Case Study - Valves S24 maya nelson

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School

Florida State College at Jacksonville *

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Course

2085C

Subject

Medicine

Date

Apr 3, 2024

Type

docx

Pages

2

Uploaded by CorporalPower2140

A&P 2 Name & N#: __Maya Nelson_________N01432187________________________________ A Case Study on Valve Function Carl arrived at the ER suffering from severe shortness of breath (dyspnea) that began approximately 12 hours earlier. He was an active 64-year-old, with no recent illness or shortness of breath before today. He had a prior history of appendicitis, but was otherwise healthy, with no known cardiovascular issues or other chronic medical conditions. A chest X-ray showed some opacity of both lungs, but his heart was not enlarged. Additional tests ruled out a myocardial infarction, but the doctor detected a noticeable murmur when listening to Carl’s heart. Carl was surprised to hear this, and reported that he had never been diagnosed with a heart murmur even though he had had regular physicals for the past 30 years. An echocardiogram (an ultrasound of the heart) showed that several of the chordae tendineae connected to the anterior leaflet of the left atrioventricular valve had ruptured. Use the following data to answer the questions below. Heart rate: 102 bpm End diastolic volume (EDV): 115 ml (within normal range) End systolic volume (ESV): 30 ml (decreased) Left ventricle size: normal Left atrial size: normal Short Answer Questions . Type or write your answers in the spaces below, changing the font for easier grading. Cite your sources. 1. Explain how the ruptured chordae tendineae are related to the newly-detected murmur. The atrioventricular valves cannot open and enter the atria due to the chordae tendinea. Both an inadequate closure of the valve and blood leakage into the atrium may be caused by a ruptured chordae tendineae attached to the anterior leaflet of the left atrioventricular valve. This is the source of the murmur as well as the inefficient and aberrant blood flow that follows. ( McGraw Hill, 19.3d) 2. Consider the path blood now takes during contraction of Carl’s left ventricle and the influence of afterload. Why is his ESV less than normal? Blood from the left ventricle enters the aorta through the opening of the aortic valve, where it is subsequently circulated throughout the body. The left ventricle of a healthy heart normally pumps blood that is oxygenated into the aorta. The resistance the left ventricle must overcome in order to pump blood into the aorta is known as afterload; it is simply the amount of effort the heart needs expend in order to pump blood. Carl's End-Systolic Volume is low as a result of his ruptured chordae tendineae, which may prevent the left ventricle from emptying fully during contraction. Consequently, at the conclusion of systole, the left ventricle will have less blood and therefore less work than it would in a heart that's functioning properly. ( McGraw Hill, 19.3d) 3. Why is Carl’s heart rate elevated?
A&P 2 Name & N#: __Maya Nelson_________N01432187________________________________ Carl may be experiencing reverse blood flow, which might be the cause of his increased heart rate. A portion of the blood pumped by the left ventricle into the left atrium reversed course in the instance of the ruptured chordae tendineae. As a result, there was less blood expelled into the systemic circulation, and the heart most likely had to pump more quickly to maintain a sufficient cardiac output . https://www.ncbi.nlm.nih.gov/books/NBK499976/ 4. Without treatment, this condition will result in enlargement of Carl’s left ventricle. Why is this the case, and what consequence(s) would this have on his cardiovascular health? Given Carl's situation and his ruptured chordae tendinea, amplification of the left ventricle is probably in store. The backflow of blood and a defective bicuspid valve might be the cause of this. A small overflow of blood into the left atrium during left ventricular contraction is likely to be caused by the valve shutting incompletely or incapably, which causes a volume excess in the left ventricle. The expansion of Carl's left ventricle may be explained by the fact that the heart has to function harder to accommodate this backflow back into the left atrium, which forces the left ventricle to pump more blood out of the aorta. (McGraw Hill, 19.3f) 5. Tests ruled out a myocardial infarction for Carl. What is a myocardial infarction? What type of test could determine if this is what he was experiencing? A heart attack is another more popular term for a myocardial infarction. It is the point at which the heart muscle starts to die as a result of inadequate blood flow and prolonged oxygen deprivation. Oxygen deprivation is the outcome of insufficient oxygen delivery to the heart by the coronary circulation. Blood tests and an electrocardiogram can determine whether a person has experienced an attack of the heart. An ECG displays electrical waves that represent the whole electrical activity of the heart, including contractile and pacemaker cells. (McGraw Hill, 19.3)
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