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CPR II Exam 1 > DSA: Clinical Approach to Stable Angina, Acute Coronary Syndrome, Aortic Dissection (Selby) > Flashcards

DSA: Clinical Approach to Stable Angina, Acute Coronary Syndrome, Aortic Dissection (Selby) Flashcards

1
Q

What is Stable Angina?

A
  • chest/pain pressure for at least 2 months that is worse with exertion or emotional stress
  • has not worsened during that time
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2
Q

What are the 3 classifications of Acute Coronary Syndrome?

A

Unstable Angina

  • new onset angina, angina at rest, inc. in freq/sever.
  • normal cardiac enzymes, possible ST seg. depress

NSTEMI

  • ST segment depression or T-wave inversions
  • ABNORMAL cardiac enzymes

STEMI

  • ST segment ELEVATION; abnormal cardiac enzyme
  • new LBBB or posterior MI
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3
Q

What lipoproteins are seen as risk factors for Coronary Artery Disease (CAD)?

A
  • low HDL < 40 mg/dL and HIGH LDL

- high non-HDL

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4
Q

What are 3 common NON-traditional risk factors for CAD development? (C/P/IS)

A
  • Chronic Kidney Disease
  • Proteinuria
  • Inflammatory States (HIV, Rheumatoid Arteritis, etc)
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5
Q

What is the classical presentation of Acute Coronary Syndrome?

What patient populations do painless AMIs occur in? (3)

A

CP: chest pain, dyspnea, nausea/vomiting, fatigue, diaphoresis (sweating)

  • silent AMIs more common in ELDERLY, FEMALE, and DIABETIC patients
    • be suspicious of atypical presentations
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6
Q

What are the 3 classic components of Angina Pectoris as defined by the Diamond-Forrester Criteria?

What are the 3 classifications of Angina based on this criteria?

A

CC:

  1. substernal chest pain or discomfort
  2. provoked by exertion or emotional stress
  3. relieved by rest and nitroglycerin

Classifications:

  • Typical Angina = has all 3 components
  • Atypical Angina = has 2 of 3 components
  • Non-Angina CP = has 1 or less of these components
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7
Q

How is Stable Angina (CAD) diagnosed? (4)

What are 3 examples of Cardiac Stress tests?

A
  • use pt. presentation, resting ECG (look for ST segment changes, T-waves, LBBB, post. MI), Cardiac Stress Testing, and Invasive Coronary Angiography

Cardiac Stress Tests: Exercise ECG, Exercise/Dobutamine ECHO, and MPI (use vasodilators to stress the heart)

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8
Q

Who should receive a Cardiac Stress Test and what happens when pts. findings are positive?

A
  • use stress tests for pts. with intermediate pretest probability of CAD (10-90% or 25-75%)
  • patients with positive stress tests should proceed to invasive coronary angiography
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9
Q

What is the difference between Exercise and Pharmacological Stress ECGs?

What do Stress ECHOs and Stress MPIs look for?

A

Exercise: performed on treadmill
Pharm:
- vasodilators: dilate coronary arteries (less blood flow)
- dobutamine: inc. oxygen demand (inc. HR/contract.)

ECHO: regional wall motion abnormalities or LV dilation
MPI: perfusion defects during rest and stress
- use IV radioisotope (technetium/thallium)

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10
Q

When can Stress ECG tests NOT be used?

A
  • cannot be used when patients already have baseline ECG abnormalities
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11
Q

How is Coronary Angiography performed?

A
  • catheter is inserted into femoral artery and snaked up to the coronary arteries, where a dye is injected allowing X-Ray imaging to visualize stenosis
  • usually do not treat unless stenosis is > 70% (significant stenosis)
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12
Q

How is Acute Coronary Syndrome (CAD) diagnosed? (3)

What are the criteria for diagnosing STEMI vs NSTEMI looking at an ECG?

A
  • resting ECG, cardiac biomarkers, invasive coronary angiography

STEMI: ST segment elev. >2 mm in continuous leads or new LBBB (cannot diagnose if known LBBB already)

NSTEMI: new ST depression >0.5 mm in two contiguous leads or T-wave inversion > 1mm in two contiguous leads with R/S ration >1

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13
Q

What causes a STEMI and NSTEMI to develop?

What is the difference between Type 1 and Type 2 variants?

A

STEMI: from COMPLETE occlusion of blood flow
NSTEMI: from partial occlusion of blood flow or in presence of complete occlusion w/collateral circulation

Type 1: infact. due to coronary atherothrombosis
Type 2: infact. due to supply-demand mismatch not the result of atherothrombosis

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14
Q

How is Stable Angina Treated? (LM/A/S/AAD)

What drugs are used for Chronic (4) vs Acute angina?

A
  • lifestyle modifications, aspirin, statin, anti-anginal drugs

Chronic: B-blockers (1st line), CCBs, nitrates (long-acting), and ranolazine

  • CCB/nitrates can be used with B-blockers
  • Ranolazine for refractory angina

Acute: nitrates (short-acting)

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15
Q

What are 3 indications for the use of Coronary Artery Bypass Grafting (CABG)?

What treatment should be considered if CABG or PCI is contraindicated?

A
  1. 3 vessels with stenosis > 70%
  2. left main disease
  3. left ventricular dysfunction
  • either CABG or PCI w/stenting used if coronary anatomy is suitable; if not suitable –> use externally enhanced counterpulsation (put on LE and inflated during diastole) = EECP therapy
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16
Q

Treatment of Acute Coronary Syndrome

What is the “MONA” mnemonic and what drugs are typically given to these patients? (A/P/H/E)

What are 3 drugs shown to improve mortality in Myocardial Infarction? (A/B/A)

A

MONA = initial management of all ACS patients
- morphine, oxygen, nitrates, aspirin

Drugs: Dual Antiplatelet Therapy (aspirin and P2Y12 inhibitors) and Anticoags (unfractionated heparin and SubQ enoxaparin)

  • aspirin, B-blockers, ACE inhibitors
17
Q

How are STEMI patients managed in a PCI capable hospital vs a non-PCI capable hospital?

A
  • always initiate therapy w/aspirin, B-blockers, nitrates, heparin

Capable: administer P2Y12 and perform PCI in < 90 mins; long-term medical therapy after

Non-Capable:

  • transfer to PCI (if possible) within < 120 minutes
  • no transfer? –> start thrombolytics < 30 minutes, then transfer to PCI capable hospital
18
Q

How are Unstable Angina and NSTEMI patients managed? (A/B/N/S)

A
  • initiate aspirin, B-blockers, nitrates, statin
  • use TIMI (predicts risk of 14 day death, recurrent MI, or urgent revascularization)
High Risk (TIMI 5-7): early invasive strat (< 24 hrs)
Mid Risk (TIMI 3-4): delayed invasive (25-72 hrs)
Low Risk (TIMI 0-2): ischemia-guided therapy
19
Q

What ECG leads and coronary arteries are associated with Myocardial Infarcts at the:

  1. Inferior Wall
  2. Septal Wall
  3. Anterior Wall
  4. Lateral Wall
  5. Posterior Wall
A
  1. leads II, III, aVF (Right Coronary Artery)
  2. leads V1-V2 (Left Anterior Descending Artery)
  3. leads V2-V4 (Left Anterior Descending Artery)
  4. leads V5/V6 or I/aVL (Left Circumflex Artery)
  5. tall R waves and ST depression in V1-V3
    • 70% originate from the RCA
20
Q

What is Dressler’s Syndrome?

A
  • postmyocardial infarction syndrome that manifests as PERICARDITIS
  • immunologically based syndrome typically occurring within weeks to months after an MI
21
Q

How are Thoracic Aortic Dissections classified? (2)

A

Stanford: Type A and Type B (FOCUS ON THIS ONE)

  • A = involve ascending aorta (67%)
  • B = arise AFTER the Left Subclavian Artery (33%)

DuBakey: Types 1, 2, and 3

  • 1: involves ascending and descending aorta
  • 2: involves ascending aorta only
  • 3: involves descending aorta only
22
Q

What are 4 risk factors for Aortic Dissection in younger patients? (C/S/C/T)

A
  1. Connective Tissue Disorders (MARFAN)
  2. Syphilis
  3. Cocaine or meth use
  4. Trauma (fall or car accident)
  • also large arteritis and bicuspid aortic valve (genetic)
23
Q

What is the classic presentation of a patient suffering from Aortic Dissection?

How does Aortic Dissection affect the pts. Renal, Neuro, and GI systems?

A

CP: sudden onset chest pain (“tearing” or “ripping” that radiates to the back) and hypertension
- pulse deficits between limbs (asymm. btwn arms)

Renal: acute renal failure
Neuro: Horner’s Syndrome (droopy eyelid, no sweat)
GI: bleeding from aortoenteric fistula; ischemia

24
Q

What are 4 ways that Aortic Dissection can be diagnosed?

A
  1. ECG/cardiac biomarkers (rule out MI)
  2. Chest X-Ray (wide mediastinum)
  3. CT ANGIOGRAPHY (most common method)
  4. Transesophageal ECHO (hemodynamically unstable)
    • can see false lumen and true lumen
25
Q

What is the medical management of Aortic Dissection? (AIT)

What 3 drugs are commonly used? (B/V/O)

A
  • Acute Impulse Therapy to lower HR and diminish force of LV ejection
  • *Goal is BP < 120 mmHg and HR < 60 BPM**
    • first line therapy: B-blockers (labetalol/esmolol)
    • can add vasodilators (nicardipine/nitroprusside)
    • Opiates for PAIN
26
Q

How should Type A and Type B Aortic Dissections be managed?

A

Type A: have a HIGHER mortality
- open surgery with synthetic graft

Type B: either medical or endovascular treatment

  • Uncomplicated = medical treatment
  • Complicated = endovascular (STENTING)

CPR II Exam 1 (15 decks)

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