CS 2: 15 points K.R. is a 46-year-old man admitted to the emergency department with unremitting chest discomfort. The pain started while he was shoveling snow from his walkway. He had experienced chest discomfort with activity previously, but the pain had subsided with rest and he sought no medical help. This time the pain did not subside and became increasingly severe, radiating to his left arm and lower jaw. In the emergency department, an ECG and cardiac enzymes were obtained. The cardiac monitor showed 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.
1.What changes in “cardiac enzymes” would be consistent with a diagnosis of MI? Troponins(I and T specific to cardiac muscle cells), elevated between 4-6 hours after the inset of an acute MI and remains elevated for 8-12 days. Myoglobin-level increase within 1-4 hours after the onset of chest pain and highly sensitive but not very specific. 2.What is the most common precipitating event for MI?
In the most cases of MI plaque rupture followed by thrombus formation at the site is the precipitating event.
3.What is the rationale 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 compound converts adjacent plasminogen into plasmin creating localized thrombolysis.
4.Why are morphine and nitroglycerin used to manage ischemic chest pain? It’s a high priority to truce myocardial stimulation by the sympathetic nervous 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 school student who is in the clinic for a sports physical prior to beginning basketball practice. He has no known significant medical history, takes no medications, and has no allergies. A review of systems reveals only that C.J. gets “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 entire precordium. An echocardiogram and cardiac cath reveals a ventricular septal defect (VSD) with moderate pulmonary hypertension.Discussion Questions
1.A VSD is usually an acyanotic defect. Why is this? The blood being shunted is oxygenated blood from the left ventricle shunted to the right 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 increased blood volume within the pulmonary circuit form the VSD. Pressure is the product of CO and vascular 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 besides VSD can produce a systolic murmur? How can character of the murmur and pattern of radiation be used to differentiate among these etiologic factors? Systolic murmurs can be produced by mitral valve prolapse, aortic or pulmonary stenosis, and mitral or tricuspid regurgitation. Heart 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 close a VSD? What are the common complications of untreated VSD? No, it is mot always imperative to close VSDs spending on patient’s age,size of defect and degree of shunt. Common complications include- pulmonary hypertension, cardiomegaly, atrial dysrhythmia and right sided heart failure.
Richard N. Fogoros, M.D. Heart Disease Expert. About health. WebMD Web site. Available at: http://heartdisease.about.com/od/heartattack/g/CardiacEnzymes.htm. Published September 10, 2014. Accessed October 21th 2014.
Anju T. Peters, Kathryn E. Hulse, Lydia A. Fibrin Deposition in Nasal Polyps Caused by Fibrinolytic Impairment through Reduction of Tissue Plasminogen Activator Expression. American Journal of Respiratory and Critical Care Medicine 189:12, 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, Issue 9, Pages 802–811
Ventricular Septal Defects.Patient.co.uk.WebMD Web site. Available at:http://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.