Cardiovascular Disorders – Congestive Heart Failure Pathology – Advanced patho week 4 response 1
Type of document Essay
1 Page
Subject area Nursing
Academic Level Master
Style APA
Number of references 3
Order description:
Please respond to jennifers post in one of the following ways and use some of the weeks readings as references Share insights on how the factor you selected impacts the cardiovascular alteration your colleague selected.
Offer and support an alternative perspective using readings from the classroom or from your own research in the Walden Library.
Validate an idea with your own experience and additional research
Week 4 Initial Discussion
Cardiovascular Disorders
According to the Centers for Disease Control (2017), heart disease is the number one cause of death in both men and when as about for one in every four deaths in America. I will be discussing the pathology of congestive heart failure (CHF) and how it is affected by a patient’s factor of age. I will also discuss the effect of hypertension and dyslipidemia on CHF.
Congestive Heart Failure Pathology
Heart failure occurs when the heart is not working adequality to pump enough blood to meet the body’s needs (Medline Plus, 2018). The weakening of the heart as a pump causes the congestion by causing blood and fluid to back up in the lungs or edema in the feet, ankles, and legs (Medline Plus, 2018). CHF is caused by left side heart failure but can result from both left and right side heart failure (Huether & McCance, 2017).
Left side ventricle failure presents commonly with dyspnea, orthopnea or paroxysmal nocturnal dyspnea (Hammer & McPhee, 2014). The causes of left ventricular failure can include volume overload, pressure overload, loss of muscle, loss contractility, and restricted filling of the heart (Hammer & McPhee, 2014). The pathology of left heart failure is complex involving hemodynamic changes, neurohumoral changes, and cellular changes (Hammer & McPhee, 2014). The contractility is reduced by diseases such as myocardial infarction, myocarditis, and cardiomyopathy, that results in ventricular remodeling which will disrupt the myocardial extracellular structures that cause a progression in contractility reduction (Huether and McCance, 2017). The stroke volume decreases and left ventricular end-diastolic volume (LVEDV) increased with the reduction in contractility which causes dilation of the heart and increases preload (Huether & McCance, 2017). The increased preload will stretch the myocardium and if it continues to increase it will lead to further reduction of contractility (Huether & McCance, 2017). The increased afterload is the results of increased peripheral vascular resistance (PVR) which is most commonly seen in hypertension (Huether & McCance, 2017). The increased afterload will cause resistance with ventricular emptying and increase the workload of the ventricle and result in hypertrophy of the ventricle (Huether & McCance, 2017). With sustained increase afterloads, the hypertrophy is mediated by angiotensin II and catecholamines that will result in an increased oxygen demand with the thickened myocardium (Huether & McCance, 2017). During the hypertrophy process, there are changes in the extracellular matrix and deposition of collagen between myocytes that will increase the chance of dilation and failure (Huether & McCance, 2017). When the cardiac output, there is a decrease in renal perfusion that results in the activation of the renin-angiotensin-aldosterone system (RAAS) that increases the PVR and plasma volume, which in turn will increase afterload and preload (Huether & McCance, 2017). Baroreceptors in the central circulation detect the decreased perfusion and response by stimulation the sympathetic nervous system (SNS) to cause further vasoconstriction and increase the production of antidiuretic hormone by the hypothalamus (Huether & McCance, 2017).
There are also neurohumoral, inflammatory and metabolic processes involved with CHF (Huether & McCance, 2017). Ang II, aldosterone, and catecholamines that are release are toxic to the myocardium that contributes to remodeling, cell death, and fibrosis (Huether & McCance, 2017). Natriuretic peptides are secreted to increase excretion of salt and water by the kidneys (Huether & McCance, 2017). Inflammatory cytokines are released that increase myocardial damage and cardiac cachexia (Huether & McCance, 2017). The metabolic processes affect the heart to decrease the ability to produce energy and increase the release of toxic metabolites (Huether & McCance, 2017).
Patient Factors with CHF
Many patient factors can contribute to or effect CHF including family history or genetics and behaviors such as alcohol abuse. There is evidence of familial aspect in 30-50% of cases in non-ischemic CHF, and there are more than 30 genetic loci that have been identified with the familial genes to contribute to CHF (MacRae, 2010). Genes control all aspects of the entire cardiovascular system, encompassing the strength of the vessel, the accumulation of plagues, to the way the cells of the heart communicate (MacRae, 2010) Any mutation of a single gene can affect the heart to develop heart disease including CHF. Chronic alcohol abuse contributes to dilated cardiomyopathy (Mouton et al., 2016). The volume overload that is the result of dilated cardiomyopathy will reduce systolic and diastolic function that will lead to CHF (Mouton, 2016).
Hypertension and Dyslipidemia Role in CHF
Hypertension and dyslipidemia have a significant role in CHF. Hypertension is mentioned in the hemodynamic changes with CHF. Hypertension will increase peripheral vascular resistance that will result in increased afterload (Huether & McCance, 2017). Dyslipidemia is more closely related to other heart diseases such as coronary artery disease and myocardial infarction. These diseases will result in the reduction of contractility that can be the initial stages of CHF and increase the progression over time. Hypertension and dyslipidemia are the starting block to congestive heart failure in patients that need to be monitored and treated as soon as they are discovered to prevent progression into CHF.
References
Centers for Disease Control. (2017). Heart disease fact sheet. Retrieved from https://www.cdc.gov/dhdsp/data_statistics/fact_sheets/fs_heart_disease.htm
Hammer, G. G., & McPhee, S. (2014). Pathophysiology of disease: An introduction to clinical medicine. (7th ed.) New York, NY: McGraw-Hill Education.
Huether, S. E., & McCance, K. L. (2017). Understanding pathophysiology (6th ed.). St. Louis, MO: Mosby
MacRae, C. A. (2010). The Genetics of Congestive Heart Failure. Heart Failure Clinics, 6(2), 223–230. http://doi.org/10.1016/j.hfc.2009.11.004
Medline Plus. (2018). Heart failure. Retrieved from https://medlineplus.gov/heartfailure.html
Mouton, A. J., Ninh, V. K., El Hajj, E. C., El Hajj, M. C., Gilpin, N. W., & Gardner, J. D. (2016). Exposure to chronic alcohol accelerates development of wall stress and eccentric remodeling in rats with volume overload. Journal Of Molecular And Cellular Cardiology, 9715-23. doi:10.1016/j.yjmcc.2016.04.010
These are this weeks readings and resources
Learning Resources
Required Readings
Huether, S. E., & McCance, K. L. (2017). Understanding pathophysiology (6th ed.). St. Louis, MO: Mosby.
Chapter 23, “Structure and Function of the Cardiovascular and Lymphatic Systems”
This chapter examines the circulatory system, heart, systemic circulation, and lymphatic system to establish a foundation for normal cardiovascular function. It focuses on the structure and function of various parts of the circulatory system to illustrate normal blood flow.
Chapter 24, “Alterations of Cardiovascular Function”
This chapter presents the pathophysiology, clinical manifestations, evaluation, and treatment of various cardiovascular disorders. It focuses on diseases of the veins and arteries, disorders of the heart wall, heart disease, and shock.
Chapter 25, “Alterations of Cardiovascular Function in Children”
This chapter examines cardiovascular disorders that affect children. It distinguishes congenital heart disease from acquired cardiovascular disorders.
Hammer, G. G. , & McPhee, S. (2014). Pathophysiology of disease: An introduction to clinical medicine. (7th ed.) New York, NY: McGraw-Hill Education. Chapter 11, “Cardiovascular Disorders: Vascular Disease”
This chapter begins with an overview of the vascular component of the cardiovascular system and how the cardiovascular system is normally regulated. It then describes three common vascular disorders: atherosclerosis, hypertension, and shock.
Required Media
Laureate Education, Inc. (Executive Producer). (2012a). Alterations of cardiovascular functions PPT lecture. Baltimore, MD: Author.
This media presentation outlines common alterations of cardiovascular function, including disorders of the veins and arteries.
Optional Resources
American Heart Association. (2012). Retrieved from http://www.heart.org/HEARTORG/
Million Hearts. (2012). Retrieved from http://millionhearts.hhs.gov/index.html
National Heart, Lung, and Blood Institute. (2012). Retrieved from http://www.nhlbi.nih.gov/
