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HLTH 502 Applied Pathophysiology
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HLTH 502 Applied Pathophysiology
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Course Code: HLTH502
University: Victoria University Of Wellington
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Country: New Zealand
Question:
Describe about the Applied Pathophysiology For Hypertensive on Medication.
Answer:
Mr. Crawford is a 56-year-old male patient who presented with retrosternal chest pain that was prolonged, radiating to the neck and described as crushing in nature. He is a known hypertensive on medication, obese with a BMI of 38 and a former smoker with 10 pack years. His vitals were deranged with a tachycardia of 105 beats per minute, an elevated blood pressure of 155/92 and a respiratory rate of 26 breaths per minute. His weight is 96 Kg and a height of 1.53 meters putting her body mass index at 38 which is obese. He was admitted for the complaints with a suspicion of an acute coronary syndrome. On admission he was given heparin 5000 units stat, reteplase 10 units iv bolus and morphine 2.5 mg iv for the pain and aspirin 300mg on the way to the hospital. A diagnostic workup was started with a 12 lead ECG and cardiac enzymes done. The ECG and biomarkers confirmed an ongoing ST-elevation myocardial infarction (STEMI). The management involved continuous monitoring of vitals and ECG, serial cardiac markers, oxygen therapy by nasal prongs and thrombolytic therapy as a definitive solution is sought.
Myocardial infarction is an acute coronary syndrome that occurs due to interruption of blood flow to the heart muscles leading to the death of myocardium otherwise named a heart attack (Kumar, Abbas, Fausto, & Aster, 2014). This blockage is in part due to blockage of coronary vessels following rupture of an atherosclerotic plaque in the artery wall that forms an occluding thrombus or an embolic phenomenon. Up to 80% are due to occluding arteriosclerotic plaque with superimposed thrombus (Burke & Virmani, 2007). Pre-existing hypertension and obesity are known risk factors for cardiovascular disorders (Thune et al., 2008). Mr. Crawford is a known hypertensive and obese.
Atherosclerotic plaques are depositions of lipid within artery wall with surrounding fibroblast proliferation and a fibrous cap (Nabel & Braunwald, 2012The pre-existing plaque acts as a nidus for thrombus formation leading to infarction of the downstream myocardium supplied by that coronary branch (Frangogiannis, 2015).
Plaque rupture activates platelet aggregation and activation of coagulation cascade due to exposure of tissue factor (Kumar, Abbas, Fausto, & Aster, 2014). This is the rationale of early antithrombosis and anticoagulation in the setting of MI as seen in the management of Mr. Crawford by the provision of aspirin, heparin, and reteplase.
The clinical presentation follows the biochemical, functional and morphological changes following ischemia of the myocardium (Kumar, Abbas, Fausto, & Aster, 2014). Due to occlusion, the myocardium stops aerobic glycolysis leading to reduced ATP and accumulation of metabolic waste in the cells (Kumar, Abbas, Fausto, & Aster, 2014). There is a rapid loss of contractility in the affected myocardium and if the injury continues this becomes irreversible (Frangogiannis, 2015). This is the rationale of dropping blood pressure in the setting of MI, a phenomenon termed cardiogenic shock. However, the blood pressure could also be elevated due to the release of compensatory sympathetic discharge and elevated levels of catecholamines (Kumar, Abbas, Fausto, & Aster, 2014). This also leads to tachycardia and nausea involved in MI. Mr. Crawford’s blood pressure was elevated at 155/92. The ischemic changes cause arrhythmias and myocardial irritability.
The cardiac biomarkers are enzymes released by dying myocytes and are good predictors of myocardial infarction (Thygesen et al., 2012) They start rising minutes after the event and some remain elevated for days. They include troponin T and I, myoglobulin, creatinine kinase and creatinine kinase MB (CKMB). They were all elevated in Mr. Crawford’s case.
Metabolic changes are linked to intracellular changes stemming from depletion of ATP stores, inability to regulate electrolyte pumps. This leads to sodium, potassium and calcium derangements. Potassium and calcium imbalance is implicated as one of the causes of ventricular arrhythmias seen in MI. Mr. Crawford had elevated potassium and hyponatremia.
The etiology of chest pain in myocardium ischemia is poorly understood but has been hypothesized to be due to the release of chemical mediators triggered by ischemic changes within the myocardium cells (Leach & Fisher, 2013). Circulatory derangements are however due to ventricular dysfunction caused by loss of myocardium (Walker & Colledge, 2013). Infarction of myocardium heals by scar formation leading to permanent loss of contractility in that area. If the dysfunction is systolic, cardiac output drops leading to a fall in blood pressure and coronary perfusion (Walker & Colledge, 2013). This has the disadvantage of potentiating the ischemia. A diastolic dysfunction will lead to increased left ventricular diastolic pressure that causes back pressure to the lungs that manifest as pulmonary congestion (Walker & Colledge, 2013). This leads to hypoxemia and difficulty breathing, impaired oxygen transport and further ischemia. A chest radiograph was requested for Mr. Crawford to access pulmonary congestion and also the cardiac profile.
References
Burke, A. P., & Virmani, R. (2007). Pathophysiology of Acute Myocardial Infarction. Medical Clinics of North America, 91(4), 553-572. doi:https://doi.org/10.1016/j.mcna.2007.03.005
Frangogiannis, N. G. (2015). Pathophysiology of Myocardial Infarction. Compr Physiol, 5(4), 1841-1875.
Kumar, V., Abbas, A. K., Fausto, N., & Aster, J. C. (2014). Robbins and Cotran pathologic basis of disease, professional edition. London: Elsevier health sciences.
Leach, A., & Fisher, M. (2013). Myocardial ischaemia and cardiac pain – a mysterious relationship. British Journal of Pain, 7(1), 23–30. https://doi.org/10.1177/2049463712474648
Nabel, E. G., & Braunwald, E. (2012). A tale of coronary artery disease and myocardial infarction. New England Journal of Medicine, 366(1), 54-63.
Thune, J. J., Signorovitch, J., Kober, L., Velazquez, E. J., McMurray, J. J., Califf, R. M., … & Pfeffer, M. A. (2008). Effect of antecedent hypertension and follow-up blood pressure on outcomes after high-risk myocardial infarction. Hypertension, 51(1), 48-54.
Thygesen, K., Alpert, J. S., Jaffe, A. S., Simoons, M. L., Chaitman, B. R., White, H. D., … & White, H. D. (2012). Third universal definition of myocardial infarction. European heart journal, 33(20), 2551-2567.
Walker, B. R., & Colledge, N. R. (2013). Davidson’s Principles and Practice of Medicine E-Book. Elsevier Health Sciences.
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