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BCACP > Acute Coronary Syndrome > Flashcards

Acute Coronary Syndrome Flashcards

1
Q

angina

A

chest discomfort not necessarily in the chest, relieved with rest or nitroglycerin

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2
Q

relief with nitroglycerin

A

does not always mean cardiac in origin

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3
Q

unstable angina

A

angina that increases with frequency and intensity, lasting longer than 20 min, not necessarily a heart attack

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4
Q

acute myocardial infarction

A

presence of positive cardiac enzymes suggestion myocyte death AND presentation of ischemic-type chest pain or changes in EKG

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5
Q

How many types of myocardial infarction (MI) are there?

A

5 (type 4 has two sub types)

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6
Q

Type 1 MI

A

spontaneous MI due to plaque erosion, rupture, or dissection

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7
Q

Type 2 MI

A

secondary to ischemia from increased oxygen demand or decreased supply

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8
Q

Type 3 MI

A

sudden, unexpected cardiac death (or cardiac arrest) with symptoms suggestive of MI, accompanied by STEMI, new LBBB, or evidence of a fresh thrombus in coronary artery by angiography or autopsy –> vtach, ACLS

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9
Q

Type 4 MI

A

associated with coronary angioplasty or stents
- 4a: MI associated with PCI
- 4b: MI associated with stent thrombus evident by angiography or autopsy

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10
Q

Type 5 MI

A

associated with CABG

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11
Q

Can you have a MI without EKG changes?

A

Yes, 5-10% of pts having an active MI can have a normal EKG

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12
Q

EKG findings in MI

A
  • T wave inversions or tall/symmetric “peaked” T-waves
  • presence of Q-waves
  • ST segment depression
  • ST segment elevations
  • new LBBB
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13
Q

atypical MI

A

active MI without chest pain; 1/3 - 1/2 of pts present this way; mainly in elderly, diabetics with neuropathy, females

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14
Q

risk factors for atypical MI

A
  • women
  • non-Caucasian
  • diabetes
  • uncontrolled or long-standing HTN
  • hyperlipidemia
  • smokers
  • family h/o CAD
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15
Q

Physical exam consistent with decreased cardiac output

A
  • anxious
  • diaphoretic
  • presence of rales
  • hypotension
  • presence of an S3
  • new or worsening mitral regurgitation
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16
Q

What are the cardiac markers?

A
  • myoglobin
  • CK-MB
  • troponin
17
Q

Initial rise of cardiac markers

A
  • myoglobin: 1-2 hrs
  • CK-MB: 3-4 hrs
  • troponin: 3-6 hrs
18
Q

Peak levels of cardiac markers

A
  • myoglobin: 4-6 hrs
  • CK-MB: 12-24 hrs
  • troponin: 12-24 hrs
19
Q

Duration of cardiac markers

A
  • myoglobin: 24 hrs
  • CK-MB: 2 days
  • troponin: 7 days
20
Q

How is troponin cleared in the body?

A

renally

20
Q

When to give oxygen? (MONA)

A

if O2 saturation is < 94%, start O2 at 4L per nasal canula and titrate as needed

20
Q

What effect does nitroglycerin have on preload and afterload?

A

decreases which decreases workload

20
Q

When is reducing the preload bad?

A

in patients that have R sided MI since they are preload dependent

20
Q

Which of the P2Y12 inhibitors is reversible?

A

ticagrelor

20
Q

In which patients is nitroglycerin recommended?

A

pts w/ persistent ischemia, heart failure, HTN, or anterior MI

21
Q

Contraindications to using nitroglycerin

A
  • Hypotension (<90 SBP or >30 decrease from baseline)
  • Brady or tachy - cardia
  • Recent use of PDE5 inhibitor (can cause profound hypotension and shock)
22
Q

If medium or high risk and invasive surgery is indicated, what antiplatelet therapy to give upon presentation?

A

DAPT

23
Q

With initial conservative strategy and diagnostic angiography not indicated, what antiplatelet therapy to give?

A
  • aspirin
  • anticoagulant + clopidogrel or ticagrelor
  • low risk: continue ASA forever, cont clopidogrel or ticagrelor up to 12 months
24
Q

With initial conservative strategy and presence of recurring symptoms, what antiplatelet therapy to give?

A
  • ASA
  • anticoag
  • Glycoprotein IIb/IIIa Inhibitors (tirofiban or eptifibatide) OR P2Y12 inhibitors (clopidogrel or ticagrelor)
  • diagnostic angiography
  • PCI: cont ASA, loading dose of P2Y12, stop anticoag
  • CABG: cont ASA, stop gp IIb/IIIa 4 hr b4 CABG, cont UFH or stop enoxaparin 12-24 hr or fonda 24 hr B4 CABG and start UFH,
25
Q

Pros and cons to using beta blockers in ACS

A
  • Pros: mortality benefit, decrease rate of reinfarction and ventricular fibrillation
  • Cons: increased risk of cardiogenic shock
26
Q

Risk factors for increased risk of shock of using beta blockers in ACS

A
  • Age > 70 y/o
  • SBP < 120
  • Bradycardia or sinus tachycardia
  • Increased time since onset of symptoms
27
Q

When is heparin indicated in ACS?

A
  • High-risk unstable angina (troponin positive)
  • NSTEMI
  • PCI
  • No evidence or concern for aortic dissection (can open up and bleed)
28
Q

Reperfusion time goal

A
  • Door to balloon (PCI): 90 min
  • Door to needle (fibrinolysis): 30 min
29
Q

Thrombolytic mechanism of action

A

converts plasminogen to the proteolytic enzyme plasmin, which lyses fibrin as well as fibrinogen

30
Q

What type of MI are thrombolytics indicated?

A

STEMI

31
Q

Thrombolytic fail rate

A

20% of infarcted arteries –> PCI

32
Q

Half-life of thrombolytics

A
  • Alteplase: 3-6 min
  • Reteplase: 13-16 min
  • Tenecteplase: 22 min
33
Q

Absolute contraindications to thrombolytics

A
  • Prior intracranial bleeding
  • Known structural cerebral vascular lesion
  • Malignant intracranial neoplasm
  • Ischemic stroke previous 3 mos
  • Aortic dissection
  • Active bleeding or bleeding disorder
  • Significant head trauma in last 3 months
34
Q

Relative contraindications to thrombolytics

A
  • Severe or poorly controlled HTN (SBP > 180 or DBP > 110)
  • Ischemia stroke > 3 months ago or dementia
  • Traumatic or prolonged CPR (> 10 min)
  • Major surgery in last 3 wks
  • Recent internal bleed in last 2-4 wks
  • Active peptic ulcer
  • Chronic anticoag w/ high INR

BCACP (12 decks)

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