Medical and Surgical Nursing: MI Case Study, ECG, and Interventions

This assignment presents a detailed case study of a patient, Bill, who arrived at the emergency department with symptoms indicative of a myocardial infarction (MI). The solution includes an analysis of the patient's symptoms, ECG findings, and the pathophysiology of MI, including crushing chest pain, diaphoresis, and nausea. It discusses the importance of heart rate monitoring, ECG interpretation (P and QRS complex analysis), and the implications of the patient's symptoms. The assignment also outlines nursing interventions, including immediate medical treatments such as oxygen therapy, analgesia, and the use of medications like diamorphine and antiemetics. Furthermore, it explores advanced interventions like Percutaneous Coronary Intervention (PCI) and fibrinolytic drugs, detailing the procedures and their mechanisms of action in treating MI. The solution provides comprehensive insights into the diagnosis and management of myocardial infarction, drawing from various medical resources.

Running head: MEDICAL AND SURGICAL NURSING
MEDICAL AND SURGICAL NURSING
Name of the student
Name of the university
Author note

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Answer 1:
The patient Bill came to the hospital’s emergency department with the problem of
Crushing chest pain, diaphoresis and nausea. His problem started at the night with
mild heart burning which increased to such a level that he came to the hospital emergency
department at 5 a.m.
It is important to measure the heart rate of Bill, if the rate is lesser than 60 beats per
second then Bradycardia is present, while if the beating is more than 100 per second it
denotes tachycardia.
Standard heart rhythm varies from 60 to 100 beats per minute. The location of P is
denoted from the ECG graph. The P wave if absent then it denotes the arterial fibrosis. The
connection between P and qrs complex is also important in ECG graph, in normal condition
the number of qrs and P should be equal. In the ECG graph of Bill it can be observed that the
qrs complex is much elevated than the P-comples , which denotes the rhythm is a ventricular
or junctional accelerated rhythm (Kamel et al., 2014). Depolarization of broken fibrous tissue
leads to the elevated level of high frequency qrs –complex after myocardial infraction. In the
case of Bill, the case can be interpreted from the ECG graph as the classic case of myocardial
infraction, as the pathophysiology matches. MI contributes to a regional declination of
electrical potential, often expressed by reduced QRS voltage or irregular Q waves; decreasing
the velocity of conduction resulted by ischemia or infarction can often reduce the potential
which have high-frequency. Hence, the average high-frequency QRS voltage after MI may be
expected to decrease. The P wave is differing from normal level in the intensity, morphology
and length. Bill complained about diaphoresis, a condition of sweating that is not normal. The
ECG analysis of Bill is indicating a case of myocardial infraction (MI). The pathophysiology
of myocardial infraction is elaborated in the next paragraphs (Acharya et al., 2017).

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Myocardial infarction widely known as "heart attack" is the permanent injury
triggered by severe ischemia and hypoxia of myocardial tissues. Myocardial infraction
(MI) mostly happens where a coronary artery get fully or partially blocked leaded by a
rupture of an atherosclerotic plaque, which contributes to a blood clot or coronary thrombosis
formation. This phenomena can also trigger vasospasm. The absolute occlusion of the vessel
it can also lead to hypoxia or ischemia. The clinical symptom of Myocardial Infraction
matches perfectly with the symptom, that Bill, the patient was facing. The Clinical symptoms
of Myocardial infraction (MI) includes extreme chest pain that increases and become
unbearable, which was the major issue with Bill (Anderson & Morrow, 2017). The other
symptom reported by Bill, was nausea and diaphoresis, an excessive sweating is also two
significant symptom of Myocardial infraction (MI) (Gokhroo et al., 2016). The other classic
symptom of the disease are dyspnea or shortness of breath, uneasy feeling of substernal
heaviness, anxiety, hypo or hyper –tension, Problem to fall asleep and comfortable sleep, and
fatigue. Nausea, a symptom complained by the patient Bill is a classic pathophysiological
indicator of myocardial infraction. It is suspected the nausea the happens during myocardial
ischemia is connected with infarction of the lower wall. However, evidence suggesting such
correlation are minimal, and an alternate theory has also been proposed that cardiac arrest
related vomiting is linked to the size of the infarct is a modern technique to get the indication
of the severity. Vomiting or nausea is a strong indicator of p lower than 0,0001 of myocardial
infarction (MI) (Malik et al., 2013). Nausea can not denote the myocardial infraction alone,
tough when associated with elevated level of CKMB, it can serve as a potential indicator of
myocardial infraction (MI). Chest pain complained by the patient Bill was acute, and severe
as he marked 9 out of 10 to the intensity of the pain This also is a commonly repoted
symptom of myocardial infraction (MI) (Malik et al., 2013). Prolapse of the mitral valve is a
complication during which a heart valve refuses to completely shut. Mitral valve prolapse has

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been linked with a number of symptoms including chest pain, palpitations and dizziness, but
it can often have no symptoms, particularly in condition where intensity prolapse is
not severe. Severe chest pressure or squeezing, a "fire" sensation, or trouble breathing is
generally defined as a classic symptom of ischemia. The patient, Bill expresses the burning
sensation in the heart, which can be a corealeted with “fire sensation.” In most of the cases
patients reports the extension of the pain in the neck, arm and left shoulder (Fox, 2015).
Every year at least five million people experiencing chest pain get admitted to emergency
departments. The assessment and evaluation of the pain shows that the 15 to 20 percent of
them has a history of coronary diseases. The symptom of coronary disease and myocardial
infraction related to chest pain is so similar that it sis quite impossible to distinguish between
them. The difference is only can be done by analyzing the ECG report. The ECG report of
Bill, give clear indication of myocardial infraction (Stroobandt, Barold & Sinnaeve, 2016).
Answer B:
Bill is a sufferer of myocardial infraction (MI), so the primary considerations of
applying intervention would be his health and comfort. For the successful delivery of
emergency drug treatment, intravenous exposure must be secure, accompanied by immediate
relocation to an environment with sufficient rates of supervisory and resuscitation services.
patient satisfaction requires oxygen management, analgesia, nitrates and antiemetics.
Myocardial infarction discomfort is commonly extreme and includes strong analgesia with
opiates. The medication of choice is intravenous diamorphine 2.5–5 mg, which can
applied repeatedly if needed. The drug is not only a effective analgesic but also known to
have beneficial anxiolytic effect (Topol, & Teirstein, 2015). Opiate usage can be linked w ith
diarrhea and vomiting and can be avoided by intravenously with the prescribed antiemetic
medications such as cyclizine 50 mg or metoclopramide 10 mg. Opiate analgesia can also be
linked with hypoxaemia of the arteries.

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Immediate management of myocardial infraction starts at home. However, in case of Bill the
home interventions are totally missed and the medical team need to start with the immediate
hospital intervention. The immediate hospital intervention starts with the veloflon insertion to
start with the other intervention process. The blood test are already done of the blood
component. The next important intervention is to intense observation and monitoring of
disease symptom which are the pulse, blood pressure, pulse oximetry analysis to understand
oxygen satuaration level, heart rate and rhythm (Xin, Chen & Hu, 2019). The patient need
emergency oxygen therapy and the administration of pain relief. Nitrate work by reducing the
preload and after load of the heart resulting the lowering of the myocardial oxygen demands.
These can indeed boost myocardial blood supply through coronary vasodilatation (Alsop &
Hauton, 2016).
PCI (Percutaneous coronary intervention):
PCI is a non-surgical technique used in the treatment of narrowing of the heart's coronary
arteries observed in coronary artery disease. Primary PCI is the immediate pharmacological
intervention of PCI in individuals with an acute heart attack, particularly when the
electrocardiogram shows signs of heart damage. PCI can be used in people with other types
of myocardial infarction or dysfunctional angina, where the possibility of more incidents is
high (Al-Lamee et al., 2018). The procedure involves integrating coronary angioplasty with
stenting, that is the procedure of the insertion of either drug eluting (DES) or bare metal
(BMS) permanent wire-meshed tube. The name balloon angioplasty is widely used to
describe a balloon's inflation inside the coronary artery to smash the so formed plaque into
the artery walls. The angioplasty catheter stent delivery balloon is expanded with media to
cause contact between the stent struts and the vessel wall (stent apposition), thus expanding
the width of the blood vessels. The technique uses coronary catheterization to image the

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blood vessels on X-ray imaging, after entering the blood supply through the femoral or radial
artery. After this, a coronary angioplasty can be conducted by an interventional cardiologist,
utilizing a balloon catheter through which a deflated balloon is advanced into the obstructed
artery and expanded to alleviate narrowing; other devices such as stents may be used to hold
the channel accessible (Morice et al., 2014). Some other procedures performed during a
percutaneous coronary intervention involve:
 Stent implantation
 Rotational or laser atherectomy
 Brachytherapy (use of radioactive source for restenosis inhibition)
The angioplasty procedure usually consists of several of the following steps and is conducted
by a group of physicians,nurse practitioners, , physician assistants, nurses endovascular
specialists and radiographers. The steps include (Morrow, 2016):
1) A needle punctures the femoral artery in the leg, or the radial artery in the arm, and a
thin wire is inserted through the artery. This technique is often called percutaneous
access.
2) Once access is obtained to the artery, a "sheath introducer" is inserted in the artery
over the wire to enable catheters to advance into the artery and to prevent bleeding.
3) A long, flexible, soft plastic tube called a "guiding catheter" is forced through this
sheath. The guiding catheter enables injection into the coronary artery of radio-opaque
dyes (usually iodine-based), so that the condition and location of the disease can be
readily assessed using real-time X-ray visualization.
4) The coronary guidewire is threaded through the guiding catheter and into the coronary
artery that is an very thin wire includes a radio-opaque, flexible end. The wire tip then
goes through the blockage.

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5) The angioplasty catheter is moved ahead slowly, and it continues to move untill the
deflated balloon get inside the blockage.
6) The balloon is then expanded and the atheromatous plaque is squeezed and the artery
wall expands to expand.
7) When a stent is on the ballon, it is inserted (left behind) to support the artery's current
stretched open position from the inside.
Fibrinolytic drug:
Fibrinolytic drug, also known as thrombolytic drug, any product that can cause a
blood clot (thrombus) to dissolve. Fibrinolytic drugs working mechanism is activating the so-
called fibrinolytic tract. The drugs working mechanism separates them from the anticoagulant
drugs (coumarin derivatives and heparin) that constrict blood clot formation by blocking the
synthesis or work of various coagulating factors ordinarily existing in the blood (Topol &
Teirstein, 2015). It is used in myocardial infarction, stroke, and in extreme venous
thromboembolism (massive pulmonary embolism or extensive deep vein thrombosis) with ST
elevation. Plasminogen forms a cleaved substance called plasmin, thrombolytic drugs kill
blood clots. Plasmin is a proteolytic enzyme that removes the cross-links between fibrin
molecules, providing the structural integrity of blood clots. The thrombolytic drugs are also
called "plasminogen activators" and "fibrinolytic drugs" because of these actions (Lal, 2017).
Fibrinolytic drugs include three main classes: streptokinase (SK), urokinase (UK) and tissue
plasminogen activator (tPA). Although drugs in these three groups are all capable of
effectively dissolving blood clots, they vary in their comprehensive mechanisms in ways that
alter their fibrin clot selectivity. Within tissue plasminogen activators are commonly
recommended over streptokinase for acute myocardial infarctions.

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References:
Acharya, U. R., Fujita, H., Adam, M., Lih, O. S., Sudarshan, V. K., Hong, T. J., ... & San, T.
R. (2017). Automated characterization and classification of coronary artery disease
and myocardial infarction by decomposition of ECG signals: A comparative
study. Information Sciences, 377, 17-29.
Al-Lamee, R., Thompson, D., Dehbi, H. M., Sen, S., Tang, K., Davies, J., ... & Nijjer, S. S.
(2018). Percutaneous coronary intervention in stable angina (ORBITA): a double-
blind, randomised controlled trial. The Lancet, 391(10115), 31-40.
Alsop, P., & Hauton, D. (2016). Oral nitrate and citrulline decrease blood pressure and
increase vascular conductance in young adults: a potential therapy for heart
failure. European journal of applied physiology, 116(9), 1651-1661.
Anderson, J. L., & Morrow, D. A. (2017). Acute myocardial infarction. New England Journal
of Medicine, 376(21), 2053-2064.
Fox, S. (2015). Human physiology. McGraw-Hill Education.
Gokhroo, R. K., Ranwa, B. L., Kishor, K., Priti, K., Ananthraj, A., Gupta, S., & Bisht, D.
(2016). Sweating: A Specific Predictor of ST‐Segment Elevation Myocardial
Infarction Among the Symptoms of Acute Coronary Syndrome: Sweating In
Myocardial Infarction (SWIMI) Study Group. Clinical cardiology, 39(2), 90-95.

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Kamel, H., Soliman, E. Z., Heckbert, S. R., Kronmal, R. A., Longstreth Jr, W. T., Nazarian,
S., & Okin, P. M. (2014). P-wave morphology and the risk of incident ischemic stroke
in the Multi-Ethnic Study of Atherosclerosis. Stroke, 45(9), 2786-2788.
Lal, V. (2017). Fibrinolytic drug therapy in the management of intravascular thrombosis,
especially acute myocardial infarction-A review. J Pharmacol Clin Res, 2(4), 555593.
Malik, M. A., Alam Khan, S., Safdar, S., & Taseer, I. U. (2013). Chest Pain as a presenting
complaint in patients with acute myocardial infarction (AMI). Pakistan journal of
medical sciences, 29(2), 565–568. https://doi.org/10.12669/pjms.292.2921
Morice, M. C., Serruys, P. W., Kappetein, A. P., Feldman, T. E., Ståhle, E., Colombo, A., ...
& Religa, G. (2014). Five-year outcomes in patients with left main disease treated
with either percutaneous coronary intervention or coronary artery bypass grafting in
the synergy between percutaneous coronary intervention with taxus and cardiac
surgery trial. Circulation, 129(23), 2388-2394.
Morrow, D. A. (2016). Myocardial Infarction: A Companion to Braunwald's Heart Disease
E-Book. Elsevier Health Sciences.
Stroobandt, R. X., Barold, S. S., & Sinnaeve, A. F. (2016). ECG from Basics to Essentials:
Step by Step. John Wiley & Sons.
Topol, E. J., & Teirstein, P. S. (2015). Textbook of Interventional Cardiology E-Book.
Elsevier Health Sciences.
Topol, E. J., & Teirstein, P. S. (2015). Textbook of Interventional Cardiology E-Book.
Elsevier Health Sciences.
Xin, Y., Chen, X., & Hu, W. (2019). Oxygen therapy in ST-elevation myocardial infarction.

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