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 blood where the atria hold the returning blood to the heart. The heart received its entire supply of blood through coronary arteries. Coronary arteries disease (CAD) occurs due to the buildup of plaque in the arteries known as atherosclerosis (reference anatomy and physiology book). 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 (reference book-pathophys). 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. (reference mayo pdf).
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The Pathophysiology of ACS can be explained in stages starting off 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. (reference book pdf). 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. (reference mayo pdf). 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. (reference book-pathophys).
ACS becomes problematic when the plaque enlarges and caused 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 (reference mayo pdf). Continuous micro tears of the cap results in more fibrous tissue build up and consequently the fatty plaque becomes hard (reference book-pathophys). 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. (reference mechanism of thrombus pdf). The sudden coronary obstruction of the artery caused by thrombus formation over a ruptured or ulverated atherosclerotic plaque is the result of ACS.(reference book-pathophys).
body 2: pharmacology management of ACS- drugs used to treat; MOA of drugs and classes (600 words)
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, nauseas and sweaty. Essential equipment paramedics need to determine severity of ACS is the Electrocardiography (ECG). ALS paramedics carry 3 lead ECG which is capable to determining if there in fact a ST Elevation Myocardial Infarction (STEMI) present and whether a MICA unit is required to do a 12 lead ECG reading. (reference Mayo pdf). 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, 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 now 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. (reference CPG). 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. (reference CPG).. 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.
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Glyceryl trinitrate (GTN) is a nitrate and has been used to treat symptoms of ACS for hundreds of years (reference GTN pdf). 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 (reference GTN 2 pdf). 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. (reference nitrates pdf ). 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 ( reference aspirin good pdf). 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 ( reference aspirin good pdf). 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 active the release of thromboxane A2 and therefore reducing platelet aggregation from occurring ( reference aspirin2 pdf).
Morphine is an analgesic and offers relief of pain and anxiety via the opioid mu (µ) 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. (find reference). The transmission of pain is via a gate control mechanism (reference pahram made easy book). 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 (reference parma book). 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.
body 3: how these relate to paramedics - use of drugs, success rates ect. (200 words)
It is evident that ACS is on the rise in Australia with more and more calls being made daily. The effects of the drug have been proven to have great effects with patients suffering
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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. Due to the increased rates of ACS calls, paramedics nationwide should educate patients on how to reduce the risk factors associated with ACS and also ways of managing symptoms of ACS at home and also the availability of drugs which can be purchased over the counter.