Week 12 Chapter 33 Case Study Describe How Atherosclerosis May Cause A Myocardial Infarction Essay

Week 12 Chapter 33 Case Study Describe How Atherosclerosis May Cause A Myocardial Infarction Essay

Week 12 Chapter 33 Case Study Describe How Atherosclerosis May Cause A Myocardial Infarction Essay

1. Describe how atherosclerosis may cause a myocardial infarction.

Depending on one’s genetic makeup, lipid buildup can start to cling to arterial walls as early as early adulthood (Gatto & Prati, 2020). As a result of the buildup being seen as foreign by the arterial walls, inflammation results. Lipid production is encapsulated by inflammatory cells. The encapsulation’s core needs to stay isolated from blood flow since the core contains a potent clotting agent. Inflammation eventually degrades the lipids’ enclosed core. A plaque rupture is what is happening here. Plaque induces clot development when it enters the bloodstream, which results in myocardial infarction.

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1. Could the patient have had microvascular angina? How does microvascular angina differ from silent ischemia? Be specific.

Microvascular angina is a kind of angina caused by issues with the coronary arteries’ tiniest blood capillaries. The microvasculature of the heart refers to the microscopic vessels. This form of angina differs from others in that it is caused by a functional issue with the arteries themselves (Pelletier-Galarneau & Dilsizian, 2020). This is known as endothelial dysfunction. It occurs more frequently in postmenopausal women and can result in myocardial ischemia. Myocardial ischemia without angina is known as silent ischemia. The patient merely complains of indigestion and not of chest discomfort. This might be the patient’s way of expressing her chest pain. The patient may be suffering from microvascular angina.     

1. Why did the nurse practitioner order an ECG? What purpose does it serve? The patient begins showing increasing PVCs on the ECG. State the cause and describe the effect if these continue to increase in frequency.

The NP requested an ECG to look for ST segment abnormalities that might indicate STEMI or NSTEMI. If the patient has unstable angina, the ECG may show hyperacute T-waves, inverted T-waves, flattening of the T-waves, and ST depression (McCance & Huether, 2019). A PVC is an additional, irregular heartbeat. Caffeine, alcohol, smoke, stimulants, and cardiovascular illness can all produce an ectopic beat. The PVCs the patient is experiencing are most likely caused by angina or restricted blood supply to their heart. Recurrent PVCs might result in ventricular tachycardia, a potentially fatal rhythm. VTACH can be used with or without a pulse. This rhythm necessitates the use of ACLS.

References

Gatto, L., & Prati, F. (2020). Subclinical atherosclerosis: how and when to treat it? European Heart Journal Supplements, 22(Supplement_E), E87–E90. https://doi.org/10.1093/eurheartj/suaa068

McCance, K.L and Huether S.E. (2019). Pathophysiology Online for Pathophysiology (8th ed.). Mosby: Elsevier. ISBN: 9780323654388

Pelletier-Galarneau, M., & Dilsizian, V. (2020). Microvascular Angina Diagnosed by Absolute PET Myocardial Blood Flow Quantification. Current Cardiology Reports, 22(2). https://doi.org/10.1007/s11886-020-1261-2

Week 12: Case Study Assignment Chapter 33

1. Discuss the contributing factors to shock in this case and the pathophysiologic changes causing the changes in vital signs.

The patient in this case is suffering from neurogenic shock and hypovolemic shock. Massive vasodilation is one of the major contributors to shock in this condition. Vasodilation is caused by the activation or inhibition of parasympathetic activity (Bahrami et al., 2020). Since sympathetic system obstruction causes loss of venous and arterial tone and a dilated peripheral venous system, these pathophysiological alterations produce changes in the patient’s vital signs. When the heart cannot fill, cardiac output decreases. This causes a high heart rate, quick breathing, and a drop in blood pressure. Furthermore, due to the nature of the occurrence, hypovolemic shock cannot be ruled out.

2. Discuss the signs and symptoms of shock, including the rationale for each, as seen in the early stage, and as compensation mechanisms respond.

• Cold and clammy skin is caused by a lack of blood because circulating blood volume generates heat (McCance & Huether, 2019).
• Pale skin is caused by blood loss via vasodilation or hemorrhage.
• Rapid pulse and respirations are caused by sympathetic activity inhibition. Sympathetic nerve system blockade causes vasodilation and a decrease in cardiac output.
• Pupillary dilation is caused by parasympathetic nervous system activity.
• Weakness and weariness are caused by insufficient blood volume, which results in a lower oxygen supply to the organs, which reduces cellular metabolism and makes the patient fatigued.
• Dizziness is caused by a drop in blood pressure.
• Changes in mental state are caused by reduced blood volume, which reduces blood flow to the brain and affects oxygen delivery, resulting in altered mental status and elevated intracranial cranial pressure.

3. Compare the types of shock, giving a specific cause, classification, and any significant changes in onset or manifestations.

There are four different forms of shock, each with a unique set of symptoms and underlying causes: hypovolemic, obstructive, cardiogenic, and distributive shock (Chioncel et al., 2020). The most frequent kind of shock, hypovolemic shock, is brought on by inadequate circulation volume, usually from bleeding, though severe diarrhea and vomiting are also possible causes. Depending on the degree of blood loss and the severity of the symptoms, hypovolemic shock is rated on a four-point scale. A quick, weak pulse caused by reduced blood flow paired with tachycardia, chilly, clammy skin, and rapid, shallow breathing are typical symptoms. Cardiogenic shock is brought on by the heart’s inability to function properly. This can be a result of myocardial infarction, which causes damage to the muscle of the heart, cardiac valve issues, congestive cardiac failure, or dysrhythmia. A blockage of the blood supply beyond the heart results in obstructive shock. Usually, a decrease in venous return causes this, however an aortic obstruction might also be to blame.

Septic, neurogenic, and anaphylactic conditions can all result in distributed shock, which is characterized by an aberrant circulation of blood to organs and tissues (McCance & Huether, 2019). The most frequent cause of distributive shock is septic shock, which is brought on by a severe systemic infection that the body’s immune system is unable to clear, leading to vasodilation and hypotension. When an allergen is exposed severely, histamine is released, resulting in widespread vasodilation and hypotension, which is what causes anaphylactic shock. The cause of neurogenic shock is central nervous system injury, which reduces heart rate and relaxes blood vessel tone, impairing cardiac function and causing severe hypotension.

References

Bahrami, A., Vafapour, M., Moazzami, B., & Rezaei, N. (2020). Hyperinflammatory shock related to COVID ‐19 in a patient presenting with multisystem inflammatory syndrome in children: First case from Iran. Journal of Paediatrics and Child Health. https://doi.org/10.1111/jpc.15048

Chioncel, O., Parissis, J., Mebazaa, A., Thiele, H., Desch, S., Bauersachs, J., Harjola, V., Antohi, E., Arrigo, M., Gal, T. B., Celutkiene, J., Collins, S. P., DeBacker, D., Iliescu, V. A., Jankowska, E., Jaarsma, T., Keramida, K., Lainscak, M., Lund, L. H., & Lyon, A. R. (2020). Epidemiology, pathophysiology and contemporary management of cardiogenic shock – a position statement from the Heart Failure Association of the European Society of Cardiology. European Journal of Heart Failure, 22(8). https://doi.org/10.1002/ejhf.1922

McCance, K.L and Huether S.E. (2019). Pathophysiology Online for Pathophysiology (8th ed.). Mosby: Elsevier. ISBN: 9780323654388

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minimum of 2 references used for each case study. References must be reputable and within 5 years. Provide a reference page for each case study. Chapter 33 in the textbook must be used for each case study as a reference. Use apa in text citation and reference page. 
WEEK 12: CASE STUDY ASSIGNMENT CHAPTER 33

The patient is 56 years of age and has been complaining of severe fatigue and “indigestion.” Her son is quite concerned and brings her to the emergency department. On arrival the nurse practitioner notes that she appears very anxious, her facial skin is cool and clammy, her BP is 90/60 and her pulse is 90 weak and irregular. The nurse practitioner orders oxygen, and IV, and an EKG. The tentative diagnosis is a myocardial infarction. The patient’s son provides information that she is a long-time smoker, is a high school biology teacher, and has recently separated from her husband. He also tells the nurse practitioner that his mother has begun to rely on “fast foods” like pizza and fried chicken and cooks infrequently. She has also had intermittent leg pain when walking or climbing stairs at work.

1. Describe how atherosclerosis may cause a myocardial infarction.
2. Could the patient have had microvascular angina? How does microvascular angina differ from silent ischemia? Be specific.
3. Why did the nurse practitioner order an ECG? What purpose does it serve? The patient begins showing increasing PVCs on the ECG. State the cause and describe the effect if these continue to increase in frequency.

WEEK 12: CASE STUDY ASSIGNMENT CHAPTER 33

A 19-year-old woman with no previous medical history, was involved in a serious automobile accident in which her best friend died. Examination by EMT personnel first on the scene revealed she had only minor scrapes and bruises and no sign of head trauma. While en route by ambulance to the hospital, the patient complained of thirst and appeared restless. Further examination indicated a rapid pulse and respirations, with her blood pressure now at 100/60 mm Hg. She appeared less responsive to the paramedics. She was slipping into circulatory shock as they checked her again for internal injuries.

1. Discuss the contributing factors to shock in this case and the pathophysiologic changes causing the changes in vital signs.

2. Discuss the signs and symptoms of shock, including the rationale for each, as seen in the early stage, and as compensation mechanisms respond.

3. Compare the types of shock, giving a specific cause, classification, and any significant changes in onset or manifestations.