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7100 > O2 Supply N Demand > Flashcards

O2 Supply N Demand Flashcards

1
Q

Ventilation

A

Movement of air in and out of the lungs

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2
Q

What are the major influencing factors of ventilation?

A
  1. Muscle function
  2. Lung compliance
  3. Airway resis
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3
Q

What happens in ventilation?

A

Regulated by chemoreceptors sending msg to brain: increase RR and tidal volume.
1. Peripheral chemoreceptors are sensitive to decreased PaO2 lvls below 60 mmhg
2. Central chemoreceptors are sensitive to increased PaCO2 lvls

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4
Q

What is the best indicator of ventilation?

A

PaCO2
Normal PaCO2: 35-45mmHg
- CO2 diffuses 20x more easily than O2

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5
Q

Why is knowing that CO2 diffusing 20x more easily than O2 important?

A

This means that despite a pathological problem with diffusion (ie. pulmonary edema causing a thickened AC membrane), CO2 will pass from the pulmonary capillary to the alveoli more easily than O2.

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6
Q

What decreases CO2 levels through exhalation?

A

the function of VENTILATION

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7
Q

Inadequate ventilation will cause: (not S&S!!)

A

*CO2 levels rise in the alveoli
*Decreasing CO2 driving pressure
*Slowed movement of CO2 from the pulmonary capillary to the alveoli

This results in elevated PaCO2 levels.

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8
Q

What is Respiratory Muscle Function (RMF)?

A

The ability/strength of the respiratory muscles

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9
Q

What happens if RMF is decreased?

A

then vital capacity will be decreased and patient may be at risk of not protecting own airway with the decreased ability to take a deep breath in and cough forcefully

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10
Q

How is RMF decreased by? (Ax)

A

Decreased by:
•Older age
•Poor nutrition
•Generalized weakness/tiredness
•Accessory muscle use
•Exhaustion (overuse: fast RR, increased WOB)
•Prolonged mechanical ventilation (underuse/muscle atrophy)

Other things to consider:
•Weak cough (think RMF)
•Tracheal indrawing (think RMF)
•Brain injury
•Diaphragm function
•spinal cord injury
•Multiple sclerosis
•Guillian-Barre
•Spinal deformity (kyphosis, scoliosis)
•Drugs: paralytics

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11
Q

When O2 supply is decreased to the brain, what are the specific S&S?

A
  • restlessness
  • agitation
  • confusion
  • decreased LOC
  • GCS change
  • pain
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12
Q

When O2 supply is decreased to the heart, what are the specific S&S?

A
  • tachycardia
  • ST changes
  • dysrhythmias
  • chest pain/angina/MI
  • MAP
  • increased troponin
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13
Q

When O2 supply is decreased to the lungs, what are the specific S&S?

A
  • increased RR
  • SOB
  • hypoxemia
  • O2 requirements
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14
Q

When O2 supply is decreased to the GI system, what are the specific S&S?

A
  • n/v
  • last BM
  • decreased bowel sounds
  • loss of appetite
  • ischemic bowel
  • elevated liver enzymes/liver failure
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15
Q

When O2 supply is decreased to the kidneys, what are the specific S&S?

A
  • decreased urine output
  • dark/amber urine
  • elevated creatinine
  • decreased eGFR
  • acute kidney injury
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16
Q

What is lung compliance?

A
  • the ease with which the lungs can be inflated (distensibility)
  • most processes decrease lung compliance
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17
Q

Lung compliance (elastic) is decreased by (Ax details):

A

Fluid in the lungs:
- crackles (fine/coarse)
- secretions/mucous/inflammation
- pulmonary edema
- productive cough
- pink frothy sputum
- thick, yellow sputum
- chest X-ray & CT finding: wet looking lungs, edema, atelectasis, infiltrates, opacities, consolidation, pneumonia, COPD, fibrosis, ARDS

Fluid outside the lungs in pleural space:
- hemothorax/pneumothorax
- pleural effusion/empyema

Lung changes:
- atelectasis

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18
Q

Lung compliance (elastic) - is increased by (Ax details):

A
  • flail chest (rib fractures) lungs can expand beyond rib cage
  • emphysema (loss of elastin) lungs get big and baggy and do not recoil back into shape leading hyperinflation of alveoli

Other things to consider:
- chest x-ray & CT findings: wet looking lungs, edema, atelectasis, infiltrates, opacities, consolidation, pneumonia, COPD, fibrosis, ARDS, etc

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19
Q

What is airway resistance?

A
  • the impedance of bringing in air to inflate the lungs
  • mainly influenced by airway diameter
  • airway resis is determined by narrowing of the airways
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20
Q

What are some airway resistance (impedance) assessment details?

A

Increased by:
- wheezes (think increased airway resistance)
- tube size (trach, OETT)
- partial/complete obstruction
- mucous plugs
- bronchospasm
- airway edema
- inflammation
- lots of secretions, especially thick mucous
- asthma/anaphylaxis

Other things to consider:
- tumour
- bronchoconstriction and bronchospasm (asthma attack, anaphylaxis)
- bronchiectasis (chronic condition where the walls of the bronchi are thickened from inflammation)
- SNS response (bronchodilation)
- bronchodilators (this will decrease airway resistance)

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21
Q

What is WOB?

A

The amount of work that must be done to overcome the “elastic” and “resistive” properties of the lungs

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22
Q

What is compliance?

A

The ease with which the lungs can be inflated, the distensibility of tissue

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23
Q

What is resistance?

A

Describes the impedance to bring in air to inflate the lungs, which is mainly influenced by the diameter of the airway

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24
Q

How will WOB be increased?

A

If lung compliance and airway resistance are abnormal and will negatively impact lung volume

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25
Q

What does WOB effect?

A
  • RR
  • tidal volume

RR x Vt = minute ventilation

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26
Q

What is tidal volume?

A

The total amount of air that moves in or out of the lungs with each respiratory cycle at rest

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27
Q

What are some assessment details to assess lung volume?

A
  • decreased breath sounds
  • shallow breathing
  • atelectasis
  • pain, rib/spinal fractures, chest tubes (think this can decrease Vt)

Other considerations:
- IPAP intended to increase Vt (BIPAP setting)
- hemo/pneumothorax, empyema, pleural effusions (any fluid in pleural space)

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28
Q

What is vital capacity?

A

The total volume of air forcefully expelled from the lungs after maximum inhalation

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29
Q

What are some assessment details for vital capacity of the lung volume?

A
  • respiratory muscle function (RMF)
  • cough strength
  • anything that decreases the strength of the muscles (spinal cord injury, ALS, GB)
  • trends in VC volume numbers
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30
Q

What is Functional Residual Capacity?

A

The amount of air left in the lungs after normal expiration

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31
Q

What are some assessment details for function residual capacity?

A
  • prolonged decreased breath sounds
  • prolonged shallow breathing
  • atelectasis

Other considerations:
- EPAP increased FRC (BiPAP setting)
- PEEP increases FRC (Ventilator setting)
- Emphysema can increase FRC

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32
Q

What is the relationship between RR and Ventilation?

A
  • increased RR (compensation) will increase ventilation (when it decreased PaCO2)
  • decreased RR (oversedation, drug OD, brain injury) will decrease ventilation when it results in increased PaCO2)
  • Kussmaul breathing will increase RR and tidal volume

Important considerations:
- pt could have healthy lungs, and the only issue with ventilation is decreased RR, this is the ventilation issue, so ventilation will be decreased for example a pt with drug OD

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33
Q

What happens in Normal Ventilation in regards to Ventilation Conclusion and PaCO2?

A
  • Normal PaCO2
  • Despite abnormal findings in lung compliance, airway resis, tidal volume, and RMF, ventilation is normal if PaCO2 is within normal range. Therefore, conclude that ventilation is normal
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34
Q

What happens in Increased Ventilation in regards to Ventilation Conclusion and PaCO2?

A
  • Decreased PaCO2
  • Despite abnormal findings in lung compliance, airway resis, tidal volume, and RMF, ventilation is increased if PaCO2 is decreased since CO2 is being blown off
  • RR and Tidal Volume have increased to normalize minute ventilation to compensate for a decrease in oxygen supply, but in this process, more CO2 is exhaled
  • when PaCO2 is decreased, conclude that ventilation is increased no matter what condition or disease is present
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35
Q

What happens in Decreased Ventilation in regards to Ventilation Conclusion and PaCO2?

A
  • Increased PaCO2
  • when lung compliance, airway resis, tidal volume and RMF are abnormal and PaCO2 is elevated, then make the conclusion of decreased ventilation
  • or if no identified ventilation issue, but RR is decreased and increased PaCO2, conclude that ventilation is decreased
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36
Q

What is the Ventilation Conclusion when PaCO2 is unavailable?

A

If assessment data and the determinants conclusions are abnormal, and the pt does not have PaCO2 value, then conclude that ventilation is decreased

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37
Q

What is alveolar gas exchange?

A

A process by which O2 and CO2 cross the alveolar-capillary membrane by diffusion between the respiratory system and the blood stream

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38
Q

Oxygenation is most affected by factors influencing gas exchange:

A
  • V/Q matching
  • diffusion
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39
Q

What do you measure in Alveolar Gas Exchange?

A

PaO2 level
- PaO2 normal is 80-100 (normal gas exchange)

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40
Q

What is the V and Q in V/Q matching?

A

V = Ventilation in lungs
Q = Blood flow in the lungs (perfusion)

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41
Q

What is V/Q matching?

A
  • Ventilation to perfusion ratio (V/Q ratio) of alveolar ventilation to alveolar perfusion at the site of gas exchange
  • used to assess adequate matching of ventilation to perfusion for sufficient gas
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42
Q

What is a shunt or shunt-like unit caused by?

A

any identified ventilation issue is a ventilation issue for the alveoli:
- crackles
- pneumonia
- COPD
- mucous plugging
- atelectasis
- pulmonary edema
- decreased RR

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43
Q

What is a dead space or dead space-like unit caused by?

A

Decreased cardiac output:
- pulmonary vasoconstriction
- pulmonary embolism
- HF
- decreased preload
- hemorrhage
- surgical blood loss
- dehydration
- or any issue that decreases perfusion to the alveoli is a perfusion problem
**Rmbr: perfusion is about blood flow when discussing dead space, not oxygenation

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44
Q

What is a shunt?

A

No ventilation but adequate perfusion (ie. mucous plug or complete obstruction)

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45
Q

What is a shunt-like unit?

A

Some ventilation with adequate perfusion (ie. partial obstruction, inflammation)

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46
Q

What is normal V/Q matching ratio?

A

adequate ventilation and perfusion

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47
Q

What is a dead space-like unit?

A

decreased perfusion but adequate ventilation (ie. decreased cardiac output)

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48
Q

What is a dead space?

A

no perfusion but adequate ventilation (ie. pulmonary embolism)

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49
Q

Define Diffusion

A

movement of molecules moving from higher to lower concentration

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50
Q

What are the factors affecting diffusion in the lungs?

A
  1. thickness of the alveolar-capillary membrane
  2. SA of the a-c membrane
  3. the solubility of the gases (diffusion coefficient)
  4. concentration gradients of the gases (driving pressures)
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51
Q

Thickness of the A-C membrane

A

A thin tissue barrier through which gases are exchanged between the alveoli and blood in the pulmonary capillaries. The thicker the a-c membrane, the slower the rate of diffusion of gases

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52
Q

Assessment Details re: Diffusion

A
  • crackles
  • secretions, mucous
  • productive cough, yellow sputum
  • inflammation, consolidation, lung infection

Other things to consider:
- chest x-ray & CT findings - wet looking lungs, edema, atelectasis, infiltrates, opacities, fibrosis, COPD, pneumonia

*Atelectasis or fluid in pleural space does NOT affect thickness of a-c membrane

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53
Q

Alveolar SA

A

The amount of area within the alveolar walls that participate in gas exchange. Process that decreases actual or potential surface

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54
Q

What are some assessment details affecting alveolar SA?

A
  • consolidation
  • atelectasis
  • prolonged shallow breathing
  • prolonged decreased breath sounds to bases

Other considerations:
- chest X-ray & CT atelectasis
- pleural effusions
- hemo/pneumo (compressed alveoli)
- bullectomy, lobectomy, pneumonectomy
- bullae formation in emphysema (destruction of alveolar walls)

55
Q

What is driving pressure?

A

The driving force for diffusion of oxygen across the alveolar membranes

56
Q

In clinical practice, driving pressure is mainly effected by what?

A

Supplemental Oxygen Therapy

57
Q

What is the driving pressure if someone is on room air?

A

Normal driving pressure if on room air

58
Q

When will you have an increased driving pressure?

A

When on Oxygen Therapy

59
Q

Driving pressure will be decreased by what reason?

A

Driving pressure will be decreased mainly due to altitude (ie. less pressure in the atmosphere at higher lvls than at sea lvl)

60
Q

What is diffusion coefficient?

A
  • The level of diffusivity of a gas to another
  • the higher the lvl of diffusivity, the faster the diffusion rate of a gas compared to another
61
Q

Why does CO2 diffuse 20x faster than O2?

A

more soluble in water

62
Q

Increase/Decrease Diffusion Coefficient

A

DOES NOT EXIST. Ratio does not change so it is not labelled increased or decreased

63
Q

What changes in diffusion coefficient?

A

Degree of lung pathology (diseases and infections) and its effects on the 2 gases

64
Q

What is a good indicator of the increased degree of lung disease?

A

O2 is significantly decreased, 20x more than CO2. When CO2 is rising, despite an increased respiration rate (compensation for decreased O2 and increased CO2)

65
Q

What happens to the O2 and CO2 level in an end-stage COPD patient?

A

these patients retain CO2, and CO2 remains high all the time despite compensation (central chemoreceptors or ABG correction). Because the lung disease is so significant, CO2 diffusion is decreased. But CO2 still diffuses 20x easier than O2 under any circumstance

66
Q

What is the best indicator of Gas Exchange?

A

PaO2

67
Q

What is PaO2?

A
  • Partial pressure of Oxygen
  • normal: 80-100 mmHg
68
Q

How do we conclude about gas exchange if there is no PaO2 level?

A

If there is not PaO2 value, but there is evidence of decreased gas exchange as concluded by the above determinants of gas exchange, conclude that gas exchange is decreased.

69
Q

Hypoxemic

A

PaO2 Below 80 mmHg

70
Q

Oxygen Transport

A

How O2 is carried in the blood to the end organs and tissues

71
Q

How is O2 transported?

A

O2 is transported from the lungs to the organs in 2 ways:
1. dissolved in plasma = 3%
2. bound to Hgb = 97%

72
Q

What is O2 transport affected by?

A
  • Hgb lvl
  • Oxyhemoglobin Dissociative Curve
73
Q

What is the main transported of oxygen?

A

Hgb

74
Q

What does the number of Hgb present mean?

A

It reflects the carrying capacity of the oxygen

75
Q

__% of available oxygen is carried to the tissues by Hgb?

A

97%

76
Q

What happens to Hgb when they travel to the lungs?

A

Bindings sites on the Hgb are fully occupied by O2 after travelling to the lungs to “pick them up”

77
Q

What is the oxygen transport conclusion if the Hgb is lower than normal?

A

Even if the Hgb is a bit lower than normal, still identify that oxygen transport is decreased since there is not enough oxygen carrying capacity

*It is not a consideration whether or not physicians choose to give blood products to correct ir or not, it is still a transport problem

78
Q

What is ODC?

A

Oxyhemoglobin Dissociative Curve:
- a graph curve that describes the relationship between saturation of Hgb (SaO2 = bound Hgb) and partial pressure of arterial oxygen (PaO2 = oxygen dissolved in plasma)
- it describes where oxygen is carried (on Hgb or in plasma) and how it is released to the tissues
- it also describes the relationship between oxygen and hemoglobin (affinity)

79
Q

What is affinity?

A

Describes the attraction of Hgb to oxygen molecules

80
Q

What does affinity influence?

A

It influences the transport of O2 to the organs and tissues by determining how Hgb “easily releases” or “does not easily release” O2 molecules

81
Q

ODC curve starts at what values of pH? Temp? PaCO2? DPG?

A
  • pH (7.35-7.45)
  • Temp
  • PaCO2 (35-45 mmHg)
  • 2-3 DPG
82
Q

What happens when there is a change in the Curve values?

A

Shifts in the curve occurs

83
Q

What is 2, 3-DPG?

A

It is a phosphate compound in RBC that facilitates the release of O2 from Hgb to tissues and organs

84
Q

Bank Blood and 2, 3 DPG

A

Banked blood may not have 2, 3 DPG because it only lasts outside of the body for about 2 weeks

85
Q

Blood transfusion and 2, 3 DPG

A

If a patient requires blood, it may not contain 2, 3-DPG and the pt will have a transport problem and a LEFT shift (Low 2, 3DPG)

86
Q

What happens when Hgb is not releasing oxygen?

A

SpO2 or SaO2 may be normal BUT PaO2 will be decreased cus Hgb is NOT releasing O2. Pts will have decreased end-organ perfusion and have S&S of decreased LOC and urine output

87
Q

What causes a shift in the ODC?

A
  • Abnormal values of pH, PaCO2, temp or 2, 3DPG
  • any ONE can shift the position of the curve to Left or Right
88
Q

What do shifts in the ODC alter?

A

Shift alters the affinity of Hgb for oxygen

89
Q

What does a shift in the ODC indicate?

A
  1. there is a change in the way O2 is picked up by Hgb at the alveoli (affinity)
  2. there is a change in the way O2 is transported to the tissues
90
Q

Left Shift in ODC indicates:
- ?? pH
- ?? pCO2
- ?? temp
- ?? 2-3, DPG

A
  • High pH
  • Low pCO2
  • Low temp
  • Low 2-3 DPG

*too sticky!!!

91
Q

Left Shift in ODC means that Hemoglobin has an ___________ affinity for O2.

A

Left shift = Hgb has an INCREASED affinity for O2

92
Q

A left shift _______ O2 delivery to the tissues because Hgb does not unload O2 as readily.

A

IMPAIRS

93
Q

Right shift in ODC indicates:
- ?? pH
- ?? pCO2
- ?? temp
- ?? 2-3, DPG

A
  • LOW pH
  • HIGH pCO2
  • HIGH temp
  • HIGH 2-3 DPG
94
Q

Right shift in ODC means that Hgb has a ________ affinity for O2.

A

Right shift in ODC means that Hgb has a DECREASED AFFINITY for O2.

95
Q

A right shift __________ O2 delivery to the tissues because Hgb unloads more readily

A

ENHANCES

96
Q

Left LOVES O2

A

Or all the lows!!
- alkoLOsis
- LOW PaCO2
- LOW temp
- LOW 2, 3 DPG
- increased affinity
- Hgb “loves” O2 (SaO2)
- does not easily move from Hgb to plasma/tissue

97
Q

Right RELEASES O2

A
  • Acidosis
  • HIGH PaCO2
  • HIGH temp
  • HIGH 2, 3 DPG
  • Decreased affinity
  • O2 easily “released” to plasma (PaO2)/tissues
  • easily moves from Hgb to plasma/tissue
98
Q

What is Cardiac Output?

A

The volume of blood ejected from the heart each minute

99
Q

How is CO expressed in?

A

CO2 is expressed in L/min (normal = 4-8 L/min)

100
Q

What is the equation for CO?

A

HR x SV

101
Q

What is the HR affected by?

A
  • ANS (Autonomic Nervous System)
  • Drugs
    1. ↑’d by ventolin
    2. ↓’d β-blocker, Ca+ channel blocker
102
Q

What is stroke volume?

A

Amount of blood ejected from the heart with each contraction

103
Q

SV is expressed in __________.
What is the normal range?

A

mL/beat
normal = 60-80 mL

104
Q

What are the factors that affect SV?

A

Preload, Afterload, Contractility

105
Q

What is PRELOAD?

A

The Volume of blood in the heart stretching the ventricles for contraction
- volume of blood in the ventricles at the end of diastole that stretches the myofibrils before each contraction

106
Q

What is AFTERLOAD?

A

The resistance encountered by the ventricles that must be overcome for blood to be ejected out
- it is the FORCE or RESIS against which the ventricles must pump in order to eject the blood

107
Q

What is CONTRACTILITY?

A

The force generated by the ventricular muscle fibers during contraction
- ability of the hearts myofibrils to change their strength and force of contraction

108
Q

What affects Preload?

A
  1. Total Circulating Volume
  2. Venous Blood Return
109
Q

DECREASED circulating volume indicates:

A
  • DECREASED Preload
  • Blood loss
  • fluid shift (LOW albumin, liver disorder)
  • fluid loss (dehydration, diuretics)
110
Q

INCREASED circulating volume indicates:

A
  • INCREASED preload
  • IV fluids
  • fluid shift
  • chronic illness (renal disease, CHF)
111
Q

INCREASED venous return indicates:

A
  • INCREASED preload
  • vasoconstriction (SNS stimulation)
  • DECREASED intra-thoracic pressure
112
Q

DECREASED venous return indicates:

A
  • DECREASED preload
  • vasodilation (fever, sepsis, nitroglycerin)
  • INCREASE in intra-thoracic pressure
113
Q

What measures preload?

A

CVP

114
Q

What is CVP?

A

Central Venous Pressure
- measures the pressure exerted by the blood (preload) in the right atrium
- it allows us to trend the patients preload

115
Q

What is the normal CVP range?

A

2-6 mmHg

116
Q

What is the afterload affected by?

A

3 Vs
- Vessel diameter mostly
Also…
- Valve stenosis
- blood viscosity

117
Q

What causes vasodilation?

A
  • hyperthermia
  • drugs
  • spinal cord injury
118
Q

What causes vasoconstriction?

A
  • hypothermia
  • drugs
  • SNS: epinephrine, norepinephrine
119
Q

_________ ventricular afterload is affected by the change in pulmonary vessel prssure and diameter

A
  • pulmonary HTN
  • pulmonary vessel constriction
  • pulmonary embolus
  • chronic pulmonary illness
120
Q

What is contractility primary determined by?

A

Preload

121
Q

What is the Frank-Starling’s Law?

A

It is the amount of preload that determines the effectiveness of contractility

122
Q

Frank-Starling’s Law of the Heart indicates that ↑ volume (preload) =

A

↑ volume (preload) = ↑ contractility and cardiac output

123
Q

Why does the Cardiac Output increases when there is an increase in volume (preload) and increase in contractility?

A

Because the ventricles will have a greater force of contraction with the bigger stretch (and resulting recoil) from the increased volume

124
Q

What is Frank-Starling’s Law of the Heart on excessive preload?

A

↑↑↑ volume (preload) = ↓ contractility and cardiac output

125
Q

Why does cardiac output decreases when there is excessive preload?

A

A decrease in cardiac output occurs when the point is reached that too much volume has OVERSTRETCHED the cardiac muscle fibres

  • “overstretch” results in a ↓’d recoil of the ventricle, which ↓’s contractility
126
Q

Decreased Contractility

A
  • inadequate or excessive PRELOAD
  • hypoxia of cardiac tissue
  • abnormal electrolytes levels
  • negative inotropic drugs
    - Ca+ channel blockers
    - β-blockers
127
Q

Increased Contractility

A
  • increasing preload (to a point)
  • circulating catecholamines
  • positive inotropic drugs
    - digoxin
    - dopamine
    - dobutamine
128
Q

What is Ejection Fraction (EF)?

A
  • the % of blood ejected from the left ventricle with each beat
  • normal is 55-75%
  • a measurement of contractility
129
Q

What is the contractility/ventricular filling time like in tachycardia?

A

Only diastole gets shorter, decreasing the time for the ventricle to fill

130
Q

What does having decreased time for filling mean?

A

decreased time for filling = ↓ preload = ↓ contractility =↓ CO

131
Q

What does having a shorter diastole mean when it comes to contractility and HR?

A

A shorter diastole also decreases coronary artery perfusion cus there is less time perfusion

↓ coronary artery perfusion = ischemia = ↓ contractility =↓ CO

132
Q

Increased preload = __________ contractility

A

increase

133
Q

excessive preload = ___________ contractility

A

decrease

134
Q
A

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