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Care Management and Leadership

Bullet point list your main concerns for this patient

  • Pain
  • Arrhythmias
  • Myocardial infarction
  • Thrombus
  • High respiratory rate

Provide a rationale/reason for this concern

The patient was admitted with the complaint of chest pain and after the failed attempt of coronary angioplasty was eventually done. Pain is the chief complaint that could have risen due to various reasons like heart failure, cardiac arrest, angina, myocardial infarction, etc. The patient underwent cardiac arrest because of the blockage in her heart and it is a painful condition it is important that the pain is managed and also because it was the chief complaint. Pain management becomes a priority. The call was made to do coronary angioplasty to relieve her of the blockage and the blood flow is resumed and the heart muscles are not under stress. Cardiac arrest can be caused due to many factors but it is due to the fact that the blood flow to the heart muscles is hampered (Sossalla & Vollmann, 2018). The risk factors associated with a cardiac arrest can be categorized under modifiable and non-modifiable risk factors. Modifiable risk factors are the one which can be modified by the patient and the recurrence can be prevented like- high level of serum cholesterol, hypertension, diabetes, obesity, sedentary lifestyle, smoking, alcoholism, stress, and diet (Smit, Coetzee & Lochner, 2019).

The non-modifiable risk factors are the one which cannot be modified by the patient like- family history, genetic predilection, age, gender and post-menopausal, etc. (Smit, Coetzee & Lochner, 2019). The most common cause of cardiac arrest is atherosclerosis which is caused by high levels of low-density lipoproteins (Suciu et al., 2018). It starts with the accumulation of low-density lipoprotein in the intima layer of arteries which is determined by the plasma concentration, the size of the molecules and the level of permeability of the arterial wall (Suciu et al., 2018). This accumulated lipoprotein undergoes oxidation and glycation which leads to inflammation and ultimately leading to the formation of atherosclerotic plaque. This affects only those arteries which are atherosclerotic in nature as the oxidized and glycated lipoproteins trigger the adhesion response and establishment of a bond between monocytes and T lymphocytes this bond facilitates the entry of plaque in the intima (Suciu et al., 2018).

After entering this there is an inflammatory response which increases the uptake of low-density lipoproteins these are called foam cells and as an attempt to close blood vessels these leave the arteries and leave a trail which is called a fatty streak. This artery is anatomically intact but is damaged which is filled with collagen and it is done to maintain the integrity of the arteries. There is overexpression of extracellular matrix proteins and there is resultant fibrous cap formation and this inflammation is the cause of death of cardiac smooth muscles (Suciu et al., 2018). As this plaque matures, the outer surface of the capsule is rich in collagen while the core of the capsule is necrotic. The arteries in order to compensate often enlarge themselves at the same time preventing lumen stenosis (Camaré et al., 2017). This enlargement is the reason the artery undergoes blockage preventing the flow of blood and the death of cardiac smooth muscles is the reason for pain (Camaré et al., 2017).

The blockage in the heart leads to improper cardiac output which leads the heart to enter into a state of irregular rhythm and it has to be managed it may lead to arrhythmia-induced cardiomyopathy or atrial fibrillation (Sethi et al., 2017). Cardiac arrhythmia is a type of arterial fibrillation which can be caused by many reasons like hypertension, genetic, ischaemic, etc. (Jensen, & Thomalla, 2019). In the present case, it is because of ischaemic though the structural heart disease cannot be judged. Arterial fibrillation is caused by the interaction of trigger in the form of rapidly firing ectopic foci which can be located in one or more pulmonary veins with abnormal atrial tissue (Chan et al., 2019). This mechanism involves the focal initiators as the focal points in the pulmonary veins are the ones that cause rapid ectopic activity. The arterial fibrillation is due to abnormal focus activity including an increase in automaticity, triggered activity and re-entry (Satomi, 2018). This has a parasympathetic predominance and is characterized by the presence of multiple wavelets of excitation around atrial myocardium. The number of wavelets determines the stability of atrial fibrillation and the re-entry is facilitated by the conduction and refractory period shortening (Satomi, 2018).

In cases of cardiac arrest due to blockage and where the coronary angioplasty is done, it is often seen that the atherosclerotic plaque is formed due to the accumulation of low-density lipoprotein in arteries (Hurtubise et al., 2016). In the present case scenario was the reason for coronary angioplasty but often it is seen the most common complication is intracoronary thrombus. Thrombus is occlusion of any blood vessel but is most commonly seen in arteries due to the blood pressure (Alberts, 2019). This occlusion is caused by the embolus and in the present case, it can be due to the dislodgement of the atheromatous plaque from the original site of placement and the lodgement of the same in another area along the blood vessel usually where the vessels are narrows (Alberts, 2019). The patient should be monitored and investigations should be done to make sure the situation remains the same and there is a positive health outcome. The pathophysiology of atherosclerosis and that of the thrombosis is a bit overlapping (Libby, Bornfeldt & Tall, 2016). The atherosclerotic plaque which is formed due to the flow of blood often can cause the detachment of the plaque from the place where it was originally formed (Zarins & Xu, 2017).

This dislodged plaque flows with the blood and where the vessels are narrow, narrower than the embolus it gets lodged and causes occlusion. The patients are often administered blood thinners and if the patient is hypertensive, anti-hypertensive drugs are given so that the pressure is reduced and the chance of dislodgement is reduced (Libby, Bornfeldt & Tall, 2016). The consequences of thrombosis can affect the organ system where the blood vessels are thinner as the blood flow is completely hampered causing formation oxidative stress. In case the thrombosis occurs in any part of the brain it reduces or may even stop the blood flow to that part of the brain. If this is prolonged, it can cause irreversible damage to the brain tissues eventually leading to cognitive impairment.

Another major concern in the given case is the development of compartment syndrome the patient is hypotensive and is at more risk for the necrosis of the tissue due to the inability of the blood flow to the extremities and inadequate drainage. This occurs due to cellular anoxia due to the increase of fluid pressure that occurs in the compartment of a muscle and usually happens in the extremities. As the fascia that encloses the compartment of the muscle is not distensible the fluid expansion increases the internal pressure of the compartment. This is due to arteriovenous pressure gradient and this increase in the pressure restricts the localized tissue perfusion where the venous pressure is increased and the arterial pressure is decreased. When the condition is prolonged it can lead to cellular anoxia and cause nerve damage (Chung, Yoneda & Mondrall, 2018).

The patient is under tachycardia and this is due to the fact the body is trying to compensate for the reduced cardiac output and resultant hypoxia and tissue anoxia in compartment syndrome.

List all the appropriate interventions in order of priority (be specific).

  • Primary assessment
  • Pain management
  • Electrocardiogram
  • Neurovascular obstruction
  • Site management
  • Blood test

Provide a rationale/reason for these interventions in order of priority

The vitals of the patient need to be managed in the case of a cardiac care unit. The patient in the given case scenario is hypotensive, tachycardic, tachypneic, normotensive and with good oxygen saturation level. The patient was admitted with the complaint of chest pain and coronary angioplasty was done due to which there should be continuous monitoring to make sure that the condition does not worsen. The vitals should be monitored hourly and the patient should not be left alone as the change in condition should be managed immediately (Harjola et al., 2018). The patient had undergone an operative procedure that would have caused immense pain to the patient and for the ease and to make sure that the body is under further stress it is better than the patient is given pain medication.

The best method of pain medication will be to provide patients with administered morphine which is an opioid analgesic (Beloeil et al., 2019). It is one of the most commonly used drugs in the case of pain management in both acute and chronic cases. The pain in the case of a cardiac event like in the present one is due immense and the patient would not be able to tolerate the pain. The assessment of pain is necessary before the pain management can be initiated for which the patient can be asked to rate the pain on a ten-point scale (van Dijk et al., 2016). Since the patient is elderly and the drug used is opioids, it is necessary to monitor the patient so that cardiovascular depression does not occur and dependency is not created.

The cardiac output, rate, rhythm, and character of the heart condition can be measured by electrocardiogram (Axell, White & Giblett, 2020). The electrocardiogram should be continuously monitored by a 12-lead electrocardiograph and any change in the condition should be immediately notified to the doctor (Axell, White & Giblett, 2020). The heart rate of the patient is high and the management for the same is given but the monitoring of the electrocardiogram will give show if the patient’s condition worsens and if arrhythmia occurs. The characteristics of the ECG reading will change as the condition of the patient changes and the in case of arrhythmia spiking of T wave is seen and there will be an alteration of the QRS complex occurs (Safa, Sriram & Karpawich, 2018).

For prevention and to avoid the complication of thrombosis the patient can be administered with antiplatelet drugs. Platelets play a significant role in atherosclerosis, development of plaque, its detachment and formation of embolus and thrombosis (Rana et al., 2019). An antiplatelet drug like aspirin is given after consultation with the doctor and this will help in the prevention of the myocardial infarction. Aspirin’s mechanism of action is by inhibition of platelet adhesion, activation, aggregation and in turn, reduces the inflammation (Li, Wu & Liu, 2017). Prevention of thrombosis is the expected outcome and it is the reason after the assessment of vitals and ECG along with the blood cholesterol levels the patient will be administered with the anti-platelet drug. This will help in the prevention of cerebrovascular accidents which is expected in case there is no intervention.

The patient is elderly and the patient had a failed attempt of coronary angioplasty in one hand and then it was done on the other hand. With age the wound healing and repair capacity of the patient reduces and it is important that wound management at the site is important to ensure there is no infection local and systemic (Lindholm & Searle, 2016). The dressing should be kept clean at all times and should be changed every day, the hand hygiene should be maintained by the healthcare providers as well as that by the carer and family members of the patient (Lindholm & Searle, 2016). The patient should also be given healthy and nutritious food so that wound healing is better and faster (Sibbald & Ayello, 2019). The patient is elderly with a heart condition and the most common cause of cardiac arrest is atherosclerosis and the blood tests need to be conducted to know the levels of low-density lipoprotein (Chen et al., 2019). The blood test will show the level of low-density lipoprotein, high-density lipoprotein, and serum cholesterol and the medication and lifestyle alterations can be done accordingly (Karr, 2017). The other blood test that needs to be conducted is to know the arterial blood gas levels as the patient is tachypneic (Willis et al., 2019).

References for Care Management and Leadership

Alberts, M. J. (2019). Clinical presentation and diagnosis of cerebrovascular disease. Vascular Medicine: A Companion to Braunwald's Heart Disease E-Book, 376.

Axell, R. G., White, P. A., & Giblett, J. P. (2020). Cardiovascular measurement. In Clinical Engineering (pp. 267-281). Academic Press. DOI: 10.1016/B978-0-08-102694-6.00016-4.

Beloeil, H., Albaladejo, P., Sion, A., Durand, M., Martinez, V., Lasocki, S., ... & Belbachir, A. (2019). Multicentre, prospective, double-blind, randomised controlled clinical trial comparing different non-opioid analgesic combinations with morphine for postoperative analgesia: The OCTOPUS study. British Journal of Anaesthesia, 122(6), e98-e106. DOI: 10.1016/j.bja.2018.10.058.

Chung, K., Yoneda, H., & Mondrall, G. (2018). Pathophysiology, classification, and causes of acute extremity compartment syndrome. Retrieved from: https://www.uptodate.com/contents/pathophysiology-classification-and-causes-of-acute-extremity-compartment-syndrome/print.

Camaré, C., Pucelle, M., Nègre-Salvayre, A., & Salvayre, R. (2017). Angiogenesis in the atherosclerotic plaque. Redox Biology, 12, 18-34. DOI: 10.1016/j.redox.2017.01.007.

Chan, C. S., Lin, Y. K., Chen, Y. C., Lu, Y. Y., Chen, S. A., & Chen, Y. J. (2019). Heart failure differentially modulates natural (Sinoatrial node) and ectopic (pulmonary veins) pacemakers: Mechanism and therapeutic implication for atrial fibrillation. International Journal of Molecular Sciences, 20(13), 3224. DOI: 10.3390/ijms20133224.

Chen, G., Farris, M. S., Cowling, T., Colgan, S. M., Xiang, P., Pericleous, L., ... & Anderson, T. (2019). Treatment and low-density lipoprotein cholesterol management in patients diagnosed with clinical atherosclerotic cardiovascular disease in Alberta. Canadian Journal of Cardiology, 35(7), 884-891. DOI: 10.1016/j.cjca.2019.04.008.

Harjola, V. P., Parissis, J., Brunner‐La Rocca, H. P., Čelutkienė, J., Chioncel, O., Collins, S. P., ... & Lainscak, M. (2018). Comprehensive in‐hospital monitoring in acute heart failure: applications for clinical practice and future directions for research. A statement from the Acute Heart Failure Committee of the Heart Failure Association (HFA) of the European Society of Cardiology (ESC). European Journal of Heart Failure, 20(7), 1081-1099. DOI: 10.1002/ejhf.1204.

Hurtubise, J., McLellan, K., Durr, K., Onasanya, O., Nwabuko, D., & Ndisang, J. F. (2016). The different facets of dyslipidemia and hypertension in atherosclerosis. Current Atherosclerosis Reports, 18(12), 82. DOI: 10.1007/s11883-016-0632-z.

Jensen, M., & Thomalla, G. (2019). Causes and Secondary Prevention of Acute Ischemic Stroke in Adults. Hämostaseologie. 40(01): 022-030. DOI: 10.1055/s-0039-1700502.

Karr, S. (2017). Epidemiology and management of hyperlipidemia. The American Journal of Managed Care, 23(9 Suppl), S139-S148. Retrieved from: https://europepmc.org/article/med/28978219.

Li, Y., Wu, C., & Liu, W. (2017). Coronary artery ectasia presenting with thrombus embolization and acute myocardial infarction: A case report. Medicine, 96(4). Retrieved from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5287974/.

Libby, P., Bornfeldt, K. E., & Tall, A. R. (2016). Atherosclerosis: successes, surprises, and future challenges. Circulation Research, 118, 531–534. DOI: 10.1161/CIRCRESAHA.116.308334.

Lindholm, C., & Searle, R. (2016). Wound management for the 21st century: combining effectiveness and efficiency. International Wound Journal, 13, 5-15. DOI: 10.1111/iwj.12623.

Murphy, P. B., & Barrett, M. J. (2019). Morphine. In StatPearls [Internet]. StatPearls Publishing. Retrieved from: https://www.ncbi.nlm.nih.gov/books/NBK526115/.

Rana, A., Westein, E., Niego, B. E., & Hagemeyer, C. E. (2019). Shear-dependent platelet aggregation: Mechanisms and therapeutic opportunities. Frontiers in Cardiovascular Medicine, 6. Retrieved from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6763557/.

Safa, R., Sriram, C., & Karpawich, P. P. (2018). Arrhythmia Identification: Stabilization and Treatment. In Cardiac Emergencies in Children (pp. 131-160). Springer, Cham. DOI: 10.1007/978-3-319-73754-6_8.

Satomi, K. (2018). Focal Atrial Tachycardia. In Catheter Ablation (pp. 119-125). Springer, Singapore. DOI: 10.1007/978-981-10-4463-2_12.

Sethi, N. J., Safi, S., Feinberg, J., Nielsen, E. E., Gluud, C., & Jakobsen, J. C. (2017). Digoxin versus placebo, no intervention, or other medical interventions for atrial fibrillation and atrial flutter: a protocol for a systematic review with meta-analysis and Trial Sequential Analysis. Systematic Reviews, 6(1), 71. DOI: 10.1186/s13643-017-0470-2.

Sibbald, G., & Ayello, E. A. (2019). Nutrition and Wound Healing: Eat Well, Live Well. Advances in Skin & Wound Care, 32(10), 437. DOI: 10.1097/01.ASW.0000581784.28913.89.

Smit, M., Coetzee, A. R., & Lochner, A. (2019). A review of the pathophysiology of myocardial ischemia and perioperative myocardial infarction. Journal of Cardiothoracic and Vascular Anesthesia. DOI: 10.1053/j.jvca.2019.10.005.

Sossalla, S., & Vollmann, D. (2018). Arrhythmia-Induced Cardiomyopathy: Causes, Clinical Significance, and Treatment. Deutsches Ärzteblatt International, 115(19), 335. DOI: 10.3238/arztebl.2018.0335.

Suciu, C. F., Prete, M., Ruscitti, P., Favoino, E., Giacomelli, R., & Perosa, F. (2018). Oxidized low density lipoproteins: the bridge between atherosclerosis and autoimmunity. Possible implications in accelerated atherosclerosis and for immune intervention in autoimmune rheumatic disorders. Autoimmunity reviews, 17(4), 366-375. DOI: 10.1016/j.autrev.2017.11.028.

van Dijk, J. F., Vervoort, S. C., van Wijck, A. J., Kalkman, C. J., & Schuurmans, M. J. (2016). Postoperative patients’ perspectives on rating pain: A qualitative study. International Journal of Nursing Studies, 53, 260-269. DOI: 10.1016/j.ijnurstu.2015.08.007.

Willis, L. H., Slentz, C. A., Johnson, J. L., Kelly, L. S., Craig, K. P., Hoselton, A. L., & Kraus, W. E. (2019). Effects of Exercise Training With and Without Ranolazine on Peak Oxygen Consumption, Daily Physical Activity, and Quality of Life in Patients With Chronic Stable Angina Pectoris. The American journal of cardiology, 124(5), 655-660. DOI: 10.1016/j.amjcard.2019.05.063.

Zarins, C. K., & Xu, C. (2017). Pathophysiology of human atherosclerosis. In Vascular surgery (pp. 37-60). CRC Press.

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