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RNSG 2539 (Healthcare Concepts) > Myocardial Infarction (+ Sudden Cardiac Death) > Flashcards

Myocardial Infarction (+ Sudden Cardiac Death) Flashcards

1
Q

What is a myocardial infarction - MI?

A

Heart attack: blockage of blood flow to the heart muscle; sustained ischemia (reduced blood flow) leading to IRREVERSIBLE myocardial death or necrosis (cell death)

**80% are because of blood clots

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2
Q

CAD

A

Coronary Artery Disease

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3
Q

What is ATHEROSCLEROSIS?

A

disease of arteries because of a collection of plaques OR fatty materials on inner walls of those arteries

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4
Q

What can ATHEROSCLEROSIS be made of?

A
  • fatty streaks
  • fibrous plaque
  • lesions
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5
Q

What are some risk factors for CAD; and ultimately MI that are NOT MODIFIBLE…

A
  • increased age
  • certain ethnicities: white & black
  • increased risk for men than women in ages under 75
  • genetics
  • family hx
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6
Q

What are some risk factors for CAD; and ultimately MI that ARE MODIFIBLE….

A
  • smoking
  • obesity
  • diabetes (type 2)
  • physical activity (limited - little)
  • HTN
  • lipid profile (increased lipids)
  • metabolic syndromes
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7
Q

What does CAD prevention look like?

A

**identify patients that are HIGH RISK + offer early management of those modifiable factors to allow for early management of CAD for these patients

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8
Q

CARDIAC DIET

A
  • balanced calories
  • monitor weight throughout
  • smaller meals + more often
  • **WHOLE GRAINS + ***HIGH FIBER
  • **MORE FRUITS + ***MORE VEGETABLES
  • NO sodas, sugary drinks
  • **LEAN MEATS
  • **SKIM DAIRY
  • moderate alcohol intake
  • **LOW SALT (2400mg/daily OR less)
  • NO deep fried OR limited; bake, broil, grill
  • **FISH-OMEGA 3 FATTY ACIDS
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9
Q

What is ANGINA?

A

ischemia (reduced blood flow) causing chest pain;
this is caused by the narrowing of coronary arteries which leads to MYOCARDIUM HYPOXIA (decreased oxygen to cardiac muscles, increased lactic acid) = PAIN;
**can be acute OR chronic

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10
Q

How can pain ANGINA pain present?

A
  • chest
  • sternum
  • neck/jaw
  • shoulder/arm
  • mid-back
  • *Can radiate from any location to any other location
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11
Q

Why does an MI have such serious effect on the heart?

A

ALL heart muscle BELOW the blockage becomes ischemic/necrotic because of LACK OF OXYGENATED BLOOD FLOW reaching that heart muscle; blockage can be complete or even incomplete; incomplete blockages restrict enough blood flow that over time the muscle still dies

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12
Q

Ischemia/Necrotic time frame:

A

**cardiac cells become ischemic 20 minutes BEFORE cell death occurs (once dead = always dead) YOU CANNOT REVERSE THIS: 30 minutes into ischemic attack, the WHOLE HEART BECOMES NECROTIC/DEAD!!!!!!!

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13
Q

MI Locations: RT Coronary Artery - RCA

A
  • occlusions lead to heart blocks
  • **this artery feeds the POSTERIOR part of the heart
  • only MASSIVE infarction of RCA = cardiogenic shock
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14
Q

MI Locations: LT Main Coronary Artery - Left Main

A

**VERY THIN, TINY and QUICKLY leads to sudden death > Widow Maker

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15
Q

MI Locations: LT Anterior Descending - LAD

A
  • leads to LT sided heart failure

* **BIG DEAL because EVERYTHING below becomes necrotic > FULL DEATH of HEART

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16
Q

MI + EKG: what type of EKG is gold standard for MI?

A

****12 LEAD EKG is ONLY EKG used to determine MI

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17
Q

EKG zones

A

EKG reads will fall into THREE-ZONES; these zones show what the heart is OR isn’t doing & gives some insight as to what is going on + how severe.

  • Zone of Ischemia
  • Zone of Injury
  • Zone of Necrosis
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18
Q

ZONE OF ISCHEMIA

A

-ST segment depression (because of lack of oxygen)
»electrical disturbance
***WORK TO RESTORE BLOODFLOW QUICKLY; there is the ability for this area to return to normal without becoming necrotic
-needs follow up but isn’t sudden death.

**ST segment depression MUST be present for AT least 1mm LOW on EKG strip

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19
Q

ZONE OF INJURY

A

(cells are NOT fully repolarizing because of the lack of oxygen)

  • INTERVENTIONS NEED TO OCCUR
  • **TREAT EFFECTIVELY & QUICKLY to prevent permanent damage!!!

**ST segment elevation must be present in TWO LEADS; for AT LEAST 1mm HIGH on EKG strip

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20
Q

ZONE OF NECROSIS

A

(ST elevation = most important part of this on EKG)
-this is where scarring starts to occur; scarring can interfere with muscle function (scarring interferes with ability to conduct electrical impulses)

***Scarring > remodeling; remodeling = increased risk of death

21
Q

MI zones severity: least > most

A

ZONE OF ISCHEMIA > ZONE OF INJURY >

ZONE OF NECROSIS

22
Q

What do you want to prevent in an MI, which can ultimately be life saving!?

A

***preventing REMODELING is very important and can safe your patients life!

23
Q

STEMI vs NSTEMI

A

STEMI = ST(segment) ELEVATED MI
^^^^^^**EMERGENT

NSTEMI = NON ST(segment) ELEVATED MI
^^^^^^***NON-EMERGENT but requires follow-up!

24
Q

STEMI (ST(segment) ELEVATED MI)

A

***MUST be determined by 12 lead EKG + MUST show up on 2 of the leads @ 1mm HIGH

> > Intervention needed IMMEDIATELY; could mean coronary artery is occluded > heart muscle death likely

25
Q

NSTEMI (NON ST(segment) ELEVATED MI)

A

-likely from an INCOMPLETE coronary artery occlusion
**chest pain likely present BUT oxygen + nutrients are still being supplied
-needs treatment/attention BUT is not emergent
»>no Q wave will be present

26
Q

Main goals for a patient with possible/likely/identified MI

A
  • minimize damage
  • preserve function
  • reperfusion of myocardial muscles
  • prevention of complications
27
Q

How can I prioritize my care as a nurse to achieve these goals?

A 
#1: Assess ABC's: airway, breathing, circulation
#2: Position for optimal gas exchange + admin oxygen
#3: Obtain vital signs
#4: 12 Lead EKG
#5: IV access
#6: Assess pain using (PQRST) 
#7a: Admin NITRO
#7b: Admin aspirin
#8: Admin morphine
#9: Continuous EKG monitoring
#10: Obtain bloodwork
#11: Chest X-Ray
#12: Admin STATINS
28
Q

1: ABC’s

A

Airway
Breathing
Circulation

29
Q

2: Position + Oxygen admin

A

Ensure your patient is upright
Admin oxygen as/if needed
**O2 goal with MI is 93% or greater

30
Q

3: Obtain vital signs

A

Frequently assess vital signs + compare to previously obtained or baseline vital signs to determine any significate changes!

31
Q

4: 12 Lead EKG

A

MI CANNOT be dx’d without a 12 lead EKG; this is gold standard for MI dx!

32
Q

5: IV access

A

you may/may not need more than one IV access site: you might need to give medications and or fluids and they may not all be compatible with each other!

33
Q

6: Assess PAIN w/ PQRST

A

P: precipitating event: what lead up to the MI/chest pain; what were you doing?

Q: quality of pain: how bad is it, what kind of pain is it?

R: radiation of pain: is the pain radiating to other locations?

S: severity of pain: how severe is the pain, what level 0-10, etc.

T: timing: how long has the pain been present?

34
Q

7a: Administer NITRO

A

NITRO can be administered Q5minutes for 15 minutes;
nitro will TANK B/P, DO NOT give if patient is HYPOtensive.

  • *Assess allergies before admin
  • **Assess previous admin before admin: was patient brought in by ambulance and given by EMT? these need to be determined before administration!
35
Q

7b: Administer Aspirin

A

Admin Aspirin after NITRO, if needed; normally 325mg chewable tablet

36
Q

8: Administer Morphine (IV)

A

IF nitro doesn’t relieve the pain, or achieve desired effect, administer morphine BUT only AFTER NITRO; same considerations for Morphine because morphine can TANK B/P and cause HYPOtension; what is B/P?

37
Q

9: Continuous EKG monitoring

A

patients with MI/possible MI are at higher risk for other dysrhythmias **A-FIB; they need to be attached to continuous monitoring to ensure these are addressed if happens

38
Q

10: Obtain bloodwork

A

Bloodwork needs to be obtained to see what is going on:

  • electrolytes
  • CBC
  • cardiac markers
39
Q

11: Chest X-ray

A

is there any cardiac enlargement? is there anything else on this x-ray that makes you think its NOT an MI? etc.

40
Q

12: Administer STATINS

A

Administer HIGH DOSE STATINS

41
Q

What S/S should I look for in my patient + what S/S should I educate my patient to look for?

A

***SUDDEN ONSET CHEST PAIN that:
-NOT relieved w/ rest OR medications
-20 minutes or longer
-the chest pain feels CRUSHING (like elephant
sitting on chest, etc.)
-neck/jaw, epigastric, sternal or back pain

**SOB
**nausea
**anxiety
**cool, pale, moist skin (grey in appearance)
**indigestion (not relieved with antiacids)
**INCREASED RR + HR (this is compensatory)
^^^ trying to blow off more CO2 to get more O2

42
Q

What is so significate about Diabetes and MIs?

A

**diabetics are KNOWN to have SILENT MIs because of their increased neuropathy (they cannot feel it because of this)

43
Q

Diabetics and MIs

A

diabetics NEED:
-continuous monitoring: this helps determine any changes that are occurring since your patient may or may not feel these changes; this also helps know what/when medications are necessary

44
Q

What else can you do for diabetics regarding MIs or possible MIs?

A
  • offer SUPPORT
  • EDUCATE the patient on what to look for
  • *prepare for POSSIBLE emergency: crash cart, intubation kit, etc.
45
Q

What labs/diagnostics are important for determining an MI?

A 
**Troponin **Lipid Profile **Chest X-Ray
The GOLD STANDARD lab for MI is:
TROPONIN (T)/(I)
TROPONIN T: 0.1+ = POSITIVE for MI
TROPONIN I: 0.04+ = POSITIVE for MI
46
Q

What is important to remember about TROPONIN?

A

TROPONIN elevation occurs 4-6 hours POST-INJURY and can last up to 10-14 days!

47
Q

What does treatment for NSTEMI patients look like?

A

1: start on antiplatelet drugs (aspirin/heparin), to prevent clot formation

^^^^increases bleed time; so monitor) #2: start on beta-blockers
^^^^decreases workload on heart #3: start ACE inhibitors/ARBs
^^^^decreases workload on heart + decreases 
       remodeling #4: start/administer NITRO (vasodilates)
^^^^reduces workload AND pain
48
Q

What type of treatments are performed in the operating room for MI patients?

A
  • coronary artery bypass graft

- off-pump coronary artery graft

49
Q

What physiological changes can occur after an MI?

A
  • leucocytes start coming to the heart and start remodeling! (DO NOT WANT)
  • necrotic muscle = THIN MUSCLE; which leaves the patient at risk for ventricular aneurysms!!!!

RNSG 2539 (Healthcare Concepts) (13 decks)

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