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?
• 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?
Differential Diagnosis
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Angina
MI
Pericarditis
Aortic Dissection
Heart Failure
Pneumonia
Pneumothorax
- PE
- GERD
- PUD
- Pancreatitis
- Costochondritis
- Anxiety
- Shingles
WHAT IS YOUR NEXT STEP IN ASSESSING THE PATIENT?
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?
Lab Tests
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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?
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?
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
.
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?
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)
Atherosclerosis
• Essentially endothelial cell damage of muscular
and elastic arteries
• Causes of endothelial cell injury?
– HTN, smoking, HLD, homocysteine etc.
Atherosclerosis
•
Cell Response is Crucial!
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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
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.
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.
Common Sites for Atherosclerosis
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Abdominal Aorta
Coronary Artery
Popliteal Artery
Internal Carotid
Artery
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
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
Resources
• http://ars.els-cdn.com/content/image/1-s2.0-S0002914900006949-gr1.gif
• http://www.med.umich.edu/anatomy/plastinate/galleries/pathological_sp
ecimens.html
• http://www.imcar.rwth-aachen.de/news/2009/03-03-carolustherapeutics-scibx/figure01.jpg
• http://o.quizlet.com/i/MXtzGl5vaPs3xycUPbp2CA_m.jpg
• http://www.jfponline.com/images/Supplements/Nov09/SupplJFP1109_CV
risk_2-fig1.jpg
• https://www.healthtap.com/#topics/best-coronary-arteriosclerosisprogram
• http://www.nlm.nih.gov/medlineplus/ency/article/007452.htm
• Goljan, Edward. Rapid Review Pathology, Elsevier 2009 Edition