Case Study Assignment - ECG

This case study assignment focuses on ECG and discusses the biophysical properties of electrocardiogram and the medications used for treatment. It also provides information on the recommended guidelines for managing a patient with acute chest pain. Read more at Desklib.

RUNNING HEAD: CASE STUDY ASSIGNMENT - ECG
CASE STUDY ASSIGNMENT - ECG
Name of Student
Name of University
Author note

1CASE STUDY ASSIGNMENT - ECG
Table of Contents
Response to question 1:..............................................................................................................2
Response to Question 2:.............................................................................................................3
Response to Question 3:.............................................................................................................5
References:.................................................................................................................................9

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Response to question 1:
The electrocardiogram of Alan reveals a typical graph with coronary ischemic
deviations mediated electrophysiology which are described in terms of its biophysical
properties. The electrical properties are altered making the resting membrane potential
negative in phase 4 and action potential’s duration is diminished to less than about 200
milliseconds, with alteration of phase 2. Consequently, there forms a voltage gradient existing
between the ischemic and normal myocytes. These biophysical changes are then recorded by
electrocardiogram in form ST segment deviations from isoelectric point. Any change in the
resting membrane potential creates ST depression during diastole, contributing to the ST
elevation on the ECG (Azoz et al., 2018). A shorter action potential marks an abnormal flow
of current during systole (in trans-mural ischemia). Direction of the ST vector towards
positive outer epicardial zones produces tall T-waves and ST elevations. Amplitude of the ST
elevation indicates a severity of the ischemia. If a marked ST depression or elevation is
observed in a range of multiple leads, it should be considered that ischemia has affected a
broader area of the myocardium. Generally, in the ST elevation area – a new elevation is seen
at J point within two of the contiguous leads that is with cut-points about more than 0.1
millivolts in all the ECG leads except the V2-V3 leads. In the leads V2-V3, cut-points are
found to be greater than (and sometimes equal) to 0.2 millivolts in the affected men who are
more than 40 years old. The reading is greater than (equal to) 0.25 millivolts in affected men
who are somewhat less than 40 years and it is greater than 0.15 millivolts in affected women.
For a T wave and ST depression changes – a new horizontal is seen with downward sloping
of the ST depression is found to be greater than (or sometimes equal to) 0.05 millivolts in two
of the ECG leads. And T wave inversion is greater than or sometimes equal to around 0.1
millivolts in the two contiguous ECG leads showing a prominently represented R wave and
R/S ratio whose value greater than the value of 1.

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Coronary artery results from an accumulation of plaque in the arterial walls of
coronary arteries supplying the walls of the heart. Plaque comprises of cholesterol deposits
and other molecules occluding the artery (Mandell et al., 2017). Plaque buildup narrows the
arteries over time, which results in total or partial blockade to the blood flow by a process
called atherosclerosis. Excessive plaque causes severe narrowing of the coronary artery
lumen obstructing blood flow greatly in the myocardial walls, lessening oxygen perfusion
causing ischemia (Elumalai and Sujitha, 2016). Myocardial ischemia is responsible for
different kinds of angina – stable, unstable and prinzmetal angina which less commonly leads
to shortness of breath (dyspnea) secondary to dysfunctional left ventricular and cardiac
arrhythmias. The mechanisms of myocardial ischemia is related with chronic coronary
insufficiency plus symptoms of stable angina (Ohman, 2016). Oxygen delivery to walls of
myocardium is proportional to oxygen transport in the blood along with the viscosity of
coronary blood flow. Oxygen transport of blood can well be disrupted readily by a sudden
and rapid fall in levels of hemoglobin. This can suddenly worsen the angina symptoms in the
patient with a history of stable angina for many years and associated anemia (Miyamoto et
al., 2015). Generally, atherosclerosis of the non-resistance coronaries of epicardium (1.5–4
mm) can have an effect by distortion of the arterial physiology while it introduces a
resistance to the established coronary flow. Newly acquired resistance have a great impact on
the reserve of coronary flow leading to reduction of sufficient levels of oxygen delivery to the
myocardium (Alderman et al., 2016).
Response to Question 2:
The medications used in the emergency department, to treat Alan’s symptoms are
glyceryl tri-nitrate, morphine and aspirin.

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Glyceryl tri- nitrate is a medication used for vasodilation that relaxes the muscles
forming the walls of arterial and venous blood vessels. This medication assists in bringing in
more amount of oxygen rich blood to the heart. Glyceryl trinitrate is efficiently used in the
treatment myocardial infarction, angina pectoris and also congestive heart failure. The
organic nitrate esters always have a great relaxant effect on the smooth muscles - dilating the
coronary arteries to enhance oxygen delivery to myocardium. Dilation of peripheral veins and
peripheral arteries reduces the volume afterload and preload, lowering consumption
myocardial oxygen but this medication causes dilation of coronary vessels reversing the
process. Inhibition of the progress of platelet aggregation is a pharmacological effect that is
of an immense therapeutic value (Hamarneh et al., 2017). The relaxing effect induced on the
walls of vascular smooth muscles along with the biological effect of platelets is due to a
stimulation of guanylate cyclase in the fluids by nitric oxide, catalyzed by enzymatic activity
of cytochrome 450, glutathione S-transferase along with the action of esterases. The cyclic
GMP created by the action of enzyme guanylate cyclase acting through the enzyme cGMP-
dependent protein kinase. The protein kinase diminishes the levels of intracellular calcium
through physiological processes causing an increased uptake to the reservoirs of intracellular
stores is crucial(Federico et al., 2017)
Aspirin also known as acetylsalicylic acid, is efficiently used as a pain reliever for
pains and to reduce fever. Aspirin is used as an anti-inflammatory drug plus a blood thinner
(Poehl, et al., 2017). Aspirin’s mechanism of action progresses through inhibition of platelet
aggregation and activation. The prime mechanism of action involves irreversible inhibition of
cyclooxygenase (COX)- platelet-dependent enzyme that prevents the process of
prostaglandins synthesis. The cyclooxygenase-1 enzyme assists in the production of
thromboxane A2 which is a powerful promoter in platelet aggregation (Feng et al., 2016).
Aspirin acts by irreversibly inactivating COX-1, blocks the thromboxane A2 production

5CASE STUDY ASSIGNMENT - ECG
leading to potential anti-platelet effect. The platelet aggregation and activation with
consequential activation of the physiological clotting cascade essentially play a critical role
leading to acute vascular events (occlusive in nature) like myocardial infarction (Fang et al.,
2015). Other mechanisms of aspirin includes blockage in the formation of many COX-
dependent potent vasoconstrictors - contributing to atherosclerosis’s endothelial dysfunction
(Gimbrone and García-Cardeña, 2016). Hence, improvement of dysfunctional endothelium
with aspirin will also better vasodilation, reducing thrombosis while inhibiting pathological
progression of the atherosclerosis. Aspirin also diminishes the severity of inflammatory
response present in patients suffering with coronary dysfunction and would also prevent
atherosclerosis progress by preventing the low-density lipoprotein from biological oxidation
(Ference et al., 2017).
Alan reported an angina ‘pain’ intensity of 9 upon 10. Hence, his discomfort and
agony has to be managed with morphine. Morphine binds to opioid receptors blocking
nociceptive signal transduction while activating the molecular signals of pain modifying
neurons (pain gate) present in the spinal cord (Mann and Carr, 2018). It also inhibits the
neuronal transmission from the afferent pain receptors present in the dorsal horn sensory
cells. Onset of action is generally within 6-30 minutes after administration. Morphine
interacts with μ–δ-opioid (Mu-Delta) receptors, whose binding sites are found in thalamus,
hypothalamus, amygdala and Substantia gelatinosa of spinal cord (Pierre et al., 2019).
Response to Question 3:
According to Australian guidelines, it is recommended that a coronary heart disease
patient with symptoms of acute chest pain must receive Electrocardiogram (ECG) assessment
within the first 10 minutes of a clinical contact which is done exactly in the emergency
department (Thomsett and Cullen, 2018). Next, cardiac troponin levels should be

6CASE STUDY ASSIGNMENT - ECG
immediately sent for testing. In the emergency department, aspirin is administered to Alan
and in addition, glyceryl tri nitrate is administered to relieve Alan’s angina. Morphine was
used to relieve the pain which is in accordance with the Australian guidelines. The above
protocols should be followed strictly to manage Alan in the emergency department. An
individualized medical care plan for Alan – a targeted low-density- lipoprotein cholesterol
(that is less than 1.8 mmol/L) level is recommended in the very first instance. Initiation of
treatment with the beta -blockers is recommended in patients with reduced left ventricular
systolic function. Relaxation, head level, anti-hypertensive medications are to be used to
control the abnormally high blood pressure which can predispose to more impaired cardiac
function. Beta blockers should be administered in case of a proper diagnosis, vitals should be
monitored for any signs of tachycardia and should be managed immediately. The given
guidelines below should be followed in medical management of Alan.
For management in emergency department, oxygen supplementation should be started
if oxygen saturation level is lower than the physiologically permissible level or due to
associated dyspnea. In case of severe angina, oxygenation can relieve the chest pain.
Australian guidelines also recommends initiation of aspirin therapy at 300 mg aspirin daily
for initial se followed by 100- 150 mg daily. Primary percutaneous coronary angioplasty is
advised for reperfusion therapy in subjects with myocardial infarction ( showing elevated ST
levels) within a 90 minutes of the first medical contact.* Fat paced strategies to be operated
for Alan in medical emergency. Protocols should be coordinated with proper planning and
decision making skills which incorporates an operative ambulance services with paramedic
functionality, primary level first line physicians with optimally functional performance of
cardiology and emergency departments. These steps are critical to achievement of acceptable
cardiac reperfusion times. Strategies which effectively lessen the time of reperfusion are -
establishing hospital functional networks along with the pre-determined medically effecient

7CASE STUDY ASSIGNMENT - ECG
management pathways, ambulance ECG devices, pre-hospital paramedic administered
fibrinolytic therapy. Patients who are treated with fibrinolytic therapy, with about 50% ST
recovery in 60 to 90 minutes along with hemodynamic instability, there should be an
immediate patient transfer for the angiography procedure with rescue angioplasty is certainly
recommended. Systems of medical should enable appropriate, immediate, earliest transfer of
the angiography patients who are treated with a fibrinolytic therapy is also recommended by
Australian guideline. Patient fitness and affected anatomies are the main determinants for the
major surgeries. Urgent re-vascularization using coronary artery bypass grafting (CABG)
should be done for Alan if percutaneous coronary angioplasty fails or if there is presence of
cardiogenic from the myocardial infarction. A multidisciplinary cardiac team should be
handling Alan’s medical management. In type 2 myocardial infarction which is to be
diagnosed further in Alan, angiography and re-vascularization is taken into consideration
when ischaemia due to hemodynamic de-compensation is continuing in spite of providing
adequate treatment for the underlying critical pathophysiology processes leading to the
causation of type 2 myocardial infarction. If Alan is confirmed with acute coronary syndrome
with presentation of an intermediate to high risk of ischemic recurrence, a P2Y12 inhibitor
that is ticagrelor 180 mg given orally and then about 90 milligram twice a day thereafter, a
prasugrel 60 milligram given orally and then 10 mg daily, clopidogrel at 300 to 600
milligram orally daily, 75 milligram thereafter is medically practiced and recommended with
the application of aspirin. Ticagrelor is to be used as the first-line of P2Y12 inhibitors due to
superior efficacy (Bhatia and Ola, 2015) . Ticagrelor is also advised for a broad range of
patients suffering from STEMI, persisting at an intermediate to a very high risk in recurrent
ischemic event while atrio-ventricular conduction disorders are absent. Prasugrel is to be
considered for coronary patients who did not receive any P2Y12 antagonists but percutaneous
coronary angioplasty is planned but the medication should not be used in patients who are 75

8CASE STUDY ASSIGNMENT - ECG
years, with low bodyweight like less than 60 kgs or who has a history of stroke or ischemic
disorder. Prasugrel or ticagrelor is preferred over the use of clopidogrel in patients who
experienced recurrent ischemic events while intake of clopidogrel or experienced stent
mediated thrombosis. Clopidogrel medication is recommended for the patients who is not fit
to take the above choice of drugs as adjunctive agent for fibrinolytic therapy and also for
those who need oral anticoagulation. Clopidogrel must be started soon after the diagnosis but
good attention is to be given to problems like ischemia and bleeding while preparing for
coronary artery bypass grafting (is recommended to patients with extensive ECG deviations
to hemodynamic instability). Prasugrel is to be started immediately after diagnosis for
patients to have a percutaneous coronary intervention for STEMI and the coronary anatomy
is to be known properly before administration. Initiation of medication Prasugrel before the
coronary angiographic procedure is not recommended. Patients who have an urgent
indication for intake of oral anticoagulation must go through a careful medical and nursing
assessment diagnosing the thrombotic risks along with bleeding risks, using CHA2DS2-
VASc, HAS-BLED scores. The given advice is and should be based on a consensus decision
of all working medical disciplines. In affected patients with very strong indication of long
term anticoagulation - intravenous glycoprotein (IIb/IIIa inhibition) along with heparin is
always recommended during percutaneous coronary intervention procedure in patients
suffering with high risks prevalent while treating complications of thrombotic origin with
acute coronary syndrome.

9CASE STUDY ASSIGNMENT - ECG
References:
Alderman, S.L., Harter, T.S., Wilson, J.M., Supuran, C.T., Farrell, A.P. and Brauner, C.J.,
2016. Evidence for a plasma-accessible carbonic anhydrase in the lumen of salmon
heart that may enhance oxygen delivery to the myocardium. Journal of Experimental
Biology, 219(5), pp.719-724
Azoz, A., Youssef, A., Alshehri, A., Gad, A., Rashed, M., Yahia, M., Alsharqi, M. and Al
Saikhan, L., 2018. Correlation between ST segment shift and cardiac diastolic
function in patients with acute myocardial infarction. Journal of
electrocardiology, 51(4), pp.592-597
Bhatia, R. and Ola, V., 2015. Dual antiplatelet therapy and newer agents: More efficacy but
lets keep the brain safe!!. Indian heart journal, 67, pp.S7-S10.
Elumalai, G. and Sujitha, A.S., 2016. Anomalies origin of left coronary artery” its
embryological basis and clinical significance. Elixir Embryology, 100, pp.43446-
43449
Fang, L., Moore, X.L., Dart, A.M. and Wang, L.M., 2015. Systemic inflammatory response
following acute myocardial pain

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Feng, X., Liu, P., Zhou, X., Li, M.T., Li, F.L., Wang, Z., Meng, Z., Sun, Y.P., Yu, Y., Xiong,
Y. and Yuan, H.X., 2016. Thromboxane A2 activates YAP/TAZ protein to induce
vascular smooth muscle cell proliferation and migration. Journal of Biological
Chemistry, 291(36), pp.18947-18958. ardial infarction. Journal of geriatric
cardiology: JGC, 12(3), p.305.
Federico, M., Portiansky, E.L., Sommese, L., Alvarado, F.J., Blanco, P.G., Zanuzzi, C.N.,
Dedman, J., Kaetzel, M., Wehrens, X.H., Mattiazzi, A. and Palomeque, J., 2017.
Calcium‐calmodulin‐dependent protein kinase mediates the intracellular signalling
pathways of cardiac apoptosis in mice with impaired glucose tolerance. The Journal
of physiology, 595(12), pp.4089-4108.
Ference, B.A., Ginsberg, H.N., Graham, I., Ray, K.K., Packard, C.J., Bruckert, E., Hegele,
R.A., Krauss, R.M., Raal, F.J., Schunkert, H. and Watts, G.F., 2017. Low-density
lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from genetic,
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Atherosclerosis Society Consensus Panel. European heart journal, 38(32), pp.2459-
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Gimbrone Jr, M.A. and García-Cardeña, G., 2016. Endothelial cell dysfunction and the
pathobiology of atherosclerosis. Circulation research, 118(4), pp.620-636.
Hamarneh A., Hardman, E., Wicks, P., Shanahan, H., Bulluck, H., Ramlall, M., Chung, R.,
Bell, R., Cordery, R., Yellon, D. and Hausenloy, D., 2017. 57 The effect of remote
ischemic conditioning and glyceryl trinitrate on perioperative myocardial injury in
cardiac bypass surgery patients: the eric-gtn study.
Mandell, D.M., Mossa-Basha, M., Qiao, Y., Hess, C.P., Hui, F., Matouk, C., Johnson, M.H.,
Daemen, M.J.A.P., Vossough, A., Edjlali, M. and Saloner, D., 2017. Intracranial

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vessel wall MRI: principles and expert consensus recommendations of the American
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