Pathophysiology of Acute Heart Condition - Myocardial Infarction

Myocardial infarction is a very serious medical issue and it needs to be treated as soon as possible. Every nurse should have the knowledge about this condition and should know how to treat a patient who is suffering from this condition. According to the Australian Bureau of statistics Ischaemic heart disease was top leading cause of death in Australia in 2017 and heart failure was number thirteen cause of death for men and number eleven for women in Australia (Australian bureau of statistics, 2018). This essay will discuss and analyse the pathophysiology of Myocardial infarction. Fist it will go through pathophysiology of ST-Elevation Myocardial Infarction, then symptoms of this condition and pathophysiology of the symptoms to analyse reasons that patient have those symptoms.

In myocardial infarction one or more than one parts of myocardium can be permanently damaged as a result of low oxygen supply because coronary arteries are blocked and they cannot transfer enough blood to cardiac muscles and myocardium cells start to die which is known as necrosis (Farrell, 2017). One of the biggest contributors to myocardial infarction is atherosclerosis and there are lots of evidence to suggest that high concentration of low density lipoproteins (LDL) in blood can start and help atherosclerosis to progress (Lu & Daugherty, 2015). First the process starts with a damage in endothelial layer, then it transfers LDL from blood into tunica intima and LDL become oxidised LDL, after that endothelial cells discharge a protein named monocyte chemoattractant protein which is responsible for bringing monocytes to the site of injury and after monocytes enter the intima they turn to macrophages. Macrophages try to fight ox-LDL and after ingesting them they eventually become foam cells. These new foam cells discharge more chemokines and monocyte chemoattractant protein forces SMCs to come into intima, then platelet-derived growth factor is secreted by Foam cells, SMCs and macrophages. Then foam cells and macrophages release Interleukin IL-12 which causes T cells to be activated and it is a contributor to plaque growth, then interferon IFN-γ is discharged by T cells and then they bring more macrophages into intima and the process repeats itself which starts to build up plaque and eventually cause atherosclerosis (Hao & Friedman , 2014). Thrombus generation at the site of plaque rupture is effected by local flow disturbances, plaque vulnerability and systematic thrombotic propensity involving platelets hyperactivity, inflammation and blood vulnerability. Platelets adhesion is initiated by binding of glycoprotein Ib-V-IX receptor to Von Willebrand factor (vWF) glycoprotein receptor binds to collagen. After adhesion platelets form monolayer at the site of rupture, they release two agonists thromboxane A ( TxA2 ) and adenosine diphosphate (ADP). These two receptors play a role in in platelets activation and activation of GPIIb/IIIa receptors. Thrombus is formed when activated GPIIb/IIIa receptors bind between platelets through fibrinogen. Thrombin promotes more platelets activation and the formation of procoagulant platelet surface and larger amounts of thrombin created. At the end thrombin converts fibrinogen to fibrin and as a result a fibrin network and platelet fibrin clot is formed (Waksman et al, .2014). Then fatty tissues and thrombus make coronary arteries narrow and interrupts blood flow to cardiac cells, if doctors do not address this issue as soon as possible myocardial cell start to die as a result of low oxygen and the body does not have the balance for oxygen supply and demand anymore (Montecucco et al., 2016).

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Myocardial infarction has many symptoms including angina, diaphoresis and, nausea, shortness of breath, elevated cardiac troponin and creatine (Jevon, 2012). All these symptoms have pathophysiology explanations and they will be analysed one by one.

Angina is usually a severe pain in the chest which can radiate to neck, jaw and left arm. It can come from Ischaemic or coronary diseases and it could be a sign of myocardial infarction (Wolters Kluwer Health, 2014). Angina is a visceral pain and visceral pain is caused by autonomic nervous system. During a cardiac pain afferent sympathetic nerve activity is affected by adenosine which is responsible for signalling pain from heart to brain. Afferent sympathetic neurones pass from myocardium to superior cardiac plexus, then they go through sympathetic ganglion chain to the dorsal horn of the spinal cord. After that they connect to neurons in Lamina I and V. it is possible that this is the point at which signals occurs between somatic and visceral afferent pathways and because cardiac sympathetic plexi, spinal cord and ganglion chain have many connections angina pain can be felt in many parts of upper body (Leach & Fisher , 2013).

The second symptom of MI is diaphoresis which means excessive sweating. There are two possible reasons for excessive sweating in MI. The first reason is sympathetic nervous system starts to stimulate and produces sweating to protect the body from pain, but this explanation does not explain the absence of sweating in other painful diseases such as trauma, burn. The second explanation is activation of the sympathetic nervous system because of hypotension which has caused by acute MI (Gokhroo et al., 2015).

Another symptom is nausea and there are two explanations for nausea in patients with myocardial infarction. The first possible reason could be injured and necrotic cardiomyocytes discharge metabolites such as pyruvic acid and lactic acid, then these metabolites stimulate autonomic nerve peripheral receptors and it causes nausea. The second explanation is reduced function of heart as a result of myocardial necrosis and occlusion of coronary arteries which can trigger Bezold-Jarisch reflex and can cause nausea (Guo et al., 2015).

One of the most important symptom is shortness of breath and it happens because when cardiac cells die and coronary arteries are occluded the body needs more oxygen and heart cannot give enough oxygen to the body , the heart receives the a signal to increase rate of breathing because oxygen demand is more than oxygen supply (Berliner et al, 2016).

Another symptom of myocardial infarction is increases level of troponin which is responsible for cardiac cells contraction. When the cardiac cells start to die, they release troponin into blood stream and it causes the troponin to elevate (Popp, 2013). Creatine also is another enzyme that exists in heart muscles and skeletal muscles and body releases creatine after infarction to blood stream (Mythili & Malathi, 2015).

So, myocardial infarction pathophysiology and symptoms of this condition have been explained. The mortality rate of MI keeps declining because of advancement in medical therapy.

References

1. Australian bureau of statistics. (2018), Causes of Death, Australia, 2017 https://www.abs.gov.au/ausstats/abs@.nsf/Lookup/by%20Subject/3303.0~2017~Main%20Features~Australia's%20leading%20causes%20of%20death,%202017~2
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