Acute Coronary Syndromes Flashcards

1
Q

Greatest specific cause of CVD mortality

A

CAD

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2
Q

Stable ischemic heart disease definition

A

Exertional chest pain (or equivalent) that is chronic
May be asymptomatic
Typically seen in the outpatient clinic setting

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3
Q

Pathophysiology of stable ischemic heart disease

A

Obstructive (collaterals) or non-obstructive coronary artery plaque
Intact fibrous cap
Minimal platelet activation, inflammation
Other conditions: aortic stenosis, HOCM

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4
Q

Angina pectoris

A

Pain or discomfort in the chest caused by
insufficient blood supply to the heart muscle
Typically brought on by exertion or emotional stress
Typically lasts 1-15minutes
Relieved by rest and nitroglycerin

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5
Q

Populations more likely to have non-classical presentation of angina pectoris

A

women, elderly, people with diabetes

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6
Q

Diagnostic value of exercise stress ECG depends on the __________________ of having coronary artery disease

A

pre test probability

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7
Q

Stress nuclear scintigraphy

A

Nuclear imaging method, areas of blood flow are “hot”, areas of infarct or ischemic tissue will remain “cold”. Pre- and post-stress results may indicate areas that will benefit from myocardial revascularization

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8
Q

Fractional flow reserve

A

Measure pressure upstream and downstream of blockage- can gauge functional (rather than anatomic) severity of a plaque

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9
Q

Treatments that relieve symptoms of stable ischemic heart disease

A

Nitrates, calcium channel blockers, beta blockers, re-vascualrization (stent/ angioplasty or CABG)

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10
Q

Treatments that prevent adverse outcomes (MI, stroke, death) of stable ischemic heart disease

A
Lifestyle measures
Aspirin
Statins
ACE-Is
P2Y12 receptor blockers
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11
Q

In stable ischemic heart disease, CABG is superior to medical therapy for two specific types of disease:

A
  • L main disease

- severe three vessel disease with reduced LV function

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12
Q

Unstable ischemic heart disease is also called…

A

acute coronary syndrome

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13
Q

Unstable ischemic heart disease definition

A

New or rapidly progressive symptoms

Typically seen in the emergency room setting

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14
Q

Unstable ischemic heart disease pathophysiology

A

obstructive coronary artery plaque; plaque rupture or erosion; platelet activation, inflammation, thrombus

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15
Q

Why do plaques rupture?

A
  • mechanical factors- shear stress
  • inflammation
  • exogenous factors ex smoking
  • endogenous factors ex catecholamines
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16
Q

Why do coronary arteries thrombose?

A
  • activation of intrinsic clotting (tissue factor)
  • platelet activation
  • endothelial dysfunction
17
Q

Platelet activation triggers

A
catecholamines
cigarette smoking
collagen
tissue factor
vWF
18
Q

Platelet activation feed back

A

ADP
Serotonin
TXA2

19
Q

Acute coronary syndrome includes:

A
  • unstable angina
  • NSTMEI
  • STEMI
20
Q

Characteristics of unstable angina

A
  • mild or no changes to ECG

- no biochemical evidence of myonecrosis

21
Q

Characteristics of NSTEMI

A
  • T inversion on ECG

- some biochemical evidence of myonecrosis

22
Q

Characteristics of STEMI

A
  • ST elevation on ECG

- much biochemical evidence of myonecrosis

23
Q

Steps in emergency assessment of acute coronary syndrome

A

Characterize discomfort onset, character, severity
Identify risk factors
Physical Examination – signs of instability
Cardiac Biomarkers (Troponin, CK-MB)
ECG (ST depression or ST elevation)
Rule out other causes of chest pain

24
Q

TIMI risk score

A

Used to risk stratify patients presenting with unstable angina/ NSTEMI

  • score of 0-2= lower risk, do stress test ECG to gain further info
  • score of 3-7= higher risk, do invasive revascularization (cath)
25
Q

Treatments that relieve symptoms of unstable angina/ NSTEMI

A

nitroglycerine, morphine

26
Q

Treatment that prevents adverse events in unstable angina/ NSTEMI

A
Anti-platelet therapy
Anti-thrombin therapy
Statins
Beta-blockers 
ACE-Inhibitors
Revascularization
Lifestyle measures
27
Q

Antiplatelet therapy agents

A

aspirin (irreversibly blocks COX1, decreased production of TXA2, less platelet activation)
P2Y12 receptor blockers (irreversibly inhibit receptor on platelet membrane to prevent formation of GpIIbIIIa complex)
GpIIbIIIa inhibitors (directly prevent fibrionogen cross linking)

28
Q

Anti- thrombin agents

A

Heparin, direct thrombin inhibitors, Factor Xa inhibitors

29
Q

Should fibrinolytic therapy be used for unstable angina or NSTEMI?

A

NO- no benefit since vessel is not fully occluded, only harm from bleeding risk

30
Q

In what cases should stents/ CABG be used for unstable angina or NSTEMI?

A
  • High risk features (L main or 3 vessel disease with reduced LV function)
31
Q

Management of STEMI

A
PROMPT Reperfusion 
Aspirin
P2Y12 Receptor blocker 
Cardiac Care Unit Care
Statin
Beta-blocker
ACE-Inhibitor
Cardiac Rehab
32
Q

List some problems with thrombolytic therapy

A

Failure to open infarct artery ~40%
Intracranial hemorrhage 1-2%
Contraindications up to 40%
Lytic outcomes consistently inferior to timely PCI

33
Q

If fibrinolytic therapy is to be used in a patient with STEMI, what is the time frame for administration?

A

30 minutes, with rescue PCI if fibrinolytic doesn’t work

34
Q

What is the ideal/ goal time frame for reperfusion by stent/ angioplasty in STEMI?

A

90 minutes

35
Q

List some complications following MI

A

Ventricular arrhythmias- poor prognosis if more than 48 hours after MI
Post-MI pericarditis
Cardiogenic shock- prognosis is very poor
Congestive heart failure

36
Q

What region of the heart is most vulnerable to infarct expansion?

A

antero-apical region- thinnest area of myocardium, greatest curvature, greatest deforming forces, site of thrombus due to stasis, site of rupture