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Assignment 2

Jandi M. Nietes

ID# 201633309

ACCN 5507

Mount Royal University

Joan Harris, Instructor

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Case 2


As a thrombolytic, Tenecteplase (TNK) would be used in this case as it breaks down the

blood clots in the coronary vessels initially by degrading fibrin with the protease enzyme

plasmin. As plasminogen binds to fibrin in the blood clots, it is activated as plasmin by tissue

plasminogen activators. As blood cells become lysed, clots continue to dissolve as plasmin

gradually breaks down fibrin and fibrinogen (Brenner and Stevens, 2018).

In order to prevent further myocardial damage, urgent fibrinolytic therapy is necessary.

The best therapeutic indication would be the resolution of chest pain and discomfort as well as

the gradual resolution of ECG abnormalities and arrhythmias, although reperfusion arrhythmias

may appear in the EKG as the clot lyse. As bleeding becomes the most relative adverse effect,

patients are closely observed. Routine evaluation of the EKG for resolution of arrhythmias is

completed. Hypersensitivity reactions are also being monitored post- administration (Yazdi, et

al., 2017).


On the other hand, the use of Aspirin or acetylsalicylic acid (ASA) in both the ER and as

well as the daily recommendation shows marked improvement in mortality post-myocardial

infarction, especially ion the first month (Xian, et al., 2015). As an antiplatelet, aspirin

irreversibly inhibits the action of cyclooxygenase by acetylation and as well as inhibiting the

release of platelet aggregation mediators such as prostacyclin and thromboxane

A2. Therapeutically, the prevention of further growth of the thrombus and thus effectively
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mitigating myocardial damage immediately post- MI episode and subsequently preventing

future myocardial infarctions are the goals for treatment ion this case (Brenner and Stevens,


Bleeding remains to be the most common adverse effect from ASA. Thus, bleeding precautions

and monitoring is initiated, prothrombin and bleeding time is expected to be prolonged.

Patients with allergic reactions, especially with tartrazine, are expected to develop more

hypersensitivity, but it is monitored nonetheless. Moreover, in prolonged therapy, a clinician

may evaluate salicylate levels to rule- out salicylate toxicity in the future (Vallerand, Sanoski and

Quiring, 2019)


As an anticoagulant, Heparin is indicated to prevent thrombus expansion and mitigate

its development. It potentiates the action of antithrombin on factor X-a and as well a thrombin

itself. When used in conjunction with Aspirin, this will increase the risk for bleeding, thus CBC,

platelet count is checked and as well as bowel movements are tested for occult blood but not

routinely. aPTT is routinely checked (Vallerand, Sanoski and Quiring, 2018). The monitoring for

effectiveness with heparin would be similar to TNK.

Further monitoring for heparin-induced thrombocytopenia is necessary should it

develop, as well as for petechial hemorrhages to the skin. Carefully monitoring skin for signs of

bleeding such as bruising or nonblanchable redness is necessary during treatment. On another

note, heparin promotes natriuresis but tends to inhibit kaliuresis, thus monitoring for serum

potassium levels is essential, especially when kidney function becomes impaired as this not only
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predisposes the patient for hyperkalemia but with increased bleeding tendencies as well

(Mulloy, et al,. 2016).


Nitroglycerin is an anti-anginal medication that is indicated for the relief and inhibition

of angina or chest pain. This also causes a decrease in blood pressure and increases cardiac

output. It acts on the coronary vessels by promoting the dilation of coronary arteries and

thereby supporting adequate coronary blood flow and promoting collateral circulation in favor

of regions of myocardial ischemia. It has a systemic effect on veins by promoting vasodilation,

lowering ventricular end- diastolic pressure and left ventricular- end diastolic volume thus

effectively lowering myocardial oxygen demand (Vallerand, Sanoski and Quiring, 2018).

Blood pressure monitoring is essential as hypotension and syncope may ensue.

Furthermore, studies suggest that efficacy off nitroglycerin should be evaluated and

intermittent dosing is favored as it shows a lesser chance for the patient to develop tolerance

(Boden, et al., 2015). Heart rate should be monitored closely as a reflex tachycardia may

develop, mores EKG should also be conducted to monitor for any changes. With excessive

vasodilation, headaches and dizziness should be monitored (Brenner and Stevens, 2018).


The use of Beta-blockers in recent MI episode has shown to decrease mortality. Being a

cardioselective and lipid- soluble beta- blocker, metoprolol causes a blockade in the beta- 1

adrenergic receptor. This effectively lowers cardiac rate and increases myocardial oxygen

demand; decreases the force and velocity of myocardial contractions; causes blood pressure
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and cardiac output to decrease thus lowering the rate pressure product; lengthens the interval

between diastole thus improving blood supply; suppresses exercise-induced catecholamine

release; decreases phase 4 depolarization and AV node conduction (Khan, 2015).

The use of beta- blockers may cause hypotension, as such blood pressure monitoring is

done. Heart rate can decrease thus observing for bradycardia is essential. Medication may

often be withheld if persistent hypotension and bradycardia develop. Moreover, an EKG is

conducted to rule- out any conduction blocks in the heart (Vallerand, Sanoski and Quiring,



Being an ACE inhibitor, enalapril is indicated as it is shown to reduce mortality and slows

the development of heart failure post- MI episode; it slows the progression of dysfunction of

the left ventricle into heart failure. By inhibiting the conversion of Angiotensin I to angiotensin

II, it lowers blood pressure. Moreover, net systemic vasodilation is expected as it increases

plasma renin levels but decreases aldosterone (Vallerand, Sanoski and Quiring, 2018).

A common adverse reaction is the development of a dry cough which is mainly due to

the release of bradykinin into the pulmonary bed. However, treatment may or may not be

discontinued depending on the patient's tolerance to the symptom. Moreover, blood pressure

is monitored closely due to its antihypertensive effect; hypotension may develop. It is

necessary to assess heart and kidney function as heart failure, and kidney failure may develop.

Observing for signs and symptoms of hyperkalemia is essential, thus observing for EKG changes

and routine serum potassium pre and during treatment must be checked (Herman and Bhimji,

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As furosemide is a loop diuretic, it promotes diuresis of excess fluids thus decreasing

blood pressure. By inhibiting Na and Cl reabsorption through the distal tubule and loop of

Henle, excretion of electrolytes and fluids is effectively done, even with impairment in kidney

function (Vallerand, Sanoski and Quiring, 2018).

Being a potent diuretic, monitoring the fluid and electrolyte sautés is vital during

treatment. Moreover, blood pressure is also cautiously checked. Assessing kidney function via

estimated GFR prior to treatment is necessary. Although uncommon, ototoxicity may develop

and should be considered especially in older adults and persons with impaired renal function.

Assessing the patient for hypersensitivity reactions is also necessary (Khan & Siddiqui, 2018).

Desired outcomes, in this case, would perhaps be related to decreased pulmonary crackles

which may be caused by pulmonary edema related to the recent MI episode.


Morphine is a potent opioid analgesic, effective in pain management, usually for

moderate to severe pain and is usually the drug of choice for pain management with

myocardial infarctions. It acts on the central nervous system (CNS) by binding to the opiate

receptors. While causing generalize CNS depression, pain response and perception are altered

(Vallerand, Sanoski and Quiring, 2018).

Response to pain management is monitored closely as this determines its efficacy as

morphine is used when nitroglycerin does not manage the pain. With decreased pain response,

there is a decreased heart rate, and this reduces myocardial oxygen demand, preventing

further myocardial damage due to schema and hypoxemia. However, like all opiates,
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respiratory rate is monitored closely for bradypnea as opiate toxicity can cause respiratory

depression. Blood pressure is also monitored due to possible hypotension due to vasoactive

properties of morphine. Bowel sounds/movement is monitored, and constipation is prevented

with laxatives as this promotes straining and further increases stress, effectively increasing

heart rate and myocardial oxygen demand (Forth & Mountfort, 2018).


The enzyme type 3 phosphodiesterase is inhibited by milrinone. Thus, it increases the

concentration of cAMP in the cardiac myocytes. It promotes the stimulation of cardiac

contractility and causes vasodilation in the smooth muscles. (Brenner and Stevens, 2018). Its

positive inotropic effect causes an increase in cardiac output by decreasing both preload and

afterload (Vallerand, Sanoski and Quiring, 2018).

It is essential to monitor the patient for the development of arrhythmia, hypotension,

and thrombocytopenia. Thus, EKG should be checked routinely as well as heart rate and blood

pressure. As patients are at higher risk for bleeding due to thrombocytopenia, platelet count

and CBC should be checked (Brenner and Stevens, 2018). As milrinone is usually used in heart

failure, there should be a decrease in HF symptoms related to acute MI. Moreover,

hemodynamic parameters such as blood pressure and cardiac output should be improving

(Vallerand, Sanoski and Quiring, 2018).

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Boden, W. E., Padala, S. K., Cabral, K. P., Buschmann, I. R., & Sidhu, M. S. (2015). Role of short-

acting nitroglycerin in the management of ischemic heart disease. Drug design,

development, and therapy, 9, 4793-805. doi:10.2147/DDDT.S79116

Brenner, G. M., & Stevens, C. W. (2018). Pharmacology (5th ed.). Philadelphia, PA: Elsevier.

Foth, C., & Mountfort, S. (2018, October 27). Myocardial Infarction, Acute, ST Elevation (STEMI).

Retrieved on November 29, 2018,


Herman, L. & Bhimji, S. (2018, October 27). Angiotensin Converting Enzyme Inhibitors (ACEI).

Retrieved on November 30, 2018,


Khan, M. I. (2015). Cardiac drug therapy (8th ed.). Totowa: Humana Press.

Khan, T., & Siddiqui, A. (2018, October 27). Furosemide. Retrieved on November 30, 2018,

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Lincoff, M., & Cutlip, D. (2018, September). Anticoagulant therapy in acute ST elevation

myocardial infarction. Retrieved on November 29, 2018,



Mulloy, B., Hogwood, J., Gray, E., Lever, R., & Page, C. P. (2016, January 01). Pharmacology of

Heparin and Related Drugs. Retrieved November 30, 2018, from

Vallerand, A. H., Sanoski, C. A., & Quiring, C. (2018). Davis's drug guide for nurses. Philadelphia,

PA: F.A. Davis Company.

Xian, Y., Wang, T. Y., Mccoy, L. A., Effron, M. B., Henry, T. D., Bach, R. G., . . . Peterson, E. D.

(2015). Association of Discharge Aspirin Dose With Outcomes After Acute Myocardial

Infarction. Circulation, 132(3), 174-181. doi:10.1161/circulationaha.114.014992

Yazdi, A. H., Khalilipur, E., Zahedmehr, A., Pouya, S. A., Pakrou, M., Ghaznavi, M. A., . . .

Rouzitalab, M. (2017, July 11). Fibrinolytic Therapy With Streptokinase vs Tenecteplase for

Patients With ST-Elevation MI Not Amenable to Primary PCI. Retrieved on November 25,