To assist in the diagnosis and aid in determining the causes and symptoms of heart disease, several diagnostics tools ( i. e. ECG), and laboratory tests such as blood serum level of enzymes can help health professional’s determine a favourable outcome in treating this disease. The heart electrical activity is recorded by using ECG; it is use to detect changes that occur during the course of myocardial infarction. For example, ECG patterns of patients with AMI may reveal “marked elevations in ST segments on ECG and are categorized as having ST-elevation MI or STEMI.
Those without segment elevation are more likely to have subendocardial infarction and are said to have non-STEMI” (Huether et al, 2008, p. 631). This abnormal elevation in ST-segment, STEMI in particular, requires immediate intervention to prevent serious damage to the heart (Huether et al, 2008). Furthermore, any abnormal readings can indicate chamber enlargement of the heart, pericardium inflammation or heart damage (Funnel et al, 2006). There are various serologic markers associated with the heart that can be utilised for additional resources for early evaluation and diagnosing of AMI.
The serum level of enzymes and isoensymes (CK-MB, lactic dehydronagenase and aspartate), myosin and troponin, electrolytes (potassium and sodium), are all determinants of AMI diagnosis( Gould, 2006 ). These elevated levels of total creatine kinase(CK) and CK-MB isoensymes and cardiac troponin , indicate confirmation of myocardial Infarction (Yuan, 2003). These enzymes are released from the myocardium into the tissue fluid and circulating blood and are a specific indication of myocardial tissue damaged during the onset of myocardial infarct in the body (Gould, 2006).
The level of cholesterol in the body correlates significantly with coronary artery disease. According to George-Gay & Chernecky (2002), people with high level of triglycerides are at more risks of coronary heart disease. Low-density lipoproteins (LDL) are considered bad cholesterols as these accumulate in the walls of the arteries. High-density liproprotein (HDL) is said to be good cholesterol as it takes cholesterol away from tissues and delivers them to the liver to be metabolised, thus preventing the formation of plaque in the arterial walls.
The desirable range for LDL, HDL, and triglycerides for people at risk/no risk are: LDL: less than 160mg/dl for persons with coronary artery disease(CAD) and less than 180mg/dl for persons without CAD; HDL: more than 45mg/dl for men and more than 55mg/dl for women; triglycerides; from 40-160mg/dl for men and 35-135mg/dl for women and finally, total cholesterol overall is less than 200mg/dl (George-Gay & Chernecky, 2002). Mathew’s diagnostic results such as ECG, serum level of troponin, triglycerides and lipids indicate abnormalities in the heart, blood serum level and cholesterol (Medical Council of Canada (2010).
This abnormality is indicative of myocardial infarction and need further investigation and intervention. Complications: According to Funnel et al. (2006), myocardial complications are attributed to left ventricular failure, arrhythmia and pericardities. It is very common for patients to feel depressed after their recovery period and this can result to non compliance with their treatment regime and may cause further infarctions (Funnel et al. , 2006).
Other complications after a heart attack include, persistent or recurrent chest pain, cardiogenic shock, rupture of ventricular septum causing ventricular defect, rupture of ventricular papillary muscle causing mitral valve insufficiency, thromboembolism and ventricular aneurism. Pharmacological Management: Treatment of myocardial infarction and angina in Mathew’s case focus in reducing the myocardial oxygen demand, relieve chest pain , stabilize the heart rhythm, and to increase blood flow to the heart; in other words treatment is focus on preserving the integrity of the myocardium (Yuan, 2004).
Drugs that may be given to Mathew to treat his myocardial infarction are believed to be the cornerstone in treating coronary heart disease and angina. These are as follows: Nitroglycerine (anginine, lycinate) is the drug of choice in treating angina because of its perfusion effects; it dilates the coronary arteries and this enables more oxygen delivery that the body needs (Bryant & Knights, 2007). Nitrates such as anginine is given to relieve pain by redistributing blood to the affected areas in the myocardium thus increasing cardiac output and reducing myocardial workload (Yuan, 2004).
Moreover, patient suffering from angina attack is given this type of drug not only to relieve pain but also as a prophylaxis measures (Tiziani, 20060). Prior to beginning treatment, nurses should check if there are other medications the patient is taking or any allergies as this may interact with the drug. The correct route of administration (i. e. anginine is to be taken sublingually) must also be taken into consideration as this may affect the bioavailability of the drug (Tiziani, 2006). Beta blockers (atenolol, bisoprolol, metoprolol etc), is used to inhibit the stimulation of the sympathetic nervous system.
This inhibition reduces the responses of the body to adrenalin, noradrenalin and isoprenaline. Beta blockers such as beta one and beta two causes inhibition of sympathetic nervous system response that results in decrease in cardiac output, myocardial oxygen demand, blood pressure, rate of impulse in the conducting system (Tiziani, 2006). Patients using this drug may experience bronchospasm, bradycardia, hypotension, diarrhoea, cold extremities, dizziness, fatigue, palpitations, wheezing and dyspnoea on exertion (Tiziani, 2006).
It is vital for a nurse to check patient’s heart rate before administering the drug and warn patient to sit or lie down at the onset of faintness. If heart rate is less than 60 beats per minute and blood pressure less than 90 systolic, this drug is not be given or initiated ( George-Gay, & Chernecky, 2002). ACE Inhibitors (captopril, enalapril, fosinopril, lisinopril) are anti-hypertensive drugs that block the conversion of angiotensin converting enzyme responsible for the conversion of angiotensin I to angiotensin II.
Angiotensin II is a potent vasoconstrictor that strongly constricts and narrows blood vessels, thereby causing the increase of peripheral vascular resistance (Bryant & Knights, 2007). Captopril for example acts to block effects of angiotensin by preventing angiotensin I from binding angiotensin II receptors; due to this, it can dilate blood vessels and increase the excretion of sodium and water, thereby reducing blood pressure (Pharmacogenomics Knowledge Base, 2010).
Nurses should advise patients taking diuretic medication as it may significantly lower their blood pressure, and patients should report any adverse reaction such as palpitations, tachycardia, chest pain, dizziness, hypotension and headache (Tiziani, 2006). Thrombolytic drugs (altepase, reteplase, streptokinase or urokinase) help to establish blood flow especially with patients with AMI; it is used to dissolve blood clots in the coronary arteries which are causing total blockage to blood circulation (Gutierrez & Peterson,2007).
It is important to note that this type of drug must be administered within the “6-hour window” from the onset of myocardial infarct to reverse the damaged to the myocardium and help resume blood flow to the heart (Gutierrez & Peterson, 2007, p. 239). According to Huether et al. (2008), patients diagnosed with non-STEMI and STEMI must be administered with this drug during the critical hour of heart attack to lessen the risk of further complications including death. On the other hand, patients not receiving this drug will be receiving other alternative drugs such as prophylaxis for venous thrombosis (Huether et al. , 2008),
Antiplatelet (aspirin, clopidogrel, dipyridamole, ticlopidine,) drugs is an important adjunct to thrombolytic therapy; it is used to enhance the effects of thrombolytic agents. For example, aspirin, its action is to inhibit the aggregation of platelet, increase platelet activity in AMI and permanently damages the platelet (George-Gay, & Chernecky, 2002). Furthermore, according to Yuan (2004), this drug should be given within 24 hours after the onset of symptoms of myocardial infarction and patient is monitored closely for any sign of bleeding as it may interact with other antiplatelet drugs or fibrinolytic agents.
Analgesics (paracetamol, NSAID, opiods ), are drugs used to relieve pain that acts in peripheral and nervous system. There are two types of this drug, opiod anlgesic (acts on the nervous system and alters a person perception and used for severe pain) and nonopiod analgesic (mostly act at the periphery and used for mild to moderate pain and doesn’t affect a person perception) (Harris, Nagy & Vardaxis, 2006).
These drugs is also use for fever, inflammation and can be use as an adjunct to other medications. The widely use aspirin (salycylates), not only control pain but also have antipyretic and anti-inflammatory effect. It relieves pain by inhibiting the inhibition of prostaglandin synthesis, reduces fever by stimulating the hypothalamus by causing vasodilatation in the peripheries and inhibits platelet aggregation.
Patient use this drug may experience nausea, vomiting, abdominal distress, hearing, loss dizziness, impaired vision, tinnitus and bleeding tendencies. Before giving initial dose, it is vital to assess potential for interactions with other prescriptions, over the counter that patient is using. Furthermore, nurse should monitor the patient for signs of bleeding, hearing and eye function, bronchospasm and report for any adverse reaction and interaction (Sutherland, 2005).