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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).
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
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. Drug Therapy
a. Beta-Blockers
1. Meds
a. Not ordered
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
Nursing Management
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.
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.