Coronary Artery Disease Flashcards

1
Q

what is coronary artery disease?

A

atherosclerosis which athere= fatty mush and skleros= hard meaning soft deposits of fat that harden with age

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2
Q

what contributes to atherosclerosis?

A

endothelial injury and inflammation
when damage occurs to the endothelial lining, a local inflammation response occurs. C-reactive protein produced by the liver is the cause of this inflammation

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3
Q

what are the 3 developmental stages of coronary artery disease?

A

1) fatty streak - fat into the muscle cells

2) fibrous plaque - collagen covers the fatty streak but again the seal decreases the blood flow

3) complicated lesion - if the problem gets worse and the place ruptures, thrombus formation which further narrow the blood flow pathway

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4
Q

what about collateral circulation?

A

a backup out body can take if the main arteries and veins are blocked or damaged. basically if the main arteries have a blockage , the RBC cant pass the part that has blockage so the Arterial anastomose will connect from the sides from one end to the other to by pass the block.

depends on
- Inherited predisposition to develop new blood vessels (angiogenesis)
- Presence of chronic ischemia

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5
Q

what are modifiable and non modifiable factors?

A

non modifiable - age, sex, ethnicity

modifiable - serum lipids, hypertension, tobacco use, obesity, or any disease thats a YOU problem like DM, Metabolic syndrome

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6
Q

what is the health promotion for CAD?

A

Physical activity, nutrition and medication (cholesterol-lowering meds and anti platelet therapy)

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7
Q

discuss chronic stable angina

A

when the myocardial oxygen exceed the ability of the coronary arteries to supply the heart with oxygen which results in myocardial schema

basically increase demand for oxygen but decrease supply of it

PRIMARY reason for this is narrowing of coronary arteries caused by atherosclerosis

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8
Q

discuss chronic stable angine on a cellular level

A

basically the myocardium becomes hypoxic within 10 seconds of coronary occlusion. With this occlusion, contractility after several minutes which leaves the myocardial cells deprived of oxygen and glucose for aerobic metabolism. Once anaerobic metabolism begins, lactic acid accumulates which is the reason why they experience pain.

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9
Q

what happens when pts participate in stable angina precipitating factors?

A

they experience intermittent chest pain

ask the onset, duration, intensity

remember the pain doesn’t change with position or breathing and can only subside if the precipitating factor is relieved

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10
Q

what do you as a nurse do if a pt has an angina attack?

A
  • give oxygen first
  • measure vitals
  • 12 lead ECG
  • fix pain
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11
Q

discuss prinzmetal’s angina

A

aka variant angina

it occurs during rest in response to spasm of a major coronary artery which is caused by you guessed it intracellular CALCIUM.

mostly occurs often in patients with history of migraines or raynaud’s

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12
Q

how does prinzmentals angina looks liken ECG?

A

ST segment elevation

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13
Q

when does prinzmental angina happen?

A

at rest especially during sleep specifically REM sleep when myocardial oxygen consumption increases

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14
Q

how is prinzmental angina treated?

A

calcium channel blockers, nitrates or both

it can also be relieved by moderate exercise or disappear spontaneously

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15
Q

discuss acute coronary syndrome

A

myocardial schema is prolonged and not immediately reversible

it is compromised of :( these are types of heart attacks)
- unstable angina
- non-ST elevation myocardial infraction
- ST-elevation myocardial infraction

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16
Q

how does ACS occur?

A

when the plaque that was stable ruptures and breaks basically stimulating platelet aggregation and local vasoconstriction with thrombus formation

17
Q

what does ACS lead to?

A

either

1) partially occluded by a thrombus (unstable angina or NSTEMI)

2) totally occluded by a thrombus (STEMI)

18
Q

discuss unstable angina

A

chest pain that is new in onset, occurs at rest or has a worsening pattern

  • chronic stable angina may lead to unstable angina
  • unpredictable and MED EMERGENCY
19
Q

discuss myocardial infraction

A

sustained schema causing irreversible myocardial cell death.

when a thrombus develops, perfusion to myocardium distal to the occlusion is halted which means necrosis

contractile function of heart stops in necrotic areas

basically this leads to necrosis of heart muscle and you will DIE

20
Q

what are the symptoms of myocardial infarction

A

Severe, immobilizing chest pain that is not relieved by rest, position
change or nitrate administration

pts will describe the pain as burning and heavy like pressure

lasts > 20 min

21
Q

what is released during myocardial infarction?

A

catecholamines (epic and more) which will increase BP and HR

how will they look? ashen, clammy and cool to touch

22
Q

discuss myocardial infarction healing process

A

enzymes released from dead cardiac cells are important for diagnostic indicates of MI

myocardium vulnerable to stress 10-14 days after MI

23
Q

what are some complications of myocardial infarction?

A

heart failure, dysrhythmias

24
Q

what is ischemia - electrocardiographic changes associated with ACS

A

occurs in response to the electrical disturbance in the myocardial cells that is caused by an inadequate supply of blood and oxygen

ST segment depression
T wave inversion

25
Q

what is injury - electrocardiographic changes associated with ACS

A

stage of worsening ischemia that is potentially reversible but may evolve to infarction (necrosis)

ST elevation

26
Q

discuss infarction - electrocardiographic changes associated with ACS

A

necrosis

ST elevation
Q wave appearance meaning heart wall involved
T wave inversion

27
Q

what is diagnostic study serum cardiac marker

A

released into the blood in large quantities from necrotic heart muscle

  • indicate whether cardiac damage is present and the approx extent of damage

3 components:
1) CK - MB
2) Troponin
3) Myoglobin

28
Q

what is diagnostic study coronary angiogram?

A

evaluate the extent of the disease

  • determines the most appropriate therapeutic treatment

x-ray to basically see the blood vessels

29
Q

discuss emergent percutaneous coronary intervention (PCI)

A

FIRST LINE OF TREATMENT

basically open the affected artery within 90 minutes of patients arrival at ED.

watch YouTube vide its like a mesh thats put into the clogged artery to create pathway basically cardiac catheterization

30
Q

what are some pros and cons of PCI?

A

PROS: alternate to surgery and ambulatory 24hrs

CONS: the artery could rupture and kill u lol

31
Q

discuss fibrinolytic therapy

A

used for patients who are in facilities without an interventional cardiac catheterization lab or pts who are unable to transfer.

basically the therapy is used to dissolve the thrombus but complication is bleeding lol

32
Q

what about nutrition therapy?

A

NPO initially
sips of water until stable
diet advanced to as tolerated but low salt, saturated fat and cholesterol

33
Q

discuss coronary revascularization

A

coronary bypass grafts if problem continues to persist - watch YouTube

34
Q

what are the 3 phases of rehabilitation after ACS

A

1) Phase 1 : hospital - activity depends on severity of angina, start sitting up in bed then ambulatory to hallway then climb stairs. Attention focused on pain management and complications

2) phase 2 : Early recovery - begins after pt discharge, activity level gradually increased under the supervision, physical activity may be resumed at home.

3) Phase 3: Late recovery - long term maintenance program is followed. lifestyle changes, individual physical activity programs are designed and implemented at home