History of presenting illness

Answer

Assignment 1: Case Study

Question 1

The coronary vessel/vessels involved:

Ben was diagnosed with an anterolateral STEMI with inferior reciprocal changes. Therefore, he experienced both anterior and lateral myocardial infarction. According to the ECG Learning Center (2016), the left anterior descending coronary artery supplies the anterolateral and the anterior walls of the left ventricle while the right coronary artery supplies the inferior portions and the right ventricle. Therefore, the coronary arteries involved in the anterolateral MI with inferior reciprocal changes were the left anterior descending coronary artery and the right coronary artery.

Myocardium and conduction system at risk:

The areas of the heart supplied by the left anterior descending coronary artery and the right coronary artery will be at risk of ischemia due to poor blood supply. The myocardium supplied by these arteries that will be at risk after occlusions are the anterolateral and the anterior walls of the left ventricle as the diaphragmatic myocardium. The anterior two-thirds of the interventricular septum that is supplied by the left anterior descending coronary artery will be also at risk. The ECG Learning Center (2016) also posits that the right coronary supplies the AV node through it AV nodal coronary artery branch. Therefore, the AV node will be the part of the conduction system at risk.

The potential complications:

According to Annenberg Center for Health Sciences (2016), the complications of STEMI are cardiogenic shock, left ventricular aneurysm, atrial fibrillation, ventricular septal defect, left ventricular thrombus, left ventricular free wall rupture, acute mitral regurgitation, and pericarditis. Ben is likely to develop the STEMI complications that are directly linked to the myocardium or the conduction system affected occluded arteries. Cardiogenic shock is likely to be developed due to the reduced strength of myocardial contractility especially in the left ventricle. The cardiac output will reduce and therefore, leading to insufficient pumping of blood to tissues. Left ventricular aneurysm is likely to develop because of inadequate blood flow in the left ventricle walls. Ventricular septal defects such as free wall rupture can occur because of thinning of the septum due to inadequate blood supply that leads to necrosis of the septal tissues.

Question 2

Actions, dose and appropriateness of each drug

The main medications administered to Ben were Aspirin, Clopridogrel, morphine, and heparin. These medications were appropriate in alleviating his symptoms of myocardial infarction and risks for further complications. According to Katzung, Masters, & Trevor (2012), the actions of Aspirin in the body include anti-inflammation, anti-coagulation, analgesic, and anti-pyretic that are achieved by the irreversible acetylation of cyclooxygenase enzyme. The acetylation inhibits the enzyme and therefore, prevents the synthesis of prostaglandins that are important mediators of pain, inflammation, fever, and coagulation. The ultimate of Aspirin’s anti-coagulation effect is inhibition of aggregation of platelet; an essential initial step in the clotting process. Aspirin is particularly appropriate in the management of STEMI due to its anti-platelet activity. The drug inhibits the formation of clots and therefore, can limit clots associated with occlusion of the coronary arteries aforementioned. Additionally, the analgesic properties of Aspirin will also regulate the pain experienced by Ben that he rated as 9/10. Katzung, Masters, & Trevor (2012) further posit that the dose of Aspirin appropriate for anti-platelet activity is 81-325mg once daily. Ben experienced a profound STEMI with the risk of its complications such as spread of emboli to the brain. Therefore, he should receive Aspirin dose of 300mg once daily.

Clopridogrel was also helpful in mitigating the progression of the pathophysiology of the STEMI. The emc+ (2016) opines that Clopridogrel is an anti-platelet drug that prevents clumping together of platelet. This action will prevent formation of thrombi on the already narrowed coronary arteries. Ben should start on the recommended loading dose of 300mg of Clopridogrel once daily (emc+, 2016). This medication will be appropriate to couple the anti-coagulation effects of Aspirin. Next, Ben experienced a very severe pain rated as 9/10. Therefore, the administration of morphine was appropriate for pain management. According to Katzung, Masters, & Trevor (2012), morphine is an opiod prototype used for the management of moderate to severe pain with an appropriate oral dose of 5 to 30mg with analgesia for 4-5 hours for adults. Therefore, Ben should receive a morphine dose of 5mg after 5 hours to avoid addiction.

Ben’s last medication was heparin. Heparin is both an anti-coagulant and anti-thrombotic drug that inactivates the various clotting factors and enables the clot lytical mechanisms to break down existing clots (Mulloy, Hogwood, Gray, Lever, & Page, 2016). The administration of heparin will be appropriate to prevent spreading of clots to the brain that might result to a cerebrovascular accident. According to Katzung, Masters, & Trevor (2012), heparin dosage should constitute an initial bolus injection of 80-100units per kg and a continuous infusion of 15-22units/kg/hour. Therefore, Ben should be given a loading intravenous dose of 80units/kg and a continuous dose of 20units/kg/hour.

The clots that formed in Ben’s coronary vessels should be lysed to enable reperfusion of the myocardium and prevent the risk of spread of clots to other parts of the body such as the brain. Katzung, Masters, & Trevor (2012) opine that fibrinolysis involves digestion of fibrin using plasmin. Therefore, fibrinolysis would involve activation of plasminogen to plasmin that then digests the fibrin clots. Fibrinolysis is an effective alternative solution to recanalization or percutaneous coronary intervention in promoting reperfusion. According to Katzung, Masters, & Trevor (2012), tissue plasminogen activator, streptokinase, and urokinase can activate the fibrinolytic pathway. Therefore, these chemicals are suitable for fibrinolytic therapy. Also, Karthikeyan, Senguttuvan, Joseph, Devasenapathy, Bahl, & Airan (2013) observed in their study that streptokinase was the most used fibrinolytic agent followed by tissue plasminogen activator, and urokinase with 18%. Therefore, streptokinase will be the drug of priority as a fibrinolytic therapy for Ben.

Nurses have a role in ensuring proper management of all the drugs aforementioned. The nurses should ensure that administration of drugs promote quality and safe care. First, the nurse must ensure that all the drugs are administered according to the physician’s prescriptions. The doctors should be consulted in a case when there is uncertainty on the formulation of a drug. Nursing management should also focus on supporting positive outcomes from the treatment and regularly monitor the progress of treatment. Most importantly, the nurse should monitor adverse reactions due to the medications and report the same to a physician immediately.

The medications are also relevant for the ongoing patient status. Ben has hypoxemia while on room air and also has tachypnea. Therefore, the continuation of oxygen therapy is suitable to ensure he has enough oxygen in blood.

Question 3

The administration of ACE inhibitor and a beta blocker were appropriate to enhance Ben’s cardiac function. Hall (2015) posits that ACE converts angiotensin I to angiotensin II that is a potent vasoconstrictor in the body. Therefore, an ACE inhibitor will prevent the conversion of angiotensin I to angiotensin II. Consequently, there will be less amount of angiotensin II circulating in the blood and the extent of vasoconstriction will be limited. The diameter of the vascular lumen will remain dilated and therefore, blood pressure will reduce. The reduction in blood pressure would mean the heart will have a minimal amount of force to pump blood against. As a result, blood flow to the tissues will be optimized despite the diminished left ventricular function. The relaxation of the blood vessels would also promote blood flow into the myocardium and therefore, supplying more oxygen to the myocardium.

Beta blockers will also promote cardiac function and prevent further complications of the myocardial infarctions. Beta blockers inhibit the effects of the adrenaline hormone that causes vasoconstriction, increases myocardia contractility, and increases the oxygen demand of the myocardial tissues (Katzung, Masters, & Trevor, 2012). The administration of a beta blocker will reverse the adrenergic effects aforementioned due to the inhibition of adrenaline. According to the American Heart Association (2015), beta blockers reduce myocardial contractility, cause vasodilation, and reduce the heart rate. These three effects relieve stress on the heart to pump blood to all the body parts. For instance, vasodilation in all the body parts lowers blood pressure and therefore, reducing the amount of force that the left ventricle must exert to pump blood to other body parts. In this case, Ben had a left ventricular dysfunction. Therefore, lowering the needed pressure for the left ventricle to pump sufficient amount of blood is beneficial in enhancing cardiac function.

The next advantage of using a beta blocker would be a reduction in the myocardial contractility. This reduction is due to the inhibition of the adrenaline hormone that activates the sympathetic system in the body. Tissue demand for oxygen depends on the level of activity of the tissue. For instance, skeletal muscles demand more oxygen when an individual is performing physical exercise than when a person is resting. Similarly, the cardiac muscle tissue in the myocardium would demand for less oxygen when their contractility is reduced by the beta blocking agent. Necrosis in myocardial infarction usually occurs when oxygen demand in the myocardium exceeds supply. Therefore, lowering oxygen demand by administering a beta blocker would limit the chances for cardiac tissue necrosis due to the lower demand for oxygen.

A beta blocker would also couple the effects of ACE inhibitors in reducing blood pressure. Hall (2015) argues that venous return is directly proportional to total blood pressure. Therefore, it can be adduced that lowering blood pressure using the beta blocker and ACE inhibitor would reduce preload because little amount of blood will be pushed back to the heart by the low blood pressure. Consequently, the pumping mechanisms of the heart in the left ventricle would not get strained because only little amount of blood would be available to be pumped out. Additionally, cardiac output will reduce because the beta blockers reduce the heart rate. The ultimate effect of low preload and reduced cardiac output would be a decrease in afterload. Therefore, the workload of the heart would reduce and this would decrease the oxygen demand in the myocardium. The low oxygen demand will ensure the cardiac cells survive despite the hypoperfusion of the myocardium. In summary, the ACE inhibitor and the beta blocker would work to reduce blood pressure, myocardial contractility, and heart rate. These effects are directed towards ensuring the heart functions with the minimal amount of oxygen supply available.