AB Med Surg > ACS > Flashcards

ACS Flashcards

From "Pitt NUR 1120 PP CV Disease - MI PPTX" (97 cards)

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1
Q

What is an Acute Coronary Syndrome?

A

Acute chest pain due to…
* unstable angina
OR
* acute myocardial infarction (MI)

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2
Q

List

8 lifestyle factors that dictate health

A
  1. sleep
  2. diet
  3. exercise
  4. glucose
  5. weight
  6. lipid/cholesterol levels
  7. BP
  8. smoking (+ alcohol)
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3
Q

List

modifiable risk factors of heart disease

8 points

A
  1. hyperlipidemia
  2. HTN (untreated)
  3. diabetes (unmanaged)
  4. metabolic syndrome
  5. obesity
  6. physical inactivity
  7. chronic inflammatory conditions
  8. chronic kidney disease
  9. smoking
  10. excessive alcohol use
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4
Q

List

non-modifiable risk factors of heart disease

4 points

A
  1. family hx/genetic profile
  2. age
  3. gender
  4. race
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5
Q

Where does the heart recieve blood from?

A

the coronary arteries

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6
Q

Fill in the blank

the coronary arteries branch off the [BLANK] and lay on the [BLANK] of the heart

A

the coronary arteries branch off the aorta and lay on the epicardium of the heart

epicardium=outer surface of the heart

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7
Q

What are the 2 main coronary arteries?

A
  1. Right coronary artery
  2. Left coronary artery
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8
Q

What are the two arteries the left coronary artery splits into?

A
  1. circumflex coronary artery
  2. left anterior descending coronary artery
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9
Q

which branch of the left coronary artery supplies the lateral and posterior walls of the heart?

A

circumflex artery

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10
Q

the right coronary artery supplies…

2 places (on the heart)

A

inferior and posterior wall of the heart

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11
Q

define

myocardial infarction

A

acute onset of myocardial ischemia that results in myocardial cell death

myo=muscle
cardial=heart
ischemia: insufficient blood flow/oxygen

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12
Q

what is the pathophysiology of how an MI occurs?

6 steps

A
  1. plaque formation
  2. the plaque ruptures
  3. platlet activation and aggregation at site of rupture (body doesn’t know not to do that)
  4. thrombus/clot formation
  5. ischemia of tissue distal to complete vessel occlusion
  6. eventually…cell death
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13
Q

What happens in a plaque rupture?

A

the built up plaque cracks and causes the weak blood vessel wall to tear and triggers a thrombus/clot formation, cutting off blood flow/oxygen to heart muscles

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14
Q

What medication should you give to a pt complaining of chest pain immediately and why?

1 med and 2 whys

A

aspirin

  1. inhibits platlet aggregation (clot)
  2. minimal risk associated with taking it, but high reward if pt having MI
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15
Q

Why is time of the essence with chest pain?
(w/ suspected MI)

3 points

A
  • necrosis is irreversible
  • dead myocardium can never contract
  • large infarction = largely useless heart = heart failure or death

infarction= the death of body tissue (necrosis) due to a lack of blood supply

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16
Q

define

when the thrombus/clot completely occludes the vessel with ischemia and necrosis/infarction

A

STEMI

seen on an EKG as ST elevation

STEMI = ST segment elevation MI

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17
Q

define

when the thrombus/clot partially occludes the vessel with ischemia and necrosis/infarction

A

NSTEMI

on EKG…ST segment depression or T wave inversion

NSTEMI = non ST segment elevation MI

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18
Q

define

when the thrombus/clot partially occludes the vessel with ischemia but NOT necrosis/infarction

ischemia causes the chest pain

A

unstable angina

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19
Q

significant difference between a proximal occlusion vs distal occlusion?

A

proxmial occlusions result in more myocardial damage and usually from plaque buildup (often linked to artery diseases like atherosclerosis)

distal occlusions usually caused by emboli/clots

a metaphor to use:
proximal= blockage at dam near the river’s source
distal= log jam further downstream

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20
Q

fill in the blank

cell death begins about [INSERT TIME] after onset of ischemia

A

cell death begins about 20 minutes after onset of ischemia

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21
Q

what does ischemic heart tissue increase the risk of?

you can see it on the monitors!

A

dysrhythmia formation

abnormal impulse impulse formation/conduction aka irregularities in rate, rhythm, and/or waveform morphology on EKG

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22
Q

pathophysiology of necrosis

4 steps

A
  1. cell is choking/gasping for air due to blockage and dies
  2. cell membrane ruptures
  3. contents of cell leaks out
  4. lymphatic system picks up cell leakage and puts it into circulation

4 is the reason why see the enzymes on a blood test

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23
Q

what cardiac enzymes are released into the blood upon cell death?

(in heart)

A
  1. troponin
  2. creatine phosphokinase
  3. myoglobin
  4. lactic dehydrogenase
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24
Q

which cardiac enzyme is the most specific, easiest to interpret, and is often tested to diagnose an MI?

cardiac enzymes = cardiac biomarkers

A

troponin

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25
What are the 3 ways an MI can be described?
1. type 2. location on heart (anterior-biggest part of heart, lateral, 3. point in time (acute or evolving) ## Footnote 1. STEMI or Non-STEMI 2. anterior (biggest part of heart), lateral, inferior, posterior 3. acute, evolving, or resolved
26
desribe an MI based on type (EKG changes)
1. STEMI (transmural or full thickness) 2. Non-STEMI (subendocardial or partial thickness) ## Footnote parentheses are how much the artery is blocked
27
what do we see on an **EKG during a STEMI**? | image included
ST elevation
28
what do we see on an **EKG during a non-STEMI**? | image included
* ST depression/no elevation and/or * T wave inversion
29
signs and symptoms of an acute MI | 9 listed
1. chest pain (unrelieved by rest or nitroglycerin) 2. new murmur, S3 or S4 hearts sounds 3. HF present if JVD, SOB, crackles 4. EKG changes/dysrhythmias...VTACH, PVC, AFIB 5. increased or decreased BP 6. cardiac arrest, shock 7. diaphoresis, n/v, anxiety, clammy skin 8. cardiac enzyme elevation 9. VS changes | JVD = jugular venous distention
30
what are significant VS changes to look out for with MI? | 3 of them
1. **BP: increased** (b/c chest pain, thus SNS stimulation, thus up BP) **or decreased** (b/c big MI, thus heart not pumping well, thus BP down) 2. HR: increased (increase CO with low SV) or decreased (special circumstance) 3. RR: up
31
why would a HR decrease during MI? | this is a special circumstance
an inferior wall MI is affecting the R coronary artery, which can slow HR because this artery also supplies the SA and AV node (aka the pacemaker)
32
what is a later sign of MI (24-48 hrs later)...and why does it occur?
low grade fever * due to necrotic tissue stimulating an immune response
33
# what to do in an MI assessment... neuro
get a baseline AAO THEN assess for symptoms of brain ischemia: 1. stroke symptoms (BEFAST) 2. restlessness 3. lightheadedness 4. anxiety
34
# what to do in an MI assessment... cardiac | 6 things to assess
* chest pain * EKG changes (w/ 12 lead EKG) * JVD (jugular vein distention) * murmurs * S3, S4 * pulses
35
# what to do in an MI assessment... pulmonary | 4 points of assessment
1. crackles 2. respiratory distress 3. tachypnea 4. if having heart failure or a pulmonary edema ## Footnote remember your ABCs!!!!
36
# what to do in an MI assessment... gastrointestinal
nausea and vomitting
37
genitourinary
urine output ## Footnote kidney will tell you if heart is failing to perfuse organs by increased BUN and creatinine, fluid retention, albumin in urine
38
# what to do in an MI assessment... skin | 4 things to check
* cool * clammy * diaphoresis * pale
39
# what to do in an MI assessment... psychosocial
feeling of impending doom, fear, denial
40
What are potential causes of chest pain that are EMERGENT? | 4 points (not related to ACS)
* aortic dissection * pulmonary embolism * esophageal rupture * pneumothorax
41
what are other causes of chest pain that aren't totally emergent? | 8 points (not related to ACS)
* pleurisy * pneumonia * pericarditis * musculoskeletal pain * esophageal reflux * costocondritis * panic disorder * acute cholecystitis
42
which patients do not present with the classic symptoms of ACS? | 4 groups
1. women 2. elderly 3. diabetics 4. heart transplant pts
43
what s/s may women with ACS present with? | 4 points
1. fatigue/dizziness 2. n/v 3. weakness 4. overall unwell
44
How do ACS symptoms differ for diabetics and eldery pts? | 1 reason
neuropathy * so they don't feel chest pain as much
45
Why do heart transplant pts not feel chest pain with ACS?
their nerve endings were cut so there are no signals to send to the brain about heart ischemia
46
what does the diagnosis of ACS involve? | 3 tests/assessments
1. history and physical 2. 12 lead EKG 3. serum enzymes
47
what EKG findings indicate myocardial **ISCHEMIA**? (no permanent damage has occured yet) | 2 possible findings
1. ST segment depression (aka below baseline) 2. T wave inversion | (no permanent damage has occured yet)
48
why isn't T wave inversion always the best indicator of MI ischemia?
it is a nonspecific finding that some drugs can cause ## Footnote it's an issue when it appears randomly!!!
49
what EKG finding indicates myocardial INJURY? ## Footnote no permanent damage yet but beginning of infarction since tissue is still viable
ST segment elevation (about baseline) | (no permanent damage yet but beginning of infarction)
50
which EKG findings indicate myocardial INFARCTION? | 2 visualizations (irreversible damage has occured)
1. pathologic Q waves 2. ST elevation | (irreversible damage has occured)
51
# describe pathologic Q waves
a deep initial deflection of QRS (goes straight down) that is permanent on the EKG
52
when do troponin levels rise?
3-6 hours after start of injury
53
when do troponin levels peak?
12-18 hours after start of injury
54
how long do troponin levels stay elevated once injury has occured?
1-2 weeks before going back to normal levels
55
how often do you test the troponin levels?
q 8hrs for 24 hours | *to ensure peak is not missed*
56
# example scenario: A pt came to the ER with chest pain. The 12 lead EKG shows ST segment elevation, but their troponin levels are normal. What is going on?
they are having a myocardial infarction ## Footnote troponin levels peak 18-24 hrs after an MI
57
what are 3 goals of MI treatment?
1. relieve symptoms 2. prevent or minimize myocardial tissue death 3. prevent complications
58
# fill in the blank the 12 lead EKG is to be read within **[INSERT TIME]** of pt arriving to ER
the 12 lead EKG is to be read within **10 minutes** of pt arriving to ER
59
what are the **guidelines for treatment of STEMI**? | 5 general things to do as soon as possible (within first 24 hours)
1. rapid transport to hospital (activate the EKG) 2. history/physical exam 3. 12 lead EKG (to be read within 10 min) 4. obtain blood for cardiac biomarkers (troponin) 5. routine med interventions (aspirin, oral beta blockers, RAAS inhibitors, anticoagulation therapy)
59
why give morphine to a pt with chest pain? | 2 points
* pain relief * vasodilation (helps w ischemia)
60
what are the **routine medical interventions** for a pt with **chest pain**? ## Footnote *hint: think of the acronym*
**MONA** 1. **m**orphine 2. **o**xygen 3. **n**itroglycerin 4. **a**spirin plus beta blockers and anticoagulants!
61
why is it important to only give oxygen (for CP) if the O2 sat is <90%?
when there is too much oxygen, the **vessels can vasoconstrict**, leading to adverse outcomes
62
why give **nitroglycerin to pt with chest pain**?
**venous vasodilator!** * increases blood and oxygen return and decreases the workload (afterload) which let's the heart chill out a bit
63
What medication is contraindicated with nitrates and why? | in pts with persistent ischemia, HR or HTN
viagra (vasodilator) taken in the past 48 because can cause too much vasodilation, making it too hard for the blood to get back to the heart
64
# explain administering 0.4 mg tab of nitroglycerin | **key things to remember!**
* 1 tab under the tongue q5 min x 3 * take BP (systolic >100) and assess pain BEFORE each dose ## Footnote **inform pt may experience burning sensation as tablet dissolves**
65
why are beta blockers give to pts with chest pain?
they block the effects of the SNS, decreasing the HR and BP, therefore letting the heart muscle rest
66
# Fill in the blank beta blockers increase time in **[diastole/systole]**, giving the heart and coronary arteries more time to fill with blood
beta blockers increase time in **diastole**, giving the heart and coronary arteries more time to fill with blood
67
what is one of the most common beta blockers (and it's dose in mg) given to chest pain pts?
metoprolol 5 mg IV
68
# define reperfusion therapy
a critical medical intervention designed to restore blood flow to organs or tissues suffering from ischemia ## Footnote tx includes...percutaneous coronary intervention (PCI/angioplasty) and fibrinolytic (thrombolytic) drugs
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