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The cardiovascular and cardiopulmonary pathophysiologic processes.

The cardiovascular and cardiopulmonary pathophysiologic processes.

The scenario provided is below
A 45-year-old woman presents with a chief complaint of the 3-day duration of shortness of breath, cough with thick green sputum production, and fevers. Patient has a history of COPD with chronic cough but states the cough has gotten much worse and is interfering with her sleep. Sputum is thicker and harder for her to expectorate. CXR reveals flattened diaphragm and increased AP diameter. Auscultation demonstrates hyper resonance and coarse rales and rhonchi throughout all lung fields.

Assignment (2-pages case study analysis). Reminder: The College of Nursing requires that all papers submitted include a title page, introduction, summary, No plagiarism and references.

In your Case Study Analysis related to the scenario provided above, 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.


Significant depressive ailment (MDD), explained by Hippocrates as melancholia 2,500 in the past, was the first medical disorders of unknown etiology to get fully recognized as being a medical organization. It is primarily manifested in a triad of symptoms: sadness and its correlates (feelings of worthlessness, guilt and suicidality); lack of pleasure or interest in activities; and low levels of energy, or fatigability. Currently, in the general population, the point prevalence of MDD is about 4% to 7%,1,2 whereas lifetime prevalence estimates range from 15% to 20%.2,3 MDD is more prevalent in women (the female:male ratio is typically 2:1, but it can be as high as 5:2) and its median age of onset is 25 years.4 Depressed patients have decreased life expectancy, and cardiovascular disease (CVD) may be one possible explanation for the increased risk of premature death in those patients.

Among grownups ≥ 2 decades outdated, the prevalence of coronary heart disease is 8.6Percent of males and 6.8Percent in women. Among adults at age 60 to 79, the prevalence is 24.4% in men and 15.1% in women. According to data from the National Health and Nutrition Surveys (NHANES), the incidence of myocardial infarction (MI) for white men is about 0.9% at ages 35 to 44 years, 3.0% at 45 to 54 years, 6.1% at 55 to 64 years, and 9.2% at 65 to 74 years. For women, the estimates are substantially lower: 0.3, 1.0, 2.4, and 5.1%, respectively. The sex ratio for incidence of coronary events narrows progressively with advancing age, but the incidence is still higher for men than for age-matched women. The incidence at ages 65 to 94 compared to ages 35 to 64 more than doubles in men and triples in women.5 But compared to men, women’s CVD (cardiovascular disease) risk is increased to a greater extent by some traditional risk factors (such as diabetes, hypertension, hypercholesterolemia and obesity), as well as by socioeconomic and psychologicalfactors.6

Despite an extensive anecdotal weblink between CVD and despression symptoms, this partnership only has been explored detailed over the past fifteen years.7 The systems connecting major depression to CVD and cardiac death will not be yet well established. There are three plausible hypotheses that could account for their co-morbidity, and each of them will be discussed in this article. We will discuss here the pathophysiological basis for the association between depression and CVD and will conclude with a discussion of the impact of pharmacological treatment of depression on CVD.

A web link between your brain along with the center was offered by William Harvey in 1628. It was only over 300 years later that the aforementioned link was first demonstrated by Frasure-Smith et al., in a study showing that patients who are depressed at the time of an acute myocardial infarction (MI) have markedly elevated mortality as compared with patients who are not depressed.8

Since that period, a lot more than 200 research has displayed a link between significant major depression and CVD.9–18 Nevertheless, the causal relationship somewhere between the two scenarios stays not clear. There are three hypotheses that can explain that relationship: 1) depression causes CVD; 2) depression is a consequence of CVD; and 3) depression and CVD share common underlying processes.

1) Theory 1: Depressive disorders like a cause of CVD There may be persuasive evidence that depression is an independent risk component for the development of CVD as well as for deteriorating prognosis once CVD is established. Depression is linked to metabolic syndrome (MetS) and CVD.11,16,19–24 as reported by the large INTERHEART multi-centric study. In that study, stress and depression were risk factors for first myocardial infarction (MI) in healthy individuals.25 The study compared 12,461 acute MI cases with 14,637 matched controls in 54 countries on eight traditional risk factors for coronary heart disease and a composite index of psychosocial factors. The population-attributable risk of the combined psychosocial factors was 33%, with 9% of this attributable to depression. The odds ratio was comparable to those reported for other major risk factors (OR: 1.55; CI 1.42–1.69). After adjustment for geographic and ethnic context, the index remained a strong predictor of MI.

Inside a prospective cohort review of healthier men and women, present or previous (in the previous 12 months) depressive disorders greater by 2.7 times the potential risk of perishing from ischemic heart problems.26 According to other would-be reports with human population samples as well as scenario-control reports, major depression in patients without coronary heart disease improves the altered relative chance for that subsequent growth and development of heart disease 1.5-retract to 2.-fold.27–34 A meta-assessment indicated that depression nearly doubles the potential risk of cardiac situations,11 much like the risk conferred through the conventional risk factors, like dyslipidemia, diabetes mellitus and hypertension.20 Another meta-examination revealed that major depression is surely an unbiased threat component for heart disease, with the all round chance ratio of 1.64.13 Numerous further meta-analyses analyzing the function of despression symptoms in cardio morbidity and death have also exhibited the connection between depression and heart disease.10,16,35–37

It can be currently apparent that major depression adversely influences the course of many cardiovascular problems. Once CVD is established, depression impacts negatively on the prognosis, increasing the risk of both further cardiac events and of mortality. Several randomized studies have shown that depression leads to poorer prognosis in patients with existing CVD. In patients who have had an acute MI, depression is a significant risk factor for recurrent non-fatal MI and cardiac mortality.19,21,35,36,38–45 In patients with preexisting CVD, depression increases the risk of death by up to 4-fold.24

Despression symptoms could be the underlying reason behind CVD by triggering alterations from the coronary heart work and flow (with and without using antidepressants), by raising coagulability and platelet aggregation, by predisposing visitors to unhealthy life styles, by altering the hypothalamic-pituitary-adrenocortical (HPA) axis, by raising soreness, by raising autonomic color, and also by causing endothelial disorder, among other much less well known functions. However, it is not possible to determine whether those conditions are caused by depression or whether they are part of the underlying co-morbidities. The mechanisms linking depression and CVD will be discussed in due course.

2) Theory 2: Depressive disorders because of CVD The frequency of major depression after an acute myocardial infarction (MI) is higher. About 20% of patients post-MI have depression, and up to 40% of patients have at least one symptom of depression.46 Another study showed that depression is three times more common in patients after an MI than in the general population.14 Therefore, it is also possible that depression is a consequence, not a cause, of CVD.

Depression results in a higher boost in the likelihood of CVD in women. Conversely, women with CVD seem to experience higher levels of depression when compared to men.6 In a compilation of 27 studies that reported rates or risks of depression in coronary disease samples,47 it was observed that all of those studies had reported clinically or statistically significant rates or risks of at least one measure of depression. Concomitantly, among depressed patients, the same compilation showed that, among 47 studies evaluating the risk of coronary disease in depressed patients, 20 reported rates or risks of coronary disease events in depressed samples. All but one study reported at least one significantly increased rate or risk of coronary disease in the depressed group compared to the non-depressed group. Several cross-sectional studies have shown that the prevalence of depression (DSM-IV criteria) in coronary artery disease patients ranges from 15 to 20%,8,48–51 which is two to four times higher than the prevalence in the general community.

Individuals with CVD can become depressed as a response to the burden of any co-morbid issue.12 In that case, the adjustments that could describe why depression would result in CVD (changes in coronary heart operate and tempo, hypercoagulability and elevated platelet aggregation, insufficient adherence to prescription medication and wholesome way of life, alterations in the HPA axis, and improved inflammation) could possibly be just markers of CVD and not its determinants.

Even so, studies that utilized danger change for cardiac and non-cardiac illness stress with their analyses showed that these variables usually do not appear to get rid of the relationship, helping the hypothesis that major depression is surely an independent forecaster of final result.52 Furthermore, depressive disorders precedes heart disease in several scientific studies.

3) Hypothesis 3: Depressive disorders and CVD discuss typical primary functions Major depression and CVD could possibly be the consequences of any disseminated vascular illness, leading to skin lesions to the brain as well as to the center, on account of vascular and up coming metabolic changes. In addition, the relationships between plasminogen activator inhibitor-1 (PAI-1), tissue plasminogen activator (tPA) and brain-derived neurotrophic factor (BDNF) could be the underlying processes common to both diseases.