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Managing the Effects of Cardiac Cachexia Heather Carlson, ANP-BC, ACHPN Ƒ Constance M

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Managing the Effects of Cardiac Cachexia Heather Carlson, ANP-BC, ACHPN Ƒ Constance M Symptom Management Series 2.3 ANCC Contact Hours Managing the Effects of Cardiac Cachexia Heather Carlson, ANP-BC, ACHPN ƒ Constance M. Dahlin, MSN, ANP-BC, ACHPN, FPCN, FAAN Although cachexia is common in cancer, it is poorly DEFINITION OF SYMPTOM understood in noncancer diagnoses. This article reviews Cardiac cachexia is defined as a complex metabolic dis- cancer cachexia in cardiac disease. The definition, pathophysiology, and assessment specific to cardiac order involving progressive weight loss accompanied by disease are delineated. Diagnostic workup is discussed. muscle wasting, fatigue, and weakness. The associated Finally, pharmacological and nonpharmacological weight loss involves both the loss of lean muscle mass as interventions are offered. well as fat and bone. Skeletal muscle wasting and loss of body weight precede loss of cardiac mass and are late signs 2,3 KEY WORDS in heart failure. Once cachexia occurs, it is impossible to reverse the muscle wasting by increasing caloric intake cachexia, cardiac cachexia, heart failure alone.4,5 Primary cachexia refers to ‘‘unintentional weight loss of more than 5% premorbid weight in a 6-month period ardiac cachexia is a symptom sequela of advanced with concurrent body mass index of less than 20 kg/m2 heart failure that was identified thousands of years in patients younger than 65 years or less than 22 kg/m2 Cago. Around 400 BC, Hippocrates first described in patients older than 65 years with albumin level of less cardiac cachexia in Greek citizens suffering from a condi- than 3.5 g/L, decreased total protein levels, anemia, elevated tion in which ‘‘the flesh is consumed and becomes water, triglycerides, elevated glucose, and elevated lactic acid.’’5-7 Ithe shoulders, clavicles, chest, and thighs melt awayI 1 Secondary cachexia is a result of unintentional weight loss the illness is fatal.’’ Although science has advanced since subsequent to altered anabolic states from noncancer con- Hippocrates’ observations, the occurrence of cardiac ca- ditions (eg, infections, chronic renal failure, and chronic chexia still remains poorly understood. heart failure).5 This phenomenon occurs in both chronic right-sided heart failure and in severe advanced stages of CASE STUDY heart failure. It has also been suggested that cachexia can develop progressively through phases of precachexia to re- Mr S. is a 76-year-old man with class III New York Heart fractory cachexia.6,8,9 Common symptoms include anorexia, Association congestive heart failure (CHF) who was recently nausea, constipation, early satiety, alteration in taste, dys- hospitalized for a CHF flare with resting dyspnea occurring pnea while eating, depression, weakness, and generalized and worsening with minimal activity. During an outpatient deconditioning.7,8 These symptoms promote further weight visit with his advanced practice registered nurse (APRN), loss, and cachexia is typically irreversible with just diet and he explained that overall he felt weak and tired. Mrs S. nutrition modifications.6 commented that Mr S. was too skinny. Mr S. noticed that his clothes felt a bit too loose. He had little interest in food or eating. He knew that he should eat, but his taste changes IMPORTANCE resulted in lack of desire. When his wife was able to coax With the aging population resulting in a higher percentage him to eat, he felt full after only a few bites. During eating, of chronic illness, the prevalence of heart failure is propor- Mr S. experienced worsened shortness of breath resulting tionally increasing. Early diagnosis of cardiac cachexia, in longer mealtimes. followed by comprehensive, multidisciplinary management, will improve quality of life. Treatment promotes restoration of body balance, maintains function, preserves safety, and Heather Carlson, ANP-BC, ACHPN, is a palliative nurse practitioner at increases survival. Palliative Care Service, North Shore Medical Center, Salem, Massachusetts. Constance Dahlin, MSN, ANP-BC, ACHPN, FPCN, FAAN, is a palliative nurse practitioner at Palliative Care Service, North Shore Medical Center, Salem, Massachusetts, and director of Professional Practice at Hospice and INCIDENCE Palliative Nurses Association, Pittsburgh, Pennsylvania. Cachexia, common in patients with advanced cancer and Address correspondence to Constance M. Dahlin, MSN, ANP-BC, ACHPN, FPCN, FAAN, Hospice and Palliative Nurses Association, One Penn Center end-stage HIV/AIDS, affects patients with other progres- West, Suite 425, Pittsburgh, PA 15276-0100 ([email protected]). sive life-limiting illnesses such chronic obstructive pulmo- The authors have no conflicts of interest to disclose. nary disease, CHF, end-stage heart disease, and chronic 3 DOI: 10.1097/NJH.0000000000000039 kidney disease. It is estimated that more than 80% of Journal of Hospice & Palliative Nursing www.jhpn.com 15 Symptom Management Series patients with advanced, noncancer illnesses experience Tumor necrosis factor " decreases albumin production cachexia. With higher frequency in the elderly, it will become in the liver. Decreased protein synthesis produces an ac- more prevalent as increased numbers of patients develop celeration of lean tissue mass loss.10 Elderly patients with heart failure.5 In 2008, 5.7 million Americans older than cardiac cachexia can develop fat malabsorption and GI 65 years were hospitalized with heart failure.10 Statistics in- protein loss.11 Again, a higher resting metabolic state in dicate that approximately 10% to 15% of patients with ad- patients with advanced CHF requires the consumption of vanced CHF develop severe progressive weight loss, and more calories just to accommodate respiratory effort. Pa- two-thirds of patients with CHF develop muscle wasting.10 tients with CHF have been found to have micronutrient 10 Studies have shown that approximately 10% of patients deficiencies of folate and vitamins C, E, and B12. Inflam- with either class III or IV New York Heart Association heart matory cytokines result in free radical production. However, failure develop cachexia annually.7 Patients who develop antioxidants and repletion of vitamins C and E have been cardiac cachexia have a 50% mortality rate in 18 months found to have the ability to suppress or decompose the from time of their diagnosis.10 Because it becomes more elevated production of free radicals.11 pronounced in end-stage disease, cachexia has been found Finally, subsequent neurohormonal abnormalities from to be an important predictor of reduced survival in heart fail- impaired cardiac function lead to the development of car- ure patients.6,7 diac cachexia. Given the complex systems involved, cachexia can occur shortly after the presentation of initial heart fail- PATHOPHYSIOLOGY ure symptoms present or 3 to 6 months thereafter. The body releases angiotensin II, which signals water and sodium Cardiac cachexia is not well understood. It is hypothesized retention in the kidneys as well increase as aldosterone that multiple pathways, including immunological, meta- secretion. These hormones release norepinephrine, which bolic, and neurohormonal processes, are intricately in- decreases energy stores, impairing the autonomic reflex re- volved in the activation of the complex mechanisms that sponse.10 Another result of cardiac cachexia is impaired result in cardiac cachexia. The precise etiology of the im- thyroid function, which affects cardiac contractility. This mune response activation within CHF has not been identi- is caused by lower nutritional and caloric intake and low fied. Congestive heart failure alters gastrointestinal (GI) levels of testosterone in males. Of note, in a study about permeability, resulting in bowel wall edema, reducing in- heart failure, low levels of testosterone were found in ap- testinal absorption. Bacteria and endotoxins are allowed to proximately 30% of men older than 65 years.10 subsequently stimulate inflammatory cytokine activation. These changes in the GI tract also result in systemic inflam- mation.7,10 It is theorized that hypoxia and the failing heart muscle are responsible for the release of inflammatory cyto- kines, specifically tumor necrosis factor ". Tumor necrosis factor " results in apoptosis or cellular death. This produces profound anorexia and exercise intolerance with simulta- neous reduction in peripheral blood flow.7,10 The metabolic process corresponds to a higher metabolic rate, further necessitating increased caloric requirements in the presence of preexisting anorexia and fatigue. This response can occur in either the catabolic state with the re- lease of the hormones leptin and growth hormone or the anabolic state with the release of ghrelin by cardiac myo- cytes and cells in the stomach lining, which increases the response to tumor necrosis factor ". The imbalance of anabolic and catabolic states leads to negative balance of energy within the body.10 Specific to cachexia caused by cardiac impairment, there is an increased muscle protein breakdown that differentiates it from cachexia caused by chronic obstructive pulmonary disease or cancer, which tends to reduce muscle protein synthesis.3,10 The inflamma- tory response resulting from heart failure leads to muscle breakdown resulting in fatigue, which significantly impacts a patient’s quality of life. This cycle of cardiac cachexia is FIGURE 1. Understanding the effects of the cachexia cycle. demonstrated in Figure 1. Based on the information in Springer et al.2 16 www.jhpn.com Volume 16 & Number 1 & February 2014 Symptom Management Series UNDERSTANDING
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