Pathophysiology Assessment

Question 1

Looking at the initial information and the known history that Sam presented with, there are a few medical diagnoses that he could possibly be presenting with. The three diagnoses that I can conclude include (1) heart failure, (2) myocardial infarction, and (3) ischemic heart disease. Heart failure would explain the loss of appetite through nausea and vertigo (Ziaeian &Fonarow, 2016). Sam’s palpitations could also be explained by his heart having added efforts to sustain his normal heart rate and beat. The Low oxygen saturation could also be explained by heart failure which is the process through which not enough blood is being released to the organs and muscles of the body. This then causes one to feel weak, tired, and dizziness which could be from a lack of oxygen running through the bloodstream in order to reach the brain. Finally, heart disease is also associated with fever which then lets one become short of breath and experience weakness in their joints, brain, and body overall (Ziaeian &Fonarow, 2016).

Myocardial infarction could help to explain his “heavy pressure” that he feels in his chest and from the pain he experiences in his shoulders and through his jaw. For women, they experience a myocardial infarction (MI) differently than men having symptoms such as jaw pain (Anderson & Morrow, 2017; Thygesen, Alpert, & White, 2007). This is not to say that men do not experience this but it is to say that women have a sign of these symptoms as being most prevalent. In the case of Sam, this could be taken into consideration. Chronic fatigue and anxiety could explain the somatic symptoms, with Sam’s existing diagnoses then being likely to have caused the other symptoms. If compelled to offer a single diagnosis in this case, the diagnosis of early-stage of myocardial infarction is perhaps most supported by the existing symptoms, Sam’s known history, and the relevant medical literature.

Ischemic heart disease supports the fact that Sam has high blood pressure, type II diabetes mellitus, and hyperlipidemia. This is because, with this disease, there is a blockage of the arteries and blood flow to one’s muscles and brain (Gardner, Thomas, Jacobs, Stegmann, & Mickael, 2017). With hyperlipidemia, there is a high amount of lipids or particles found within the blood which makes it difficult for other particles to pass through the blood cells. This is extremely important as we would want certain things such as oxygen and nutrients to pass through one’s bloodstream in order to reach certain organs for the body’s proper functioning. There are certainly reasons for Sam to feel anxious or to have had a panic attack at once, but the range of symptoms detectable in her case is more consonant with non-somatic explanations such as heart failure and ischemic heart disease.

Question 2

Based on the added assessment information and his known history, the previous diagnosis that I would feel is Sam’s condition is MI or myocardial infarction. I say this because of the pain that he is in which means his body is in pain. He states that he has heavy pressure throughout his body which is mostly in his chest, should, and jaw area. His legs are swelling while his abdomen has some tenderness. His skin is cool and pale which is also a sign of MI as there is little blood flow throughout the body and irregular flow to the heart and brain. Lastly, his cardiac assessment seams normal which is often a way for MI to go undetected. One might experience an instance of calmness when in actuality the cardiac symptoms will soon start up again (Wellings et al., 2018).

Question 3

The pathophysiology for his condition has passed over time. In the following bullet points, I will present in detail the pathophysiology of his condition and my conclusion. I will start with the etiology, progress into the pathophysiology changes, and then to the cellular level (Gabriel-Costa, 2018).

There is a change in the vessel’s endothelium. Here, this is the tissue of the cells aligning the blood cells that are then changed, making the blood vessels, heart, and lymphatic cells more vulnerable and susceptible to under-functioning.

There is then the build-up and accumulation of plaque within the vessels. Here, the blood vessels become clogged and trap even more plaque, blocking adequate blood flow and necessary nutrients needed through the body. This then supports the fact that Sam has had high blood pressure. High blood pressure leads to an enlarged and less efficient heart, which struggles to pump sufficient blood through blood vessels. In this context, it should be noted both that Sam has a history of high blood pressure and that his oxygen saturation is low (94%). Sam’s high blood pressure is a predisposing factor in myocardial infarction.

Blood clotting or thrombus begins to form within the blood vessel. This causes some blood platelets to stick to one another which further hinders blood flow. This could possibly be the cause of Sam feeling the tightness in his chest and the swelling in his legs. Hyperlipidemia results in both the deposit of fat cells in arteries and damage to the epithelial cells in arteries, both of which obstruct blood flow and therefore contribute to atherosclerosis and atherosclerosis-driven heart failure. Sam is already known to have hyperlipidemia, which is in independent precipitating factor in atherosclerosis and therefore heart disease attendant on atherosclerosis.

Then an area of infarction is formed. Here at the site of injury, death to the tissue begins to form.

The ventricular makeup is then changed. This is also known as ventricular remodeling. This is all due to the thinning, inflammation, and scarring of the tissue and vessels leading to the heart. In the context with Sam, this is leading to the chest pain and feelings of weakness and shortness of breath.

An integrated account of myocardial infarction consistent with the known and new information in Sam’s case can be provided as follows. Sam presented with symptoms that are consistent with myocardial infarction. Sam’s pre-existing diabetes mellitus likely caused damage to cells responsible for (a) the relaxation of blood vessels and (b) regulation of blood flow and also inflamed cells within blood vessels that would not otherwise have been inflamed. The cellular volume of Sam’s red blood cells is, because of the predisposing factor of hypertension, also likely to be low, representing another pathway to the pathophysiology of myocardial infarction. Finally, Sam’s hyperlipidemia likely resulted in the deposit of fat cells in his arteries and damage to the epithelial cells of his arteries, both increasing the odds of atherosclerosis and thereby of myocardial infarction.

Question 4

Three medicines can be recommended to Sam based on the available data and existing diagnosis. First, Sam can take beta-blockers. Beta-blockers are commonly prescribed for heart failure and other diseases or matters of the heart (Ouwerkerk et al., 2017). Beta-blockers have two therapeutic properties that are likely to be useful to Sam: They result in a reduction in blood pressure by means of slowing the heartbeat, and they can also open up the arteries to higher blood flow (Ouwerkerk et al., 2017). Second, Sam can take an angiotensin-converting enzyme (ACE) inhibitor (Ouwerkerk et al., 2017). According to Sam’s medical history, Sam is already taking the ACE known as Lisinopril, the dosage of which might be increased in light of the diagnosis of myocardial infarction, or which might be combined with a beta-blocker. Third, Sam could take an angiotensin II receptor blocker (ARB) to achieve the same pharmacological effect as an ACE. Beta-blockers, ACEs, and ARBs were chosen because they have complementary mechanisms of action (Ouwerkerk et al., 2017); of these options, I would recommend a beta-blocker, because, especially in conjunction with the ACE that Sam is already taking, it is likely to be more effective in terms of slowing down the work rate of Sam’s heart and opening his arteries.

Question 5

Sam has returned to the emergency department. New information has been collected that can inform both diagnostic conclusions and proposed therapeutic interventions. Before examining the new data, it seems likely that Sam’s elevated heart rate and dizziness are both consistent with the prior diagnosis of heart failure. Likely due to atherosclerosis (which itself was expressed in terms of the collective pathophysiology of diabetes mellitus, hypertension, and hyperlipidemia, all of which Sam has had), insufficient blood is reaching Sam’s brain, muscles, and organs. His heart is working too hard, and not enough blood is flowing through his arteries, resulting in his falling episode and in his ongoing elevated heart rate. However, the new data offer added guidance.

Of immediate note is Sam’s low (106 / 74) blood pressure, which indicates that his hypertension might have been managed too aggressively. His skin is warm, indicating that sufficient blood is reaching the extremities. Sam’s troponin level of 0.90 ng/ml is very concerning, as any troponin value over 0.40 ng/ml suggests that the test subject has had a heart attack (Based on the high troponin level, it can be concluded that Sam has had a heart attack. Given that Sam had three independently predisposing conditions or risks for heart failure (diabetes mellitus, hyperlipidemia, and high blood pressure), it is not necessarily surprising that Sam has had a heart attack.

At this point, Sam should have a cardiac CT scan or MRI, either of which can reveal the extent of the damage to his heart likely to have resulted from the heart attack (Bakos et al., 2013). Given Sam’s high troponin levels, which are well beyond the reference range there is no real diagnostic need for an echocardiogram or angiogram, as it can safely be concluded that, in fact, Sam has cardiac/arterial damage. Of more diagnostic interest at this stage in Sam’s treatment is an evidence-based assessment of the extent of the damage caused by his heart attack. The troponin levels ought to be taken as constituting sufficiently compelling proof that Sam has a heart attack, and the CT / MRI should now be pursued as the most informative means (Bakos et al., 2013) of establishing the extent of the structural damage to Sam’s cardiac structure.

The plan of care should, therefore, be as follows. First, either a cardiac CT or a cardiac MRI ought to be ordered. It is likely, based on these results and the other facts of the case, that Sam will be a candidate for coronary angioplasty or other related surgical interventions. Oxygen therapy should be pursued because of Sam’s low oxygen saturation. The target for Sam’s oxygen saturation should be 96%, based on a well-established recommendation (O’driscoll, Howard, & Davison, 2008) from the British Thoracic Society (BTS). The BTS recommended an oxygen saturation range between 94% and 98%, so the choice of 96% falls in the middle of the BTS’s recommendations.

The objective of the plan of care is to keep Sam stable while his cardiac CT / MRI are performed and while surgical interventions such as coronary angioplasty are planned. It is almost certain that Sam has had a heart attack, and it is also almost certain that there will be a surgical intervention during his inpatient stay. Given these parameters, the task of the nursing staff is to ensure that Sam is appropriately stabilized and monitored. After the likely surgical intervention, Sam’s medications will likely have to be readjusted to reduce the risk of his incurring low blood pressure (which might have been responsible for his initial fall), and there will also have to be a more serious lifestyle intervention to address Sam’s rapidly increasing risk of morbidity from heart disease.

Question 6

Sam has likely had a stroke or blessing in the brain. The initial diagnosis of heart failure and myocardial infarction as precipitated by atherosclerosis (which itself was worsened by Sam’s precipitating factors of hyperlipidemia, hypertension, and diabetes mellitus) should stand because it is still the best explanation of the entire range of Sam’s symptoms and history. However, based on further analysis, it is also possible that Sam has had a stroke. Both stroke and bleeding of the brain can account for the symptoms of irregular pulse, urinary incontinence, vomiting, and increased blood pressure. With having a stroke and bleeding brain, one would lose their ability to have balance and would usually feel sick, dizzy, and weak. Without further diagnostic information, it is impossible to determine whether Sam has had another heart attack or a stroke, but these two diagnoses should be explored as soon as possible. At the moment, however, the medical and ethical necessity is to stabilize Sam and ensure his survival.

References

Anderson, J. L., & Morrow, D. A. (2017). Acute myocardial infarction. New England Journal of Medicine, 376(21), 2053-2064.

Bakos, Z., Markstad, H., Ostenfeld, E., Carlsson, M., Roijer, A., & Borgquist, R. (2013). Combined preoperative information using a bullseye plot from speckle tracking echocardiography, cardiac CT scan, and MRI scan: Targeted left ventricular lead implantation in patients receiving cardiac resynchronization therapy. European Heart Journal–Cardiovascular Imaging, 15(5), 523-531

Gabriel-Costa, D. (2018). The pathophysiology of myocardial infarction-induced heart failure. Pathophysiology, 25(4), 277-284.

Gardner, V., Thomas, K., Jacobs, J., Stegmann, T., & Mickael, F. L. A. A. (2017). U.S. Patent Application No. 15/641,649.

Ouwerkerk, W., Voors, A., Anker, S., Cleland, J., Dickstein, K., Filippatos, G., . . . Ter Maaten, J. (2017). Determinants and clinical outcome of uptitration of ACE-inhibitors and beta-blockers in patients with heart failure: A prospective European study. European Heart Journal, 38(24), 1883-1890.

Thygesen, K., Alpert, J. S., & White, H. D. (2007). Universal definition of myocardial infarction. Journal of the American College of Cardiology, 50(22), 2173-2195.

Wellings, J., Kostis, J. B., Sargsyan, D., Cabrera, J., Kostis, W. J., System, M. I. D. A., & Group, S. (2018). Risk factors and trends in incidence of heart failure following acute myocardial infarction. The American journal of cardiology, 122(1), 1-5.

Ziaeian, B., & Fonarow, G. C. (2016). Epidemiology and etiology of heart failure. Nature Reviews Cardiology, 13(6), 368-378.