Acute Coronary Syndromes Flashcards

1
Q

What is ACS?

A

acute myocardial ischemia resulting from an imbalance between myocardial oxygen demand and supply

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2
Q

Spectrum of conditions

A

silent ischemia
SIHD
UA
NSTEMI
STEMI

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3
Q

Development of ischemia

A

rupture of atherosclerotic plaque –> platelet adherence, activation, aggregation and activation of the clotting cascade –> fibrin and platelets form clot –> ischemia

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4
Q

Classification

A

type 1: spontaneous MI - atherosclerotic plaque rupture
type 2: MI secondary to ischemic imbalance - Oxygen supply or demand mismatch to heart (examples: vasospasm, anemia, hypotension)

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5
Q

Epidemiology

A

Median age at ACS presentation is 68 years
Males are more likely to have ACS: Ratio of males:females is approximately 3:2
For some patients, ACS is the initial presentation of CAD
In the United States, >780000 persons per year will experience an ACS: Approximately 70% of these will have NSTEMI

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6
Q

Risk factors

A

obesity, smoking, genetics, older age, male, positive FH of CAD, presence of peripheral arterial disease, diabetes, prior MI, renal insufficiency, sedentary lifestyle

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7
Q

Precipitating factors

A

exertion, emotional stress, cold air/extremes in temperature, recent exercise, diet - large meal, emotions - fright/anger, coitus, smoking, walking against the wind

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8
Q

Signs and symptoms

A

Retrosternal chest pain: May radiate to shoulder, down the left arm, to the back or to the jaw; Most often at rest
Nausea or vomiting Diaphoresis
Shortness of breath

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9
Q

Atypical symptoms

A

more likely in:
* Elderly
* Females
* Diabetics
* Impared renal function
* Dementia
Symptoms:
* Epigastric pain
* Indigestion
* Stabbing or pleuritic pain
* Increasing dyspnea in the absence of chest pain

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10
Q

Patients with chest pain and high- risk features such as…

A

continuing chest pain
severe dyspnea
syncope/presyncope palpitations
Should transported by emergency medical services when available

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11
Q

Delay in care

A

Patients with STEMI do not seek medical care for approximately 1.5 to 2 hours after symptom onset: Patient delay times are often longer in women, blacks, the elderly, and Medicaid patients Reasons for delay
1. Inappropriate reasoning that symptoms will be self-limited or are not serious
2. Attribute symptoms to other preexisting conditions
3. Fear of embarrassment should symptoms turn out to be a “false alarm”
4. Reluctance to trouble others unless “really sick”
5. Preconceived stereotypes of who is at risk for a heart attack, especially women
6. Lack of knowledge of the importance of rapid action, the benefits of calling EMS or 9-1-1, and the availability of reperfusion therapies
7. Attempted self-treatment with prescription and/or nonprescription medications
Healthcare providers should educate patients to recognize and respond to an acute event!

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12
Q

Diagnosing ACS

A

All patients with acute chest pain should have an ECG within 10 minutes of arrival at an emergency facility
All patients presenting to the ED with acute chest pain and suspected ACS should have troponin measured as soon as possible after presentation

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13
Q

ECG STEMI

A

STEMI: Persistent electrocardiographic
(ECG) ST elevation
Q wave changes: Often not present on initial ECG, but develops over hours to days; Electrical ‘hole’- scar tissue cannot conduct electricity; May disappear after early reperfusion if stunned tissue can recover; Often remain permanently

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14
Q

ECG NSTEMI and UA

A

NSTEMI and UA:
May have normal ECG; ST depression, transient ST-elevation, or new T-wave inversion are possible; Q wave changes unlikely; No ST elevation

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15
Q

Myocardial injury biomarkers

A

Released from necrotic myocytes (injured heart cells) into bloodstream
Troponin is the gold standard: High sensitivity troponin- PREFERRED - Measured in ng/L; Greater sensitivity and negative predictive values; Shorter time from onset of chest pain to a detectable concentration
Conventional troponin: Measured in ng/mL

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16
Q

What is the difference between sensitivity and specificity?

A

sensitivity: likelihood of detecting a disease when it exists (true positive rate)
specificity: likelihood of not detecting a disease when it does not exist (true negative rate)

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17
Q

Myocardial injury biomarkers: troponin

A

Troponin: Highly sensitive results specific for detecting
myocardial injury
Normal value is undetectable: High sensitivity troponin < 14ng/L; Conventional troponin < 0.05ng/mL
Need to check trend: 3 levels over 12 hours; Initial may be negative
troponin may be elevated by other conditions

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18
Q

Myocardial injury biomarkers: CK MB

A

Creatinine kinase myocardial band (CK MB): No longer used (no benefit); Less sensitive than troponin, and substantially more tissue injury is required for its detection

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19
Q

Stable angina vs unstable angina

A

Stable angina: Chest pain occurs during physical
exertion - Predictable; Relieved by rest; Lasts a short time (<5 minutes)
Unstable angina: Chest pain may occur at rest, while sleeping, or with little physical exertion; Comes as a surprise; Is more severe and lasts longer than stable angina (may be >30 minutes)

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20
Q

Unstable angina vs NSTEMI

A

Closely related conditions
Depends on the degree of
ischemia:
UA - Less ischemia; Does not lead to detectable
quantities of troponin
NSTEMI - Troponin is elevated

21
Q

NSTEMI vs STEMI

A

NSTEMI: Chest pain; Troponin is elevated; No ST elevation on ECG (may have ST depression or T wave inversion)
STEMI: Chest pain; Troponin is elevated; Persistent ST elevation on ECG

22
Q

Thrombolysis in myocardial infarction (TIMI) risk score

A

Risk of experiencing either death, myocardial infarction or urgent need for revascularization within 14 days
low risk: 0-2 points
medium risk: 3-4 points
high risk: 5-7 points

23
Q

Complications of ACS

A

heart failure, valvular dysfunction, arrhythmias, bradycardia/heart block, pericarditis, stroke secondary to LV thrombus, cardiogenic shock, death

24
Q

Ventricular remodeling

A

Changes in the size, shape and function of the left ventricle after an ACS: Many factors involved - Activation of the renin-angiotensin-aldosterone system; Hemodynamic factors (increased preload and afterload)
Leads to heart failure - increased morbidity and mortality
Preventing ventricular remodeling is an important therapeutic goal

25
Q

Major adverse cardiac events (MACE)

A

Often used as a composite endpoint in cardiology trials
Definition can vary, but usually includes: Stroke; MI; Cardiovascular death

26
Q

Short term goals of therapy

A

restore blood flow, provide relief of ischemia (chest pain), prevent morbidity, prevent re-occlusion of artery, prevent mortality

27
Q

Initial recommendations

A

12-Lead ECG:
Within 10 mins of arrival at an emergency facility
If the initial ECG is NOT diagnostic but the patient remains symptomatic and there is a high clinical suspicion for ACS, serial ECGs should be performed - Every 15-30 mins for the first hour

Serial Troponin Levels:
Troponin = heart damage
Levels should be obtained at presentation and 3-6 hours after symptom onset
High sensitivity troponin is preferred Repeating troponin levels will identify a rising and/or falling pattern

28
Q

UA/NSTEMI treatment

A

MONA
Reperfusion: Early invasive strategy vs. ischemia- guided strategy; No fibrinolytic
Antiplatelets: APT = ASA + P2Y12 inhibitor - 12-month duration; Ticagrelor or prasugrel preferred; +/- GPIIb/IIIa inhibitor (unlikely to use)
Anticoagulation : LMWH or UFH
BB
ACE-I or ARB
Statin
Nitroglycerin PRN

29
Q

STEMI treatment

A

MONA
Reperfusion: PCI vs fibrinolytic Antiplatelets: DAPT = ASA + P2Y12 inhibitor -
12-month duration; Fibrinolytic: clopidogrel preferred; PCI: ticagrelor or prasugrel preferred
+/- GPIIb/IIIa inhibitor Anticoagulation: UFH or bivalirudin
BB
ACE-I or ARB
Statin
Nitroglycerin PRN

30
Q

MONA

A

early hospital care immediately upon arrival
M = morphine
O = oxygen
N = nitroglycerin
A = aspirin

31
Q

Morphine

A

To relieve chest pain
Initial dose: 4-8 mg IV, followed by 2-8
mg IV q5-15mins
Side effects: Sedation; Respiratory depression; Nausea/vomiting
AVOID NSAIDs during hospitalization (except aspirin)
Discontinue home NSAIDS and do not initiate new therapy NSAIDs lead to sodium and water retention = increased risk of MACE

32
Q

Oxygen

A

maintain oxygen saturation >90%

33
Q

Nitroglycerin

A

Vasodilator = increases blood flow to the heart
Sublingual NTG: 0.3-0.4 mg q5min × 3 for ischemic pain
IV NTG: for persistent ischemia, HF, or HTN: Start at 10 mcg/min; Titrate by 5 mcg/min q5min (MAX: 200 mcg/min)
Side effects: Headache; Hypotension

34
Q

Nitrogylcerin transdermal

A

Transdermal NTG is NOT recommended in the setting of ACS
The onset of action is not rapid enough (~15-60 min)

35
Q

Nitroglycerin tolerance

A

Tolerance to nitrates develops after > 24 hours of continuous use: Increase the dose or change to intermittent administration (aim for > 10 hours of a NTG-free period/day)
Tachyphylaxis = when a drug loses part of or its entire efficacy over time as the body develops tolerance to it

36
Q

Nitrates contraindications

A

Nitrates are contraindicated with recent use of a phosphodiesterase inhibitor!
sildenafil, vardenafil, tadalafil

37
Q

Aspirin

A

162-325 mg chewable aspirin x 1 dose
Given to ALL patients without contraindications ASAP
enteric coated aspirin can be used if it is chewed

38
Q

Reperfusion strategies

A

percutaneous coronary intervention (PCI)
coronary artery bypass graft (CABG)
fibrinolytic

39
Q

Coronary angiography

A

Shows which arteries in the heart have blockages!
1. A catheter is inserted into the radial and femoral artery and fed up to the heart.
2. Dye is injected into the coronary arteries.
3. An x-ray picture is taken and shows the
blocked arteries.
4. A stent is placed in blocked arteries, if needed.

40
Q

Percutaneous coronary intervention

A

This procedure uses a small balloon to reopen a blocked artery to increase blood flow. A stent is placed, if needed, to keep the artery open long-term.

41
Q

Coronary artery bypass graft

A

Open-heart surgery!
A vein or artery from another part of the body is removed and attached to the heart to “bypass” the blocked artery/arteries.

42
Q

Fibrinolytics

A

clot busters
fibrinolytic - conversion of plasminogen to plasmin, plasmin can degrade fibrin clots

43
Q

Fibrinolytics drugs

A

tenecteplase
reteplase
alteplase
streptokinase (not used)

44
Q

Reperfusion therapy: STEMI

A

PCI or fibrinolytic
Reperfusion therapy should be administered to ALL eligible STEMI patients whose symptoms began in the past 12 hours!
PCI (preferred)&raquo_space;> fibrinolytic
Higher rates of infarct artery patency; Lower rates of recurrent ischemia, reinfarction, and emergency repeat revascularization procedures; Lower rates of intracranial hemorrhage; Lower rates of death

45
Q

Door-to-needle time

A

within 30 min of hospital arrival

46
Q

Door-to-balloon time

A

within 90 min of hospital arrival

47
Q

Fibrinolytic therapy is recommended for STEMI patients at

A

non-PCI-capable hospitals

When ≥ 120 mins away from a PCI-capable hospital
Ensure patient does not have any contraindications to fibrinolytics
Should be administered within 30 mins of hospital arrival
Better outcomes when given promptly!: A meta-analysis demonstrated that a 60-minute reduction in time from symptom onset to delivery of a fibrinolytic resulted in a 17% reduction in mortality during hospitalization*; The 60-minute reduction was due to pre-hospital administration of fibrinolytics

48
Q

Reperfusion therapy: NSTEMI/UA

A

early invasive vs ischemia-guided
Fibrinolytics are NOT recommended!
Early Invasive = Coronary Angiography +/- Revascularization: Preferred for patients with high-risk features: Refractory angina New-onset heart failure; Rising troponin; New ST-segment depression
Ischemia-Guided = “Medical” Management: Treatment with evidence-based medications
No heart catheterization - Unless the patient has refractory or recurrent ischemic symptoms or becomes hemodynamically unstable