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Heart Disease Annotated Bibliography
Anand, S.S., Islam , S., and Rosengreen, A., (2008). Risk factors for myocardial infarction in women and men : insights from the interheart study. European heart journal . 29 (7), 932-940.
The article is about Coronary heart disease (CHD) which has been described as being amongst the leading cause of death amongst adults worldwide. Women have been found to be developing CHD about ten years after it has developed in men, but there are no clear reasons why this is so. The authors aimed at establishing if disparities in the distribution of risk factors are found amongst men and women across various categories of ages in order to assist in explaining the reasons for women developing acute MI several years after men have developed it.
The authors found out that on average most women develop their initial acute MI at least 9 years after men have developed it. There were nine variable risk factors that were found to be critically related to acute MI in both genders. This was used in explaining more than 90% of the PAR. There are disparities in age if the initial MI is narrated by the high degree of risk factors in men and young ages in comparison to women. Compared to other articles this article was more informative in nature for it explained the reasons for lower incidents of CHD in women before the age of 50 years.
It also explained that after this age CHD tends to increase with strategies that are usually seen in men in the eighth decade. However, as much as the Framingham study defined risk factors that impact CHD in women it was limited to only White Caucasians residing in America. It was thus not able to explain the future age of the initial occurrence of myocardial infarction (MI) amongst women in relation to men. This source was thus very useful.
Heart Disease Annotated Bibliography
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Bray G.A. (2013) Risks of obesity. Endocrinology Metabolism Clinics of North America, 32 (4), 787-804.
According to the authors of this article even though obesity leads to an increase of lots of chronic diseases it is not all obese people that develop these diseases. In the recent past a subset of individuals who were obese got free of chronic diseases. The metabolic problems that have been perceived as the causes of these diseases were pointed out in the research literature.
The population is typified by intense insulin sensitivity, ordinary blood pressure and good levels of cholesterol in spite of excess adiposity. It is now referred to as metabolic health obese. The authors indicate that there has been a rapid interest to point out fresh insights in the processes of chronic diseases. The objective of this article is thus to translate outcomes into treatment alternatives.
The disparity it has with other articles on this subject matter is the fact that it does not make a clear indication of whether Individuals that are MHO have been protected from the chronic diseases adverse effects as well as the mortality characteristic of obesity. Numerous longitudinal studies on the development of chronic diseases in MHO individuals have not exhibited any increased risk of the disease.
For instance St Pierra et al. followed 1800 men from Canada for a decade and a half and found that they were not at risk of heart diseases because they had MHO.A number of findings portray protection while other researchers have found out that MHO represents an impediment in the progression of diseases in subpopulations. Answers to these queries would provide critical implications for the policy on public health; however there is a lot of equivocalness in the existing literature. In spite of these findings the article was very useful.
Harris, T.B. (2007), carrying the burden of Cardiovascular risk in old age: Associations of weight and weight change with prevalent cardiovascular disease, risk factors and health status in the cardiovascular study. American journal of clinical Nutrition, 66 (3), 837-844.
As obesity and overweight rates rapidly increase in the US and globally the disease burden is becoming considerable and is likely to decrease life expectancy. As much as obesity has rapidly been related to augmented risks of cardiovascular diseases (CVD) few research studies have assessed whether the deliberation of permanent change in BMI could offer extra information on CVD prediction. Previous observational studies support the notion that the lowest CVD risk could be amongst those that have a stable weight.
The loss and gain of weight are related to poorer status of health and an increased rate of CVD mortality. In the assessment of BMI change there is a need for observational studies to be cautious so as to reduce confounding factors for instance likely underlying malignancy, smoking status and physical activity. The aim of this study was to employ potential data from a wide cohort with permanent follow up to effectively comprehend how BMI change is related to CVD risk.
It also aims at finding out if the BMI trajectory consideration can add analytical information beyond the existing BMI knowledge. The study thus assessed how BMI change in the past eight years was related to the main CVD events risk amongst 13,000 healthy men for 13 years. A rising and higher BMI were related to an increased CVD risk, however, increased BMI did not increase analytical information upon considering the existing BMI. Contrastingly, a decline in BMI was linked to an augmented CVD risk that was autonomous of the existing BMI. The article was thus very useful.
Bray G.A. (2013) Risks of obesity. Endocrinology Metabolism Clinics of North America, 32 (4), 787-804.
Harris, T.B. (2007), carrying the burden of Cardiovascular risk in old age: Associations of weight and weight change with prevalent cardiovascular disease, risk factors and health status in the cardiovascular study. American journal of clinical Nutrition, 66 (3), 837-844.
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Death of the Heart muscle
Question for discussion
Mr. Smith was lifting a heavy piece of furniture when he experienced crushing pain in his chest, began sweating heavily, and was nauseated. His wife drove him to the hospital, where he was diagnosed with a myocardial infarction (MI, also called a heart attack) and given intravenous drugs to dissolve a clot that was obstructing a major coronary artery. After his hospitalization, Mr. Smith?s doctor told him that some of his heart muscle had died. Explain the Pathological processes associated with the death of the heart muscle
Pathological processes associated with the death of the heart muscle
The function of heart relies on a complex network of cells’ ‘the cardiomyocytes for its appropriate function. These cells are the contracting cells in the heart, that exist in a three dimensional network of endothelial cells, vascular smooth muscle, an abundant fibroblasts and transient populations of immune cells. Gap junctions electrochemically coordinate the contraction of the individual cardiomyocytes, and their contraction to the extracellular matrix that transduces force and coordinates the overall contraction of the heart. In the cells, the repeating units of actin, as well as the myosin form the sarcomere structure, the basic functional unit of the cardiomyocyte.
The sarcomere has more than 20 proteins form connections between extracellular matrix and myocytes that regulate muscle contraction. The dysfunction occurs due to the disruption in the interaction in the complex activity that exist between multimeric complexes and many proteins. The heart can tolerate a variety of pathological insults, even then if the adoptive responses that aim to maintain functions eventually fail, they result in a range of functional deficits of cardiomyopathy. (Pamela and Leslie,2011).
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Patho-physiological processes of cell injury
Tissue injury and cell death occur due to ischemic insult, is determined by the magnitude and duration of the blood supply and the changer induced due to reperfusion. Prolonged ischemia, reduces the ATP levels and intracellular PHdue to anaerobic metabolism and accumulation of lactate. This results in the dysfunction of ATPase dependent ion transport mechanisms, that contribute to increasing intracellular mitochondrial calcium levels, swelling of the cell and the rupture of the cell, ultimately resulting in the death of the cell by necrotic, necroptotic. Apoptopic and autophagic mechanisms. (Theodore et.al,2012).
Reversible and irreversible cell injury
Reversible cell injury
Reversible cell injury denotes pathological changes that can be reversed, provided the stimulus is removed and the cellular injury is mild. Cellular injury can be recovered only to a certain point.(Farber et.al,1981)
Irreversible cell injury
Irreversible cell injury is a pathological change that is permanent and can cause cell death and cannot be reversed to normal state.(Farber et.al,1981)
Sustaining heart attack
The cell injury causes loss of phosphorylation in mitochondria, increase in anaerobic glycolysis, slowing down of the pumping of sodium, failure of active transport. The morphological changes that include swelling of the cell, loss of microvilli and blebs. All these abnormalities can be reversible if the oxygenation is restored.
Chief Complaint (CC): “I have been experiencing shortness of breath and fatigue in the last two weeks.”
History of Present Illness (HPI): Patient complains of shortness of breath, and general fatigue. Patient has been experiencing swelling of the feet and has been having difficulty in completing tasks that she would normally.
Past Medical History (PMH): measles at age 3, mumps at age 4
Past Surgical History (PSH): None
Family history;
Father died at age 65 y/o due to CAD.
Mother 70 y/o, alive diagnosed with hypertension
Brother (35) alive and healthy
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Personal and Social History:
She is born and raised in this community. She is a college graduate with a diploma in business management. She works as an assistant in one of healthcare facilities within the community. She lives with her daughter. She interacts with the community members. Pt denies smoking, but takes a lot of salt. The pt takes two cups of caffeine. Pt states that she is physically inactive.
Review of Systems:
HEENT: EOMI, PERRL,
CV: RRR, S3 present, m/r/g absent
RESP: breathing symmetrical, SOB, CTAB x mild crackles
Healthy dietary is recommended to boost the immune system
Maintain hygiene to protect themselves from communicable diseases.
Reflections
Congestive heart failure (CHF) is the leading cause for hospitalization in this community. There is no cure of the disease, but can effectively be managed through therapeutic and non-pharmacological measures (Esposito, Bagchi, and Verdier, 2009). My preceptor and I were on the same page in during care delivery and treatment of this pt. From the comprehensive assessment, I learnt that the patient was non-compliant to medication.I was assigned to research on the strategic ways that would be used to educate the patient and to ensure that she adhered to the recommended medication (Bickley, 2013
Esposito, D., Bagchi, A., Verdier, J.M. (2009). Medicaid beneficiaries with congestive heart failure: Association of medication adherence with healthcare use and costs. The American journal of managed care 15(7); 437-445
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Myocardial Infarction: Case Study
Causes, Incidence, and Risk Factors for Myocardial Infarction
Myocardial infarction (MI) is an impairment of heart functioning characterized by diminished blood supply to cardiac muscles following myocardial ischemia (Wong et al., 2012). Myocardial cells are destroyed but not repaired as the rate of their degeneration exceeds the capacity of repair mechanisms, which are usually slowed by poor blood supply. The causes of MI include myocardial ischemia that results when metabolic needs of the heart are too high and exceeding a certain threshold or ischemia that results after the coronary circulation is inefficient and affecting oxygen and nutrient delivery to heart muscles (Wong et al., 2012). In some cases, the two causes may co-occur and eventually result in MI.
The prevalence of MI in Australia is significantly high with data indicating a correlation between disease occurrence, age and sex (Wong et al., 2013). Statistics indicate higher prevalence among older persons, with more than 3,800 cases of male patients 85 years and above having been reported in 2011. On the other hand, about 11 cases of female patients of ages between 25 and 34 were recorded on the same year. Nevertheless, MI prevalence in Australia was reported to have been decreasing between the years 2007 and 2011 (Heart Foundation, 2014).
Studies indicate that risk factors for MI are those that also increase people’s susceptibility to atherosclerosis. These include tobacco use, being of the male gender, a positive family history for the condition, and pre-occurring conditions such as diabetes mellitus (DM), hypertension, and hyperlipidemia (Gehani et al., 2015). The risk of MI is highest in persons with multiple predisposing factors.
In the case of Mr. Savea, several factors could have predisposed him to MI. These include his history of tobacco use, being clinically obese, having high blood pressure, being at a considerably advanced age, and of course being a male. Research links components of tobacco to damage of blood vessels hence increasing the risk of atherosclerosis and MI. Obesity is also linked to diabetes and hyperlipidemia, both which are risk factors for MI (Gehani et al., 2015). Age and gender are unavoidable risk factors for MI.
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5 Common Signs and Symptoms of MI
Signs and symptoms of MI
Underlying pathophysiology
Chest pain likened to a sensation of squeezing caused by application of pressure at the mid-thorax (Haasenritter et al., 2012)
Caused by hypoxia and ischemia result in MI. Impaired cardiac function also contributes to pain as muscles in other body parts do not get sufficient supply of oxygen and nutrients, hence becoming weak and unable to contract and relax normally. Reduced cardiac output also contributes to dyspnea hence causing the squeezed sensation.
Loss of consciousness (Heart Foundation, 2015a)
Patients of MI may become unconscious due to poor blood supply to the brain as manifested in the disease. The occurrence results from cardiogenic shock whereby the heart is unable to pump blood efficiently since cardiac muscles are damaged.
Tachycardia and hypertension (McSweeney et al., 2010)
Patients with MI often present with tachycardia and hypertension. The phenomena are linked to anxiety and pain that patient experience when they get other symptoms of the disease. The anxiety and pain stimulates the sympathetic system hence causing cardiac activation and vascular constriction. As a result, patients develop hypertension and tachycardia as secondary manifestations.
Shortness of breath and dyspnea (Heart Foundation, 2015a)
The symptom is associated with the damage and impairment of heart muscles that occur in MI. The functioning of the left ventricle is affected hence reducing its pumping ability. Consequently, ventricular failure precedes pulmonary edema. Accumulation of fluid in the lungs in turn reduces the pulmonary volume, and hence causes difficulties in breathing.
Increased perspiration (Heart Foundation, 2015a)
Diaphoresis that characterizes MI is due to the activation of the sympathetic pathway. Usually, the pathway is activated as a counter mechanism for the maintenance of arterial pressure which is usually high in patients with MI. The activation of the pathway is a compensatory mechanism effected via baroreceptor response following decreased cardiac output.
Pharmacological Treatment of MI
Several classes of drugs have been approved for the treatment of MI in Australia. These include beta-blockers and angiotensin converting enzyme inhibitors (ACEIs). Drugs in the same class often work in the same mechanism in MI treatment.
ACEIs
The pharmacodynamics of these drugs in treating MI includes causing vascular dilation, hence reducing the myocardial afterload (Clauss et al., 2015). So as to attain optimal effectiveness, treatment is initiated with a low dose of an ACEI that has a short half-life (Song et al., 2015). The dose is then titrated upwards until a stable maintenance dose is achieved within 24 to 48 hours. The short-acting agent may then be continued at the maintenance dose or replaced with a longer-acting agent.
Angiotensin receptor blockers (ARB) may be co-administered with ACEIs if the patient is intolerant to the latter (Gadzhanova et al., 2016). ACEIs are recommended for diabetic and hypertensive patients while contraindicated for those with low blood pressure or patients of kidney failure (Blood Pressure Lowering Treatment Trialists’ Collaboration, 2014). Some of the commonest ACEIs used in the management of MI include captopril, lisinopril, and ramipril (Monroy et al., 2014). Patient data collected in Mr. Savea’s case suggest high applicability of ACEIs.
Beta Blockers
The physiological effects of beta blockers include decreasing the force and rate of myocardial contraction and subsequent reduction of oxygen demand in cardiac muscles (Atrial Fibrillation Association Australia, 2014). The medication should be administered the earliest possible after the onset of symptoms, preferably within the first 12 hours of diagnosis (Scot, 2010). Early treatment with beta-blockers does not only reduce the incidence of re-infarction, recurrent ischemia, and ventricular arrhythmias, but it also decreases the size of the infarct and so the chances of short-term death (Scot, 2010).
The medications are particularly essential when the disease condition is characterized by poor oxygen supply owing to the drugs’ effects on reducing oxygen demand in the myocardia. Common beta-blockers used in MI management include carvedilol, atenolol, and metoprolol (Martin et al., 2014). The drugs are also associated with hypotensive effects, and therefore, their use is safe in the case of Mr. Savea.
Post-Admission Nursing Care Strategies for Mr. Savea
Nursing care for the presented patient should prioritize on patient comfort and safety (Martin et al., 2014). Measures that should be taken to ensure safety for the patient include facilitating the accessibility of intravenous drug therapy services. Safety should also be promoted by ensuring that the patient has the access of resuscitation facilities, and he can be easily monitored and supervised. On the other hand, measures to increase the comfort of the patient include early administration of oxygen therapy, pain relievers, vasodilators, and anti-emetic medications.
Oxygen Therapy
The registered nurse should ensure that Mr. Savea receives oxygen therapy so as to avert arterial hypoxaemia that could occur within 24 hours of admission (Martin et al., 2014). The strategy would also facilitate the use of medications such as opioid analgesics whose use could cause hypoxia. Research also indicates that administration of oxygen to patients of MI would counter the development of infarcts hence reducing the possibility of short-term mortality, and subsequently increasing survival chances for the victims (Burgess, 2012).
Pain and Emesis Management
Mr. Savea presents with severe chest and abdominal pain, and therefore, the registered nurse should prioritize on relieving the pain. Opioids such as diamorphine would be applicable in analgesia as they are considerably highly potent. However, such drugs could induce emesis and it would be necessary to counter the side effect using anti-emetic agents. Such drugs include metoclopramide and cyclizine (Department of Health and Human Services, 2012). The hypoxaemic effects of opioid analgesics should be countered by the use of oxygen therapy.
Vasodilation
The nurse should prioritize on increasing blood flow to the heart by using vasodilators. Nitrates would be an applicable class of drugs as they would reduce myocardial oxygen demand by decreasing both the preload as well as the afterload (Branson & Johannigman, 2013). By promoting cardiac blood flow, the drugs would also help in reducing pain associated with ischemia (National Prescribing Service, 2010).
Administration of Anti-Clotting Agents
After stabilizing the patient, the nurse should proceed with long-term measures to protect the victim’s myocardia. The approach involves re-canalizing the affected blood vessels so as to promote cardiac function (National Prescribing Service, 2010). Drugs that may be used for this case include aspirin. The patient may take the drug at a low dose on a daily basis if he can tolerate it. Thrombolytic agents may also be used for the protection of the myocardium. Streptokinase is an example of an intervention that is thrombolytic and applicable in the management of MI (Heart Foundation, 2015b).
Blood Pressure Lowering Treatment Trialists’ Collaboration. (2014). Effects of blood pressure lowering on cardiovascular risk according to baseline body-mass index: a meta-analysis of randomised trials. The Lancet, 385(9571), 867-874.
Branson, R. D., & Johannigman, J. A. (2013). Pre-hospital oxygen therapy. Respiratory Care, 58(1), 86-97.
Burgess, S. (2012). Oxygen therapy for myocardial infarction. Australian Journal of Paramedicine, 8(2), 1-3.
Clauss, F., Charloux, A., Piquard, F., Doutreleau, S., Talha, S., Zoll, J., & Geny, B. (2015). Angiotensin-converting enzyme inhibition prevents myocardial infarction-induced increase in renal cortical cGMP and cAMP phosphodiesterase activities. Fundamental & Clinical Pharmacology, 29(4), 322-361.
Gadzhanova, S., Roughead, S., & Bartlett, L. (2016). Long-term persistence to mono and combination therapies with angiotensin converting enzymes and angiotensin II receptor blockers in Australia. European Journal of Clinical Pharmacology, 2016(1), 1-7.
Gehani, A., Hinai, A, Zubaid, M., Almahmeed, W., Hasani, M., Yusufali, A., & … Yusuf, S. (2015). Association of risk factors with acute myocardial infarction in Middle Eastern countries: the INTERHEART Middle East study. Preventive Cardiology, 21(4), 400-410.
Haasenritter, J., Stanze, D., Widera, G., Wilimzig, C., Abu Hani, M., Sönnichsen, A. C., & Donner-Banzhoff, N. (2012). Does the patient with chest pain have a coronary heart disease? Diagnostic value of single symptoms and signs – a meta-analysis. Croatian Medical Journal, 53(5), 432–441.
Martin, L., Murphy, M., Scanlon, A., Naismith, C., Clark, D., & Faraoukwe, O. (2014). Timely treatment for acute myocardial infarction and health outcomes: An integrative review of the literature. Australian Critical Care, 27(3), 111-118.
McSweeney, J. C., Cleves, M. A., Zhao, W., Lefler, L. L., & Yang, S. (2010). Cluster Analysis of Women’s Prodromal and Acute Myocardial Infarction Symptoms by Race and Other Characteristics. The Journal of Cardiovascular Nursing, 25(4), 311–322.
Monroy, F., Ferrario, C. M., Hernandez, C., & Martinez, L. (2014). Comparative Effects of a Novel Angiotensin-Converting Enzyme Inhibitor versus Captopril on Plasma Angiotensins after Myocardial Infarction. Pharmacology, 94(2), 21-28.
Scot, I. (2010). Up the dose of beta blockers after MI. Medical Journal of Australia, 2010(160), 435-442.
Song, P. S., Seol, S., Seo, G., Kim, D., Kim, K., Yang, J. & Kim, D. (2015). Comparative study of angiotensin 2 receptor blockers. Journal of Cardiovascular Drugs, 12(4), 43-54.
Wong, C. X., Sun, M. T., Lau, D. H., Brooks, A. G., Sulivan, T., Worthley, I. M., & Sanders, P. (2013). Nationwide Trends in the Incidence of Acute Myocardial Infarction in Australia, 1993–2010. AJC, 112(2), 169-173.
Wong, C., Brooks, A., Leong, D., Thompson, K., & Sanders, P. (2012). The Increasing Burden of Atrial Fibrillation Compared With Heart Failure and Myocardial Infarction: A 15-Year Study of All Hospitalizations in Australia. Arch Intern Med, 172(9), 739-742.
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