Case Study: Pathophysiology of Myocardial Infarction Analysis

This assignment presents a case study of a 55-year-old patient, Ms. X, who presents with symptoms of fatigue and indigestion, leading to a diagnosis of myocardial infarction. The case study explores the patient's risk factors, including smoking, age, lack of physical activity, unhealthy diet, family history, and stress. It delves into the pathophysiology of myocardial infarction, discussing the process of artery blockage, heart muscle damage, and the resulting chest pain. The assignment analyzes the patient's symptoms, including low blood pressure, cool and clammy skin, a weak and irregular pulse, and anxiety, and provides insights into the underlying causes. The analysis covers diagnostic methods, such as serum enzyme and electrolyte level tests and ECG, and discusses the implications of premature ventricular contractions (PVCs). Treatment measures, including lifestyle changes, medication (thrombolytic and anticoagulant agents), and stress management, are also explored. Furthermore, the assignment examines the progression of cardiogenic shock and the body's compensatory mechanisms, ultimately leading to the patient's demise, which is attributed to cardiogenic shock of the left ventricle.

Running head: PATHOPHYSIOLOGY 1
Pathophysiology
Student’s Name
Institutional Affiliation

PATHOPHYSIOLOGY 2
Question 1
 Smoking
 Older age
 Inadequate physical activity
 Unhealthy regimen
 Family history of a heart attack.
 Stress
Question 2
When the plague builds up the artery, its wall thickens narrowing the channel within the
blood vessel hence declining the flow of blood. When the artery is seriously blocked, it causes
damage to a section of the heart muscle called myocardium causing a heart attack (Bentzon,
Otsuka, Virmani & Falk, 2014).
Question 3
When a portion of the heart muscle is temporarily unable to acquire sufficient blood and
oxygen because of the thinned arteries, the heart muscle fails to function properly causing
tentative chest pain.
Question 4
Low blood pressure: It is happening because of the interference of blood flow to the cardiac
muscle.
Cool and clammy facial skin: It is due to her pain, anxiety as well as low blood oxygen level.
Weak and irregular pulse: This occurs because of myocardial contractility along with conduction
loss due to the exhausted oxygen to the heart.

PATHOPHYSIOLOGY 3
Anxiety: It is due to her extreme tiredness, pain, and admission to the emergency department.
Question 5
The pulse of Ms. X is under the standard range but it is weak. Also, her blood pressure is
marginally low. Her diagnosis is enhanced since she is in the initial shock stages and she can
quickly be maintained prior to the fall of her blood pressure and pulse and lead to injury to other
organs. The intermitted leg pains, as well as fatigue, indicate a hardening of the arteries along
with atheromas (Sheng, Budin, Ishak, Nor & Anuar, 2019) which are plagues affiliated with
thrombi which are an elegant clinical talk for blood clots. It aggravates her diagnosis since the
elevated thickening of the blood vessels and her susceptibility for blood clotting can lead to
pulmonary embolus or a second myocardial infarction. Ms. X should be cured with thrombolytic
or anticoagulant agents to reduce the clotting. Moreover, an aspirin treatment may be used for
indelible therapy of her illness.
Question 6
Serum enzyme levels indicate the number of enzymes in the bloodstream and an increase
in these enzymes reveals that the heart tissue is injured by myocardial infarction. On the other
hand, electrolyte levels indicate the levels of potassium and sodium in the bloodstream.
Abnormal levels of sodium along with potassium also indicate myocardial infarction.
Question 7
ECG records the electrical operation of the heart. It diagnoses any anomalies of the heart
rate, structure, and performance, depolarization of the P wave, and depolarization of ventricles in
QRS wave and ventricular repolarization of the T wave.
Question 8

PATHOPHYSIOLOGY 4
PVCs are caused by infarct in the anterior left ventricle which leads to extra pulses from
ventricular muscle cells. Before the atria could replenish the PVCs with blood, the heart ventricle
contracts and ventricular fibrillation develops if the PVC frequency is increased. Ms. X will have
a broad QRS than normal because there will be P waves and abnormal rate on the ECG.
Question 9
Measures include; nutrition changes that embrace a low-fat and low-salt regimen with
diet counseling, increment in physical activity and exercise, up-to-date vaccination as well as
smoking cessation (Brinks, Fowler, Franklin & Dulai, 2017).
Question 10
Stress led to a marked escalation in sympathetic nervous system activity and an
outpouring of adrenaline. The escalated sympathetic simulation raised oxygen demand by
elevating heart rate, and cardiac contractility. Stimulation of α sympathetic receptors elevated
coronary vascular tone, declining oxygen provision. Moreover, escalated ventricular inotropy
along with coronary tone changes altered the shear blood stress against a vulnerable
atherosclerosis plague leading to plague fracture hence myocardial infarction (Hering,
Lachowska & Schlaich, 2015).
Question 12
Ms. X's cardiogenic shock was a result of ventricular fibrillation which is an arrhythmia
in which lower chambers quiver. Her weak and irregular pulse leads to dangerous rhythms hence
causing cardiogenic shock.
Question 13
The sympathetic nervous system, as well as the adrenal medulla, tries to escalate heart
rate, escalate the heart contractions and escalate systemic vasoconstriction to elevate blood

PATHOPHYSIOLOGY 5
pressure. As a result, renin, angiotensin, along with aldosterone is produced to elevate the blood
volume. From the kidneys and vasoconstriction, the antidiuretic hormone is secreted to prompt a
rise in water reuptake. Glucocorticoids are unleashed to cool the vascular system and acidosis
boosts respiration which sequentially escalates oxygen and minimizes carbon dioxide.
Question 14
The cells will gradually lose their performance and the issue will be hard to counter since
the tissues along with cells deliberately fails and the compensation approach farther improves the
condition. After, more bodily problems like acute respiratory distress syndrome, septic shock,
depression of the cardiac function, disseminated intravascular coagulation, acute kidney disease,
hepatic failure, and general multiorgan collapse occur. On the verge of multiorgan decline, the
body cannot recuperate and death occurs.
Question 15
Demise of Ms. X was as a result of cardiogenic shock, precisely of the left ventricle. The
heart’s inefficiency to appropriately pump blood blocked the flow of blood via the heart.

PATHOPHYSIOLOGY 6
References
Bentzon, J. F., Otsuka, F., Virmani, R., & Falk, E. (2014). Mechanisms of plaque formation and
rupture. Circulation Research, 114(12), 1852-1866.
Brinks, J., Fowler, A., Franklin, B. A., & Dulai, J. (2017). Lifestyle modification in secondary
prevention: beyond pharmacotherapy. American journal of lifestyle medicine, 11(2), 137-
152.
Hering, D., Lachowska, K., & Schlaich, M. (2015). Role of the sympathetic nervous system in
stress-mediated cardiovascular disease. Current hypertension reports, 17(10), 80.
Sheng, S. S., Budin, S. B., Ishak, I., Nor, F. M., & Anuar, N. N. M. (2019). Review of sudden
deaths due to cardiac abnormalities. Jurnal Teknologi, 81(5).