Nursing: Myocardial Infarction and Recent Clinical...

Patient’s failure to call 999 is a major cause of delay in treatment for acute myocardial infarction. It’s been suggested that delaying to call 999 among the older patients is a common feature. Older patients who had a previous cardiac problem often do not wish to call for help in order not to trouble the out of hours services (BHF, 2006).
This was the case of Mr.JH the 72yrs old male Caucasian patient. He was due to be seen in our outpatient clinic as a routine visit. Mr. JH is a cheerful, well presented retired air traffic controller known to have DM type II in 1999, previous AMI in 2000(no interventions, he was thrompolysed), and advanced Ca. colon. I saw Mr.JH with his wife and started my routine procedures. Mr.JH was quiet unlike him, so I started with a simple question how are you? His answer was with a nod and with a faint voice “I’m fine” which was very odd. His wife jumped to add he was having chest pain all weekend. I turned to Mr. JH and asked him tell me more about it.
It is essential to let the patient express their chief complaints using their own word. An accurate description from the patient will provide an insight to the origin of the illness and help to identify if the patient is trying to deny having a cardiac problem (Davis L, 2004). It’s also essential to ask the correct relevant questions to determine the origin of the pain cardiac or non cardiac. A thorough history highlights all important symptoms, evaluates severity of the symptoms, past medical (any previous CHD) and family history, current medication, review of systems(Coady E, 2002).
Mr. JH said he had for 2 days central chest discomfort, radiating to his neck, not relieved by GTN spray, mild SOB. No other symptoms associated. He reported his discomfort was not trigged by any physical activity and actually it came during rest on Saturday. I tried to exclude any positional pain, pain associated with breathing, abdominal pains (NICE, 2010). At the clinic; he had mild chest discomfort. His BP was 208/110mmhg on the Lt Arm, 190/110mmgh on the RT arm, pulse 100bpm, RR 25/min, Spo2 on air 92%. He was pale, not sweating. ECG was done immediately showing sinus tachycardia Ventricular Rate 100/min, Tall Twave, ST depression on lead II and III. Q waves appeared in anterior and inferior leads. Immediate medical help was called. Mr.JH was transferred to acute medical unit where he was cannulated and started on O2 therapy. He was attached to cardiac a monitor and bloods for Trop T, U+E, FBC, ABG and CKMB were collected. He was reviewed by cardiology on call and after assessment an initial Non STMI was suggested pending on cardiac markers; Bisoprolol 25mg, ASA 300mg and Clopidogrel 300mg PO, diamorphine 2.5mg IV, clexane sc 40mg was initiated and ECHO and CXR were booked (NICE, 2010). GTN infusion was also started to lower blood pressure. Mr. JH was for conservative management at this point (ESC, 2007).
In patients with Non STMI two strategies are possible, either routine invasive strategy (PCI) or conservative strategy. Patient will undergo a risk stratification score to determine which strategy is suitable. The 3 most commonly used are TIMI, GRACE and PURSUIT. Recent clinical trials are being conducted to evaluate the benefit of early invasive strategy vs. conservative for USA and Non STMI (Texas Heart, 2010). The theory behind this; acute coronary syndrome conditions share the similar pathophysiology, which leads to the instability and rupture of atherosclerotic plaques. However, they are differentiated by their severity and prolonged ischemia leading to a damage to the myocardium. When an existing atherosclerotic plaque ruptures, it causes damage to the endothelial and activation of the clotting cascade. As a result of this damage, platelets adhere to the vessel lining and become activated and secrets an array of substances, including fibrinogen. Fibrinogen then forms bridges between platelets by binding to GB IIb/IIIa receptors causing

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