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Coronary Artery Disease: A Time for Nutrition Intervention
Hilary Shone
March 25, 2015
Queen of the Valley Medical Center
INTRODUCTION
Patient Background & ER Course
On February 9, 2015, PG was highly encouraged to visit the ER by his family after having
an unusual episode of chest pain while doing paperwork in his home office. Upon admission to
the ER, PG reported this time was unlike any other chest pain he had experienced; this pain was
felt at rest whereas other chest pains he has reportedly felt intermittently and upon exertion or
physical activity. An immediate EKG was performed and PG was discovered to be in rapid atrial
fibrillation. This finding immediately triggered the administration of Metoprolol which was not
found to be highly effective in controlling his heart rate. He was then placed on a Diltiazem drip
which helped to control his blood pressure and chest pain. Additionally, he was given Plavix to
offset any adverse blood clotting after a possible heart attack. The plan at this point was to
hold the patient overnight and refer him to a cardiologist for evaluation in the morning,
possibly for eventual cardiac catheterization, continue Diltiazem drip for atrial fibrillation,
nitroglycerin for the chest pain and continue anticoagulation therapy with the administration of
Lovenox.
Admission Physical Data-Vital Signs
General: Pleasant, alert male, currently in no acute distress
Vital signs: Blood pressure initially 192/148 w/heart rates ranging between 115 and 143,
respirations 19, afebrile
Cardiovascular: Tachycardic and irregular
Abdomen: Positive bowel sounds. Soft, nontender
Extremities: No clubbing, cyanosis or edema
Admission Biochemical Data
Lab
Hgb
Hct
Na
K
BUN
2/9
15.8
46.5
135
3.5
16
Normal Range
12.5-16.3 g/dL
36.7-47.1%
136-145 mg/dL
3.5-5.1 mg/dL
6-20 mg/dL
GFR
82
Albumin
5.2
Glucose
90
Troponin I
0.72*
*Indicates average value for that day
> 90 mL/min
3.5-5.0 g/dL
70-118 mg/dL
< 0.04 ng/dL
Past Medical/Surgical & Family History
There was a not a significant medical history for this patient, in the ER there was a
question of hypertension and this was confirmed later in the patient’s hospital stay. Upon
consultation by the cardiothoracic surgeon, the patient was also discovered to have a history of
heavy alcohol consumption but had recently discontinued. Because the patient reported that
he has felt irregular heartbeats for the past few years, he was determined to have had atrial
fibrillation for the past 3 years. Past surgical history includes varicose vein stripping. PG was
not taking any outpatient medications upon admission.
Family history of cardiovascular conditions are significant for this patient, father passed
away at age 35 secondary to angina, son had a CVA at age 12 of unknown etiology and brother
has a history of atrial fibrillation. This significant family history for cardiovascular disease likely
played a large role in PG’s admitting symptoms, eventual medical diagnoses and necessary
course of treatment.
Hospital Medical/Surgical Data
Upon cardiologist evaluation the morning after admission, PG’s laboratory data was
evaluated, specifically cardiac biomarkers, showing an elevated troponin I of 0.82 ng/mL initially
and 0.97 ng/mL on reassessment. According to the literature, abnormal levels of troponin T
and CK-MB, an isoform of creatinine phosphokinase, are two biomarkers used for diagnosis of
myocardial infarction, however cardiac elevated troponin I, lactate dehydrogenase I, an isoform
of lactate dehydrogenase, and myoglobin are all indications of cardiomyocyte ischemia and/or
necrosis (Nelms, 2011). There is some discrepancy between the normal range of troponin I in
the literature and the normal range at QVMC; the literature considers a value greater than 0.5
ng/dL to be indicative of cardiomyocyte ischemic damage whereas QVMC considers a value
between 0.04-0.49 ng/mL to indicate acute coronary syndromes and a value greater than 0.49
ng/mL to indicate myocardial necrosis. Provided these differential units, these standards are
still significantly different (0.04 ng/mL = 4 ng/dL). Nevertheless, PG was evaluated according to
QVMC standards and was ruled in for a myocardial infarction considering his two elevated
troponin I levels and a 12-lead ECG showing atrial fibrillation with rapid ventricular response
and inferolateral ST depression. This wave depression on the ECG is indicative of altered
electrical activity of the cardiac myocytes, further indicating ischemic cardiac tissue as a normal
electrical wave is not able to conduct a normal PRQST wave (Kavya & ThulasiBai, 2012). Given
the presence of unstable angina, unpredictable chest pain upon rest, and occurrence of acute
myocardial infarction, PG was determined to have acute coronary syndrome with strong
possibility of underlying coronary artery disease. The pathophysiological connections of all of
these symptoms and diagnoses will be discussed in a later section.
Provided these findings and new conclusions, PG was recommended for cardiac
catheterization and coronary angiogram, further evaluating the need for surgical intervention.
Future treatment recommendations were to be made based on the findings of the angiogram.
As a result of the angiogram, PG was determined to be an appropriate surgical
candidate for urgent revascularization, or placement of a Coronary Artery Bypass Graft (CABG).
This particular type of surgical intervention was chosen on the basis of the number of occluded
coronary arteries, specific arteries which were found to be occluded and recent occurrence of
other acute cardiac events, specifically the myocardial infarction. Specific eligibility
requirements as relevant to PG include left main artery stenosis, stenosis of the left anterior
descending and circumflex arteries, 3-vessel disease, NSTE-ACS (non-ST elevation acute
coronary syndrome), classified by the American College of Cardiology and American Heart
Association (Bilal & Lange, 2014). PG was found to have mildly depressed ventricular function,
a tight left main (coronary artery) and circumflex artery as well as high-grade stenosis of the left
anterior descending artery; at this time PG was diagnosed with coronary artery disease. The
CABG placement took place the following morning, and a total of 2 grafts were used to bypass
the occluded arteries. After surgery, the patient was fairly hemodynamically stable and was
transferred to ICU and temporarily intubated and sedated. Once the patient was extubated, he
remained hemodynamically stable, erring on the side of hypertension. In a study conducted by
Green et al, the majority of patients who are extubated experience hemodynamic instability,
particularly rapid blood pressure drops into hypotensive ranges (Green, 2012).
OVERVIEW OF DISEASE STATE
Coronary artery disease (CAD), also known as ischemic heart disease, is the result of the
continued result of atherosclerosis, or buildup of lipid-based plaque in the coronary
vasculature. As this plaque grows within the blood vessel, the vessel becomes continually
occluded and a lesser volume of blood can perfuse past the atherosclerotic plaque. The overall
result of this reduced blood flow is a decreased amount of oxygen and nutrients delivered to
the cardiac muscle, resulting in ischemic conditions and potential necrosis of the myocytes. A
myocardial infarction occurs when the oxygen demands of the heart are not met by the oxygen
delivery in the blood, resulting in cardiomyocyte death and the subsequent release of certain
biomarkers from these necrotic cells, several of which are used for diagnostic purposes. As a
result of the infarction, a small area of cardiac muscle may have become necrotized, the patient
could experience cardiac rhythm abnormalities from damage to the neural pathways of the
heart and even sudden cardiac death can result. If this type of severe blood flow restriction
occurs within a vessel in the brain, a stroke (cerebrovascular accident) can occur (Nelms, 2011).
At the heart of CAD is atherosclerosis. Because atherosclerosis and coronary artery
disease are so inextricably linked, the risk factors for both conditions are very similar.
Significant risk factors include the male sex, greater than 65 years of age, obesity (BMI > 30
kg/m2), dyslipidemia (abnormal blood lipid panel), hypertension (> 140/90 mmHg), physical
activity, atherogenic diet, diabetes mellitus, impaired fasting glucose and metabolic syndrome,
and cigarette smoke. With the exception of low HDL, PG’s lipid panel was surprisingly normal.
A recent study by Tietjen et al. (2012) found a correlation between decreased levels of HDL
production, due to mutations in genes coding for essential HDL proteins, and increased risk for
myocardial infarction and CAD; stronger correlation was found in the group with known family
history of low HDL levels as compared to the group with unknown family history of low HDL
levels. The initiation of atherosclerosis is thought to begin as an inflammatory response to
endothelial cell injury, typically from hypertension or vasospasm. This injury attracts circulating
monocytes, a phagocytic immune cell, which then travel into the subendothelial space,
differentiate into macrophages and take up oxidized LDL cholesterol, transforming them into
foam cells. The capture of LDL cholesterol relates to the atherogenic diet as a strong risk factor
for the onset and development of atherosclerosis. An atherogenic diet or “westernized diet” is
one that is high in saturated fat and sodium and low in fiber, usually resulting in obesity and
abnormal lipid profiles (elevated serum LDL cholesterol, total cholesterol and triglycerides
paired with low serum HDL cholesterol). Given this dietary-dyslipidemic relationship, the
greater the concentration of LDL cholesterol circulating in the blood, the greater chance of
oxidized LDL uptake by the subendothelial macrophages. It is for this reason, monitoring
saturated fat and sodium intake can be primary prevention measures despite the presence of
other atherosclerotic risk factors (Nelms, 2011).
As the foam cell formation process continues, these cells form what is known as a fatty
streak in the extracellular space in the vessel lumen. The fatty streak is usually the first visible
sign of atherosclerosis as it begins the occlusion process of the artery. At the initial formation
of the injury, circulating platelets are also drawn to the lesion, forming a small thrombus, or clot
at the site. With continued platelet accumulation, these platelets begin to release growth
factors and ADP which results in the migration of smooth muscle cells and fibroblasts to the site
of injury. The combination of these blood and immune cells is the formation of a collagenous
and fibrous extracellular matrix. The formation of the thrombus plays an important role in the
later occurrences of myocardial infarctions and strokes. As these processes continue, the
plaque grows larger, at first compensated by the elasticity of the vessel, however eventually the
plaque grows to a size and rigidity that the vessel can longer accommodate the reduction in
lumen diameter and occlusion begins. The larger the plaque becomes, the more unstable its’
adhesion to the endothelial wall. A myocardial infarction results when the occlusion becomes
so great that the cardiac myocytes receive an inadequate amount of oxygen as a result, or the
plaque ruptures, and releases a thrombus which causes stenosis of a coronary vessel,
preventing adequate oxygen delivery. The definition of CAD includes all forms of heart disease
categorized by the narrowing or stenosis of the blood vessels; once this process is detected
through angiography, CAD may be considered as a likely diagnosis (Nelms, 2011).
Acute coronary syndrome is essentially the acute on chronic of CAD. It applies to
individuals who experience an acute myocardial infarction or unstable angina. Through
evaluation of laboratory data, diagnostic testing, and self-report, PG was found to have both of
these occur within a very short time. Compared to stable angina, which is chest pain felt upon
exertion or physical activity, unstable angina is chest pain that occurs at rest and usually
without warning. Angina is the primary symptom of CAD as it indicates diminished blood flow
and oxygen delivery to the cardiac muscle (Nelms, 2011). Although the exact chronology of
PG’s cardiac events is unclear, it is likely that the unstable angina gave a short warning of the
sustained myocardial infarction and part of the angina episode was in fact the infarction.
Following an infarction, there is potential for several additional adverse cardiac events
to occur. One of these events is cardiac arrhythmias; as a result of the necrotized tissue, the
tissue adjacent to this area becomes irritated and can interfere with the neural pathways of the
cardiac muscle. As the neural pathways, the sinoatrial and atrioventricular node, are
responsible for maintaining the electrical activity of the heart, if these pathways become
interrupted or damaged, electrical conductivity and subsequent contractility can become
altered and irregular. Ventricular fibrillation is the common manifestation of this process,
particularly after an infarction and occurs when the ventricles contract uncontrollably as a
result of the altered electrical activity. Despite the exact chronology of cardiac events
remaining unknown, PG was discovered to be in atrial fibrillation with rapid ventricular
response. Atrial fibrillation is similar to ventricular fibrillation regarding the uncontrolled
contractility however, the rapid ventricular response is a specific rapid contractility in the
ventricles as a result of the abnormally contracting atria (Nelms, 2011). Given the unstable
angina, followed by an infarction and presenting with atrial fibrillation with rapid ventricular
response upon admission, the described order of these events may have been synonymous
with PGs’ course that evening.
The goals of nutrition therapy following a myocardial infarction are aligned with the
medical treatment goals: stabilize cardiac function, decrease pain and if indicated, initiate
rehabilitation after the acute infarction period. Directly following the infarction, oral intake
may be reduced as a result of pain, fatigue and anxiety. While receiving medical care, the diet
may begin as a clear liquid diet omitting caffeine to reduce the risk of arrhythmias, and progress
to a soft texture diet, consumed as small, frequent meals. Once the patient can tolerated a
regular texture diet, the dietary guidelines of the Therapeutic Lifestyle Changes (TLC) diet
should be adhered to and individualized, considering the patient’s specific risk factors (Nelms,
2011). The components of the TLC diet will be elaborated upon when the nutrition
interventions performed with the patient are discussed.
PATIENT PROFILE
PG is a 59 year old male who is married with one son and lives in Napa. He works from
home and is in the furniture restoration business. Both he and his wife report he has been
physically inactive for most of his life, although recent efforts have been made by both of them
to increase the frequency and type of physical activity they engage in. According to the
patient’s wife, he is an ‘alcoholic’ consuming a bottle of vodka or six pack of beer every day.
PG’s wife claims she has previously tried multiple intervention strategies to limit his alcohol
intake however none were permanently successful; PG reports he has been sober since
December 26, 2014 and does not plan to drink again until ‘maybe this coming New Year’s Eve’.
This is evident throughout the patient’s hospital notes. As previously noted, PG’s wife and son
have been encouraging him to receive medical treatment for his chronic intermittent chest pain
but it was only until this most recent episode he agreed due to the abnormal nature and timing
of the pain.
Nutrition Assessment in Cardiovascular Disease
Specific to cardiovascular disease, nutritionally assessing a patient involves gathering
their anthropometric data, biochemical data especially lipid profile, social and past medical
history, typical dietary intake, person in family responsible for cooking and preparing
meals/meal preparation methods, and physical observations. Relevant to hospitalized patients,
results and history of medical and diagnostic tests also play an important role in nutritional
assessment and proceeding with the remainder of the nutrition care process (Nutrition Care
Manual).
Food and nutrition-related history was obtained from both PG and his wife in the days
immediately before and after his CABG placement. PG gave a fairly comprehensive outline of a
typical day reporting breakfast is typically “a bowl of oatmeal (made with water) with
blueberries, maple syrup and walnuts”, lunch is usually “yogurt, 3 pieces of fruit or vegetables,
a handful of almonds and 3 pieces of meat, usually salami or other lunch meat and cheese” and
dinner “could be many things, often we have chicken, mashed potatoes and a vegetable side”.
Typical fluid choices are “water and non-fat milk”; when asked to estimate consumed quantities
of the foods listed, PG used rough approximations and vague hand gestures, indicating his wife
does the meal preparation. Red meat is not consumed often but when it is, he and his wife
share a steak. PG was sure to note that “not a lot of salt is used in anything” and he and his
wife “started eating healthier a few years ago” when he learned his brother was experiencing
atrial fibrillation, and likely considered his strong family history for cardiovascular-related
complications as a motivation factor for change.
Preparation and cooking methods were obtained from PG’s wife. She stated all cooking
is done with olive oil and butter is “used not often but when the food calls for it”. She endorsed
PG’s claim of minimal salt usage in cooking, stating she still salts boiling water for pasta but was
considering changing this cooking habit. She also endorsed PG’s statement of infrequent red
meat consumption, verifying they share a steak once in a while. This prompted her to admit
salami is purchased and consumed fairly frequently, evident by PG’s report of his typical lunch
meal. Both PG and his wife report they do not eat out often.
In addition to obtaining food and nutrition-related history, an essential part of assessing
a cardiovascular patient is the calculation of estimated energy, protein and fluid needs. In
order to perform these calculations, the patient’s basic anthropometric data is needed as well
as some preliminary weight calculations. PG’s anthropometric data and weight calculations are
as follows:
Height
Weight
BMI
UBW
6’2” (188 cm)
104 kg (240 lbs)
29.5 kg/m2
~220 lbs
Adjusted BW
IBW
% IBW
92 kg (202 lbs)
86.4 kg (190 lbs)
121%
Although an adjusted body weight was calculated, it is the policy of the hospital’s
dietetic department to only utilize the adjusted body weight value for obese patients, defined
as having a BMI > 30 kg/m2. To estimate PG’s energy needs throughout his hospitalization, the
Mifflin St-Jeor predictive equation was used per department policy and Nutrition Care Manual
recommendation (Nutrition Care Manual).
CHRONOLOGY OF MEDICAL TREATMENTS AND MEDICAL NUTRITION THERAPY
Admission Nutrition Assessment
At the time PG was first assessed on February 11, 2015, he was on the telemetry patient
floor and scheduled to have the CABG surgery the following morning. Continued from the day
prior, he was on Lopressor and Lisinopril to control his hypertension and had underwent the
coronary angiogram the day before, determining the need for the CABG surgery. Medical
treatments up this point included cardiac stabilization with medication in the ER, and cardiac
catheterization and coronary angiogram; future medical treatments included the scheduled
CABG surgery. Treatment goals included the revascularization of the cardiac muscle and
restoration of blood perfusion to the heart through bypass of the occluded coronary arteries.
Upon the result of the coronary angiogram, the patient was started on Aspirin, Lisinopril,
Lopressor, and Lipitor; in preparation for surgery he was started on heparin that evening. See
APPENDIX B for full list of medications.
Nutrition-related labs assessed:
Lab
Hgb
Hct
Na
K
BUN
GFR
Albumin
Triglycerides
LDL Cholesterol
HDL Cholesterol
2/10
14.4
42.0
137
3.7
14
98
X
151
79
28
2/11
13.7
40.1
132
3.8
14
93
3.8
X
X
X
Normal Range
12.5-16.3 g/dL
36.7-47.1%
136-145 mg/dL
3.5-5.1 mg/dL
6-20 mg/dL
> 90 mL/min
3.5-5.0 g/dL
<150 mg/dL
< 100 mg/dL
40-59 mg/dL normal
> 60 mg/dL
cardioprotective
Total Cholesterol
137
Glucose
87
Hemoglobin A1C
5.5
Troponin I
0.97
*Indicates average value for that day
X
X
X
0.65
< 200 mg/dL
70-118 mg/dL
4-5.9%
< 0.04 ng/dL
Given PG’s upcoming CABG surgery, the day prior to this surgery was an appropriate time for
nutrition intervention, specifically discussing the Therapeutic Lifestyle Changes (TLC) diet.
Because his nutritional intervention was going to be primarily an educational experience, the
main topics discussed would likely need reinforcement and additional instruction after his
surgery and with his wife. Although several nutrition diagnoses would have been appropriate
for PG’s nutritional issues at this time, his admission nutrition diagnosis was:
“Overweight R/T excessive energy intake prior to admission AEB abnormal BMI of 29.5”
Based on the patient’s anthropometric data, including the most current weight, estimated
needs were determined as follows:
Mifflin St. Jeor: 1931 kcals (REE)
Estimated Energy Needs: 2125-2511 kcals (1.1-1.3 x MSJ)
Estimated Protein Needs: 125-146 g (1.2-1.4 g/kg BW), BW used 104.2 kg
Estimated Fluid Needs: 2125-2511 mL (1 mL/kcal)
According to the Nutrition Care Manual, the recommended activity factor for sedentary
individuals with cardiovascular disease is 1.3 and a 500 kcal per day subtraction from the
estimated energy requirements for permitted weight loss. Considering PG’s overweight status
and requirement to provide at minimum the REE, a lower set of activity factors were applied to
guarantee provision of at least the REE and avoid recommending a lower number of calories by
deducting 500 kcals for permitted weight loss. His first measured weight was used for all
estimated needs throughout his hospitalization as this was likely his truest weight, any
apparent weight gain was likely due to fluid gains. Protein needs were estimated in greater
consideration of PG’s recovery from major surgery than cardiovascular disease. Per the
QVMC’s dietetic department policy, estimated protein needs following a major surgery range
from 1.2-1.5 g/kg with individual patient discretion encouraged. In retrospect, the factors used
to determine protein needs were likely higher than the patient’s needs and should have been
closer to the recommended 0.8-1 g/kg (Nutrition Care Manual). Fluid needs were determined
according to the dietetic department’s policy of 1 mL/kcal for all patients assessed.
Upon admission, PG was placed on the Cardiac AHA Heart Healthy diet which provides:
1700-2100 kcals
85-110 grams protein
45-60 grams fat (20-32% kcals)
At the time of this nutrition assessment, PG’s average meal intake was 100% except for the
several hours he was ordered to be NPO for the angiogram. Using an average of 1900 kcals
provided daily by the Cardiac diet, this diet technically did not meet the patients’ needs
however given his overweight, nearly obese status, this diet was determined to be adequate
and potentially permissive of weight loss. Per the QVMC diet manual, ‘this diet is restricted in
total fat, saturated fat and sodium content as compared to the Regular Diet and provides a
daily average of < 10% calories from saturated fat, 2 grams sodium, < 200 mg cholesterol and
no caffeine’. Goals of this diet coincide with overall nutrition therapy goals for cardiovascular
disease and include ‘reduction of elevated blood cholesterol and/or triglyceride levels, control
intake of saturated fat, total fat, cholesterol and sodium’. Because the nutritional aspects and
goals of this diet are closely aligned with those of the TLC diet, PG’s diet order was used as an
initiative for education on the TLC diet.
The majority of the nutrition intervention given at this assessment was education on the
TLC diet. Prior to delving into the core components of the diet, food and nutrition-related
history was obtained to better gauge the presentation of certain aspects of the diet and
increase educational efficacy. The four main components of the TLC diet were emphasized:
limiting saturated fat, increasing intake of unsaturated fats, limiting sodium intake and
increasing dietary fiber intake, especially soluble fiber. Sensitive to PG’s likely emotional state
the day before a major surgery, a relatively light education was provided on these topics,
however more attention was given to sodium intake and sources of fat. Different types and
sources of fat were discussed, emphasizing that the percentage of calories from fat in the TLC
diet does change significantly, rather it is the source of fat (unsaturated rather than saturated).
Interestingly, a recent study conducted with myocardial infarction-induced rats found that
when fed a diet high in saturated fat, the cardiac muscle in the high fat-fed mice group was able
to restore function and metabolic phenotype to a greater extent than the group fed a ‘normal’
diet; findings even suggested a cardioprotective effect in the rats fed a diet high in saturated fat
as compared to the normal diet group (Berthiaume et al, 2012). Another recent study
examined the associations between self-reported dietary saturated fat intake and risk of
subsequent coronary events and mortality in patients with established CAD and interestingly
found no correlation between reported dietary intake of saturated fat and incidence of
coronary events or mortality (Puaschitz, 2015). Both of these studies provide new insight into
standard dietary recommendations for cardiac patients and may initiate a larger scale reexamination of current dietary guidelines and the credos of the TLC diet.
So as not to overwhelm him just prior to surgery, PG was not left with any physical
educational materials but was informed additional education would be provided after surgery
and throughout his stay at the hospital. Nutritional monitoring and evaluation proceeding
forward after the CABG surgery included any new or changed medical conditions and planned
treatments, medical and nutritional recovery from surgery, nutrition-related lab trends and
assessing education readiness. A study examining the nutrition knowledge and attitudes of
cardiac patients just prior to meeting with their cardiologists found that although perceived
importance of nutrition knowledge and treatment in cardiac disease was very high, actual
knowledge was significantly less, suggesting the need for routine and frequent formal nutrition
education counseling from a dietitian (Plous et al., 1995).
The CABG surgery took place early in the morning on Thursday, February 12th and from
the surgery notes, all procedures and administration of medications went as planned with the
exception of a brief intraoperative atrial fibrillation episode which was immediately resolved
with cardioversion. A chest tube was placed for fluid drainage. The surgery lasted several
hours and at its completion, PG was transferred to the ICU where he was intubated and started
on Propofol to maintain sedation. For the purposes of the surgery, PG was ordered to be NPO
after midnight the day prior to surgery and remained NPO for approximately 8 hours after
surgery. At this time, the patient was extubated per pulmonologist recommendation, weaned
off of Propofol and started back on the Cardiac AHA Heart Healthy diet without any
intermediate transition diet(s). The indication for re-initiating the Cardiac diet without
transition was that PG did not have any biting, chewing or swallowing problems that would
require a softer-textured diet; interestingly, left and right upper quadrant bowel sounds were
not present at the time of transition to oral intake. Due to the recency of PG’s operation,
sedative state and lack of need for immediate nutrition intervention at that time, PG was not
formally nutritionally assessed that day.
Nutrition Intervention: Education
On Friday, February 13, POD #1, PG remained on the ICU and was scheduled for transfer
back to the telemetry floor in the afternoon. Gastrointestinal parameters were within daily
limits, including the return of bowel sounds. PG complained of sternal pain at the incision site
and still had a chest tube in place for drainage. Medical diagnoses included acute left main
coronary artery disease treated with CABG x2 placement, improved acute coronary syndrome,
resolved atrial fibrillation with rapid ventricular response and worsened hypertension,
continued on Lisinopril. Treatment goals included achieving hemodynamic stability, restoring
blood perfusion through coronary vasculature and a stable recovery. Although PG was not
formally nutritionally assessed at this visit, laboratory values were still evaluated, consistent
with quality of care measures for the patient.
Nutrition-related labs assessed:
Lab
2/12
Hgb
11.2*
Hct
33.1
Na
139*
K
4.3*
BUN
11
GFR
98
Glucose
118*
2+
Ionized Ca
4.4*
*Indicates average value for that day
2/13
11.3
32.7
133
4.2
10
103
125*
X
Normal Range
12.5-16.3 g/dL
36.7-47.1%
136-145 mg/dL
3.5-5.1 mg/dL
6-20 mg/dL
> 90 mL/min
70-118 mg/dL
4.64-5.28 mg/dL
This visit was an additional nutrition intervention and educational opportunity for PG
but more importantly for his wife and son who were also present. PG’s wife expressed her
gratitude multiple times for the nutritional attention to her husband’s care and was extremely
receptive of the information throughout the education. It was at this time the more complete
food and nutrition-related history described above was obtained. A handout outlining key
components of the TLC diet served as the structure of the education, providing a more in-depth
review for PG from the first visit and new information for his wife. The thorough explanation
and review of the handout allowed PG’s wife to ask many questions, provide current dietary
habits and gain a detailed understanding of the foods recommended and not recommended on
the TLC diet. At the conclusion of the education, a follow up assessment date was established
for the coming Monday. As this was Friday, and the patient would not be seen by a dietitian
over the weekend, monitoring and evaluation efforts were to be retrospective and acted upon
Monday at the next assessment. These parameters included nutrition-related laboratory
values, any significant weight changes, new or changed medical treatments and assessing
education readiness and retained knowledge regarding the TLC diet.
On the weekend of February 14-February 15th, which were POD # 2 and 3, PG remained
on the telemetry floor and was monitored for any aberrant cardiac activity or post-operative
complications. Over the course of those two days, PG’s ongoing medical conditions including
CAD, acute coronary syndrome, and atrial fibrillation had significantly stabilized, improved or
resolved. Administration of Lopressor and Lisinopril continued to treat the ongoing and even
noted ‘worsened’ hypertension. He continued on the cardiac diet which was still meeting 100%
of his estimated energy needs and approximately 77% of his estimated protein needs due to
the elevated estimated protein calculation.
As before, nutrition-related laboratory values were evaluated as part of patient quality care
measures:
Nutrition-related labs assessed:
Lab
Hgb
Hct
2/14
11.7
34.1
2/15
10.6
31.5
Normal Range
12.5-16.3 g/dL
36.7-47.1%
Na
131
134
K
4.2
4.0
BUN
13
21
GFR
98
82
Glucose
102*
105*
*Indicates average value for that day
136-145 mg/dL
3.5-5.1 mg/dL
6-20 mg/dL
> 90 mL/min
70-118 mg/dL
The final cardiologist progress note was written on February 15 th and included a referral to a
cardiac rehabilitation outpatient program which is standard protocol for QVMC after a CABG
surgery. The chest tube was still in place but removal was planned for the following day.
Follow-up Nutrition Assessment
On Monday, February 16, the follow-up as well as final nutrition assessment was
conducted; upon viewing PG’s nursing notes it became clear his discharge was planned for early
afternoon that day. Given the patient’s upcoming discharge and overall medical stability, only
one point of care (POC) glucose reading was recorded, comprising the only recorded laboratory
value that day.
Nutrition-related lab value:
Lab
2/16
Glucose
118
Normal
Range
70-118 mg/dL
PG’s chest tube was removed and had begun ambulating around the telemetry patient floor to
initiate light physical activity. Just prior to the final visit, PG’s diet order was noted to be the
cardiac diet and average meal intake remained 100%. Because the nutrition interventions
provided for PG were largely educational experiences and intended for future application, it
seemed appropriate to focus his final nutrition diagnosis around a behavioral issue:
“Food and nutrition-related knowledge deficit R/T new diagnosis of acute MI, atrial fibrillation
and coronary artery disease AEB need for CABG placement and lack of prior cardiac diet
education”
This diagnosis was applicable at any point in PG’s hospital course but it seemed most fitting just
prior to discharge as he received his final cardiac diet education and reinforcement before
hopefully implementing some changes once at home. PG’s estimated energy, protein and fluid
needs were not changed from the previous assessment; it was decided these calculations still
aligned with the patient’s medical status, nutrition status and needs at the time of the
assessment. They remained as follows:
Mifflin St. Jeor: 1931 kcals (REE)
Estimated Energy Needs: 2125-2511 kcals (1.1-1.3 x MSJ)
Estimated Protein Needs: 125-146 g (1.2-1.4 g/kg BW), BW used 104.2 kg
Estimated Fluid Needs: 2125-2511 mL (1 mL/kcal)
While the estimated energy and fluid needs were likely appropriate for the patient at this time,
the elevated estimated protein needs still should have been lowered, calculated with lower
factors such as 1.1-1.3 g/kg. The rationale for continuing to recommend this elevated protein
range was the post-operative status and subsequent perceived increased protein needs for
healing purposes. Because the protein recommendations did not change throughout PG’s
hospital course, the recommendation was likely more appropriate at this assessment as
compared to the admission assessment, again given the perceived increased protein needs for
skin and muscle healing. It should be noted however that his BMI of 29.4 kg/m2 was 0.6 kg/m2
away from qualifying as obese and in that case an adjusted body weight would have been used,
lowering the estimated protein needs even with the elevated protein factors utilized. Once
again, although PG’s weight at discharge was 109 kg, a 6.5 kg ‘gain’ over his admitting weight of
102.5 kg, this was likely due to fluid gains as it is rare true weight gain occurs in the hospital
setting. For this reason, his lowest recorded weight, which was the admit weight, was used for
all calculations.
As the final nutrition intervention, an additional education was provided regarding the
four key components of the TLC diet, as was emphasized in the initial nutrition assessment
although this time in more detail. A brief and concise rationale for each component was given,
including physiological effects of each nutrient, to increase comprehension, connection to
medical condition and promote long-term retention, ultimately equipping PG for success upon
discharge. Suspected current and future problematic foods as related to the TLC such as high
fat meats and sweets were again discussed, reiterating their reason for limitation or omission
on this diet plan. PG had several questions about the incorporation of dietary fiber into his
daily diet, especially soluble fiber since this type of fiber was highlighted in the education for its
cholesterol-lowering properties. Several sources of soluble fiber were discussed that were
already in or would be probable additions to PG’s diet, these foods included apples, potatoes
(leaving the skin on), oatmeal, broccoli, oranges, bananas, flaxseed, raisin bran and kidney
beans; this information was summarized on a handout and given to the patient. Creation of a
sample meal plan was offered but PG expressed he ‘thinks he gets the food changes in the new
lifestyle’. The final part of the education was a discussion on potential behavioral and
emotional barriers to implementing dietary changes. A recent review of current literature on
the long-term diet and exercise outcomes in patients who underwent CABG surgery showed
mixed results for each area of lifestyle modification; the literature demonstrated positive
impacts of physical activity on psychosocial wellbeing and physical fitness however only
indicated short-term effectiveness on dietary and exercise-related interventions, with
diminished long-term efficacy (Coyan et al., 2014). While the reason for these study results
could be multifactorial, this does demonstrate a need for a realistic and thorough integration
plan of the proposed lifestyle changes at the time of hospitalization for surgery and at frequent
follow up sessions. Upon asking PG to identify any predicted obstacles, he could not think of
anything concrete and replied ‘I don’t know, I just know I never want to go through this again’.
Sensing that PG had received and absorbed all of the education he could at that point to be at
least initially successful, a final empowering talk was given emphasizing positive lifestyle
changes and assuring him that once a few changes were made, other aspects of his overall
health profile (hypertension, weight, long-term prognosis and prevention of cardiac event
reoccurrence) would more naturally fall into place.
DISCHARGE PLAN
At the time of his discharge, PG had received an extensive amount of nutrition
education regarding the TLC diet. Aside from the formal nutrition education he received on this
topic, some dietary education was provided in the discharge instructions from PG’s cardiologist
regarding the importance of adhering to a ‘sodium-restricted, low cholesterol-low fat diet’. He
was prescribed 8 outpatient medications: Colace, Aspirin (Ecotrin), Acetaminophen, Lipitor,
Lopressor, Pacerone, Protonix and Lisinopril. According to Brackbill and Sytsma (2004),
initiation of an antihyperlipidemic agent and provision of antihyperlipidemic education during
the hospitalization for a CABG results in greater long term patient adherence and compliance
with continuing antihyperlipidemic therapy as well as monitoring of cholesterols levels by the
patients’ primary care provider in a 5 and 12 month follow up. As a sternal precaution, PG was
advised to begin physical activity slowly and seek immediate medical attention for any detected
chest pain. Lastly of nutritional relevance, PG was also instructed to contact his doctor if he
noticed any significant or rapid weight gain.
SUMMARY
A likely combination of modifiable and non-modifiable risk factors led to an acute
exacerbation of a previously unknown chronic condition: coronary artery disease. Throughout
PG’s hospital course, medical diagnoses included acute myocardial infarction, acute coronary
syndrome, left main coronary artery disease, atrial fibrillation with rapid ventricular response
and he was admitted with unstable angina which is a primary symptom of coronary artery
disease. Treatments included a cardiac catheterization and coronary angiogram which
determined his need and eligibility for the CABG surgery. Nutritional interventions were
provided before and after surgery as well as on day of discharge, as education regarding the
recommended dietary guidelines of the TLC is important to conduct at the soonest possible
opportunity and as frequently as possible to promote comprehension and retention.
For the duration of PG’s hospital stay, he was prescribed and remained on the Cardiac
AHA Heart Healthy diet, which was an appropriate diet given its’ parallel guidelines to the TLC
diet. This diet provided an average of 1900 kcals per day which met approximately 83% of PG’s
estimated energy needs (using a median 2300 kcals to represent needs), and 50 grams of
protein per day which met approximately 38% of his estimated protein needs (130 g protein
used). As mentioned before, his BMI was just below the obese category and had an adjusted
body weight been utilized for this calculation, the estimated protein needs would have been
calculated at a much lower value. Despite this observation, PG’s protein needs were still
calculated to be higher than was medically and nutritionally indicated. Protein factors should
have been 0.8-1 grams protein/kg body weight or even 1.0-1.2 g/kg prior to surgery and
perhaps increased to 1.1-1.3 g/kg post-operatively. With the exception of his first meal after
the CABG surgery, intake at every meal during his hospitalization was 100% which confirmed his
consistently reported ‘good’ appetite. Because he was screened as a moderate nutritional risk
upon admission, PG was not seen until his third day in the hospital per dietetic department
policy. After his initial nutrition assessment, PG was visited each week day of his hospital stay
with the exception of the day of CABG operation. As evidenced by his excellent PO intake and
lack of diet order changes, no encouragement was needed for nutritional adequacy.
Encouragement was however needed for receiving education regarding the TLC diet and
conceptualizing the implementation of the recommended dietary changes into his daily meal
plan.
Another key to educational success was the establishment of a good rapport and
relationship with both PG and his wife. It was important to educate them almost equally as
they are engaged in a lifestyle together and serve as each others’ support system. While PG
was the primary recipient, his wife was and will be a key component of his success as the meal
preparer and otherwise caregiver for the short and long term period. Although the information
was new, both PG and his wife were incredibly receptive to the proposed dietary and lifestyle
changes, especially his wife. At multiple points within the joint education, she expressed her
gratitude for the education and personalized suggestions made, based on the lifestyle
information she and PG had shared. With each education, recommendations were increasingly
tailored to PG’s current and hopefully future diet as more about his lifestyle was learned. At
the conclusion of the joint and final nutrition intervention and education sessions, both PG and
his wife verbalized their motivation and readiness to incorporate the proposed guidelines into
cooking and consuming meals. They both displayed good comprehension and verbalized their
understanding by asking numerous questions, broad and specific which demonstrated their
application of the concepts to their own lives.
Reflecting on PG’s experience at QVMC, appropriate nutritional interventions were
provided for his primary diagnosis of coronary artery disease and subsequent CABG placement.
While his treatment was by great majority medical, the nutrition interventions PG received
played an essential supporting role in his immediate success and overall health prognosis. As a
vital part of PG’s interdisciplinary health care team, the role of the dietitian in providing him
medical nutrition therapy was well-recognized by his primary health care team in addition to his
wife and most importantly, himself. Equipped with the resources for nutritional success and
armed with knowledge and motivation, PG has all of the tools he needs to pave a long and
smooth path toward longevity and health. His road to recovery is solely in his hands now;
compliance with medical and nutritional recommendations will assure him a prosperous future
in health.
REFERENCES
Academy of Nutrition and Dietetics. (2015). Coronary Artery Bypass Graft (CABG) Nutrition Therapy,
Nutrition Assessment in Clients with Cardiovascular Disease.
Berthiaume, J.M., Young, M.E., Chen, X., McElfresh, T.A., Yu, X. & Chandler, M.P. (2012). Normalizing the
metabolic phenotype after myocardial infarction; impact of subchronic high fat feeding. Journal
of Molecular and Cellular Cardiology, 53(1), 125-133. doi: 10.1016.j.yjmcc.2012.04.005
Bilal, R.H. & Lange, R.A. (April 4, 2014). Coronary Artery Bypass Grafting. Retrieved from:
http://emedicine.medscape.com/article/1893992-overview
Brackbill, M.L. & Sytsma, C. (2004). Secondary prevention of hyperlipidemia after coronary artery bypass
graft: from acute care to primary care. American Journal of Critical Care, 13(15), 411-415.
Retrieved from: http://ajcc.aacnjournals.org/content/13/5/411.long
Coyan, G.N., Reeder, K.M. & McDowell, A.V. (1995). Nutrition Knowledge and Attitudes of Cardiac
Patients. The Physician and Sports Medicine, 42(2), 119-129. doi: 10.3810/psm.2014.05.2064
Crowe, J.C. & Pronsky, Z.M. (2012). Food-Medication Interactions (17th ed.). Birchrunville, PA: FoodMedication Interactions.
Green, R.S., Edwards, J., Sabri, E. & Ferguson, D. (2012). Evaluation of the incidence, risk factors, and
impact on patient outcomes of postintubation hemodynamic instability. Canadian Journal of
Emergency Medicine, 14(2), 74-82. Retrieved from: http://www.cjem-online.ca/v14/n02/p74
Kavya, G. & ThulasiBai, V. (2012). Abnormality diagnosis in ECG signal using Daubechies wavelet.
Biomedical Engineering and Informatics, 418-421. doi: 10.1109/BMEI.2012.6512962
Nelms, M., Sucher, K.P., Lacey, K., & Long, Roth, S. (2011). Disease of the Cardiovascular System. In T.
Pujot, J. Tucker & J. Barnes. (Eds.), Nutrition Therapy & Pathophysiology (284-320). Belmont, CA:
Wadsworth
Plous, S., Chesne, R.B. & McDowell, A.V. (1995). Nutrition Knowledge and Attitudes of Cardiac Patients.
Journal of the American Dietetic Association, 95(4), 442-446. Retrieved from:
http://www.andjrnl.org/article/S0002-8223(95)00119-0/pdf
Pollehn, T., Brady, W.J., Perron, A.D. & Morris, F. (2002). The electrocardiogram differential diagnosis of
ST segment depression. Emergency Medicine Journal, 19(2): 129-135. doi:10.1136/emj.12.2.129
Puaschitz, N.G., Strand, E., Norekval, T.M., Dierkes, J., Dahl, L., Svingen, G.F.T., Assmus, J., SchartumHansen, H., Oyen, J., Pedersen, E.K.R., Drevon, C.A., Tell, G.S. & Nygard, O. (2015). Dietary Intake
of Saturated Fat is Not Associated with Risk of Coronary Events or Mortality in Patients with
Established Coronary Artery Disease. Journal of Nutrition, 145(2), 299-305. doi:
10.3945/jn.114.203505
Tietjen, I., Hovingh, G.K., Singaraja, R., Radomski, C., McEwen, J., Chan, E., Mattice, M., Legendre, A.,
Kastelein, J.J.P. & Hayden, M.R. (2012). Increased risk of coronary artery disease in Caucasians
with extremely low HDL cholesterol due to mutations in ABCA1, APOA1 and LCAT. Biochimica et
Biophysica Acta (BBA) – Molecular and Cell Biology of Lipids, 1821(3), 416-424. doi:
10.1016/j.bbalip.2011.08.006
Appendix A
Laboratory Value Summary
Lab
Value
Normal Range
2/9
15.8
46.5
135
3.5
16
82
5.2
X
X
X
2/10
14.4
42.0
137
3.7
14
98
X
151
79
28
2/11
13.7
40.1
132
3.8
14
93
3.8
X
X
X
2/12
11.2*
33.1*
139*
4.3*
11
98
X
X
X
X
Total Cholesterol
X
Glucose
90
Hemoglobin A1C
X
Troponin I
0.72*
Ionized Ca2+
X
*Indicates average value for that day
137
87
5.5
0.97
X
X
94.5*
X
0.65
X
X
118*
X
X
4.4*
Hgb
Hct
Na
K
BUN
GFR
Albumin
Triglycerides
LDL Cholesterol
HDL Cholesterol
Lab
2/13
Hgb
11.3
Hct
32.7
Na
133
K
4.2
BUN
10
GFR
103
Glucose
125*
*Indicates average value for that day
Value
12.5-16.3 g/dL
36.7-47.1%
136-145 mg/dL
3.5-5.1 mg/dL
6-20 mg/dL
> 90 mL/min
3.5-5.0 g/dL
< 150 mg/dL
< 100 mg/dL
40-59 mg/dL (normal)
> 60 mg/dL cardioprotective
< 200 mg/dL
70-118 mg/dL
4-5.9%
< 0.04 ng/mL
4.64-5.28 mg/dL
Normal Range
2/14
2/15
2/16
11.7
10.6
X
12.5-16.3 g/dL
34.1
31.5
X
36.7-47.1%
131
134
X
136-145 mg/dL
4.2
4.0
X
3.5-5.1 mg/dL
13
21
X
6-20 mg/dL
98
82
X
> 90 mL/min
102*
105*
118
70-118 mg/dL
From 2/13-2/16, albumin, lipid panel, troponin I and ionized calcium were not measured
Appendix B
Medication Summary
Medication
Start Date
Stop Date
Function
Amiodarone HCl
Route of
Administration
IV/PO
2/13
2/14
2/14
2/16
Antiarrhythmic
Diltiazem
IV
2/9
2/10
Heparin sodium
IV
STK-MED Inj.
IV
2/10
2/12
Antiangina,
antihypertensive
Anticoagulant
2/9
2/10
2/12
2/13
2/9
2/10
2/13
2/16
Sodium replacement
2/9
2/11
2/10
2/13
2/13
Discharge
2/9
2/11
2/12
2/13
2/16
Antihypertensive,
antiangina, CHF
treatment, MI
treatment
Sodium chloride
Insulin (Humulin)
Metroprolol
(Lopressor)
Subcutaneous
injection
PO
IV Inj.
Fast-acting insulin
Docusate sodium
PO
2/13
Discharge
2/16
Stool softener, laxative
Aspirin
PO
2/10
2/13
Discharge
2/10
2/16
To prevent CVA or MI,
platelet aggregation
inhibitor
Potential Nutrition
Implications
Avoid grapefruit/related
citrus, anorexia, N/V,
constipation
Avoid natural licorice
Abdominal pain, GI
bleed, constipation
None significant
Hypoglycemia,
↓serum/urinary glucose
Recommended ↓
dietary Na & kcal, ↓in
BP w/possible
hypotension, avoid
natural licorice
(↑[cortisol], ↑Na
reabsorption, water
retention, K excretion
and BP)
High fiber w/1500-2000
mL fluid to prevent
constipation, altered int
abs of water &
electrolytes
N/V, dyspepsia, black
tarry stools, limit
caffeine, limit foods that
Lisinopril
PO
2/10
2/13
Discharge
2/12
2/16
ACE inhibitor,
antihypertensive, acute
MI adjunct
Pantoprazole sodium
PO
2/13
Discharge
2/16
Anti-GERD
Multivitamins
Nitroglycerin
PO
Topical
STK-MED Inj.
Subcut inj.
Anticoagulation
None significant
Fentanyl citrate
STK-MED Inj.
2/16
2/9
2/12
2/12
2/9
2/10
2/10
2/12
Repletion
Antiangina
Enoxaparin sodium
2/13
2/9
2/10
2/12
2/9
2/10
2/10
2/12
affect coagulation,
anorexia
Avoid salt subs, caution
w/ K supplement, ↑
serum K
HCTZ: ↓ serum Na, Cl,
K, ↑ glc (urinary
excretion)
May ↓abs of Fe, B12,
↓gastric acid secretion,
↑gastric pH, diarrhea
Mixture unknown
None significant
Analgesic
Midazolam HCl
STK-MED Inj.
2/10
2/12
2/10
2/12
Anesthesia adjunct
Chlorhexidine
gluconate
Magnesium sulfate
Cefazolin sodium
Oral rinse
2/11
2/12
2/12
2/12
2/11
2/12
2/12
2/12
EENT anti-infection
Dry mouth, dyspepsia,
N/V, abdominal pain,
C/D
↓wt, ↑app, limit
caffeine to < 400-500
mg/day
None significant
Magnesium sulfate
Antibiotic
↑serum Mg2+
None significant
2/12
2/12
Alkalinizing agent
2/12
2/12
Increases cardiac
contractility
Belching, caution
w/HTN, take Fe suppl
separately, caution
w/Ca suppl
None significant
Sodium bicarbonate
STK-MED Inj.
STK-MED IV Inj.
IV
STK-MED Inj.
Dobutamine HCl
STK-MED Inj.
Propofol
IV Inj.
2/12
2/12
Anesthesia, sedative
Protamine sulfate
Calcium chloride
STK-MED Inj.
STK-MED Inj.
2/12
2/12
2/12
2/12
Antiheparin agent
Calcium replacement
Morphine sulfate
IV
2/12
2/12
Analgesic
Famotidine
IV Inj.
2/12
2/13
Antiulcer, Anti-GERD,
Antisecretory
Ibuprofen
PO
2/13
2/16
Analgesic, NSAID
Atorvastatin
PO
2/10
2/13
Discharge
2/12
2/16
HMG-CoA Reductase
Inhibitor
Clopidogrel
PO
2/9
2/9
Use >72 hr low fat diet
(1.1 kcal/mL),
hypotension,
↑triglycerides, ↑chol
Possible drop in BP
Take separate from
large amounts of high
fiber, oxalate or phytate
foods, vit D ↑ Ca abs
Dry mouth, ↓gastric
motility, N/V, C/D
Bland diet may be rec.,
↓Fe & Vit B12 abs, Mg
↓ drug abs, ↓gastric
acid secretions,
↑gastric pH
Caution w/GI irritants,
limit caffeine to ↓GI
effects, ↓appetite, N/V,
dyspepsia, abdominal
pain
Caution
w/grapefruit/related
citrus, ↓serum chol, TG,
LDL, VLDL, ↑ HDL
Food significantly ↑
bioavailability,
dyspepsia, abdominal
pain, GI bleeding
Acute coronary
syndrome treatment,
prevention of repeat
MI, CVA or Vascular
event, platelet
aggregation inhibitor
Crowe, J.C. and Pronsky, Z.M. (2012). Food-Medication Interactions (17th ed.). Birchrunville, PA: Food-Medication Interactions.
http://www.rxlist.com/dobutamine-drug/side-effects-interactions.htm
http://www.rxlist.com/protamine-drug/side-effects-interactions.htm