Sloan Hall

April 5, 2022
NSG 461 – Professor Timalonis
Disease Deep Dive

The 54-year-old black female presents with symptoms most likely linked to acute

coronary syndrome (ACS). This patient is presenting with dyspnea, chest discomfort on exertion,

postural lightheadedness, heart palpitations, and cannot climb one flight of stairs, and the patient

is currently in mild distress. The symptoms of chest discomfort on exertion, palpitations, and

fatigue with not being able to climb one flight of stairs are connected some way to ACS.

According to McCance and Huether (2019), myocardial ischemia that is seen within women may

not present with typical angina, which is chest pain; the common symptoms that are seen in

women include atypical angina, palpitations, a sense of uneasiness, and severe fatigue (p. 1080).

However, this patient’s symptoms of postural lightheadedness and dyspnea may or may not be

connected to ACS, as with any ischemia, the cells within the heart do not have the ability to

contract and cardiac output is decreased and oxygen can no longer get to tissues quickly

(McCance & Huether, 2019, p. 1079). This would explain the postural lightheadedness. The

dyspnea could be either from the patient’s mild distress she is experiencing or could be from the

ACS itself. According to Zhao et al., (2021), the authors stated that chest pain that is presented

with or without cardiac symptoms and dyspnea are the most common symptoms seen in women

who have been diagnosed with ACS (p. 60).

After reviewing the history, I am convinced that this patient does not have pernicious

anemia and will eliminate it. I chose to eliminate pernicious anemia due to this patient’s

presenting symptoms and her history, which do not add up. Typically, early on in pernicious

anemia, you will see infections, mood disorders, and diseases pertaining to the gastrointestinal
and cardiac systems, and even conditions affecting the kidneys (McCance & Huether, 2019, p.

933). These symptoms are usually ignored due to the vagueness of them (McCance & Huether,

2019, p. 933). Once the hemoglobin drops down to 7-8 g/dL, the typical symptoms of anemia are

seen, such as, weakness and exhaustion; loss of feeling in the feet and fingers; ataxia; poor

appetite, abdominal discomfort and reduction in weight; and a smooth, but beefy red, sore tongue

that is due to atrophic glossitis (McCance & Huether, 2019, p. 933). The skin may become pallor

or look lemon-yellow (McCance & Huether, 2019, p. 933). The patient has been experiencing

symptoms of shortness of breath for one week, has a history of hypertension, Epstein Barr Virus,

and osteoporosis; hysterectomy; smoke one pack per day and drink 3-5 alcoholic beverages per

week for 10 years. Her blood pressure, pulse, and respirations are elevated, and she is 93% O2

on room air. She takes candesartan for hypertension, as well as a multivitamin and calcium

supplement. Upon reviewing her symptoms and history, I feel confident eliminating pernicious

anemia.

This patient’s chief complaint is dyspnea, chest discomfort on exertion, postural

lightheadedness, palpitations, and a functional limitation of less than one flight of stairs, and she

is in mild distress. Her history revealed worsening shortness of breath for one week, has

hypertension, hysterectomy, smokes one pack per day, consumes 3-5 alcoholic beverages per

week for 10 years, BP 136/92, 108 P, 22 R, 98.9 temp, and O2 is 93% RA. The review of

systems revealed she has gained six pounds of weight over two months, has weakness, fatigue,

occasional migraines; positive JVD; positive for dyspnea, chest discomfort, hypertension,

palpitations, and trace peripheral edema in lower legs and feet; has a poor appetite; occasional

nocturia; joint pain that goes away with moving, occasionally has tingling feelings in her lower

extremities and occasional tremors when anxious. All of her lab results were normal range,
except hemoglobin (10.2 g/dL, normal 12-18 g/dL), hematocrit (32%, normal 37%-54%),

potassium (3.2 mEq/L, normal 3.5-5 mEq/L), glucose (226 mg/dL normal 75-110 mg/dL), BUN

(52 mg/dL, normal 24-49 mg/dL), creatinine (1.4 mg/dL, normal 0.6-1.2 mg/dL), and LDH (256

units/L, normal 110-220 units/L) (McCance & Heuther, 2019). With all reported, I still believe

this patient is experiencing ACS, with myocardial infarction (MI). Although troponin I is most

specific of indicating a MI (McCance & Huether, 2019, p. 1086), her level was 0.50 ng/mL.

According to Ferry et al. (2019), they concluded that with a diagnosis of myocardial infarction, 1

in 3 women were only identified as having such condition by using a high-sensitivity cardiac

troponin I assay (p. 7). This patient should have another troponin level drawn 6-9 hours after and

12-24 hours after since her previous sample was negative, but border line (McCance & Huether,

2019, p. 1086). Also, her LDH is another biomarker that can detect MI and hers is elevated

(McCance & Huether, 2019, p. 1086). Her glucose is also elevated, which can be true with MI

(McCance & Huether, 2019, p. 1086), and her A1C is normal, ruling out diabetes. The elevation

of glucose is due to the release of norepinephrine, through stimulation of liver and skeletal

muscle cells, suppressing pancreatic B-cell activity and reducing insulin secretion (McCance &

Huether, 2019, p. 1084). Her hemoglobin, hematocrit, potassium, BUN, and creatinine could be

caused by decreased cardiac output that comes with ischemia (McCance & Huether, 2019, p.

1079).

The pathophysiology of ACS begins with a thrombus that forms within a blood vessel

due to plague is lodged and occludes the vessel for a prolonged period, cutting off blood supply

and myocyte necrosis sets in and causes cell death (McCance & Huether, 2019, p. 1083-1084). If

the thrombus breaks up, this MI will present with a non-STEMI (McCance & Huether, 2019, p.

1084). If it does not break up, the infarction extends through the myocardium, into the
endocardium, and into the epicardium, causing severe cardiac dysfunction, presenting a STEMI

(McCance & Huether, 2019, p. 1084). With this thrombus, cellular injury occurs, and the cells

can withstand ischemic conditions for only 20 minutes before cellular death occurs (McCance &

Huether, 2019, p. 1084). Irreversible hypoxic injury causes the cellular death and tissue necrosis

is evident, and this results in the release of intracellular enzymes, such as troponin, where

lymphatics pick up the enzymes and transport them into the bloodstream (McCance & Huether,

2019, p. 1085). After the MI has been caught and perfusion is restored, structural and functional

changes occur, then the repair of the “wounds” take place, and it depends on how severe the

infarction was to determine the severity of functional impairment (McCance & Huether, 2019, p.

1085). According to Mechanic, Gavin, and Grossman, (2021), an inflammatory response

happens as a result from an atherosclerotic rupture, where monocytes and macrophages rush to

the site and thrombus formation and platelet aggregation takes place. After this response, the

deliverance of oxygen is reduced through the coronary artery, leaving the myocardium oxygen-

deprived (Mechanic et al., 2021). Without oxygen, adenosine triphosphate (ATP) is not able to

be produced in the mitochondria and this results in the ischemic attack, where apoptosis (cell

death) of the endocardium occurs and the infarction is evident (Mechanic et al., 2021). Also, the

authors explained that the presenting symptoms in women are usually not typical symptoms and

can experience no chest pain at all and can present with abdominal discomfort and dizziness

(Mechanic et al., 2021). The authors also indicate that lightheadedness, anxiety, irregular

heartbeat (palpitations), tachycardia, and high blood pressure are seen, and that distention of

neck veins may be present, indicating right ventricular heart failure and edema may be evident in

the lower extremities (Mechanic et al., 2021). This patient is presenting with all the above and

the symptoms coincide with the pathophysiology .

Ferry. A. V., Anand, A., Strachan, F. E., Mooney, L., Stewart, S. D., Marshall, L., Chapman, A.

R., Lee, K. K., Jones, S., Orme, K., Shah, A. S. V., Mills, N. L. (2019). Presenting

symptoms in men and women diagnosed with myocardial infarction using sex-specific

criteria. Journal of the American Heart Association, 8(17), 1-9.

https://doi.org/10.1161/JAHA.119.012307

McCance, K. L., & Heuther, S. E. (2019). Pathophysiology: The biologic basis for disease in

adults and children (8th ed.). Elsevier

Mechanic, O. J., Gavin, M., Grossman, S. A. (2021). Acute myocardial infarction. StatPearls

Publishing. https://www.ncbi.nlm.nih.gov/books/NBK459269/

Zhao, Y., Sivaswamy, A., Lee, M. K., Izadnegahdar, M., Chu, A., Ferreira-Legere, L. E.,

Humphries, K. H., & Udell, J. A. (2021). A feasibility study for CODE-MI: High-

sensitivity cardiac troponin-Optimizing the diagnosis of acute myocardial

infarction/injury in women. American Heart Journal, 234, 60-70.

https://doi.org/10.1016/j.ahj.2021.01.008