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Cardiology - MI (Myocardial Infarction) (Coronary Blood Supply Summary…
Cardiology - MI (Myocardial Infarction)
Coronary Blood Supply Summary
Right Dominant Coronary Artery Circulation
note that 85 - 90% of people are right dominant in RCA producing the Posterior Descending Artery
*Post MI Complicaions / Sequelae
go by number of days post MI for the risks of different things happening
most common is mitral valve paillary mucsle rupture
Post MI Mitral Valve Papillary Muscle Rupture
happens 3-5 days post MI
severe pulmonary edema
--> way to tell difference with superacute RV failure
Clinical Cases
Clinical Case
Notes
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note that
Clinical Case
Post MI papillary muscle rupture case
Notes
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note that the posterior descending artery supplies the entire bottom of the heart in right dominant people
--> this also supplies the postermedial papillary muscle that holds the chorda tendinae for the mitral valve
there is also an anterior and annulus papillary muscles
Clinical Case
Free Wall Rupture
longest = within 2 weeks of MI
high mortality
Clinical Cases
Clinical Case
Notes
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note that
Clinical Case
Clinical Case
Notes
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Clinical Case
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note that free wall rupture usually happens in the LV anterior portion of the heart where there is the most pressure and LAD = widow maker
if occluded proximal enough you get transmural infarction and necrosis
--> high risk for free wall rupture
RV failure
acute - within 72 hours
clear lungs, hypotension and peripheral edema
Clinical Cases
Clinical Case
Notes
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note that
Clinical Case
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ACUTE - within 3 days
--> first RV failure due to volume overload
subacute - 1-3 days = ruptures due to stress
mitral papillary muscles
--> MV regurge
interventricular septum rupture
--> new holosystolic murmur
free wall rupture
--> cardiac tamponade triad
--> distant heart sounds, hypoTN, JVD and JVP
Interventricular septum rupture
subacute - 3 - 5 days
new loud holosystolic murmur
Clinical Cases
Clinical Case
Notes
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note that
Clinical Case
*Classifying MI by Location, ECG leads and Coronary Arteries
When you get an MI, don't be such a
SALI
S = superior
A = anterior
L = lateral wall
I = Inferior
MI by *ECG Leads
When you get an MI, don't be such a
SALI
look at the leads of the ECG starting in order at V1 and go through V1 -6 and then the other leads
S = superior = v1 , v2
A = anterior = v3, v4 (also v1 and v2) = LAD
L = lateral wall = v5, v6
I = Inferior = IVF and other inferior leads
Septal MI
leads v1 and v2
Notes
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Anterior MI
leads v3 and v4 mainly (v1 and v2 also)
most common from the LAD = widowmaker
Notes
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Lateral MI
leads v5 v6 aVL and lead 1
Tetralogy case
Notes
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note that
Clinical Case
Notes
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Inferior MI
leads I, II and IVF
think INFerior = IVF and all downward facing leads
Acute Inferior MI treatment for Bradycardia
Tx = IV Atropine = Muc ACh Antagonist
need to lower the vagal tone to the heaart to increase the HR
Atropine for MI and bradycardia case
Notes
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note that
Clinical Case
Notes
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note that inferior MI are in lads 1 2 and AVF
from blood supply to inferior part of the heart = RCA / RPD = right posterior descending artery
note that right coronary artery supplies all the nodes and initial cardiac conduction system up to the proximal part of the bundle of HIS and first part of right bundle
rest is supplied by the LCA
thus RCA and inferior MIs present with very slow conduction and bradycardia
Tx = stop the vagal tone by ACh antagonist = Atropine IV
MI by *Coronary Arteries
NOtes
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MI by *STEMI
*Damage of MI and Repair
< 30 min = reversible changes
.> 30 min = IRReversible changes
ATP and Adenosine Stores loss and Lactate accumulation
3 / 3 / 30 rule for ATP loss and Adnosine stores loss
3 seconds post total MI = switch to anarobic metabolism happens in
3 minutes post total MI = ATP remains normal for about 3 minutes then rapid decline
30 minutes post total MI = Adenosine stores that keep coronary arteries dilated runs out
--> irreversible damage happens at this point
Clinical Cases
Clinical Case
Notes
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note that
Clinical Case
Ischemia and Reperfusion Injury = RI
releaase of creatine kinase
causes of RI = think all things that blood return to the damaged tissue
O2 free radicals from the returning perfusion
return of areobic respiration in the mitochondria
--> mitochondrial damage
blood brings WBCs
--> general inflammation once the blood returns and WBCs notice the cell is damaged
Clinical Cases
Clinical Case
Notes
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note that
Clinical Case
