Case Study Analysis: Medical Examination and Drug Therapy

CASE STUDY ANALYSIS
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Introduction
Medical examination is critical in reviewing the status patients. Patient Betsy overall
medical history review and significance of medication care process initiated are discussed in
this review. Assesment of acute coronary symptom state of the patient and in-depth
discussion on drug therapy has been illustrated.
The rationale for the ECG request
ECG assessment is essential in establishing the diagnostic assessment for the electrical
and muscular ability of the heart. Heart function affects the flow of oxygen thus causing
shortness of breath. The patient has occasioned shortness of breath which in most cases is an
indication of underlying lung and heart function, relating to the removal of carbon dioxide
and problem linked to breathing effects processes (Ripoll et al., 2016).
Breathing regulation is undertaken by the interaction of complex activities between
various processes of air and blood. The levels of oxygen and carbon dioxide tend to increase
in the blood; this signals the heart to increase the breathing rate. The levels of the oxygen
tend to rise leading to deep breaths of oxygen leading to increase and elevated heartbeat rates
(Paliakaitė et al., 2018). This increases the overall breathing rate and causes a sensation of
shortness of breath. Thus the ECG assessment will indicate the breathing patterns of the
patient and how it may signal other functions and facilitate diagnosis to be much faster and
easier.
References
Paliakaitė, B., Petrėnas, A., Henriksson, M., Skibarkienė, J., Kubilius, R., Sörnmo, L., &
Marozas, V. (2018). Atrial fibrillation frequency tracking in ambulatory ECG signals:
The significance of signal quality assessment. Computers in biology and medicine, 102,
227-233.
Ripoll, V. J. R., Wojdel, A., Romero, E., Ramos, P., & Brugada, J. (2016). ECG assessment
based on neural networks with pretraining. Applied Soft Computing, 49, 399-406.
Angina path physiology

3
Angina is a state of chest pain occurring due to lack of enough blood to the heart
muscle. One of the causes is the obstruction of the coronery arteries. The underlying
mechanism of the Angina relates to the development of myocardial ischemia which occurs
due to inadequate blood flow resulting from aerobic and anaerobic metabolism which
progresses with an impairment of the metabolic, electrical and mechanical functions (Dewey
et al., 2016). The key critical manifestation of Angina is the clinical manifestation of
myocardial ischemia. It is related to the cause of the mechanical and clinical action of the
sensory and the nerve ending afferent located in the coronary vessels and the myocardium
region. The endings of the nerve tend to extend from the spinal nerves thoracic site through
the spinal cord of the thymus in the cerebral cortex.
Adenosine interacts on angina as a pain chemical mediator. In ischemia state, the ATP
causes degradation of the adenosine occasioned by the diffusion on the extracellular space
which leading to the stimulation of A receptors located in the nerve endings (Gao et al.,
2018).
The heart rate, myocardial wall tension, and the myocardial isotropic state are highest
myocardial activity determinant linked to demand of oxygen which increases the heart rate
and the activity of the myocardial leading to elevated levels of oxygen demand. It increases
after loads and preload states leading to increase in the wall tension of myocardial wall and
increasing the demand for oxygen. This leads to a net effect o supply of oxygen in
determining the flow of blood and oxygen extraction. This resultant net effect of oxygen
imbalance leads to elevated demand of oxygen due to decline supply related to obstruction of
the coronary (de Souze et al., 2018).
Stable angina refers to chest pains or discomfort which occurs at the emotional stress.
The heart muscle often needs a constant supply of oxygen which allows the coronary arteries
to carry oxygen in the heart. When there is a need for more oxygen, the heart muscle tends to
pump harder leading to symptoms of angina on low blood flow to the heart muscle.
Unstable angina at times referred to the acute coronary syndrome leads to unexpected
chest pain which occurs at resting state. The key common cause is due to reduced blood flow
on the muscles of the heart due to constricted coronary arteries due to atherosclerosis which
cause injury on the coronary blood vessel leading to blood clotting blocking the blood flow to
the heart muscle.

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Non-STEMI stands for non-ST elevation in the myocardial infarction which signals to a
type of heart attack. Myocardial infarction feeds to heart attack leading to illustrations on ST
using ECG assessment tracing the heart attack diagnosis. The diagnosis of the NSTEMI is
undertaken with blood markers of heart damage and by the tracing of the heart patterns of ST
elevation occurrence son the EKG (Lüscher, 2016).
STEMI referring to ST elevation on myocardial infarction indicates a serious type of
heart attack which causes blockage of the major arteries. The ST elevation leads to an
abnormality which is detected on the 12 lead ECG. If often depicts a life-threatening state
associated with coronary heart state, (Mozaffarian et al., 2016).
Risk factors
The patient Betsy is experiencing various risk factors which increased her rate of
coronary heart which include;
- Hypertension
- Diabetes
References
Dewey, M., Rief, M., Martus, P., Kendziora, B., Feger, S., Dreger, H., ... & Hamm, B.
(2016). Evaluation of computed tomography in patients with atypical angina or chest
pain clinically referred for invasive coronary angiography: randomised controlled trial.
bmj, 355, i5441.
Lüscher, T. F. (2016). The management of acute coronary syndromes: towards optimal
treatment of STEMI and non-STEMI.
Mozaffarian, D., Benjamin, E. J., Go, A. S., Arnett, D. K., Blaha, M. J., Cushman, M., ... &
Howard, V. J. (2016). Heart disease and stroke statistics-2016 update a report from the
American Heart Association. Circulation, 133(4), e38-e48.
Molecular Mechanisms of the Arterial Wall in Acute Coronary Syndromes. In Endothelium
and Cardiovascular Diseases (pp. 473-483). Academic Press.