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NRSG 327 > Week 3- ACS > Flashcards

Week 3- ACS Flashcards

(75 cards)

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1
Q

characteristics of GI pain

A

burning
cramping

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2
Q

respiratory characteristics of chest pain

A

sharp
changes with inhalation and exhalation

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3
Q

cardiac characteristics of chest pain

A

crushing
pressure

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4
Q

three types of chest pain

description

A

burning
stabbing
pressure

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5
Q

Gi causes of chest pain

A

GERD
Esophageal
Abnormal motility

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6
Q

Hyperadrenergic status causes of chest pain

5

A
  • stress induced
  • cardiomyopathy
  • cocaine intoxication
  • methamphetamine intoxication
  • pheochromocytoma (tumor of adrenal gland)
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7
Q

chest wall causes of chest pain

A

msk
nerve pain

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8
Q

psychogenic/psychosomatic causes of CP

2

A

panic disorder
depression

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9
Q

pulmonary causes of CP

PPPPAC

6

A

PE
pulmonary htn
cor pulmonale
lung parenchyma (pneumonia, cancer)
asthma/COPD
pneumothorax

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10
Q

cardiovascular causes of CP

3

A

Ischemic:
- CAD
- Vasospasm
- Cardiac syndrome X
Non ischemic
- pericarditis, myocarditis, acute aortic syndromes
Valvular

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11
Q

progression of atherosclerosis

A
  • chronic endothelial injury (damaged endothelium)
  • fatty streak (lipids accumulate and migrate into smooth muscle cells
  • fibrous plaque (collagen covers the fatty streak, vessel lumen is narrowed, blood flow is reduced, fissures can develop)
  • complicated lesion (plaque rupture, thrombus formation, further narrowing or total occlusion of vessel)
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12
Q

Risk factors for atherosclerosis

A

Smoking
HTN
Diabetes
High cholesterol
Obesity
Fam hx
Age >65
Alcohol/drugs
Diet
inactivity
Stress

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13
Q

VIRCHOWS TRIAD

A

contributors to a DVT or other clots
1) venous stasis
2) vessel wall damage
3) coagulation

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14
Q

causes of hypercoagulability

M M P I I I I A E D

10

A
  • major surgery
  • malignancy
  • pregnancy
  • inherited thrombophilia
  • infection/sepsis
  • IBD
  • autoimmune condition
  • estrogen therapy
  • inflammation
  • dehydration
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15
Q

causes of vascular damage

7

A
  • thrombophlebitis
  • cellulitis
  • atherosclerosis
  • indwelling catheter / heart valve
  • venipuncture
  • physical trauma, strain or injury
  • microtrauma to vessel wall
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16
Q

causes of circulatory stasis

CLAVVI

A
  • immobility
  • venous obtruction
  • varicose veins
  • a fib or left ventricle dysfunction
  • congenital abnormalities, affecting venous anatomy
  • low HR and BP
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17
Q

PE caused by

A

obstruction of the pulmonary artery or one of its branches by a thrombi

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18
Q

PE originates in

3

A

venous system or RA or RV

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19
Q

risk factors for DVT

HATP

A
  • associated with trauma
  • pregnancy
  • HF
  • > 50
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20
Q

thrombotic and embolic causes of PE

A

DVT, Afib

fat, amniotic, air

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21
Q

S/S of PE

A

Depend on the size of thrombus and the area where the occlusion occurs
- Dyspnea
- Tachypnea
- CP sudden onset – pleuritic
- pale
- diaphoretic
- decreased SpO2
- hemoptysis
- panic, anxiety
- tachycardia

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22
Q

hemoptysis

A

pink frothy sputum

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23
Q

nursing intervention PE

A
  • get help (call bell)
  • O2
  • Increase fowlers
  • call MRP
  • ensure working IV
  • heparin (PE DVT and cardiac)
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24
Q

MRP orders for suspected DVT

8

A
  • CXR
  • CT PE (with contrast dye)
  • ABG
  • ECG
  • coags
  • D-dimer
  • trops
  • C reactive protein (general inflammation)
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25
thromboembolism treatment
Anticoagulants
26
role of anticoagulants
- don't actually thin your blood, rather delay clotting time - goal is to prevent thrombus from growing and fragmenting - prevent new thrombus formation
27
unfractionated heparin
whole, standard IV heparin
28
LMWH
fractionated heparin - dalteparin, enoxaparin, nadroparin - great if higher risk of clotting - great when we don't want a heavy hitter
29
fondaparinux use
- given sc - to act more like a thrombolytic (kind of think about it like an off label use that some drugs have). - We use either use this stand-alone (usually AFTER we are unable to give TNKase or we can give in conjunction). - it does not have as much bleeding effects as say a LMWH
30
warfarin
oral anticoagulant - a fib - mechanical heart valves
31
new oral anticoagulant (NOACs) | examples uses
apixaban rivaroxaban dabigatran - a fib dont use for mechanical valves
32
when would give anticoagulants post op | types of surgery
- ortho surgery - cardiac surgery (stable waiting for surgery, prevent clot formation)
33
if someone found to have a fib
will start with IV or subcu and then transferred to an oral to sustain the levels
34
nursing considerations for anticoagulants
watch for bleeding check coags before (INR, PTTs, Platelets, hgb)
35
Factors which may determine peri-op myocardial ischemia and infarction | 2
- ↓ myocardial O2 supply - ↑ myocardial demand
36
↑ myocardial demand | 3 STD
↑ myocardial wall stress Dysrhythmia Changes in body temperature
37
↓ myocardial O2 supply | 3
Hypoxia ↓BP (stress will bring it up) Coronary vasospasm
38
common non modifiable risk fators
- fam hx - age - male
39
women after menopause
more at risk for cardiac issues
40
modifiable RF | 5
- diet - HTN - Activity level - Stress level - Alc/drug use (messes with coagulation)
41
downers vs uppers
resp depression, decrease LOC uppers: cocaine, meth= stimulant, increase RR, HR, BP will cause stress on body, meth is given for ADHD (as you age make sure get assessed for cardiac functioning)
42
risk factors for high cholesterol
- high Lp (a) - High LDL - Low HDL
43
LDL HDL
low density, light and fluffy, (marshmallow sticks everywhere) <2 mmol: normal person <1.8 mmol: cardiac issue dense, will slip down (rock) >1.03 higher the better
44
Lp(a)
- newly discovered, target should be less than 100 - Risk of cardiac disease will get the test done once in your life
45
statins
lower LDL increase HDL
46
Chest pain that is the result of
myocardial ischemia
47
types of angina
Stable*** Acute Coronary Syndrome*** Variant (Prinzmetal) atypical
48
stable angina
- predictable, have small clots but not fully occluded - will come on with stress or exercise - relieved by rest
49
ACS is a umbrella term for
1- unstable angina 2- NSTEMI 3- STEMI
50
variant CP
Coronary vasospasm, constriction but not actually caused by a clot. Doesn’t follow MI type of pain
51
unstable angina | 5
Narrowing and worsening No longer responds to rest Wake up in middle of the night No platelet aggregation Small thrombus formation
52
NSTEMI
- Both thrombus and platelet aggregation - Large coronary artery we do not get complete blockage - Incomplete blockage of the large coronary arteries - Can also see a complete blockage but in small coronary arteries - Will not elevate ST segment
53
STEMI
Full occlusion of the coronary artery Platelet has covered artery 0 blood flow
54
3 main coronary arteries
LAD Left circumflex Right coronary artery LAD and left circumflex come off left main.
55
woman and people with diabetes | 3
- diffuse epigastric pain - flu like symptoms - nausea
56
coronary bridging
Coronary arteries are on top of heart This is when the coronary artery is inside the heart muscle when contracts causes chest pain
57
COLLATERAL CIRCULATION
Arterial branching Develops over time in response to chronic ischemia Rapid onset CAD no time to develop collateral circulation
58
query MI what to do next
Quick bedside 12 lead ECG (#1) Cardiac enzymes *troponin (most specific) - CKMB (heart muscle) - Myoglobin (general muscles)
59
leads are
different views of the heart
60
ST elevation=
myocardium does not have enough oxygen, getting shift in electrical conduction
61
ECG=
electrical conduction of the heart, any kind of movement in the muscle we need electrical conduction
62
ECG
usually resting 12 lead most common left ventricle rate, rhythm, st elevation or not
63
P wave: QRS complex: T wave: Atrial relaxation
- atrial depolarization (contracting) - ventricular depolarization (ventricles bigger so longer) - ventricular repolarization (ventricles relaxing) - is happening behind the ventricle contracting
64
ST elevation YES= NO= | algorythms
YES= STEMI NO then look if cardiac markers raised no= unstable angina Yes= NSTEMI
65
cardiac enzymes
CK CKMB troponin
66
CKMB onset peaks normalizes
Creatine kinase myoglobin Onset 2-3h Peaks 15-24 Normalizes 3 days
67
troponin o p n
Onset 4-6h Peaks 10-24h Normalizes 10-15 days
68
How do we know when they are done having their heart attack
Serial troponin (looking for a decline, want to know what was the highest mark) are they still having an MI 3 troponins 6 hours apart What if its still climbing- order another one
69
Meds for MI | 5
- (#1) P2Y12 receptor antagonist – Clopidogrel (Plavix), Ticagrelor (Brilinta) - (#2) ASA (Aspirin) - Nitroglycerin Spray - Beta Blocker - ACE-I or ARB
70
when nitro not good
not good if already hypotension, aortic stenosis), look at BP and history
71
why give BB ACEI and ARBS
reduces contractility and decrease myocardial demand
72
Mi interventions
depends where you are - large tertiary hospital PCI - smaller hospital determine if enough time to wait for PCI - Fibrinolytic is no time CABG
73
ABSOLUTE Contraindications of thrombolytics 1. (3) 2. (2) 3.
Brain Problems: - Intracranial Hemorrhage (ICH) - Recent ischemic stroke <3months - Brain CA Bleeding Problems: - Aortic Dissection - Recent (within 3 months) Trauma/Active Bleeding Uncontrolled Hypertension
74
RELATIVE Contraindications thrombolytics
Brain Problems: - Ischemic stroke > 3months - Other neuro issues Bleeding Problems: - High INR, anticoagulant use - Recent bleeding - Traumatic CPR Controlled Hypertension
75
primary rescue planned PCI
Primary PCI * - PCI is the first intervention for the blockage Rescue PCI * - PCI is the secondary intervention for the blockage - Gave clot buster but still some left on the sides Planned PCI* - May not have had an acute event but block (ages) are known from a previous Selective Coronary Angiogram (SCA)

NRSG 327 (5 decks)

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