Running head: CONGESTIVE HEART FAILURE

Congestive Heart Failure

Linda Elliston
The Robert B. Miller College
Pathophysiology BSRN 420
Theresa Dawson
October 12, 2011

CONGESTIVE HEART FAILURE

Introduction
Congestive Heart Failure (CHF) is a condition that describes the heart when it is failing
to meet the demands of the body. It can be caused by a number of different conditions that
require an increased work demand on the heart. The heart can usually compensate for this
demand, but over time, it fails. When the heart begins to fail, patients start to feel the effect. If
the heart failure is left untreated, the end result is usually death. To prevent CHF, people need to
be aware of the preventative measures in regards to their health and seek treatment for any
underlying disease process that might lead to heart failure; if they are already diagnosed with
CHF, they need to seek treatment right away to prevent further damage to their heart. The
purpose of this paper is to discuss diagnosis and treatment of a 60-year-old man who presents in
the emergency room with symptoms of CHF.
The heart is an organ, the size of a fist, located in the middle of your chest, behind and
slightly to the left of your breastbone (sternum) (Anatomy of the heart, 2011, para. 2). It is held
in place by the pericardium, which is a double-layered sac filled with fluid. The fluid in between
the layers of the pericardium allows the heart to contract or beat. The main purpose of the heart
is to circulate blood throughout the body and each day, the average heart beats 100,000 times,
pumping about 2,000 gallons (7,571 liters) of blood" (Anatomy of the heart, 2011, para. 1). The
blood is important for supplying oxygen and nutrition to the cells, and then carrying their waste
products away to be eliminated by the kidneys. In order to supply the entire body with blood, the
heart is made up of four chambers: the upper chambers are called the left and right atria, and the
lower chambers are called the left and right ventricles (Anatomy of the heart, 2011, para. 3).
Blood from the body flows into the right atrium from the Superior Vena Cava, and then is

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pumped into the right ventricle. The right ventricle pumps the blood through the pulmonary
artery to the lungs for exchange of carbon dioxide for oxygen. After picking up oxygen, the
blood travels down the pulmonary vein and empties into the left atrium. The left atrium passes
the blood to the largest chamber of the heart, the left ventricle. When the heart contracts again,
oxygen-rich blood from the left ventricle is pumped through the aorta to the rest of the body.
The four chambers of the heart are divided by muscle and valves. The upper atria
chambers of the heart and lower ventricle chambers are divided by a muscle called the septum.
The heart valves control the flow of blood traveling through the heart chambers. There are four
valves in the heart: the tricuspid valve is between the right atrium and right ventricle, the
pulmonary valve is between the right ventricle and the pulmonary artery, the mitral valve is
between the left atrium to the left ventricle, and the aortic valve is between the left ventricle and
the aortic artery. Oxygen-rich blood is delivered to the body through the aortic artery, and then
the veins return the blood to the heart.
In order to make the blood flow throughout the body, the heart muscle (myocardium)
has to be stimulated to contract by electrical impulses. This electrical signal originates from the
sinoatrial (SA) node located at the top of the right atrium. The impulse from this natural
pacemaker (SA node) travels through the muscle fibers of the atria and ventricles, causing them
to contract (Anatomy of the heart, 2011, para. 5). The SA node usually sets the heartbeats at a
certain rate, but this rate can change to compensate for certain demands of the body. For
instance: if a certain area of the body needs more oxygen and/or nutrition, it can signal the heart
though the Sympathetic Nervous System (SNS). When stimulated by the SNS, the heart can
increase in the strength and rate of its contractions to compensate.

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The heart can normally compensate for the bodys increased demands; however, if the
heart muscle is damaged, or if the demand is prolonged due to some other disease process, the
heart can begin to fail. Depending on the initial cause of the heart failure, the ventricles may
become weaker or they might become thicker (hypertrophy); both processes, weaker ventricle
or thicker, less compliant ventricle, result in diminished cardiac output (Pathophysiology of
CHF, n.d., para. 1 ). Decreased oxygen and nutrition to the body activates a vicious cycle of
compensation and de-compensation. The Sympathetic Nervous System (SNS) tries to
compensate by increasing the heart rate and constricting the blood vessels. By increasing the
peripheral vascular resistance and the heart rate, the heart is forced to work harder, causing more
damage to the left ventricle. The kidneys activate the renin-angiotensin-aldosterone system
(RAAS). This system compensates to the low blood supply by reabsorbing more sodium and
water, and then the heart begins to fail more, due to the increase in blood volume. If the blood
flow to the brain is decreased, the brain will try to compensate by secreting anti-diuretic hormone
(ADH). This hormone also increases the amount of salt and water that is reabsorbed in the
kidneys, adding more blood volume to the overloaded circulation system (preload).
There are a lot of conditions and risk factors that can lead to Congested Heart Failure. For
instance: the muscles of the ventricles can be weakened by heart attacks, infections
(myocarditis) or toxins (alcohol, some chemotherapy agents). The diminished pumping ability of
the ventricles due to muscle weakening is called systolic dysfunction (Kulick, D, 2011, p.1).
Some conditions can cause stiffening of the heart muscle and impair the ventricles' capacity to
relax and fill; this is referred to as diastolic dysfunction (Kulick, D, 2011, p. 1). High blood
pressure and hemochromatosis (iron overload) are diastolic dysfunctions, which can lead to a
hypertrophied heart. Another type of CHF is high output heart failure. This type of CHF is seen

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in patient with hyperthyroidism or anemia when the heart has to work hard due to an
abnormally high oxygen demand by the body's tissues (Kulick, D, 2011, p. 1). Other
conditions or risk factors that can lead to weakening or stiffing of the heart include: coronary
artery disease, cardiomyopathy, valve disease, kidney disease, diabetes, and heart defects (Heart
disease, n.d.). To prevent CHF, people need to stay healthy and see their doctors regularly to
diagnosis and treat any underlying conditions that could lead to heart failure, such as coronary
artery disease, high blood pressure, high cholesterol, diabetes or obesity (Mayo Clinic staff,
2011, para. 3). Preventive measures should also include lifestyle changes, such as exercising,
reducing the salt in your diet, managing stress, treating depression, and especially losing excess
weight (Mayo Clinic staff, 2011, para. 2).
History of Patient
As mentioned above, the purpose of this research is about a 60-year-old man who
presents himself to the emergency room with sign and symptoms of CHF. His symptoms
included: dyspnea, (that was worse when he was lying down), weakness, fatigue, and edema in
the lower extremities. He states he frequent has to get up in the middle of the night to sit by an
open window to catch his breath, and that he has to urinate frequently during the night but
doesnt need to void as much during the day. He also complains of being short of breath on
exertion, coughing up frothy blood-tinged fluid, a rattling sound form the trachea, periods of
confusion, pain in the upper right quadrant, and occasional nausea and vomiting.
Criteria for Diagnosis
Signs and Symptoms of CHF depend on the severity of the damage and whether the
patient has right-sided heart failure, left sided heart failure, or both. When damage is present on
either side, they both have similar forward effects due to decreased oxygen and blood supply to

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the tissue; these symptoms include: fatigue and weakness, dyspnea, and shortness of breath
especially with exertion, exercise intolerance, cold intolerance, and dizziness (Gould & Dyer,
2011, p. 299). The cold intolerance, fatigue and weakness are usually due to the body trying to
compensate by shunting the blood to the vital organs, leaving the rest of the body without
adequate oxygen and nutrition. Both right and left sided CHF also have similar compensation
symptoms such as: tachycardia and pallor, secondary polycythemia, and daytime oliguria
(Gould & Dyer 2011, p. 299). The backup effects are the symptoms that can vary depending on
the side of the heart that is damaged. For the patient who presents with left sided CHF, these
effects could include: orthopnea, cough, shortness of breath, paroxysmal nocturnal dyspnea,
hemoptysis, and rales. Backup symptoms present in patients with right sided failure include:
dependent edema in feet, hepatomegaly, splenomegaly, ascites, distended neck veins, headache,
and flushed face (Gould & Dyer, 2011, p. 299). Unfortunately, our patient presents at the
emergency room with signs and symptoms of both right and left sided heart failure. He
complains of fatigue and weakness, which are common symptoms for both sides. His dyspnea
and coughing up blood is due to the extra blood backing up into the lungs from the left ventricle
failure, especially at night when the patient is lying down. His lack of urination during the day
with urinary frequency at night is consistent with right-sided failure and decreased perfusion to
the kidneys while standing up. The confusion and edema in his ankles is due to the increase
fluid in his circulation and the high pressure in his right atrium. The pain in his right upper
quadrant and the nausea is due to congestion in his liver and digestive system.
On his physical examination, his blood pressure is 110 over 60. This high pulse
pressure usually means he has some underlying cardiovascular disease or stiffing of the arteries.
His pulse is weak, with tachycardia probably due to SNS response to the poor cardiac output. He

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has rapid shallow breathing with moist aspirator rales and bilateral pleural effusions due to left
ventricular failure. His jugular vein distention is due to right ventricular failure and the increased
preload (high pressure) in the superior vena cava. A systolic outflow murmur is also noted,
which usually means heart valve defect.
If a patient presents with symptoms of CHF, a thorough medical history should be
obtained to find any underlying disease process that could have caused the heart failure.
Diagnostic test are also conducted. Lab results, such as a B-type natriuretic peptid level (BNP),
is typically elevated from heart failure and can aid in the diagnosis, and can be useful in
following the response to treatment of congestive heart (Kulick, D, 2011, p. 3). Other
diagnostic tests could include: electrocardiogram, chest x-ray, echocardiogram, heart
catheterization, and/or a biopsy of the heart tissue. Pertinent diagnostic test to diagnose CHF on
this man included: an ECG which shows alterations that are consistent with left ventricular
hypertrophy, A Chest x-ray revealing biventricular chamber enlargement with marked pulmonary
edema -- "butterfly" patterns in the perihilar areas. AN ultrasound image analysis revealing aortic
stenosis and left ventricular hypertrophy and his abdominal x-rays reveals liver enlargement due
to congestion. With these test results, our patients underlying problem is probably related to
aortic stenosis-valve dysfunction, which was left untreated, causing the left sided heart failure to
progress to the right side. The valve dysfunction could have been caused by his age and some
underlying atherosclerotic heart disease, or maybe he had a history of rheumatic fever. The
patients lab results show a slight elevation in the blood urea nitrogen (BUN) and significant
proteinuria and granular casts in his urinalysis. CHF can lead to multiple organ failure, and after
reviewing these tests results, I would say his kidneys, lungs, and liver are starting to fail.

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Treatment options for CHF include diet control and lifestyle changes. A low sodium diet
with a fluid restriction will help decrease the fluid that accumulates in the body. Usually no
more than 2 grams (2000 milligrams) of sodium per day is generally advised and patients with
more advanced cases of congestive heart failure are often advised to limit their total daily fluid
intake from all sources to 2 quarts (Kulick, 2011, p. 4). Alcohol should not be consumed and
the patient should weigh himself frequently. An increase in weight may occur even before
shortness of breath or swelling in the legs and other body tissues (edema) is detected (Kulick,
2011, p. 4). If the patient notices a increase of two to three pounds over two to three days he
should be instructed to call his doctor, who may order an increase in the dose of diuretics
(Kulick, 2011, p. 4). Exercise, within the patients limitations, is also recommended. Further
treatment options for CHF depend on the underlying cause. Some medical treatments could
include heart catherization/ angioplasty to increase blood supply to the heart, surgical correction
of any heart valve abnormities, and/or blood pressure control. The patient that came into ER
would need to be treated aggressively with fluid restriction, and diuretics. Diuretics, (like Lasix),
will help this patient breath by stimulating the kidneys to excrete the extra fluid. To help the
patient breath better, oxygen could be ordered and the head of the bed should be elevated. Other
medications that could be used include: ace inhibitors, beta blockers, Digoxin, and angiotensin
receptor blockers (ARBs). Ace inhibitors, like Vasotec, are used to treat hypertension and to
block the formation of angiotensin II. Beta blockers, like Coreg, can lower the blood pressure,
but are primary used to decrease the hearts force of contraction by blocking the beta receptors
from being stimulated by hormones. Digoxin can be used to decrease the heart rate and
strengthen the contractions. ARBs, like Cozaar, act on the same hormonal pathway as the ACE
inhibitors, but instead block the action of angiotensin II at its receptor site directly (Kulick,

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2011, p. 5). If the patient is basically in good health, other than his heart, a heart transplant is
another option for long-term treatment.

Prognosis (Outcome)
Prognosis varies patient-to-patient depending on the underlying cause, the patients
response to the medications, the patients age, and the degree of damage to other organs in the
body. In some newly diagnosed patients a significant spontaneous improvement is not
uncommonly observed, even to the point where heart function becomes normal (Kulick, 2011,
p. 7). Prognoses can also be determined based on the patients ability to function, and the
patients ability to function is based on a scale I to IV:
1. Class I is patients with a weakened heart but without limitation or symptoms.
2. Class II is only limitation at heavier workloads.
3. Class III is limitation at everyday activity.
4. Class IV is severe symptoms at rest or with any degree of effort (Kulick, 2011, p. 7).
Comparing the patient in the emergency room to this scale, I would put him in Class II or III.
His short-term prognosis should be good after treating him in the hospital with diuretics, oxygen,
a low salt diet, and fluid restrictions. Healthcare professions can educate him on the purpose of
his new medications, the need for daily weights, and how to prevent further episodes. His B-type
Natriuretic peptid level (BNP) initially will be high, but should decrease after successful
treatment. During his hospital stay, his potassium level should be monitored since some diuretics
can alter it. Some of his limitations for taking care of himself might include: emotional and
financial burdens caused by frequent doctors visits, prescription drug coverage, and the decrease
in his ability to do things without becoming short of breath. Diet modification, fluid restriction,
and cessation of any alcohol might also be a burden. There is usually no cure for CHF, but with
treatment he should do well for another five to ten years.

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As this patient gets older, his symptoms and his heart failure will probably get worse.
To monitor his status, frequent lab work should be done. A BNP can show the progress of his
heart failure. A complete metabolic profile (CMP) should be done periodically to monitor his
electrolytes and to watch for any indications of liver failure. Some medications can either
increase or decrease his potassium level, which could lead to sever arrhythmias. If he starts to
retain sodium he could become confused and not take his medications appropriately. If he is
taking digoxin, this level should be monitored since it can easily become toxic. His BUN and
creatine should be monitored for any signs of renal failure. A complete blood count (CBC) can
indicate whether hes body is trying to compensate for low cardiac output by producing more red
blood cells (polycythemia). As time goes by, this patient might become depressed due to the
frequent lab draws and hospitalizations, increased shortness of breath, and his decreased level of
function. Mortality rates increase as patients getting older: in the group 55 years old, the 15year total mortality rate was 39.1% for women and 71.8% for men (Schocken et al, 1992, p.
301). There is no cure for CHF, but with treatment, the patient should be able to live a
productive life.
Supportive Role of teaching/community resources
Healthcare professions have a very important role when it comes to educating patients
about their Congestive Heart Failure. Our patient in the emergency room needs to be taught all
the signs and symptoms of heart failure, and told to call his doctor if he notices any of them. He
should be encouraged to keep a list of his current medications and to bring them to every
doctors appointment. If he needs help with his prescription coverage, he should be told about the
resources available for him. Healthcare providers need to educate the patient regarding lifestyle
changes such as: low salt diet, exercise, fluid restrictions, quitting smoking, no alcohol, and daily

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weights. Patients should be warned against taking over-the-counter medications without

checking with their doctors first, especially since nonsteroidal anti-inflammatory drugs
(ibuprofen, naproxen and others), cold medications and diet pills may worsen heart failure and
lead to fluid buildup (Mayo Clinic, 2011, para. 4). If the patient has any questions or needs
clarification, he should be encouraged to write them down so he will remember to ask the doctor
when he sees him. The American Heart Association, the Mayo Clinic, and the Heart Failure
Society of America, are just a few of the community resources that offer information to patients
with CHF. They have educational web sites available with information on the disease, treatment,
and prevention. They also have pictures and videos available for patients to view.
In the future, the number of people developing CHF and the mortality rate will probably
increase due to the baby boomers getting older. One way to prevent this is through research.
Scientists are discovering new methods for treating and preventing heart failure every day.
Another way to prevent CHF is though education. Public service announcements and physicians'
offices should teach people preventive lifestyle choices such as low fat diets, exercise, and seeing
their doctors regularly. Frequent visits to the doctor are important to catch any underlying
disease process before it causes heart failure, (high blood pressure, diabetes, coronary artery
disease, etc.). The emergency room patient should have a long life as long as he is compliant
with his treatment plan and has support from his family and friends.
As mentioned above, scientists are working on new treatments for CHF. One study in
particular, from the American Heart Association, studied patients with wide surface QRS
(18022 ms) and the benefits of having a pacemaker that can stimulate both atria chambers, and
then both ventricular chambers, with a delay for filling in between. This study is important for
the treatment of some patients with severe heart fail since sometimes the left and right side of
the heart don't beat in rhythm (Kulick, 2011, p. 7). In this study, they evaluated immediate

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changes in hemodynamic function during brief periods of atrial-synchronous ventricular pacing

(American Heart Association, Inc., 1999, para. 4). While monitoring the pressures in the
chambers of the heart, the pulmonary artery, and the aorta they tried this new pacemaker. They
paced the heart for 5 beats, and then let the heart do 15 beats on its own. The end results
concluded that CHF patients with sufficiently wide surface QRS benefit from atrialsynchronous ventricular pacing, [left ventricular] LV stimulation is required for maximum acute
benefit, and the maximum benefit at any site occurs with a patient-specific [atrial ventricular] AV
delay (American Heart Association, Inc., 1999, para. 6).
Long-term treatment options for this 60-year-old man should include treatment of the
underlying cause of the CHF. If he has a valve defect, surgery may be an option. If he has
coronary artery disease, diet modifications to control his cholesterol and lipid reducing
medications might be ordered. Other treatment options could include: coronary bypass, heart
pumps, and/or heart transplant. Cardiac arrhythmias are significant cause of death in patients
with heart failure; one major advance has been the finding that nonsurgical placement of
automatic implantable cardioverter/defibrillators (AICD) in individuals with severe congestive
heart failure (defined by an ejection fraction below 30%-35%) can significantly improve
survival. (Kulick, 2011, p. 7).
Prevention is the best medicine for Congestive Heart Failure. People need to take care of
themselves. They need to see their doctors regularly to have their cholesterol, blood sugar, and
blood pressure checked. They should report any changes in their health to their doctors. Healthy
choices in living include: exercise, weight loss, stress reduction, appropriate amount of sleep,
alcohol in moderation, and not smoking. For our patient who is diagnosed with CHF, he needs to
take his medication regularly, keep track of his weight, limit his fluid intake, and stay on follow a
low-salt diet. Staying healthy is the name of the game.

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References

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