Cardiac case studies Essay

CS 2 15 points K.R. is a 46-year-old man admitted to the need department with unremitting chest discomfort. The irritation started while he was shoveling power point Celsius from his walkway. He had experienced chest discomfort with activity previously, but the upset had subsided with rest and he sought no medical help. This time the pang did not subside and became increasingly severe, radiating to his left arm and degrade jaw. In the emergency department, an ECG and cardiac enzymes were obtained. The cardiac monitor showed venous sinus tachycardia with occasional premature ventricular complexes. K.R. was treated with 2 L nasal oxygen, tissue plasminogen activator, sublingual nitroglycerin, and IV morphine sulfate. When he was pain free, he was transferred to the cardiac unit for monitoring.Discussion Questions1.What changes in cardiac enzymes would be consistent with a diagnosis of MI? Troponins(I and T specific to cardiac pass cells), elevated between 4-6 hours after the inset of an acute MI and the Great Compromiser elevated for 8-12 days. Myoglobin-level increase within 1-4 hours after the onset of chest pain and extravagantlyly sensitive but not very specific. 2.What is the most roughhewn precipitating event for MI?In the most cases of MI governance rupture followed by thrombus formation at the site is the precipitating event.3.What is the principle for using tissue plasminogen activator in the management of ACS? Tissue plasminogen activator if fibrin specific. It binds to the fibrin of fresh clots and the resulting abstruse converts adjacent plasminogen into plasmin creating localized thrombolysis.4.Why are morphine and nitroglycerin apply to manage ischemic chest pain? Its a high priority to truce myocardial stimulation by the sympathetic flighty system. Morphine sulfate reduces anxiety and catecholamine secretion and it can reduces preload. And nitroglycerin decreases preload and reduces MVO2.CS 3 15 points C.J. is a 16-year-old high s chool student who is in theclinic for a sports physical prior to beginning basketball practice. He has no known significant medical history, takes no medications, and has no allergies. A polish of systems reveals only that C.J. ticks winded earlier than most boys on the team. He attributes this to needing to get in better shape. The physical exam is unremarkable except for a grade III systolic murmur heard over the perfect precordium. An echocardiogram and cardiac cath reveals a ventricular septal defect (VSD) with moderate pulmonic hypertension.Discussion Questions1.A VSD is usually an acyanotic defect. Why is this?The kin being shunted is oxygenated blood from the left ventricle shunted to the mightily because pressures on the left are higher. 2.What is the mechanism and significance of pulmonary hypertension? The mechanism of pulmonary hypertension is due to change magnitude blood volume within the pulmonary circuit form the VSD. Pressure is the increase of CO and vascul ar resistance. From this case pressure is high secondary to increased CO and the primary pulmonary hypertension, the cause is increased pulmonary vascular resistance. Pulmonary hypertension can lead to cor pulmonale and right-sided heart failure.3.What other disorders alike VSD can produce a systolic murmur? How can face of the murmur and pattern of radiation be used to differentiate among these aetiologic factors? Systolic murmurs can be produced by mitral valve prolapse, aortic or pulmonary stenosis, and mitral or tricuspid regurgitation. mall sounds are produced in some different areas of the heart and have different characteristics Aortic stenosis- right second intercostal space, mid systolic, crescendo decrescendo and radiates to the neck.4.Is it necessary to smashed a VSD? What are the common complications of untreated VSD? No, it is mot always absolute to close VSDs spending on patients age,size of defect and degree of shunt. Common complications include- pulmonary hype rtension, cardiomegaly, atrial dysrhythmia and right sided heart failure.ReferenceRichard N. Fogoros, M.D. Heart Disease Expert. About health. WebMD Web site. forthcoming at http//heartdisease.about.com/od/heartattack/g/CardiacEnzymes.htm. create September 10, 2014. Accessed October 21th 2014.Anju T. Peters, Kathryn E. Hulse, Lydia A. Fibrin Deposition in Nasal Polyps Caused by Fibrinolytic decline in quality through Reduction of Tissue Plasminogen Activator Expression. American Journal of Respiratory and unfavorable Care Medicine 18912, 1487-1493 Sepideh Jabbari, Hassan Ghassemian. Modeling of heart systolic murmurs based on multivariate matching pursuit for diagnosis of valvular disorders. June 21, 2011. Volume 41, get by 9, Pages 802811Ventricular Septal Defects.Patient.co.uk.WebMD Web site. Available athttp//www.patient.co.uk/doctor/ventricular-septal-defects. Published Mar 31, 2014.Accessed October 21th 2014. Alyson A. Tamamoto, MD.Acyanotic Congenital Heart Disease. Case based pediatrics.WebMD Web site. Available at http//www.hawaii.edu/medicine/pediatrics/pedtext/s07c02.html.Published July 2013. Accessed October 21th 2014.