Heart Failure: A Case Study
Michelle Lane
University of San Francisco
Based on the information presented, what do you think the Chest X-ray would show and why? Describe the pathophysiological changes in the heart that occur as a result of heart failure. Can other factors come into play with the development of heart failure?
Mrs. Smith is probably presenting with acute or sub acute left sided mild to moderate congestive heart failure (CHF) ( American Heart Association, 2016 ). The Chest X-ray would most likely show cardiomegaly, cephalization of blood vessels, increased interstitial markings and pleural effusion. Because Mrs. Smith presents with fatigue and dyspnea on exertion, she is probably retaining excess fluid related to decreased cardiac output which is affecting perfusion to her muscles, especially the legs and respiratory accessory muscles (Figueroa & Peters, 2006).
CHF involves both the inability of the heart muscle to maintain adequate oxygen delivery to the body (structural abnormality), and a cardiovascular (systemic) response that is attempting to compensate for poor perfusion by activation of the renin-angiotensin system. When the renin-angiotensin system is activated, preload (volume of blood entering the left ventricle) is increased by retention of sodium and water. This leads to increased vasoconstriction and increased afterload (impedance of blood flow from the left ventricle [LV]), and adds to contractility. Initially this is a good compensatory response, but if prolonged it will result in the loss of myocytes and extracellular matrix (Figueroa & Peters, 2006). The myocardium undergoes remodeling (molecular, cellular and interstitial changes) which manifests as change in size, shape and function of the heart muscle. As myocytes stretch, local norepinephrine activity and angiotensin and endothelin release are increased. The end result is additional deterioration in cardiac performance and increased neurohormonal activation. Increased activation of aldosterone and cytokines may also stimulate collagen synthesis, leading to fibrosis and remodeling of the extracellular matrix. (Cohn, Ferrari & Sharpe, 2000).
A further result of remodeling and dilation is damage to the kidneys, muscles, and blood vessels. Remodeling also results in additional cardiac decompensation from complications including mitral regurgitation and cardiac arrhythmias from atrial remodeling.
This process has detrimental effects on the functioning of the lungs. Elevated preload leads to increased pulmonary artery pressures. With the initial pressure increase, the pulmonary capillaries compensate by enlarging their capacity to accommodate the increased volume. As pressure continues to increase however, volume is diverted from the alveoli to the interstitium and fluid forms in the interlobular septae. With continued sodium retention, peripheral edema and pleural effusion develop (Figueroa & Peters, 2006).
Describe what happens when someone suffers from dilated cardiomyopathy.
According to McCance & Huether (2014), the cardiomyopathies are a group of myocardial diseases distinguished by their tissue characteristics, genomics and hemodynamic effects. Dilated cardiomyopathy (DCM) is one of four types and is characterized by diminished myocardial contractility. Cardiomyopathies are myocardial disorders in the absence of definite disease able to cause pathology (Sisakian, 2014). DCM is the most common cardiomyopathy, comprising approximately 60% of all cardiomyopathies. It is characterized by LV dilation and systolic dysfunction and, in the majority of cases, no definite cause is found. DCM is considered to be either primary (genetic, mixed or predominantly familial nongenetic, or acquired) or secondary (inflammatory, autoimmune, or thyrotoxic) and is diagnosed in association with recognized cardiovascular disease. In the majority of cases no definite cause is found (Sisakian, 2014). However, in the last several years more attention has been given to takotsubo (stress) cardiomyopathy. First described in 1990, this disease derives its name from the Japanese word takotsubo (“octopus pot”) describing the characteristic ballooning of the left ventricular apex. Generally recognized as a benign disorder, the disease is characterized by transient systolic and diastolic LV dysfunction with a variety of wall-motion abnormalities. It predominantly affects elderly women and is often preceded by an emotional or physical trigger, but the condition has also been reported with no evident trigger. The clinical presentation is often similar to that of acute coronary syndrome. Although the cause of takotsubo cardiomyopathy is unknown, the role of the brain–heart axis in the pathogenesis of the disease has been described (Templin et al., 2015, p. 930).
The most common symptoms of DCM are dyspnea and fatigue. The patient may experience pulmonary congestion, palpitations, emboli and non specific chest pain. Clinically the patient will usually manifest hypotension and possibly extra heart sounds and/or cardiac murmur (McCance & Huether, 2014).
What current evidence based practice and standards of care are there for heart
failure?
The primary goals of initial treatment in acute heart failure (AHF) are hemodynamic stabilization of the patient, alleviation of symptoms, reduction of congestion, and prevention of further organ damage (Teichman, Maisel & Storrow, 2015). According to The American College of Cardiology Foundation/American Heart Association Guidelines (Yancy et al., 2013), all patients presenting with dyspnea should be evaluated for heart failure and all should undergo a medical history, physical exam, lab testing, chest radiograph (CXR) and a 12-lead electrocardiogram (ECG). Recommended labs include a complete blood count, urinalysis, serum electrolytes (with calcium and magnesium), blood urea nitrogen, serum creatinine, glucose, fasting lipid profile, liver function tests, and thyroid-stimulating hormone. CXR can identify cardiomegaly, pulmonary congestion and alternate causes of the patient’s symptoms. A two-dimensional echocardiogram with Doppler (2-D echo) is recommended to assess ventricular function, wall motion and valve function. Measurement of brain natriuretic peptide or N-terminal probrain natriuretic peptide levels can support clinical decision regarding diagnosis. Measurement of other biomarkers of myocardial injury or fibrosis should be considered. Biomarkers are useful in HF management as they may reflect pathophysiological changes indicative of HF.
Pharmacological treatment includes loop diuretics as a primary method to reduce fluid imbalance. The American College of Cardiology Foundation/American Heart Association guidelines (2013) recommend that if symptomatic hypotension is absent, use of intravenous nitroglycerin, nitroprusside, or nesiritide may be considered an adjuvant to diuretic therapy for relief of dyspnea in patients admitted with AHF. Current evidence supports the use of ACE inhibitors and beta-blocker therapy to impede LV remodeling and low left ventricular ejection fraction (LVEF).
According to Teichman et al., (2015), the management of AHF remains clinically challenging due to patients co-morbidities, and effects of medications and myocardial changes due to the HF itself. Despite advancements in clinical knowledge, an incomplete understanding in the processes of HF still exists. “The lack of evidence-based guidelines for interventions that improve morbidity and mortality in AHF reflects the lack of progress in the development of such therapies despite extensive efforts. Clinical experience and judgment in this setting is key to identifying those patients at higher risk and then tailoring available therapies as best as possible” (p.15).
What would be appropriate for managing Mrs. Smith’s condition?
I believe Mrs. Smith should be admitted for observation. She should be on bed rest with legs elevated above heart level. Oxygen flow via nasal cannula should be at 6 liters to maintain oxygen saturation between 94-98%. Normal CBC could rule out differential diagnosis of pneumonia. However COPD would increase intrathoracic pressure contributing to a decrease in right atrial pressure and thus a decrease in ventricular filling. Mrs. Smith should be on a telemetry monitor. We do not know if her “non-specific Q wave changes” are pathological or due to lead placement error, but it is possible that she has had a previous myocardial infarct.
What pharmacological interventions would be appropriate for Mrs. Smith? Why? What would influence choice of these interventions in her case?
Intravenous nitroglycerin would help to alleviate dyspnea while lowering her blood pressure. According to Teichman et al. (2015) “low doses of nitrodilators have been shown to improve some aspects of dyspnea shortly after administration, and early treatment with high-dose nitrodilators was found to improve arterial oxygenation and possibly lower the risk of myocardial infarction” (p. 18). Mrs. Smiths BNP is slightly elevated, indicating the need to terminate the renin-angiotensin system with an ACE inhibitor, thus reducing afterload. The ventricles, in response to increased pressure and volume load produce BNP, it functions to counteract the effect of renin-angiotensin by causing vasodilation, diuresis, natriuresis and decreased smooth muscle proliferation. A beta blocker would be used to reduce the catecholamine surges, and a diuretic would reduce preload, as well as dyspnea caused by water retention (Figueroa & Peters, 2006).
Heart failure can be a chronic condition. What health promotion practices would you address with Mrs. Smith?
Because heart failure can be so complex, Mrs. Smith needs a personalized treatment plan that takes her physiological characteristics, resources, motivation and support system into account. She requires education regarding her disease, pharmacologic therapy and need for lifestyle changes. A teach back method should be used to assure patient understanding and increase her chance of compliance.
Mrs. Smith must understand the effects of her medications, and the need to avoid grapefruit juice and caffeine products. The importance of diet including adjustment in sodium intake, and the importance of regular physical activity for weight loss and maintenance should be explained. She also needs to understand the importance of controlling her blood pressure and the possible triggers (stress) to increased BP. She should be warned about the risks of tobacco and alcohol consumption, and instructed on timely follow up with her healthcare team. Mrs. Smith also needs to receive her influenza and pneumococcal vaccines to avoid significant illness and further stress on her system. Family members should be included in her health education plan.
What techniques and medications would you employ in a larger similar population with heart failure?
I would hold community education classes regarding the diverse causes of heart failure, stressing the causes and exacerbating risk factors that could possibly be controlled by the individual such as hypertension, coronary artery disease, medications, alcohol, and nutritional disorders. I would explain that Hispanic and African Americans have higher rates of CHF, due to higher rates of risk factors for HTN, diabetes and obesity, and that it affects more men than women and its prevalence increases with age ( Bui, Horwich & Fonarow, 2011). I would emphasize healthy nutrition and exercise as well as compliance with medication and follow up appointments. I would explain symptoms and clinical manifestations of heart failure encouraging immediate physician follow up if symptoms worsen. I would provide resources to websites regarding the disease of heart failure, as well as referral to cardiac rehab programs.
What methods would you use to assess quality improvement in this disease?
Challenges exist in measuring outcomes in patients with heart failure because symptoms vary greatly, as evidenced by the New York Heart Association (NYHA])classes I through IV, and treatment varies according to symptoms and their severity. However, because admission and readmission for HF remains high, as a CNL I would emphasize the importance of the appropriate diagnosis of HF by skilled clinicians, proper administration of polypharmacy, effective patient education about HF and preventive strategies, and counseling of patients about their care and prognosis (Krumholz et al, 2000).
To begin, I would meet with the interdisciplinary team to define measurable goals that we would like to attain. I would initiate improvement tools that promote evidence based care regarding identifying patients with heart failure, developing a plan of care at admission, medication safety, team communication and discharge/follow-up care. I would collect data reflecting the volume of admissions/readmission and length of stay.
Next I would assess the process of care to determine if physicians follow practice guidelines and review patient charts to determine whether they received diagnostic tests and therapies that have been shown to increase survival or improve health-related quality of life (such as reduced symptoms of breathlessness and fatigue) as well as vaccinations against influenza and pneumonia. Anticoagulation for atrial fibrillation, evaluation of ischemia, and treatment of hyperlipidemia for coronary artery disease are also important indicators of quality of care (Krumholz et al., 2000). I would take baseline measurements of patients upon admission and then have a 3 and 6 month follow up with a predetermined number of patients by interview to assess symptoms and determine which quality of care measures apply, and to determine improvement or deterioration in the patients functional capacity.
I would suggest a program be put into place to initiate ongoing assessment and improvement criteria for HF. Other outcome measures could include mortality, readmission, resource consumption, health status, and satisfaction with care.
References
American Heart Association (2016 ). New York Heart Association Classification of
Congestive Heart Failure.
http://www.heart.org/HEARTORG/Conditions/HeartFailure/AboutHeartFailure/
Classes-of-Heart-Failure_UCM_306328_Article.jsp#.V_BSpjuambA
Bui, A., Horwich, T. & Fonarow, G. (2011). Epidemiology and risk profile of heart
failure.
Nature Reviews Cardiology, 8 (1), 30-41. doi:10.1038/nrcardio.2010.165
Cohn, J., Ferrari, R. & Sharpe, N. (2000). Cardiac remodeling-concepts and clinical
implications:
A consensus paper from an international forum on cardiac remodeling. Journal ofthe
American College of Cardiology, 35 (3), 569-582. http://dx.doi.org/10.1016/S0735-
1097(99)00630-0
Figueroa, M. & Peters, J. (2006). Congestive heart failure: Diagnosis, pathophysiology,
therapy, and implications for respiratory care. Respiratory Care, 51(4), 403– 412.
Krumholz, H., Baker, D., Ashton, C., Dunbar, S., Friesinger, G., Havranek, E.,…Spertus, J.
(2000). Evaluating quality of care for patients with heart failure. Circulation, 101
(12), 1-19. doi: http://dx.doi.org/10.1161/01.CIR.101.12.e122
McCance, K. &Huether, S. (2014). Pathophysiology: The biologic basis for disease in
adults and children. Missouri: Mosby
Sisakian, H. (2014). Cardiomyopathies: Evolution of pathogenesis concepts and
potential for new therapies. World Journal of Cardiology, 6(6), 478-494.
doi:10.4330/wjc.v6.i6.478
Teichman, S., Maisel, A. & Storrow, A., ( 2015). Challenges in acute heart failure clinical
management: Optimizing care despite incomplete evidence and imperfect drugs.
Critical Pathways in Cardiology: A Journal of Evidence-Based Medicine, 14 (1), 12-
24. doi:10.1097/HPC.0000000000000031
Templin, C., Ghadri, J.R., Diekmann, J., Napp, L.C., Bataiosu, D.R., Jaguszewski, M., …&
Luscher, T.F. (2015). Clinical features and outcomes of takotsubu (stress)
cardiomyopathy. New England Journal of Medicine, 373 (10), 929-938.
Yancy, C., Jessup, M., Bozkurt, B., Butler, J., Casey, D., Drazner, M….& Wilkoff, B. (2013).
2013 ACCF/AHA guideline for the management of heart failure.
Journal of the American College of Cardiology, 62 (16), e147-e239.
doi:10.1016/j.jacc.2013.05.019