Alright, here is the post to reply to for week 4 (by Hi. At.):
If you can, please dumb it down as much as possible. The last paper had a 71% similarity score. Thank you.
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Heart diseases are amongst the leading causes of death worldwide. A normal physiologically functioning heart has two sounds. S1 heart sound represents the closure of the tricuspid and mitral valves during ventricular contraction. The S2 heart’s sound represents the closing of the aortic and pulmonic valves during ventricular repolarization or relaxation. However, a third (S3) or fourth (S4) heart sound auscultated over the apex of the heart may develop in cases of pathological origin, although physiological conditions too can lead to S3 heart sounds. According to Katz et al. (2018), the S3 sound frequently referred to as the “third heart sound†can be an important sign of systolic heart failure from dilated cardiomyopathy. It is because the myocardium is often overly compliant, resulting in left stretched ventricles. This dilation allows for turbulent blood to fill the ventricles
Some other causes of the S3 heart sound may also include aortic regurgitation, mitral regurgitation. With valvular regurgitations, the valve leaflets, inability to shut up completely, facilitates blood flow to continue even when the valves are seemingly closed (Huether et al. 2020). The damage to the heart valves, result in incompetence that lead to the ineffectual overfilling of the heart chambers. Continuation over prolonged periods, the ventricles dilate to accommodate the increase in blood volume into the ventricles leading to reduced contractility and reduced cardiac output. The case involving Mrs. K‘s presentation of shortness of breath, inspirational lung crackles, worsening peripheral edema, and rumbling S3 gallop via auscultation appears to point to worsening systolic heart failure.
Katz et al. (2018), observed that the pathophysiology of systolic heart failure is usually regarded as failure of the cardiovascular system to deliver sufficient oxygenated blood to the body. As the heart failure continues, the cardiac output is decreased. The ejection fraction measures of the amount of blood that is ejected by the ventricles per beat. According to Huether et al. (2020), heart failure with reduced ejection fraction, or systolic heart failure, is defined as an Ejection Fraction of <40% and an inability of the heart to generate an adequate cardiac output to perfuse vital tissues.
Still, there are others factors implicated in the causation of heart failure. These include \”hemodynamic overload, myocardial infarction, ventricular remodeling, excessive neuro-humoral stimulation, abnormal myocyte calcium cycling, excessive or inadequate proliferation of the extracellular matrix, and genetic mutations,†De Paris et al., (2019. Compensatory mechanism to boost cardiac output through the Renin-Angiotensin-Aldosterone system temporarily increases heart rate, blood pressure and reduces urine output. As the fluid is pull back into the systemic circulation, it further exacerbates the heart failure. Now when fluid accumulates in the ventricles, it try to find outlet into the pulmonary system resulting in wet capillary beds as evident by Mrs. K inspiratory crackles, and dyspnea.
References
Brashers, V.L., & Huether, S.E. (2020). Alteration of pulmonary function in children. In S.E. Huether, K.L. McCance, V.L. Brashers & NS. Rote (Eds.), Understanding pathophysiology (7th ed., pp. 590-625). Elsevier.
De Paris V, Biondi F, Stolfo D, (2019). Pathophysiology. In: Sinagra G, Merlo M, Pinamonti B, editors. Dilated Cardiomyopathy: From Genetics to Clinical Management Cham (CH): Springer; 2019. Chapter 3. Available from: https://www.ncbi.nlm.nih.gov/books/NBK553848/ doi: 10.1007/978-3-030-13864-6_3
Katz, S. D. (2018). Pathophysiology of Chronic Systolic Heart Failure A View from the Periphery. Annals of the American Thoracic Society, 15, S38-S41. https://doi.org/10.1513/AnnalsATS.201710-789KV
NSG 530: Week 4 Reply
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NSG 530: Week 4 Reply
Response to Hi. At.
The initial discussion was about the pathophysiology of the S3 heart sound. The student provided a comprehensive discussion regarding the issue. Therefore, this response is meant to support, as well as provide additional information on what the student provided in the initial discussion. Heart disease may be silent and go undiagnosed until one experiences symptoms of heart attack or heart failure (Dornbush & Turnquest, 2022). Heart sounds can signify the presence of heart disease. Heart sounds are normally created when blood flows through the chambers of the heart as the cardiac valves open and close during the cardiac cycle. The vibrations originating from the flow of blood lead to audible sounds. As the blood flow becomes more turbulent, more vibrations are created. The same variables that determine the turbulence of flow in all fluids apply to blood flow (Dornbush & Turnquest, 2022). These variables include density, viscosity, velocity, and the diameter of the column in which the blood is flowing.
The anatomy of the heart is complicated. The heart has four chambers, including the right ventricle, the right atrium, the left ventricle, and the left atrium. The atrioventricular valves are situated on the floor of the atria and empty their content to the ventricles. The tricuspid valve separates the right atrium from the right ventricle (Dornbush & Turnquest, 2022). The mitral valves help in separating the left ventricle from the left atrium. There are other valves such as the semilunar valve and the pulmonary valve. The heart valves help in allowing forward flow of blood and prevent backward regurgitant flow.
The S1 heart sound is created when the mitral and tricuspid valve close in systole. These hemodynamic and structural change produces vibrations that can be heard in the chest wall. The louder portion of the S1 heart sound is when the mitral valve is closing (Dornbush & Turnquest, 2022). The S2 heart sound is normally created at the closure of the aortic and pulmonary valves in the diastole. The aortic valve is believed to be the first to close before the pulmonary valve, and it is often the loudest component of the S2 heart sound. This incidence happens because the pressure in the aorta is often higher than that in the pulmonary artery.
The third heart sound (S3) is a low-frequency, brief vibration produced in early diastole at the end of the rapid diastolic filling period of the right or left ventricles. The S3 heart sound is often the most commonly auscultated with mitral regurgitation among valvular diseases (Shono et al., 2019). The S3 heart sound is the initial signal suggesting left heart failure and is often associated with severe mitral. In agreement with the student, damages caused to the heart valves may lead to incompetence causing ineffective overfilling of the heart chambers (Shono et al., 2019). This response has provided both new knowledge and support based on what the student discussed in the initial discussion.
References
Dornbush, S., & Turnquest, A. (2022). Physiology, Heart Sounds. https://www.ncbi.nlm.nih.gov/books/NBK541010/
Shono, A., Mori, S., Yatomi, A., Kamio, T., Sakai, J., Soga, F., & Hirata, K. I. (2019). Ultimate Third Heart Sound. Internal Medicine, 58(17), 2535-2538. https://doi.org/10.2169/internalmedicine.2731-19