ICS-STEMI Flashcards

(69 cards)

1
Q

Clinical Scenarios for Chronic Stable Angina

A

identified by obtaining a detailed history from the patient (patient is usually pain free at the time)

 a. Stable angina means the pain is predictable 2. Acute onset of chest pain
 a. Rest angina: angina is prolonged (usually > 20 minutes) and occurs at rest
b. New-onset angina: at least CCS Class III severity 
c. Increasing angina: previously diagnosed angina that is more frequent, longer in duration, or lower in threshold (increased CCS Class within 2 months to at least CCS Class III)
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2
Q

ST-segment elevation requiring immediate reperfusion therapy (STEMI)

A

AMI

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3
Q

ischemia is severe enough to cause sufficient myocardial damage and the release of markers of myocardial injury

A

NSTEMI

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4
Q

Pathophysiology of STEMI

A

Vulnerable plaque, plaque rupture, thrombus formation

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5
Q

Triggers for plaque rupture

A

physical exertion, mechanical stress, pulse rate, BP, and vasoconstriction

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6
Q

Initial Recognition of STEMI in the ED

A
  1. ST-segment elevation  0.1 mV in greater than or equal to 2 contiguous leads indicates STEMI and patients should be considered for immediate reperfusion therapy
    - > 90% of patients will have elevated serum cardiac markers
    - ST-segment depression indicates UA or NSTEMI
    - Biochemical markers distinguish between these diagnoses
    - If initial EKG is nondiagnostic, serial EKG at 15-30 minute intervals may be performed
  2. Biomarkers of cardiac injury
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7
Q
  1. Preferred test due to cardiac specificity
  2. Low sensitivity early in MI (< 6 hours)
  3. Remain elevated for 5-14 days
A

Cardiac-specific troponins (TnT and TnI)

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8
Q
  1. Principal serum cardiac marker until recently
  2. Lack of cardiac specificity due to many isoforms
  3. Useful for early detection of MI (within 4 hours)
  4. Peak in 24 hours and may remain elevated for 3-4 days
A

Creatine kinase isoenzymes (CK-MB)

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9
Q
  1. Not cardiac specific but is released more rapidly from infarcted myocardium than CK-MB or troponins
  2. Detected as early as 2 hours but is elevated for less than 24 hours
A

Myoglobin

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10
Q

When are Serial enzyme sets (CK-MB, troponin, myoglobin) ordered

A

at 3 to 6 hour intervals

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11
Q

Other laboratory tests besides cardiac specific biomarkers

A

CBC, INR, aPTT, electrolytes and Mg, BUN, creatinine, glucose, serum lipids

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12
Q

Initial Management of ACS in the ED

A

MONA -

  1. Morphine (Analgesia)
  2. Oxygen for patients with PaO2 < 90%
  3. Nitroglycerin
  4. Aspirin
  5. Beta-blockers
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13
Q

Why give Morphine for ACS

A

Pain contributes to increased sympathomimetic activity
In addition to analgesic and anxiolytic effects, morphine causes venodilation and may further reduce myocardial oxygen demand
- does not decrease mortality

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14
Q

Dose of Morphine for ACS

A

Morphine sulfate 2-4 mg IV repeated at 5 to 15 minute intervals as needed

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15
Q

Adverse effects of Morphine

A

respiratory depression, nausea and vomiting, hypotension

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16
Q

AVOID in ACS patients

A

AVOID NSAIDS and Cox-2 inhibitors (except aspirin

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17
Q

When can oxygen be given for ACS

A

Can be administered for all patients within first 6 hours

- no mortality benefit

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18
Q

Dose of Nitroglycerin for ACS

A

a. SL NTG 0.4 mg q5min X 3 doses then assess the need for IV NTG
b. IV NTG indicated for relief of ongoing ischemia, control of HTN or management of pulmonary congestion
- Titrate until signs of ischemia are relieved or SBP does not tolerate
- no mortality benefit

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19
Q

DO NOT ADMINISTER IV Nitroglycerin IF

A
  1. SBP < 90 mm Hg or more than 30 mm Hg below baseline
  2. Severe bradycardia (< 50 bpm)
  3. Tachycardia (> 100 bpm)
  4. Suspected RV infarction
  5. Use of PDE for erectile dysfunction within the last 24 hours (48 hours for tadalafil)
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20
Q

can be used as an alternative or once patients have been pain free for 12 – 24 hours on IV NTG

A

Oral or topical nitrates

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21
Q

Dose of Aspirin in ACS

A

162 mg to 325 mg chewed if not taken before presentation to the ED
- Decreases mortality in patients with ACS (23% RRR in 35-day mortality)

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22
Q

Contraindications for beta-blockers

A
  1. Signs of heart failure, low output state or risk for cardiogenic shock
  2. Active asthma or reactive airway disease
  3. Heart block
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23
Q

Prompt IV therapy of beta-blockers can be used alternatively if

A

if tachyarrhythmia or hypertension is present

- decreased mortality in patients with ACS by the end of day 1 (prior to the reperfusion era) (IV or PO)

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24
Q

Dose of Metoprolol for ACS

A
  1. 5 mg IV q5min X 3 doses
  2. 50 mg PO q6h X 48 hours
  3. 100 mg PO twice daily thereafter
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25
Dose of atenolol for ACS
1. 5 mg IV q10min X 2 doses 2. 50 mg PO q12h X 2 doses 3. 100 mg PO once daily thereafter
26
In patients with contraindications to beta-blockers, what may be used
diltiazem or verapamil many be used but only if there are no signs of CHF, LV dysfunction or AV block
27
Additional Therapies for STEMI
1. Reperfusion therapy 2. Anticoagulation therapy 3. Additional antiplatelet therapy 4. Inhibitors of renin-angiotensin-aldosterone-system 5. Lipid Management
28
in the first 6 to 12 hours while the affected myocardial zone is undergoing necrosis majority of patients have
Majority of patients have persistent occlusion of the infarct artery
29
Goal of reperfusion therapy
restore blood flow to the infarct zone as soon as possible
30
Recommended for ALL patients with STEMI due to evidence of improved survival (reperfusion therapy)
Fibrinolytic therapy
31
Mechanism of fibrinolytic therapy
initiate thrombolysis by converting plasminogen to plasmin (a fibrinolytic enzyme that dissolves the fibrin clot)
32
Efficacy of fibrinolytic therapy
a. 35-day mortality reduction (18% RR) | b. Survival benefit maintained up to 10 years
33
Door-to-needle time for fibrinolytic therapy
30 minutes | - May also be administered in the pre-hospital setting by EMS
34
Fibrinolytic agents
Streptokinase, Alteplase, Reteplase, Tenectoplase-tPA
35
Contraindications (absolute) of Fibrinolytic therapy
a. Any prior intracerebral hemorrhage b. Active bleeding (excluding menses) c. Significant trauma or ischemic stroke within three months i. Except acute ischemic stroke within 4.5 hr d. Uncontrolled hypertension
36
1. Suitable for 90% of patients | 2. Should be performed within 90 minutes of first medical contact (otherwise fibrinolytic therapy is preferred)
Percutaneous coronary angiography (PCI) | - Preferred reperfusion strategy
37
PCI preferred, especially if
1. Patient is at a high risk of bleeding 2. STEMI diagnosis is questionable 3. Lower mortality rates 4. Opens 90% of occluded arteries
38
Fibrinolytic therapy is preferred if
PCI is unavailable and patient cannot be transferred to an alternate center with PCI performed within 120 minutes of initial medical contact - opens <60% of occluded arteries
39
Goal of anticoagulant therapy
establish and maintain patency of the infarcted artery, prevent DVT/PE, LV mural thrombus and/or cerebral embolism
40
UFH for STEMI
- Used in conjunction with fibrinolysis or PCI Dose: 1. 60 U/kg bolus (max = 4000 units) 2. 12 U/kg/hr (max = 1000 units/hr) - Duration: minimum of 48 hours and preferably for the length of hospitalization or up to 8 days
41
Enoxaparin for STEMI
Evidence for use with fibrinolytic therapy
42
ASSENT-3 Trial for Enoxaparin
a. TNK + UFH 60 units/kg bolus then 12 units/kg/hr was compared to TNK + enoxaparin 30 mg IV bolus then 1 mg/kg SC q12h b. Primary endpoint: composite of 30-day mortality, in-hospital reinfarction, or in-hospital refractory ischemia i. 15.4% UFH vs. 11.4% enoxaparin (p < 0.0001) c. Non-cerebral major bleeding was greater in patients > 75 years of age
43
Extract-TIMI 25 Trial for Enoxaparin
a. Thrombolytic therapy with either: i. UFH 60 units/kg bolus then 12 units/kg/hr ii. Enoxaparin 30 mg IV bolus then 1 mg/kg SC q12h in patients < 75 years of age iii. Enoxaparin 0.75 mg/kg SC q12h in patients > 75 years of age iv. Enoxaparin 1 mg/kg SC q24h in patients with CrCl < 30 ml/min b. Primary endpoint: composite of death or non-fatal recurrent MI in the first 30 days after randomization i. 12% UFH vs. 9.9% enoxaparin (p< 0.001) c. Rates of major bleeding were greater in patients treated with enoxaparin
44
Dosing options for Enoxaparin
a. Patients < 75 years of age: 30 mg IV bolus then 1 mg/kg SC q12h (current guideline recommendation) b. Patients > 75 years of age: 0.75 mg/kg SC q12h (NO BOLUS) c. Patients with CrCl < 30 ml/min: 1 mg/kg SC q24h d. Treat for the length of hospitalization up to 8 days
45
OASIS-6 trial
Fondaparinux | - Not indicated for PCI – it is recommended to use an anticoagulant with anti-IIa activity
46
Dosing of Fondaparinux if fibrinolytic strategy is used
1. 2.5 mg IV, then 2.5 mg SC q24h 2. Continue for length of hospitalization 3. NOT FDA approved for this indication at this time
47
HORIZONS-AMI trial
Bivalirudin - May be used as an alternative anticoagulant in select patients undergoing PCI - Reasonable to use in patients with high bleeding risk
48
ADP Inhibitors
i. May be used as an alternative to aspirin if the patient has a true aspirin allergy ii. Should be used in combination with aspirin in ALL patients who receive PCI with stent implantation
49
Duration of therapy of ADP inhibitors
a. 12 months of dual antiplatelet therapy for bare metal stents implanted b. Continue therapy beyond 12 months if a drug eluting stent (sirolimus or paclitaxel-eluting stent) is used
50
Prasugrel clinical trial
b. TRITON-TIMI 38: i. 13, 608 patients with ACS managed by PCI randomized to prasugrel at doses above or clopidogrel 300 mg loading dose then 75 mg daily ii. Primary efficacy endpoint (composite of death due to CV causes, nonfatal MI or non-fatal stroke) was significantly less with prasugrel (2.2% absolute reduction, 19% relative reduction) iii. Rates of major bleeding were higher with prasugrel and net-harm was observed in 3 subgroups: 1. Patients with history of TIA or stroke 2. Patients > 75 years of age 3. Patients with body weight < 60 kg
51
Dose of Prasugrel
60 mg loading dose then 10 mg once daily
52
Dose of Clopidogrel
600 mg loading dose before or when PCI is performed then 75 mg once daily
53
PPI controversy with Plavix
1. 2C19 inhibitors: inhibit breakdown of clopidogrel to its active form 2. Strong inhibitors: Omeprazole, lansoprazole, rabeprazole 3. ACC does not prohibit use of PPIs with clopidogrel
54
2 clinical trials with Plavix in pts receiving fibrinolytic therapy
a. CLARITY-TIMI 28: 300 mg loading dose followed by 75 mg daily for a maximum of 8 days demonstrated a significant 36% relative reduction in a composite endpoint b. COMMIT: 75 mg daily until hospital discharge or up to 4 weeks demonstrated a significant 9% relative reduction in a composite endpoint
55
Recommendation for Short-term use of clopidogrel in STEMI patients who receive fibrinolytic therapy, aspirin and anticoagulation with heparin or LMWH
75 mg once daily for at least 14 days (300 mg loading dose may be given to patients < 75 years of age) - Any patient needing CABG should have clopidogrel discontinued for at least 5 days prior to the procedure
56
Oral, reversible, direct-acting inhibitor of the ADP receptor that has a more rapid onset and more pronounced platelet inhibition than clopidogrel
Ticagrelor
57
Dose of Ticagrelor
Load 180 mg followed by 90 mg bid
58
Clinical trial for Ticagrelor
d. PLATO trial i. Ticagrelor vs clopidogrel in ACS patients ii. Resulted in reduced rates of death 9.8% ticagrelor vs 11.7% clopidogrel
59
ASA dose with Ticagrelor
81 mg
60
Duration of therapy of ticagrelor
a. 12 months of dual antiplatelet therapy for bare metal stents implanted b. Continue therapy beyond 12 months if a drug eluting stent (sirolimus or paclitaxel-eluting stent) is used
61
Any patient needing CABG should have clopidogrel discontinued when
at least 5 days prior to the procedure
62
MOA of GP IIb/IIIa inhibitors
block GP IIb/IIIa receptor on platelet surfaces and prevent binding of fibrinogen during platelet aggregation for STEMI patients undergoing PCI (abciximab has strongest evidence)
63
GP IIb/IIIa inhibitors
Abciximab (ReoPro) Eptifibatide (Integrelin) Tirofiban (Aggrastat) - Agents: not interchangeable
64
Leads to pts developing HF after MI
a. Left ventricular remodeling: alterations in ventricular mass, chamber size and shape due to myocardial injury i. Myocyte hypertrophy, fibroblast hyperplasia and collagen deposition in non-infarcted myocardium ii. Acute dilatation and thinning on infarcted area resulting in extra workload on residual function myocardium (leading to hypertrophy) iii. RAAS and local production of angiotensin II within the endothelium are important stimuli for the remodeling process
65
Which ARB to use post MI
valsartan according to VALIANT trial
66
clinical trial for aldosterone antagonists
i. EPHESUS Trial 1. Compared eplerenone 25-50 mg daily vs. placebo in 6642 patients within 3-14 days of AMI 2. Patients required documented LVEF  0.4 plus one documented sign of heart failure 3. Results: a. 15% RR in all-cause mortality b. 13% reduction in CV death or hospitalization for CV causes c. Significantly higher rates of hyperkalemia (especially with CrCl < 50 mL/min)
67
e. ACC/AHA recommendation for post-STEMI
i. Initiate oral ACEI therapy within 24 hours of STEMI and continue indefinitely ii. Initiate valsartan in patients intolerant to ACEI who have clinical or radiological signs of heart failure or LVEF  0.4 1. May also be used as alternative in patients tolerant of ACEI iii. Long-term aldosterone blockade for post-STEMI patients who are receiving therapeutic doses of ACEI, have an LVEF  0.4, and have either symptomatic heart failure or diabetes 1. SCr should be < 2.5 mg/dL in men and < 2.0 mg/dL in women 2. Potassium level should be < 5 mEq/mL
68
Secondary Prevention for all pts
``` Smoking cessation HTN (goal is <130/80 per JNC-8) Lipid management Physical activity Weight management Diabetes management Influenza vaccination ```
69
should be initiated or continued in all patients with STEMI and no contraindications
High intensity statin therapy