Solution Manual for Medical Nutrition Therapy A Case-Study Approach, 5th Edition

Solution Manual for Medical Nutrition Therapy A

Case-Study Approach, 5th Edition

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Answer Guide for Medical Nutrition Therapy: A Case Study Approach 5th ed.
Case 6 – Heart Failure with Resulting Cardiac Cachexia
I. Understanding the Disease and Pathophysiology

1. Outline the typical pathophysiology of heart failure. Onset of heart failure usually can be traced to damage
from an MI and atherosclerosis. Is this consistent with Mrs. Maney's history?

• Many different events can lead to the development of congestive heart failure.
• Previous myocardial infarction, valve defect, or increased work demand on the heart from other conditions
such as hypertension all can damage the heart.
• This damage results in a decreased ability of the heart to pump adequately.
• When there is reduced blood flow to tissues, the body compensates in several ways.
• The kidney responds to decreased blood flow by secreting renin and aldosterone, causing
vasoconstriction and an increase in blood volume.
• The heart then has to work even harder to handle the increased blood volume.
• Over time, the heart enlarges (cardiomegaly) with its attempt to handle the increased workload.
• Cardiac output and stroke volume decrease.
• Compensation mechanisms do work for a time but eventually the heart muscle weakens.
• Dr. Maney’s medical history is consistent with the typical pathophysiology of heart failure. She has a long
history of coronary artery disease, hypertension, and mitral valve disorder. She also experienced a
myocardial infarction. Her previous medical diagnoses are all indicative of damage to the heart muscle,
which is the first step in the progression of heart failure.

2. Identify specific signs and symptoms in the patient’s physical examination that are consistent with heart
failure. For any three of these signs and symptoms, write a brief discussion that connects them to
physiological changes that you described in question #1.

• Jugular venous distention

• Ascites
• 2+ pedal edema
• Shortness of breath
• Increased pulse (110) respirations (24), lower blood pressure (90/70)
• Rales
• Skin - gray
a) Rales
Due to decreased cardiac output and the resulting low blood pressure present in HF, the RAAS is
activated by the kidneys. This system attempts to raise blood pressure by increasing sodium and water
retention. Fluid accumulates in the pulmonary vein and backs up into pulmonary circulation, which
increases pressure in the pulmonary capillaries. This increased pressure pushes fluid into the lungs, causing
pulmonary congestion/edema. The presence of fluid in the lungs can be heard through a stethoscope as
rales or crackles as the air tries to move through the fluid with each breath. Because the system lacks the
oncotic pressure to pull the fluid back into the capillaries, it continues to accumulate in the lungs, leading to
labored breathing and dyspnea. This, in turn, leads to tachypnea, as the patient must breathe more rapidly to
get enough oxygen into the lungs.
b) 2+ pedal edema
As the heart enters right-sided HF, it remains unable to pump blood efficiently. The right side of
the heart cannot maintain cardiac output, so blood volume decreases. The decrease in renal blood flow
again activates the RAAS to increase sodium and water retention, which then causes fluid to back up into
the systemic circulation.5 This increased venous pressure in the systemic circulation causes fluid to leak
from the capillaries into the third spaces near the ankles and feet (largely due to gravity) leading to pedal
edema. Again, the heart is not strong enough and the vessels lack the oncotic pressure needed to pull the
fluid back into circulation, so it continues to accumulate, increasing the severity of the edema.
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c) Tachycardia
As the failing heart works to increase cardiac output to normal levels, it must beat harder and faster to
do so. The release of hormones by the sympathetic nervous system not only cause vasoconstriction and
activation of the RAAS, but also increase the heart rate and contractility.

3. Heart failure is often described as R-sided failure or L-sided failure. What is the difference? How are the
clinical manifestations different?

Heart failure can involve the left side, the right side, or both sides. However, it most often begins with the left
ventricle. In left-sided HF, the left side of the heart experiences dysfunction and is unable to adequately maintain
cardiac output. In right-sided HF, the right side of the heart cannot maintain cardiac output. Because the left and
right sides of the heart have different functions, the resulting signs and symptoms caused by their failure are
different. Though initial compensation by the body occurs, it cannot be maintained, and one-sided HF often expands
to the entire heart, leading to decompensated HF.
Left-sided HF is typically the result of end-stage CAD or MI. When the left ventricle is damaged, it becomes
weakened and cannot pump blood adequately to the systemic circulation. This can be further classified as systolic or
diastolic. In systolic left-sided HF, the left ventricle has diminished contractility and cannot fully empty. In diastolic
left-sided HF, the left ventricle experiences impaired relaxation and is unable to fill completely. Both of these
situations lead to a decreased cardiac output and a resulting activation of the RAAS system in order to restore blood
volume by increasing sodium and water reabsorption by the kidneys. The increase in fluid causes a backup of blood
into the pulmonary circulation. The excess fluid in the pulmonary vein causes an increase in pressure in the
pulmonary capillaries, and fluid is forced out of the vessels and into the lungs. This fluid makes it difficult to
breathe, leading to dyspnea and tachypnea. Because the blood vessels lack the oncotic pressure to pull the fluid back
out of the lungs, blood pressure remains low, and the system continues to stimulate the RAAS system to try to bring
the body back to homeostasis. This leads to additional fluid accumulation and further pulmonary congestion.
Right-sided HF is most often the result of left-sided HF.3 When the right side of the heart begins to fail, it
cannot maintain cardiac output to the pulmonary trunk. Again, the RAAS system is stimulated to retain sodium and
water. This causes blood to back up into the systemic circulation. The high pressure in the periphery causes fluid to
leak out into the third spaces near the feet and ankles as well as the liver and abdominal organs, resulting in pedal
edema and ascites as well as splenomegaly and hepatomegaly. Additionally, venous pressure remains high, which
results in the distention of the jugular vein in the neck and cerebral edema, which causes headache.
Both left- and right-sided HF lead to fatigue, dyspnea, and generalized weakness. Furthermore, the presence of
edema in the abdominal region and dyspnea together cause a decrease in appetite/increase in satiety. This has
many nutritional implications, including malnutrition and cardiac cachexia.

II. Understanding the Nutrition Therapy

4. Mrs. Maney’s husband states that they have monitored their salt intake for several years. What is the role of
sodium restriction in the treatment of heart failure? What level of sodium restriction is recommended for the
outpatient with heart failure? What difficulties may a patient have in following a sodium restriction?

• Some level of sodium restriction is necessary in the treatment of heart failure because of the complications
associated with severe fluid retention. Sodium in the body attracts fluid, meaning that an excess of sodium
from the diet will cause additional fluid retention. Excessive fluid retention causes peripheral edema,
ascites, and pulmonary congestion in heart failure patients. The clinical manifestations of fluid overload
can increase the patients' energy expenditure (increased work of breathing/respiration rate), while causing
eating difficulties (dyspnea, ascites pressing against the stomach). It is essential that these patients control
their intake of sodium, which in turn controls their level of fluid retention.
• A 2,000 mg sodium diet is a standard initial recommendation.
• Adjustments to levels of 1,000 mg or 500 mg may be prescribed depending on an individual patient’s
medical condition—specifically, fluid and volume states as well as overall oral intake.
• These levels of sodium restriction are a challenge to manage outside a hospitalized setting, so it is critical to
evaluate the patient’s actual PO intake to determine the level of sodium the patient is consuming prior to
putting any further modifications in place. However, in malnourished or cachectic patients who have
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anorexia, caution should be exercised. This is because the first priority in the HF patient is to ensure they
are getting enough nutrients to maintain weight and support healing.
• Such difficulties include: sodium's high prevalence in Western/processed foods, salt's prominent role in
flavor/taste, and salt's high use in foods at restaurants

5. Why is Mrs. Maney placed on fluid restriction? How will this assist with the treatment of her heart failure?
What specific foods are typically "counted" as a fluid?

• On admission she was had fluid retention and had prerenal azotemia.
• Physical exam reveals 2+ pedal edema that demonstrates her fluid overload
• The patient’s creatinine and BUN are also elevated.
• These findings are compatible with low kidney perfusion.
• Fluid restriction will improve clinical symptoms and quality of life.
• Foods “counted” as fluid: All beverages (including water, milk, juices, coffee, tea, soft drinks),soups,
gelatins, fruit ice, Popsicles™, liquid nutritional supplements, ice cream, puddings, custard, sherbet, ice,
soups, and anything liquid (or that melts) at room temperature.

6. Identify any common nutrient deficiencies found in patients with heart failure.

Common nutrient deficiencies found in patients with heart failure include: potassium, magnesium, thiamin,
riboflavin, pyridoxine, folate, B-12, calcium, and zinc. Many of these nutrient deficiencies are caused by drug-
nutrient interactions. A common drug-nutrient interaction in heart failure patients is the loss of water-soluble
nutrients when a combination of multiple diuretics is used to remove excess fluid from the body. Sdditional
research is being done to determine the appropriate use of some supplements, such as omega-3 fatty acids and
coenzyme Q10, in HF patients. While results do not suggest any strong evidence for the supplementation of
either of these substances, there remains a possibility that they may help the HF patient. L-arginine and
carnitine are also being investigated for potential supplementation .

III. Nutrition Assessment

7. Identify factors that would affect interpretation of Mrs. Maney’s weight and body composition. Look at the
I/O record. What will likely happen to Mrs. Maney's weight if this trend continues?

• Ascites and peripheral edema

• Mrs. Maney’s I/O record shows an overall net fluid retention of 408 mL over a 24-hour period since her
admission. If this trend continues, Mrs. Maney’s measured weight will increase to reflect additional fluid
retention. A negative net I/O value would correlate with a decrease in measured weight.
Mrs. Maney also has signs of muscle wasting (temporal wasting and weak handgrip) which may indicate a
loss of lean body mass. These may be masked due to fluid retention.

8. Calculate Mrs. Maney’s energy and protein requirements. Explain your rationale for the weight you have
used in your calculation.

• Mrs. Maney’s IBW (50 kg) is used for calculations as her current weight is masked by fluid retention. This
is within 10% of her current weight.
• Energy: energy needs for cardiac cachexia may be calculated using the American Chest Physician’s
nomogram. 50 x 25 = 1250 kcal 50 x 35= 1750 kcal Range: 1250-1750 kcal

• Protein: AND EAL recommends 1.37 g/kg for heart failure patients.
47.7 kg  1.37 = 65 g/day

9. Do you have any evidence that Mrs. Maney may be malnourished? Identify factors that may support a
diagnosis of malnutrition using the latest AND/ASPEN proposed guidelines for malnutrition diagnosis.
• Yes, there is evidence that Mrs. Maney is malnourished
• Muscle loss at her temporal region
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• Fluid accumulation is present: ascites, 2+ pedal edema (though, her heart failure complicates this clinical
evidence for malnutrition) and would be difficult to interpret.
• Weak grip strength
• < 27% energy intake (per 2 cans of Boost daily)

10. Malnutrition in heart failure is often referred to as cardiac cachexia. What is cardiac cachexia? What are
the characteristic symptoms? Explain the role of the underlying heart disease in the development of
malnutrition.
• Cardiac cachexia is a wasting syndrome caused by heart failure that results in a metabolic imbalance
favoring catabolism over anabolism. Losses in lean and fat tissue, in addition to bone mineral density, can
be observed and is not always reversible upon feeding (like starvation).
• Signs and symptoms: increased plasma TNF-α, decreased GI tract perfusion (slowed peristalsis, early
satiety, and impaired nutrition absorption), and endothelial dysfunction (leading to a reduction in skeletal
muscle nutrient supply).
• Heart failure promotes the development of malnutrition through inflammatory pathways, elevated levels of
B-type and atrial natriuretic peptides, aldosterone, and cortisol, and anorexia.

11. Do you feel that Mrs. Maney may benefit from enteral feeding? What guidelines would you use to make this
decision? Outline a nutrition therapy regimen for her that includes formula choice, total volume, and goal
rate.

• Yes, Mrs. Maney would benefit from enteral feeding since she is consuming < 5% of her meals and
consumed < 27% of her energy needs prior to admission
• ASPEN guidelines should be used to make this decision; since she is malnourished and critically ill at
admission
• Formula choice: Two-Cal HN (high-protein formula that provides 2 kcal/mL) = 1800 kcal
• Total volume: 900 mL
• Goal rate: 38 mL/hr
• Osmolality of Two-Cal NH is 725 mOsm/kg H2O; therefore, the initial rate should be 20 mL/hr for first 8
hours, then advanced 10 mL/hr every 4 hours until goal rate is reached.

12. Identify any abnormal biochemical values associated with Mrs. Maney's heart failure or CVD and assess
them using the following table:

Name of Normal Patient’s Reason for Abnormality

Laboratory Value Value Value &
Date
Sodium (mEq/L) 136-145 132 (2/14) Fluid overload resulting in dilution of serum sodium
133 (2/16)
135 (2/20)
BUN (mg/dL) 6-20 32 (2/14) Decreased renal perfusion; Cardiac cachexia (protein
34 (2/16) catabolism, muscle wasting)
30 (2/20)
Creatinine serum 0.6-1.1 1.6 (2/14) Decreased renal perfusion; Cardiac cachexia (protein
(mg/dL) 1.7 (2/16) catabolism, muscle wasting)
1.5 (2/20)
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Name of Normal Patient’s Reason for Abnormality

Laboratory Value Value Value &
Date
Bilirubin, direct <0.3 1.0 (2/14) Abnormal liver function; hepatomegaly resulting from edema in
(mg/dL) 1.1 (2/16) liver
0.9 (2/20)
Protein, total (g/dL) 6-7.8 5.8 (2/14) Fluid overload resulting in dilution of serum protein
5.6 (2/16)
5.5 (2/20)
Albumin (g/dL) 3.5-5.5 2.8 (2/14) Fluid overload resulting in dilution of serum albumin; increased
2.7 (2/16) protein catabolism due to cardiac cachexia
2.6 (2/20)
Prealbumin 18-35 15 (2/14) Fluid overload resulting in dilution of serum prealbumin;
(mg/dL) 11 (2/16) malnutrition (cardiac cachexia); possible abnormal liver
10 (2/20) function (hepatomegaly)
ALT (U/L) 4-36 100 (2/14) Impaired liver function resulting from edema in liver
120 (2/16) (hepatomegaly); Damage to heart muscle;
115 (2/20)
AST (U/L) 0-35 70 (2/14) Impaired liver function resulting from edema in liver
80 (2/16) (hepatomegaly) Damage to heart muscle;
85 (2/20)
CPK (U/L) 30-135 180 (2/14) Damage to heart muscle;
200 (2/16)
205 (2/20)
Troponin T (ng/L) <0.03 0.035 Past cardiac injury (myocardial infarction)
(2/14)
0.037
(2/16)
0.036
(2/20)
Troponin I (ng/L) < 0.2 0.026 Past cardiac injury (myocardial infarction)
(2/14)
0.028
(2/16)
0.027
(2/20)
HDL-C (mg/dL) >59 30 (2/14) History of coronary artery disease; genetic, lifestyle and diet
31 (2/16) may contribute.
30 (2/20)
LDL (mg/dL) <130 180 (2/14) History of coronary artery disease; genetic, lifestyle and diet
160 (2/16) may contribute.
152 (2/20)
LDL/HDL ratio <3.22 5 (2/14) History of coronary artery disease; genetic, lifestyle and diet
5.23 (2/16) may contribute.
4.97 (2/20)
WBC ( 103/mm3) 4.8-11.8 12 Inflammation and overall disease state
12
10.5

13. The following drugs/supplements that were prescribed for Mrs. Maney. Give the medical rationale for the
use of each. In addition, describe any nutritional concerns for Mrs. Maney while she is taking these
medications.

Medication Rationale for Use Nutrition Implications

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Medication Rationale for Use Nutrition Implications

Lanoxin Increases myocardial
contraction.
Lasix Diuretic used in edematous
states to improve fluid
balance; sometimes used to
lower blood pressure.
Dopamine Increases myocardial
contraction and has a pressor
effect to help support blood
pressure when low.
Thiamin Diuretic use can lead to
thiamin deficiency.
Side effects of this medication include diarrhea, loss of
appetite, stomach pain, nausea, and vomiting; all of these
side effects can make eating difficult and unpleasant,
resulting in suboptimal oral food and nutrient intakes.
Avoid avocado, high fiber foods within 2 hours of taking
medication, limit sodium, avoid milk, Ca supplements, iron,
antacids or aluminum salts 2 hours before or 6 hours after
taking medication. Avoid K containing salt substitutes, limit
garlic, ginger, gingko, and horse chestnut
Hypokalemia, hypomagnesemia, thiamin deficiency,
calcium deficiency; supplementation may be necessary
depending of severity of electrolyte or nutrient deficiency.
Side effects include potential decrease in serum potassium,
proteinuria, nausea, and vomiting; may require potassium
supplementation or high-potassium diet choices; nausea and
vomiting may inhibit adequate caloric intake.
NA

IV. Nutrition Diagnosis

14. Select two nutrition problems and complete a PES statement for each.
• Inadequate oral food/beverage intake related to poor appetite as evidenced by few sips of liquids, soft
foods, and “trying to take Ensure.”
• Inadequate intake from enteral nutrition related to intolerance secondary to uncontrolled diarrhea as
evidenced by ___ (more data would be needed regarding the specific amount that was either provided or
withheld during this period of time, e.g. “only X mL of formula compared to goal rate”).
• Malnutrition related to anorexia and SOB as evidenced by consumption of <75% of estimated energy
needs, moderate temporal wasting and reduced handgrip strength.

V. Nutrition Intervention

15. Mrs. Maney was not able to tolerate the enteral feeding because of nursing report for diarrhea. What
recommendations could be made to improve tolerance to the tube feeding?

• The formula could be changed to one with added fiber (such as Jevity) or fiber could be added to Mrs.
Maney's medications.
• It is important to remember that fiber supplements should not be added separately to the enteral formula or
placed down the feeding tube. It may cause interactions with the formula and could result in a tube
blockage.
• Additionally, an antidiarrheal agent such as loperamide could be used.
• Depending the osmolality of the formula, it may be advisable to have a lower initiation rate to lower the
"water-pulling" effect that the higher osmolar formula may have in the intestinal tract.

16. The tube feeding was discontinued because of continued intolerance. Parenteral nutrition was not initiated.
What recommendations could you make to optimize Mrs. Maney's oral intake?

• If she is able to eat, provide her with foods that she likes with increased nutrient density.
• Small, frequent feedings work well to minimize the volume of food consumed and stress on both the
cardiac and respiratory systems.
• Within her fluid allowance, use of a nutrient-dense liquid supplement may be easier than attempting to
consume solid food.
Solution Manual for Medical Nutrition Therapy A Case-Study Approach, 5th Edition

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• Consume fluids between meals to prevent their contribution to fullness during mealtime

17. Outline steps you would take to assist Mrs. Maney as she prepares for discharge. Include the specific
nutrition education that you would include.
• Assess readiness/motivation for change
• Educate the importance of sodium and fluid restriction and their implications on the clinical manifestations
and exacerbations of her cachexic state (increased work of breathing due to pulmonary congestion,
anorexia, etc.)
• Educate Mrs. Maney on nutrient density – steps to add both kcal and protein to her diet. Suggest that Mrs,
Maney have assistance with meal preparation and grocery shopping. Attempt to get at least 1/3 of her kcal
at the meal where she is hungriest. Could also suggest spreading meals over 5-6 small feedings rather than
only three. Discuss the use of high calore and high protein supplements. Every bite of food should provide
both kcal and protein –discourage consumption of empty calorie foods.
• Educate Mrs. Maney on fluids:
o See question 5. for examples
o How to optimize/reduce intake (e.g. avoid salty foods, drink only when thirsty, etc.)
• Educate on low-sodium and avoidance of high-sodium options:
o Low sodium: fresh or frozen vegetables, fruits, unprocessed meats, noodles, rice, English muffins,
etc.
o High-sodium: processed foods, salty snack foods, soups, sauces, fast foods, pickles, etc.

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