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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:
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:
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:
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.
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.
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.
Goal / Outcome:
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:
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.
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.
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:
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