Acute Coronary Syndromes Flashcards
What is the 3 step pathogenesis to cause acute coronary syndromes (ACS)?
Unstable angina –> MI –> irreversible heart necrosis
What type of occlusion can cause a NSTEMI and NQMI?
Partial occlusive thrombus
Unlike unstable angina, what happens to the myocardium in a NSTEMI?
myocardial necrosis
So what type of occlusion leads to a STEMI or QwMI?
complete obstruction of coronary artery –> severe ischemia and necrosis
Which 2 important intrinsic chemical substances can cause plaque disruption, leading to rupture?
g-interferon, MMP
What is the main physical stress which can lead to plaque rupture?
BP
In atherosclerosis, there can be decreased amounts of NO and prostacyclin, which leads to what abnormality of the vessel?
Loss of vasodilation.
What 2 chemicals can over-run the vasodilators, causing a contractile events in endothelial dysfxn?
Thromboxane and serotonin
If you find a pt with ST depression and/or T-wave inversion, what can u use to differentiate a NSTEMI and unstable angina?
Serum biomarkers
Where do the serum markers come from to Dx a NSTEMI and STEMI?
Myocytes. They’re damaged so they leak em out.
These markers are absent in a healthy person, so detection of these markers is specific for myocyte damage.
Troponins (TnC, TnI)
When is the onset to serum troponin markers after MI?
they rise after 3-4 hours
When is the peak of serum troponin markers in an MI?
18-36 hours
This is the form of creatine kinase that is used as a cardiac marker for MI’s.
CK-MB
Besides the heart, where else in the body can u find CK-MB?
Small amts in the uterus, prostate, gut, diaphragm, and tongue.
In MI, how much greater is the CK-MB than the CK?
> 2.5%
When is the rise, peak, and return to normal for CK-MB during an MI?
rise 3-6 hours
peak at 24
fall to normal from 48-72 hours
What are the 3 drugs you can give to the potential STEMI/NSTEMI/UA patient to prevent ischemia?
B-blocker, Nitrates, +- Ca++ channel blocker
If a STEMI patient comes into ER, if you can’t do an emergent PCI within 90 minutes, what type of drug therapy should you give?
Fibrinolytic therapy
What is the score to asses risk in UA and NSTEMI?
TIMI score
If the UA or NSTEMI ranks high on the TIMI score, what is the appropriate management?
Invasive therapy (PCI or CABG)
Bradycardia, bronchospasm, decompensated HF, and hypoTN are contraindications to which drug that reduces the sympathetic drive of the heart?
B-blockers
If B-blockers and nitrates don’t work, which class of drugs can you give to prevent ischemia by decreasing HR and contractility?
CCB
Which antithrombolytic is given with aspirin to block the P2Y12 ADP receptor to reduce CV mortality, recurrent cardiac events, and strokes?
Clipidogrel
Which thieopyridine deriviative also blocks the P2Y12 ADP receptor to further reduce coronary events in ACS pts who undergo PCI?
Plasurgel
Abciximab, eptifibate and tirofiban are of which class of drugs that blocks the final common pathway of platelet aggregation to decrease adverse coronary events in pts undergoing PCI?
Glycoprotein IIb/IIIa receptor antagonists
This anticoagulant binds to antithrombin, which increases the potency of the plasma protein in the inactivation of the clotting forming thrombin.
UFH
How do u measure the dose adjustments when using UFH?
aPTT
test question lol
This anticoagulant interacts with antithrombin but prefers to inhibit coagulation factor Xa, is more predictible than UFH, and given via 1 or 2 subQ injections (rahter than IV).
LMWH (like enoxapirin)
This anticoagulant also blocks factor Xa but has less bleeding complications than LMWH.
Fondaparinux
This anticoagulant is a direct thrombin inhibitor and has superior clinical outcomes compared to the combo of UFH + GP IIb/IIIa receptor blocker.
Bivalarudin
How many of these factors must you have to begin antithrombolytic therapy?
a. Age >65 y/o
b. > 3 risk factors for CAD
c. Known coronary stenosis of >50% by prior angiography
d. ST segment deviations of the ECG at presentation
e. At least 2 anginal episodes in prior 24 hrs
f. Use of aspirin in prior 7 days
g. Elevated serum troponin or CK-MB
3
So if a pt comes into the ER with a total coronary artery occlusion and a STEMI, you give drugs like ASA, UFH, B-blockers, and nitrates, but that doesn’t actually treat the condition- it just stalls it. Which class of drugs must you give to treat the thrumbus to reperfuse the heart?
Fibrinolytics
This class of fibrinolytics work by stimualting the natural fibrinolytic system of the body, which transforms the inactive plasminogen into plasmin, which lyses fibrin clots.
tissue-type Plasminogen activators
So if you give a fibronolytic (like t-PA) within 2 hours of STEMI Sx, what is the % decrease in mortality compared to those who receive it 6 hours later?
50%
Boom. You give the t-PA. Sx disappear, ST segments go back to baseline, markers peak earlier than normally. How can you prevent immediate vessel reocclusion?
Antithrombotics (ASA, UFH or LMWH, and clopidogrel)
Obviously t-PA can cause a lot of bleeding. Which pt’s is t-PA a contraindication?
PUD, bleeding disorders, recent stroke, recovering from recent surgery
If you have the access, what is the alternative therapy to fibrinolytics to treat pts with acute STEMIs?
PCI
If you can get the PCI done within 90 mins, what is the optinal flow rate of the newly opened coronary vessels?
95%
True or False: the contraindications for PCI are the same as those for giving fibrinolytics.
True
The most important of post-MI outcome is the extent of damage to which part of the heart?
LV
What are the 4 classes of drugs u send the pt home with after they are treated for ACS?
ASA, B-blocker, Statin, and an ACEi (if the pt has a LV contractile dysfxn)
True or False: episodes of V-fib that occur during the first 48 hours of MI are often related to TRANSIENT electrical activity.
True!
This is the condition when blood demand to a portion of the heart is higher than the supply of oxygenated blood.
Ischemic Heart Disease (IHD)
What is the main culprit in IHD?
Atherosclerotic plaque occluding the coronary arteries.
True or False: IHD is the leading cause of death worldwide, killing 500k Muricans/year.
True
If an atherosclerotic plaque isnt the culprit causing the narrowing of the arterial lumen, what can be the other 2 causes to cause IHD?
thombosis and vasospasm
True or False: Angina is substernal recurrent chest pain that is from ischemia leading to necrosis.
False. It doesnt lead to necrosis.
This type of angina is the most common, caused by exertion or stress, and relieved at rest.
Stable/typical
This type of angina has a pattern of increasing frequent pain of prolonged duration with less and less exertion to trigger it.
Unstable/crescendo
This type of angina is caused by coronary artery spasm and occurs at rest.
Prinzmetal
This is the most important form of IHD, where there is death of cardiac muscle due to prolonged severe ischemia.
MI
After what time after ischemia do the cells show myofibrillar relaxation, glycogen depletion, cell and mitochondrial swelling?
just 60 seconds.
Thats just nutty. Like a…. nevermind.
However, these changes to myocytes after 60s are reversible, right?
Yes.
So when does myocytes have irrversible damage after ischemia?
2-4 hours
Give me 1 patient with all the risk factors for an MI. DO IT.
a 60 year old ham planet with a previous MI, who’s a smoker, has HTN and dyslipidemia, diabetic, lazy, stressed about being lazy, drug user, and who’s family also has a Hx of MI’s as well.
You said all that, right?
Which one of these causes ST elevation: transmural infarcts or subendocardial infarcts
Transmural infarcts
Food for thought: is an “in-fart” the thing when your bowel grumbles?
True or False: transmural infarcts are the most common form of infarct and involve the full thickness of the ventricular wall.
True
How much of the wall does a subendocardial MI involve?
limited to inner 1/3-1/2 of ventricular wall
Why is the subendocardial zone the most vulnerable to any reduction in coronary flow?
it’s one of the least perfused region of the myocardium
This is the time span after an MI when reversible injury occurs.
0-0.5 hours
This is the time span after an MI when there is no gross features, and there is viarable waviness of fibers at the border.
0.5-4 hours
This is the time span after an MI when there is dark mottling of the heart, and u can see early coagulation necrosis, edema, and hemorrhage.
4-12 hours
This is the time span after an MI when you see dark mottling, ongoing coagulation necrosis, pykinosis, myocyte hypereosinophilia, marginal contraction band necrosis, early neurtophilic infiltrate
12-24 hours
This is the time span after an MI when there is mottling with yellow-ran infarct, coagulation necrosis with LOSS OF NUCLEI and striatins, and brisk interstitial infiltrate of neutrophils
1-3 days
At 3-7 days after an MI, there is a hyperemic border with central yellow-tan softening, and what happens to the dead myocytes?
the dead ones disintegrate by phagocytosis from myocytes
When does granulation tissue begin to form after an MI?
7-10 days
During the 7-10 day period after an MI, there is well established granulation tissue, which brings about the appearance of what 2 things?
- new blood vessels
2. collagen deposition
Ok so the granulation tissue is set and we’re trying to rebuild the heart, but it usually doesnt happen to like how it was. What happens during the 2-8 week span to decreased cellularity?
increased collagen deposition
After what time is the scarring of the heart complete with the formation of a dense collagenous scar?
> 2 months
This may be obvious, but what is the best way to limit and stop MI damage?
Reperfusion
BUT WAIT. There are problems with FURTHER injurying tissue after a certain period of ischemia. When is it important to reperfuse the area after an MI?
before 4 hours
This is the syndrome when the MI knocks out LV function, leading to pump failure, which has a 70% mortality rate.
Cardiogenic shock
True or False: the size, area, and thickness of the infarct is DIRECTLY related to MI complications.
True
This is the condition that results when the myocardium becomes soft and weak from the necrotic and inflammed destruction.
Myocardial rupture
literally your heart explodes lol
Where is the most common location of myocardial rupture?
Ventricular free wall
If your ventricular free wall ruptures, where does blood accumulate? What is the condition resulting from this?
Hemopericardium –> cardiac tamponade
Once again, if like gives you tampons, you make tamponade.
This is a complication of an MI where fiberous or fibrohemorrhagic formations of the pericardium develops around the 2nd or 3rd day.
Pericarditis (dressler syndrome)
Which other chamber can have an infarction when there is ischemic injury to the adjacent chambers?
RV
True or False: infarcts can spread to adjacent tissues from weakening of the necrotic muscle.
True
This is a complication of an MI when the combination of a local abnormality in contractility (causing stasis) and endocardial damage can result in a specific formation.
Mural thrombus
This is a complication of an MI when the ventricals can buldge as a result of a complication of large transmural infarcts.
Ventricular aneurysm
The dysfunction of these muscles is a complication of an MI, resulting in mitral regurgitation.
Papillary muscles
