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Cardiovascular > SM 129 Acute Coronary Syndromes Pathophysiology > Flashcards

SM 129 Acute Coronary Syndromes Pathophysiology Flashcards

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?

A

Diabetics, women, elderly patients

24
Q

How does Abciximab work?

A

Antibody against GPIIbIIIa receptors

25
Q

What can be done to reduce ischemia in an MI?

A

Use a beta blocker

26
Q

What is Heparin neutralized by (not the reversal agent)?

A

Platelet Factor 4 released by platelets on aggregation neutralizes Heparin

LMWH are unaffected

27
Q

How can recurrence of ACS be prevented?

A

Several medications prevent recurrence:

ASAB

Aspirin
Statins
ACE Inhibitors
Beta Blockers

28
Q

Compare and contrast NSTEMI to STEMI?

A

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
Q

Within what time frame can blood flow be restored to avoid myocardial damage?

A

Restoring flow within 12 hours avoids damage from ischemia

30
Q

How can fibrosis be prevented in ACS?

A

Aldosterone receptor antagonists = Spironolactone

31
Q

What trait is the hallmark of ACS?

A

Symptoms present without obvious provocation (ie occur in the absence of physical activity or psychological stress)

32
Q

What factors determine the outcome of an ACS?

A

Extent of Obstruction and Presence or Absence of Residual Flow

33
Q

What can be done to decrease spasm?

A

Use nitrates which act as coronary vasodilators

34
Q

Compare and contrast Troponins to CK-MB?

A

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
Q

Why do beta blockers reduce Myocardial Oxygen demand?

A

Beta blockers result in lower heart rate and anti-inotropic effects, decreasing Myocardial oxygen needs

36
Q

What additional symptoms may accompany ACS?

A

PNLS

Perspiration
Nausea
Lightheadedness
Syncope

37
Q

What factors promote the rupture of a clot?

A

A large lipid pool separated from circulation by a thin membrane

Presence of an inflammatory reaction

38
Q

How does STEMI present on ECG?

A

Elevated ST interval

39
Q

Why are cardiac enzymes a good marker for MI?

A

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
Q

How does Unstable Angina present on ECG?

A

May or may not show changes on ECG

May show ST segment depressions or T wave inversions

41
Q

Which cardiac enzyme is preferred for detecting a less recent MI?

A

Tropnonins I/T, since they decline over the course of 7-14 days

42
Q

What options exist for myocardial revascularization?

A

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
Q

What is PTCA?

A

Percutaneous Transluminal Coronary Angioplasty

Uses a stent to restore blood flow to a blocked artery

44
Q

What is stable angina not an ACS?

A

ACS are acute - stable angina is chronic

45
Q

What is the basic pathology of an ACS?

A

Acute rupture or erosion of a coronary atherosclerotic plaque that leads to intravascular clot formation

46
Q

What drugs are used for NSTEMI?

A

LACA

LMWH or Heparin
Aspirin
ADP Receptor Antagonist = Clopidogrel
IIbIIIa blocker = Abciximab

47
Q

What are the basic goals of acute care of ACS?

A 
Restore blood flow ASAP
Stop clot formation
Relieve pain
Reduce ischemia
Control potential vasospasm
48
Q

Which type of MI requires restoring blood flow ASAP?

A

STEMI requires restoring Blood Flow asap

Restoring blood flow within 12 hours of onset reduces myocardial damage

49
Q

What drugs are used for STEMI?

A

HAC/P/T

Heparin
Aspirin
Clopidogrel/Prasugrel/Ticagrelor (Platelet agent)

50
Q

How are ACS classified?

A

ACS are classified by the changes noted on ECG during time of presentation as well as cardiac enzymes

51
Q

What is the common final pathway to platelet aggregation?

A

GPIIbIIIa receptors

52
Q

How does the duration of ACS compare to Stable Angina?

A

ACS lasts much longer (30+ min) as opposed to Stable Angina (2 min max)

53
Q

What is the preferred method of restoring blood flow for NSTEMI?

A

Mechanical revascularization; thrombolytics have never been shown to have an effect

54
Q

How do Thienopyridines exert anti-platelet effects?

A

Clopidogrel and Ticagrelor block the ADP pathway of platelet activation

Act synergistically with Aspirin

55
Q

What factors determine the clinical syndrome caused by acute rupture or erosion of a plaque?

A

Degree of obstruction to blood flow

Duration of obstruction

Amount of residual flow provided by collaterals

56
Q

What are the residual flow outcomes of an ACS?

A

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
Q

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

A

NSTEMI

Cardiovascular (25 decks)

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