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Cardiology Week 3 > Acute Coronary Syndromes (ACS) > Flashcards

Acute Coronary Syndromes (ACS) Flashcards

1
Q

what percentage block usually causes heart attacks?

A

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

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2
Q

transmural infarction

A

complete blockage of coronary artery leads to infarct of entire wall of myocardium

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3
Q

sub endocardium infarct

A

involves only the innermost layers of the myocardium…usually due to partial bloockage and not enough flow to inner layers

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4
Q

why is there a risk of arrhythmia with MI?

A

the accumulating lactic acid causes sodium and other ion changes that lead to abnormal electrolyte levels that can cause an arrhythmia

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5
Q

macroscopic feature of MI less than 4 hours

A

nothing

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6
Q

macroscopic feature of MI 4-12 hours

A

some dark mottling

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7
Q

macroscopic feature of MI 12-24 hours

A

dark mottling

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8
Q

macroscopic feature of MI 1-3 days

A

mottling and developing yellow tan necrotic center

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9
Q

macroscopic feature of MI 3-14 days

A

yellow/tan and soft with red borders

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10
Q

macroscopic feature of MI 2-8 weeks

A

gray white scarring form border to core of infarct

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11
Q

long term macroscopic feature of MI

A

scarring

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12
Q

microscopic feature of MI less than 4 hours

A

usually nothing

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13
Q

microscopic feature of MI 4-12 hours

A

wavy fibers, early coagulative necrosis

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14
Q

microscopic feature of MI 12-24 hours

A

coagulative necrosis, nuclear pyknosis, early PMN

contractile bands denature

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15
Q

microscopic feature of MI 1-3 days

A

coagulative necrosis, total loss of nuclei and interstitial PMN

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16
Q

microscopic feature of MI 3-14 days

A

macros and granulation tissue start to appear, disintegration of dead myocytes

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17
Q

microscopic feature of MI 2-8 weeks

A

no cellularity and increasing collagen

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18
Q

microscopic feature of MI permanent

A

collagenous scar

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19
Q

what happens to myocytes surrounding the infarct?

A

they hypertrophy

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20
Q

hypokinesis definition in MI

A

local area with reduced contraction

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21
Q

akinesis definition in MI

A

local area with NO contraction

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22
Q

dyskinesis definition in MI

A

local area that bulges out with contraction

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23
Q

what are the two types of diastolic dysfunction in MI?

A

increased ventricular filling pressures and reduced compliance

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24
Q

what is ischemic preconditioning?

A

brief ischemia actually leads tissue to better handle future episodes of severe ischemia

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25
Q

how do we get left ventricular failure from MI?

A

stenosis of all coronary vessels

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26
Q

two complications following a infarct and MI?

A

arrhythmias and extension of infarct or emboli

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27
Q

with a transmural infarct…what can happen to the ventricular wall?

A

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

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28
Q

pericardial tamponade definition

A

when myocardial wall ruptures and you bleed into pericardial cavity

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29
Q

what can happen to papillary muscle following an MI?

A

it can rupture…leads to regurgitation of mitral valve

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30
Q

aneurysm following MI

A

wall bulges during systole following transmural MI…and predisposes to rupture

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31
Q

mural thrombosis after MI

A

very deadly after an MI..systemic emboli

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32
Q

clinical symptoms of MI

A

pain in chest, radiate to left arm…nausea…diaphoresis and cool clammy skin
fever shortness of breath

33
Q

physical exam findings of MI

A 
rales
S4
dyskinetic apical pulse
mitral regurg
diaphoresis
HR and BP UP
34
Q

when do we care about T wave inversion with an MI?

A

if the symptoms are there from the patient then inverted T waves are worth worrying about

35
Q

where should ST segment fall on Y axis of the ECG?

A

should be isoelectric with the PR interval

36
Q

ST depression

A

N-STEMI partial occlusion likely

37
Q

ST elevation

A

STEMI transmural

38
Q

how large must depressions must be of the ST segment be to worry?

A

over 1 mm or more than 1 small box

39
Q

what must you have to diagnose an N STEMI or a STEMI?

A

rise and fall in troponin

40
Q

do you need troponin changes for unstable angina?

A

NO how we differentiate between NSTEMI and angina

41
Q

when does troponin show up?

A

it will show in serum levels 3-4 hours after chest pain begins…negative troponin dont mean shit if it is early on

42
Q

do troponin levels directly correlate with size of MI?

A

YES

43
Q

what do you have to have to be ST elevation?

A

ST elevation in two contiguous leads of greater than 1 mm

44
Q

what leads are associated with inferior of heart? and vessels is this?

A

II, III and aVF…RCA

45
Q

what leads are associated with anterior of heart? and vessels is this?

A

V2-V4 and LAD

46
Q

what leads are associated with anteroseptal of heart? and vessels is this?

A

V1-V4 and LAD

47
Q

what leads are associated with lateral of heart? and vessels is this?

A

I, AVL, V5, V6 and LCx

48
Q

an LBBB means what portion of heart for MI and what vessel?

A

anterior and LAD

49
Q

if V1 and V2 have depressions what portion of heart for MI and what vessel?

A

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

50
Q

what are diagnostic criteria for a pathological Q wave?

A

must be more than 1 mm wide, in contiguous leads, and be greater than 25% of the QRS amplitude

51
Q

what is variant (prinzmetal) angina?

A

coronary artery spasm without atherosclerosis leads to chest pain and ST elevation…but IS NOT an MI

52
Q

what type of MI is only type to get pathological q waves?

A

STEMI…none ever in N STEMI or unstable angina

53
Q

what type of MI has worst prognosis and why?

A

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

54
Q

How do we rate risk for MI?

A

TIMI risk score

55
Q

what are factors for TIMI risk score (7)

A 
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
56
Q

what is the main anti-ischemic drug for NSTEMIs? and why do we give this?

A

beta blockers are given to reduce need for Oxygen and to slow heart rate

57
Q

after an NSTEMI, how long do you give beta blockers?

A

permanently

58
Q

what is another anti-ischemic drug after an NSTEMI and why?

A

nitroglycerin..leads to venous dilation which leads to lower preload of heart and less O2 demand for heart wall

also gives coronary vasodilation

59
Q

when should you not give nitorglycerin?

A

if the patient is in right heart ischemia…they need higher preload to fill enough blood in RV

60
Q

what is another drug options for patients with NSTEMI?

A

calcium channel blockers like the verapamil and diltiazem

61
Q

name the three drugs to give NSTEMI patient

A

beta blockers, nitroglycerin, and calcium channel blockers

62
Q

what two antiplatelet drugs do you give NSTEMI? and are these permanent?

A

Aspirin and clopidogrel

63
Q

what anticoag to give NSTEMI?

A

heparin or LMWH

64
Q

if you cannot give NSTEMI heparin, what other anticoag can you give?

A

fondaparinux..facto X1 inhibitor

65
Q

what drug is used for anticoagulation exclusively in the cath lab?

A

bivalirudin

66
Q

what are the two styles of treatment you have option of with NSTEMI, and when should you switch from one to other?

A

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

67
Q

if no cath lab available following a STEMI…what drug do you give and why?

A

alteplase (tpa)…it is a fibrinolytic that can bust up the clot

68
Q

what mechanisms lead to arrhythmias after MI?

A
  1. impaired perfusion of conduction system
  2. accumulation of toxic metabolites
  3. a autonomic changes
  4. arrhythmogenics we give as meds
69
Q

what is the early cause of VT after MI?

A

transient electrical instability…most common cause of death after an MI

70
Q

what is the later cause of VT after an MI?

A

structural scar and electrical reentry

71
Q

what vessel supplies the SA/AV node?

A

RCA

72
Q

what parts of conduction pathway does the LAD provide?

A

bundle of his, RBB, LBB

73
Q

what three things does an IABP do?

A

increases coronary blood flow, improves left ventricle unloading and improves cardiac output

74
Q

what is an IABP and why do we give it after an MI?

A

intra aortic balloon pump….given to help increase left heart failure

75
Q

what is the treatment for right ventricular infarction?

A

VOLUME of blood and reperfusion

76
Q

what leads have ST elevation in right heart usually?

A

lead III greater than lead II and move lead V4 to right side and will get ST elevation

77
Q

three ruptures that can happen post MI

A

papillary muscle like valves
IV septum
ventricular wall

78
Q

how do we get thromboemboli after MI?

A

from stasis of blood around the infarcted region of the heart

79
Q

name the two drugs we can give people to help lower cholesterol and prevent further MI?

A

ACE inhibitors and statins

Cardiology Week 3 (15 decks)

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