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Cardiovascular > SM 129 Acute Coronary Syndromes Pathophysiology > Flashcards

SM 129 Acute Coronary Syndromes Pathophysiology Flashcards

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1
Q

How long do ACS last?

A

At least 30 min

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2
Q

What is a Type 1 MI?

A

Spontaneous MI from ischemia related to plaque erosion and/or rupture

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3
Q

How do the symptoms of ACS compare to Angina Pectoris?

A

The symptoms are similar, but ACS is more severe

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4
Q

What is a Type 3 MI?

A

Sudden unexpected cardiac death

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5
Q

How does NSTEMI present on ECG?

A

ST segment depression or T wave inversion

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6
Q

What are the goals of long-term treatment of ACS?

A

Prevent recurrence
Prevent left ventricular remodeling (STEMI only)
Prevent fibrosis

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7
Q

What does Heparin bind inadvertently?

A

Heparin binds non-specifically to plasma proteins in patient to varying extents, lowering its anti-coagulative properties

LMWH is unaffected

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8
Q

How does Aspirin mediate anti-platelet effects?

A

Irreversible acetylation of COX enzymes, preventing release of Thromboxane A2

Act synergistically with Aspirin

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9
Q

What enzymes are commonly used as cardiac makers?

A

Troponin I and T, as well as CK-MB

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10
Q

Within what time frame of arrival should mechanical ventilation be pursued?

A

90 min within arrival

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11
Q

Why are Thienopyridines and Aspirin able to act synergistically?

A

They both inhibit platelet activity through different pathways; specifically, Theinopyridines inhibit ADP-dependent activation through P2Y12 while Aspirin irreversibly acetylates COX to block Thromboxane A2 production

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12
Q

What are Acute Coronary Syndromes?

A

A spectrum of diseases ranging from unstable angina to non ST elevated MI (NSTEMI) to ST elevated MI (STEMI)

Does not include stable angina

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13
Q

What two pathways contribute to coronary clot formation?

A

Clotting Cascade + Platelet Aggregation = Coronary Clot

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14
Q

Under what circumstances can pursuing mechanical ventilation be delayed?

A

A patient who presents with NSTEMI and troponin elevation can receive PTCA beyond 90 min and within 1-3 days if no symptoms of ongoing injury are present

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15
Q

What form of Thrombin can Heparin not neutralize?

A

Heparin cannot neutralize Thrombin bound to Fibrin

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16
Q

How does Tirofiban work?

A

Small molecule blocker against GPIIbIIIa receptors

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17
Q

How can the peak value of a cardiac enzyme be shifted?

A

Cardiac enzymes peak earlier if blood flow is restored

12 hours vs 24

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18
Q

List the thrombolytic agents, and what is their purpose?

A

Thrombolytic agents help break clots to restore blood flow

tPA
Streptokinase
Tenecteplase

Alternatively, use mechanical dilation via PTCA

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19
Q

What pathology underlies Total Obstruction w/o Adequate Residual Flow?

A

STEMI

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20
Q

How can left ventricular remodeling in ACS be prevented?

A

ACE Inhibitor

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21
Q

What is a Type 2 MI?

A

MI secondary to ischemia due to an imbalance of O2 supply an demand, as from coronary spasm, embolism, anemia, hypotension

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22
Q

What are the common antithrombin therapies?

A

Unfractionated Heparin + Low Molecular Weight Heparin

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23
Q

What groups are more likely to have silent ACS?

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A

Diabetics, women, elderly patients

24
Q

How does Abciximab work?

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A

Antibody against GPIIbIIIa receptors

25
What can be done to reduce ischemia in an MI?
Use a beta blocker
26
What is Heparin neutralized by (not the reversal agent)?
Platelet Factor 4 released by platelets on aggregation neutralizes Heparin LMWH are unaffected
27
How can recurrence of ACS be prevented?
Several medications prevent recurrence: ASAB Aspirin Statins ACE Inhibitors Beta Blockers
28
Compare and contrast NSTEMI to STEMI?
STEMI involves total occlusion of an artery and requires PTCA within 90 minutes of ischemia onset NSTEMI involves partial occlusion of an artery and requires PTCA within 1-3 days of ischemia onset
29
Within what time frame can blood flow be restored to avoid myocardial damage?
Restoring flow within 12 hours avoids damage from ischemia
30
How can fibrosis be prevented in ACS?
Aldosterone receptor antagonists = Spironolactone
31
What trait is the hallmark of ACS?
Symptoms present without obvious provocation (ie occur in the absence of physical activity or psychological stress)
32
What factors determine the outcome of an ACS?
Extent of Obstruction and Presence or Absence of Residual Flow
33
What can be done to decrease spasm?
Use nitrates which act as coronary vasodilators
34
Compare and contrast Troponins to CK-MB?
Both peak around 12 hours with blood flow restoration or 24 hours without blood flow restoration CK-MB declines over 2-3 days while Troponins decline over 7-14 days
35
Why do beta blockers reduce Myocardial Oxygen demand?
Beta blockers result in lower heart rate and anti-inotropic effects, decreasing Myocardial oxygen needs
36
What additional symptoms may accompany ACS?
PNLS Perspiration Nausea Lightheadedness Syncope
37
What factors promote the rupture of a clot?
A large lipid pool separated from circulation by a thin membrane Presence of an inflammatory reaction
38
How does STEMI present on ECG?
Elevated ST interval
39
Why are cardiac enzymes a good marker for MI?
Normally, cardiac enzymes are intracellular proteins and present in the blood in small amounts Elevations of these enzymes in the blood indicates myocardial damage specifically
40
How does Unstable Angina present on ECG?
May or may not show changes on ECG May show ST segment depressions or T wave inversions
41
Which cardiac enzyme is preferred for detecting a less recent MI?
Tropnonins I/T, since they decline over the course of 7-14 days
42
What options exist for myocardial revascularization?
Mechanical reperfusion with PTCA for STEMI within 90 minutes since complete vessel occlusion is common Mechanical reperfusion with PTCA for NSTEMI within 1-3 days since complete vessel occlusion is rare CABG for urgent need
43
What is PTCA?
Percutaneous Transluminal Coronary Angioplasty Uses a stent to restore blood flow to a blocked artery
44
What is stable angina not an ACS?
ACS are acute - stable angina is chronic
45
What is the basic pathology of an ACS?
Acute rupture or erosion of a coronary atherosclerotic plaque that leads to intravascular clot formation
46
What drugs are used for NSTEMI?
LACA LMWH or Heparin Aspirin ADP Receptor Antagonist = Clopidogrel IIbIIIa blocker = Abciximab
47
What are the basic goals of acute care of ACS?
``` Restore blood flow ASAP Stop clot formation Relieve pain Reduce ischemia Control potential vasospasm ```
48
Which type of MI requires restoring blood flow ASAP?
STEMI requires restoring Blood Flow asap Restoring blood flow within 12 hours of onset reduces myocardial damage
49
What drugs are used for STEMI?
HAC/P/T Heparin Aspirin Clopidogrel/Prasugrel/Ticagrelor (Platelet agent)
50
How are ACS classified?
ACS are classified by the changes noted on ECG during time of presentation as well as cardiac enzymes
51
What is the common final pathway to platelet aggregation?
GPIIbIIIa receptors
52
How does the duration of ACS compare to Stable Angina?
ACS lasts much longer (30+ min) as opposed to Stable Angina (2 min max)
53
What is the preferred method of restoring blood flow for NSTEMI?
Mechanical revascularization; thrombolytics have never been shown to have an effect
54
How do Thienopyridines exert anti-platelet effects?
Clopidogrel and Ticagrelor block the ADP pathway of platelet activation Act synergistically with Aspirin
55
What factors determine the clinical syndrome caused by acute rupture or erosion of a plaque?
Degree of obstruction to blood flow Duration of obstruction Amount of residual flow provided by collaterals
56
What are the residual flow outcomes of an ACS?
Total Obstruction w/o Adequate Residual Flow Total Obstruction w/ Adequate Residual Flow Partial Obstruction w/o Adequate Residual Flow Partial Obstruction w/ Adequate Residual Flow
57
What pathology underlies Partial Obstruction w/o Adequate Residual Flow?
NSTEMI

Cardiovascular (25 decks)

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