Presentation on theme: "What other questions would you like to ask this man?"— Presentation transcript:
1What other questions would you like to ask this man? HPIA 56 year old man is brought to the ED complaining of chest discomfort for around 90min. He has had occasional symptoms for about a month he thinks, but it is notably worse today. The symptoms began as he was walking up a flight of stairs at his home. He describes the discomfort as a pressure sensation in the left substernal chest area to go along with shortness of breath and a mild sweat. The pain does not radiate anywhere today, but his wife claims he has complained of left arm pain and facial numbness in the past.What other questions would you like to ask this man?
2What is your differential? PmHx: patient denies any current health issues, claims that he has not seen a physician in years, though his wife has been on him about it since his brother passed away from an MI 6months agoAll: NoneMeds: NoneHos/Sx: Tonsillectomy at age 12, Rhinoplasty at age 23FmHx: Mother with DM2, Father with HLD, only brother died of an MI 6months ago at age 62.Social Hx: works as a zamboni driver for the Indianapolis ice. Lives at home with his wife, and 4 cats. He has 2 children both in college. Smokes 1/2ppd, and drinks 2-3 Mikes Hard Lemonade’s a day. Denies any illicit drug use since his college days.What is your differential?
3Differential Diagnosis Angina PEMI GERDPericarditis PUDAortic Dissection - PancreatitisHeart Failure CostochondritisPneumonia AnxietyPneumothorax - ShinglesWhat is your next step in assessing the patient?
4What would you like to do next? Physical ExamVitals:T 98.8, HR 105, RR 18, BP 190/95, Ht 5’10, Wt 260General: appears anxious and worried, he is an obese man, who appears somewhat pale.CV: regular rhythm without murmur, but you do notice an S4 gallop, 2+ pulses in radial and dorsal pedalis arteriesLung: CTAHEENT: neck has faint carotid bruit on left, minimal JVDAbd: normalExtremities: trace edema, warm to touch, no clubbing, no cyanosisWhat would you like to do next?
5What would you like to do next? Lab TestsCBC: NormalBUN/Cr: WNLPT: 13 secPTT: 27 secINR: 1.4Troponins: elevatedCKMB: > 5%What would you like to do next?
6Initiate treatment! MONA Morphine – this can achieve an adequate analgesia which will decrease the levels of circulating catecholamine's, thus reducing myocardial oxygen consumptionOxygen – 2-4 L via nasal cannulaNTG – sublingual administration ever 5minAspirin – 325mg chewed and swallowed.Now What?
7Diagnostic Testing Not all MI’s will show ECG and/or CXR abnormalities. 12 Lead EKGST elevationsCXRAcute MI now with Pulmonary edema
8How does any of this relate to pathology? Definitions to KnowAngina Pectoris- severe pain around the heart caused by a relative deficiency of oxygen supply to the heart muscle.MI – cardiac muscle death caused by a partial or complete occlusion of one or more of the coronary arteries.New York Heart Association Functional Classification of AnginaI : angina with unusually strenuous activityII : Angina with slightly more prolonged or slightly more vigorous activity than usualIII : Angina with usual daily activityIV : Angina at rest.Unstable Angina – Angina of new onset, angina at rest or with minimal exertion, or a crescendo pattern of angina with episodes of increasing frequency, severity or durationHow does any of this relate to pathology?
9Atherosclerosis!Atherosclerosis leading to plaque rupture, cascading to coronary artery thrombosis is the cause of acute MI approximately 90% of the time.(With this in mind, remember that many different conditions can lead to angina)
10AtherosclerosisEssentially endothelial cell damage of muscular and elastic arteriesCauses of endothelial cell injury?HTN, smoking, HLD, homocysteine etc.=
11Atherosclerosis Cell Response is Crucial! Macrophages and platelets adhere to damaged endothelium, this results in a release of cytokines that cause hyperplasia of medial smooth muscle cells.Smooth muscle cells migrate to the tunica intimaPlaque (fibrous cap) develops – composed to inflammatory cells, smooth muscle, foam cells, and extracellular matrixThese plaques reduce blood flow through arteries, when the plaques become disrupted a thrombosis often occurs
12Atherosclerosis Thrombosis leads to Acute MI, Strokes, Small Bowel Infarctions etc.Here is occlusive coronary atherosclerosis. The coronary at the left is narrowed by 60 to 70%. The coronary at the right is even worse with evidence for previous thrombosis with organization of the thrombus and recanalization such that there are three small lumens remaining, one of which contains additional recent thrombus.
13Here is a closer view of the gross appearance of a coronary thrombosis Here is a closer view of the gross appearance of a coronary thrombosis. The thrombus occludes the lumen and produces ischemia and/or infarction of the myocardium. Atherosclerosis is an ongoing process that takes years to decades for clinically apparent problems to appear.
14Common Sites for Atherosclerosis Abdominal AortaCoronary ArteryPopliteal ArteryInternal Carotid Artery
15Primary Treatment Mainstays of treatment remain prevention. BP control, Lipid Control, Smoking Cessation, Healthy Diet, Exercise.Know who is at riskRisk Factors : Males over 40, HTN, Tobacco Abuse, DM, Cocaine Use, HLD, Family Hx of CAD, Postmenopausal Status, Homocystinemia
16Pearls Angina is the most frequent symptom of intermittent ischemia Physical exam is normal in many patients with anginaMONA are the initial mainstays of treatmentTime is MyocardiumMain complications of atherosclerosis include aneurysms, thrombosis, and ischemiaAbdominal Aorta = most common site for atherosclerosis because no vasa vasorumFibrous Cap = pathognomonic for atherosclerosisMain players in atherosclerosis = endothelial cell injury leading to macrophages and platelet activation