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202A > Test #2 > Flashcards

Test #2 Flashcards

1
Q

How does surfactant work

A

It reduces surface tension by lowering the amount of pressure needed to inflate the alveoli, which makes them less likely to collapse

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2
Q

What is lung compliance

A

How well the lungs can expand (fluid in your lungs, like from pneumonia, makes your lungs less compliant, which means it is harder for them to inflate)

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3
Q

What is the most common pulmonary function test? What is? What does it test?

A

Spirometer - where you take a deep breath and exhale as hard and as fast as you can (think of that one guy yelling at that girl during her test)

Tests how much air you can inhale, exhale, and how much air is in the lungs

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4
Q

What kinds of things do pulmonary function tests diagnosis

A

Things like asthma, emphysema, bronchitis

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5
Q

Should you do a pulmonary function test when you’re sick

A

No, we want to do these tests when your lungs are healthy, we want baseline

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6
Q

What is tidal volume

A

The amount of air inhaled and exhaled during normal breathing

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7
Q

What is expiratory reserve volume

A

Additional air that can be forcefully exhaled after a normal breath

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8
Q

What is residual volume

A

The amount of air left in the lungs after exhaling as much as you can

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9
Q

What is inspiratory reserve volume

A

Maximum volume of air that you can inhale after already inhaling (you take a breath in and then take another breath in)

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10
Q

What is total lung capacity

A

Maximum amount of air that lungs can contain

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11
Q

What is functional residual capacity

A

The amount of air left in the lungs after exhaling

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12
Q

What is vital capacity

A

Total volume of air that can be exhaled after inhaling as much as you can

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13
Q

What is inspiratory capacity

A

Volume of air that can be inhaled after an expiration

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14
Q

What is forced vital capacity

A

The amount of air that can be quickly and forcefully exhaled after maximum inspiration

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15
Q

What is forced expiratory volume

A

The amount of air exhaled in first seconds of the test

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16
Q

What is minute volume

A

Total amount of air that is exhaled per minute

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17
Q

What is forced midexpiratory flow

A

Measurement of airflow rate in the middle half of forced expiration

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18
Q

What is maximal voluntary ventilation? What is this one used for?

A

Deep breathing as rapidly as possible for a specific amount of time

Can be used to determine exercise capacity

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19
Q

What is peak expiratory flow rate? What can it test for?

A

How fast you can blow air out of your lungs.

Can test for asthma

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20
Q

What is SaO2 measuring

A

The oxygen saturation of both functional and non-functional hemoglobin in arterial blood

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21
Q

What is SPO2

A

The oxygen saturation of only functional hemoglobin

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22
Q

How is SaO2 data gathered? What about SPO2?

A

SaO2 is through extracting arterial blood, while a pulse ox can be used for SPO2

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23
Q

What is PAO2? What is it telling us? What is a normal level?

A

PAO2 is the partial pressure of oxygen dissolved in the plasma in arterial blood.

Normal 80-100 (which equals at or above 94% for SpO2)

*This stuff is on page 470

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24
Q

What are the mold, moderate ans severe levels of hypoxemia according to PaO2

A

Mild PaO2 = 60-79, which is 90 SpO2

Moderate PaO2 = 40-59, which is 88 SpO2

Severe PaO2 = less than 40, which equals 75 SpO2

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25
Q

Why does oxygen diffuse out into the blood from the alveoli

A

Because the alveoli have a higher tension than in the pulmonary capillaries, such oxygen will diffuse down the concentration gradient into the pulmonary capillaries (opposite is true for carbon dioxide - that’s why it diffuses out of the blood and into the alveoli)

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26
Q

What is the purpose of the oxyhemoglobin dissociation curve

A

To show how likely hemoglobin is to release oxygen to the tissues or hold onto oxygen based on the needs of the body

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27
Q

With the oxyhemoglobin dissociation curve, what does it mean when we say we are shifting to the right? What things cause this?

A

Hemoglobin is giving oxygen to the tissues, so there will be a higher PO2 amount (dissolved oxygen)

Causes:
- Acidosis (you have more hydrogen ions binding to hemoglobin, which reduces hemoglobins attraction or desire to hang onto oxygen)
- Hyperthermia (uses more oxygen in the tissues, so hemoglobin will be releasing a lot more oxygen to the tissues)
- Hypercapnia (increased altitude) (excessive CO2)
- Increased 2,3 DPG (decreases hemoglobin affinity for oxygen)

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28
Q

With the oxyhemoglobin dissociation curve, what does it mean when we say we are shifting to the left? What things cause this?

A

Hemoglobin will bind more readily with oxygen

Causes:
- Alkalosis (less hydrogen ions to take up hemoglobin)
- Hypothermia (tissues aren’t needing as much oxygen)
- Hypocapnia (low altitude) (less CO2)
- Decreased - 2,3 DPG

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29
Q

Do we like to see quick shifts in the oxyhemoglobin dissociation curve

A

NO! Quick shifts maybe life threatening.

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30
Q

Basically, what is the difference between PaO2 and SaO2

A

PaO2 is the amount of oxygen in the arterial blood BEFORE it has attached to hemoglobin

SaO2 is the amount of oxygen that has bound to hemoglobin

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31
Q

Good video for oxygen dissociation curve https://www.youtube.com/watch?v=wQ2eCRN02f4

A
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32
Q

What is capnography

A

Non invasive display of CO2 concentration that is exhaled

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33
Q

Why might we use capnography 4

A

For continuous monitoring during:
- Surgical and procedural anesthesia
- Post op recovery
- Critical care
- Evaluate the effectiveness of compressions during codes
(basically monitors the effectiveness of ventilation)

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34
Q

What does the V and Q stand for in the V/Q ratio

A

V = ventilation
Q = perfusion

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35
Q

What is the V/Q ratio

A

Shows us how much air is moving into the alveoli (ventilation) compared to how much blood is going through the pulmonary capillaries (perfusion)

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36
Q

What is a normal V/Q ratio

A

V = 4 liters of air flowing into the alveoli
Q = 5 liters of blood flowing past the alveoli

4/5 = 0.8

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37
Q

What happens if the V/Q ratio is greater than 0.8? What if it is less?

A

Greater = Too much air is blowing by but not enough air is getting too the tissues

Smaller = Not enough air is getting in to go to the tissues

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38
Q

Where does the largest pulmonary capillary perfusion (gas exchange) occur in the lungs

A

It is gravity dependent - so where ever gravity is lowest based on the position of the lungs

For example - in an upright position the most gas exchange is occurring in the lower lungs

In a person laying on their tummy it will be the anterior part of the lungs

See pg 297 in high acuity for examples

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39
Q

Why is it important to know where “good” gas exchange occurs in the lungs (“good lung down”)

A

We want to position patients in a way that no long conditions, like pneumonia, will impair their gas exchange.

Like if they have pneumonia in the upper lobes then we want to keep them upright so gas exchange occurs in the healthy lower lobes

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40
Q

What are examples of ventilation problems affecting the V/Q ratio?

What are examples of perfusion problems affecting the V/Q ratio?

A

Ventilation = Asthma, COPD, atelectasis (obstructive things)

Perfusion = pneumonia, pulmonary hypertension, pulmonary fibrosis, pulmonary embolism (not getting enough perfusion to alveoli due to pneumonia secretions)

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41
Q

What is a pulmonary shunt

A

Amount of cardiac output that flows from the right heart into the left heart without undergoing pulmonary gas exchange

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42
Q

What are the two types of pulmonary shunts

A
  1. Anatomic
  2. Capillary
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43
Q

What is an anatomic pulmonary shunt? What are the two types?

A
  1. Normally occurring, where 2-5% of the blood doesn’t pass through alveoli, so it doesn’t go through gas exchange
  2. Abnormal anatomic shunt - like a ventricular septal defect, where there is a hole in the heart wall dividing the right side from the left
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44
Q

What is a capillary shunt? Where do we most commonly see capillary shunts?

A
  • Where blood passes through an unventilated alveoli, which causes it to not participate in gas exchange (basically the alveolis are not functioning correctly, so they cant do gas exchange)
  • Most commonly seen in high acuity patients usually caused by atelectasis, consolidation or fluid in the alveoli
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45
Q

Will supplemental oxygen help improve shunting

A

No - because it’s an issue with the blood and alveoli, not about getting enough oxygen (basically no matter how much oxygen is administered, diffusion cannot take place if alveoli are completely bypassed or nonfunctioning)

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46
Q

What things can affect ventilation of alveoli (alveoli from working properly) 6

A
  • Atelectasis (collapsed alveoli)
  • Alveolar fibrosis
  • Alveolar capillary destruction (like from emphysema)
  • Alveolar consolidation (like from pneumonia)
  • Interstitial edema (swelling pushing the alveoli in to collapse)
  • Frothy secretions (like pulmonary edema)
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47
Q

What things can affect ventilation of alveoli (alveoli from working properly) 6

A
  • Atelectasis (collapsed alveoli)
  • Alveolar fibrosis
  • Alveolar capillary destruction (like from emphysema)
  • Alveolar consolidation (like from pneumonia)
  • Interstitial edema (swelling pushing the alveoli in to collapse)
  • Frothy secretions (like pulmonary edema)
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48
Q

What is an absolute shunt

A

The combined amount of the anatomic shunt and a capillary shunt

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49
Q

What percentage of shunting (so percentage of blood not getting oxygenated) can lead to severe respiratory failure

A

More than 15%

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50
Q

If a patient has ARDS, what is their typical shunt percentage

A

Usually having more at least 20% of their blood shunted (not getting oxygenated)

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51
Q

What is the hallmark symptom of ARDS

A

Refractory hypoxemia (where no amount of supplemental oxygen will help the patient, because it is an issue with the blood and alveoli, not the oxygen)

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52
Q

What is the P/F ratio

A

PaO2 (partial pressure of arterial oxygen)
/
FiO2 (fraction of inspired oxygen, expressed as a decimal)

(basically tells us how well our patient’s oxygen level is based on what type of oxygen they are on (room air or supplemental)

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53
Q

Give an example of the P/F ratio

A

PaO2 = measures 60
/
FiO2 21% or 0.21 (room air)
= 285

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54
Q

What can the P/F ratio tell us

A

Tells us the level of hypoxemia our patient’s may be experiencing
- Used to trend progression of respiratory failure, who might need to be intubated…

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55
Q

What is a normal P/F ratio

A

350-450

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56
Q

What is the minimally clinically acceptable P/F ratio level

A

286 (anything less than is worrisome)

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57
Q

How do you calculate FiO2

A

20% + 4 x (liters per minute)

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58
Q

Calculate the FiO2 if someone is on 5 liters of oxygen

A

20% + 4 x (5 liters per minute) = 40% FiO2

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59
Q

What is the FiO2 of room air

A

21%

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60
Q

What is chronic respiratory insufficiency

A

Where your body maintains an acceptable level through cardiopulmonary compensatory mechanisms, because the respiratory insufficiency is progressive and slow, it gives the body enough time to compensate (like how COPDers can live at 88% oxygen)

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61
Q

If you have chronic respiratory insufficiency, what can cause you to decompensate

A

Stressors, like an acute infection, where your body doesn’t have enough time to compensate

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62
Q

What are signs of impending respiratory failure (a lot)

A
  • Tachypnea
  • Tachycardia
  • Increased use of accessory muscles
  • Nasal flaring
  • Abnormal chest wall movements
  • Labored breathing
  • Decreasing SpO2
  • Restlessness/anxious
  • Air hunger
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63
Q

Looking at a patient’s ABGs, how will we know if they are in acute respiratory failure (ARF)? If they are in ARF, what might we be prepared to do>

A

They will have:
- PaCO2 greater than 50
- pH less than 7.30 and/or a PaO2 less than 60

  • If an ARF, prepare for possible mechanical ventilation
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64
Q

What is acute ventilatory failure

A

Caused by alveolar hypoventilation, where air cannot move into the alveoli, which decreases gas exchange and leads to a buildup of CO2, which causes respiratory acidosis

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65
Q

What can cause acute ventilatory failure

A

Anything that can affect air flow like:
- Brain trauma
- Neuromuscular dysfunction
- ARDS
- Heart failure
- Ineffective airway clearance
- Drug induced central nervous system depression

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66
Q

What are the signs and symptoms of acute ventilatory failure

A

S/S of hypercapnia, where the high levels of CO2 are causing vasodilation, can be referred to as CO2 narcosis
- Tachypnea
- Headache
- Flushed, wet skin
- Bounding pulse
- Increased BP
- Increased HR
- Lethargic
- Drowsy
- Coma (CO2 narcosis)

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67
Q

Looking at ABGs, how can we diagnosis Acute Ventilatory Failure

A

PaCO2 greater than 50 and pH less than 7.3

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68
Q

What is happening in acute oxygenation failure

A

Hypoxemia (low oxygen) is occurring, where CO2 is diffusing quicker than oxygen, so CO2 leels remain normal, but oxygen levels show they are low

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69
Q

What is happening in acute oxygenation failure

A

There is SHUNTING occurring, where perfusion is fine, but normal alveolar ventilation is lacking, so blood is trying to pick up oxygen in the alveoli, but the alveoli are not working properly, so the blood can’t pick up the oxygen leading to poor oxygenation

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70
Q

For acute oxygenation failure, are we seeing a low or high V/Q ratio

A

A low V/Q ratio, because the ventilation number is going to be low, due to the alveoli not working, but the perfusion number will be fine, because it’s not impacted

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71
Q

What are some disorders that may cause acute oxygenation failure

A
  • Asthma
  • Pneumonia
  • COPD
  • Atelectasis
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72
Q

What ABG number shows oxygenation failure

A

PaO2 less than 60

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73
Q

What are s/s of oxygenation failure

A
  • Dyspnea
  • Tachypnea
  • Increased BP
  • Increased HR
  • Cardiac dysrhythmias
  • Altered LOW
  • Cyanosis
  • Thready pulse
  • Restlessness
  • Confusion
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74
Q

Picture of s/s of hypoxemia

A
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75
Q

Picture of s/s of hypercapnia

A
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76
Q

Obviously if someone is having acute respiratory failure where the body’s organs are not getting enough oxygen, it will lead to organ hypoxia, but what if that person also has decreased cardiac output?

A

The patient is at risk for hypoperfusion or hypoxic organ shock complications like multiple organ dysfunction syndrome (MODS)

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77
Q

What can hypercapnia cause in the body

A

Impaired cellular function and the increase in CO2 can cause vasodilation, which can lead to increased intracranial pressure and decreased cardiac output

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78
Q

Which is worse, oxygenation or ventilation failure? Basically not enough oxygen or too much CO2?

A

Ventilation failure - the buildup of CO2 creating an acidic environment can cause more damage to the body, more quickly

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79
Q

How do negative pressure ventilators work

A

In general, an NPV lowers the air pressure around part of your body, making the pressure “negative.” This creates a vacuum effect that expands your lungs and chest, pulling air into your lungs. Then the machine removes that lower pressure to let your lungs and chest contract, helping you exhale.

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80
Q

What are the benefits of negative pressure ventilators

A
  • Improved communication
  • Ability eat & drink
  • No need for pressurized air or oxygen
  • Lower acuity care
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81
Q

Basically, what is the difference between positive and negative pressure ventilators

A

Positive - increasing pressure on the outside to force air into your lungs
Negative - decreasing pressure on the outside so air will be pulled into your lungs

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82
Q

What is the benefit of non-invasive positive pressure ventilators

A

They are non-invasive, so you don’t have to force an artificial airway into someone and put them at risk for complications like infections and injuries to their airway

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83
Q

What are 3 examples of non-invasive positive pressure ventilators

A
  • BIPAP
  • CPAP
  • Hi-flow nasal cannula
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84
Q

What is the key difference between BIPAP and CPAP

A

CPAP just adjusts the pressure going into your lungs, where a BIPAP can also adjust the pressure coming out of your lungs

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85
Q

What are non-invasive positive pressure ventilators effective for? What are they not effective for?

A

Effective for COPDers and CHF exacerbations

Less effective for ARDS and pneumonia

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86
Q

What are two requirements for a person on a non-invasive positive pressure ventilators

A
  • They have to be alert
  • They can’t be restrained

That way if they vomit or something they can wake up and pull off their mask and roll over

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87
Q

What does a CPAP do? Will the pressure change?
What will the pressure be maintained at?

A
  • Provides continuous positive airway pressure
  • Level of pressure remains the same throughout the breathing cycle
  • Pressure will be between 5-20
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88
Q

What two pressures does a BIPAP utilize

A
  • Inspiratory positive pressure (PIP)
  • Expiratory positive airway pressure (PEEP)

(helps you breath in oxygen and expel CO2)

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89
Q

Is a BIPAP titrated based on FiO2 or LPM?

A

FiO2

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90
Q

What is cool about BIPAPs? Who is this helpful for?

A

They come with a mode called average volume-assured pressure support (AVAPS), which can automatically adjust tidal volumes based on the patients needs.

This is very helpful for hypercapnic patients

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91
Q

What are contraindications for CPAP and BIPAP 6

A
  • Unstable hemodynamic status (unstable cardiac output, etc)
  • Cardiac dysrhythmias
  • MIs
  • Inability to clear one’s own secretions
  • Vomiting
  • Improper mask fit
  • Patient’s in restraints
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92
Q

What should we always check for people on BIPAPs

A

Skin integrity

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93
Q

What are the benefits of a high-flow nasal cannula

A
  • Humidified
  • More comfortable than a BIPAP
  • Allows the pt to eat or drink
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94
Q

How does a high-flow cannula work

A
  • Provides oxygen with compressed air
  • Can go up to 100% FiO2
  • Flow can be up to 60 L/min
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95
Q

What is important teaching about the high-flow nasal cannula

A

Have the pt try to keep their mouth closed, because the PEEP can drop when the mouth is open

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96
Q

Is mechanical ventilation a decision

A

Yes - someone people may not want this “life support”

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97
Q

How do we keep the diaphragm from working during mechanical ventilation

A

We give the pt a paralytic

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98
Q

What do you need from the pt (unless emergent) in order to imtubate

A

Consent

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99
Q

What do we need for intubation (look over)

A

Soft –cuffed ET tube in size requested
Stylet to guide tube in place
Topical anesthetic
Laryngoscope (with blade attached and functional light source)
Suction set up
Syringe for cuff inflation
Water-soluble lubricant (will be applied to tube)
ET holding device or adhesive tape to secure the ET tube post insertion
PPE
Sedative medications
IV access
Stethoscope
Manual resuscitation bag and mask (BVM)

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100
Q

Why might a nasotracheal tube be used during intubation instead of a endotracheal tube 3

A
  • Oral surgery is needed
  • Patient has a limited ability to open their mouth
  • Mandible fractures
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101
Q

What are examples of medications that may be used for intubation - what is important to remember? what is a major side effect of these meds to be aware of?

A

Paralytics:
Rocuronium
Vecuronium
Succinylcholine

Sedatives:
Ketamine
Propofol
Versed
Etomidate

Analgesia:
Fentanyl

Remember that if you’re giving a paralytic, you will also want to give a sedative so the pt doesn’t feel themself being paralyzed

Most can cause hypotension

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102
Q

Who should not receive succinylcholine

A

Those with myasthenia gravis or another neuromuscular disorder

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103
Q

Where can we find these medications for intubation

A

Rapid Sequence Intubation (RSI) kits

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104
Q

What things should we do once a pt has been intubated 4

A

First: listen to the lungs bilaterally to confirm ETT placement
Second: observe for color change on CO2 detector
Third: obtain an order for a chest xray to confirm placement
Fourth: secure airway, noting location of tube at teeth and document (basically want to make sure we know the tube length in case it moves)

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105
Q

Us and who else is is responsible for the day to day care of an intubation? What things are we checking for?

A

RT

Proper placement, oral care, etc.

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106
Q

What if we see someone’s ET tube is not in the right place

A

Call a rapid response (may even be a code), stay with the patient and try to maintain their airway

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107
Q

Should we routinely suction an intubated pt? Why or why not?

A

Not routinely, only as needed. Suctioning is a risk because it can cause sudden respiratory distress, so it should only be done when necessary

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108
Q

What is spontaneous breathing trial

A

Taking the pt off the ventilator for periods of time to see how they do, and slowly start increasing the length of time as they do better and better

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109
Q

What infection is a high risk for ventilated pts

A

Ventilator associated pneumonia, because we’re sticking a tube directly into someone’s airway, which increases the risk of introducing pathogens

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110
Q

Should a pt just randomly be removed from a ventilator

A

NO! They should be weaned off

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111
Q

What are the 4 ventilator modes

A

AC or CMV: Assist Control or Controlled Mandatory Ventilation
Ventilator initiates the breath, ends the breath, or both.
SIMV: Synchronous Intermittent Mandatory Ventilation
Patient does most of the work, but the ventilator intermittently supplies a pre-set breath.
PSV: Pressure Support Ventilation Mode
Decreases the work of breathing by supplying additional pressure to overcome airway resistance. (pt initiates every breath - so pt is regulating everything)
Spontaneous: A mode that allows the patient to breathe on their own. It has a backup rate in case the patient goes apneic.

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112
Q

What is PEEP

A

Applied positive pressure into the airway at the end of expiration to prevent the alveoli from collapsing

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113
Q

Why do we want to keep the alveoli from collapsing using PEEP

A

Peep will keep the alveoli open throughout the breathing cycle, which increases gas diffusion time, which increases gas exchange and stops shunting.

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114
Q

What is peak inspiratory pressure

A

The amount of pressure it takes to deliver the amount of volume needed based on airway resistance and lung compliance

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115
Q

What is a desirable peak inspiratory pressure number

A

Usually 40 or less

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116
Q

What if we see an increase in peak inspiratory pressure

A

This means that the pt is needing more pressure to deliver the preset tidal volume, which means that their pulmonary condition may be worsening (we want to see less pressure needed)

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117
Q

What are the two types of alarms on ventilators

A

High and low pressure alarms

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118
Q

What is a high pressure alarm? What do we do?

A

Telling us that there is an increase in airway resistance

Check pt first!

Look for any coughing, biting on the tube, bucking, secretions in the airway or water in the tubing (all things that may be blocking the tube)

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119
Q

What is a low pressure alarm? What do we do?

A

Indicates no resistance

Check pt first!

Check the connections for an air leak, cuff leak (maybe it deflated), disconnection in the tubing

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120
Q

What are complications from mechanical ventilation

A
  • Hypotension due to increased intrathoracic pressure (because we’re adding more pressure into the chest, which may decrease venous return to the heart, which can lead to low cardiac output)
  • Barotrauma/volutrauma (barotrauma - increased pressure rupturing alveoli - greatest risk with noncompliant lungs, like COPDers, volutrauma - large tidal volumes to noncompliant lungs)
  • Oxygen toxicity
  • Ventilator associated pneumonia
  • Gastric ulcers
  • Increased ICP and decreased cerebral perfusion
  • Tracheomalacia (weaking or erosion of tracheal cartilage)
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121
Q

What are signs that a pt’s airway might not be clear on a ventilator

A

If they are tachycardic, tachypneic or restless

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122
Q

What type of lungs sounds may indicate a need for suctioning

A

Coarse (wet/Rales) lung sounds

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123
Q

What is coughing an indicator of

A

A need to be suctioned

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124
Q

What things can help prevent ventilation complications (picture)

A
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125
Q

Do we want our pt to be sedated if they are intubated

A

Yes

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126
Q

What scale can we use to help guide us on how sedated our pt should be if they are intubated

A

The Richmond Agitation-Sedation Scale (RASS) (basically helps us determine how to titrate their sedation medications so they aren’t overly or underly sedated)

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127
Q

What are signs that a pt may be ready to be extubated

A
  • Cause of respiratory failure is resolved or significantly improved
  • Adequate oxygenation- FiO2 less than 50% and PEEP less than 8 (shows that pt doesn’t need as much support)
  • Spontaneous ventilatory effort
  • Successful spontaneous breathing trial
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128
Q

Besides the obvious (like giving breaths with a bag valve mask, etc), what else do you need to do if someone self-extubates or there is an accidental extubation

A

Turn off the sedation/analgesia

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129
Q

If a tracheostomy tube doesn’t have an inner cannula, what can we use to help keep the area open when we clean

A

An obturator

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130
Q

What is the difference between a cuffed and uncuffed tracheostomy tube

A

Uncuffed (balloon deflated) - allows for airway clearance but doesn’t protect from aspiration (these are for long-term, where there isn’t a need for mechanical ventilation and there isn’t a high risk for aspiration - like the guy I saw at Jiffy Lube, they can eat and talk better with these)

Cuffed (inflated balloon)- allows for secretion clearance, mechanical ventilation and some protection from aspiration

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131
Q

What does it mean if a trach tube is fenestrated

A

It has a little hole in the top of the tube that allows for air to pass, which can help promote spontaneous breathing and possibly allow for “talking” (without a hole here, air can’t get out)

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132
Q

Even if a person has a fenestrated tube or a speaking valve, can they talk if the cuff is inflated?

A

NO, because air is not able to get out and up past the tube

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133
Q

What is some good trach care to know (that isn’t obvious)

A
  • Performing suctioning only as needed (remember the risks of scheduled suctioning)
  • Inner cannula changes if disposable
  • Use sterile technique
  • Clean the stoma with a moist cotton tip swab
  • Change trach ties if wet or soiled
  • Makes sure ties are tight enough so they won’t become dislodged (only one finger should fit underneath (book says 2 fingers))
  • Dressing goes under face plate
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134
Q

What safety things should you have at the bedside if someone has a trach

A
  • Obturator at the bedside
  • New tracheostomy of the same size and one size smaller (so if you can’t fit the same size one back in, you can use the one size smaller)
  • Oxygen
  • Suction
  • Ambu-bag

(these supplies need to go everywhere with the pt, like even to imaging or somewhere else in the hospital)

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135
Q

What are ventilator bundles

A

Ways that we can help prevent ventilator associated pneumonia (VAP)

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136
Q

How can we prevent VAP

A
  • Provide oral care every 2-4 hours
  • Keep HOB between 30-45 degrees
  • Keep ET tube cuff pressure between 20-25 to minimize aspiration risk
  • Hand washing

Other interventions:
- Stress ulcer prophylaxis
- DVT prophylaxis
- Daily sedation breaks and spontaneous breathing trials

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137
Q

When would you call a rapid response

A
  • Changes in mental status
  • Altered level of consciousness
  • Seizures
  • Rapid change in neuro status
  • Changes in vital signs- hypotension, bradycardia, tachycardia
  • Respiratory problems
    Your “gut feeling”
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138
Q

Can anyone call a rapid response

A

yes

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139
Q

What is a code blue or code 99

A

The pt doesn’t have a pulse and/or respirations

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140
Q

What are some code medications to know

A
  • Epinephrine (helps with dysrhythmias, like asystole)
  • Atropine (can help with bradycardia)
  • Sodium bicarbonate (treat acidosis)
  • Amiodarone (for ventricular dysrhythmias)
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141
Q

Be familiar with the roles during a code

A
  • Recorder- Typically the primary nurse
  • Medication administrator- should be familiar with code drugs.
  • Compressor- a team of people should be available to prevent fatigue. Feedback on compression quality is important.
  • Airway- typically respiratory therapy if they are available.
  • Monitor/Defibrillator: May be assigned to the leader or recorder. They pay attention to the rhythm, vital signs, ETCO2.
  • Leader-someone who is ACLS trained, typically a provider, may be a rapid response nurse.
  • Family supporter-typically the chaplain if they are available (we can all be family supporters)
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142
Q

Is bleach/drain cleaner acid or alkaline

A

Alkaline

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143
Q

Does hydrogen ions cause the pH to become more or less acidic

A

More acidic

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144
Q

It’s quick for us to blow off CO2, but how do we excrete fixed acids

A

These need to be excreted from the kidneys, which can take days (they cannot be excreted through expirations)

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145
Q

Do we normally have acid in our body?

A

Yes, acids are a product of normal metabolism (like from carbs) or from abnormal metabolism (like from ketone diets)

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146
Q

What is our base? What does our base do?

A

Bicarbonate HCO3 - it acts like a buffer (where it can combine with hydrogen protons to make the body less acidic)

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147
Q

What organ primarily produces HCO3

A

Kidneys

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148
Q

So how does the carbonic acid-bicarbonate buffer system work (probably don’t need to know)

A

Say you have excess CO2 that your body needs to get rid of, so water will combine with this excess CO2 creating carbonic acid, which then frees

149
Q

So how does the carbonic acid-bicarbonate buffer system work (probably don’t need to know)

A

Say you have excess hydrogen floating around creating an acidic environment, to help create a balance in the pH, bicarbonate will combine with these excess hydrogens (why it’s called a buffer) to form sodium bicarbonate (basically bicarbonate soaks up the extra hydrogen ions)

150
Q

What is the normal PaCO2 level

A

35-45

151
Q

What is the normal HCO3 level

A

22-26

152
Q

What are the compensatory mechanisms that our body has to help adjust to changes in the pH 3

A
  • Buffering (where bases can form with excess hydrogen ions or let hydrogen ions go depending on what is needed)
  • Respiratory - the depth and rate of respirations can adjust based on acid imbalances
  • Kidneys - can adjust the amount of bicarb and hydrogen that is reabsorbed or excreted
153
Q

What are some causes or respiratory acidosis

A
  • COPD (emphysema/bronchitis)
  • Hypoventilation
  • Oversedation
  • Overdose
  • Neuromuscular disease
  • Underventilation on mechanical ventilation
  • Pulmonary edema
  • Atelectasis
  • Pneumonia
  • Bronchospasm
    (basically anything that inhibits you from blowing off CO2)
154
Q

What are some causes of metabolic acidosis 6

A
  • Kidney disease
  • Build up of waste products due to renal failure
  • Buildup of acids due to ketoacidosis
  • Excess losses of bicarb, like from severe diarrhea
  • Accumulation of lactic acid, which can happen during sepsis
  • Aspirin poisoning
155
Q
A
156
Q

What are some causes of metabolic alkalosis

A
  • Extreme loses of chloride or hydrogen ions like from extreme vomiting for gastric suctioning
  • Hypokalemia
157
Q

What type of test do we use when checking for the patency of arteries before drawing ABGs

A

The Allen test

158
Q

Can we obtain an ABG from a central line? Why or why not?

A

No - because central lines are venous

159
Q

Visual review of how the kidneys and lungs work to help normalize the pH

A
160
Q

Visual review of how the kidneys and lungs work to help normalize the pH

A
161
Q

What is happening during resp acidosis

A

pH is low
HCO3 is normal or high
PCO2 is high

(remember ROME, respiratory opposite, metabolic equal)

162
Q

What is happening in resp alkalosis

A

pH is high
HCO3 is normal or low
PCO2 is low

163
Q

What is happening in metabolic acidosis

A

pH is low
HCO3 is low
PCO2 is normal or low

164
Q

What is happening in metabolic alkalosis

A

pH is high
HCO3 is high
PCO2 is normal or high

165
Q

Another helpful picture of acid base imbalances

A
166
Q

What is happening in respiratory alkalosis

A

The lungs are eliminating too much CO2

167
Q

Basically what is causing resp alkalosis? What conditions can cause you to do this?

A

Caused by hyperventilation, where we are “blowing off” too much CO2

Hyperventilation can be caused by:
- Hypoxia
- Brain injury
- Fever
- Overventilation on a ventilator
- Pain
- Anxiety
- Fear

168
Q

Besides hyperventilation, what else can cause resp alkalosis 5

A
  • High altitudes
  • Tumors
  • Trauma
  • Anemia
  • Liver disease
169
Q

What are symptoms of resp alkalosis

A
  • Hyperventilation
  • Dizziness
  • Light-headedness
  • Confusion
  • Headache
  • Tachycardia
  • Dysrhythmias due to hypokalemia
  • N/V
  • Tetany
  • Numbness, tingling in extremities
  • Seizures

(think about when I had a panic attack)

170
Q

How can alkalosis in general impact potassium? What about acidosis?

A

It can cause hypokalemia because it causes the body to excrete potassium and the kidneys are less likely to absorb it

Acidosis can cause hyperkalemia

171
Q

Why does the paper bag trick work for resp alkalosis

A

Well we want to try and increase our CO2 level, so if we are exhaling into a paper bag, then when we inhale we can reabsorb that CO2

172
Q

Besides hyperventilation, what else can cause resp alkalosis 5

A
  • High altitudes
  • Tumors
  • Trauma
  • Anemia
  • Liver disease
173
Q

What is happening in resp acidosis

A

Lungs aren’t blowing off enough CO2, so we have hypoventilation

174
Q

What can cause resp acidosis 8

A
  • Shock
  • Strokes
  • Oversedation
  • Overdose
  • Brain injury
  • Neuromuscular disease
  • Pulmonary edema
  • Pneumonia
  • Bronchospasm
  • Severe atelectasis

(anything that isn’t letting you breath enough)

175
Q

What are symptoms of resp acidosis (a lot)

A
  • SOB
  • Fatigue
  • Exhaustion
  • Headache
  • Drowsiness
  • Confusion
  • Sweating
  • Flushed skin
  • Memory loss
  • Irregular sleep patterns
  • Tremors
  • Difficulty walking
176
Q

What is chronic resp acidosis usually associated with

A
  • COPD
  • Emphysema
  • Chronic bronchitis
177
Q

What can resp acidosis cause in the body

A
  • Shock
  • Organ failure
  • Seizures
  • Increased ICP (remember too much CO2 leads to vasodilation - which can increase the pressure in the brain)
  • Coma
  • Severe kidney disease
178
Q

What are tx for resp acidosis

A
  • Medications to help widen bronchi
  • Anti-inflammatory meds
  • CPAPs and BIPAPS
  • Stopping smoking
    (basically what can we do to help decrease the cause)
179
Q

What is the base excess of deficit

A

A measure of the amount of buffer required to return the blood to a normal pH, this is specific for metabolic imbalances

180
Q

What is the normal range of a base excess deficit?

What is showing metabolic alkalosis, where there is too much base?

What is showing metabolic acidosis, where there isn’t enough base

A

+/- 2 mEq/L

Greater than +2 (basically anything positive is alkalosis)

Less than 2 (basically anything negative show acidosis)

181
Q

What does this base excess of deficit tell us

A

How much bicarbonate or carbonic acid is needed to help normalize pH

182
Q

What can cause metabolic alkalosis

A
  • Overuse of alkaline drugs, like Tums
  • Loss of gastric fluids, like from vomiting or gastric suctioning
  • Steroids
  • Excessive diuretics
  • Overuse of bicarbonates with CPR
  • Baking soda
  • Severe dehydration
  • Cystic fibrosis
  • Electrolyte imbalances
183
Q

What are symptoms of metabolic alkalosis

A
  • Irritable
  • Muscle twitching
  • Muscle cramping
  • Muscle spasms
  • Fatigue
  • Confusion
  • Tremors
  • Tingling and numbness
  • Arrythmias due to hypokalemia
  • Seizures
  • Coma
184
Q

What is the tx for metabolic alkalosis

A
  • Saline infusion
  • Give potassium
  • Give hydrochloric acid
  • Stopping any meds, like diuretics that are causing it
185
Q

What can cause metabolic acidosis (body is producing too many acids for the kidneys to keep up with)

A
  • Diabetic ketoacidosis
  • Uremia with increased phosphates and sulfates
  • Ingestions of acids (aspirin (salicylate) overdose)
  • Lactic acidosis
  • *Diarrhea (you’re loosing too many HCO3s to help balance the acid)
  • GI fistulas
  • Loss of body fluids from GI drains
  • Laxative overuse
  • Hyperaldosteronism
186
Q

What are symptoms of metabolic acidosis

A
  • Accelerated HRs
  • Confusion
  • Dizziness
  • Lethargic
  • Loss of appetite
  • Headaches
  • Nausea
  • Weakness
  • Fruity smelly breath if (ketoacidosis)
187
Q

What are tx for metabolic acidosis

A
  • Sodium citrate
  • IV fluids
  • Insulin drip if dka
  • Remove toxins, like from an overdose
188
Q

What is the anion gap

A

Helps us determine the cause of metabolic acidosis so we know how to treat it based on the difference between cations (sodium, potassium) and anion (chloride, bicarbonate) (basically how many more cations there are than anions)

189
Q

What can cause an elevated anion gap

A

Things that can increase organic acid like the following:
- aspirin toxicity
- DKA
- Uremia

190
Q

What can cause a normal anion gap (compared to a high anion gap)

A
  • GI loss of bicarbonate, like from diarrhea
  • Failure of the kidneys to excrete acids
191
Q

So basically what does a high anion gap tell us? What does a normal anion gap tell us?

A

High = there has been an increase in acid in the body

Normal = bicarb is being lost or the kidneys can’t excrete the acids (more of a body issue)

192
Q

What can anion gap acidosis cause (disturbance of negatively charged anions)

A
  • N/V
  • Malaise
  • Hypercapnia
  • Fatigue
  • Cardiac disfunction
193
Q

What is our tx for anion gap acidosis

A
  • Treat the cause
  • For example, if the anion gap is normal, then give the pt bicarb
194
Q

What are things that can cause anion gap metabolic acidosis (picture)

A
195
Q

What causes an increase in lactic acid (think about when you work out)

A

Impaired tissue oxygenation (either from decreased oxygen delivery or deficient mitochondrial utilization)

196
Q

What are the most common causes of severe lactic acidosis

A
  • Sepsis (where too little oxygen is reaching the body tissues - which is true for all of the below)
  • AIDS
  • Alcoholism
  • Cancer
  • Cirrhosis
  • Cyanide poisoning
  • kidney failure
  • Respiratory failure
  • Severe dehydration
  • DKA
197
Q

What are the primary symptoms of lactic acidosis

A
  • N/V
  • Weakness
198
Q

What is the normal lactic range

A

0.5-1.5

199
Q

What is the tx for lactic acidosis 3

A
  • Treat the underlying cause
  • Administer sodium bicarb
  • Admin IV fluids
200
Q

What are normal ph, bicarb (HCO3) and CO2 levels

A

pH = 7.35-7.45
HCO3 = 22-26
CO2 = 35-45

201
Q

Practice ABGs - know uncompensated, partially and fully compensated.

A
202
Q

What is ARDS

A

A life threatening sudden onset of respiratory failure not caused by heart failure or fluid overload

203
Q

What can cause ARDS 6

A
  • Pulmonary injuries
  • Aspiration pneumonia
  • Sepsis
  • Blood transfusion reactions
  • TBIs
  • Shock
204
Q

What is happening in ARDS? What are the 3 phases?

A
  • Rapid, onset, widespread inflammation of the lungs caused by a condition such as sepsis
    1. Injury/Exudative phase - This leads to an increase in pulmonary capillary permeability, where fluid accumulates and causes alveoli surfactant to wash away leading to alveoli collapse. This leads to shunting, where it doesn’t matter how much oxygen you give, blood won’t get oxygenated (refractory hypoxemia)
    2. Reparative or proliferative phase - Lung tissue gets invaded by neutrophils, monocytes, lymphocytes and fibroblasts (leads to an increase in fibrosis, as these immune system cells destroy pulmonary vascular) Continued shunting and airway resistance
    3. This increase in fibrosis causes remodeling of the lung leading to poor lung compliance
205
Q

What are the early symptoms of ARDS 4 (usually develops within 48-72 hours of the precipitating event)

A
  • SOB
  • Wet lungs/crackles
  • ABG could should respiratory alkalosis from hyperventilation
  • Chest x-ray can show some infiltrates
206
Q

What are late symptoms of ARDS

A
  • Severe SOB
  • Accessory muscle use
  • Increased anxiety
  • Decreased LOC
  • Cyanosis
  • Diaphoresis
  • Tachycardia
  • Cough with sputum
  • Switching over from resp alkalosis to resp acidosis
  • Organ disfunction
  • x-ray shows diffuse infiltrates “White out”
207
Q

How do they diagnosis ARDS

A

They will rule out other conditions, like HF, if other conditions aren’t causing it then they determine it’s ARDS

208
Q

What are complications of ARDS

A
  • Infections- CAUTI, VAP (ventilator associated pneumonia), CLABSI
  • Respiratory- O2 toxicity, barotrauma (explosion of the alveoli during mechanical ventilation), pulmonary emboli, pulmonary fibrosis
  • GI- hypermetabolic state, paralytic ileus, pneumoperitoneum, stress ulcerations & hemorrhage
  • Renal- acute kidney injury (if pt goes into shock, because ARDS puts a pt at a high risk for kidney injuries)
  • Cardiac- decreased cardiac output, dysrhythmias
  • Hematologic- anemia, DIC, thrombocytopenia, VTE
  • ETT related- airway injuries
  • CNS- delirium, PTSD, sleep deprivation, impaired memory
209
Q

What kind of care do we provide to pt’s with ARDS (a lot)

A
  • Oxygenation
  • Possible ventilation
  • Maintain PEEP to stop alveoli from closing
  • Use low tidal volume to stop overdistention of alveoli since they are already damaged from ARDS due to the fibrosis (the alveoli can’t withstand much pressure)
  • Diuretics to try and get rid of fluid
  • Corticosteroids
  • Reposition every 2 hours
  • Prone positioning
  • Permissive hypercapnia (letting there be a little more CO2 than normal so we don’t push too much air into the alveoli and destroy them)
  • Oral care every 4 hours
210
Q

What are warning sign from a pt with ARDS that they might need more care

A
  • Decreased urine output
  • desatting (hypoxemia)
  • Persistent hypotension
  • Really high, extended fever
211
Q

Why is the prone position good for someone with lung issues and accumulate of fluid in lungs?

A
  • In the prone position, the lungs aren’t being compressed by the heart and abdominal organs, like it is in the supine position
  • The prone position redistributes blood and airflow evenly, which helps improve gas exchange
  • Helps with the removal of secretions
  • These pts may require less help from mechanical ventilation, which can help reduce the risks of ventilation, like barotrauma.
  • May improve heart function in some patients
  • Constrictions of the lungs be decreased
212
Q

Why might prone positioning be bad

A
  • Difficult to move patients into this position
  • Can be difficult if intubated
  • Can develop hemodynamic instability
  • Can cause someone people to have worse oxygenation
  • ET tube can get knocked out
213
Q

What drugs can we give for ARDS

A
  • Corticosteroids (want to give early in low doses (do not give high doses or late)
  • Nitric oxide
  • Neuromuscular blockages (paralytics)
  • ECMO
214
Q

What can we use to check how paralyzed someone is (for when they are on a ventilator)

A

Use the “train of four”
“looking for 4 twitches, which indicates baseline”
“go to baseline after receiving paralytic, test with the device looking for 2 twitches, if there are 4 then the pt is too paralyzed, if there are less than 2 then they are not paralyzed enough”

215
Q

What is the purpose of giving someone a paralytic while on a ventilator 2

A
  • Helps with compliance with the ventilator
  • Improves PaCO2 and decreases CO2
216
Q

What is a risk with neuromuscular blockades

A

They can cause profound weakness

217
Q

What is ECMO

A
  • A machine used to bypass the lungs when the lungs are not working, where CO2 is taken out and oxygen is put in.
218
Q

Does an ECMO only help the lungs

A

No, it can also be used to help increase the BP when the oxygenated blood is put back in, which can help cardiac output, because you can either put blood back into the veins (where you would not be affecting pressure or you can put it back into the arteries, where you could increase the pressure to help with cardiac output)

219
Q

What are the indications of ECMO

A

ARDS per definition and at least one of the following:
- PaO2/FiO2 ratio <150
- Murray Score ≥3
- And/or pH <7.2 for at least 3 hours despite standard care at transferring facility
- Age ≤ 80
- Mechanical ventilation for ≤ 7 days
- No known CNS catastrophe or chronic CNS deficit

220
Q

As we get older, what happens to our respiratory system 6

A
  • Diaphragm flattens
  • Chest wall becomes more rigid due to cartilage calcification
  • Respiratory muscles weaken
  • Anterior-posterior diameter of the chest increases
  • Decreased lung compliance
  • Increased air trapping (where we retain air during exhalation, which can lead to an increase in CO2 retention)
221
Q

How can we protect the lungs of our older adults

A
  • Decrease their risks for aspiration
  • Vaccines
  • Encourage exercise
  • Coughing
  • Deep breathing
  • Regular check-ups
  • Watching their weight
222
Q

Picture of age related changes

A
223
Q

What is asthma

A

Bronchial hyperreactivity with reversible expiratory airflow limitation

224
Q

Asthma is known to cause air trapping, what can this lead to?

A

Can trap expiratory air, which is CO2, which can lead to an increase in CO2 in the body, which is respiratory acidosis

225
Q

What is the “triad” of symptoms of asthma

A
  • Dyspnea
  • Wheezing
  • Cough
226
Q

What are the big 3 things that are happening to a pt’s airway if they have asthma (aka the big 3)

A

inflammation in your airway, the muscle bands around your airways constricting (bronchospasm), increase in mucous

227
Q

What does a rescue inhaler do for asthma pts

A

Helps to loosen the tight muscle bands

228
Q

Does a rescue inhaler help decrease the inflammation? What if it doesn’t?

A

No - it only helps loosen the tight muscles

This is why you need a controller medication to help decrease the inflammation

229
Q

Once an asthma pt has a flare up and it’s been treated, what are they at an increased risk for

A

Having another flare up within a few days

230
Q

What is some good pt teaching to avoid asthma triggers

A
  • Avoid stressors
  • Know your triggers
  • Avoid getting sick, as this might trigger an attack
231
Q

If someone is having persistent asthma, where they are having constant inflammation in the airways, what are they at risk for (why we want to avoid these asthma attacks)

A

Irreversible Remodeling of the lung tissue

232
Q

Why might someone develop asthma

A
  • Genetics
  • Environmental (smoke, pollen, etc)
  • GERD
  • Exercise induced
  • Respiratory infections as a child
233
Q

What are the two categories of asthma medications that someone might take

A
  1. Quick relief (rescue) medications
  2. Long-term control medications
234
Q

What is our rescue medication? What is the most common med?

A

Short acting beta-adrenergic agonist (SABA), most common - albuterol

235
Q

What do SABAs do? How long do they last? What is the risk? What is good teaching?

A
  1. They stimulate beta adrenergic receptors in the bronchioles to produce bronchodilation
  2. They work within minutes and can last for 4-8 hours
  3. Should be used cautiously in pts with cardiac disorders, because they can increase BP, HR and increase the risk for dysrhythmias
  4. Don’t want to overuse this drug - because overuse can decrease effectiveness
236
Q

What are our long-term treatments for asthma

A
  1. Inhaled corticosteroids (like Flovent)
  2. Leukotriene modifiers (like Singulair) can be used to block leukotrienes, which decreases inflammation and helps promote bronchodilation.
  3. Long-term beta agonists (LABAs) () open the airway and reduce swelling for 12 hours
237
Q

What are our long-term treatments for asthma 4 (she’s not going to ask specific names - just have a general idea)

A
  1. Inhaled corticosteroids (like Flovent)
  2. Leukotriene modifiers (like Singulair) can be used to block leukotrienes, which decreases inflammation and helps promote bronchodilation.
  3. Long-term beta agonists (LABAs) (solumedrol) open the airway and reduce swelling for 12 hours. Only taken in combination with corticosteroids.
  4. Long acting Muscarinic (if LABAs don’t work) (combined with steroids)
238
Q

What does it mean if someone is status asthmaticus

A

They are not responding to the standard tx of asthma

239
Q

What are the signs of status asthmaticus

A
  • Use of accessory muscles
  • Reduced peak expiratory flow rate
  • Inability to speak
  • Severe SOB
  • Anxiety
  • *Fatigue
  • *Decreased LOC
  • ABGs showing hypoxemia
240
Q

What can status asthmaticus die from

A
  • Hypoxemia
  • Sudden cardiac arrest
  • Complications from mechanical ventilation
241
Q

What is the “silent chest”

A

When a pt has been wheezing, and then suddenly there is an absence of wheezing and the pt is struggling to breath (this is a life-threatening emergency and can be a sign of status asthmaticus)

242
Q

How do we classify the severity of asthma? What are the different levels?

A

We classify using a peak flow meter

Mild (green) = FEV1 greater than 80%

Moderate (yellow) = FEV1 between 50-80%

Severe (red) = FEV1 less than 50% (this is a medical emergency

243
Q

If someone has had a lot of asthma exacerbations in the past, what are they at risk for

A

Having a severe attack

244
Q

Why do we see resp. acidosis in our asthma pts

A

Because they are hyperventilating, and their airways are constricting, so they can get some air in, but they can’t get air out, so that CO2 gets trapped in there (remember - hyperventilation = CO2 retention)

245
Q

What is our tx for asthmaticus

A
  • Give IV corticosteroids
  • Give SABA
  • Theophylline (help promote muscle relaxation and get rid of extra fluid) (nasty side effects/drug interactions, need to have levels monitored)
  • Anticholinergics (Ipratropium bromide) (helps with bronchodilation - more effective for COPDers)
  • Helium/oxygen mixture
246
Q

What is a last resort for asthma pts? Why?

A

Ventilation

  • Bronchoconstriction can worsen directly after placement of ET tube
  • Also the increase pressure from ventilation can damage the airway
247
Q

What is heliox

A

A mixture of lower density oxygen and helium that can be used to decrease the resistance and work of breathing

248
Q

What are indications for mechanical ventilation for asthma pts

A
  • RR over 40
  • Can’t talk
  • Accessory muscle use
  • Intercostal retractions
  • Fatigue
  • Solumence
  • Hypoxia
  • Hypercapnia
249
Q

If an asthma pt is on a ventilator, what do we want to do

A
  • Have the ventilator set to a low tidal volume (so we’re not forcing air into airways that are constricted, otherwise we can make air trapping worse)
250
Q

What is COPD

A

Chronic inflammation that causes the obstruction of airflow being able to get out

251
Q

Generally, do COPDers have both bronchitis and emphysema

A

Yes

252
Q

What is the inflammation in COPD doing to the lungs

A
  • Changing and narrowing of lungs
  • Increases goblet cells (increase in thick mucus)
  • Scar formation
  • Long-term narrowing
  • Destruction of alveoli walls, which leads to a decrease in elasticity and recoil
  • Thickening of lining of airway due to hypertrophy
253
Q

What is chronic bronchitis in COPDers? What is it termed as?

A

Presence of a cough and sputum production for at least 3 months in each of the 2 consecutive years

Termed blue bloaters

254
Q

How can you get exacerbations of bronchitis in COPDers

A

When things like allergens or an infection triggers it

255
Q

What is the emphysema in COPDers

What are they known as

A

Destruction of alveoli without fibrosis

Pink puffers

256
Q

What does a pink puffer look like (emphysema)

A
  • Purse their lips on expiration (why they’re called puffers)
  • Barrel chest due to hyperinflation of the lungs (air is trapped in the lungs)
  • Thin (burning off a lot of calories from breathing so much)
  • SOB
  • Severe dyspnea (happens early compared to bronchitis)
  • HYPERVENTILATION (these guys are going to be breathing fast to try and get rid of CO2)
  • Hypoxemia occurs late
  • Damage occurs distally, so they don’t have an issue getting CO2 out early in the disease
257
Q

What do blue bloaters (chronic bronchitis look like)

A
  • Overweight (due to air trapping)
  • Cyanotic (hypoxemia occurs early)
  • Peripheral edema
  • Rhonchi and wheezing
  • Chronic cough
  • Have CO2 retention because the damage occurs distally in the bronchioles, therefore trapping CO2
  • Dyspnea later (compared to emphysema)
258
Q

What are COPDers at risk of developing (besides lung cancer)

A

Heart disease

259
Q

Basically what is happening in COPD

A

It’s obstructive - so you can’t get the air out

260
Q

What is interesting about COPD exacerbations

A

Sometimes we can find a cause, like smoking, but others don’t have a cause at all (it’s random)

261
Q

What is our tx for COPD exacerbations

A
  • Positive pressure ventilation
  • Mechanical ventilation
  • Small, frequent meals to conserve energy
  • Plan care appropriately to conserve energy
262
Q

What are signs of a COPD exacerbation

A
  • Chest tightness
  • Tachycardia
  • Decrease in energy
  • Decreased LOC (due to CO2 retention)
  • Increase in sputum
  • Increase in wheezing
  • Increase in accessory muscle use
263
Q

What medications can we give for COPD exacerbations

A
  • Increased dose of a SABA (like albuterol)
  • Antibiotics if they have an infection
  • Oxygen
  • IV corticosteroids
  • CPAP, BIPAP, ventilator
264
Q

What can the end stages of COPD lead to

A
  • Spontaneous pneumothorax
  • Cor pulmonale (enlarging of heart)
265
Q

Why is pursed lip breathing good

A

It allows better expiration by increasing airway pressure, which can help keep air passages opening during exhalation leading to an increase in CO2 exhalation (so we’re not retaining so much CO2)

266
Q

Healthy people (non COPDers) are stimulated by high levels of CO2 to breath, what about COPDers?

A

They are actually stimulated by oxygen to breath, so if you give them a bunch of oxygen they will lose their drive to breath (Max 2 liters)

267
Q

Where do PEs often end up at in the lungs

A

The lower lobes

268
Q

What most often causes PEs

A

DVTs

269
Q

What condition is the leading cause of preventable in-hospital deaths

A

PEs (basically preventing PEs from occurring can save a lot of people)

270
Q

What are the 4 different types of PEs

A
  • Fat embolism
  • Amniotic embolism
  • Septic embolism
  • Venous air embolism
271
Q
  1. What are causes of a fat embolism?
  2. What are signs of a fat embolism?
  3. What is the tx for a fat embolism?
A
  1. Long bone trauma and/or orthopedic surgery (basically fat in our bones can become dislodged and travel)
  2. Petechiae, tachypnea, hypoxia, confusion, drowsiness, fever, tachycardia, dyspnea, coma. (symptoms occur 12-72 hours after event)
  3. Supportive care, no specific tx
272
Q
  1. What causes an amniotic embolism?
  2. What are signs of amniotic embolism?
  3. What can it cause?
  4. What is the tx?
A
  1. When amniotic fluid mixes with mom’s blood and the mother suffers an immune response from the baby’s blood, which can lead to hypercoagulability, which puts them at a greater risk for clots.
  2. Shock, severe hypoxemia, DIC, neurologic changes (seizures).

3.Obstruction, vasoconstriction, coagulopathy and ARDS.

  1. Treat the heart and lung failure, CPR, DIC (treat hemorrhage), replenish volume

(this one sounds really serious, and sounds like it puts women at a high risk of death - treat as if they are coding)

273
Q
  1. What are risk factors for developing a septic embolism
  2. What are symptoms?
  3. How do we treat?
A
  1. IV drug use, central lines, endocarditis, implanted devices, periodontal disease.
  2. Fever, cough, hemoptysis (coughing up blood)
  3. Treat the infection with antibiotics and/or remove the infection source
274
Q
  1. How does someone get a venous air embolism?
  2. What is the lethal amount of air that can kill someone?
  3. What does an air embolism cause?
A
  1. Can be from air in an IV line, from trauma where air enters into circulation, from a surgery with an incision above the heart, scuba divers can have this happen.
  2. 3-5 mL/kg
  3. Vasoconstriction in the lungs, pulmonary HTN, injury to capillary epithelium, pulmonary edema.
  4. Oxygen, position on the left side in Trendelenburg
275
Q

Why do we want to position a pt with an air embolism on their left side in Trendelenburg

A

Prevents the air bubble from traveling out of the right ventricle and into the lung

276
Q

Why do we want to position a pt with an air embolism on their left side in Trendelenburg

A

Prevents the air bubble from traveling out of the right ventricle and into the lung

277
Q

What three things (Virchow’s triad) puts someone at higher risk for developing clots

A
  • Venous stasis (from immobility, severe varicose veins, polycythemia vera (thickening of the blood and high RBC count)
  • Hypercoagulability (genetic, birth control pills, sepsis, pregnancy, cancer)
  • Venous (endothelial injury) (like from surgery, trauma, infection, central venous catheters)
278
Q

What are signs/symptoms of PEs

A
  • Tachypnea
  • Dyspnea
  • Pleuritic chest pain (pain with inspiration, especially on the side where the embolism is lodged)
  • Apprehension (Sense of impending doom)
  • Cough
  • Fever
  • Tachycardia
  • Findings of a DVT
  • Hemoptysis (coughing up blood)
  • Shock
279
Q

When we’re doing an assessment on someone with a possible PE, what might we oberve

A
  • Crackles, wheezing in lungs
  • Fever
  • Massive PEs we see hypoxemia, decreased LOC, hypotension, feeling of impending doom
280
Q

What are the 3 categories of PEs

A
  • Massive (5% of people)
  • Submassive (20-25%)
  • Usual (majority)
281
Q

What can severe PE cause

A

Hemodynamic issues like:
- Pulmonary HTN (all this blood is trying to get to the area that is blocked, this increases the pressure in the lungs)
- Right sided failure (caused by heart working really hard to get blood to the blocked part of the lung)
- Sustained hypotension, where SBPs are less than 90 for over 15 minutes

282
Q

Some people can get small little PEs consistently overtime, what does this do to the heart?

A

It can cause right sided heart failure, because the heart has been working so hard to overcome those blockages.

283
Q

What are complications from PEs 2

A
  • Pulmonary infarction (death of lung tissue) which can cause alveolar necrosis, hemorrhage, pleural effusions or abscesses
  • Pulmonary hypertension (occurs when over 50% of the pulmonary vasculature bed is affected - usually from multiple PEs)
284
Q

What are risk factors for developing pulmonary infarction

A
  • When the occlusion is in the medium-large vessels
  • When there is insufficient collateral blood flow
  • When there are 2 or more pre-existing lung conditions
285
Q

How do we diagnosis a PE

A
  • Spiral CT using contrast
286
Q

What if a pt can’t have contrast

A

They can do a V/Q scan (ventilator/perfusion) - it examines airflow and perfusion in the lungs

287
Q

What are our txs for PEs

A
  • Give oxygen
  • Anticoagulation to help prevent further emboli (either unfractionated heparin or lower molecular weight heparin) (warfarin started and pt should continue at home use for 3-6 months)
  • Thrombolytic therapy (tpa) for severe cases to dissolve the clot (risk for bleeding)
  • Embolectomy (removing the emboli) (requires bypass - very big surgery!)
  • Vena cava filter to prevent the migration of clots if someone is having a lot of them or they can’t go on anticoagulant therapy
288
Q

What do we give a PE pt if they go into shock

A
  • Fluid
  • Vasopressors
289
Q

What is a good test for DVTs

A

Homans sign, where there may be a DVT present if there is pain when the foot is flexed

290
Q

What are signs of DVTs

A
  • Unilateral leg swelling (one leg)
  • Pain/tenderness
  • Cramping
291
Q

What are nursing considerations for PEs

A
  • Monitoring their ABGs
  • Lung assessments
  • O2 therapy
  • Monitor ptt if on heparin
  • Platelets if they’re having thrombocytopenia
  • Monitor for heparin induced thrombocytopenia (HIT)
  • Monitor for signs of bleeding (bruising, etc)
  • Monitor INR if on warfarin.
292
Q

What is heparin induced thrombocytopenia HIT? What might indicate that someone has it?

A

Low platelets (platelets are needed to clot blood)

Normal platelet range is 150,000-400,000

293
Q

What is a normal INR? What if you’re on warfarin?

A

Normal = less than 1

On warfarin = 2-3

294
Q

What is a normal ptt? What if you’re on heparin?

A

Normal = 30-40 seconds

On heparin = 47-70 seconds (2 times the normal value)

295
Q

What is flail chest

A

When 3 or more adjacent ribs are fracted in two or more places causing the segment to separate from the rib cage, this causes the lung to deviate when inhaling and exhaling (very painful!)

296
Q

What are signs of a flail chest

A
  • Pain!!!
  • SOB
  • Tachypicnia
  • Increase in HR
  • Shallow breathing (taking big breaths is painful) = causes hypoxemia
  • *Paradoxical chest movements (chest isn’t moving symmetrically)
  • Crepitus
297
Q

What can a flail chest lead to

A

Pneumo or hemothorax

298
Q

What is the tx for flail chest

A
  • Pain meds
  • Surgery (may also heal on its own)
  • Possible ventilation to fix hypoxemia
299
Q

What is a pneumothorax

A

When air enters the pleural cavity

300
Q

What are the 2 ways that a pneumothorax can be classified? What are they?

A
  • Open (air is coming in through the chest wall from the outside, like from a penetrating wound)
  • Closed (No external wound, but a rib may have punctured it)
301
Q

After trauma to the chest wall, what should we always expect

A

Pneumothroax

302
Q

What is a spontaneous pneumothorax? What can cause it?

A
  • Small blebs (air-filled sacs) on the surface of the lung rupture, which can lead to a pneumothorax
  • Causes: COPD, asthma, cystic fibrosis, pneumonia, tall and thin patients, asthma, smoking, pneumonia
303
Q

What can cause an iatrogenic pneumothorax

A

Healthcare procedure

304
Q

What is a tension pneumothorax

A

When air enters the pleural space but it can’t get out, this increase in pressure causes the lung to collapse.

305
Q

What is a chylothorax

A

Presence of lymphatic fluid in the pleural space due to trauma or malignancy

306
Q

What are signs of a pneumothorax

A
  • Signs of chest trauma
  • Tachypnea
  • Tachycardia with possible dysrhythmias
  • SOB
  • Diminished or absent breath sounds on the affected side
  • ABG (see a decrease in PaO2 and SaO2, and respiratory alkalosis
  • Sharp pain on the affected side
  • Shallow breaths
307
Q

If symptoms of a pneumothorax are pretty severe, what do we think it is

A

Tension pneumothorax

308
Q

What are the signs of subcutaneous emphysema? Does it need to be treated?

A
  • Tenderness over the site (usually around the chest tube and crepitus)
  • It usually doesn’t need to be treated as it will typically resolves on its own by being reabsorbed.
309
Q

What is a tension pneumothorax

A

Where air is sucked in, basically through a one way valve, and can’t get back out (think of the valve on my paddle board)

310
Q

Besides the lung collapsing, what is also bad about a tension pneumothorax

A

It increases pressure on things like your trachea, heart, esophagus, and great vessels and shifts them towards the unaffected side.

311
Q

What are the symptoms of a tension pneumothorax

A
  • SOB
  • Chest pain
  • Tachycardia
  • decreased or absent breath sounds on affected side
  • Severe dyspnea
  • Profuse diaphoresis
  • Hypotension and shock
  • *Tracheal deviation (late sign)
312
Q

Picture of emergency management of chest injuries

A
313
Q

What emergency supplies should you have at the bedside for chest tube patients

A
  • rubber tipped hemostat (clamps)
  • Sterile water (she didn’t say this one in lecture)
  • Occlusive petroleum dressing
314
Q

What are nursing duties for the insertion of a chest tube

A
  • Position pt with the affected side’s arm raised above their head
  • HOB at 30-60 degrees
  • Prepare local anesthetic like lidocaine for the provider
  • Cover chest tube site with occlusive dressing with petroleum jelly
  • Give pain medications
  • Check connections
  • Make sure they get an x-ray to confirm placement
315
Q

What are the 3 chambers on a chest tube drainage device and what do they do?

A
  1. Collection chamber (collects air or fluid)
  2. Water seal chamber (acts as a one-way valve allowing air out but preventing air from flowing back into the patient)
  3. Suction control chamber (regulates the amount of negative pressure that is being exerted into the pleural space)
316
Q

What is the goal of chest tubes

A

To restore the negative pressure in the thoracic cavity

317
Q

How do we confirm placement of chest tube

A

X-ray

318
Q

How often do you assess blood/fluid in the chest tube collection chamber

A

assess amount, color and consistency every 1 hour after insertion of chest tube for the first 8 hours then once every 8 hours and prn.

319
Q

How much water goes into the water-seal chamber

A

2cm of sterile water

320
Q

Is brisk bubbling in the water seal chamber expected upon insertion

A

Yes, usually right when the chest tube is placed there will be brisk bubbling

321
Q

What is tidaling? Is it expected? When will it go away?

A

Movement of water in the chamber with breathing

It is expected and should go away once a lot of air has been removed and the lung is getting back to normal

322
Q

Would we be concerned if a new chest tube is not tidaling

A

yes!

323
Q

When should we notify the provider about possible issues

A

More than 100mL of drainage within the 1st hour of placement

Drainage turns from a dark brown color to a bright red color

Eyelets sticking out (cover and notify the doctor)

(note - changing positions can cause an increase in output or changes in drainage color, etc)

324
Q

What might tell us that there is an air leak?

A

Continuous bubbling

325
Q

Is intermittent bubbling ok?

A

Yes, it usually happens when the pt is moving around, this just indicates that there is still air in the intrapleural space

326
Q

Should we ever clamp a chest tube for long periods of time? Why or why not?

A

No - it can cause a tension pneumo

327
Q

What are the two types of chest tube suction chamber

A
  1. Dry
  2. Water
328
Q

For water suction chamber chest tubes (not dry), what does high or low levels of water produce?

A

High levels of water = more suctioning

Low levels of water = less suctioning going on

329
Q

In a water system suction chamber, would we see constant bubbling

A

Yes, we will see continuous bubbling.

330
Q

Can we “milk” clots out of a chest tube? What about stripping

A

Yes, we can use gentle “milking”, but no stripping

331
Q

How can we find an air leak? What do we do if we find it in the chest or at the insertion site?

A

Start with clamping the tube close to the chest - if the bubbling stops, then we know that the leak is coming from the insertion site or in the chest.

Reinforce the dressing and notify the provider

332
Q

If a pt with a chest tube is going to imagining, should we clamp their chest tube?

A

NO! This may cause a tension. Their drainage system can go with them.

333
Q

What do we do if a chest tube becomes dislodged 4

A
  1. Immediately cover insertion site with sterile occlusive petroleum dressing
  2. Tape three sides of the dressing, leaving one side open for air to escape.
  3. Notify provider asap.
  4. Stay with the pt and monitor for signs of respiratory distress.
334
Q

What do we do if the chest tube itself becomes disconnected

A

Reestablish the water seal by immersing the tube into sterile water while a new system can be setup

335
Q

What are signs that the chest tube may be ready to come out

A
  • Pt status has improved
  • Decreased drainage (less than 100 mLs/24 hours)
  • Air leak resolved
  • X-ray shows re-inflated lung
336
Q

What are the 4 different thoracotomy’s

A
  1. Pneumonectomy: removal of one entire lung
  2. Lobectomy: removal of one or more lobes of the lung
  3. Segmentectomy: removal of one or more portions of a lobe
    4.Wedge resection: removal of a small wedge (triangle shape) section of the peripheral lung
337
Q

Is shallowing breathing ok after a chest surgery

A

NO! We want them to deep breath to avoid getting pneumonia.

338
Q

What are some complications of a pneumonectomy

A
  • Possible vocal cord dysfunction
  • Pulmonary edema
  • Empysema (collection of pus in the pleural cavity)
  • Postpneumonectomy syndrome (where there is a medial sternal shift towards the side where the lung was removed -causing tracheal obstruction)
339
Q

What are symptoms of postpneumonectomy syndrome

A
  • Dyspnea
  • Cough
  • Stridor
  • Dysphagia
340
Q

How can we treat postpneumonectomy syndrome

A

Usually will have to have surgery to have a prosthetic placed to keep the sternum from shifting

341
Q

What is the most common reason why someone might have a pneumonectomy

A

Lung cancer

342
Q

What is a pneumonectomy

A

The whole lung and associated vessels are removed leaving an empty space that eventually fills with fluid

343
Q

Where are we cutting in a median sternotomy

A

Right down the middle, like for heart surgeries

344
Q

Where are anterior and post lateral thoracotomies on the body (where they make incisions)

A

Right under the boob in the front (laterally - like horizontal)

Right under the shoulder on the back (horizontal as well)

Between the 4th and 5th intercostal space

345
Q

What is the benefit of video assisted thoracoscopic surgery

A

It is minimally invasive

346
Q

What kinds of procedures may use video assisted thoracoscopic surgery 3

A
  • Diagnosis conditions like obtaining biopsies
  • Lung resections (like taking out a small piece of lung)
  • Pleural effusions
347
Q

What things should we do post-op

A
  • Pain control (especially because we want to encourage them to cough and deep breath, which they are more likely to do if they are not in pain)
  • IS, coughing, deep breathing
  • Splinting
  • “Huff coughing” (get a little bit up at a time)
  • Monitor CBC, especially watching hemoglobin, as low hemoglobin can lead to hypoxia (oxygen doesn’t have anything to bind with)
348
Q

What is a normal hemoglobin count

A

12-18

349
Q

What is pulmonary vascular resistance

A

There is so much resistance in the pulmonary system, that the right ventricle has to work really hard to pump blood out to the lungs, but it can’t pump it all out, so this leads to an increase in afterload, which leads to right heart failure.

350
Q

What can cause pulmonary vascular resistance

A

constriction

351
Q

What things can cause pulmonary vascular resistance

A

Conditions that cause chronic hypoxia will increase vascular resistance through constriction, edema, etc.

352
Q

What does pulmonary vascular resistance lead to

A

Pulmonary hypertension

353
Q

What is pulmonary hypertension

A

Elevated pulmonary artery pressure due to an increase in resistance to blood flow - typically pressure is greater than 25 at rest and 30 with exercise (normal should be 12-16)

354
Q

What are the 2 types of pulmonary hypertension

A
  1. Idiopathic (unknown)
  2. Caused by a condition
355
Q

What are signs of pulmonary hypertension

A
  • SOB
  • Extreme fatigue
  • Syncope
  • Symptoms worsen with movement
  • Dizziness
  • High HR
  • Chest pain
  • Palpitations
  • Peripheral edema (they have edema because fluid and backed up into their body)

(it causes right sided HF, so think of symptoms of right sided HF)

356
Q

What is another name for right sided HF

A

Cor pulmonale

357
Q

What is a definitive diagnosis of pulmonary hypertension

A

Cardaic Catheterization looking for the average pressure in the pulmonary artery (high pressure at 25 at rest or 30 with exercise can indicate pulmonary hypertension )

358
Q

What are the txs for pulmonary hypertension

A
  • Oxygen
  • Sildenafil (viagra) = vasodilation
  • Epoprostenol (Flolan)
  • Lung transplant
  • Calcium channel blockers to decrease HTN
  • Furosemide to decrease preload
  • Warfarin to decrease clotting
359
Q

What is flash pulmonary edema

A

In the alveoli and interstitial spaces, where there is a rapid accumulation of fluid (don’t confuse with pleural effusion, where pleural effusion is fluid in the pleural space)

360
Q

What can cause flash pulmonary edema 4

A
  • *Left sided HF (where fluid is backing up into the lungs)
  • Complication from thoracic surgery
  • Hypertensive crisis
  • ABRUPT change in heart condition (body doesn’t have time to compensate)
361
Q

What are symptoms of flash pulmonary edema

A
  • *pink/red colored froth sputum
  • SOB
  • Decreased O2
  • Tachycardia
  • Chest pain
  • Cold clammy skin
  • Dizziness
  • Diaphoresis
  • Anxiety
  • Fear (feelings of drowning)
362
Q

What tx can we give for flash pulmonary edema

A
  • Oxygen
  • Diuretics to get rid of sudden excessive fluid
  • Nitro to help open up constricted vessels
  • Morphine to help with SOB feeling
  • Ventilation if needed
363
Q

What is pleural effusion

A

Abnormal collection of fluid in the pleural space

364
Q

What are the two types of pleural effusions

A
  1. Transudative (caused by protein poor fluid, *HF (most common cause), liver disease)
  2. Exudative (caused by inflammation usually from infection, where there can be empyema (which is a collection of purulent fluid in the pleural space))
365
Q

What are symptoms of pleural effusion

A
  • Chest pain that is usually worse in coughing and deep breathing
  • Fever
  • Chills
  • Rapid breathing
  • SOB
  • Diminished breath sounds over that area
366
Q

What are txs of pleural effusion

A
  • Thoracenteisis
367
Q

What can rapid thoracentesis cause

A

Rapid removal of too much fluid can lead to hypotension, hypoxemia, or re-expansion of pulmonary edema (this is why we want to remove fluid slowly and not too much so we don’t cause this)

368
Q

What is a tx if someone keeps having pleural effusion

A

Chemical pleurodesis, which uses chemicals to create fibrous tissue to help prevent the effusion

202A (5 decks)

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