Coronary Artery Disease Flashcards

1
Q

What is coronary artery disease?

A

Disease of coronary arteries that supply the heart.

Can be asymptomatic or develop into stable angina

Unstable angina + MI = more serious manifestations of CAD (acute coronary syndrome)

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2
Q

What is the major cause of CAD?

A

ATHEROSCLEROSIS

  • deposition of lipids within the intima of the artery
  • C-reactive protein (CRP) is released by the liver and is increased during system inflammation AND unstable plaques and oxidation of LDLs
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3
Q

Steps of atherosclerosis

A

1) Damaged endothelium
- d/t hypertension, smoking, hyperlipidemia, hyperhomocysteinemia, diabetes, infection, toxins

2) Fatty streak
- lipids accumulate and migrate into SMCs

3) Fibrous plaque
- collagen covers the fatty streak
- vessel lumen is narrowed, reducing blood flow
- fissures can develop

4) Complicated lesion
- plaque rupture
- thrombus formation
- further narrowing or total occlusion of vessel

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4
Q

Stable Angina vs unstable angina

A

STABLE

  • occlusion that is reversible w/ rest + use of nitroglycerin
  • onset, pattern, and duration is predictable and same each time

UNSTABLE

  • unstable plaque and lesion that intermittently occludes and opens
  • may lead to a complete MI
  • irreversible cell death and necrosis
  • different type and quality of pain than that of stable angina
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5
Q

What is collateral circulation?

A

Arterial anastomoses or connections

  • the body’s way of compensating when an artery becomes occluded due to atherosclerosis or CAD
  • grwoth of connections increases in the presence of chronic ischemia
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6
Q

Is there collateral circulation in rapid onsets of CAD?

A

NO
When CAD has a rapid onset, or coronary spasm occurs, there may not be enough time for collateral circulation development
Diminished arterial blood flow ==> more severe ischemia ==> infarction

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7
Q

2 types of angina

A

Angina is the clinical manifestation of reversible ischemia

CHRONIC STABLE

  • chest pain that occurs intermittently over a period w/ the same pattern of onset, duration, and intensity of symptoms
  • constrictive, squeezing, heavy, choking, suffocating sensations
  • pain is brief (3-5 mins) and goes away w/ rest
  • precipitated by physical demand

PRINZMETAL ANGINA

  • chest pain that occurs at rest randomly
  • spasms of a major coronary artery
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8
Q

What should you do when a pt complains about chest pain?

A

1) take vitals
2) administer O2
3) 12 lead ECG

4) Administer nitrates and baby aspirin
- nitroglycerin spay

5) listen to heart sounds
S3 - transient - related to hyperdynamic state
- lots of fluid - makes a swishing sound against ventricle walls
- usually the first symptom of congestive heart failure

S4 - pathological sound

  • usually there all the time
  • resistance to ventricular filling bc they are stiff and noncompliant
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9
Q

Goals

A

Goals
- Pain relief
- Preservation of myocardium
- Immediate and appropriate treatment
- Effective coping w/ illness-associated anxiety
- Participation in a rehabilitation plan
- Reduction of risk factors
- Health promotion
○ Therapeutic lifestyle changes to reduce cardiac risk factors

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10
Q

How to diagnose CAD

A
ECG
BLOOD WORK 
- cardiac markers (myoglobin, CK-MB, Troponin I)
- CK-MB and troponin I are specific to cardiac muscle cells; are released when cells are dying 
- lipid profile to assess risk factors
- CBC
- chemistry
-pt/INR
CXR
2D ECHO
CARDIAC ANGIOGRAM
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11
Q

Goal of drug therapy in CAD

A

Increase O2 supply

Decrease O2 demand

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12
Q

What meds are given to pts w/ CAD

A

ASPIRIN

  • inhibit COX1 + COX2 (to prevent the production of thromboxane A2, a platelet activator)
  • administer as soon as acute coronary syndrome is suspected

PLAVIX

  • inhibit platelet aggregation
  • alternative for pts who cannot use aspirin
  • decrease risk of blockage
NITRATES
- promotes peripheral vasodilation
- decreases preload and afterload 
promote coronary artery vasodilation 
- reduces myocardial O2 consumption 

BETA BLOCKERS ** preferred**

  • inhibit symNS stimulation of heart
  • reduce HR and contractility
  • decrease afterload
  • reduces workload and O2 demands

CA2+ CHANNEL BLOCKERS

  • prevent Ca2+ entry into myocytes and vascular SMCs
  • promote coronary and peripheral vasodilation
  • reduce HR + contractility
    • reduce workload + O2 demand

ACEi

  • prevent conversion of angiotensin I –> angiotensin II
  • decrease endothelial dysFN
  • useful in treating heart failure, tachycardia, MI, hypertension, diabetes, CKD
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13
Q

non-modifiable risk factors for CAD

A
age 
gender: risk is > men 
ethnicity: caucasian 
family Hx
genetic predisposition
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14
Q

Modifiable risk factors for CAD

A
  • elevated serum lipids: blood cholesterol, LDL > HDL
  • HTN: BP > 140/90
  • tobacco use
  • physical inactivity
  • obesity: higher LDLs + HTN
  • diabetes: incidence is 2-4X higher
  • metabolic syndrome
  • psychological states: type A personalities (greater stress, suppress anger)
  • homocysteine level: breakdown of methionine that occurs when the inner lining of BVs becomes damaged
  • substance use
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15
Q

What does health promotion involve for CAD?

A
ID high-risk individuals
management for high-risk pts
physical activity
health education in schools
nutritional therapy 
- lower LDLs, increase HDLs
- diet high in complex carbs + fiber
- omega 3 FAs reduce risks associated w/ CAD
- pts w/ CAD are encouraged to take EPA and DHA supplements
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16
Q

location of:

  • nasogastric
  • nasoenteric
  • gastrostomy
  • jejunostomy
A

NG - stomach
Nasoeneteric - duodenum
Gastrostomy - stomach
jejunostomy - jejunum

17
Q

What to document after gastric tube insertion

A
  • length, size, type of gastric tube used
  • location of insertion
  • pts tolerance of the procedure
  • character of gastric contents and pH
  • results of radiography
  • intake output