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Nurs 400;ICU > ACS > Flashcards

ACS Flashcards

1
Q

What are the signs and symptoms of acute coronary syndrome?

A

CV: Palpitations, tachycardia or bradycardia, abnormal BP, weakened/irregular pulse, pericardial friction rub

Pulmonary: Dry cough, SOB, Crackles, JVD, dyspnea, hypoxia

GI: N/V

Neurologic: weakness, cold perspiration, anxiety, restlessness, sense of doom, decreased LOC, unexplained fatigue

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2
Q

Right Coronary artery

A
  • Feeds the RA (SA & AV nodes)
  • Feeds RV and inferior LV

If occluded, an inferior wall MI of the LV will occur or a RV MI will occur

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3
Q

Left anterior descending artery (LAD)

A
  • Feeds the anterior wall of LV and the RV
  • Feeds the apical wall and anterior 2/3 of septum (Bundle of His)

Occlusion of this artery will cause Anterior wall MI, Septal wall MI (during a bundle block)

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4
Q

Left main coronary artery

A

Feeds the lateral wall and posterior wall (via the OM)
Occlusion will cause lateral wall MI and/or posterior wall MI

-clot in the left main stops blood flow to the LV, LA, RV

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5
Q

Acute coronary syndrome

A

Spectrum of acute myocardial ischemia and/or infarction- a continuum with differing severity

Includes:
- Unstable angina (UA)
- Non-ST elevation Myocardial Infarction (NSTEMI)
-ST Elevation Myocardial Infarction (STEMI)

*these three are indistinguishable based on s/s

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6
Q

How is chest pain from ACS different from chronic angina?

A

New-onset angina or rest angina not relieved by NTG or rest; lasts >20min; occurs while at rest or sleeping

Accelerating angina: more severe, prolonged, or easily provoked (worse than baseline)

*chest pain that lasts more than 15-20min and doesn’t improve is an indicative sign of ACS

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7
Q

ACS clinical presentation in women

A

Fatigue and sleepiness
Dizzy/faint
Hot, flushed,
Numbness in hands or fingers
Pain may be in high chest, throat/jaw, top of shoulders, left breast, between shoulder blades

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8
Q

How does a coronary artery plaque cause an MI?

A

When the plaque ruptures, platelets and T cells release creating a thrombus on the pre-existing plaque
Vasoconstriction

  • to stop platelets form forming, aspirin is used
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9
Q

What causes a coronary artery plaque to rupture?

A

Inflammation or infection: arterial narrowing causes plaque destabilization or rupture and thrombus formation

Mechanical obstruction: Progressive atherosclerosis after PCI d/t clot formation

Dynamic obstruction: coronary spasm or vasoconstriction

Secondary: underlying CAD and increased myocardial O2 demand (fever, tachycardia, etc.) or decreased supply (hypotension, hypoxemia, anemia)

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10
Q

Why do some patients wake up with chest pain?

A

Circadian rhythm!
- physical, mental, and behavioral changes follow roughly a 24-hour cycle
-people are hypercoagulable between 0600-1200

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11
Q

What does Lead I view?

A

Lateral wall of the LV

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12
Q

What does lead II view?

A

Inferior wall of the LV
-used most for monitoring heart activity
-RCA is involved with SA node

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13
Q

What does lead III view?

A

Inferior wall of the LV
-straight up towards the left shoulder

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14
Q

What does lead avL view?

A

Inferior wall of the LV

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15
Q

What does lead avF view?

A

Lateral wall of the LV
-circumflex is the artery involved

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16
Q

On what layer of the heart do the coronary arteries sit?

A

On top of the epicardial surface of the heart; branches will go in deeper.

17
Q

What is a transmural MI?

A

Transmural = full thickness MI; takes hours (from onset) to evolve

18
Q

What are the three zones of injury in a transmural MI?

A

Zone of ischemia
- cells can be reversed with intervention

Zone of injury
- cells can be saved, but will never return to 100% normal function

Zone of necrosis
-Cells cannot be revived; will be replaced with fibrous tissue

19
Q

What factors determine which type of ACS occurs?

A

How much occlusion is produced by the thrombus plaque
How long the occlusion lasts

20
Q

Upon arriving to the ED with positive ACS signs, how long does the nurse have to obtain an ECG on the patient?

A

Must obtain an ECG within 10 minutes of presentation to ED

21
Q

What type of ECG is seen with myocardial ischemia?

A

T wave inversion and/or ST depression

22
Q

What type of ECG is seen with myocardial injury?

A

ST wave elevation
-injury must be full thickness for ST elevation to occur

23
Q

What type of ECG occurs with myocardial Infarction (necrosis)?

A

Q wave

24
Q

What is unstable angina?

A

Flow is restricted enough to produce symptomatic ischemia, but no cell injury
-occurs when a plaque is disrupted and a thrombus forms, but it is non-occlusive

Pt will have same symptoms as someone with an MI
-t wave inversion and/or ST depression
-cardiac markers will be normal

25
Q

What is an NSTEMI?

A

Non-ST Elevation MI: ischemia with non-transmural cell death
Ischemia is severe enough to cause non-transmural necrosis
-occurs when the thrombus is non-occlusive or only transiently occlusive, but plot aggregates and portions of the disrupted plaque microembolize downstream

-T wave inversion and/or ST depression
-cardiac markers will be elevated (only thing that differentiates unstable angina from NSTEMI)

26
Q

What is a STEMI?

A

ST Segment Elevation MI: Transmural cell necrosis
-occurs when a thrombus on a disrupted atherosclerotic plaque is totally occlusive and persistent

ST elevation= indication of COMPLETE coronary occlusion producing transmural injury
-cardiac markers are elevated

27
Q

What are the cardiac serum biomarkers and when is each elevated?

A

Troponin I: Rises 4-6hours after event, peaks at 10-24hours and returns to normal after 4 days

Troponin T: Rises 4-6hours after event, peaks at 10-24hours, returns to normal after 10 days

CK-MB: Rises within 4 hours, peaks at 18-24hours, and returns to normal in 2-3 days

28
Q

What are the main therapeutic goals for treating ACS?

A
  1. Increase coronary blood supply & restore blood flow
    — Antiplatelet therapy
    —anticoagulant therapy
    — Anti-ischemic therapy: Nitrates
    — for STEMI: revascularize via PCI or fibrinolytics
  2. Decrease Myocardial O2 demand by decreasing workload
    —BB, pain relief, nitrates

Want to increase O2 supply and decrease demand

29
Q

What is the order of actions to treat a patient presenting with unstable angina or NSTEMI?

A
  1. 12 lead ECG
  2. Initiate anti-ischemic treatment
    —O2, NTG to vasodilate, Morphine sulfate for symptoms not relieved by NTG
  3. Antiplatelet treatment (need aspirin and one other)
    —aspirin continued indefinitely
    —P2Y inhibitor (clopidogrel or ticagrelor >12 months) or GP IIb/IIIa inhibitor if high risk or PCI
  4. Anticoagulants
    —Unfractionated heparin, enoxaparin, bivalirudin, fondarparinux

NO NSAIDS FOR LIFE

30
Q

What is the protocol for treating a STEMI patient?

A

*TOTAL ISCHEMIC TIME WITHIN 120 MIN

  1. Initial anti-ischemic treatment
    —O2, NTG, MS

2.Reperfusion treatment: PCI** (within 90-120min) or Fibrinolytics

  1. Immediate Antiplatelet treatment
    —ASA (continued indefinitely), P2Y, GP IIb/IIIa inhibitor (if PCI)
  2. Anticoagulant treatment
    —heparin or alternative

continuous treatment: BB within 24 hours continued indefinitely, ACEI within 24 hours, Statin continued indefinitely

31
Q

Percutaneous coronary intervention (PCI) in STEMI

A

Angioplasty with stent within 12hrs of symptom onset
-preferred method unless there’s too much time delay (must be within 120 minutes)j
—FMC (first medical contact) to device= 90min or less. ***

32
Q

When is fibrinolytic therapy used in STEMI patients?

A

Only used if PCI is not available or cannot perform PCI in time
**door to drug time: <30 min

33
Q

What are complications of AMI?

A

ALL dysrhythmias- especially ventricular

Recurrent ischemia- must monitor for ST or T wave changes
—>50% of patients don’t have chest pain as a s/s

Anterior wall:
- mobitz type II & 3rd AV block
- LV dysfunction/HF
- Cardiogenic chok

34
Q

What are inferior wall complications associated with AMI?

A

Inferior wall:
- bradycardia
- 1st degree & Mobitz type I AV block
-Hypotension
- RV dysfunction
- Psuedoaneurysm

35
Q

What are the mechanical complications associated with MI?

A
  • emergency mitral valve replacement
    -psuedoanuerysm
    -Free wall rupture
    -Ventricular septal defect
36
Q

Patient/family education if they have early signs of MI

A

Take 1 NTG, if not improved or worsens within 5 min, call 911 and chew one non-enteric coasted ASA

Nurs 400;ICU (3 decks)

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