The vital signs depicted, that is, Pulse 100; BP 150/120; Resp 18; are fit to describe several diagnoses. In this case, the likely diagnoses that may be represented include Myocardial infarction, Ischemic heart disease and Cardiac Tamponade. Among the three possible diagnoses, myocardial infarction is the most likely diagnosis whose pathophysiology is characterized by the development of a clotting cascade which is usually triggered by a significant disruption of the atherosclerotic plaque. This could lead to a partial or total occlusion of an epicardial coronary artery (Chou, 2015). Atherosclerosis occurs due to a gradual but fast build up of a mass of cholesterol as well as other fibrous materials within the walls of the arteries. Continued atherosclerosis causes inflammation of the arterial walls a condition that can be described as myocardial injury whose extent is determined by the duration and intensity of metabolic demand (Thygesen et al., 2012).
As the myocardial injury continually extends, there could occur a rupture of the plaque formed on the arterial walls leading to the formation of a blood clot. This blood clot will now essentially occlude the artery and in the case of coronary artery, the walls of either the left ventricle or the right ventricle are damaged irreversibly (Arenja et al., 2013). This is usually triggered by the impaired inflow and outflow of blood within the heart caused by the prevailing clot in the artery. In the event of the death of the cardiac cells, a condition referred to as necrosis, then this part of the heart forms a collagen scar (Alherbish et al., 2013). This implies that the heart apart from experiencing impaired blood flow it will also experience abnormal rhythms and this is worsened by the situations of high metabolism when demand for oxygen is high (Thygesen et al., 2012).
The occlusion of the artery has several implications on the normal functionality; the blockage results in the impaired inflow and outflow of blood where by the clot causes a buildup of pressure in the other arteries as well as the affected artery (Chou, 2015). This explains the elevated blood pressure as would be seen in the case study where the blood pressure, 150/120 is beyond the normal BP levels (120/80). As the demand for oxygen increases and the abnormal rhythm negatively affect the ability of the heart to sustain enough blood supply to the demanding organs, the heart has to overwork and this is explained by the high pulse rate (100) (Arenja et al., 2013).
A high pulse rate on the other hand, and an irregular blood supply are translated as deficiency of oxygen in the blood and causing an elevated respiratory rate (18) that is actually in a state of unstable angina and could result to chest pains (Chou, 2015). Normal respiratory rate in a resting state is 12. In the heart, there occurs a diminished muscular force during each heart beat characterized by elevated systolic and systolic motions of the already impaired walls (Chou, 2015).
References
Alherbish, A., Westerhout, C.M., Fu, Y., White, H.D., Granger, C.B., Wagner, G. and Armstrong, P.W., 2013. The forgotten lead: Does aVR ST-deviation add insight into the outcomes of ST-elevation myocardial infarction patients?. American heart journal, 166(2), pp.333-339.
Arenja, N., Mueller, C., Ehl, N.F., Brinkert, M., Roost, K., Reichlin, T., Sou, S.M., Hochgruber, T., Osswald, S. and Zellweger, M.J., 2013. Prevalence, extent, and independent predictors of silent myocardial infarction. The American journal of medicine, 126(6), pp.515-522.
Chou, R., 2015. Cardiac screening with electrocardiography, stress echocardiography, or myocardial perfusion imaging: advice for high-value care from the American College of Physicians. Annals of internal medicine, 162(6), pp.438-447.
Fröbert, O., Lagerqvist, B., Olivecrona, G.K., Omerovic, E., Gudnason, T., Maeng, M., Aasa, M., Angerås, O., Calais, F., Danielewicz, M. and Erlinge, D., 2013. Thrombus aspiration during ST-segment elevation myocardial infarction. New England journal of medicine, 369(17), pp.1587-1597.
Thygesen, K., Alpert, J.S., Jaffe, A.S., White, H.D., Simoons, M.L., Chaitman, B.R., Katus, H.A., Apple, F.S., Lindahl, B., Morrow, D.A. and Clemmensen, P.M., 2012. Third universal definition of myocardial infarction.Journal of the American College of Cardiology, 60(16), pp.1581-1598.
