Respiratory Assessment Flashcards

(217 cards)

1
Q

PPV-Increased FRC

A
  • FRC is the volume in the lungs at the end of a tidal breath
  • When PEEP/CPAP is used
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2
Q

Alveolar Minute Ventilation (VA)

A

More accurately represents the effective ventilation (the minute volume actually responsible for maintaining the PaCO2)

ṾA = RR x (VT-VDphys)

So it requires accurate measurement of VDphys

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3
Q

Lower Infection Point

A

lower inflection point on inspiratory limb = place where there is a sudden increase in compliance (set PEEP here to maintain FRC)

Change in the slope at the lower end of the inspiratory curve

Some think that this point can be used to help recruitment of all/most/some of the collapsed and recruitable alveoli -> helps at setting PEEP

The above assumption has been questioned because there are many limitations to this approach: recent ventilation history, variability due to underlying lung disease, presence of decreased compliance of the abdominal and chest wall, the greater importance of the expiratory component of the curve.

pig tail at the bottom indicates patient triggering (bigger the pig tail, higher the WOB to trigger breath)

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4
Q

Diagnostics

A

Sputum Culture and Sensitivty

Bronchoalveolar Lavage

Diagnstic Imaging-CXR, CT, V/Q Scan

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5
Q

PPV and Nervous System

ICP and Cerebral Perfusion

A

CPP=MAP-ICP

May decrease CPP secondary to a decreased in mean BP (compromised cardiac function)

CPP can be affect from both sides because MAP may decrease and ICP will increase

ICP increases secondaryto a increased CVP (as venous return from the head may be reduced)

Hyperventilation (PaCO2 < 35) causes cerebral vasoconstriction therefore decreases CP and ICP

This is a temporary effect!

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6
Q

PC CMV Absolute Pressure

Decreased Ti sec

A

Ti tot Decreased

Te Increase

I:E Decrease

Pmean Decrease

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7
Q

Tracheostomy Tubes Assessment

A
  • Size/type
  • Cuff pressure
  • Inspection of stoma site
  • Inspection and assessment of securing method
    • The ties should be just snug enough to get two fingers underneath
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8
Q

Types of Deadspace

A
  • Anatomical Deadspace (VDanat)
    • Volume of gas in the conducting airways
    • ~ 1 mL/lb = 2.2 mL/kg
  • Alveolar deadspace (VDalv)
    • Volume of gas ventilating unperfused alveoli
  • Physiological deadspace (VDphys)
    • The total of anatomical and alveolar deadspace
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9
Q

Arterial Partial Pressure of Oxygen

A

Abbreviation: PaO2

Description: Oxygen content in arterial blood

Normal: 100-80 mmHg

Measured: ABG

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10
Q

Low Anion Gap

A

= disruption of anion balance; usually due to a loss of HCO3- balanced by an increased Cl-

  • Gastric losses of HCO3-
  • Diarrhea
  • (Note: not vomiting—this causes hypochloremia and alkalosis)
  • Renal loss of HCO3-
  • Renal tubular acidosis
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11
Q

PC CMV Absolute Pressures

Decreased in Compliance

A

Vt Decrease

Ve Decrease

Ti dyn Decrease

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12
Q

PaCO2

A

The best index of effective ventilation

Is dependant upon the balance of CO2 production and alveolar minute ventilation

It is the inverse of VA (Avleoar minute ventilation; and how fast we are blowing off CO2)

If you have a high CO2 the you are not ventilating

If you have a low CO2 you at least have the ability to do so but we still need to figure out why you are doing it

VCO2 is how fast we are producing CO2

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13
Q

PPV Shunt and Deadspace

A

There is increased deadspace ventilation as well as an increased shunt in a mechanically ventilated patient resulting in an overall V/Q mismatch

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14
Q

PC CMV Absolute Pressure

Increased in PEEP

A

PIP Decrease

Pplat Decrease

Pmean Increased

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15
Q

Types of Trach Tubes

A

Fenestrated-If both the inner and outer cannula are fenestrated suctioning can go through both tubes and poke someone in the back of the neck

Cuffed

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16
Q

PPV and GI System

A

Increased permeability of gastric mucosa

Increased GI bleeds and gastric ulcers in mechanically ventilated patients

Consider use of antacids or H2-blocking agents to reduce gastric secretions

Potential for gastric distension if PPV done via mask

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17
Q

PC CMV Delta Pressure

Decreased Rate

A

Ve Decreased

Te Increases

I:E Decrease

Pmean Decrease

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18
Q

PC CMV Delta Pressure

Increased Ti sec

A

Ti tot Increased

Te Decrease

I:E Increased

Pmean Increased

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19
Q

Ventilator Associated Lung Injury

A

Ventilator-Induced Injury also be called Ventilator Associated Lung Injury (VALI), which will capture other problems that can be associated with PPV

VAP, air-trapping, ventilator-patient dsy-synchrony (vent is not responsive to patient’s breathing efforts which is uncomfortable and can be dangerous if there are double breaths)

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20
Q

VC VMC Decreased Resistance

A

PIP Decreases

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21
Q

IPPA

A

The first thing that should be done is a visual inspection to make sure that the patient is stable

Should repeat the appropriate part of the assessment (at a minimum) after an intervention is completed

Trends are always important

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22
Q

Measuring Compliance Clinically

A

Truly we are measuring total compliance (Ctotal)

The compliance of the lung (CL) and chest wall (CW) combined

Does CTOTAL = CL + CW ?? NO!

Because the lung and chest wall work in opposite directions, the compliance is effectively half the original components

Ctotal = (CL * CW) / (CL + CW)

The assumption is made that the chest wall compliance is unchanging, thus; changes in Cstat can reflect changes in CL.

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23
Q

PC CMV Absolute Pressure

Increased Rate

A

Ve Increase

Te Decrease

I:E Increase

Pmean Increase

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24
Q

What determines how long for breath to get out of the body

A

It is passive so compliance, resistance, (time constant)

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25
VC-CMV Vt Increased
Everything will increase with the exception of Ve which decrease and I:E Ratio which increased (specifically the E portion of this ratio will decrease)
26
PPV-Increased Deadspace Ventilation
* Normal VD/Vt is 0.25-0.40 but is increased to 0.40-0.60 in mechanical ventilation * Distribution of a positive pressure breath goes more to the apices and less to the bases compared to a spontaneous breath * This happens because in the apices the whole weight of the lung will be pulling down so that the alveoli is already stretched/opened * Ex. When the patient is standing up the lung will be pulling down
27
PPV and the CVS
* Positive pressure ventilation will impede venous return and may result in decreased CO and therefore decrease BP * Hypotension rarely occurs in normal individuals receiving PPV due to the body’s compensatory mechanisms * Altered right and left ventilicular function * Decrease endocradial blood flood
28
Peak Inspiratory Pressure
The maximum pressure delivered during Does not necessarily reflect pressures in the lungs
29
VC VMC Increased Resistance
PIP Increases
30
Lung Protective Strategies-Ensure the correct placement of ETT
Want 3-5 cm above the carina as the tube will move as the head moves, and if we do not have a buffer zone it can extend too far
31
Compliance
A measure of the distensibility of the lung Reciprocal of elastance Normal is 60-100 mL/cmH2O \< 25 - 30 cmH2O in ARDS
32
PC CMV Delta Pressures Resistance Decreased
Ti dyn Decreased
33
Disorders and changes in Cstat and CL
Dirsorders in which changes in Cstat may not be reflective of changes in the CL!
34
VC CMV PEEP Decrease
PIP Decrease Pplat Decrease Pmean Decrease
35
How if Oxygen Carried in the Blood
1) Hemoglobin (Hb) * Oxyhemoglobin * Major carrier of O2 * 1.34 of O2 per gram of Hg (when fully saturated) 2) Dissolved in plasma * Determined by Henry’s Law * Account for a small percent of O2 transport * 0.003 mL/dL/mmHg * PO2\*0.003=ml/dl dissolved O2
36
CvO2 Calculation
CvO2=(Hb x 1.34 ml/g) \* SvO2 + (PvO2 x 0.003 ml/100ml/mmHg)
37
Shunt fraction %
\<10%-Compatible with normal lungs 10%-19%-Seldom requires significant ventilatory support 20%-29%-Significant abnormality; requires PEEP or CPAP 30% or more-Severe disease; life-threatening; requires aggressive mechanical ventilation with PEEP
38
Anion Gap
The anion gap is the difference between the measured cations and the measured anions Helps determine whether a decrease in HCO3- is due to disruption of normal anion balance or the presence of an abnormal acid anion (i.e. cause of a metabolic acidosis) Anion Gap = (Na+) - (Cl- + HC03-) Normal: 9 – 14 mmol/L
39
PC CMV Pressure Control Delta Increased PC
PIP Increased Pplat Increased Vt Increased Ve Increased Pmean Increased
40
Non-Invasive Interface Assessment
Assess mask fit/leak Patient comfort Observation of skin necrosis/irritation
41
VC CMV Increased Compliance
PIP Decrease Pplat Decrease
42
What Forces need to be Overcome for Breathing
When it comes to ventilation the pt. has to overcome reistance (non-elastic resistance-diamater of the airways) and compliance (elastic resistance), and these are not static forces
43
PPV-Air Trapping
* With increased airway resistance more time is needed for exhalation * Pt. still in exhalation when the ventilator gives next breath so the air that was not exhaled is now trapped * If there is not enough time before the next breath it will result in air-trapping * Air-trapping or auto-PEEP, can also be a result of obstructive lung disease (asthma, COPD) * Auto-PEEP can be measured through an expiratory pause maneuver
44
Atelectrauma
* Injury that results due to a **repeated opening and closing of the alveoli** at low lung volumes * Can also result in volutrauma because air will only want to enter the open alveoli * The collapse itself it not always damaging even though it can cause V/Q mismatching but where atelectrauma is damaging is the repeated opening and closing * Associated with **inadequate PEEP** as an appropriate PEEP will prevent de-recruitment of alveoli * Physiologic PEEP is generally 3-5 cmH2O and is caused by the backpressure in the larynx when the vocal cords are closed * Minimum PEEP is 5 cmH2O * In neonates can be associated with inadequate CPAP * A longer Ti and higher PEEP will also allows for more alveoli to open * Usually occurs in dependent area
45
Mean Airway Pressure
The average pressure delivered over one minute, as measured by the ventilator
46
Oxygen Saturation
**Abbreviation:** SpO2 **Description:** Oxygen content in arterial blood **Normal**: \>90% **Measured:** Pulse Oximeter
47
PPV and Renal System
* Response from hemodynamic changes * Urinary output (UO) when CO causes renal perfusion * Endocrinological Effects * Increased ADH release * Decreased ANP release * Activation of the renin-angiotensin-aldosterone system * Abnormal ABGsPaO2 results in decreased renal function and UO * Function is dramatically decreased when \< 40 mmHg * PaCO2 \> 65 mmHg decreases kidney function
48
When assessing Oxygenation and Ventilation What do we Look at
Ventilator Settings ABG, SpO2, ETCO2, TC Ventilator Orders
49
Endotracheal Tube Assessment
* Size/Type * Depth * Should be the same as confirmation on CXR or adjusted to such * Position in the Mouth * Should be repositioned Q24 or more frequently * There are ETT attachment devices that will allow you to easily move the ETT without undoing everything and to help prevent pressure sores * Cuff pressure * There are automated cuff pressure monitors * Inspection and assessment of the securing method * Look for any skin necrosis/irritation
50
PPV and Muscle Function
Any muscle not being used is subject to atrophy In patient’s with prolonged mechanical ventilation both muscle endurance and strength is compromised
51
VC CMV Decreased Compliance
PIP Increases Pplat Increase
52
PC CMV Delta Pressure Decreased Ti sec
Ti tot Decreased Te Increase I:E Decrease Pmean Decrease
53
Lung Protective Strategies-Sigh Breaths
Avoid sigh breaths with high tidal volumes and long inspiratory pauses These sigh breaths are not used very much anymore
54
Alveolus Partial Pressure of Oxygen
**Abbreviation:** PAO2 **Description:** The oxygen content at the alveolus **Calculation:** PAO2= [FiO2- (Pbaro-PH2O)] - PaCO2/0.80
55
PC CMV Delta Pressures Increased in Compliance
Vt Increase Minute Ventilation Increase Ti Dyn Increased
56
Where is the air in a subcutaneous emphysema
Where is the air in a subcutaneous emphysema is when the air collects underneath the skin
57
Causes of a High Anion Gap
= presence of an abnormal acid * Lactic acidosis * Ketoacidosis * Diabetes or alcohol abuse * Toxins * Methanol * Ethylene glycol * Propylene glycol * Aspirin (acetylsalicylic acid) * Uremia (kidney failure)
58
Oxygen Toxicity
Want to try and keep FiO2 lower than 60% as above which this risk for O2 toxicity will greatly increase So just because a blood gas looks good does not mean there is no work to do
59
VC CMV Increased Flow
PIP Increased Tidyn Decreased Titot Decreased Te Increase I:E Decreased
60
PC CMV Absolute Pressure Decreased Rate
Ve Decreased Te Increases I:E Decrease Pmean Decrease
61
Deadspace (VD)
The volume of gas that is inhaled but does not take part in gas exchange VDphys = VDanat + VDalv As deadspace increases the work of breathing to maintain alveolar ventilation is increased For a given PaCO2, as the VD is increased the ṾE must increase as well, in order to maintain PaCO2 At ṾE \> 10 LPM there is increased probability of respiratory failure developing 2° to muscle fatigue
62
Lung Protective Strategies-Minimize De-Recruitment and Atelectrauma
Use the appropriate PEEP By minimizing the risk of these VILI will minimize the release of inflammatory mediators and the resultant biotrauma
63
A reliable index of poor oxygenation...
A reliable index of poor oxygenation is if FIO2 \> 0.50 and PaO2 \< 100 mm Hg and this means that the patient is getting a lot of oxygen but for some reason it is not getting into their blood
64
PPV-Increase Intrapulmonary Shunt
Perfusion will go to gravity dependent areas and ventilation will go to gravity independent areas The gravity dependent areas will be located on the posterior side when the patient is lying on their back
65
Oxygen Index
OI = (FiO2 \* MAP \*100) / PaO2 A calculation that takes into account the mean airway pressure (MAP) If you are using FiO2 as a decimal then times by 100 if you are using it was a whole number then you do not need to multiple by 100 Positively correlated with mortality risk You want a low OI (the lower the better) with \<5 being normal When you are in the 20 you need to begin to look at things such as ECMO because you lungs can no longer properly oxygenate the blood
66
Assessing Ventilatory Mechanics
* Always looking to see if the follwing are changed * Compliance * Resistance * Auto-PEEP * Done through an assessment of the: * Ventilating pressures/volumes * Waveforms
67
P(A-a)O2 Critical Number
Critical Numbers \> 350 mmHg when a person is on oxygen
68
Biotrauma
The lung will release inflammatory mediators that will attack lung tissue, as a result of volutrauma and/or atelectrauma This results in lung injury that resembles ARDS **The inflammatory mediators can also enter the systemic circulation and result in injury in other organs.** Meaning that poorly manage ventilation can lead to serious organ dysfunction in other areas of the body. All of the blood in the body will pass through the lungs which is why the inflammatory mediators can travel to the other parts of the body. This also means that severe injury/infection from other parts of the body can result in ARDS from the inflammatory mediators released from other parts of the body
69
Arterial O2 Content
**Abbreviation:** CaO2 **Description:** Total amount of oxygen contained in arterial blood (going to the body) **Calculation:** CaO2=(Hb x 1.34 ml/g) \* SaO2 + (PaO2 x 0.003 ml/100ml/mmHg) **Normal**: 16-22 mL/dL (vol %)
70
Lung Volume Recruitment Maneuver
Over time the alveolar units will collapse when awake we will sigh or yawn to help prevent this collapse, when a patient is sedated and paralyzed they will be unable to yawn or sigh meaning we will have to do it for them Use high pressure at 30-40 and hold for 30-40 seconds
71
VC-CMV-Decreased Rate
Minute Ventilation Decreases Te Increases I:E Decrease
72
Oxygen Dissociation Curve-Left Shift
* **Increased Affinity for Oxygen** * Decreased temp * Decreased 2-3 DPG * Decreased [H++] * Increased pH * CO * Because once it has bound to CO it will want to bound with more O2 but it is still easier to bond with CO because there is a stronger affinity
73
The Transmission of Positive Pressure
* Positive pressure ventilation (and use of PEEP) will increases intrapleural pressure, because how much of the pressure we are pushing in it transmitted to pleural membrane, as well as and intrathoracic pressures * The extent of the transmission is dependent on: * **Amount of PEEP and PPV** * This become more and more of an issue and PEEP and PPV becomes higher * **Lung compliance** * Low C (e.g. ARDS): Pressure transmission significantly reduced * Low compliance means that there is a higher elastic recoil (stiff lungs) and the lungs pulling inwards working against our positive pressure ventilation trying to push outwards * High C (e.g. COPD): Pressure transmission is highest * Can be regionally affected due to disease process-eg. pneumonia, atelectasis * **Thoracic compliance** * Thoracic compliance is the resistance of the chest to expansion * Hemodynamic compromise is most likely to occur when thoracic compliance is low (e.g. Abdominal distension, thoracic deformities-Kyphoscoliosis)
74
VC CMV Decreased Flow
PIP Decrease Tidyn Increases Titot Increases Te Increases I:E Increases
75
Plateau Pressure
Reflects the pressure in lung at end inspiration Requires an inspiratory pause maneuver to measure
76
PC CMV Absolute Pressures Resistance Increased
Ti dyn Increase
77
Murray Lung Injury Score
* Quantifies the level of lung injury in ALI/ARDSe * A composite score that takes into account the following four factors: * CXR findings * PaO2/FiO2 * PEEP setting * Lung compliance * No lung injury would be a score of 0 * Not commonly used clinically but can be used more in research * The specific scoring will not be testable (but what is above will be)
78
P/F Normals
Normal P/F ratio is 400 to 500
79
VC CMV PEEP Increase
PIP Increase Pplat Increase Pmean Increases
80
VC-CMV-Increased Rate
Minute Ventilation Increases Te Decreases I:E Increases
81
Ventilator-Induced Injury
The effect of PPV on the respiratory system
82
DOPE
When a person deteriorates rapidly well on a mechanical vent we can use the acronym of DOPE, which stands for * **D**isplacement of ETT * **O**bstruction of ETT * At this point try to suction the placement, and if the suction gets stuck it means that there is an obstruction * **P**neumothorax * Preventing air from entering the lungs. * When there is a rapid deterioration you will not have enough time to get an x-ray so it is at this time you will want to use your IPPA to determine the likelihood of a pneumothorax * **E**quipment Malfunction
83
PC CMV Absolute Pressures Resistance Decreased
Ti dyn Decreased
84
Shear Stress
Related to atelectrauma This is the strain exerted on the alveolar wall between the expanded lung unit and de-recruited lung unit Occurs in interstitial space between the open and the closed alveoli Capillary injury and release of inflammatory mediators results This can be a common problem in neonates as the alveoli can collapse easily, and is why we tend to use CPAP with neonates to keep the lung open
85
Therapeutic Interventions
Chest Tubes Humidity Bronchopulmonary Hyigene- VAP Protocol, CPT, bronchoscopy Ventilator Strategies-Lung proctective, LVRM, prone proning Readiness for weaning
86
PC CMV Delta Pressures Decrease in Compliance
Vt Decrease Minute Ventilation Decrease Ti Dyn Decrease
87
Lung Protective Strategies-Appropraite Volumes
* Use appropriate volumes and make sure not to over ventilate * 6-8 mL/kg in normal lungs and 4-6 mL/kg in ARDS * Maintain alveolar pressure \<30 cmH2O * Consider permissive hypercapniaWe don’t always need to ventilate to normal blood gases as sometimes a high CO2 can be used as a protective strategy * People will not die because there high CO2 is high they will die because their O2 is low, meaning we should sacrifice ventilation before we sacrifice oxygenation * It is more important to monitor pH than CO2, but we can get orders to just keep pH higher than 7.25
88
PC CMV Absolute Pressure Decreased in PEEP
PIP Increased Pplat Increased Pmean Decreased
89
Monitors
Pulse oximeters Co-Oximeters Capnographers Transcutaneous
90
Pharmacological Intreventions
Inhaled Medications Systemic Respirtory Medications Specialty Gases
91
Ventilator Assessment
Because this is a complexed task it overlap different assessment categories * **Basic Assessment** * Basic respiratory parameters * Because ventilator is ventilating the lung, part of chest assessment is checking the ventilator * **Non-Patient Assessment** * Circuits * Device check * Preventative Maintenance * **Monitoring and Diagnostics** * Continuous display of waveforms/parameters * Lung mechanics and WOB * **Therapeutic Intervention** * Supports respiratory system
92
PPV-Pulmonary Vascular Resistance
* May decrease due to an improved ABGs * Giving oxygen will dilate vasculature * May be increased due to compression of alveolar capillaries and over distension of alveoli * Can also result in a decreased pulmonary perfusion * This means that both hypoxemia and high pressure from PPV can cause higher PVR, so in order to reverse it we need to known the mechanism that it causing it * This is difficult to determine at the bedside, but new technology is coming out in order to make this easier
93
Where is the air in a Pneumothorax
Pneumothorax is when air leaks into the space between the lung and chest wall
94
PPV and Thoracic Pump
* **Spontaneous Breath** * Diagram contracts to create a negative pressure and the negative pressure will also stretch the vena cava and pulls the venues blood from extremities against gravity, ultimately improving venous return to the heart. * **Positive Pressure Breath** * The opposite is occurring because we are pushing pressure in and making atrium smaller and restricting venous return. * We are also assuming the right ventricular output will decrease as well. * What the picture below is showing will not happen for all pt. as some pt. may be more susceptible than others
95
Disorders that cause Increase Compliance
**Increased Lung Compliance** * Improvement in any of the above, pulmonary emphysema **Increased Thoracic Compliance** * Improvement in any of the above, flail chest, position change—sitting patient up
96
Non-Patient Assessment-Ventilator Related
* Ventilator Circuit Changed * Scheduled Change * Soiled * Leak Test Failure * Humidification Delivery Changes * Ventilator Change * Routine Change for PM * Changed- Mechanical Failure * Not Changed-Patient Unstable * Device Checks Performed * Automated * Pressure Test
97
PC CMV Absolute Pressures Increased in Compliance
Vt Increase Ve Increase Ti Dyn Increased
98
Oxygen Dissociation Curve-Right Shift
* **Reduced Affinity (tendency to bind) for Oxygen** * Increased temp * Increased 2-3 DPG * Increased [H++] * Decreased pH * A decrease in the amount of O2 associated with hemoglobin in response to a decreased pH is known as the Bohr Effect
99
Non-Patient Assessment
Airway Safety Equitment Suction Equitment Humidification Equitment Vent/Circuit Maintenance
100
Oxygen-Dissociation Curve
As each of the four binding sites on a Hgb molecule binds to an O2 molecule its attraction to other O2 molecules will increase. This is why there is the steep curve at the beginning. Once all the binding sites have been filled up (hemoglobin is saturated) the curve will plateau. This point will be at a saturation of 90% and a PaO2 of ~60 mmHg. **Above this point big changes in oxygenation will result in small chnges in PaO2.** At sat of 50% there is a PO2 of 27 Review curve shifts Right sided shift- increased temp, increased CO2, decreased pH (increased hydrogen ion concentration), increased 2,3 DPG. So increased everything except pH which decreases
101
PPV and Psychological States
The continued stress of mechanical ventilation can result in: * Insomnia/Sleep Deprivation * Anxiety/Frustration * Withdrawal Syndromes * Depression * Feelings of helplessness, loss of control * Can become psychologically dependent upon the machine * Fear
102
VC-CMV Vt Decrease
Everything will decrease with the exception of Ve which increase and I:E Ratio which decreased (specifically the E portion of this ratio will increase)
103
VC CMV Decreased Insp. Pause
Titotal Decrease Te Increase I:E Decrease Pmean Decrease
104
TIME CONSTANT
**Time Constant=Resistance x Compliance** ## Footnote A single time constant is the time it will take to inflate 63% of alveolar units Five time constants is when all alveolar units are expanded RR can be broken down to inspiratory time and by default exhalation time If exhalation time is too short then we can have air trapping Strategies to increase Te= Decrease Ti
105
Causes of a High P(A-a)O2
**Oxygen is not being effectively transferred from alveoli to the blood** ## Footnote V/Q Mismatch Right to Left Shunt Alveolar hypoventilation Diffusion Defect
106
PPV-Mechanical Bronchodilation
Positive pressure dilates the conducting airway
107
Volutrauma
Related to a **high transpulmonary pressure** that results in a **overdistension of the alveoli,** as air will always follow the path of least resistance and will then over distend the non diseased alveoli sac If the sac becomes rupture and not just over distended then it is considered to be barotrauma not volutrauma The stretch in the alveoli will cause a “leaky” AC membrane (gaps between the alveoli cells) which cause **edema formation** in the area which results in the release of inflammation mediators and a presentation that is similar to ARDS (massive inflammation in the lungs) and the edema can leak secondary into the alveoli
108
P/F Ratio \< 300 and \<200
\< 300 = in acute lung injury (ALI) also known as early ARDS \< 200 = in acute respiratory distress syndrome (ARDS)
109
Hypoxemia Classifications
Normal PaO2= 100-80 mmHg Mild PaO2= 60-79 mmHg Moderate PaO2= 40-59 mmHg Severe PaO2= Less than 40 mmHg
110
Barotrauma
The most acute, immediate, and severe form of VILI Risk increases with the level of alveolar pressure (Pplateau) and the extent of lung injury or previous lung disease Will occur from trying to push air in too fast Results in air outside of the alveoli (extra-alveolar air) due to the positive pressure rupturing the A/C membrane Can result in air-leak disease (diseases when air collects outside of the alveoli)-Subcutaneous emphysema, pneumothorax, pneumomediastinum
111
PC CMV Absolute Pressure Increased Ti sec
Ti tot Increased Te Decrease I:E Increased Pmean Increased
112
PC CMV Delta Pressures Resistance Increased
Ti dyn Increase
113
PC CMV Delta Pressure Increased in PEEP
PIP Increased Pplat Increased Pmean Increased
114
PaO2/FiO2 Ratio Definition
The ratio of partial pressure arterial oxygen and the fraction of inspired oxygen Will help to determine the degree of any problems with how the lungs transfer oxygen to the blood
115
Lung Protective Strategies-PEEP
Use PEEP cautiously in patients predisposed to alveolar rupture Monitor for auto-PEEP
116
Pressure vs. Volume Loop-Compliance
Compliance (imaginary line between start of inspiration and expiration) **Increased Compliance** * Left Shift of the curve * Ex. Advanced Emphysema **Decreased Compliance** * Decreased volume for pressure change * Will be a right shift of the curve * Ex. Pulmonary Fibrosis
117
Where is the air in a Pneumomediastinum
Pneumomediastinum is when air collect into the mediastinum
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What is Vol %
Vol% is equal to ml O2/ 100 ml of blood The amount of O2 in mls that is in 100 ml of blood
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VD/VT
The ratio of physiological deadspace to tidal volume Normal VD/VT = 0.2-0.4 ICU common to be \>0.70 \>0.60, patient is unlikely to sustain spontaneous ventilation VD/ VT = (PaCO2 - PECO2) / PaCO2 When CO2 goes up, pH will go down For end tidal CO2 (PaCO2) which DOES NOT EQUAL PeCO2 which is the total amoutn of CO2 removed in one minute PeCO2 will be given whenever we have to calculate deadspace
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PPV and the Liver
Impaired liver function 2° to decreased CO PEEP has more impact on hepatic blood flow than PPV (PIP)does
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Where is the air in a Interstitial emphysema
Interstitial emphysema is when air collects in the lung supportive tissue known as pulmonary interstitium
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PC CMV Pressure Control Delta Decreased PC
PIP Decrease Pplat Decrease Vt Decrease Ve Decrease Pmean Decrease
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Some results from an IPPA will require an action before a complete assessment can be completed
* Tactile Fremitus and Crackles on Auscultation * Complete suctioning * High WOB * Adjust ventilator settings
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When a wedge pressure is higher the 18 what are we concerned about
When a wedge pressure is higher the 18 non cardiogenic pulmonary edema is likely to occur
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P(A-a) Normals
In a healthy pt. 21% O2 (room air) will produce a gradient of 5-15 mmHg (10-20 in elderly) Normal A-a gradient=Age divided by 4 plus 4 Ex. A 40 year year old should have an A-a gradient of less than 14 100% O2 gradient is 100-150 mmHg The normal range will change depends on how much oxygen the patient is on. This means that the value of using A-a calculation for determining oxygenation will decrease as the patient is on an increased FiO2 (most useful when on room air)
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Non-Patient Assessment-Suction Equipment
* Reason for Changing Open Suction Catheter * Soiled * Faulty Valve * Sticky Catheter * Cutting of Sleeve * Faulty Instill Pot * Suction Equipment Changed * Yankuer * Yankuer Holder * Closed Suction Catheter * Suction Tubing * Canister Liner
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Auto PEEP
**Extrinsic PEEP (= PEEPext = PEEPset)** * Directly set on the vent **AutoPEEP or Intrinsic PEEP (= PEEPauto = PEEPint)** * Cannot be determined by simple observation of the ventilatory pressures; can be determined to be present through inspection of the expiratory flow waveform * Requires an *expiratory pause maneuver* to measure (i.e. quantify) **Total PEEP (PEEPtot)** * Reflects the total pressure in lung at end expiration PEEPtot= PEEPext + PEEPauto
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Upper Inflection Point
upper inflection point = maximum setting for peak airway pressure Has been proposed as a way to detect overdistention in the lungs, but this approach appears to be too simplistic as other parts of the lungs will already be over distended by the prior to reaching this point ‘Beak’ or ‘duckbill’=increase in airway pressure without any appreciable increase in volume
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Shunt: QS/QT Calculation
Qs/Qt= (CcO2-CaO2)/(CCo2-CvO2) Where: Qs = Pulmonary Physiologic Shunt (mL/min) Qt = Cardiac Output (mL/min) CCO2 = End-pulmonary-capillary Oxygen Content CaO2 = Arterial oxygen content CVO2 = Mixed Venous Oxygen Content
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Alveolar Air Oxygen Difference P(A-a)O2
This is a measure of the difference between the alveolar concentration of oxygen and the arterial concentration of oxygen Will be used to help diagnose the source of hypoxemia and whether it is an intrapulmonary or extrapulmonary problem Will help to assess the intgreity of the alveolar capillary unit
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Ventilator-Induced Injury Categories
Ventilator-Induced Injury can be divided into the following categories * Barotrauma * Volutrauma * Atelectrauma * Biotrauma * Oxygen Toxicity
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Time Constant
The time required to inflate (or deflate) a lung region Complete filling requires 5 time constants 1 TC = 63% 2 TC = 86% 3 TC = 95% In a pressure-controlled breath can be determined by the time it takes for equilibration to occur Time Constant= Resiatance x Compliance
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PPV and CVS- Pt. Most at Risk
Most people will not be affected by this as the body will be able to compensate it is the septic, spinal injury patient that will be very problematic as we exceed the body’s capacity to compensate Hemodynamically unstable patients (low BP etc.) Patients with high lung compliance or low thoracic compliance (as transmission of the positive pressure to the thoracic space is greatest in these patients) Worst case is a COPD pt. (higher lung compliance) with low thoracic compliance
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PC CMV Delta Pressure Increased Rate
Ve Increase Te Decrease I:E Increase Pmean Increase
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How Can the Pressure versus Volume Loop Be Measured
Can be measured as a dynamic or static technique Dynamic: Requires a square inspiratory wave form to interpret – constant flow and no inspiratory pause Static: Requires paralysis and measures of pressure with small incremental in volume
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Shunt: QS/QT
The shunt equation looks at the extent to which venous blood bypasses the capillaries (oxygenation) of the lungs Increased if pulmonary venous admixture occurs (mixed venous blood exits A/C membrane unchanged)
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Alveolar- Air Oxygen Difference
**Abbreviation:** P(A-a)O2 **Description:** A measure of the difference between the alveolar concentration of oxygen and the arterial concentration of oxygen **Normal:** Age divided by 4 plus 4 **Calculation**: PAO2 - PaO2
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Bronchopulmonary Hygiene
When assessing bronchopulmonary hygiene we need to look for * Color * Consistency * Tolerance by the patient * Cough * Spontaneous * With Stimulation * Not Present * Assess for Trends * Total passes of suctioning needed
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Dynamic vs. Static Compliance
**Dynamic Compliance:** Done during dynamic conditions (i.e. airflow), thus is impacted by Raw! Not too useful clinically. Cdyn = VTeff/ (PIP - PEEPtot) **Static Compliance:** Done during static conditions (i.e. no airflow), thus is a reflection of compliance only! Cstat = VTeff/ (Pplat - PEEPtot)
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At the core of it what is ABGs measuring
Gas Exchange
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Oral and Trach Care
Oral and trach care can and often is done at the same time
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Non-Patient Assessment-Airway Equipment
* Bedside Respiratory Safety Equipment * Manual Resuscitator * Masks * Airway * Airway * PEEP Valve * Trach Bag * Oxygen Tank * Wire Cutters * Intubation Supplies * Cricothyrotomy Tray
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PC CMV Pressure Control Absolute Increased PC
PIP Increased Pplat Increased Vt Increased Ve Increased Pmean Increased
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Pressure vs. Volume Loop
A graphical representation of the relationship between pressure and volume during inspiration and expiration Spontaneous breaths go clockwise and positive pressure go counter clockwise In pressure control or PS the loop is almost square because of pressure limiting during inspiration Bottom of loop is either 0 or PEEP level Top of loop = PIP
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Disorders that Increase Resistance
Small ETT, plug in ETT, biting on ETT Increased bronchospasm, mucosal edema, secretions, and/or airway obstruction Increased inspiratory gas flow rate
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VC CMV Increased Insp. Pause
Titotal Increase Te Decrease I:E Increase Pmean Increases
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PC CMV Pressure Control Absolute Decreased PC
PIP Decrease Pplat Decrease Vt Decrease Ve Decrease Pmean Decrease
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Minute Ventilation
VE Will typically be monitored by the ventilator VE=RR x Vt
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Pressure Volume Loop-Leaks or Air Trapping
Loop won’t meet the bottom
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Resistance
The frictional resistance to gas flow Varies; is dependant on the driving pressure Changes throughout inspiration and expiration thus, most commonly, and more simply, calculated during constant flow (ie. VCV) Normally 1 to 2 cmH2O/L/sec Intubated, probably 5 to 10 cmH2O/L/sec or more Raw = (PIP – Pplat) / flow Transwairway Pressure is (Pm – Palv)
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Disorders that Result in Decreased Compliance
**Decreased Lung Compliance** * Atelectasis, pneumonia, pulmonary edema, ALI/ARDS, pneumothorax, fibrosis, bronchial intubation **Decreased Thoracic Compliance** * Obesity, ascites, chest wall deformity
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Difference between hypoxemia and hypoxia?
Hypoxemia is defined as a condition where arterial oxygen tension (Pao2) is below normal (normal Pao2 = 80–100mmHg). Hypoxia is defined as the failure of oxygenation at the tissue level. Generally, the presence of hypoxemia suggests hypoxia. However, hypoxia may not be present in patients with hypoxemia if the patient compensates for a low Pao2 by increasing oxygen delivery. This is typically achieved by increasing cardiac output or decreasing tissue oxygen consumption. Conversely, patients who are not hypoxemic may be hypoxic if oxygen delivery to tissues is impaired or if tissues are unable to use oxygen effectively. Nevertheless, hypoxemia is by far the most common cause of tissue hypoxia.
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PC CMV Delta Pressure Decrease in PEEP
PIP Decrease Pplat Decrease Pmean Decrease
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Disorders that Decrease Resistance
Bronchodilator administration Suction and airway care Use of lower inspiratory gas flow rate
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PPV and Metabolism
* PPV takes over all or part of the WOB * Decreased O2 consumption and CO2 production by respiratory muscles but… * Hypermetabolism is associated with major illnesses/surgical procedures * Proper nutritional intake for patient’s size and illness; malnutrition a major concern * But we now have a tube down their throat blocking their ability to swallow making it more difficult to provide nutrition * Morphine will also slow down time to move food throughout the body making even more of a problem because the body needs more nutrients
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Oxygen Saturation of 90%
This is the minimum oxygen concentration that is needed to provide enough oxygen to prevent ischemia in the tissues Once the O2 sat falls below 90%, the PaO2 drops quickly into the dangerously hypoxic range as fewer and fewer oxygen molecules are bound to Hgb. We want to try to keep O2 saturation above 90%.
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Pressure vs. Volume Loop-WOB
Line drawn down middle of loop On inspiration (area to right side of line) On expiration (area to left side of line)
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When we are trying to improve oxygenation in ventilation in a pt. what can we do?
1) Increase PEEP 2) Increase FiO2 3) Increase Titotal * Increase mean airway pressure by increasing the I:E ratio * 1:1 is a higher I:E ration compared to 1:4 (think of it as 1/1 and ¼ and then then answer for 1:1 is 1 and for 1:4 is 0.25)
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PRVC Increased Compliance
PIP Decreases Pplat Decreases Tidyn Increases Pmean Decreases
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PRVC Decreased Compliance
PIP Increases Pplat Increases Tidyn Decreases Pmean Increases
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PRVC Decreased Compliance
Decreased Tidyn
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Aspects of WOB
* Mechanical * Elastic and non-elastic work * Metabolic * Oxygen consumption * Relationship of work, rate and depth of breathing to muscle fatigue * Readiness to Wean from ventilator
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WOB- Inspiration
Associated with the amount of negtaive pleural pressure that is generated during a ventilatory effort 2/3 Due to Elastic Resistance 1/3 due to Non-Elastic Resistance
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WOB- Expiration
Normally passive High Raw may need more expiratory muscle wokr
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Directly Measuring WOB
Uses an esophageal pressure monitor to reflect intrapelural pressure changes The pressure time product is calculated from the area underneath the generated curve PTP is a simpler measure than WOB and will parelle the change in effort and VO2 cost of breathing
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Pressure Volume Curve
Will be narrow and long in restrictive diseases Will be wide in obstructive lung diseases
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WOB in Normal States
We will try to breath while using a minimal amount of work A normal healthy young adult will have a Vt of 500-600ml
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Work of Breathing in Diseased States
Fast breathing will produce high flow rates which increases Raw Large tidal volumes will require a strech in the lung and increase elastic work Both of the above will increase WOB but the body will adapt a RR and Vt in mimize WOB
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Oxygen Cost of Breathing
The amount of O2 that is consumed by the ventilatory muscles (VO2R) will give and estimate of respiratory effort Noral is 2-5% of total VO2 Upon dsypnea this can increase to 30% and even up to 10 times normal amount in COPD. Will also increase with obseity, fibrosis and congestive failure Measures by (not commonly used) **VO2R=VO2 in active breathing-VO2 apnea**
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Patient-Ventilator Synchroncy
The compatability between the patient bretahing effort and the ventilator Important to consider: Mode, Phase Variables
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Patient-Ventilator Synchroncy-Triggering
Can be seen on patient assessment as well on the monitor it will look like random swiggly lines in between breath
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Patient-Ventilator Synchroncy- Limit Varible
In volume control if the limit variable is not set properly we may not be meeting inspiratory demands of the patient and instead of a straight steady increase on the pressure waveform there will and a depressed upwards curve In pressure control the patient will be able to compenstate for the limit varaible through varying flow and volumes
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Patient-Ventilator Synchroncy- Time Cycling
Ideally we want to see pressure equilibrium at the end of inspiration in pressure limited mechanical breaths
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Patient-Ventilator Synchroncy- Flow Cycling
Many vents will allow for the adjustment of the flow cycle level Tailor to pt, and situation
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Pulse Oximetry
Non-invasive measurement of arterial oxygen saturation An oximeter is an instrument that measures the amount of light absorded/ transmited through the blood Based on photoplethysmography and spectrophotometry
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Photoplethysmography
Uses light absorption to detect tiny volume changes that occur in the tissues due to blood pulsing in the vascular beds The amount of light that is absorbed is proportional to the amount of blood flow Maximum absorption during systols and minimum during diastole So this detects perfusion/ pulsatile blood flow
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Spectrophotometry
Is the science taht uses light wavelengths to measure light absorption through a substance in this case blood There are two wavelengths that are used in pulse oximetry: Red light (660nm) and infrade light (940 nm)
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Lambert Beer Law
Basis of spectrophotometry The amount of light a substance will absorb depends on the amount of substance and on the concentration of the substances in the sample. As the concentration of a substance increase so will the light absorded
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Pulse Oximeter-The Oximeter
Designed to measure either transmitted or reflected light Uses LEDs to send the light wavelengths Has a photodetector to measure the transmitted (or reflected) light
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Appropraite Oximtery Sites
Finger, Toe Ear Bridge of Nose Forehead Infant: Across the foot or hand
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Pulse Oximeter-Displayed Values
The displayed value: SpO2 This is called a **functional saturation** (not to be confused with fractional saturation) **Functional saturation** is the ratio of HbO2 to the total Hb available for binding with O2 Functional saturation does not take into account the dysfunctional hemoglobin's, like HbCO or metHb
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Pulse Oximetery Accuracy
+/- 3-5% You can have false high readings when SpO2 is \<80% The lower the sat the more likely it will read to high which is why it is important to compare against blood gas
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Factors the affect pulse oximeter accuracy
Motion Low perfusion External lights False nails/ Nail polish Wrong type of sensor Incorrect placement (too tight or loose) Dysfunctional Hb, anemia Vascular dyes
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How to Trouble Accuracy with Pulse Oximetry
•Motion interference Low perfusion Dysfunctional Hb present Anemia Venous pulsation Ambient light interference Electrical interference Optical cross talk Optical shunt
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Masimo Radial 7
Uses different wavelengths to calculate and display SpO2 SpMet- Altered shape of hemoglobin making it difficult to bind to an incorrect number of Fe and can be caused by tropical anaesthetics (Lidocaine) SpCO SpHb SpOC
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Venous Oximetry
Combines fibre-optics with an indwelling catheter to allow for **continuous** monitoring of SvO2 (via PAC) SjvO2 (via catheterization of the jugular vein) Based on reflectance spectrophotometry
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Co-Oximetry
=Hemoximetry Based on the principal that different forms of Hb absords light differently at different wavelengths Uses four (or more) wavelengths to measure Hb, HbO2, HbCO, and MetHb
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Co-Oximetry Measurement
The saturation we see from a co-oximeter is the **fraction saturation** **Fractional Saturation:** Ratio of Hb bound with O2 compared to the total amount of Hb present Total Hb includes HbO2, Hb, and dsyfunction Hb
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Capnography
**Capometry**: Measurement of CO2 in exhaled gases; provides digital display of EtCO2 value (i.e. a number) **Capnography** is a graphic display of CO2 level as they change dueing breathing
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Capnography Methods
Infraded absorption spectroscopy is the most common method Can be main stream (directly in line with flow) which is more accurate. Or side stream which is a line coming off the flow tubing and can easily get damaged or filled with secretions or fluid
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Clinical Relevance of Capnography
End tidal CO2 is closely related to PaCO2 A normal PetCO2 averages 3-5 mmHg less than PaCO2 A PaCO2 greater than ETCO2 is indicative of a V/Q mismatch Can help in confirmation of ETT placement and the effectiveness of CPR A sudden increase in the P(a-et)CO2 can indicate a pulmonary embolus.
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Suptum Culture and Sensitivity
**Culture:** Determines the presence and identification of bacteria or fungi in the sputum **Sensitivity:** Determines which antibotics the culture is sensitive too and will be the most effective
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Bronchoalveolar Lavage (BAL)
A bronchoscope is advanced into a lung segment and wedged in the bonchus Sterile saline is flushed into the segment and then suctioned back up thru the bronchoscope The sample is collected in a sterile container and is analyzed via a culture and sputum Can also help determine if an inflammatory process is under way due to the presence of neutrophils, and can somtimes detect food particles is aspiration has occured
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CT (Computed Tomography)
Takes on multiple cross sectional images of the chest (or other) about 1 cm apart Helical CT take these images very quickly and can allow for an *angiography* to occur when a contrast dye is administered intravascularly
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V/Q Scan
The perfusion scan is obtained by injecting radiolabeled albulmin intravanesously The ventilation scan is obtained by having the patient breathe in a radiolabled gas A gamma camera collects the images
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Lung Mapping
Provide imagining (a "map") of the distribution of ventilation, allowing localization and quantification of areas of injury "Quiet" regions are those without ventilation and will not be seen in the scan Is dynamic monitoring and can provoke continuous monitoring or a spot check Can help to evaulet optimal PEEP levels and the effect of recruitment maneuver, and other aspects of ventilation
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What are the two Methods of Lung Mapping
1) Electrical Impedance Tomography 2) Acoustic Respiratory Monitoring (ARM)
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Lung Mapping-Electrical Impedance Tomography
Uses 16-32 electrodes placed around the chest Impedance between the electrodes is measured A video reconstruction of ventilation will be created
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Lung Mapping-Acoustic Respirtory Monitoring
Uses a series of stethscopes placed around the chest Ventilation map is created from the sounds
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Chest Tubes
Chest tubes are used to help manage pleural diseases There are a range of sizes Will typically be connected to either a Heimlich valve or thoracic drainage unit CXRs are helpful in assessing location and depth for insertion, as well as resolution of the original problem Percussion and auscultation can be helpful in assessing the effectiveness of this therapy An assessment of the dressing and/or site can reveal onset of infection and/or air leaks
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Passive Humidification
Most common method for our adult patients Achieved through the use of an HME or HMEF
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Active Humidity
Heated humidifier and heated wires in the circuit Indications * Bloody secretions * Thick, tenacious sputum * Hypothermia (core temp \<32 °C) * Burn patients * Patients where HME contraindicated * Neonates; small peds * High MV or large leaks leakscausing Vte\< 70% of inhaled
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VAP
Ventilator-associated pneumonias are caused by the micro-aspiration of the micro-organisms in oral and gastric secretions 30-Cuff Pressureto keep secretions out (25-30) 30-HOB at 30 degree angle 30-Suction on EVAC tube
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Reducing VAP
Perform gentle suctioning Minimize circuit changes Use MDI’s (not SVNs) for med delivery to intubated patients Daily SATs and SBTs (to reduce duration of intubation) Use NIV when possible Perform oral hygiene every 4 hours at minimum Oral, not nasal, gastric tubes Measuring gastric residual volumes Many institutions have a “ventilator bundle” where two or more strategies to reduce nosocomial pneumonia and VAP are combined.
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ALI and ARDS Ventilator Strategy
The low compliance necessitates smaller VTto keep plateau pressures \< 30 cmH2O VT in the 4-6 mL/kg range PEEP is important to maintain recruitment High levels of PEEP may be indicated Can use the static (or low-flow) V-P curve to help determine ABG targets * The low VT often results in a permissive hypercapniastrategy * PaCO2 allowed to climb as long as pH \> 7.25 * Minimal FiO2 to keep SpO2 \> 90% (typically)
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TBI Ventilator Strategy
* (Typical) ABG targets: * Low-normal PaCO2 (35-40 mmHg) * High-normal pH (7.40-7.45) * Slightly vasoconstricts vessels to the brain resulting in decreased ICP * PaO2 80-120 mmHg * Ventilator settings: * Typically normal lungs so follow settings for normal lungs
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Obstructive Disorders Ventilator Strategies
**COPD vs Asthma** * Problems with airway resistance, but by different mechanisms * Asthma: bronchoconstriction; narrowed airway lumen * Maximize time * Push breath in fast and give it time to exhale (increase flow or Ti) * COPD: the high lung compliance results in “floppy” airways and airway collapse on forced exhalation * Inhalation is easy and exhalation is difficult * Both have high time constants resulting in prolonged expiration time required; auto PEEP is common * Ventilator settings: * Main goal is to maximize expiratory time in order to decrease the auto PEEP
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Criteria for D/C of Ventilatory Support:
Original reason for mechanical ventilation is resolved Patient has stable vital signs/hemodynamics Patient should be able to manage WOB on their own This is where weaning parameters help
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Criteria for extubation:
Able to maintain their airway Good LOC or has TT in place Cuff leak is present Is able to protect their a/w Presence of cough and gag reflexes Is able to manage their secretions Look at sxn history, effectiveness of cough
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Weaning Parameters
Spontaneous VT4-6 mL/kg \*RR \< 35 bpm \*VC \> 10 mL/kg \*NIP (MIP) \> 20 cmH2O f/VT\< 105 (also known as the RSBI or Tobin score) MV \< 12-15 LPM So this is what we used to assess know there are also other things we look for as studies have shown that these weaning parameters are not a good indice of how well they will wean
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Trends in Weaning
Using weaning parameters alone are not good predictors of succesful weaning and the **best parameter in the SBT** Studies have shown that 75% of patients need NO weaning Weaning should take on the form of screening for readiness for discontinuation from mechanical ventilation rather than an approach that steadily reduces ventilatory support Still need to balance FVS vs. PVS until SBT is passed
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Spontaneous Breathing Trial
Ideall done once daily in combination with a SAT Patient will be placed on a mode that provides minimal assisstance (PSV, CPAP, T-piece) Can assess the patient’s spontaneous breathing from 30 min up to 120 min The longer they have been ventilated, the longer the SBT Tobin Score and WOB assessed throughout
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Ventilator Dependance
**Respiratory Factors**-Increased ventilatorydemand, muscle atrophy, abnormal lung mechanics (R or C) **Cardiovascular Factors-**MI, arrhythmias, hemodynamic instability **Neurological Factors**-Decreased drive to breathe, impaired neurotransmission **Psychological Factors-**Fear of removal of life support, anxiety, stress, depression, sleep deprivation
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MDI
Most common; typically used to deliver bronchodilators and ICS Requires a special actuator to adapt the MDI to the ventilator circuit (ideally has a chamber to increase aerosol delivery to lung) Requires timing of the actuation with inspiration Often the dose is adjusted due to “loss” to the circuit
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Nebulizers
Nebulization during inspiration only results in greater delivery of the drug If the nebulizer is external to the vent it can add to the delivered tidal volume and interfere with triggering These disadvantages and the increased risk of contamination mean we typically use MDIs Inhaled antibiotics (e.g. Gentamicin, vancomycin) or mucolytics(i.e. drugs not available in MDI) may be given via nebulized treatment
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Nitric Oxide (NO)
A colourless, odorless gas It is produced endogenously in vascular endothelial cells and is a potent vasodilator Because it is inhaled it is selective to the pulmonary system and thus is a potent pulmonary vasodilator Administered via the INOvent T’s in NO, servo-controls and analyzes levels Common Uses-ARDS, Pulmonary hypertension, Neonates (PPHN, congenital heart defects)
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Effects of Nitric Oxide
The pulmonary vasodilation results in: Decreased PVR Decreased pulmonary artery pressures Decreased intrapulmonary shunting Better V/Q matching as NO increases blood flow only to ventilatedalveoli by relaxing the smooth muscles of the capillaries supplying these alveoli Improved oxygenation Effects are limited to the pulmonary circulation because after diffusing into the capillaries NO immediately binds to hemoglobin