ASSIGNMENT HELP | CHF Exacerbation/orthopnea

76-year-old female patient complains of weight gain, shortness of breath, peripheral edema, and abdominal swelling. She has a history of congestive heart failure and admits to not taking her diuretic, as it makes her “have to get up every couple hours to go to the bathroom.” She now has to sleep on two pillows in order to get enough air.
1-page case study analysis)
In your Case Study Analysis related to the scenario provided, explain the following
• The cardiovascular and cardiopulmonary pathophysiologic processes that result in the patient presenting these symptoms.
• Any racial/ethnic variables that may impact physiological functioning.
• How these processes interact to affect the patient.

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Reading
McCance, K. L. & Huether, S. E. (2019). Pathophysiology: The biologic basis for disease in adults and children (8th ed.). St. Louis, MO: Mosby/Elsevier.
• Chapter 32: Structure and Function of the Cardiovascular and Lymphatic Systems; Summary Review
• Chapter 33: Alterations of Cardiovascular Function (stop at Dysrhythmias); Summary Review
• Chapter 35: Structure and Function of the Pulmonary System; Summary Review
• Chapter 36: Alterations of Pulmonary Function (stop at Disorders of the chest wall and pleura); (obstructive pulmonary diseases) (stop at Pulmonary artery hypertension); Summary Review
• 4961993

J Clin Med. 2016 Jul; 5(7): 62.
Published online 2016 Jun 29. doi: 10.3390/jcm5070062
PMCID: PMC4961993
PMID: 27367736
Heart Failure: Diagnosis, Management and Utilization
Arati A. Inamdar1,2,* and Ajinkya C. Inamdar2
Salvatore De Rosa, Academic Editor
Author information Article notes Copyright and License information Disclaimer
This article has been cited by other articles in PMC.
Abstract
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1. Introduction
1.1. Background
Heart failure (HF) is a clinical syndrome caused by structural and functional defects in myocardium resulting in impairment of ventricular filling or the ejection of blood. The most common cause for HF is reduced left ventricular myocardial function; however, dysfunction of the pericardium, myocardium, endocardium, heart valves or great vessels alone or in combination is also associated with HF. Some of the major pathogenic mechanisms leading to HF are increased hemodynamic overload, ischemia-related dysfunction, ventricular remodeling, excessive neuro-humoral stimulation, abnormal myocyte calcium cycling, excessive or inadequate proliferation of the extracellular matrix, accelerated apoptosis and genetic mutations [1].
1.2. Classification of HFs

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Heart failure can be classified as predominantly left ventricular, right ventricular or biventricular based on the location of the deficit. Depending on the time of onset, HF is classified as acute or chronic. Clinically, it is typically classified into two major types based on the functional status of heart: heart failure with preserved ejection fraction (HFpEF) and heart failure with reduced ejection fraction (HFrEF). In patients with HFpEF who are mostly females and older adults, EF is usually more than 50%; the volume of the left-ventricular (LV) cavity is typically normal, but the LV wall is thickened and stiff; hence, the ratio of LV mass/end-diastolic volume is high [2]. HFpEF is further categorized as borderline HF if the EF stays between 41% and 49% and improved HF if EF is more than 40% [1]. In contrast, in patients with HFrEF, the LV cavity is typically dilated, and the ratio of LV mass/end-diastolic volume is either normal or reduced. At the cellular level, both cardiomyocyte diameter and the volume of myofibrils are higher in HFpEF than in HFrEF [1]. As far as treatment and outcome are concerned, patients with HFrEF respond favorably to the standard pharmacological treatment regimen and demonstrate better prognosis. In contrast, patients with HFpEF have not been shown to respond to standard pharmacological treatments, except for nitrates, and therefore, have a poor prognosis, especially during the decompensated phase of HF [2,3,4]. In addition, based on cardiac output, HF is also classified as high-output failure and low-output failure. High-output failure is an uncommon disorder characterized by an elevated resting cardiac index of greater than 2.5–4.0 L/min/m2 and low systemic vascular resistance. The common causes of high output failure are severe anemia, vascular shunting, hyperthyroidism and vitamin B1 deficiency. This occurs as a result of ineffective blood volume and pressure, which stimulate the sympathetic nervous system and renin-angiotensin-aldosterone system (RAAS), causing the release of antidiuretic hormone (ADH), which all together ultimately lead to ventricular enlargement, negative ventricular remodeling and HF. Low output failure is much more common than high-output failure and is characterized by insufficient forward cardiac output, particularly during times of increased metabolic demand. Left ventricular dysfunction due to large MI, right ventricular dysfunction due to an acute pulmonary embolus and biventricular dysfunction are important causes of low output failure. More recently, exercise intolerance in HFpEF is proposed to be due to a decrease in oxygen delivery to or impaired oxygen utilization by the exercising skeletal muscles. Oxygen utilization is being calculated as the arterial–venous oxygen content difference (A-VO2 Diff), rather than reduced cardiac output (CO) [5,6]. Considering the slowed down oxygen uptake kinetics in HF along with peripheral muscle function impairment, exercise rehabilitation seems to be a logical and essential factor in improving the inflammatory imbalance, relieving elevated cardiac filling pressures, restoring exercise capacity, quality of life and reducing morbidity and mortality associated with HF. Hence, exercise training, mostly high intensity as opposed to moderate, in HFpEF patients has been significantly shown to improve rate of oxygen consumption or VO2 without affecting endothelial function [7,8].
The New York Heart Association (NYHA) functional classification defines four functional classes as:
• Class I: HF does not cause limitations to physical activity; ordinary physical activity does not cause symptoms.
• Class II: HF causes slight limitations to physical activity; the patients are comfortable at rest, but ordinary physical activity results in HF symptoms.
• Class III: HF causes marked limitations of physical activity; the patients are comfortable at rest, but less than ordinary activity causes symptoms of HF.
• Class IV: HF patients are unable to carry on any physical activity without HF symptoms or have symptoms when at rest.
The American College of Cardiology/American Heart Association (ACC/AHA) staging system is defined by the following four stages:
• Stage A: High risk of heart failure, but no structural heart disease or symptoms of heart failure;
• Stage B: Structural heart disease, but no symptoms of heart failure;
• Stage C: Structural heart disease and symptoms of heart failure;
• Stage D: Refractory heart failure requiring specialized interventions.

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2. Clinical Presentation of HF
The clinical presentation of HF comprises symptoms of shortness of breath (SOB)/dyspnea (sensitivity of 84%–100%, but a specificity of 17%–34%); orthopnea/SOB on lying own (sensitivity of 22%–50% and a specificity of 74%–77%); paroxysmal nocturnal dyspnea (sensitivity 39%–41%, specificity from 80%–84%); fatigue/weakness/lethargy (due to HF-induced circulation-related abnormalities in skeletal muscles); edema, abdominal distention and right hypochondrial pain (most likely due to right-sided heart failure with sensitivity and specificity of 23% and 80%, respectively) [9,10]. Due to compensatory mechanisms, early stages of HF lack specific signs; however, late stages of HF demonstrate the following signs: tachycardia (99% specificity and 7% sensitivity); pedal edema (93% specificity and 10% sensitivity); increased jugular venous pressure (JVP) (usually > 6 cm; specificity of 92% and sensitivity of 39%), abnormal lung sounds (crackles) (specificity of 78% and sensitivity of 60%); S3 gallop (specificity of 99% and sensitivity of 13%). Other signs, such as hepatojugular reflux and ascites, are not found frequently in HF, but have a specificity of 96% and 97%, while a sensitivity of 24% and 1%, respectively [11,12]. Recent research has uncovered the microvascular dysfunction and subsequent decrease in O2 supply or mismatch with the O2 supply vs. demand in HF patients. Therapeutic strategies to improve muscle microvascular and oxidative function via exercise training, anti-inflammatory and antioxidant agents have been proposed to be essential to provide better exercise tolerance and quality of life [13].
HF has primarily been recognized as a disease of the elderly population (>60 years) and is reported to affect about 2%–3% of people in the United States. Of these include 10% of males and 8% of females. Unfortunately, these numbers are on a gradual increase due to the on-going prevalence of HF with increasing age. In the USA itself, about more than three million physician visits per year have been accounted for patients with HF as the primary health issue. In 2013, the total number of HF patients were 5.1 million, and direct costs were equal to $32 billion; and this cost is being projected to increase by about three-fold by 2030 [14]. As of 2011, the estimated lifetime cost of HF per individual patient was $110,000/year, with more than three-fourths of this cost consumed by ‘in-hospital care’ [15]. Interestingly, the five-year mortality rate for HF was reviewed to be approximately 50%, which is significantly higher than that of some cancers [16]. Among Medicare patients, 30-day all-cause, risk-standardized mortality rates for HF are 10%–12%, while 30-day, all-cause, risk-standardized readmission rates after hospital discharge are 20%–25% [17]. There is indeed a slight decrease in HF-related mortality from 2000 to 2014. The age-adjusted rate for HF-related mortality was 105.4 per 100,000 population in 2000 and reached 84.0 per 100,000 in 2014. Similarly, the percentage of in-hospital HF-related deaths declined from 42.6% in 2000 to 30% in 2014 [18]. Furthermore, although in a nursing home or long-term care facility, the percentage of deaths have been decreased from 30.1% in 2000 to 26.7% in 2014, such deaths have increased in the patients in residence and in outpatient clinics or hospice care by about 10% and 7%, respectively. Although the prognosis of other cardiac conditions, such as acute coronary syndrome (ACS), severe hypertension, valvular and congenital heart diseases, has improved over the past decade, the prevalence of HF has increased in a relatively exponential manner [18]. An increase in the prevalence of co-morbid conditions and risk factors, such as increased body mass index (BMI), metabolic syndrome, elevated apolipoprotein B/apolipoprotein A ratio and cigarette smoking, in these populations with relatively increased life expectancy may be some of the reasons behind the increased prevalence of HF [19]. Furthermore, available treatment options for HF only offer symptomatic relief and lack definitive curative treatment for the affected heart. As far as hospitalization is concerned, acute decompensated heart failure (ADHF) is the most common form of heart failure that accounts for ~80% of hospitalizations related to heart failure [19]. The common causes of ADHF include non-adherence to medication or dietary restrictions; uncontrolled hypertension; acute coronary syndrome/ischemia; dysrhythmia/arrhythmias and COPD exacerbation; alcohol intoxication or excess; thyroid conditions; pregnancy; and other iatrogenic conditions, such as postoperative fluid replacement or administration of steroids or non-steroidal anti-inflammatory drugs; all directly or indirectly leading to the progression of the underlying disease [19].
The underlying pathogenesis of HF also involves silent inflammatory and immune-regulatory responses, the activation of which still has not been completely understood. It has been proposed that in HF, excessive neuroendocrine activation leads to the activation of neuro-hormones and pro-inflammatory cytokines following an initial cardiac insult. Many of these pro-inflammatory and anti-inflammatory cytokines and their receptors, released endotoxins, adhesion molecules, nitric oxide and reactive oxygen species have been associated with various pathological aspects of HF [20,21]. The pro-inflammatory cytokines include tumor necrosis factor-α (TNF-α), sTNFR19 (soluble tumor necrosis factor receptor 1/2), soluble Fas protein, TNF-α-related apoptosis-inducing ligand (TRAIL), interleukin 6, activin A, myeloperoxidase, pentraxin-3, regulated on activation, normal T cell expressed and secreted (RANTES), C reactive protein, monocyte chemotactic protein 1 (MCP1) and macrophage inflammatory protein 1-α (MIP-1-α) [22]. Many of these inflammatory markers (such as IL-6, TNF-α, CRP) have been found to be upregulated in HF patients, especially in the ADHF phase. In light of these findings, several clinical trials have been designed, and drugs targeting inflammatory markers, nitric oxides and reactive oxidative species, such as etanercept, infliximab, glucocorticoids, statins and anti-oxidants, are being tested [21]. A newer pathological mechanism “gut hypothesis of heart failure” has been proposed. Here, HF-associated decreased CO and alteration of systemic circulation which lead to reduced intestinal perfusion and mucosal ischemia, thus causing disruption in intestinal barrier, increased gut permeability, increased bacterial translocation and increased circulating endotoxins. This in turn contributes to the elevated pro-inflammatory response reported in patients with HF. For example, the fasting plasma trimethylamine-N-oxide (TMAO) is reported to be elevated in HF patients and has recently been correlated to higher long-term mortality risk independent of other HF risk factors [23]. For this reason, several strategies have been designed to retain the normal micro-biome and maintain metabolic homeostasis in HF patients [24].
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3. Diagnosis of HF
The evaluation for HF is performed using various parameters: physical examination to determine the presence of clinical symptoms and signs, blood tests, including complete blood count, urinalysis, complete metabolic profile for levels of serum electrolytes (including calcium and magnesium), blood urea nitrogen, serum creatinine, glucose, fasting lipid profile, liver function tests and thyroid-stimulating hormone.
Other HF-specific laboratory tests (especially in patients with a high possibility of heart failure) include brain natriuretic peptide (BNP) with 70% sensitivity and 99% specificity and N-terminal proBNP (NT-proBNP) with 99% sensitivity and 85% specificity, the measurement which has been recommended both in outpatient and in the hospital settings [1]. BNP is a neuro-hormone, which is an activated form of proBNP, the 108-amino acid polypeptide precursor, stored as secretory granules in both ventricles and, to a lesser extent, in the atria. In response to volume expansion and pressure overload, proBNP is secreted into ventricles and breaks down into its two cleaved forms, the 76-peptide, biologically-inert N-terminal fragment, NT-proBNP, and the 32-peptide, biologically-active hormone BNP. NT-proBNP and BNP have clinical significance both as diagnostic and prognostic markers in the management of HF. During the diagnosis of HF, in patients presenting with acute dyspnea, BNP levels of less than 100 pg/mL have a 90% negative predictive value (NPV), and values of more than 500 pg/mL have an 81% positive predictive value (PPV) [25]. The BNP level is a strong predictor of risk of death and cardiovascular events in patients previously diagnosed with heart failure or cardiac dysfunction. It is to be remembered that elevated BNP levels have also been associated with renal failure, pulmonary embolism, pulmonary hypertension and chronic hypoxia while obese and overweight individuals have relatively lower BNP levels. Furthermore, there has been no clinically significant difference between BNP and NT-proBNP in terms of the diagnostic and prognostic values, except for the longer half-life time of NT-proBNP (72 h) as opposed to 4 h for BNP and that NT-pro-BNP levels are less affected by obesity [9,26]. A recent review by Simons et al. discussed the criteria and cut off values for the diagnosis, prognosis and treatment guidance [27]. Accordingly, single measurement of natriuretic peptides (BNP ≤ 100 pg/mL or NTproBNP ≤ 300 pg/mL) rules out HF clinically, while BNP ≥ 500 pg/mL or NTproBNP ≥ 1800 pg/mL has been proposed to have a relatively lower level of evidence in clinical settings. Nevertheless, both BNP and NT-proBNP levels aid in decisions regarding admission/ discharge and risk stratification for HF patients. Patients with BNP level of less than 200 pg/mL at admission have been associated with 2% mortality rate as opposed to 9% mortality rate seen in patients with admission BNP level of more than 200 pg/mL [28]. NT-proBNP level equal to or higher than 5000 pg/mL at admission has been shown to be associated with in-hospital mortality rate of 22.5% and longer length of stay in remaining surviving patients [29].
Biomarkers not only provide valuable information about the pathophysiology of the disease, but also shed light on the severity of ongoing disease. As far as biomarkers for HF are concerned, the National Academy of Clinical Biochemistry has set forth comparable goals in a consensus document stating that a biomarker in HF ideally enables clinicians to: (i) identify possible underlying (and potentially reversible) causes of HF; (ii) confirm the presence or absence of the HF syndrome; and (iii) estimate the severity of HF and the risk of disease progression.
Multiple biomarkers have been classified depending on their putative functional impact on cardiac myocytes and the resulting pathophysiological changes in patients with HF and include (a) myocyte stretch biomarkers; (b) myocyte necrosis biomarkers; (c) systemic inflammation biomarkers; (d) oxidative stress biomarkers; (e) extracellular matrix turnover biomarkers; (f) neuro-hormone biomarkers; and (g) biomarkers of extra-cardiac processes, such as renal function. The specific biomarkers are shown in Table 1 along with the underlying mechanisms leading to their expression in HF patients. The details of the commonly-used HF biomarkers and other emerging biomarkers are described in other review articles authored by Ahmad et al., 2012, Gaggin and Januzzi, 2012, and van Kimmenade et al., 2013 [30,31,32].
Table 1

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Rubric

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Develop a 1- to 2-page case study analysis, examing the patient symptoms presented in the case study. Be sure to address the following:

Explain both the cardiovascular and cardiopulmonary pathophysiologic processes of why the patient presents these symptoms. 28 (28%) – 30 (30%)
The response accurately and thoroughly describes the patient symptoms.

The response includes accurate, clear, and detailed reasons, with explanation for both the cardiovascular and cardiopulmonary pathophysiologic processes supported by evidence and/or research, as appropriate, to support the explanation. 25 (25%) – 27 (27%)
The response describes the patient symptoms.

The response includes accurate reasons, with explanation for both the cardiovascular and cardiopulmonary pathophysiologic processes supported by evidence and/or research, as appropriate, to support the explanation. 23 (23%) – 24 (24%)
The response describes the patient symptoms in a manner that is vague or inaccurate.

The response includes reasons for the cardiovascular and/or cardiopulmonary pathophysiologic processes, with explanations that are vague or based on inappropriate evidence/research. 0 (0%) – 22 (22%)
The response describes the patient symptoms in a manner that is vague and inaccurate, or the description is missing.

The response does not include reasons for either the cardiovascular or cardiopulmonary pathophysiologic processes, or the explanations are vague or based on inappropriate or no evidence/research.
Explain how the cardiovascular and cardiopulmonary pathophysiologic processes interact to affect the patient. 28 (28%) – 30 (30%)
The response includes an accurate, complete, detailed, and specific explanation of how the cardiovascular and cardiopulmonary pathophysiologic processes interact to affect the patient. 25 (25%) – 27 (27%)
The response includes an accurate explanation of how the cardiovascular and cardiopulmonary pathophysiologic processes interact to affect the patient. 23 (23%) – 24 (24%)
The response includes a vague or inaccurate explanation of how the cardiovascular and cardiopulmonary pathophysiologic processes interact to affect the patient. 0 (0%) – 22 (22%)
The response includes a vague or inaccurate explanation of how the cardiovascular and cardiopulmonary pathophysiologic processes interact to affect the patient.
Explain any racial/ethnic variables that may impact physiological functioning. 23 (23%) – 25 (25%)
The response includes an accurate, complete, detailed, and specific explanation of racial/ethnic variables that may impact physiological functioning supported by evidence and/or research, as appropriate, to support the explanation. 20 (20%) – 22 (22%)
The response includes an accurate explanation of racial/ethnic variables that may impact physiological functioning supported by evidence and/or research, as appropriate, to support the explanation. 18 (18%) – 19 (19%)
The response includes a vague or inaccurate explanation of racial/ethnic variables that may impact physiological functioning, and/or explanations based on inappropriate evidence/research. 0 (0%) – 17 (17%)
The response includes a vague or inaccurate explanation of racial/ethnic variables that may impact physiological functioning, or the explanations are based on inappropriate or no evidence/research.
Written Expression and Formatting – Paragraph Development and Organization:
Paragraphs make clear points that support well-developed ideas, flow logically, and demonstrate continuity of ideas. Sentences are carefully focused—neither long and rambling nor short and lacking substance. A clear and comprehensive purpose statement and introduction are provided that delineate all required criteria. 5 (5%) – 5 (5%)
Paragraphs and sentences follow writing standards for flow, continuity, and clarity.

A clear and comprehensive purpose statement, introduction, and conclusion are provided that delineate all required criteria. 4 (4%) – 4 (4%)
Paragraphs and sentences follow writing standards for flow, continuity, and clarity 80% of the time.

Purpose, introduction, and conclusion of the assignment are stated, yet are brief and not descriptive. 3 (3%) – 3 (3%)
Paragraphs and sentences follow writing standards for flow, continuity, and clarity 60%–79% of the time.

Purpose, introduction, and conclusion of the assignment are vague or off topic. 0 (0%) – 2 (2%)
Paragraphs and sentences follow writing standards for flow, continuity, and clarity < 60% of the time.

No purpose statement, introduction, or conclusion were provided.
Written Expression and Formatting – English Writing Standards:
Correct grammar, mechanics, and proper punctuation 5 (5%) – 5 (5%)
Uses correct grammar, spelling, and punctuation with no errors. 4 (4%) – 4 (4%)
Contains a few (1 or 2) grammar, spelling, and punctuation errors. 3 (3%) – 3 (3%)
Contains several (3 or 4) grammar, spelling, and punctuation errors. 0 (0%) – 2 (2%)
Contains many (≥ 5) grammar, spelling, and punctuation errors that interfere with the reader’s understanding.
Written Expression and Formatting – The paper follows correct APA format for title page, headings, font, spacing, margins, indentations, page numbers, running heads, parenthetical/in-text citations, and reference list. 5 (5%) – 5 (5%)
Uses correct APA format with no errors. 4 (4%) – 4 (4%)
Contains a few (1 or 2) APA format errors.

MODEL ANSWER

CHF/Orthopnea

Congestive heart failure (CHF) is a condition resulting from the failure of the heart muscles to pump | PLACE YOUR ORDER NOW AT writtask.com | cause of morbidity and mortality in the elderly across the | PLACE YOUR ORDER NOW AT writtask.com | of this paper is to explain the cardiovascular and cardiopulmonary pathophysiologic processes that result in a 76-year-old female patient presenting symptoms of shortness of breath, peripheral edema, abdominal | PLACE YOUR ORDER NOW AT writtask.com | variables that may impact physiologic functioning and how the processes interact to affect the patient will be explored.

The principal pathophysiology of the symptoms is the decline in the efficiency of heart muscles caused due to damage or | PLACE YOUR ORDER NOW AT writtask.com | decrease is the effect of either systole or diastole dysfunction or both. The reduced centrality of the heart muscles enhances end-systolic | PLACE YOUR ORDER NOW AT writtask.com | of the heart muscle is caused by the decreased ability of actin and myosin fibers to cross-link in the process of contraction and relaxation of the heart (McCance & Huether, 2019).

Numerous functional and structural changes occur in a CHF patient and these factors interact to result in the pathophysiology of | PLACE YOUR ORDER NOW AT writtask.com | size increases, it also causes an increase in the thickness of the myocardium. As a result, with time, the workload of the heart | PLACE YOUR ORDER NOW AT writtask.com | modulated by chronic activation of the neurohormones such as the | PLACE YOUR ORDER NOW AT writtask.com | result in structural changes in the left ventricle, which becomes spherical rather than elliptical, and also causes fibrosis and dilation of vessels that supply the heart (McCance & Huether, 2019).

The vascular tone control is interfered with in the process resulting in low nitric acid production hence leading to vascular stiffening and | PLACE YOUR ORDER NOW AT writtask.com | overload in the cell reduces and causes changes in gene expression patterns of the proteins hence resulting in increased fibrosis. The cardiovascular reserve rises hence increasing the severity of heart failure (Denham et al., 2018).

According to Leigh et al., (2016), incidences of CHF are highest among African Americans followed by Hispanics | PLACE YOUR ORDER NOW AT writtask.com | for the high CHF risk among African Americans are hypertension, chronic kidney disease, overweight, and low levels | PLACE YOUR ORDER NOW AT writtask.com | of African Americans who develop CHF have high blood pressure.

In conclusion, CHF is a serious life-threatening condition if left untreated. Patients must seek immediate medical attention and adhere to treatment plans to manage | PLACE YOUR ORDER NOW AT writtask.com | is one of the effective ways to manage the condition

References

Denham, N. C., Pearman, C. M., Caldwell, J. L., Madders, G. W., Eisner, D. A., Trafford, A. W., & Dibb, K. M. (2018). Calcium in the pathophysiology of atrial fibrillation and heart failure. Frontiers in Physiology, 9, 1380.

Díez-Villanueva, P., & Alfonso, F. (2016). Heart failure in the elderly. Journal of Geriatric Cardiology: JGC, 13(2), 115.

Leigh, J. A., Alvarez, M., & Rodriguez, C. J. (2016). Ethnic minorities and coronary heart disease: an update and future directions. Current Atherosclerosis Reports, 18(2), 9.

McCance, K. L. & Huether, S. E. (2019). Pathophysiology: The biologic basis for disease in adults and children (8th ed.). St. Louis, MO: Mosby/Elsevier.