NSTEMI and Unstable Angina Flashcards

1
Q

Pathophysiology of NSTE ACS

A

Four processes that lead to thrombus formation
1. Disruption of an unstable coronary plaque due to plaque rupture, erosion, or a calcified protruding nodule that leads to intracoronary thrombus formation and an inflammatory response.
2. Coronary arterial vasoconstriction
3. Gradual intraluminal narrowing
4. Increased myocardial oxygen demand produced by conditions such as fever, tachycardia and thyrotoxicosis in the presence of fixed epicardial coronary obstruction

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2
Q

Clinical presentation of Unstable angina

A

Chest comfort that is severe and has at least one of three features:
1. Occurence at rest (or with minimal exertion)
lasting >10 min
2. Relatively recent onset (w/n the prior 2 weeks)
3. Crescendo pattern, distinctly more severe, prolonged, or frequent than previous episodes

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3
Q

Clinical presentation of NSTEMI

A

Clinical features of unstable angina and evidence of myocardial necrosis , as reflected in abnormally elevated levels of biomarkers

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4
Q

3 major noninvasive tools in the evaluation of NSTEMI-ACS

A
  1. ECG
  2. Cardiac biomarkers
  3. Stress testing
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5
Q

TIMI risk stratification components

A
  1. Age >=65
  2. Three or more of the traditional risk factors for coronary heart disease
  3. Known hx of CAD or coronary stenosis of at least 50%
  4. Daily aspirin use in the prior week
  5. More than one anginal episode in the past 24h
  6. St segment deviation of at least 0.5 mm
  7. Elevated cardiac specific biomarker above the upper limit of normal
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6
Q

Initial treatment for NSTEMI ACS

A
  1. Bed rest
  2. Nitrates
  3. Beta adrenergic blockers
  4. Inhaled O2 in patients with O2sat <90% and/or in those with heart failure and rales
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7
Q

Absolute contraindication to the use of nitrates

A
  1. Hypotension
  2. Recent use of Phosphodiesterase type 5 inhibitor, sildenafil, or vardenafil (within 24h) or tadalafil (within 48h)
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8
Q

When to avoid beta blocker

A

-PR interval (ECG) >0.24s
-2nd or3rd degree AV block
-HR <50 bpm
-SBP <90 mmHg
-Shock
-LV failure
-Severe reactive airway disease

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9
Q

Target HR of beta blockade

A

50-60 bpm

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10
Q

Recommended for patients who have persistent symptoms or ECG signs of ischemia after treatment with full-dose nitrates and beta blocker and in patient with contraindications to either class of agents

A

Heart-rate slowing calcium channel blockers (Verapamil or diltiazem)

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11
Q

When to avoid calcium channel blockers

A

-Pulmonary edema
-Evidence of LV dysfunction (for diltiazem or verapamil)

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12
Q

Contraindications to use of antiplatelets

A

-Severe active bleeding
-Aspirin allergy

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13
Q

High risk patients who will benefit from invasive strategy

A

-Patients with multiple clinical risk factors
-ST segment deviation
-and/or positive biomarkers

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14
Q

Patients that may require immediate invasive treatment (within 2h)

A

-Refractory angina
-Signs and symptoms of HF or new or worsening MR
-Hemodynamic instability
-Recurrent angina or ischemia at rest or with low-level activities despite intensive medical therapy
-Sustained ventricular tachycardia or ventricular fibrillation

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15
Q

Patients that requires early invasive treatment (within 24h)

A

-None of factors requiring immediate tx, but GRACE risk score >140
-Temporal change in troponin
-New or presumably new ST segment depression

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16
Q

Delayed invasive (within 25-72h)

A

-None of the factors requiring immediate tx, but with DM
-Renal insufficiency (egfr <60 ml/min pr 1.72 m2)
-Reduced LV systolic function (EF <0.40)
-Early post infarction angina
-Percutaneous coronary intervention w/n 6 mo prior
-Prior coronary artery bypass graft surgery
-GRACE risk score 109-140 or TIMI risk score >=2

17
Q

Ischemia guided strategy

A

-Low-risk score (TIMI 0-1 or GRACE <109)
-Low risk , troponin negative female patients
-Patient or clinician preference in the absence of high risk features

18
Q

A syndrome of severe ischemic pain that usually occurs at rest and is associated with transient ST -segment eevation

A

Prinzmetal angina

19
Q

Pathophysiology of Prinzmetal variant angina

A

-caused by focal spasm of an epicardial coronary artery with resultant transmural ischemia and abnormalities in LV function

20
Q

Clinical feature of Prinzmetal variant angina

A

Detection of transient ST segment elevation with rest pain

21
Q

Diagnostic hallmark of Prinzmetal angina

A

Transient coronary spasm

22
Q

Main therapeutic agents of Prinzmetal Angina

A

Nitrates and calcium channel blockers