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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. 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(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