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CVS/Shock > ACS > Flashcards

ACS Flashcards

1
Q

Define unstable angina

A

Chest pain 10-20 mins

No myocardial necrosis therefore no biomarkers released

No ST elevation, with tissue ischemia there may be ST depression or T wave inversion

Partially occluded coronary artery

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2
Q

Define NSTEMI

A

Severe chest pain lasting >20 mins

Ischemic changes associated with ST depression and T wave inversion persist even after relief of pain

Cardiac biomarkers are released
Usually mostly injury with infarction not the complete thickness of the myocardium therefore recovery of injured cells is possible

Partial occluded coronary artery

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3
Q

Define STEMI

A

Severe chest pain lasting >30 mins

Ischemic changes to myocardium are associated with ST elevation >1mm

Cardiac biomarkers are released
Tissue injury and necrosis to full thickness of myocardium

Pronounced Q wave is possible

Total vessel occlusion- pain not relieved by nitro/rest/o2

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4
Q

What can new BBB indicate

A

Anterior and or septal STEMI

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5
Q

non modifiable risk factors of ACS

A

Age M>45, F>55
First degree family hx
Race Asian, black, native

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6
Q

Modifiable risk factors of ACS

A 
Tobacco use
Dyslipidemia - inc LDL, dec HDL
HTN
Inactivity
Obesity (esp abdominal)
DM
Stress
Excessive alcohol
Metabolic syndrome
Depression
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7
Q

What cluster of symptoms represents metabolic syndrome

A

Abdominal obesity, high serum blood glucose, dyslipidemia, HTN

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8
Q

Functions of the endothelium

A

blood compatible container, separating it from the tissues around it
regulates vascular tone and growth
regulates thrombosis and fibrinolysis
role in immune and inflammatory reactions

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9
Q

Name the 4 major coronary arteries and myocardial areas they vascularize

A

Circumflex - L atrium, lateral and posterior LV
LAD - Septum, anterior walls of LV
RCA(R marginal) - RV, posterior and inferior LV
RCA(posterior descending) - R atrium

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10
Q

Name 4 major coronary arteries and conduction systems they vascularize

A

Cirumflex - SA Node 50% and AV node 10%
LAD - Septum - contributes to BBB
RCA(R marginal) - AV Node 90%, proximal bundle of His
RCA(post descending) - SA node 60%

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11
Q

which leads look at inferior heart?

A

II, III, aVF

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12
Q

which leads look at L lateral heart?

A

I, aVL, V5, V6

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13
Q

which leads look at Anterior heart

A

V3, V4

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14
Q

which leads look at septum?

A

V1, V2

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15
Q

whats the role of nitric oxide in endothelium

A

is released by normal non injured endothelium, regulates vasodilation and inhibits platelet aggregation

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16
Q

what causes endothelial injury

A

ineffective shear stress, modifiable and nonmedifiable risk factors, chronic inflammation from bacteria and viruses

17
Q

what is shear stress

A

drag force exerted by blood flow on endothelium

  • when shear stress is ineffective, and in areas of turbulent flow, such as at bifurcations in blood vessels plaque forms
  • low shear stress allows gaps in endothelial cells, nice place for plaque formation
18
Q

atypical chest pain S/S?

A
  • feeling unwell/fatigue
  • nausea/epigastric pain
  • indigestion
  • neck pain
  • jaw pain
  • SOB
  • Sense of impending doom
19
Q

what signs on ECG indicate MI

A
  • ST segment elevation, 1mm up, 1.5mm from J point
  • pathologic Q waves, 1/3 the length of R and one little box across
  • Q wave with no ST elevation indicates previous MI
20
Q

what signs on ECG indicate myocardial ischemia/injury

A

ST segment depression, T wave inversion

21
Q

Inferior infarct caused by blockage in what coronary artery

A 
RCA 
leads II, III, aVF
Feeds Inferior RV, post/inf LV
-dec co. pump failure and dec contractility
Feeds SA node -55%, AV 90%
-SA pauses/arrests
-AV blocks and bradycardia
22
Q

Lateral infarct caused by blockage in what coronary artery

A 
Circumflex
leads I, aVL, V5, V6
Feeds Lateral LV
-some dec contractility
Feeds SA node at least partially
-Sinus Pauses/arrests, leading 
-Bradydysrhythmias in secondary pacemakers
23
Q

Septal infarct caused by blockage in what coronary artery

A 
LAD
leads V1, V2
Leads to rhythm and conducting problems
-BBB
-Junctional/Ventricular rhythms
24
Q

Anterior infarct caused by blockage in what coronary artery

A 
LAD
leads V2-V4
Can cause:
-Anterior LV disfunction causing
   -dec contractility
   -pump failure - dec CO
   -pulm edema
-Rhythm changes such us
   ST. VT, VF
25
Q

R ventricular infarct caused by blockage in what coronary artery

A

RCA
Leads V1R-V6R
Often occurs in conjunction with Inferior post infarct
Sensitive to preload

26
Q

Absolute contraindications of thrombolytic therapy

A

BASS C-N-L

  • Any hx of hemorrhagic stroke
  • Ischemic stroke in past 3 months (>past 3 hrs)
  • Known cerebral lesion
  • Known intracranial neoplasm
  • Active internal bleeding
  • suspected aortic dissection
  • Significant closed head or facial trauma, past 3 mths
27
Q

Relative contraindications of thrombolytic therapy

A

HACSIS HTN, AC, CPR, Stroke, Intracranial path, Sx

  • Severe uncontrolled hypertension
  • Hx prior ischemic stroke >3mths, other intracranial pathology e.g. dementia
  • Use of anticoagulants
  • Traumatic/prolonged CPR
  • Major sx < 3 weeks
28
Q

Nursing considerations for throbolytic reperfusion therapy

A
  • Have adequate IV access, as should not venipuncture within 24hrs of thrombolytics
  • Ensure adequate cardiac output in order for drug to circulate
  • No shaving/brushing teeth 24-48 hrs
  • ensure pain relief and ST segment normalization post procedure
  • No automatic BP cuffs, cause hematoma
  • ongoing assessment for bleeds
29
Q

Mechanical complications of MI

A

LV wall rupture - lethal - 1%
AV septum rupture - 0.5%
Papillary rupture - lethal 5% 2-7 days post MI

30
Q

NOPQRST

A 
N-ormal baseline
O-nset of pain
P-resipitating/palliating factors
Q-uality of pain
R-egion/radiation
S-everity
T-iming
31
Q

Complications of MI

A
  • cariogenic shock - dec contract of LV primarily, and or dec preload from atrial failure
  • mechanical complications - ruptures
  • emboli - PE, DVTs
  • electrical complications - dysrhythmias depending on coronary involved and node perfusion problems
32
Q

Aspirin for ACS

A

Single most important drug to prevent mortality in ACS
Mech of Act
-Blocks formation of Thromboxane A - preventing platelet aggregation
Effect on O2 S/D
-prevents platelet aggregation, thereby increasing intraluminal flow, allowing o2 rich blood to tissues/end organs
Contraindications
-GI bleed
-hypersensitivity

33
Q

Nitro for ACS

A

Mech of Act
-Converts to nitric oxide - potent vasodilator, primarily venous effects
Effect on O2 S/D
-Increases venous capacitance, thereby dec preload, and contractility with starling’s law, decreasing myocardial o2 demand
-Coronary vasodilation - increased (or restores) supply
Contraindications
-Avoid in RV infarct
-Avoid in cardiogenic shock

34
Q

Morphine for ACS

A

Mech of Act
-mimics endogenous endorphins-analgesic
Effect on O2 S/D
-vasodilatory effect - increase o2 supply to myocardium
- dec afterload
-Decreased pain-dec contractility-dec o2 demand

CVS/Shock (9 decks)

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