Acute Coronary Syndromes (ACS) Flashcards
what percentage block usually causes heart attacks?
it is normally the 30-40% blocks because they have a smaller fibrous cap that ruptures easily allowing a thrombus to form and block the whole thing
bigger blocks have well formed caps that dont rupture as easily
transmural infarction
complete blockage of coronary artery leads to infarct of entire wall of myocardium
sub endocardium infarct
involves only the innermost layers of the myocardium…usually due to partial bloockage and not enough flow to inner layers
why is there a risk of arrhythmia with MI?
the accumulating lactic acid causes sodium and other ion changes that lead to abnormal electrolyte levels that can cause an arrhythmia
macroscopic feature of MI less than 4 hours
nothing
macroscopic feature of MI 4-12 hours
some dark mottling
macroscopic feature of MI 12-24 hours
dark mottling
macroscopic feature of MI 1-3 days
mottling and developing yellow tan necrotic center
macroscopic feature of MI 3-14 days
yellow/tan and soft with red borders
macroscopic feature of MI 2-8 weeks
gray white scarring form border to core of infarct
long term macroscopic feature of MI
scarring
microscopic feature of MI less than 4 hours
usually nothing
microscopic feature of MI 4-12 hours
wavy fibers, early coagulative necrosis
microscopic feature of MI 12-24 hours
coagulative necrosis, nuclear pyknosis, early PMN
contractile bands denature
microscopic feature of MI 1-3 days
coagulative necrosis, total loss of nuclei and interstitial PMN
microscopic feature of MI 3-14 days
macros and granulation tissue start to appear, disintegration of dead myocytes
microscopic feature of MI 2-8 weeks
no cellularity and increasing collagen
microscopic feature of MI permanent
collagenous scar
what happens to myocytes surrounding the infarct?
they hypertrophy
hypokinesis definition in MI
local area with reduced contraction
akinesis definition in MI
local area with NO contraction
dyskinesis definition in MI
local area that bulges out with contraction
what are the two types of diastolic dysfunction in MI?
increased ventricular filling pressures and reduced compliance
what is ischemic preconditioning?
brief ischemia actually leads tissue to better handle future episodes of severe ischemia
how do we get left ventricular failure from MI?
stenosis of all coronary vessels
two complications following a infarct and MI?
arrhythmias and extension of infarct or emboli
with a transmural infarct…what can happen to the ventricular wall?
the IV septum can rupture or the lateral walls can rupture
if septum ruptures you get left to right shunt and if wall ruptures you get bleeding into pericardial cavity
pericardial tamponade definition
when myocardial wall ruptures and you bleed into pericardial cavity
what can happen to papillary muscle following an MI?
it can rupture…leads to regurgitation of mitral valve
aneurysm following MI
wall bulges during systole following transmural MI…and predisposes to rupture
mural thrombosis after MI
very deadly after an MI..systemic emboli
clinical symptoms of MI
pain in chest, radiate to left arm…nausea…diaphoresis and cool clammy skin
fever shortness of breath
physical exam findings of MI
rales S4 dyskinetic apical pulse mitral regurg diaphoresis HR and BP UP
when do we care about T wave inversion with an MI?
if the symptoms are there from the patient then inverted T waves are worth worrying about
where should ST segment fall on Y axis of the ECG?
should be isoelectric with the PR interval
ST depression
N-STEMI partial occlusion likely
ST elevation
STEMI transmural
how large must depressions must be of the ST segment be to worry?
over 1 mm or more than 1 small box
what must you have to diagnose an N STEMI or a STEMI?
rise and fall in troponin
do you need troponin changes for unstable angina?
NO how we differentiate between NSTEMI and angina
when does troponin show up?
it will show in serum levels 3-4 hours after chest pain begins…negative troponin dont mean shit if it is early on
do troponin levels directly correlate with size of MI?
YES
what do you have to have to be ST elevation?
ST elevation in two contiguous leads of greater than 1 mm
what leads are associated with inferior of heart? and vessels is this?
II, III and aVF…RCA
what leads are associated with anterior of heart? and vessels is this?
V2-V4 and LAD
what leads are associated with anteroseptal of heart? and vessels is this?
V1-V4 and LAD
what leads are associated with lateral of heart? and vessels is this?
I, AVL, V5, V6 and LCx
an LBBB means what portion of heart for MI and what vessel?
anterior and LAD
if V1 and V2 have depressions what portion of heart for MI and what vessel?
posterior and RCA…you should move some leads to the back and check for elevation so you know if it is STEMI versus N STEMI
what are diagnostic criteria for a pathological Q wave?
must be more than 1 mm wide, in contiguous leads, and be greater than 25% of the QRS amplitude
what is variant (prinzmetal) angina?
coronary artery spasm without atherosclerosis leads to chest pain and ST elevation…but IS NOT an MI
what type of MI is only type to get pathological q waves?
STEMI…none ever in N STEMI or unstable angina
what type of MI has worst prognosis and why?
N STEMI with depressed ST segment…this is because these patients usually have the worst comorbidities…so it isnt actually due to the MI itself
How do we rate risk for MI?
TIMI risk score
what are factors for TIMI risk score (7)
age greater than 65 known CAD risk factors for CAD Aspirin use more than 2 episodes of angina in 24 hours ST changes greater than 0.5 mm elevated cardiac markers
what is the main anti-ischemic drug for NSTEMIs? and why do we give this?
beta blockers are given to reduce need for Oxygen and to slow heart rate
after an NSTEMI, how long do you give beta blockers?
permanently
what is another anti-ischemic drug after an NSTEMI and why?
nitroglycerin..leads to venous dilation which leads to lower preload of heart and less O2 demand for heart wall
also gives coronary vasodilation
when should you not give nitorglycerin?
if the patient is in right heart ischemia…they need higher preload to fill enough blood in RV
what is another drug options for patients with NSTEMI?
calcium channel blockers like the verapamil and diltiazem
name the three drugs to give NSTEMI patient
beta blockers, nitroglycerin, and calcium channel blockers
what two antiplatelet drugs do you give NSTEMI? and are these permanent?
Aspirin and clopidogrel
what anticoag to give NSTEMI?
heparin or LMWH
if you cannot give NSTEMI heparin, what other anticoag can you give?
fondaparinux..facto X1 inhibitor
what drug is used for anticoagulation exclusively in the cath lab?
bivalirudin
what are the two styles of treatment you have option of with NSTEMI, and when should you switch from one to other?
early invasive…straight to cath lab
or conservative with meds
should go to cath lab and not be conservative if recurrent or you have positive stress test
if no cath lab available following a STEMI…what drug do you give and why?
alteplase (tpa)…it is a fibrinolytic that can bust up the clot
what mechanisms lead to arrhythmias after MI?
- impaired perfusion of conduction system
- accumulation of toxic metabolites
- a autonomic changes
- arrhythmogenics we give as meds
what is the early cause of VT after MI?
transient electrical instability…most common cause of death after an MI
what is the later cause of VT after an MI?
structural scar and electrical reentry
what vessel supplies the SA/AV node?
RCA
what parts of conduction pathway does the LAD provide?
bundle of his, RBB, LBB
what three things does an IABP do?
increases coronary blood flow, improves left ventricle unloading and improves cardiac output
what is an IABP and why do we give it after an MI?
intra aortic balloon pump….given to help increase left heart failure
what is the treatment for right ventricular infarction?
VOLUME of blood and reperfusion
what leads have ST elevation in right heart usually?
lead III greater than lead II and move lead V4 to right side and will get ST elevation
three ruptures that can happen post MI
papillary muscle like valves
IV septum
ventricular wall
how do we get thromboemboli after MI?
from stasis of blood around the infarcted region of the heart
name the two drugs we can give people to help lower cholesterol and prevent further MI?
ACE inhibitors and statins
