BALIUAG UNIVERSITY

College of Nursing
Baliuag, Bulacan

In partial fulfillment of the

requirements in
Medical Ward Rotation

SUBMITTED BY:
Buenaventura, Anjelica
Cabrera, Eiz
Confessor, Daniel Jr.
Dela Paz, Ryan
De Vera, Roberto
SUBMITTED TO:

HEART FAILURE

Definition:
 Congestive heart failure (CHF), congestive cardiac failure (CCF) or just heart
failure, is a condition that can result from any structural or functional cardiac disorder
that impairs the ability of the heart to fill with blood or pump a sufficient amount of
blood through the body. It is not to be confused with "cessation of heartbeat", which is
known as asystole, or with cardiac arrest, which is the cessation of normal cardiac
function with subsequent hemodynamic collapse leading to death.
Congestive heart failure also contrasts with high output heart failure. CHF denotes
a pathological process intrinsic to the myocardium, whereas in high output failure,
cardiac function is actually normal or even supra-normal, but the demand of end-organs
and other tissues outstrips what the heart can provide, occurring in the context of severe
anemia, beriberi (vitamin B1 / thiamine deficiency), thyrotoxicosis, Paget disease,
arteriovenous fistulas or malformations, and inappropriate tachycardia.
Congestive heart failure is often undiagnosed due to a lack of a universally agreed
definition and difficulties in diagnosis, particularly when the condition is considered
"mild". Even with the best therapy, heart failure is associated with an annual mortality of
10%. It is the leading cause of hospitalization in people older than 65.

Signs and Symptoms:

Symptoms
Symptoms are dependent on two factors. The first is based on the side of the
heart, right or left, that is involved. The second factor is based on the type of failure,
either diastolic or systolic.

Left sided failure

The most common symptoms are respiratory in nature. Failure of the left ventricle
causes congestion of the pulmonary capillaries. The patient will have dyspnea (shortness
of breath) on exertion and in severe cases, dyspnea at rest. Easy fatigueability and
exercise intolerance are also common complaints. Increasing breathlessness on reclining,
called orthopnea, occurs. It is often measured in the number of pillows required to lie
comfortably, and in severe cases, the patient may resort to sleeping while sitting up.
Another symptoms of heart failure is paroxysmal nocturnal dyspnea, a sudden nighttime
attack of severe breathlessness, usually several hours after going to sleep.

Right sided failure

The right side of the heart pumps blood returned from the tissues to the lungs,
where CO2 is exchanged for O2. Right ventricular failure leads to congestion of systemic
capillaries. This leads to peripheral edema or anasarca and nocturia (frequent nighttime
urination when the fluid from the legs is returned to the bloodstream). In more severe
cases, ascites (fluid accumulation in the abdominal cavity) and hepatomegaly (painful
enlargement of the liver) may develop. Hepatic congestion may actually impair liver
function, and jaundice and even coagulopathy may occur.
Heart failure may decompensate easily. this most commonly results from an
intercurrent illness, myocardial infarction, arrhythmias, uncontrolled hypertension, and
patient non-compliance with diet or medication. Other classic precipitating factors are
anemia and hyperthyroidism. These place additional strain on the heart muscle, which
may cause symptoms to rapidly worsen. Excessive fluid or salt intake (including
intravenous fluids for unrelated indications, but more commonly from dietary
indiscretion), and medication that causes fluid retention (such as NSAIDs and
thiazolidinediones), may also precipitate decompensation.

Signs

Left sided heart failure

 Signs on physical exam indicating left ventricular failure are a laterally displaced
apex beat and a gallop rhythm in case of decompensation. Heart murmurs may indicate
the presence of valvular heart disease, either as a cause or as a result of the heart failure.
Common respiratory signs are tachypnea and increased work of breathing, rales or
crackles, which suggests the development of pulmonary edema, dullness of the lung
fields to percussion and diminished breath sounds at the bases of the lung, which suggests
the development of a pleural effusion that is transudative in nature, and cyanosis which
suggests hypoxemia, caused by the decreased rate of diffusion of oxygen from fluid-filled
alveoli to the pulmonary capillaries.

Right sided heart failure

The exam can reveal peripheral edema, ascites, and hepatomegaly. Jugular venous
pressure is frequently assessed as a marker of fluid overload, which can be accentuated
by the hepatojugular reflux. Systemic venous pressure in general is elevated, and this can
be seen even in veins in the hand, which are distended when dependent, but which will
flatten when the force of gravity overcomes right atrial pressure
CAUSES:

Right-sided: pulmonary hypertension (primary

Left-sided: hypertension (high pulmonary arterial hypertension versus hypoxic
blood pressure), aortic and mitral vasoconstriction and capillary destruction due to
valve disease, aortic coarctation chronic lung disease), pulmonary or tricuspid valve
disease.
May affect both sides: Ischemic heart disease (due to insufficient vascular supply, usually
as a result of coronary artery disease); this may be chronic or due to acute myocardial
infarction (a heart attack), chronic arrhythmias (e.g. atrial fibrillation), cardiomyopathy of
any cause, cardiac fibrosis, chronic severe anemia, thyroid disease (hyperthyroidism and
hypothyroidism. Left sided failure commonly results in right sided failure.)

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 as diverse an array of conditions as 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 contractility, or force of contraction, due to overloading of the ventricle.
• A reduced stroke volume, as a result of a failure of systole, diastole or both.
• 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.
• 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.
• Hypertrophy (an increase in physical size) of the myocardium, caused by the
terminally differentiated heart muscle fibers increasing in size in an attempt to
improve contractility.
• 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, 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.
• Increased sympathetic stimulation also causes the hypothalamus to secrete
vasopressin (also known as antidiuretic hormone or ADH), which causes causing
fluid retention at the kidneys.
• 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 vasocontriction, and stimulate
increased secretion of the steroid aldosterone from the adrenal glands.
• 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.
• Reduced perfusion of skeletal muscle causes atrophy of the muscle fibers. This
can result in weakness, increased fatigueability and decreased peak strength - all
contributing to exercise intolerance.

DIAGNOSIS:

Imaging
Echocardiography is commonly used to support a clinical diagnosis of heart
failure. This modality uses ultrasound to determine the stroke volume, the end-diastolic
volume, and the SV in proportion to the EDV, a value known as the ejection fraction.
Echocardiography may also aid in deciding what treatments will help the patient, such as
medication, insertion of an implantable cardioverter-defibrillator or cardiac
resynchronization therapy. Echocardiography can also help determine if acute myocardial
ischemia is the precipitating cause, and may manifest as regional wall motion
abnormalities on echo
Chest X-rays are frequently used to aid in the diagnosis of CHF. In the
compensated patient, this may show cardiomegaly (visible enlargement of the heart).
Blood tests
Blood tests routinely performed include electrolytes (sodium, potassium),
measures of renal function, liver function tests, thyroid function tests, a complete blood
count, and often C-reactive protein if infection is suspected. An elevated B-type
natriuretic peptide (BNP) is a specific test indicative of heart failure. Additionally, BNP
can be used to differentiate between causes of dyspnea due to heart failure from other
causes of dyspnea.
Angiography
Heart failure may be the result of coronary artery disease, and its prognosis
depends in part on the ability of the coronary arteries to supply blood to the myocardium
(heart muscle). As a result, coronary catheterization may be used to identify possibilities
for revascularization through percutaneous coronary intervention or bypass surgery.

TREATMENT:
• Diuretics
• ACE inhibitors
• Vasodilators
• Digoxin
• Beta-adrenergic blockers
 • Sodium-restricted diet
• Antiembolism stockings
• Surgical valve replacement
• Coronary artery bypass grafting

NURSING CONSIDERATIONS:

During the acute phase

• Place the patient in Fowler’s position and give him supplemental oxygen to help
him breathe.
• Weigh the patient daily, and check for peripheral edema.
• Make sure the patient has continuous cardiac monitoring during acute and
advanced stages.
• Assist the patient with ROM exercises.
• Enforce bed rest and apply antiembolism stockings.
Preparing the client for discharge

• Advise the patient to avoid foods high in sodium.

• Explain the need for possible potassium supplement because of diuretic therapy.
• Tell the patient to notify the physician if his pulse is unusually irregular or
measures less than 60 beats / min.