Coronary Heart Disease Parts I & II Flashcards

1
Q

What is Chronic Stable Angina?

A

Stable plaque causing ischemia due to an imbalance of supply and demand

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2
Q

Which population is especially at risk for Stable Angina?

A

Incidence in age groups 45-65 is far higher in African American women.

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3
Q

What re the Sx of Stable Angina?

A
  1. Substernal or left chest pain/tightness/pressure/burning, lasting less than 3 minutes (sometimes up to 15)
  2. That increases with physical activity, stress and/or a big meal, and
  3. Decreases with rest, Nitro.

Typical Angina has all three

Atypical has 2 of 3

Asymptomatic has 1 of 3

NOTE: rarely will a patient refer to angina as “pain”

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4
Q

PE findings in Stable Angina

A
  • Levine Sign (clenched fist to chest)
  • PMI shifted to left
  • Apical systolic murmur at mitral valve
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5
Q

Risk Factors/Hx re Stable Angina

A

Hyperlipidemia

Diabetes

Smoking

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6
Q

How do you diagnos Stable Angina?

A

Hx + Risk Factors + EKG

Then Exercise Tolerance Test for

  • Every patient with “typical” angina
  • Men >40, women >50 60 with atypical
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7
Q

What are the four classifications of Stable Angina?

A

Class 0: Asymptomatic

■ Class 1: Angina with strenuous exercise

■ Class 2: Angina with moderate exertion

■ Class 3: Angina with mild exertion

■ Class 4: Angina at any level of physical exertion

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8
Q

Stable Angina Rx

A

Acute/Active: a dose of Nitro

(.3,.4, .5 mg sublingual tablet or .4 mg buccal spray)

every 3-5 minutes up to 3 doses.

If no releif after 5 minutes call 911

Chronic: Long term Nitroglycerin (patch),

Calcium Channel Blockers or Beta Blockers

NOTE: Nitro can go through the skin so only the patient should handle it and should be seated. Blood pressure can drop suddenly.

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9
Q

What are predictors of the severity of Angina?

A
  • # diseased vessels
  • severity and location of obstruction (LAD is bad)
  • Left Ventricular funtion
  • Hx of arrhythmia
  • Accelerating Angina (more frequent, more severe)
  • Duke Treadmill Score
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10
Q

Secondary prevention of Stable Angina?

A
  • Risk Modification (lower cholesterol and HTN, stop smoking, take statins, wt loss, exercise/cardiac rehab)
  • Long acting nitrates
  • Beta Blockers
  • Calcium Channel Blockers
  • Ranolazine
  • Aspirin or clopidogrel (post PCI, post MI)
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11
Q

What patient education is needed about Stable Angina?

A
  • Give prognosis and explain
  • Lifestyle modifications
  • Information about all meds
  • Instructions on Nitro usage
  • Importance of secondary prevention
  • CPR for family members
  • Resources: online or hard copy
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12
Q

What is follow up for a patient with Stable Angina?

A

Every 4-6 months 1st year, then annually.

EKG when change in Sx severity/frequency.

ETT every 1-3 years depending on risk category and/or change in Sx.

Inquire about:

  1. Changes in physical activity
  2. Changes in frequency/severity of angina
  3. Adverse effects of Tx
  4. Adherence to meds and lifestyle changes
  5. Knowledge about CAD
  6. Changes in comorbidities
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13
Q

The coronary arteries can compenstate for atherosclerosis until they are ___% occluded

A

75%

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14
Q

What is the sequence of atherosclerosis?

A

○ Fatty streak formation

○ Leukocyte recruitment

○ Macrophages → Foam cells

○ Development of lipid rich core

○ Accumulation of smooth muscle cells

○ Large atheroma with fibrous surface cap

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15
Q

What is the progression of atherosclerosis?

A

Chronic: slowly encroaches on lumen

Acute: suddenly encroaches on lumen due to plaque destabilization and clot formation.

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16
Q

What are the Coronary Artery Risk Factors?

Which are modifiable?

A

Major Risk Factors: Advanced age, Family history of CAD , Male gender, Hypertension Lipid abnormality, Diabetes mellitus, Cigarette smoking

Other Risk Factors: Physical inactivity, Abdominal obesity, Emotional stress, Low intake of fruits and vegetables , Excessive alcohol intake

Modifiable in italics.

17
Q

What is the difference between

Ischemia, Injury and Infarction?

A

Ischemia: Insufficient blood flow, cytokine release (“pain”), tissue can survive

Injury: occurs with sustained ischemia, release of initial cardiac biomarkers,

Infarction: irreversible cell death and necrosis, decrease in cardiac funtion, release of later biomarkers

18
Q

What are the EKG findings for

Ischemia, Injury and Infarction?

A

Ischemia: ST depression +/- T wave inversion

Injury: ST elevation +/- hyperacute T waves,

T wave inversions, new LBBB

Infarction: ST elevation +/- pathologic Q waves

(2.5 deep, 2 wide in 2 contiguous leads)

19
Q

Who automatically gets and EKG?

A

Every patient with a Hx of chest pain

20
Q

What are EKG indictions of current infarction or increased risk of infarction?

A

○ Evidence of ischemia, injury, or infarction

○ LV Hypertrophy → hypertension → increased risk for infarction

○ Atrial fibrillation → previous infarct vs. increased risk of infarction

○ Bundle Branch Blocks → if new LBBB, increased risk of infarction, masked ischemia, injury, and infarct

21
Q

What can an ambulatory EKG/Holter Monitor tell you?

A

Paroxysmal dysrhythmias (SVT, Afib)

Periods of Ischemia (in conjuntion with angina journal, detecting silent ischemia) (NOT ideal for this)

22
Q

What is the Duke Treadmill Score?

A

Assessment based on Bruce Protocol time in minutes, amount of ST depression on EKG, and degree of angina. Used for insurance purposes.

Low Risk > or = +5

High risk: < or = -11

23
Q

What are the cons of a Nuclear Study (Myocardial Perfusion Scan)?

A

Takes 4 hours

Expensive so not all centers have it

Hard to read so inter-reader variability

24
Q

What are the indications and risks of

Coronary Angiography?

A

Definitive Dx of CAD but…

Contraindictions: invasive, contrast media allergy/anaphylaxis, kidney damage

Thus: indicated ONLY if PTCA/stenting or CABG is a consideration

25
Q

Which cardiac biomarkers appear first and how long do they last?

A

Myoglobin rises first and peaks at 5 hours

Creatine Kinase rises second and peaks at about 15 hours

Troponin rises slowly until about 15 hours, then shoots up and peaks at about 25 hours and declines slowly.

Note: these enzymes are not specific to MI, but WITH chest pain, they are!

26
Q

What is Percutaneous Coronary Intervention PCI?

A

Stenting and angioplasty

to reduce Sx (Recently disproven by a double blind study with 200 pts)

NO improvement in lifespan

Metal stents can cause clots or inflammatory response

Drug Alluding Stents have endothelial cells growing on them so they are hidden from the immune system

27
Q

What is Coronary Artery Bypass Grafting CABG?

A

Internal mammary or saphenous vein used to bypass occluded coronary arteries. Only done if multiple vessel disease.

Mortality: 1-8% depending on health of pt

Will add years to life

28
Q

What are complications of PCI?

A

Intimal dissection

Stent thrombosis

MI (esp if not on anticoag)

29
Q

What is accelerating angina?

A

Change in pattern such as

  • Greater ease of provocation
  • Longer episodes
  • Greater severity
  • Longer recovery
  • More frequent use of Nitro

May be unstable angina or acute coronary syndrome such as MI.

30
Q

What do you give in the office if you realize a patient is having a STEMI?

A

MONA:

Morphine, oxygen, Nitro. aspirin

31
Q

What is a coronary vasospasm?

AKA Prinzmetal Angina

AKA Variant Angina

A

Atherosclerotic arteries plus parasympathetic innervation

leads to coronary vasocontriction

(usually parasympathetic leads to nitric oxide to vasodilation)

32
Q

What are the risk factors for Coronary Vasospasm?

A

Smoking

Cocaine

Hyperventilation

Provocative Agents (ACh, Ergotovine, Histamine, Serotonin)

33
Q

What are the Signs/Sx of Coronary Vasospasm? q

A

Typical Anginal Sx BUT

  • Occur at REST, not exertion
  • Perhaps only a small lesion (25%)

May also have CAD so may also have typical angina Sx

34
Q

What is the treatment for acute Coronary Vasospasm?

A
  • Treat as Acute Coronary Syndrome until R/O significant atherosclerosis: Nitro, Aspirin, Statins, +/- Heparin/Integrillin, Beta 1 selective beta blockers
  • Avoid nonselective Beta Blockers re risk of unopposed alpha receptor mediated coronary vasoconstriction
  • Monitor with serial biomarkers (Troponin, CK), telemetry until vasospasm ends.
35
Q

How do you treat chronic Coronary Vasospasm?

A

Eliminate causes (smoking, cocaine)

Vasodilators: Calcium Channel Blockers

+/- Long acting Nitrates

36
Q
A