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Module 7 (Critical Care) > Respiratory Part 1 > Flashcards

Respiratory Part 1 Flashcards

1
Q

Acid-Base Balance

A

The process of regulatingthe pH, bicarbonateconcentration, and partialpressure of carbon dioxideof the body fluids

Regulated through respiratory and renal functions

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2
Q

Gas Exchange

A

oxygen is transported to the cells and carbon dioxide is transported from the cells

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3
Q

Perfusion

A

flow of blood through arteries and capillaries delivering nutrients and oxygen to cells and removing cellular wastes

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4
Q

Upper Respiratory Tract anatomy

A

Nasopharynx
Oropharynx
Laryngopharynx

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5
Q

Lower Respiratory Tract anatomy

A

Bronchioles (Trachea)
R and L lung
- alveolar ducts
- alveoli

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6
Q

What the different airway obstructions?

A
  • blockage from alveolar compromise (Pulmonaryedema)
  • collapsed lungs (Atelectasis)
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7
Q

Pulmonary edema (cardiogenic) caused by

A

backup of fluid that the heart cannot clear

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8
Q

Non-cardiogenic PE caused by

A

inflammation from injury and/or infection
ARDS (trauma to the lungs causing redness and swelling)

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9
Q

Atelectasis is caused by

A

collection of air or blood outside the lung but within the pleural cavity - a portion of the lung collapses
- Pneumothorax
- Hemothorax

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10
Q

Pulmonary embolism occurs when

A

blood clot that is lodged in a blood vessel in the lungs blocking blood flow to part of the lung.
- Surgical pts, clotting disorders prone

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11
Q

Perfusion obstruction includes

A

pulmonary embolism

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12
Q

Tidal volume

A

the volume of air exchanged with each breath

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13
Q

6-8mL/kg is approximately what in mL of tidal volume

A

400-500

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14
Q

FiO2 is

A

fraction of % of inspired O2

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15
Q

RA FiO2

A

21%

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16
Q

Nasal Cannula 4-6L FiO2

A

37-45%

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17
Q

High Flow 60L/min FiO2

A

100%

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18
Q

MAP normal

A

> 65 mmHg (perfuse organs)

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19
Q

If the MAP is extremely high, what is happening

A

no perfusion
- no cap refill, mottling

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20
Q

What is the formula for MAP?

A

SBP + 2 (DBP) / 3

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21
Q

MAP shows

A

how much Oxygen is being perfused in the tissues

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22
Q

ABGs is used to

A

maintain homeostasis
- Respiratory CO2
- Metabolic HCO3

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23
Q

pH normal

A

7.35-7.45

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24
Q

< 7.35 pH

A

acidic

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25
Q

> 7.45 pH

A

alkalosis

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26
Q

PaO2 normal

A

80-100 (how much O2 is in arterial blood)

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27
Q

SaO2 normal

A

> 95%

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28
Q

PaCO2 normal

A

35-45 mmHg

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29
Q

<35 PaCO2

A

hypercapnic

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30
Q

> 45 PaCO2

A

hypercapnic (retaining too much

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31
Q

HCO3 normal

A

22-26

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32
Q

CO2 is the

A

ACID component of our blood
- lungs regulate the CO2 levels within minutes

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33
Q

To compensate for acidosis

A

RR and depth will increase to blow off CO2

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34
Q

To compensate for alkalosis

A

the RR and depth will decrease to retain CO2

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35
Q

PaO2/FiO2 Ratio is used to determine

A

determine lung injury

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36
Q

Normal Lung ratio

A

300-500

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37
Q

Acute lung injury ratio:

A

200-300

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38
Q

ARDS: < 200

A

very significant injury

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39
Q

ARDS: <100

A

severe injury with high mortality

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40
Q

Acute lung injury is like ARDS but has

A

less of a shunt resulting in hypoxemia

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41
Q

Normal lungs require

A

little outside O2 to maintain a normal PaO2
- 21%

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42
Q

As lungs become injured, they require

A

higher concentrations of supplemental O2

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43
Q

Lung injury formula

A

PaO2 (arterial O2) divided by FiO2 (oxygen %)

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44
Q

V/Q is the

A

ventilation to perfusion ratio​

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45
Q

(V)

A

air moving in & out of the lung​
- bringing oxygen in to /removing CO2 from the alveoli

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46
Q

(Q)

A

blood circulating to areas of the lung ​
- removing O2 from the alveoli and adding CO2 so the Co2 can be blown off by the lungs

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47
Q

In the lungs normally, V and Q are

A

the volume of blood perfusing the lungs and the amount of gas reaching the alveoli are almost identical

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48
Q

Why is the V/Q ratio important?

A

the ratio between the ventilation and the perfusion is one of the major factors affecting the alveolar (and therefore arterial) levels of oxygen and carbon dioxide

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49
Q

If the V and Q are imbalanced, the patient will develop

A

hypoxemia on RA
- providing O2 will correct until the true cause can be addressed

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50
Q

A clot in the vascular or perfusion side prevents blood from circulating effectively in the pulmonary capillary in that area where some of the alveoli are, so even if the alveoli bring in O2 the blood stream cannot pick it up in that area – it is a _________ issue.

A

perfusion

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51
Q

If pneumonia secretions are sitting in the alveoli preventing breathed in oxygen to reach the pulmonary capillary of those alveoli the blood rushes by but is unable to pick up oxygen in that area – it is a ____________ issue.
These situations create a VQ mismatch and in these cases cause a respiratory failure event.

A

ventilation

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52
Q

Hypoxemia Respiratory Failure

A

decreased O2 gas exchange
- V/Q mismatch or impaired diffusion at alveolar level
- ventilation or perfusion failure

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53
Q

Early hypoxemia PaO2

A

<80

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54
Q

Late hypoxemia PaO2

A

<60

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55
Q

Hypoxemia leads to

A

Inadequate alveolar ventilation causing hypoventilation

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56
Q

Inadequate alveolar ventilation causing hypoventilation

A
  • alveolar blockage
  • perfusion blockage
  • airway obstruction
  • respiratory depression
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57
Q

Alveolar blockage includes

A

pulmonary edema
pneumonia
ARDS
cystic fibrosis

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58
Q

Perfusion blockage

A

pulmonary embolism

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59
Q

Airway obstruction

A

Asthma
COPD
Anaphylaxis
Atelectasis
Bronchospasm

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60
Q

Respiratory depression

A

opioids overdose

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61
Q

Hypercapnia

A

decreased CO2 removal
- causes ventilation failure

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62
Q

Late hypercapnia PaCO2

A

> 50

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63
Q

Early hypercapnia PaCO2

A

> 45

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64
Q

Hypercapnia can lead to

A

inadequate alveolar ventilation causes hypoventilation and CO2 retention

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65
Q

Hypoventilation and CO2 retention caused by

A
  • CNS (spinal cord injury and opioid overdose)
  • Neuromuscular (MS and ALS)
  • Barrel chest, kyphosis, trauma - open thorax wound
  • COPD and Cystic fibrosis
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66
Q

Hypoxia is the 1stsign of

A

hypoxemia …

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67
Q

Hypoxia is the

A

reduction of O2 at the tissue level (SaO2)

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68
Q

Hypoxemia is the

A

reduction of arterial oxygen tension or partial pressure of oxygen PaO2

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69
Q

S/S of hypoxemia respiratory failure

A

Dyspnea
Tachypnea & tachycardia
Coughing
Wheezing
Confusion
Cyanosis (Bluish/purplish) color in skin, fingernails, and lips

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70
Q

Hypercapnic respiratory failure is also known as

A

ventilatory failure
- decreased ventilation or CO2 removal

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71
Q

COPD patients typically have a higher rate of

A

CO2

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72
Q

S/S of Hypercapnic

A

Hypoventilation (dyspnea) – unable to remove CO2 from body
Tachycardia
Diaphoresis
Headache
Restlessness
Change in consciousness – CO2 sedates – so very lethargic

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73
Q

Consequences of hypercapnia

A

slow changes in CO2 allow for compensation (tolerate high CO2 better than low O2)
- TX PRIMARY CAUSE BEFORE THEY DETERIORATE

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74
Q

When CO2 levels cannot be maintained within normal limits by the respiratory system, one of two primary problems exists:

A

(1) an increase in CO2 production
(2) a decrease in alveolar ventilation.

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75
Q

Hypoventilation caused by

A

Blockage in alveoli
Airway obstruction
Perfusion blockage
Issues with mechanical movement of thorax

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76
Q

What happens in hypoxemia or hypercapnia?

A

Diffusion limitation
Shunting
Alveolar hypoventilation

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77
Q

Shunting

A

blood exits the heart without taking part in gas exchange as this is a perfusion issue:

  • i.e. cardiac-like septal defect, cardiogenic pulmonary edema
  • PE is not going to be perfused
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78
Q

Diffusion limitation occurs when

A

gas exchange across the alveolar-capillary membrane is compromised by either the destruction of the alveoli or blockage within the pulmonary capillaries

SO EITHER PERFUSION AND/OR VENT ISSUES: i.e., ARDS, pulmonary edema

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79
Q

Alveolar hypoventilation

A

decrease in ventilation that causes hypercapnia and hypoxemia which is typically caused by vent issues:

  • i.e. CNS conditions, acute asthma, chest wall dysfunction (respiratory paralysis, flail chest)
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80
Q

S/S of early respiratory failure

A

mental status changes (confusion)
dyspnea
tachypnea
tachycardia
hypotension
refusal to take oral fluids
decreased urination (concentration)
wheezing
persistent cough

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81
Q

Late s/s of respiratory failure

A

bradycardia
bradypnea
increased CO2 HA morning, decreased LOC and RR
lethargic
unresponsive
cyanosis (PaO2 is < 45)

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82
Q

What does cyanosis look like in darker skin tones?

A

purple (lips, oral mucous, clubbing
pallor (hands, conjuctivia)

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83
Q

ARDS is

A

pulmonary edema due to trauma or infection

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84
Q

Causes of ARDS

A

Aspiration of gastric contents
Near drowning
MVC
Chemical Inhalation (paints etc.) – need to wear a mask
Sepsis
COVID-19
Viral pneumonia, fat emboli, decreased surfactant production, fluid overload, and shock

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85
Q

S/S of ARDS

A

Changes in LOC
Severe dyspnea and coughing
Tachypnea and shallow
Inspiratory crackles – Rice Krispies
Hypoxemia unresponsive to O2
Tachycardia
Cyanosis
Orthopnea – can’t breathe when lying down (sit them up)
increased WBC
respiratory distress

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86
Q

These s/s of ARDS cn lead to what intervention
- Profound dyspnea,
hypoxemia,
increased WOB
respiratory distress

A

endotracheal intubation

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87
Q

A chest x-ray of ARDS shows

A

white out and plural effusions

88
Q

ARDS can lead to

A

severe hypoxemia
hypercapnia
metabolic acidosis
organ dysfunction

89
Q

ARDS phases

A

Exudative
Proliferative
Fibrotic

90
Q

ARDS Exudative phase

A

Cell injury and inflammation
Alveolar edema decreases ventilation > hypoventilation occurs
- Low PaO2 and elevated PaCO2
- Whiteout on chest xray
Respiratory failure
- Classic sign >refractory hypoxemia (PaO2 < 60 mmHg)
Assisted ventilation needed

91
Q

ARDS Proliferative phase

A

Edema fluid resorption
Recovery phase

92
Q

ARDS Fibrotic phase

A

Fibrosis of lungs
Ventilator dependent breathing

93
Q

Nursing interventions for ARDS

A

Assess respiratory rate, depth, and vitals
Administer oxygen
Fowler’s position (45 degrees)
Mobility – passive ROM, TCDB, turn the whole body (turn on the good side (good lung) to cause secretions)
Restrict fluid intake (Daily wts and I&Os)
Breathing treatments (AIMS)
Administer diuretics and/or glucocorticoid steroids (Furosemide and K
Prepare for intubation and mechanical ventilation if the patient declines

94
Q

What position should a patient with ARDS lay on

A

the good side to get rid of secretions

95
Q

What respiratory secretions are Rx to ARDS patients?

A

AIMS
- 1st Albuterol
- Inhaled and IV steroids

96
Q

Blood sugar does what on steroids

A

goes up

97
Q

If K is low

A

dysrhythmias and muscle weakness

98
Q

Atelectasis causes

A

Pneumos: VALI (Ventilator Induced Lung Injury) – high PEEP and/or Tidal Volumes on vents
Either: Trauma
– MVC, gunshot wound,

99
Q

Pneumothorax

A

open/closed wound causing air to enter chest wall

100
Q

Hemothorax

A

blood in the pleural space causing atelectasis

101
Q

S/S of Atelectasis

A

Tachycardia
Hypotension
Tachypnea
Shallow breathing
Hypoxia
Chest pain
Tension Pneumo = tracheal deviation

102
Q

Pneumothorax causes

A

blunt or penetrating chest injury, certain medical procedures (high tidal volumes on mechanical vents), or lung disease

103
Q

VALI

A

(Ventilator Induced Lung Injury) caused by high PEEP levels and/or Tidal Volume too high on ventilator; car crash with rib fractures causing either pneumo and/or hemo.

104
Q

PEEP

A

Positive End-Expiratory Pressure

105
Q

On a dry suction chest tube, the orange bellow means

A

connection to suction

106
Q

Dry chest tube suction

A

stays at the suction on the dial regardless of the suction on the wall

107
Q

Bubbling in the wet chest tubes suction chamber intervention

A

nothing normal (expected)

108
Q

The water seal chamber should not

A

constantly bubble
= air leak

109
Q

If pneumothorax in the water seal chamber bubbles

A

occasionally okay not constant
on expiration

110
Q

If the chest tube becomes dislodged then

A

place in sterile water and place a 3 sided dressing on the incision site

111
Q

What type of pressure is the chest tube restoring

A

negative pressure with releasing air or blood

112
Q

Pneumothorax chest tubes are placed in

A

upper portion

113
Q

Hemothorax chest tubes are placed in

A

placed in the lower portion

114
Q

Nurses should assess for what in atelectasis patients

A
  • Absent breath sounds on the affected side
  • Cyanosis
  • Dyspnea
  • Decreased chest expansion unilaterally
  • Hypotension
  • Sharp chest pain
  • Subcutaneous emphysema – CO2 or air leaking into the skin causing crepitus (crackling) feeling in skin
  • Tracheal deviation to the unaffected side with a tension pneumo
    =Tension pneumos seen with closed pneumos from closed-chest wounds or mechanical ventilation
    =Creates a “one way” valve which allows air out of the lung, but not out of the pleural space creating a tracheal deviation
  • Monitor skin around insertion site
  • Keep patient moving by turning frequently
  • Keep sterile gauze at the bedside to place over site if the tube becomes dislodged
115
Q

Mobility for atelectasis patients

A

ROM
TCDB
Turn frequently

116
Q

Care of chest tubes

A

Dislodged from patient
Sterile dressing over site, taped on 3 sides, andcall the physician immediately
System breaks
Insert tube into sterile water or saline
Milking, stripping or clamping
NOT recommended

117
Q

The drainage chamber is marked each

A

shift for output

118
Q

If the drainage chamber is full,

A

chnage out system with a new one

119
Q

Miking, clamping, striping could cause increase of

A

pneumo or cause a pneumo if the patient has a hemo

120
Q

What to do if chest tube becomes dislodged?

A

Cover the site with a sterile dressing, and tape on three sides (this allows air to escape and prevent tension pneumothorax) and notify physician immediately.

121
Q

What do you do if the System breaks?

A

Insert the tube 1 inch into a bottle of sterile water or sterile normal saline and obtain a new system.

122
Q

Milking or stripping tubing?

A

Not recommended anymore because it creates too much negative pressure (always follow hospital policies)

123
Q

Clamping tubing?

A

Increase risk of patient developing a tension pneumothorax. Never do it without an order and follow hospital policies.

124
Q

Wet system type of chest tube

A

suction control uses water for the pressure

125
Q

Dry system type of chest tube

A

suction control has a bellow (orange) for the pressure.

126
Q

If the patient has a pneumothorax, the drainage chamber will have

A

nothing to monitor

127
Q

Wet system suction chamber

A

needs water to suction
- refill PRN to Rx pressure as it evaporates overtime
- continuous bubbling noted as expected in wet system
- connect to suction

128
Q

Dry system suction chamber

A

connected to suction and the orange bellow needs to be seen in the suction control window.
- There is no water in the suction control chamber with a dry system

129
Q

Water seal chamber (wet and dry)

A

continuous bubbling = leak in system
- normal for tidaling (water move up and down) with inspiration

130
Q

How do you identify crepitus?

A

Palpate around chest tube insertion site
- air leaking under the skin

131
Q

Pulmonary embolism

A

Embolus lodged within the pulmonary system

132
Q

PE causes

A

DVT (common), cancer, fat emboli (trauma – pelvic fx)

133
Q

PE s/s

A

Severe dyspnea, tachypnea
Hypoxemia unresponsive to oxygen therapy
Chest pain
Tachycardia, diaphoresis
Changes in mental status
Syncope
Cyanosis
Pallor

134
Q

How do you dx PE?

A

D Dimer lab – elevated levels from proteins that break down blood clots
CT Scan (1st)

135
Q

What drugs combined can cause DVT - PE?

A

Dextromethorphan (Niquil) contraindicated with antidepressants
- Straddle

136
Q

PE nursing interventions

A

Assess respiratory rate, depth, and vitals (1st)
Elevate HOB
Oxygen
Heparin therapy (PT, black stools-GI and stomach)
Warfarin (takes several days)
Mobility - cautious (ROM, TCDB, frequent turning)
Nutrition - deficits, calories, tube feedings, oral eating
Teaching about anticoagulant therapy

137
Q

Coumadin (Warfarin) needs to limit

A

Vitamin K (moderation)
- green leafy veggies

138
Q

Everything involving respiratory nursing mgmt

A

Assessment (VS, lung sounds, rate and depth of breaths, work of breathing)
Positioning (HOB, aspiration = side-lying, unilateral/bilateral
O2 Therapy (PaO2 > 60, SaO2 >95%)
Dx (CBC = WBC, RBC, H&H, platelets, ABG (sedative - retaining too much CO2)
- Chest Xrays = infiltrations, confirm chest tube placements (Hemothorax if white at the bottom)
Pharmacologic therapy and reassessments
Nutritional therapy
Mobility
sleep
pt education

139
Q

If the patient is on a ventilator, then the patient should be

A

prone to move secretions

140
Q

ARDS has a fluid

A

restriction

141
Q

COPD patients with CO2

A

rely on the hypoxic drive to breathe.
- chemoreceptors that recognize CO2 are less sensitive to Co2.
- lack of oxygen that causes them to breathe.
-too much oxygen, they might become severely hypoxic because their drive to breathe is high CO2 and not high O2 levels.
But remember, never withhold oxygen from a hypoxic patient

142
Q

O2 Delegation

A

cannot be delegated to UAP unless it is already in place.
RNs must assess and evaluate the patient before delegation**

143
Q

When should you start enteral feedings with a respiratory/ventilator?

A

within 48 hours to keep gut working

144
Q

Verify OG or HG tube with

A

xray confirmation prior to using it

145
Q

What type of diet will a repsiratory patient eat

A

high protein promote healing

146
Q

Parenteral feedings are through a

A

central line

147
Q

Turn the pateint every

A

2 hours if tolerated

148
Q

ROM or PROM should be done

A

every shift

149
Q

If the patient is not vented then encourage

A

ambulation (early)

150
Q

Sleep deprivation decreases

A

healing

151
Q

T/F: Paralytic patients can still hear

A

yes

152
Q

Pt edu for patient with respiratory problems

A

Labs and what they mean – understand what they are for so you can pass this along to your patients and their families
Oral care for vented patients
Medications – what are they for? What side effects?
Mobility – Incentive spirometer, ambulation
Sleep – importance of rest

153
Q

Respiratory Meds - Bronchodilators

A

Beta blockers (1st albuterol)
Anticholinergic (2nd Ipratropium)
Methylxanthines
BAM and SLaM

154
Q

Respiratory Meds - Anti-inflammatory

A

Steroids (Beclomethasone and Flutaxaxone – inhaled steroids)
Leukotriene inhibitors –(Montelukast)
Mast Cell stabilizers

155
Q

Beta 2 Agonist

A

Albuterol 1st line for ashtma attack
- dilate bronchodilators
- immediate action

156
Q

What are the expected s/s of Beta 2 agonists?

A

wheezing to diminish and hearing clear breath sounds

157
Q

Anticholinergics med type

A

(Ipratropium – 2nd)

158
Q

What are the expected s/s of Anticholinergics

A

– dry mucous membranes, tachycardia, hot/dry skin

159
Q

Methylxanthines MOA

A

Bronchodilator and stimulatory effects
- LONG TERM CONTROL OF ASHTMA
caffeine

160
Q

1st and 2nd Ashtma attack meds

A

Albuterol – 1st line used for asthma attack
Ipatropium – 2nd line for asthma attack

161
Q

How to take bronchodilators?

A

Shake it before you take it
Breathe out, then inhale puffs
2-4 puffs every 20 mins

162
Q

Nebulizer Bronchodilators if not effective after

A

3 doses = call HCP

163
Q

Which inhaler goes first?

A

Bronchodilator
steroid inhalers

164
Q

Nebulizer Bronchodilators are effective if

A

decrease in RR and O2 sats increased >90%

165
Q

Nebulizer bronchodilator side effects (expected)

A

Tachycardia, Tremors, and insomnia (feels like adrenaline rush)

166
Q

Steroids med types

A

(Beclomethasone and Flutaxaxone – inhaled steroids)

167
Q

Steroids onset

A

Slow onset so not used as first line for asthma attack.

168
Q

Inhaled steroids

A

need to rinse mouth or perform oral care – DO NOT SWALLOW WATER - as these can cause thrush
- swish and spit

169
Q

Inhaled steroids on BG

A

not affect blood sugar, only IV (prednisone) does

170
Q

Leukotriene inhibitors med type

A

Montelukast

171
Q

Leukotriene inhibitors onset

A

Slow onset (1-2 weeks) but opens airway
- not a rescue drug

172
Q

What is expected with Leukotriene inhibitors?

A

cough, sore throat, fatigue, headache

173
Q

Mast Cell Stabilizers onset

A

Acts fast but is not rescue inhaler

174
Q

Take Mast Cell Stabilizers 15 minutes before

A

exercise to reduce exercise induced asthma

175
Q

DO NOT USE _______________ or _____________ as a primary for an asthma attack.

A

Salmeterol or Fluticasone
- long term inflammatory control of the bronchioles

176
Q

How do I know if respiratory drugs are working?

A

Lung sounds, go down on FiO2 and stats go up, regular, rate

177
Q

After an inhaled steroid on a ventilator patient, what needs to be done?

A

oral care

178
Q

What diuretics could help respiratory illnesses?

A

furosemide, hydrochlorothiazide, bumetanide
spironolactone

179
Q

What anticoagulants could help respiratory illnesses?

A

Injection: heparin, enoxaparin
Oral: warfarin, apixaban, rivaroxaban

180
Q

What anti-inflammatory steroids could help respiratory illnesses?

A

Oral: prednisone
Oral or injection: methylprednisolone, dexamethasone, betamethasone
Inhaled: beclomethasone, fluticasone

181
Q

Diuretics decrease

A

BP, decrease fluid (causing increased urination), and dehydrate

182
Q

Furosemide or HCTZ: potassium

A

wasting

183
Q

Spironolactone potassium

A

sparing

184
Q

Nutrition education for Furosemide and HCTZ

A

encourage high potassium foods
Bananas, Oranges, Green leafy vegetables, Liver, avocado

185
Q

Hypokalemia ECG

A

> flat T waves, prolonged QT, ST depression, U waves

186
Q

ICU patients K needs to be

A

4-5

187
Q

Spirinolactone nutrition

A

avoid K

188
Q

Hyperkalemia ECG

A

peaked T waves, maybe ST elevation, P wave
Hyperkalemia KILLS

189
Q

Anticoagulants do what

A

decrease the body’s ability to clot and prevent clots from forming allowing the body time to reabsorb and break down clots in the body already. They do not break down clots
**prevnt forming new clots and growth of existing clots

190
Q

Heparins MONITOR

A

platelets (do not give if less than 100,000 mcL

191
Q

Heparin Labs

A

PTT 46-70

192
Q

Antidote for Heparin

A

Protamine Sulfate

193
Q

Actions if PTT >70 or signs of bleeding from Heparin

A

STOP the heparin gtt and notify provider
Prepare antidote
Reassess labs in 1 hour

194
Q

Warfarin Labs

A

INR levels for warfarin- therapeutic levels 2-3

195
Q

Antidote for Warfarin

A

Vitamin K

196
Q

Actions if INR > 4 in Warfarin

A

Assess for bleeding
Prepare Vitamin K

197
Q

Actions if INR > 2 in Warfarin

A

Give warfarin to increase INR to 2.5

198
Q

Which anti-coagulant is fast acting?

A

Heparin

199
Q

Which anti-coagulant is slow-acting?

A

Warfarin
- 5 days therapeutic levels

200
Q

PE patients in the hospital should be started on

A

Warfarin
- unless apixaban is Rx

201
Q

Apixaban and rivaroxaban begin working within

A

few hours of taking so they can start after the heparin therapy. Can start on discharge. Does not require INR testing.

202
Q

Nutrition education for anticoagulants

A

consistent levels of leafy green vegetables or liver which are high in Vitamin K. They do not have to avoid these but keep it in moderation.

203
Q

ASA and clopidogrel

A

antiplatelets

204
Q

Glucocorticoids used to

A

suppress immune responses like inflammation.

205
Q

Prednisone and prednisolone are intermediate acting and have a half life up

A

36 hours

206
Q

Dexamethasone and betamethasone are longer acting and have a half life up to

A

50 hours

207
Q

Which glucocorticoid is only give orally?

A

prednisone

208
Q

Side effects of Glucocortoids

A

Hyperglycemia, infection, insomnia, polydipsia, polyphagia
- No need to report to HCP as this is an expected finding, but should be part of patient teaching

209
Q

Hypokalemia can occur with what interaction cobination: glucocorticoid and

A

HCTZ and loop diuretics

210
Q

Glucocorticoids can cause insomnia so take

A

early in the day

211
Q

Patient with severe asthma presents to the ER with the following vital signs: HR 120 BPM, RR 32 BPM, O2 Sat 90% on room air and a Peak Expiratory flow of <40%. What medication would you give? Select all that apply
- Inhaled salmeterol
- Albuterol inhaler
- Nebulizer ipratropium
- IV Methamphetamines
- IV Methylprednisolone

A
  • Albuterol inhaler
  • Nebulizer ipratropium
  • IV Methylprednisolone

Think AIM – albuterol, ipratropium, steroid
BAM and SLaM

212
Q

The emergency department nurse is assessing a client who has sustained a blunt injury to the chest wall. Which finding would indicate the presence of a pneumothorax in this client?
1. A low respiratory rate
2. Diminished breath sounds
3. The presence of a barrel chest
4. A sucking sound at the site of injury

A
  1. Diminished breath sounds

Rationale:
This client has sustained a blunt or closed-chest injury. Basic symptoms of a closed pneumothorax are shortness of breath and chest pain. A larger pneumothorax may cause tachypnea, cyanosis, diminished breath sounds, and subcutaneous emphysema. Hyperresonance also may occur on the affected side. A sucking sound at the site of injury would be noted with an open chest injury.

213
Q

The nurse instructs a client to use the pursed-lip method of breathing and the client asks the nurse about the purpose of this type of breathing. The nurse responds, knowing that the primary purpose of pursed-lip breathing is to promote which outcome?
1. Promote oxygen intake
2. Strengthen the diaphragm
3. Strengthen the intercostal muscles
4. Promote carbon dioxide elimination

A
  1. Promote carbon dioxide elimination

Rationale:
Pursed-lip breathing facilitates maximal expiration for clients with obstructive lung disease. This type of breathing allows better expiration by increasing airway pressure that keeps air passages open during exhalation. Options 1, 2, and 3 are not the purposes of this type of breathing.

214
Q

The nurse is assessing a client with multiple trauma who is at risk for developing acute respiratory distress syndrome. The nurse should assess for which early sign of acute respiratory distress syndrome?
1. Bilateral wheezing
2. Inspiratory crackles
3. Intercostal retractions
4. Increased respiratory rate

A
  1. Increased respiratory rate

Rationale:
The earliest detectable sign of acute respiratory distress syndrome is an increased respiratory rate, which can begin from 1 to 96 hours after the initial insult to the body. This is followed by increasing dyspnea, air hunger, retraction of accessory muscles, and cyanosis. Breath sounds may be clear or consist of fine inspiratory crackles or diffuse coarse crackles.

215
Q

A client has experienced pulmonary embolism. The nurse should assess for which symptom?
1. Hot, flushed feeling
2. Sudden chills and fever
3. Chest pain that occurs suddenly
4. Dyspnea when deep breaths are taken

A
  1. Chest pain that occurs suddenly

Rationale:
The most common initial symptom in pulmonary embolism is chest pain that is sudden in onset. The next most commonly reported symptom is dyspnea, which is accompanied by an increased respiratory rate. Other typical symptoms of pulmonary embolism include apprehension and restlessness, tachycardia, cough, and cyanosis.

Module 7 (Critical Care) (22 decks)

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