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Complex > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

primary goal of pre hospital mgmt

A

move pt to location that will provide definitive treatment

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2
Q

priorities in trauma situation (5) pre hospital

A
  1. Maintain airway
  2. Ensure adequate ventilation
  3. Control external bleeding and prevent shock
  4. Maintain spine immobilization
  5. Transport to appropriate facility
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3
Q

golden hour

A

first hour following trauma

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4
Q

what is the responsibility of the EMTs

A

stabilizing and resuscitating

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5
Q

3 Ts

A

Triage, treatment, transport

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6
Q

primary goal of in hospital mgmt

A

adhering to trauma Care protocol to allow for efficient ID of life threatening conditions

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7
Q

D2N

A

door to needle
TPA
60 minutes

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8
Q

D2B

A

door to balloon
PTI
90 minutes

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9
Q

3 things to diagnose STEMI

A

chest pain
EKG changes
elevated cardiac biomarkers (troponin, CK-MB)

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10
Q

what EKG changes do you see for ischemia

A

Can have ST depression and/or T wave inversion

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11
Q

what does ST elevation indicate

A

injury
QRS does not come back to baseline

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12
Q

what does Q wave indicate

A

infarct = death of tissue
usually happens in hours

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13
Q

what population may not complain of chest pain

A

diabetics

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14
Q

how to avoid ST elevation?

A

thrombolytic (TPA, alteplase)

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15
Q

how to know if a thrombolytic works?

A

ST will go back down

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16
Q

what is CABG?

A

Coronary artery bypass grafting
Healthy artery or vein is grafted to the blocked coronary artery –> One end is attached to the aorta with the other end attached to the block coronary distal to the occlusion → bypasses blocked portion of artery allowing blood flow to the cardiac tissue

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17
Q

why would you do a PCI vs. CABG?

A

PCI is for one area in one vessel
CBG - may be better for someone with weak heart that needs revascularization

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18
Q

normal troponin level

A

0.04

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19
Q

what is troponin?

A

Cardiac troponin I and T are proteins expressed exclusively in the heart, are a specific marker or muscle damage
Can be elevated within 4 hours of injury and can stay elevated for 10 days

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20
Q

what is creatine kinase

A

general marker of cellular injury
Released from cells in brain, skeletal muscle, and cardiac tissues after muscle damage has occurred

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21
Q

what is CK-MB and when does it show up

A

CK isoenzyme marker specific to cardiac tissue
When myocardial damage occurs, CK-MB is released from cells
Can show up 3-36 hours

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22
Q

what does ACS include

A

unstable angina, NSTEMI, STEMI

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23
Q

what does telemetry show

A

rate and rhythm only

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24
Q

when did triage start

A

Triage started in 1854 during Crimea war - Florence Nightingale

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25
Q

when/where/who created first US Clinical shock trauma unit

A

1961, Baltimore, R. Adams Crowley

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26
Q

who is R. Adams Crowley

A

father of the golden hour

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27
Q

when/where first civilian trauma unit

A

1966, Cook County, Chicago
where 3 levels of trauma were first identified

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28
Q

what did the 1966 highway safety act say

A

Said each state must include emergency medicine services as part of highway safety
Mobile intensive care unit EMS

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29
Q

what is the emergency medical services act

A

1973
15 components
Most important: identifies what type of emergency care an ED must have if designated as a trauma center
Trauma nurse certification course

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30
Q

what is included in primary survey during in hospital mgmt

A

Airway management
Breathing
Circulation
D - identify disability that is obvious to you (broken bone), neuro assessment
Exposure - measure to completely undress patient so that obvious and potential injuries

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31
Q

what is part of the tertiary survey (and ex)

A

Includes variables that will compact trauma
Ex: Pt over 75 or w/ substance abuse issue has a greater risk of not doing as well

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32
Q

5 priorities in hospital mgmt

A

primary survey
secondary survey
tertiary survey
fluid resuscitation
damage control/definitive care

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33
Q

ESI

A

emergency severity index, a five level system

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34
Q

ESI level 1

A

Presents with a life threatening condition at a resuscitation level
First is worst, most severe

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35
Q

ESI level 2

A

needs attention quickly, assessed by a nurse in 15 minutes
Examples: unstable, listless child, significant dehydration, severe pain

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36
Q

ESI level 3

A

urgent, has the potential to progress, assessed in 30 minutes.
Examples: acute abdominal pain, chest pain without diaphoresis

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37
Q

ESI level 4

A

less urgent, less potential for deterioration, needs to be assessed within an hour
Examples: burning on urination, elevated temp less than 101 degrees

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38
Q

ESI level 5

A

no acute problem
Examples: suture removal, medication renewal

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39
Q

what is part of RN triage assessment (5)

A

-history of presenting complaint
-pertinent medical history
-physical assessment
-vital signs with orthostatics, pulse ox
- current meds, allergies

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40
Q

orthostatics

A

BP lying, sitting, and standing with a minute b/w each reading

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41
Q

what does a + orthostatic mean

A

Positive orthostatics if greater than 10% difference
What would you look for? HR will go up and BP will go down

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42
Q

5 nursing interventions in triage

A

Fever medications as per protocol
All lacerations must be dressed
All suspected fractures need to be immobilized
Antihypertensive medications as per protocol
Pain medications as per protocol

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43
Q

possible causes of unconscious patient (7)

A

head and neck trauma,
drug/ETOH overdose,
meningitis,
metabolic conditions like hypoglycemia,
cardiac arrest,
toxins,
acute stroke

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44
Q

clinical manifestations of unconscious patient

A

unarguable, altered neuro assessment and vital signs, pupillary changes, involuntary movements

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45
Q

how to tx unconscious patient

A

NARCAN and glucose

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46
Q

LOC: alert and oriented

A

Name, where they are, month/date/year, why are they in the hospital

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47
Q

LOC: lethargic

A

Drowsy but will follow simple commands and makes sense

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48
Q

LOC: obtunded

A

Arousable with stimulation, can follow simple commands

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49
Q

LOC: stuporous

A

Hard to arouse, inconsistently following commands, limited spontaneous movements

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50
Q

LOC: semi comatose

A

Movements are purposeful when stimulated but not following commands or speaking coherently

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51
Q

LOC: comatose

A

Patient may respond with reflexive posturing
Can still be breathing on their own and maintain BP and HR
Light vs deep coma

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52
Q

level 1 trauma center

A

serves a region

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53
Q

level 2 trauma center

A

serves a community

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54
Q

level 3 trauma center

A

Stabilizes and transfers to trauma center

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55
Q

level 4 trauma center

A

is a clinic that serves as an entry into the system

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56
Q

blunt trauma

A

w/o penetration of skin- don’t know extent of injury
Common with MVAs, sports injuries, falls
CT scan is most valuable tool

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57
Q

penetrating trauma

A

Injury from moving object that interrupts the skin
Firearms, knives, etc.
Can’t tell extent of internal damage
Do not remove whatever is there - it is removed in OR

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58
Q

what age is injury rate the highest

A

15-24 y.o

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59
Q

is trauma more common in males or females

A

2.5x higher for males than females - more likely

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60
Q

is incidence of trauma higher in rural or urban areas

A

rural areas

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61
Q

is incidence of trauma higher in low income or high income areas

A

low income

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62
Q

3 mediators of injury response

A

Underlying medical conditions
Drug ingestion
Age related variances

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63
Q

what is AVPU

A

baseline evaluation of patient’s neurological status
A-V-P-U
A = alert
V = response to voice
P = response to pain
U = unresponsive

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64
Q

warning signs for airway

A

Stridor
A crowing noise on inspiration
Gurgling
Hoarseness

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65
Q

3 interventions for airway

A

c-spine immobilization
Jaw thrust maneuver
endotracheal intubation

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66
Q

purpose / dangers of removing all clothing (e- exposure)

A

Purpose: allow entire body to be examined for evidence of trauma
Important: preserve forensic evidence
Danger: hypothermia

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67
Q

automaticity

A

ability to spontaneously generate an electrical impulse

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68
Q

conductivity

A

transmission of electrical impulse to another cardiac cell

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69
Q

excitability

A

ability to respond to electrical impulse

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70
Q

contractility

A

ability to contract after impulse is received

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71
Q

rhythmicity

A

ability to send impulses in a regular, paced manner

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72
Q

refractory period

A

cells’ inability to respond to another impulse during a certain time in the cardiac cycle

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73
Q

conduction system transmission steps

A

SA node → AV node → into ventricles through Purkinje fibers and right and left bundles

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74
Q

which comes first: electrical or mechanical activity

A

electrical

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75
Q

CO equation

A

HR x SV

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76
Q

what is SV

A

Stroke volume = blood ejected from LV after ventricular contraction

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77
Q

normal CO for healthy adult

A

4-8L per minute

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78
Q

SA node intrinsic rate

A

60-100 bpm

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79
Q

AV node intrinsic rate

A

40-60bpm

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80
Q

ventricle intrinsic rate

A

20-40 bpm

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81
Q

purpose of EKG

A

register heart’s electrical activity
used to diagnose/look for ischemia and infarct

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82
Q

P wave

A

Positive deflection that appears in the beginning of the normal EKG complex
Represents atrial depolarization

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83
Q

QRS complex

A

3 different waves, represents ventricular depolarization

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84
Q

Q wave

A

an initial negative deflection
Q represents pathology
If you see a Q - means MI

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85
Q

R wave

A

positive deflection

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86
Q

S wave

A

any subsequent negative deflection

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87
Q

T wave

A

Positive deflection following QRS complex
Represents ventricular repolarization
Have to have T wave in order to stimulate the heart cells and start depolarization all over again

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88
Q

P-R interval

A
  • Measured from the beginning of P wave to beginning of QRS
  • Normal - 0.12 - 0.20 seconds
  • Represents length of time for impulse from SA node to get through atria and to AV node to start ventricular depolarization
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89
Q

QRS complex

A

Measured from the beginning of the Q (or R if there is no Q) to the end of the S
Start from beginning of deflection
Normal is 0.05 - 0.11 seconds
-reflects the amount of time for ventricles to depolarize

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90
Q

what if the QRS is longer than .12 seconds?

A

there is some sort of pathology that is making the time it takes to get the ventricles ready to contract much longer (i.e. bundle branch block)

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91
Q

what is the QT interval

A

Measured from beginning of the Q to the end of the T wave
Indicates the total time interval from the beginning of depolarization and end of repolarization
normal is < .44 seconds

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92
Q

ST segment

A

Beginning of the end of the S to the beginning of the T
It is not measured but the shape and location are evaluated
elevated in STEMI

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93
Q

normal sinus rhythm characteristics

A
  • P, QRS, T
  • P - P equal
  • R - R equal
  • PR interval is between .10 and - .20
  • QRS complex b/w .05-.11
  • HR is between 60-100 bpm
94
Q

sinus brady characteristics

A

P, QRS, T
P - P is equal
R - R is equal
PR interval is between .12-.20 seconds
QRS complex between .05.-.11 seconds
HR is below 60, usually between 40-60 bpm

95
Q

causes of sinus brady

A

Well trained athlete
Sleep
Increased ICP
Medications - BBs, CCBs
Vagal stimulation
Ischemia from an anterior wall MI

96
Q

symptoms of sinus brady

A

hypoperfusion s/s
Dizziness
Cold, clammy skin
diaphoresis

97
Q

tx for sinus brady

A

atropine 0.5 mg IV bolus followed by 3-5 minute wait, NS in between, and then another dose (3 times total)
If it doesn’t work - pacing

98
Q

sinus tachy characteristics

A

P, QRS, T
P - P is equal
R - R is equal
PR interval is between .12-.20 seconds
QRS complex between .05.-.11 seconds
HR: 100-140, usually not greater than 160
Gradual onset and gradual resolution

99
Q

causes of sinus tachy

A

Anxiety, fear
Pain
Fever
Certain meds (Bronchodilators)
Drugs (crack, cocaine)
Shock
Heart failure (heart rate will increase in a compensatory way)

100
Q

s/s of sinus tachy

A

Chest pain - because heart is filling in diastole

101
Q

nursing interventions for sinus tachy

A

Monitor vital signs
Check blood pressure
Treat underlying cause
If symptomatic w/ ST of greater than 150 bpm - should give adenosine 6 mg IV, then 12 mg IV, then 12 mg IV (3 doses)
-If that doesn’t work → cardioversion

102
Q

sinus arrhythmia characteristics

A

P, QRS, T
P - p are unequal
R- R are unequal
P-R interval within normal limits
QRS complex within normal limits
HR = 60-100 bpm

103
Q

nursing interventions for sinus arrhythmia

A

Normal variation that occurs with the respiratory cycle
Monitor vital signs
Rate should have no greater difference than 10%

104
Q

Least serious rhythm disturbance

A

premature atrial contractions

105
Q

characteristics of PACs

A

P, QRS, T wave
P - P = except for premature beat
R - R = except for premature beat
P-R interval is normal
QRS complex normal
Ventricular rate = 60-100 bpm

106
Q

what are PACs

A

ectopic beats that occur within the context of other rhythms

107
Q

unifocal PACs

A

If they come from one atrial pacemaker cell

108
Q

multifocal PACs

A

Come from multiple atrial pacemaker cells

109
Q

couplet

A

two PACS together

110
Q

frequent PACs

A

more than 6 per minute

111
Q

bigeminy PACs

A

every other beat is a PAC

112
Q

trigeminy

A

PAC falling every 3rd beat

113
Q

short burst PACs

A

6 in a row

114
Q

4 causes of PAC

A
  1. Can be caused by excessive caffeine, stress, fatigue
  2. Can also occur in the presence of organic heart disease
  3. Increasing PACs can often be one of the initial signs of HF
  4. low K+
115
Q

Paroxysmal Atrial Tachycardia (PAT) characteristics

A

Sudden onset w/ sudden stop
Abnormal P wave
Rapid heart rate
P, QRS, T wave
P - P are equal
R - R = equal
PR interval = normal
QRS complex = normal
Ventricular rate from 160/180-220/250 bpm

116
Q

causes of PAT

A

Emotional stress
Physical fatigue
Stimulants
Organic heart disease, especially in those that involves pressure changes in the heart

117
Q

why can PAT precipitate HF

A

Because it is beating so fast
blood from ventricles can lead back into atria and back into pulmonary systems

118
Q

symptoms of PAT

A

Palpitations
Vertigo
Precordial pain
Anxiety
Signs of decreased CO

119
Q

tx of PAT

A

if stable - CA channel blockers (CCBs), Adenosine (6 mg, 12 mg, 12 mg)
unstable - Cardioversion
less common - Increase vagal tone - Carotid sinus massage, Valsalva maneuver
Sedation

120
Q

AE of amiodarone

A

Liver, thyroid, pulmonary toxicity

121
Q

atrial flutter characteristics

A

Absent P wave → not SA node, atria takes over
QRS complex
T wave
Sawtooth waves = F, flutter, waves
F-F is equal
R is R is equal usually
No P-R interval
QRS complex is normal
Ventricular rate and atrial rate are not the same

122
Q

8 causes of atrial flutter

A

-Rapid, strong ectopic impulse in the atria beats fast, from 250- 350 times per minute
-The AV node acts as a gatekeeper
-Rheumatic Heart Disease
-Mitral Heart Disease
-Pericarditis
-Cor Pulmonale
-Thyroid disease
-CHF, AMI

123
Q

nursing interventions for atrial flutter

A

Monitor BP
If hemodynamically stable → vigilant observation
If hemodynamically unstable → digitalis, beta blockers
Lastly - cardioversion
*Danger in atrial flutter is the loss of the atrial kick

124
Q

how to determine atrial rate

A

Number of boxes between one f wave and divide into 1500

125
Q

atrial fibrillation characteristics

A

Absent P wave
QRS complex present
T waves present
P wave not present, instead small “f” fibrillatory waves - cannot plot of the “f”s
R-R totally irregular
No PR interval
QRS complex is normal
VR and AR totally different
Chaotic atrial activity 350-1000 bpm

126
Q

controlled a fib

A

< 100 bpm

127
Q

uncontrolled a fib

A

> 100 bpm
No time to fill → decreased CO – also blood moving backwards through pulmonary vein → into capillaries and alveoli (crackles produced)

128
Q

causes of a fib

A

-Rheumatic Heart Disease
-Mitral Heart Disease
-Pericarditis
-Cor Pulmonale
-Thyroid disease
-CHF, AMI
-seen after coronary artery bypass surgery and chest trauma
-Common rhythm disturbance in the elderly

129
Q

tx for atrial fib

A

If a common rhythm disturbance in a hemodynamically stable patient → might be no treatment
Digitalis, CCBs, BBs
Cardioversion if unstable

130
Q

danger of a fib

A

reduced CO, thrombus formation leading to stroke
Blood hangs out in atria → predisposed to clotting, thrombus formation → can lead to stroke

131
Q

PVC characteristics

A

P, QRS complex, T wave
P-P is equal, except for premature beat
R-R is equal, except for premature beat
P-R interval is normal
QRS complex is normal - Will be wide and bizarre
PVCs can occur in any ventricular rate
Are ectopic beats that occur in context of other rhythms.
Wide, bizarre, early beats

132
Q

causes of PVCs (7)

A

Caffeine, smoking, stress
Sudden fear
Hypokalemia
Digitalis toxicity
Hypoxia
Myocardial ischemia
Acute Myocardial infarction (AMI)

133
Q

tx for PVCs

A

Occasional require no treatment - Check K and O2 stat, Seen with hypokalemia
(Rule on cardiac units: Keep K above 4 and Mg above 2 to avoid rhythm)
Treat those with acute MI (most common rhythm disturbance) if systematic or sustained
Treat with amiodarone (150 mg IV over 10 mins bolus then drip), lidocaine rarely used (is neurotoxic)

134
Q

unifocal PVCs

A

If they come from one ventricular pacemaker cell

135
Q

multifocal PVCs

A

Come from multiple ventricular pacemaker cells

136
Q

two PVCs in a row

A

couplet

137
Q

3 PVCs in a row

A

triplet or three beat run of VT

138
Q

PVC ever other beat

A

bigeminy

139
Q

trigeminy PVC

A

PVC falling every 3rd beat

140
Q

salvo

A

short burst = 4 in a row - nonsustained ventricular tachy

141
Q

V Tach characteristics

A

Deadly rhythm
100-250 beats per minute
Only wide, bizarre looking complexes
QRS complex is greater than .12 seconds and wide and weird looking

142
Q

tx for v tach

A

Patient is awake and alert with adequate vital signs → amiodarone - 150 mg IV bolus over 10 minutes
Might add BB to prevent from coming back

If patient has inadequate vital signs and is not awake → treat with defib/cardioversion

143
Q

what is ventricular fibrillation also called

A

sudden cardiac death

144
Q

characteristics of ventricular fibrillation

A

Deadly rhythm
Rhythm does not generate a pulse
Completely uncoordinated electrical activity without any discernible complexes
All waves are fibrillatory waves

145
Q

tx for ventricular fibrillation

A

Defibrillate
CPR
Defibrillate
CPR, epinephrine 3-5 mins
Defibrillate
Continue with CPR, ACLS protocol
Second drug of choice = amiodarone

146
Q

what is cardioversion

A

Delivers a shock that is synchronized w/ heart’s activity

147
Q

defibrillation

A

Indicated in pulseless ventricular tachycardia and ventricular fibrillation
Shock delivered
Be prepared to deliver subsequent shocks per ACLS protocol
Biphasic defibrillators use less current so there is less damage to the heart

148
Q

asystole characteristics

A

Cardiac standstill/flatliner
Rhythm is associated with death
Less than 5bpm
No complexes associated with this rhythm

149
Q

when is asystole seen

A

head trauma and significant drug abuse

150
Q

tx for asystole

A

intubate
resusitate
look for reversible causes

151
Q

Hs of asystole reversible causes

A

hypovolemia,
hypoxia,
hydrogen ions (acidosis, DKA),
hypo or hyperkalemia,
hypothermia

152
Q

Ts of asystole reversible causes

A

tension pneumothorax,
cardiac tamponade,
toxins,
pulmonary thrombosis (embolus),
coronary thrombosis (acute MI with blood clot)

153
Q

3 goals of treatment for patient with CAD

A
  1. reduce symptoms
  2. improve quality of life
  3. improve survival
154
Q

5 cardiac risk factors

A

Family history - under age of 60
DM
HTN
Dyslipidemia
smoking/tobacco use history

155
Q

what is S1

A

Closure of the mitral and tricuspid valves
Beginning of systole

156
Q

what is s2

A

Closure of aortic and pulmonic valves
Beginning of diastole

157
Q

where is chest pain usually?

A

usually in the front of the chest (retrosternal) but can also be in the upper abdomen, neck, jaw, left arm or left shoulder.

158
Q

where does chest pain radiate?

A

neck
jaw
back
left or right arm

159
Q

if chest pain is due to ischemia, what might it feel like

A

tight and crushing

160
Q

s3

A

happens in heart failure
cadence of a galloping horse

*innocent in children and young adults but never over 30

161
Q

s4

A

occurs before the 1st
is abnormal
occurs with ventricular hypertrophy, coronary heart disease, dilated cardiomyopathy, hyperdynamic circulation, arrhythmia and heart block.

162
Q

what does an electrocardiogram (EKG) record

A

-Records electrical impulses traveling through the heart
-Detects abnormal conduction
-Identifies dysrhythmia
-Detects left ventricular enlargement
-Diagnostic for acute MI

163
Q

what labs are drawn for a cardiac patient

A

-troponin
-K+
-BUN
-creatinine
-CBC
-H&H
-coags (INR, aPTT, PTT especially if on anticoags)
-lipids
-BNP

164
Q

troponin

A

Cardiac troponin I and T are proteins expressed exclusively in the heart, are a specific marker or muscle damage

Can elevated within 4 hours of injury and can stay elevated for 10 days

165
Q

what is creatinine kinase

A

Released from cells in brain, skeletal muscle, and cardiac tissues after muscle damage has occurred

166
Q

what is CK-MB

A

CK isoenzyme marker specific to cardiac tissue
When myocardial damage occurs, CK-MB is release from cells
Can show up 3-36 hours

167
Q

what can a chest XR show

A

Visualizes vascular and cardiac shapes
Evaluates size,
pulmonary congestion,
pleural and pericardial effusions,
position of central lines

168
Q

what is the gold standard for evaluating coronary artery lumen

A

cardiac catheterization (angiography)

169
Q

Hemodynamic monitoring

A

Arterial, central venous, and pulmonary artery catheters

170
Q

nursing responsibilities with catheters

A

Check all connections to be certain they are tight
Assess circulation to the cannulated limb
Inspect skin color, temperature, capillary refill and distant pulses, motor function and sensation of the cannulated limb
Monitor wave forms

171
Q

what is the normal wedge pressure (pulmonary artery occlusion pressure)

A

8-12 mm hg

172
Q

what does it mean if the wedge pressure is over 18

A

systolic dysfunction d/t MI damage

173
Q

what does the wedge pressure measure

A

LV end diastolic pressure
indicator of LV function

174
Q

how do crackles develop?

A

patient with systolic dysfunction that leads to poor cardiac outputs and low BP bc of decreased volumes being pumped into systemic circulation..The blood ends up going “backwards” into pulm circulation, causing fluid build up in alveoli = crackles

175
Q

why are we concerned with MI?

A

Sets someone up for arrhythmia
Damages muscle → loses systolic function

176
Q

what does an echo measure?

A

structures of heart, valvular dysfunction/disease, wall thickness, and pressures in chambers

177
Q

what is normal ejection fraction

A

65-75%

178
Q

what does an EF of 40% indicate

A

myocardial dysfunction

179
Q

what does an EF of 30 indicate

A

may need automatic defibrillator to avoid v tach or v fib

180
Q

what does EF of 20 indicate

A

severe
Medications: positive inotropes, ACE, or ARBs

181
Q

what does EF of 10 indicate

A

critically ill, will be referred for transplant

182
Q

what causes increased o2 demand

A

-increased HR
-contractility
-BP
-preload = venous return
-afterload

183
Q

what is o2 supply

A

-coronary artery patency
-diastolic pressure
-diastolic time / filling time
- o2 extraction (hb, saO2)

184
Q

how to measure preload

A

Measure central venous pressure in superior or inferior vena cava

185
Q

how to increase preload

A

fluid, blood products

186
Q

what is afterload

A

pressure heart has to squeeze against to eject blood from heart

187
Q

how to manipulate afterload

A

Decrease afterload w/ nitroglycerin, relax vessel walls with ACE inhibitors, ARBs, diuretics
First line = diuretics

188
Q

what are two types of stents

A

BMS (bare metal)
DES (drug eluting)

189
Q

what are DES stents

A

emits chemotherapeutic agent in vessel to decrease scar tissue formation
Need to be on anti platelet therapy for longer than BES (1 year vs 3 months)

190
Q

what is dual antiplatelet therapy

A

aspirin + clopidogrel/ticagrelor

191
Q

two options for reperfusion therapies

A

PCI or fibrinolytics

192
Q

contraindications for fibrinolytics/thrombolytics

A

recent stroke within 3 months
on anticoags

193
Q

5 types of PCI procedures

A

-balloon
-laser
-directional atherectomy
-rotational atherectomy
-stenting

194
Q

nursing interventions: pre-PCI

A

Cardiac monitor, BP, and pulse oximetry
O2 if indicated
Premedicate w/ PPI, benadryl and IV solumedrol
VS before procedure
Nursing assessment
Explain the procedure
Verify NPO status
Check labs- INR, any kidney injury?
Verify allergies
Informed consent (nurse should witness)
IV assess

195
Q

nursing interventions - peri PCI

A

Continuous VS, O2, LOC, and cardiac rhythm monitoring
Alert physician of any changes
Be prepared for CPR/ACLS
Emergency equipment and medications nearby

196
Q

nursing intervention: post PCI

A

Monitor VS and rhythm
Check catheterization site –radial or femoral
Check distal pulses
Post EKG for changes
Keep extremity straight
Maintain IV infusion per physician’s order/protocol
Supplemental O2 as needed
Encourage PO fluids – kidney fx?
Check coagulation studies before sheath removal

197
Q

2 complications post arterial stick

A

pseudoaneurysm (PSA)
arteriovenous fistula

198
Q

what will a bruit sound like with a PSA

A

turbulent flow, swishing sound - will be pulsatile b/c with arterial flow
More common with femoral sticks

199
Q

what will a bruit sound like with AVF

A

Bruit - continuous sound - flow is continuous

200
Q

what must occur prior to procedure

A

time out
-Verify right patient
Verify right procedure
Verify consent signed and matches procedure
Verify right laterality
Verify labs
Verify premedications

201
Q

indications for CABG

A

Older
More advanced CAD
Impaired LV function
Previous CABG surgery

202
Q

what vein is used for CABG

A

saphenous

203
Q

avg life of bypass graft

A

10 years

204
Q

epicardial temporary pacing

A

temporary pacing wires are placed on the epicardial surface of the heart and brought out of the chest wall.
V wires on Left and Atrial wires typically on right.
Can be hooked up to a generator and pace the heart.

205
Q

Demand pacing

A

demand is pacing that withholds a stimulus when generator senses an adequate intrinsic heart rate

206
Q

asyncronous pacing

A

asynchronous is pacing at a set and fixed rate regardless of intrinsic activity of the heart

207
Q

where are pacing wires placed

A

Right side - atrial pacing
Left side - ventricular pacing

208
Q

what is the function of a water seal chamber of a pleurovac

A

prevents air going back to the patient; filled to -2 cm H2O which maintains a slight negative pleural pressure and prevents air entering the pleural space when off suction and on water seal.

209
Q

what does the collection chamber of a pleurovac do

A

collects fluid with air passing through

210
Q

indication for intra-aortic balloon pumping (4)

A

cardiogenic shock
MI
post op LV failure
unstable angina

211
Q

when is the IABP balloon inflated and what is the result

A

diastole
increases blood flow to coronary arteries

212
Q

when is the IABP balloon deflated and what is the result

A

balloon is deflated quickly as heart starts to squeeze → helps pull blood out of LV, decreases LV outflow resistance (afterload)

213
Q

therapeutic effect of IABP (5)

A

increase CO
increase CA perfusion
increase aortic pressure (BP)
decrease myocardial o2 consumption
decrease cardiac afterload

214
Q

how often to check IABP insertion site

A

hourly, note any oozing

215
Q

nursing interventions IABP

A
  1. Palpate DP & PT pulses in affected leg hourly; mark the location of pulses & compare them to the other extremity
  2. Firmly secure the IABP & possibly restrain the affected extremity to maintain it in a straight position
  3. Keep HOB lower than 30 degrees
  4. Note any sudden decrease in urinary output or any differences in BP between both arms
  5. Maintain appropriate timing-trigger off of EKG or Aline
216
Q

5 potential complications of IABP

A
  1. Distal extremity ischemia
  2. Balloon migration (toward the renal arteries with occlusion of those arteries or toward the aortic arch with occlusion of the subclavian arteries)
  3. Potential perforation of the aorta during insertion or with inadvertent patient movement
  4. Inappropriate timing causing hypotension & dysrhythmias
  5. Psychological consequences (anxiety, loss of control, & sleep alteration
217
Q

what is the purpose of a ventricular assist device

A

It assists the patient’s own heart to pump blood throughout the body, decreasing the work of the left ventricle

218
Q

what does a LVAD do

A

receives blood from the left ventricle and delivers it to the aorta

219
Q

what does an RVAD do

A

receives blood from either the right atrium or right ventricle and delivers it to the pulmonary artery

220
Q

pulsatile VAD

A

fills with blood, then pumps, and continues

221
Q

non pulsatile VAD

A

whirling and continuous.
no palpable pulse

222
Q

complications of acute STEMI (8)

A

-Rhythm disturbances (A fib, v tach)
-Cardiogenic shock - LV pump failure (Elevated PA pressure, elevated wedge pressure, Tachycardia)
-HF
-Pericarditis
-Embolisms
-Papillary muscle dysfunction
-Interventricular septal rupture
-Ventricular aneurysms

223
Q

HFpEF

A

heart failure with preserved ejection fraction - diastolic dysfunction

224
Q

HFrEF

A

heart failure with reduced ejection fraction - systolic dysfunction

225
Q

what is BP an indirect measure of?

A

afterload

226
Q

what would indicate an unstable patient

A

Rapid RR, diaphoresis, thready pulses, cool clammy skin, poor cap refill, neurologic impairment

227
Q

max number of pts waiting in traige

A

5

228
Q

main threat for circulation following trauma

A

hemorrhage

229
Q

tx for hemorrhage

A

0.9% NS/LR

230
Q

secondary survey

A

performed after the primary survey is complete and lifesaving interventions have been initiated. This survey identifies the other injuries that the primary survey did not assess along with pertinent information about the patient such as other comorbidities.
- assess vitals, pain

231
Q

which tool to use to look at viability of heart tissue

A

MRI

232
Q

when can fibrinolytics be given

A

within 30 minutes of arrival to hospital

Complex (3 decks)

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