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Cardiology > Lectures 23-24: Acute Coronary Syndrome > Flashcards

Lectures 23-24: Acute Coronary Syndrome Flashcards

1
Q

Critical parts of coagulation cascade

A

Tissue factor liberated due to plaque rupture + Factor VII –> Factor Xa, turns prothrombin –> thrombin, turns fibrinogen –> fibrin –> MESH CLOT

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2
Q

Where is Factor Xa in the coagulation cascade?

A

Intersection of ex and intrinsinc pathways

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3
Q

How do we inhibit clots? Where do these proteins arise?

A

Antithrombin (inhibits thrombin w/ heparan on endothelial cells); Protein C/S/thrombomodulin; Tissue Factor Pathway Inhibitor; ALL FROM ENDOTHELIAL CELLS

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4
Q

How do we destroy clots? Relation to endothelial cells?

A

Lysis via plasmin, converted from plasminogen by TPA, which is secreted by endothelial cells

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5
Q

Interaction between endothelium and platelets (healthy, 2 main ways)

A

Inhibit platelet aggregation via NO, PGI and conversion of ADP into Adenosine; promote vasodilation

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6
Q

What does an activated platelet do?

A

Aggregate due to factor release (ADP) and FIBRIN linking via glycoproteins (IIb-IIIa) on platelet surfaces

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7
Q

Why do plaques rupture?

A

Chemical factors (cytokines, enzymes), physical stresses (high blood pressure, emotional upset)

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8
Q

Hypokinesis

A

Reduced contraction

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9
Q

Akinesis

A

Loss of contraction

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10
Q

Dyskinesis

A

Outwad bulging during contraction

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11
Q

Why is there diastolic dysfunction during MI?

A

Relaxation is a process that requires ATP, leads to reduced compliance and increase filling pressure

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12
Q

What is ischemic preconditioning?

A

Increased ischemic threshold with continued exercise is protective against MI

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13
Q

Define ventricular remodeling

A

Changes in cardiac size, shape, structure, physiology which can be pathological

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14
Q

Early remodeling occurs where and includes

A

At site of injury, infarction zone thinning and elongation

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15
Q

Late remodeling occurs where and includes

A

Diffuse process with hypertrophied myocytes and increased interstitial collagen

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16
Q

What does a remodeled heart look like (late)

A

Spherical

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17
Q

Early/late remodeling: good or bad?

A

Early may be adaptive by increasing stroke volume in setting of decreased CO; late is bad because of hypertrophy and pathological shape

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18
Q

How do we prevent remodeling?

A
  1. Early reperfusion (prevent large infarct); 2. Medical therapy (ACE-I, ARBs, beta-blockers)
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19
Q

Type 1 and 2 of MIs

A

Type 1: classic plaque rupture; Type 2: supply-demand inbalance w/ no plaque rupture (anemia)

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20
Q

Q wave MI

A

Transmural

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21
Q

Non-Q wave MI

A

Subendocardial

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22
Q

Type 3 MI

A

Cardiac death

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23
Q

Type 4/5 MI

A

Revascularization process

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24
Q

Some nonatherosclerotic causes of acute MI and patient profile

A

Young OR no coronary risk factors: valve problems, inflammatory disorders (vasculitis), peripartum female, cocaine abuse

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25
How does cocaine abuse cause acute MI?
Vasospasm decreases O2 supply, increased HR/inotropy increases O2 demand AND chronic abuse increases atherosclerosis risk
26
First step of flow chart of ischemic discomfrot at rest
ST segment elevation
27
Ischemic discomfort at rest can ultimately be due to...
Unstable angina, Non-Q-wave MI, Q-wave MI
28
A non-occlusive thrombus can cause either...what's the difference between these two outcomes?
Unstable angina or Non-ST elevation myocardial infarction (NSTEMI); NSTEMI causes necrosis while unstable angina does NOT
29
An occlusive thrombus causes...
ST-elevation myocardial infarction (STEMI)
30
Comparing unstable angina to MI
Severe, longer duration chest pain compared to stable angina not improved with rest; large sympathetic response (diaphoresis, nausea, tachycardia, cool skin); shortness of breath
31
Physical findings of MI (4)
S4 (atrial contraction into a concompliant LV), S3 (volume overload), systolic murmur (rupture or papillary dysfunction), low grade fever (inflammation)
32
Some items on MI differential
Pericarditis (painful with inspiration), aortic dissection (ripping pain, look for BP asymmetry), PE, GI problems
33
Why BP assymetry on aortic dissection?
If dissection is proximal to subclavian, you will get different BPs in right arm vs left arm
34
What might you see on EKG for unstable angina/NSTEMI? How can you differentiate NSTEMI from USA?
T wave inversion or ST Depression OR normal; biomarkers elevated in NSTEMI
35
For STEMI, discuss EKG and biomarkers
ST segment elevated, biomarkers elevated
36
Lateral wall leads, what artery?
I, aVL, V5, V6; Left circumflex
37
Inferior wall leads, what artery?
II, III, aVF; Right coronary
38
Anteroseptum leads, what artery?
V1 - V4; LAD
39
Overtime, an unreated ST segment elevation MI will evolve into what on EKG?
Q wave; absence of electrical force in that segment
40
3 biomarkers of myocardial necrosis
Troponin core complex (TnI and TnC); creatine kinase myocardial band (CK-MB), and myoglobin
41
Discuss positive troponin test and MI?
Elevated cTnI (cardiac troponin) is NECESSARY but NOT sufficient for diagnosis of cardiac MI
42
When are cTnI levels highest?
Begin to rise within 3-4 hours and pea at about 1 day, slow deline
43
What is CK?
Enzyme involved in generation of ATP
44
Describe kinetics of elevated CK in MI
Rises and peaks faster (24 hours) but clears faster
45
Why is using both CK-MB and cTnI helpful?
If they had multiple MIs in short period of time, CK-MB would be high again (though cTnI might not have fallen)
46
Goal of STEMI treatment
IMMEDIATE RESTORATION OF BLOOD FLOW TO OCCLUDED VESSEL
47
Approaches to NSTEMI
Conservative vs invasive approaches
48
Anti-ischemic drug classes (3)
Beta-blockers, nitrates, Ca2+ channel blockers
49
Beta-blockers do what in context of ACS?
Relieve ischemic pain, reduce infarct size, and life threatening arrhythmias --> mortality benefit
50
What categories of patients do we NOT give nitrates to?
Hypotensive and STEMI patients with inferior MI/RV infarction (must fill RV to allow for heart function)
51
Are Ca2+ channel blockers used in ACS?
Not really, no mortality benefits
52
Anti-thrombotic therapy: drug classes and why it works
Inhibit thrombin reduces platelet aggregation proliferation (but do not reduce size); includes antiplatelets and anticoagulants
53
Anti-platelet therapy drugs and mechanism
Aspirin (COX inhibitor), Clopidogrel (blocks ADP at P2Y12 receptor), Anti GPIIb-IIIa (binds fibrinogen)
54
What do statins due in setting of ACS?
Stabilize plaque
55
Who gets aspirin?
Any patient with acute MI
56
Two P2Y12 ADP receptor blockers
Clopidogrel and prasugrel
57
Clopidogrel is indicated in...What's a problem with clopidogrel?
All patients with USA/NSTEMI unless surgery planned; substantial variability in response
58
Prasugrel is different from clopidogrel how?
More consistent effect at inhibition of platelets with increased risk of bleeding
59
Describe GPIIb-IIIA receptor antagonists
Very potent because they inhibit the final common pathway of platelet aggregation so platelets CANNOT aggregate
60
T/F: GPIIb-IIIA receptor antagonists are commonly prescribed
False! Use is declining
61
Anti-coagulation therapy drugs do what? Name drugs
Inhibit some step of coagulation cascade; heparin, direct thrombin inhibitors (bivalirudin), factor Xa inhibitor (now a major target)
62
Descibe mechanisms and delivery of two types of heparin
Unfractioned heparin (IV, must test levels): binds antithrombin which binds both factor Xa and thrombin; Low molecular weight heparin (SQ, don't have to check levels) only binds factor Xa
63
USA/NSTEMI conservative approach vs invasive approach
Medications alone until sx worsen vs urgent cardiac catheterization with revascularization if indicated
64
How do we decide to use conservative or invasive approach?
TIMI risk score calculator (higher than 2-3 will benefit from aggressive treatments)
65
What do we do to reperfuse STEMI?
Fibrinolysis vs mechanical revasularization (PCI or CABG)
66
What does fibrinolysis refer to?
Medical therapy to enzymatically break down fibrin clot
67
Fibrinolytic agent that is still used today
tPA
68
Compare primary PCI vs fibrinolysis for STEMI
PPCI is better for flow and reduced risk of hemorrhage (compared to fibrinolysis) --> generally favor PCI
69
When is fibrinolysis preferred?
Early presentation (
70
When is invasive strategy preferred? (5)
Skilled PCI lab available, high STEMI risk (shock), fibrinolysis contraindicated (risk of bleeding), late presentation (>3 hours, lytic therapy won't work), diagnosis of STEMI is in doubt
71
Additional therapies for STEMI patients...
Antiplatelets, anticoagulants
72
Do you give GBIIb-IIIa inhibitors if lytics are chosen for STEMI patients?
NOPE, no role for them
73
What other drugs do we give to MI patients?
ACE-I (prevent remodeling), statins (stabilize plaque and eventually lower atherosclerosis), prolonged anticoagulation (in certain patients)
74
When would be prescribe LT anticoagulation?
LV thrombus, Afib
75
MI complications: electrical
Vfib, supraventricular arrhythmias (brady and tachycardias), conduction blocks
76
MI complications: mechanical
Left: pulmonary congestion; Right: JVD and hypotension
77
T/F: MIs can cause sytolic and dystolic dysfunctions
True!
78
What arrhythmia are we particularly concerned about with MI?
V fib! Can cause SCD
79
You've occluded the RCA...consequence...treatment...
Damage to right ventricle --> JVD --> hypotension (cannot get blood into R ventricle) --> treatment is volume to get blood into right ventricle
80
Posterior wall MI has what kind of EKG?
Will demonstrate ST depression in anterior leads (as opposed to ST elevation)
81
Other MI complications (3)
LV aneurysm: true and pseudoaneurysm; papillary muscle rupture; pericarditis
82
What is a pseudoaneurysm. Treatment?
Essentially a mycocardial rupture that is contained by sac; surgical emergency
83
What can a papillary muscle rupture cause? Treatment?
Severe mitral regurgitation and death; surgery
84
Two flavors of pericarditis
Acute (due to inflammation) vs later, called Dressler syndrome (autoimmune system may be involved)

Cardiology (22 decks)

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