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What other questions would you like to ask this man?

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Presentation on theme: "What other questions would you like to ask this man?"— Presentation transcript:

1 What other questions would you like to ask this man?
HPI A 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?

2 What 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 ago All: None Meds: None Hos/Sx: Tonsillectomy at age 12, Rhinoplasty at age 23 FmHx: 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?

3 Differential Diagnosis
Angina PE MI GERD Pericarditis PUD Aortic Dissection - Pancreatitis Heart Failure Costochondritis Pneumonia Anxiety Pneumothorax - Shingles What is your next step in assessing the patient?

4 What would you like to do next?
Physical Exam Vitals: T 98.8, HR 105, RR 18, BP 190/95, Ht 5’10, Wt 260 General: 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 arteries Lung: CTA HEENT: neck has faint carotid bruit on left, minimal JVD Abd: normal Extremities: trace edema, warm to touch, no clubbing, no cyanosis What would you like to do next?

5 What would you like to do next?
Lab Tests CBC: Normal BUN/Cr: WNL PT: 13 sec PTT: 27 sec INR: 1.4 Troponins: elevated CKMB: > 5% What would you like to do next?

6 Initiate treatment! MONA
Morphine – this can achieve an adequate analgesia which will decrease the levels of circulating catecholamine's, thus reducing myocardial oxygen consumption Oxygen – 2-4 L via nasal cannula NTG – sublingual administration ever 5min Aspirin – 325mg chewed and swallowed. Now What?

7 Diagnostic Testing Not all MI’s will show ECG and/or CXR abnormalities.
12 Lead EKG ST elevations CXR Acute MI now with Pulmonary edema

8 How does any of this relate to pathology?
Definitions to Know Angina 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 Angina I : angina with unusually strenuous activity II : Angina with slightly more prolonged or slightly more vigorous activity than usual III : Angina with usual daily activity IV : 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 duration How does any of this relate to pathology?

9 Atherosclerosis! 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)

10 Atherosclerosis Essentially endothelial cell damage of muscular and elastic arteries Causes of endothelial cell injury? HTN, smoking, HLD, homocysteine etc. =

11 Atherosclerosis 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 intima Plaque (fibrous cap) develops – composed to inflammatory cells, smooth muscle, foam cells, and extracellular matrix These plaques reduce blood flow through arteries, when the plaques become disrupted a thrombosis often occurs

12 Atherosclerosis 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.

13 Here 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.

14 Common Sites for Atherosclerosis
Abdominal Aorta Coronary Artery Popliteal Artery Internal Carotid Artery

15 Primary Treatment Mainstays of treatment remain prevention.
BP control, Lipid Control, Smoking Cessation, Healthy Diet, Exercise. Know who is at risk Risk Factors : Males over 40, HTN, Tobacco Abuse, DM, Cocaine Use, HLD, Family Hx of CAD, Postmenopausal Status, Homocystinemia

16 Pearls Angina is the most frequent symptom of intermittent ischemia
Physical exam is normal in many patients with angina MONA are the initial mainstays of treatment Time is Myocardium Main complications of atherosclerosis include aneurysms, thrombosis, and ischemia Abdominal Aorta = most common site for atherosclerosis because no vasa vasorum Fibrous Cap = pathognomonic for atherosclerosis Main players in atherosclerosis = endothelial cell injury leading to macrophages and platelet activation

17 Resources https://www.healthtap.com/#topics/best-coronary-arteriosclerosis-program Goljan, Edward. Rapid Review Pathology, Elsevier 2009 Edition


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