Running head: CONGESTIVE HEART FAILURE

Congestive Heart Failure

S. Schneider
**** **** College

Running head: CONGESTIVE HEART FAILURE

Congestive Heart Failure

Definition
Congestive heart failure (CHF), formerly referring to just left sided heart failure, is a common,
yet complex, clinical disorder that can result from any functional or structural cardiac disorder that
impairs the ventricles ability to fill with or eject blood.(Figueroa, M. and Peters, J., 2006, pg. 402).
Congestive heart failure may be acute or chronic and ranges from mild to severe in nature. There are
two sub-types: systolic and diastolic. Systolic heart failure results when the heart has insufficient
strength to contract forcefully enough to eject adequate amounts of blood into the circulation. Diastolic
heart failure occurs when the left ventricle cannot relax adequately during diastole (relaxation phase)
which prevents the ventricle from filling with sufficient blood to ensure normal cardiac output and
tissue perfusion.(Ignatavicius, D., and Workman, L., 2013, pg. 715). Within this paper we will be
focusing in systolic heart failure.
Risk factors
There are major unmodifiable and modifiable risk factors to congestive heart failure. The major
unmodifiable risk factors include age (over 65), family history, congenital heart defects, valvular heart
disease, past myocardial infarction (heart attack), irregular heart rhythms, and coronary artery disease.
(Mayo Clinic Staff, 2015). The major modifiable risk factors include sedentary lifestyle, obesity,
uncontrolled diabetes mellitus, uncontrolled hypertension, poor diet and nutrition, alcohol use, and
tobacco use (smoking, chewing, etc.) (American Heart Association (AHA), 2015).
Pathophysiology
Congestive heart failure (CHF) is both an acute and chronic disorder that develops when the heart is
unable to maintain adequate ejection of blood and perfusion of organs. Cardiac dysfunction causes a
drop in cardiac output which leads to the activation of several neurohormonal pathways. (Gorbunova,
S., n.d.). As noted by Hobbs, R., & Boyle, A. (2014, March 1), in systolic dysfunction the body

Running head: CONGESTIVE HEART FAILURE

activates the sympathetic nervous system (through neurohormonal tracts) that increases heart rate and
strength of contractions, which results in vasoconstriction that stimulates secretion of renin from the
juxtaglomerular apparatus of the kidney due to loss of perfusion. Stimulation of the renin-angiotensin
system as a result of increased sympathetic stimulation and decreased renal perfusion results in further
vasoconstriction, sodium and water retention, and release of aldosterone. An increased aldosterone
level, in turn, leads to sodium and water retention, and other complications. Preload and afterload
increase as sodium and water are retained. Angiotensin II furnishes ventricular changes resulting in
advancing myocyte contractile dysfunction. Natriuretic peptides are neurohormones that work to boost
vasodilation and diuresis through sodium excretion in the kidney tubules. Brain naturietic peptide
(BNP) is produced and excreted by the ventricles when the client has fluid volume excess from CHF.
(Ignatavicus, D. & Workman, L., 2013). Another compensatory mechanism is the enlargement of the
cardiac muscle, with or without the increase in ventricular size. These walls thicken to increase the
force of contractions but may hypertrophy faster than collateral circulation can supply adequate blood
supply. (Ignatavicius, D., & Workman, L., 2013).
Complications
The complications of CHF arise from the decrease in tissue perfusion. This decrease in
perfusion leads to serious tissue damage and in turn congestion of the circulatory system. Such
complications that can arise are: kidney damage/failure, heart valve problems, and liver damage. The
kidney damage and/or failure arises from the decrease in blood flow which may require dialysis for
treatment. Heart valve problems arise from the damage sustained from high pressure or from the
enlargement of the heart muscle. Liver damage is done via the fluid backup which leads to scarring of
the liver making it hard for the liver to function properly. (Mayo Clinic, 2015 August 18).

Running head: CONGESTIVE HEART FAILURE

Table 1
Client to Textbook Comparison
Textbook

Client

Clinical Manifestations

1. Cough
2. Breathlessness
3. Weakness
4. Dizziness
5. Acites
6. Peripheral Edema
7. JVD
8. Cardiomegaly
9. Decreased Mentation
10. Decreased SpO2
11. Reduced Kidney Function
12. Chest Pain
13. Weight Gain

1. None upon assessment

2. Exertional related to pain from
RLE infection
3. Present, unable to hold self
over while turning in bed.
Weak to moderated grips and
plantar/dorsifelxion.
4. None noted upon assessment
5. None noted upon assessment
Abdominal obesity.
6. +2-3 pitting edema on
bilateral lower extremities,
and +1 on bilateral upper
extremities.
7. None upon assessment or
admission
8. None noted upon admission
9. Some
forgetfulness/disorientation at
times. Re-orientated easily.
Noted that opioid pain
medications have caused this
in the past.
10. Upon admission O2 Sat was
in high 90s but currently in
low 90s.
11. GFR 66/57
12. None upon assessment or
admission
13. Upon admission had gained
2-4 lbs; diuresing with Lasix.
Current weight 80.28 kg.

Diagnostic Labs, Tests,

Procedures

1. History and Physical

1. Past smoker history for 30
2. Urinalysis
years (quit in 2006), HTN,
3. Troponin
COPD, cataracts (surgeries in
4. BNP
08 and 13) worked as a sales
5. Serum Electrolytes
manager at a department store
6. Arterial Blood Gases
and homemaker.
7. Hemoglobin and Hematocrit 2. Clear, straw colored, voided
8. BUN and Creatinine & Protein 25 mL, Sp. Gravity 1.004
9. Chest X-Ray
(low), pH 5.0 - 9/14/15.
10. Echocardiogram
3. <0.04 - 9/15/15

Running head: CONGESTIVE HEART FAILURE

H&P

Medical Management

11. EKG
12. MUGA

4. 216 9/14/15
5. K+ = 3.8, Na+ = 137,
CO2 = 26
6. Not ordered
7. HgB: 10.3, Hct: 31.2
9/15/15
8. Protein: 3.9 6/5/15, BUN
and Creatinine not ordered
9. Cardiac silhouette and
pulmonary vasculature show
mildly prominent congestion,
increased opacity in bases
5/19/15
10. Not ordered
11. Normal Sinus 9/14/15
12. Not ordered

1. Past Medical History

2. Home Meds
3. Vitals and Pain
4. Respiratory Status
5. Family Hx.

1. Hx. COPD, essential

hypertension, cataracts
(surgeries in 08 and 13),
obesity, hyperlipidemia,
anemia and depression.
2. ASA 81 mg qd, Celexa 20 mg
qd, ferrous sulfate 325 mg (65
mg Fe) qd, Hydralazine 50 mg
bid, Imdur 30 mg qd, Cozaar
50 mg qd, Multivitamin qd,
Simvastatin 20 mg qPM,
Spiriva inhal 18 mcg qd,
Vitamin B-12 500 mcg qd.
3. Bp: 149/48 (0755 9/15/15)
150/49 (1200 9/15/15); Temp:
98.2 (0755 9/15/15) 98.1
(1200 9/15/15); Pulse: 78
(0755 9/15/15) 74 (1200
9/15/15); SpO2: 93% RA
(0755 9/15/15) 94% RA
(1200 9/15/15); Pain: 0 (0755
9/15/15) 10/10 (1200
9/15/15).
4. Room air, unlabored
breathing, equal chest
expansion, lungs CTA.
5. Not on file

1. Drug Therapy
a. Beta-Blockers

1. Meds
a. Not ordered

Running head: CONGESTIVE HEART FAILURE

b. ACE-inhibitors
c. Angiotensin Receptor
Blockers
d. Hydralazine and Nitrates
e. Aldosterone agonists
f. Diuretics
g. Digoxin
h. Heparin
2. CPAP
3. Cardiac Resynchronization
Therapy
4. Investigative Gene Therapy
5. Oxygen Therapy
6. Diet Therapy
7. Fluid Restriction
8. Strict I&O

b. Not ordered
c. Cozaar 50 mg qd
d. Hydralazine 50 mg bid,
Imdur 30 mg qd.
e. Not ordered
f. Lasix 40 mg qd
g. Not ordered
h. Heparin 5,000 units q 8hr
for DVT prevention
2. Not indicated for pt.
3. Not indicated for pt.
4. Not indicated for pt.
5. Room air
6. Cardiac, Low Na diet.
7. Not ordered
8. Not ordered

Surgical Management

1. Heart Transplant
2. Ventricular Assist Devices
3. Partial Left Ventriculectomy
4. Endoventricular Patch
5. Acorn Cardiac Support Device
6. Myosplint

1. Not indicated for pt.

2. Not indicated for pt.
3. Not indicated for pt.
4. Not indicated for pt.
5. Not indicated for pt.
6. Not indicated for pt.

Nursing Management

1. Administer Meds as Ordered

2. Health Teaching and
Promotion
3. Assess Patient for Clinical
Manifestations
4. Monitor Vital Signs
5. Monitoring I&O and Weight
6. Monitoring Lab Studies
7. Maintaining HOB Elevation

1. RN assigned to patient
administered medications as
ordered.
2. Taught client: how to use the
incentive spirometer and to
breathe in deeply and slowly
to increase the amount of
oxygen the body receives,
choosing healthy choices for
food, and importance of doing
some physical activity (even if
it is just ROM exercises).
3. Completed physical
assessment on patient and
noted no other signs of
congestive heart failure (CHF)
except for edema, and some
weakness.
4. Monitored vital signs in the
morning and afternoon.
5. Charted when patient voided
urine. Check chart for updated
weight.

Running head: CONGESTIVE HEART FAILURE

6. Looked up lab studies for

patient. 0500 labs were
resulted, however no
additional labs were
ordered/resulted.
7. Maintained HOB at 30-45
degrees unless patient was
eating then at 90 degrees and
when placing patient on
bedpan and taking patient off
bedpan lowered head of bed.
(Winkelman, C., 2013, pp. 351-355) (Ignatavicius, D., & Workman, L., 2013, pp. 751-754)
Contributing Factors Relating to the Pathology
This is a 85 year old female that also suffers from COPD, anemia, obesity, hyperlipidemia,
essential hypertension and depression. She is currently 28.6 pounds overweight for her age and height.
While at the hospital she does not have much of an appetite. She does not exercise regularly due to age,
weakness, COPD, and going to cancer appointments with her husband. She complains of right lower
extremity pain. She is also a past pack a day smoker for 30 years and quit in 2006. Upon review of this
patient's health history, the contributing factors leading to her development of CHF include obesity,
hyperlipidemia, COPD, hypertension, sedentary lifestyle, age, and previous smoking history.

Running head: CONGESTIVE HEART FAILURE

References
American Heart Association (AHA). (2015, July 29). Causes and Risks for Heart Failure. Retrieved
September 20, 2015, from
http://www.heart.org/HEARTORG/Conditions/HeartFailure/UnderstandYourRiskforHeart
Failure/Causes-and-Risks-for-Heart-Failure_UCM_002046_Article.jsp
Hobbs, R., & Boyle, A. (2014, March 1). Heart Failure. Retrieved September 20, 2015, from
http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/cardiology/heartfailure/Default.htm
Figueroa, M., & Peters, J. (2006). Congestive Heart Failure: Diagnosis, Pathophysiology, Therapy, and
Implications for Respiratory Care. Respiratory Care, 51(4), 402-412. Retrieved September 14,
2015, from http://www.rcjournal.com/contents/04.06/04.06.0403.pdf
Gorbunova, S. (n.d.). What is Heart Failure? Retrieved September 18, 2015, from
http://www.queri.research.va.gov/chf/products/nurse_education/What-is-Heart-Failure.pdf
Ignatavicius, D., & Workman, L. (2013). Medical-surgical nursing: Patient-centered collaborative
care (7th ed., pp. 747-758). St. Louis, MO: Saunders/Elsevier.
Mayo Clinic. (2015, August 18). Heart failure (R. Mankad, Ed.). Retrieved September 19, 2015, from
http://www.mayoclinic.org/diseases-conditions/heart-failure/basics/complications/con20029801
Mayo Clinic. (2015, August 18). Heart failure (R. Mankad, Ed.). Retrieved September 16, 2015, from
http://www.mayoclinic.org/diseases-conditions/heart-failure/basics/risk-factors/con-20029801
Winkelman, C. (2013). Clinical companion, Ignatavicius Workman, Medical-surgical nursing: Patientcentered collaborative care. (7th ed., pp. 349-355). St. Louis, MO: Elsevier Saunders.