal physical activity does not cause fatigue, Jog/walk 8km/h
palpitations and dyspnoea
II (slight) Normal physical activity causes fatigue, dyspnoea Walk 7km/h on level
and palpitations/angina ground
III Comfortable at rest, light physical activity causes Walk 4km/h
(moderate) fatigue, dyspnoea and palpitations/angina
IV (Severe) Symptoms present at rest; any physical activity Unable to perform any of
increases discomfort the above activities
 This score documents severity of symptoms, and can be used to assess response to
treatment. While its use is widespread, the NYHA score is not very reproducible and doesn't
reliably predict the walking distance or exercise tolerance on formal testing.

D. Clinical Manifestations and Underlying aetiology

Common clinical manifestations of CHF are presented below:

Signs Aetiology
Pulmonary venous congestion causes inadequate blood oxygenation and
Dyspnoea fluid extravasation into pulmonary tissues with secondary pleural effusion
causing symptoms.
Recumbent position reduces blood pooling in the extremities, improving
Orthopnoea
venous return that exacerbates pulmonary congestion.
Paroxysmal Improved venous return, reduced ventricular adrenergic innervation during
nocturnal dyspnoea sleep and nocturnal depression of respiratory center.
Fatigue Reduced CO - poor perfusion of skeletal muscles leads to fatigue
Underperfusion of kidneys during the day, adequate perfusion restored by
Nocturia
supine position at night.

Symptoms Aetiology
Venous congestion of abdominal viscera leads to fluid
Ascites
extravasation into peritoneal cavity.
Generalised oedema (anasarca), Peripheral vascular congestion alters Starling forces in tissues,
dependent oedema causing fluid extravasation into interstitial spaces.
Hepatic congestion and fluid extravasation cause hepatomegaly,
Right upper quadrant pain
stretching the hepatic capsule, causing pain.
Elevated Jugular venous Blood congestion and decreased right ventricular output
pressure (JVP) increases atrial filling, giving a higher JVP.

E. Pathophysiology

Heart failure is caused by any condition which reduces the efficiency of the myocardium,
or heart muscle, through damage or overloading. As such, it can be caused by a wide number of
conditions, including myocardial infarction (in which the heart muscle is starved of oxygen and
dies), hypertension (which increases the force of contraction needed to pump blood) and
amyloidosis (in which protein is deposited in the heart muscle, causing it to stiffen). Over time
these increases in workload will produce changes to the heart itself:

 Reduced force of contraction, due to overloading of the ventricle. In a healthy heart,

increased filling of the ventricle results in increased force of contraction (by the Frank–
Starling law of the heart) and thus a rise in cardiac output. In heart failure this mechanism
fails, as the ventricle is loaded with blood to the point where heart muscle contraction
becomes less efficient. This is due to reduced ability to cross-link actin and myosin
filaments in over-stretched heart muscle.
 A reduced stroke volume, as a result of a failure of systole, diastole or both. Increased
end systolic volume is usually caused by reduced contractility. Decreased end diastolic
volume results from impaired ventricular filling – as occurs when the compliance of the
ventricle falls (i.e. when the walls stiffen).
 Reduced spare capacity. As the heart works harder to meet normal metabolic demands,
the amount cardiac output can increase in times of increased oxygen demand (e.g.
exercise) is reduced. This contributes to the exercise intolerance commonly seen in heart
failure. This translates to the loss of one's cardiac reserve, or the ability of the heart to
work harder during strenuous physical activity. Since the heart has to work harder to
meet the normal metabolic demands, it is incapable of meeting the metabolic demands of
the body during exercise.
 Increased heart rate, stimulated by increased sympathetic activity in order to maintain
cardiac output. Initially, this helps compensate for heart failure by maintaining blood
pressure and perfusion, but places further strain on the myocardium, increasing coronary
perfusion requirements, which can lead to worsening of ischemic heart disease.
Sympathetic activity may also cause potentially fatal arrhythmias.
 Hypertrophy (an increase in physical size) of the myocardium, caused by the terminally
differentiated heart muscle fibres increasing in size in an attempt to improve contractility.
This may contribute to the increased stiffness and decreased ability to relax during
diastole.
  Enlargement of the ventricles, contributing to the enlargement and spherical shape of the
failing heart. The increase in ventricular volume also causes a reduction in stroke volume
due to mechanical and contractile inefficiency.

The general effect is one of reduced cardiac output and increased strain on the heart. This
increases the risk of cardiac arrest (specifically due to ventricular dysrhythmias), and reduces
blood supply to the rest of the body. In chronic disease the reduced cardiac output causes a
number of changes in the rest of the body, some of which are physiological compensations, some
of which are part of the disease process:

 Arterial blood pressure falls. This destimulatesbaroreceptors in the carotid sinus and
aortic arch which link to the nucleus tractussolitarii. This center in the brain increases
sympathetic activity, releasing catecholamines into the blood stream. Binding to alpha-1
receptors results in systemic arterial vasoconstriction. This helps restore blood pressure
but also increases the total peripheral resistance, increasing the workload of the heart.
Binding to beta-1 receptors in the myocardium increases the heart rate and make
contractions more forceful, in an attempt to increase cardiac output. This also, however,
increases the amount of work the heart has to perform.
 Increased sympathetic stimulation also causes the posterior pituitary to secrete
vasopressin (also known as antidiuretic hormone or ADH), which causes fluid retention
at the kidneys. This increases the blood volume and blood pressure.
 Reduced perfusion (blood flow) to the kidneys stimulates the release of renin – an
enzyme which catalyses the production of the potent vasopressor angiotensin.
Angiotensin and its metabolites cause further vasoconstriction, and stimulate increased
secretion of the steroid aldosterone from the adrenal glands. This promotes salt and fluid
retention at the kidneys.
 The chronically high levels of circulating neuroendocrine hormones such as
catecholamines, renin, angiotensin, and aldosterone affects the myocardium directly,
causing structural remodelling of the heart over the long term. Many of these remodelling
effects seem to be mediated by transforming growth factor beta (TGF-beta), which is a
common downstream target of the signal transduction cascade. initiated by
 catecholaminesand angiotensin II, and also by epidermal growth factor (EGF), which is a
target of the signaling pathway activated by aldosterone
 Reduced perfusion of skeletal muscle causes atrophy of the muscle fibres. This can result
in weakness, increased fatigueability and decreased peak strength – all contributing to
exercise intolerance.

The increased peripheral resistance and greater blood volume place further strain on the
heart and accelerates the process of damage to the myocardium. Vasoconstriction and fluid
retention produce an increased hydrostatic pressure in the capillaries. This shifts the balance of
forces in favour of interstitial fluid formation as the increased pressure forces additional fluid out
of the blood, into the tissue. This results in edema (fluid build-up) in the tissues. In right-sided
heart failure this commonly starts in the ankles where venous pressure is high due to the effects
of gravity (although if the patient is bed-ridden, fluid accumulation may begin in the sacral
region.) It may also occur in the abdominal cavity, where the fluid build-up is called ascites. In
left-sided heart failure edema can occur in the lungs – this is called cardiogenic pulmonary
edema. This reduces spare capacity for ventilation, causes stiffening of the lungs and reduces the
efficiency of gas exchange by increasing the distance between the air and the blood. The
consequences of this are dyspnea (shortness of breath), orthopnea and paroxysmal nocturnal
dyspnea.

The symptoms of heart failure are largely determined by which side of the heart fails. The
left side pumps blood into the systemic circulation, whilst the right side pumps blood into the
pulmonary circulation. Whilst left-sided heart failure will reduce cardiac output to the systemic
circulation, the initial symptoms often manifest due to effects on the pulmonary circulation. In
systolic dysfunction, the ejection fraction is decreased, leaving an abnormally elevated volume of
blood in the left ventricle. In diastolic dysfunction, end-diastolic ventricular pressure will be
high. This increase in volume or pressure backs up to the left atrium and then to the pulmonary
veins. Increased volume or pressure in the pulmonary veins impairs the normal drainage of the
alveoli and favors the flow of fluid from the capillaries to the lung parenchyma, causing
pulmonary edema. This impairs gas exchange. Thus, left-sided heart failure often presents with
respiratory symptoms: shortness of breath, orthopnea and paroxysmal nocturnal dyspnea.
 In severe cardiomyopathy, the effects of decreased cardiac output and poor perfusion
become more apparent, and patients will manifest with cold and clammy extremities, cyanosis,
claudication, generalized weakness, dizziness, and syncope.

The resultant hypoxia caused by pulmonary edema causes vasoconstriction in the

pulmonary circulation, which results in pulmonary hypertension. Since the right ventricle
generates far lower pressures than the left ventricle (approximately 20 mmHg versus around 120
mmHg, respectively, in the healthy individual) but nonetheless generates cardiac output exactly
equal to the left ventricle, this means that a small increase in pulmonary vascular resistance
causes a large increase in amount of work the right ventricle must perform. However, the main
mechanism by which left-sided heart failure causes right-sided heart failure is actually not well
understood. Some theories invoke mechanisms that are mediated by neurohormonal activation.
Mechanical effects may also contribute. As the left ventricle distends, the intraventricular septum
bows into the right ventricle, decreasing the capacity of the right ventricle.

F. Fictitious Case

Mr. Solomon is a 63-year old gentle man who has been under your care for a variety of
medical problems during the past 5 years. He has been treated for two myocardial infarctions,
hypertension, non-insulin dependent diabetes and stasis dermatitis of the left leg. He had an
aorto-coronary bypass one year ago.

Today he presents in the office with shortness of breath which has been progressive over
the past five days. He has, however, experienced episodes of shortness of breath during the past
four months, especially when exerting himself. He fatigues easily and has lost "all my energy to
do anything." He also complains of anorexia. Last night he awoke suddenly from sleep because
"I couldn’t catch my breath" and developed a dry cough. The breathing problem improved when
he sat on the edge of his bed for an hour. He generally sleeps with two, sometimes three pillows.
He has not experienced chest pain, leg pain or fainting spells.

Examination in the office reveals an undernourished man who appears depressed and
older than his stated age. He is unkept and unshaven. His shoes are untied. His breathing is
labored and his lips have a blue tinge.
 Vital Signs: Blood Pressure 98/82mmHg in the right arm; Heart Rate 110/min;
Respiratory Rate 26/min; Temperature 98oF. Examination of the lungs reveals dullness to
percussion in both bases with decreased excursion of the diaphragms. Course rhonchi and moist,
inspiratory crackles are heard bilaterally in the lower lung fields.

Examination of the cardiovascular system: Neck veins are prominent and distended to the
mandible when the patient is sitting upright. The apical pulse is palpated in the 5ICS, left of the
MCL. S3 is palpable at the apex. S1 and S2 are diminished. S3 is heard at the apex. A grade 3/6
holosytolic murmur is heard best at the apex; it radiated to the left axilla.

Examination of the abdomen: The anterior wall is round and soft. The liver edge is
palpable and tender. The spleen is not palpable. Examination of the extremities revealed
diminished peripheral pulses. There is an irregular pulse. There is pitting edema of both lower
extremities.

G. Nursing Care of CHF

Nursing Diagnosis:

1. Activity intolerance related to fatigue due to a decrease of cardiac output and pulmonary
congestion as manifested by dyspnoea, tachycardia, and feelings of weakness and shortness
of breath.

Nursing Interventions and Rationales:

 Encourage alternative restas well as activity periods to reduce cardiac workload.

 Provide emotional and physical rest to reduce oxygen consumption and to relieve
dyspnoea and tiredness.
 Observe cardiorespiratory response to activity to establish amount of activity that can be
performed.
 Educate patient and significant other the particular approaches of self-care to decrease
much needed oxygen consumption.
  Assist todecide on activities in keeping with physical, psychological and social
capabilities to establish the amount of activity that can be carried out.
 Work with the help of healthcare professional, physiotherapist and even recreational
therapists to plan and observe action plan.

Goal / Outcome:

 Oxygen saturation within expected range in response to activity.

 Heart rate within expected rate in response to activity.
 Respiratory rate within expected rate in response to activity.
 ECG within normal limits.
 Skin colour within normal limits.
 Reported activities of daily living performance.
 Systolic blood pressure in expected range in response to activity.
 Diastolic blood pressure in expected range in response to activity.

2. Altered Tissue Perfusion and Impaired Gas Exchange

Nursing Diagnosis:

 Altered tissues perfusion and impaired gas exchange due to insufficient heart
contractility.
 Modified tissue perfusion describes a scenario where the actual cells don't receive
sufficient oxygen and so the tissues where they're located in the body tend to receive less
oxygenation and in danger for damage tissue.
 Gas exchange occurs within the alveoli of the lungs and when heart failure occurs, the
lungs can become congested consisting blood as a result it reduces its capability to
function the gas exchange process thus results in an altered tissues perfusion.
 In order to minimize this, the nurse can perform within its nursing scope to address these
types of problems and alleviate anxiety and distressed such as:
Nursing Interventions and Rationale:

 It is important to administer oxygen as ordered by physician to increase tissue

oxygenation and therefore prevents hypoxia (deprived of oxygen supply to the tissue) and
hypoxemia (deficiency of oxygen in arterial blood)
 Auscultate (listen) to breathe sounds noting areas of reduced or absent ventilation as well
as presence of adventitious sounds within the lungs in order to assess congestion
promptly.
 Ensure that you maintain the delivery device of oxygen from mask to nasal prongs while
the patient is doing activity of daily living in order to sustain the level of oxygen to the
tissues.
 Monitor the effectiveness of oxygen delivery by evaluating oxygen saturation in order to
identify hypoxaemia and determine oxygen saturation.
 Ensure that the patient’s bed position in the head area is elevated (semi fowler position)
to alleviate anxiety, improve ventilation and decreasing venous return to the heart
therefore allowing the patient to breathe easily in a comfortable position.
 If the patient is mobilizing less due to activity intolerance or movement intolerance as a
result of inability to breathe properly make sure that you inspect for any skin wounds or
pressure ulcer areas to prevent further complications such as infections or sepsis. When
the cell tissues receive less oxygen there may be a high risk of infection especially when
wound occurs in the body.
 Reassure the patient frequently as providing reassurance helps the patient feel comforted
and thus reduces anxiety.
 Ensure that the patient’s call bell is within reach and side rails of the bed is up in placed
to prevent falls or if in any case the patient develops confusion due to hypoxia (decreased
oxygen in the tissue) the patient might suddenly get up on his/her own therefore this
prevents accident or falls to occur.
 Ensure that the patient is on restricting fluids if ordered by a physician, therefore it
prevents excess fluid volume in the cells.
 Instruct patient’s food intake to avoid consumption of high sodium (salt) intake in his/her
diet to prevent hypernatraemia (elevated sodium level in the blood).
Goal / Outcome:

 The expected outcome of the nursing interventions for congestive heart failure is that the
patient’s gas exchange in the lungs is able to function well allowing the patient to receive
sufficient oxygenation in the tissues.

3. Excess fluid volume related to cardiac heart failure

Nursing Diagnosis:

 Excess fluid volume related to cardiac heart failure as evident by dyspnoea, tachycardia,
increased weight gain and oedema in ankles or other parts of the body.

Nursing Interventions and Rationales:

 Monitor patient’s serum electrolyte levels to assess the underlying condition and
therefore preventing electrolyte imbalances.
 Monitor patient’s weight by weighing daily as ordered to determine if patient’s weight is
increasing drastically possibly due to fluid retention and if this occurs inform the doctor
in order to start an assessment or order by a physician.
 Monitor respiratory breathing pattern to determine if symptoms of respiratory difficulty
occurs and for early detection of pulmonary congestion.
 Monitor for renal function including intake and output in order to determine fluid balance

4. Anxiety
Nursing Diagnosis:

 Anxiety related to dyspnoea as evident by expressions of feeling scared, irritability and

restlessness.

Nursing Interventions and Rationales:

 Ensure that each procedure administered by a nurse ordered by a physician must be

thoroughly explained in an appropriate manner in order to promote sense of comfort and
security.
 Encourage and educate patient by using relaxation techniques in order to alleviate
anxiety.
 Always reassure patient in a calm and appropriate approach to maximize patient’s
confidence and relieve anxiety.
 Develop an atmosphere suitable for a patient in order to facilitate trust between patient
and nurse relationship. In this example make sure that you answer the call bell promptly,
making yourself available frequently as well as making frequent checks in order to help
alleviate anxiety and promoting sense of security.
H. WOC of CHF
 BOOK LIST

Dumitru, I., Baker, M.(2010). Heart Failure. Retrieved on 11th August 2010, from
http://emedicine.medscape.com/article/163062-overview

http://nurseslabs.com/congestive-heart-failure-av-block-nursing-care-plans/

http://nanda-nursing.blogspot.com/2010/10/nursing-care-plan-for-congestive-heart.html