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The cardiovascular system is complex and is one of the key fundamentals of keeping humans alive. The function of the heart is to pump circulating blood to the surrounding organs in the body. Ventricles pump blood out of the heart, where the atria's hold the returning blood from the body. The heart receives its entire supply of blood through coronary arteries. Coronary artery disease (CAD) occurs due to the buildup of plaque in the arteries known as atherosclerosis (Marieb & Hoehn, 2007). Acute coronary syndrome (ACS) refers to the obstruction of the coronary arteries due to atherosclerosis, the process of arterial walls thickening and hardening caused by plaque buildup (McCane, Huether, Brasher, & Rote, 2010). ACS is accompanied by chest pain, radiating from the left arm, along with nausea and sweating. ACS arises generally due to acute myocardial ischemia and can show clinical conditions such as angina. Angina then tiers down to two other symptoms such as stable and unstable angina where their clinical presentation may present similarly but differ in severity of outcome (Kumar, &Cannon, 2009).
The Pathophysiology of ACS can be explained in stages beginning with the initiation of atherosclerosis. Atherosclerosis is an ongoing process throughout an individual's lifetime. Atherosclerosis has many contributing risk factors such as hypertension, smoking, diabetes and obesity(Imaizumi, 2011). These risk factors cause damage to the endothelium layer and as a result cause endothelium dysfunction. Once the endothelium has been damaged inflammatory mediators come to the site and the progression of atherosclerotic plaque is now in progress. Monocytes are first to react as a result of the inflammation and undergoes its transformation into macrophages (Kumar, &Cannon, 2009). It is the role on the macrophages to then engulf oxidized low-density lipoprotein (LDL), which have been increased due to the risk factors mentioned earlier, as they will penetrate the arterial wall forming fatty streaks and foam cells resulting in plaque buildup at the injured site. The macrophages release chemoattractants and cytokines which signal additional macrophages to the site of the plaque (McCane, Huether, Brasher, & Rote, 2010).
ACS becomes problematic when the plaque enlarges and causes partial block or full occlusion of the artery or when the plaque ruptures. The growth of the plaque is a result in a tear of the plaques fibrous cap. The tear of the cap allows contact between the plaque and the circulating blood. Inflammatory mediators then promote further coagulation to close the cap, which leaves the cap weakened and vulnerable to tear again (Kumar, &Cannon, 2009). Continuous micro tears of the cap results in more fibrous tissue build up and consequently the fatty plaque becomes hard (McCane, Huether, Brasher, & Rote, 2010). Thrombus formation occurs when the tear exposes majority of the plaque content into the blood stream which activates platelets. In addition the activation of platelets results in the changeover of the glycoproteins IIb/IIIa receptors which are fundamental to thrombus formation, due to the fact that this is where fibrinogen combines to form the fibrin mesh and platelet aggregates (Furie, & Furie, 2008). The sudden coronary obstruction of the artery caused by thrombus formation over a ruptured or ulcerated atherosclerotic plaque is the result of ACS (Kumar, &Cannon, 2009).
Upon suspicion of ACS, paramedics need to have appropriate equipment to correctly diagnose and treat the patient accordingly. Paramedics need to look for the classic signs and symptoms in which ACS produce, which are chest pain with radiation down the left arm, nausea and appear sweaty. An essential equipment paramedics require in order to determine the severity of ACS is the Electrocardiography (ECG). ALS paramedics carry 3 lead ECG which are capable of determining if there is in fact a ST Elevation Myocardial Infarction (STEMI) present and whether a MICA unit is required to do a 12 lead ECG reading (Kumar, &Cannon, 2009). Paramedic's response time to the patient is a crucial factor in the survival of patients with ACS and early management by the paramedics may determine life or death. Close monitoring of the patient is required as patients with ACS can go into a full cardiac arrest. The Clinical Practice Guidelines (CPG) states that patients who are suffering from ACS are administered with nitrates and antiplatelets followed by pain relief. If the patients systolic BP > 110, Glyceryl trinitrate (GTN) is administered 300mcg sublingual/buccal if no previous administration or 600mcg sublingual/buccal if previous administration. A repeat of the initial dose is to be administered after 5 minutes unless the patient's blood pressure has dropped below 110 mmHg systolic. If that is the case then a GTN patch of 50mg is to be applied until systolic BP is below 90 mmHg (Clinical Practise Guidleine: For Ambulance and MICA Paramedics, 2012) . Aspirin is then given once at a 300mg oral chewable tablet, and also the administration of morphine up to 5mg IV and repeating the dose with a 20mg as a maximum dose (Clinical Practise Guidleine: For Ambulance and MICA Paramedics, 2012) .
Before administering morphine, paramedics need to consider the amount of pain in which a patient is suffering. A pain score out of 10 is asked of the patient which paramedics can then indicate how much morphine to administer in order to achieve a lower pain score outcome. D.O.L.O.R is an acronym often used to also determine the patient's pain, where D stands for description where the paramedics ask the patient to describe the type of pain, whether it be sharp, stabbing, burning or dull. O is onset of the pain which paramedics can determine when the pain had occurred used in conjunction with L for location of the pain. This helps to determine if the chest pain is central or if the pain may radiate to other parts of the body, typically down the left arm. O is for other signs and symptoms which may be associated with the primary ACS symptoms and can include the patient feeling nauseous and dizziness. R is for the relief of pain, where paramedics ask the patient whether they have taken any medications or drugs to try and relieve the pain prior to the paramedics arrival. Generally patients with ACS chest pain may have their own anginine spray or have even taken a couple of aspirin tablets before the paramedic's arrival.Patient with successful treatment will begin to display no or reduced symptoms compared to initial assessment. Paramedics need to transport the patient to the nearest hospital for further treatment.
Drugs; Mechanism of Action:
Glyceryl trinitrate (GTN) is a nitrate and has been used to treat symptoms of ACS for hundreds of years (Csont, Szilvassy, Fulop, Nedeiani, Pali, Tosaki, Dux, & Ferdinany, 1999) . GTN is currently a drug used within Ambulance Victoria in the treatment of ACS. GTN is used for its smooth muscle relaxant properties and also vasodilator effects. GTN reduces the demand of myocardial oxygen to the heart by decreasing preload. Furthermore it also dilates large coronary arteries and enhances myocardial oxygen delivery to ischemic areas such as the myocardium (Ignarro, Lippton, Edwards, Baricos, Hyman, Kadowitz, & Gruetter, 1981).GTN works by releasing a free radical known as nitric oxide (NO). The NO then activates guanylate cyclase in vascular smooth muscle which catalyses guanylate cyclase to cyclic guanosin monophosphate (cGMP). The result of cGMP is that it then reduces intracellular calcium levels which in turn lead to relaxation. (Nossaman, Nossaman, &Kadowitz, 2010). These effects may reduce chest pain sensation in the patient.
Aspirin is the most common non-steroidal anti-inflammatory drug (NSAID) and is administered orally which is rapidly absorbed. It is used for its antiplatelet agents and to reduce thrombus formation. Aspirin is used as a treatment of ACS by Ambulance Victoria paramedics as it prevents platelet aggregation by inhibiting the production of thromboxane A2 ( Eisenberg, & Topol, 1996). Thromboxane A2 is produced in platelets and is released in an inflammatory response, which may include the rupture of atherosclerotic plaque. Aspirin permanently inhibits the production of thromboxane A2 as it inactivates the cyclooxygenase pathway ( Eisenberg, & Topol, 1996). The role of the cyclooxygenase (Cox) enzyme is to break down arachadoinc acid into inflammatory substances (thromboxane and prostaglandins). Blocking the Cox enzyme therefore stops inflammatory mediators to activate the release of thromboxane A2 and therefore reducing platelet aggregation from occurring (Vane, 1971).
Morphine is an analgesic and provides relief of pain and anxiety via the opioid mu (Âµ) receptor. Pain can arise from nociceptors which are found in nearly all organs but the brain. Nociceptors are naked nerve endings that first register the pain stimulus. There are two types of nociceptors type A-delta fibres and C-fibres. Both A-delta and C-fibres perceive pain but differentiate in sensation. The transmission of pain is via a gate control mechanism (Dawson, 2002). Pain stimulus travels in an afferent transmission via the spinal cord through the dorsal horn, then to the cortex where the pain is registered. Opioid receptors bind to g-protein coupled receptors which regulates the opening and closing of potassium and calcium channels. Inhibiting the opening of calcium channels decreases the release of excitatory neurotransmitters which causes pain. Morphine stimulates opioid receptors which inhibits the release of substance P, involved in bringing upon pain, inflammation and smooth muscle contraction in the dorsal horn, and closes the gate which prevents the afferent transmission to occur ( Bryant & Knights, 2011). Therefore by closing the gate, pain stimuli are unable to register in the cortex, and as a result pain is decreased or no longer felt.
It is evident that ACS is on the rise worldwide with increasing calls being made to emergency services daily. The effects of the drugs have been proven to have vast effects with patients suffering from ACS. This is evident through the Ambulance Victoria's Clinical Practice Guidelines (2012) for ACS as GTN, aspirin, and morphine are vital drugs to be used when treating the patient for the most successful outcome. GTN is the preferred drug used during treatment as drug dose can be easily controlled and altered, duration is short acting and peak of the drug lasts between 5-10 minutes compared to many other smooth muscle relaxant drugs available in the market (Bang, Nojgaard, Andersen & Matzen, 2008). Aspirin is the preferred antiplatelet drug classified as a schedule 2 drug class; it is cost effective, works efficiently and has minimal side effects to the patient, as well as being easily administered in difficult situations. Drugs assist paramedics in the management of pain. Morphine helps in reducing initial chest pain associated with ACS or completely masks the patients' pain. Although morphine may have its side effects such as CNS depression, respiratory depression and bradycardia, its beneficial effects of reducing pain outweighs the side effects the patient experience.
The role of the paramedic in ACS is crucial as it can determine the outcome of the patient. The key responsibility for paramedics is early intervention with treatment as well as dealing with other signs and symptoms and immediate transport. Calling upon MICA backup is also important for their use of a 12 lead ECG to depict severity. A delay in treatment may have consequential actions such as a cardiac arrest and death. Paramedics are able to successfully treat patients with ACS without complications arising due to the advanced machines and a wide range of drugs made available for the paramedics to use. Due to the increased rates of ACS calls, paramedics nationwide should educate patients on how to reduce the risk factors associated with coronary artery disease, acute coronary syndrome, ways of managing symptoms of ACS at home and also the availability of drugs which can be purchased over the counter.