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SEE/BOARD STUDY > AA APEX: RESPIRATORY: PHYSIOLOGY > Flashcards

AA APEX: RESPIRATORY: PHYSIOLOGY Flashcards

1
Q

Anatomic dead space begins in the mouth and ends in the:

A

Terminal Bronchioles

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2
Q

The airway is functionally divided into 3 zones: ​ What are the 3 zones?

A

conducting, respiratory, transitional.

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3
Q

The conducting zone is from the

A

nares and mouth to the terminal bronchioles

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4
Q

What zone of the airway is the anatomic dead space?

A

Conducting zone

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5
Q

The respiratory zone is where gas exchange occurs. This region extends from the

A

respiratory bronchioles to the alveoli.

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6
Q

In what respiratory zone does gas exchange occurs?

A

The respiratory zone

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7
Q

What is ventilation ?

A

Ventilation is the process of exchanging gas between the atmosphere and the lungs.

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8
Q

Explain the 2 cricical function of the gas exchange process during ventilation?

A

O2 is delivered to hemoglobin to support aerobic metabolism.

CO2 (the primary end-product of aerobic metabolism) is eliminated from the blood. ​

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9
Q

Breathing Muscles: To effectively ventilate, we need a mechanism that repeatedly changes______ over time. By changing the lung volume, we create a pressure gradient that transfers gas into and out from the lungs.

A

lung volume; pressure gradient that transfers gas into and out from the lungs.

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10
Q

Contraction and relaxation of the breathing muscles allow us to produce cyclic changes in ________throughout the respiratory cycle.

A

thoracic volume

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11
Q

Inspiration–> Contraction of the inspiratory muscles

A

Contraction of the inspiratory muscles reduces thoracic pressure and increases thoracic volume. This is an example of Boyle’s law.

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12
Q

What happens during inspiration ? What muscles are involved.

A

The diaphragm and external intercostals contract during inspiration (tidal breathing).

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13
Q

What muscle increases the superior-inferior dimension of the chest?

A

The diaphragm

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14
Q

What muscles increase the anterior-posterior diameter.?

A

The external intercostals

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15
Q

Accessory muscles of inspiration include which 2 muscles?

A

include the sternocleidomastoid and scalene muscles.

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16
Q

What is the drive for Exhalation?

A

Exhalation is usually passive; this process is driven by the recoil of the chest wall.

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17
Q

Active exhalation is carried out by which muscles?

A

abdominal musculature (rectus abdominis, transverse abdominis, internal obliques, and external obliques).

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18
Q

Active exhalation is done by which muscles ?

A

Mnemonic: ​ I let the air out (exhale) of my TIREs (Transverse abdominis, Internal oblique, Rectus abdominis, External oblique).

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19
Q

The internal intercostals serve a secondary role in

A

active exhalation

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20
Q

When does Exhalation becomes an active process? when

A

minute ventilation increases or in patients with lung disease, such as COPD.

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21
Q

A forced exhalation is required to

A

cough and clear the airway of secretions

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22
Q

What is the vital capacity needed for an effective cough?

A

vital capacity of at least 15 mL/kg is required for an effective cough.

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23
Q

Functional Divisions of the Airway

A

conduit (or a tube) to transfer gas between the atmosphere and the blood -

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24
Q

Which part of the airway zone serves as both air conduit and gas exchange?

A

Transitional Zone

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25
Q

2 that would be considered would be considered part of the transitional zone

A

respiratory bronchioles and alveolar ducts

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26
Q

The respiratory zone begins at the respiratory bronchioles. It also includes the alveolar ?

A

alveolar ducts and alveolar sacs.​

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27
Q

The conducting zone begins at the ______and ends where?

A

nares and mouth and ends with the terminal bronchioles.

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28
Q

What are the last structures perfused by the bronchial circulation?

A

The terminal bronchioles are the

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29
Q

Does the conducting zone participate in gas exchange?

A

The conducting zone does not participate in gas exchange - it is anatomic dead space.

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30
Q

Airway Patency
For air movement (and gas exchange) to occur, the airways must remain patent (open). To prevent airway collapse, What pressure balance must occur?

​

Alveolar pressure is the pressure inside the airway.
Intrapleural pressure is the pressure outside the airway.
Transpulmonary pulmonary pressure (TPP) is the difference between the pressure inside the airway and the pressure outside of the airway.
​

A

the pressure inside the airway must be greater than the pressure outside of the airway.

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31
Q

Alveolar pressure is the pressure

A

inside the airway.

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32
Q

Intrapleural pressure is the pressure

A

outside the airway.

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33
Q

Transpulmonary pulmonary pressure (TPP) is the difference between the

A

pressure inside the airway and the pressure outside of the airway

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34
Q

What happens when the transpulmonary pressure is positive?

A

If TPP is a positive value, then the airway stays open.

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35
Q

What happens when the transpulmonary pressure is negative?

A

If TPP is a negative value, then the airway collapses.

​

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36
Q

Aside from pathologic states, such as_____ the only time that intrapleural becomes positive is during

A

pneumothorax; forced expiration.

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37
Q

Alveolar pressure becomes slightly_______during inspiration and slightly _____during expiration. When is there no airflow?

A

negative during inspiration
positive during expiration

There is no airflow at FRC or end-inspiration.

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38
Q

Transpulmonary pressure is always

A

positive (keeps the airway open).

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39
Q

Intrapleural pressure is always negative

A

(keeps lungs inflated).

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40
Q

What is the primary determinant of carbon dioxide elimination?

A

Alveolar Ventilation

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41
Q

Tidal Volume: What is tidal volume?

​

​
.

A

A tidal volume (Vt) is the amount of gas that is inhaled and exhaled during the breath.

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42
Q

Tidal Volume: What is tidal volume?

A

A tidal volume (Vt) is the amount of gas that is inhaled and exhaled during the breath.

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43
Q

When you take a breath, part of the Vt is delivered to the respiratory zone

A

(gas exchange occurs here), while the remainder of the Vt sits in the conducting zone (dead space).

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44
Q

When the patient exhales,______is removed first followed by _______of respiratory zone gas.

A

conducting zone gas (anatomic dead space) is removed first.

This is followed by exhalation of respiratory zone gas.

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45
Q

Any condition that increases dead space makes it more difficult to
Therefore, increased Vd widens the PaCO2-EtCO2 gradient and causes CO2 retention.

A

eliminate expiratory gases from the lungs.

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46
Q

Any condition that increases dead space makes it more difficult to

A

eliminate expiratory gases from the lungs.

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47
Q

An increased Vd widens the_______ and causes ___________

A

PaCO2-EtCO2 gradient and causes CO2 retention.

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48
Q

The ventilation rate is the

A

Volume of air moved into and out of the lungs in a given period of time. We care about minute ventilation and alveolar ventilation.

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49
Q

Minute ventilation (VE) is the amount of (think about the formula)

A

air in a single breath (Vt) multiplied by the number of breaths per minute (RR)

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50
Q

MV formula is

A

MV = TV x RR

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51
Q

Alveolar ventilation only measures

A

fraction of VE that is available for gas exchange. Said another way, it removes dead space gas from the minute ventilation equation.

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52
Q

Alveolar ventilation (VA) =

A

( TV - deadspace) x RR

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53
Q

Alveolar ventilation(VA) (related to PaCO2)

A

CO2 production / PaCO2

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54
Q

VA is directly proportional to

​

A

Carbon dioxide production (a higher CO2 production stimulates the body to breathe deeper and faster so it can eliminate more CO2)

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55
Q

VA is inversely proportional to

A

PaCO2 (faster and deeper breathing reduces PaCO2).

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56
Q

Conditions that increase dead space tend to

A

increase the volume of the conducting zone or reduce pulmonary blood flow.

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57
Q

Dead space is reduced by anything that reduces the volume of the conducting zone or increases pulmonary blood flow. Examples include an

A

ETT, LMA, or neck flexion.

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58
Q

Dead space is reduced by anything that

A

reduces the volume of the conducting zone or increases pulmonary blood flow

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59
Q

Which conditions will MOST likely increase the PaCO2 to EtCO2 gradient? ​ (Select 3.) HPA

A

–HYPOTENSION
–POSITIVE PRESSURE VENTILATION
–ATROPINE

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60
Q

Hypotension AND THE PaCo2 and ETCO2 gradient? Atropine is a bronchodilator, so it increases anatomic dead space by increasing the volume of the conducting zone. ​
Positive pressure ventilation increases alveolar pressure, which increases ventilation relative to perfusion. This is another way of saying that dead space increases.

A

reduces pulmonary blood flow, which increases alveolar dead space.

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61
Q

How does Atropine affect the PaCo2 to ETCo2 gradient? is a bronchodilator, so it

A

Atropine is a bronchodilator and it increases anatomic dead space by increasing the volume of the conducting zone. ​

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62
Q

How does Positive pressure ventilation affect the PaCo2 to ETCo2 gradient?

A

It increases alveolar pressure, which increases ventilation relative to perfusion. This is another way of saying that dead space increases.

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63
Q

What are the 4 types of dead space?

A

Anatomic
Alveolar
Physiologic
Apparatus

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64
Q

Anatomic dead space definition? and example?

A

Air confined to the conducting airways/ Examples Nose/mouth –> terminal bronchioles.

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65
Q

Alveolar dead space definition? and example?

A

Alveoli that are ventilated but not perfused

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66
Q

Physiologic dead space.

A

Anatomic Vd and Alveolar Vd

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67
Q

Apparatus dead space? Example

A

Vd added by equipment ; face mask, heat moisture exchange

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68
Q

Dead Space to Tidal Volume Ratio (Vd/Vt) is the fraction of the

A

The fraction of the tidal volume that contributes to dead space is called the Vd/Vt ratio.

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69
Q

Factors that alter dead space or the V/Q relationship will alter the

A

Vd/Vt ratio.

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70
Q

In the spontaneously ventilating patient, we assume that dead space is 2 mL/kg or 150 mL in a 70 kg patient. Therefore…

A

Vd/Vt = 150ml/450 ml = 0.33

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71
Q

***The most common cause of increased Vd/Vt under general anesthesia is a.

A

reduction in cardiac output

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72
Q

If the EtCO2 acutely decreases, you should first rule out

A

hypotension before considering other causes of increased dead space.

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73
Q

ETT tube on dead space

A

Decreases dead space.

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74
Q

Face mask on dead space

A

Increases dead space.

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75
Q

Does an LMA Reduces or increases Vd? HOW?

A

An LMA reduces Vd because it bypasses much of the anatomic Vd between the mouth to the glottis (similar to the ETT)

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76
Q

Does atropine increases or decreases Vd?

A

Atropine increases Vd, because its bronchodilator action increases the volume of the conducting airway. ​

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77
Q

Does neck extension increase or decrease Vd?

A

Neck extension increases Vd, because it opens the hypopharynx and increases its volume.

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78
Q

3 airway equipments that decreases Vd?

A

ETT
LMA
Tracheostomy

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79
Q

3 airway equipments that increases Vd?

A

FM
HMEs
PPV

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80
Q

Drugs that increase Vd>

A

Anticholinergics because they bronchodilates

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81
Q

Age and increased Vd

A

Old age increases Vd

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82
Q

Neck position on Vd

A

Extension increase Vd

Flexion decrease Vd

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83
Q

Pathophysiology: What can cause an increased in Vd. as far as CO, Pulmonary blood flow

A

Decreased CO and Pulmonary blood flow both increased vd.

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84
Q

2 conditions that can cause an increased in Vd?

A

PE caused by thrombus, air, amniotic fluid, bone

COPD

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85
Q

Sitting position on Vd

A

Increase

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86
Q

Positions that decreases Vd.

A

Supine

Head down positions

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87
Q

If dead space increases,

​

A

minute ventilation (RR, Vt, or both) must increase to maintain a constant PaCO2. For example, if the Vd/Vt ratio is 0.8 – 0.9 as a result of severe chronic bronchitis, then minute ventilation must increase to 30 – 50 L/min to maintain a normal PaCO2!

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88
Q

In the circle system, dead space begins at the

A

y-piece. Anything proximal to the y-piece does not influence dead space nor does increasing the length of the circuit.

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89
Q

Circle system dead space begins at the Y piece, The only exception to this rule is

A

an incompetent valve in the circle system. In this situation, the entire limb with the faulty valve becomes apparatus dead space.

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90
Q

This equation allows us to calculate physiologic dead space?

A

Physiologic dead space can be calculated with the Bohr equation

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91
Q

The Bohr equation compares the

A

partial pressure of carbon dioxide in the blood vs. the partial pressure of carbon dioxide in exhaled gas

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92
Q

Many clinicians use the difference between

A

PaCO2 and end-tidal CO2 as a gross estimation of dead space. This estimation does not determine the cause of dead space, but only that dead space has changed.

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93
Q

A patient is in the sitting position. When compared to the apex of the lung, which of the following are higher in the base?

A

Partial pressure of alveolar carbon dioxide

Blood flow

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94
Q

The non-dependent region (apex in the sitting position) has a
The dependent region (base in the sitting position) has a

A

Higher PAO2 and a higher V/Q ratio (V > Q)

Higher PACO2 and has a lower V/Q ratio (V < Q).

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95
Q

As far as the alveolar compliance curve ventilation is ____L/min and perfusion is _______L/min yielding to an overall V/Q ration of

A

4; 5; 0.8

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96
Q

Compliance formula is

A

Change in volume/ Change in pressure.

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97
Q

Where is ventilation the greatest in the lung and why?

A

Ventilation is greatest at the lung base due to higher alveolar complaince.

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98
Q

Where is perfusion the greatest in the lung and why?

A

Greatest at the lung bases due to gravity .

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99
Q

Ventilation in the alveoli in the apex ? The slope of the curve is

A

alveoli in the apex have the poorest ventilation, because they have the poorest compliance. The slope of the curve is less steep in this region, so there’s a smaller volumetric change throughout the respiratory cycle.

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100
Q

The alveoli in the base have the_____why?

A

greatest ventilation, because they have the greatest compliance. The slope of the curve is more steep in this region, so there’s a larger volumetric change throughout the respiratory cycle (i.e., better ventilation).

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101
Q

At a lung volume below FRC (a low lung volume), compliance will be

A

less

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102
Q

Alveolar Perfusion (Q): 2 that affect the distribution of blood flow to the lung.

A

Gravity and hydrostatic pressure affect the distribution of blood flow to the lung.

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103
Q

When standing upright, Explain where in the lung the blood flow is greatest and where it is the lowest?

A

There is less blood flow towards the apex of the lung, and there is more blood flow towards the base. This explains why there are higher V/Q ratios towards the apex and lower V/Q ratios towards the base.

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104
Q

Gas that remains equal in dependent and nondependent region of the lung

A

PAN2

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105
Q

Alveolar Ventilation, compliance and PACO2 in the nondependent region vs dependent region?

A

Nondependent –> Decrease alveolar ventilation and decrease alveolar compliance, and decrease PACO2 and increased PAO2

Dependent –> Increase alveolar ventilation and Increase alveolar compliance, and Increase PACO2 and decreased PAO2

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106
Q

Blood flow, vasculature pressure and vasculature resistance in the nondependent region vs dependent region?

A

Nondependent: Decrease Blood flow, decrease Vascular pressure, increase resistance
Dependent: Increase blood flow, increase vascular pressure, decrease resistance.

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107
Q

2 True statements about HPV :

A

Bronchioles constrict to minimize zone 1.

Blood passing through underventilated alveoli tends to retain CO2.

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108
Q

Hypoxic pulmonary vasoconstriction minimizes

A

shunt (not dead space).

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109
Q

V and Q are perfectly matched where the what 3 lines intersect.

A

V/Q ratio
Pulmonary blood flow
Ventilation

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110
Q

Towards the apex: ​ V ___Q

Towards the base: ​ V ____Q

A

> ;

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111
Q

Towards the apex: ​ V ___Q (blood flow or CO)

Towards the base: ​ V ____Q (blood flow or CO)

A

> ;

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112
Q

What is the most common cause of Hypoxemia in the PACU?

A

V/Q mismatch (specifically atelectasis) is the most common cause of hypoxemia in the PACU

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113
Q

V/Q mismatch (specifically atelectasis) is the most common cause of hypoxemia in the PACU. As FRC becomes smaller (the result of anesthesia and surgery), there is

A

less radial traction to hold the airways open. The result is atelectasis, right-to-left shunt, V/Q mismatch, and hypoxemia.

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114
Q

Treatment of hypoxemia in the PACU includes

A

humidified O2 and maneuvers designed to reopen the airways (mobility, coughing, deep breathing, and incentive spirometry).

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115
Q

Consequences of V/Q Mismatch: What Happens in Underventilated Alveoli?

A

Blood passing through underventilated alveoli tends to retain CO2 and is unable to take in enough oxygen.

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116
Q

Consequences of V/Q Mismatch: What Happens in OVERventilated Alveoli?

A

Blood passing through overventilated alveoli tends to give off an excessive amount of CO2. Remember that CO2 diffuses 20 times faster than oxygen. Even though this blood can eliminate a large amount of CO2, it cannot take up a proportionate amount of O2. This is explained by the flatness of the oxyhemoglobin dissociation curve.

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117
Q

With the oxyhgb dissociation curve, Once the PaO2 reaches 100 mmHg, hemoglobin is

A

fully saturated, and any additional oxygen that enters the blood must be dissolved in the blood (this is a very small amount). Said another way, an alveolus can transfer much more CO2 than it can O2. ​

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118
Q

A lung with V/Q mismatch does what to CO2?

A

eliminates CO2 from overventilated alveoli to compensate for the underventilated alveoli. This is why the PACO2-PaCO2 gradient usually remains small with V/Q mismatch. CO2 retention indicates failure of this compensation mechanism. ​

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119
Q

A lung with V/Q mismatch

A

cannot absorb more oxygen from overventilated alveoli to compensate for underventilated alveoli. This is why the PAO2-PaO2 gradient is usually large with V/Q mismatch.

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120
Q

What is the compensation for a V/Q mismatch?

A

The body responds to these imbalances by attempting to match ventilation to perfusion. ​To combat dead space (zone 1), the bronchioles constrict to minimize ventilation of poorly perfused alveoli. To combat shunt (zone 3), hypoxic pulmonary vasoconstriction reduces pulmonary blood flow to poorly ventilated alveoli.

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121
Q

What does the law of Laplace states?

What are the variables of the equation?

A 
The law of Laplace states that as the radius of a sphere or cylinder becomes larger, the wall tension increases as well.
The variables in this equation include: 
Tension
Pressure
Radius
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122
Q

The law of Laplace describes the relationship between

A

pressure, radius, and wall tension.

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123
Q

Cylinder shape Law of laplace equation? Examples are

A

Tension = pressure x radius ;

Examples: blood vessels, cylindrical aneurysms

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124
Q

Spherical shape Law of laplace equation?

A

Tension = Pressure x radius /2

Examples: Alveoli/ cardiac ventricles/ Saccular aneurysms.

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125
Q

Surfactant is a

A

A thin layer of water coats the alveoli. This increases surface tension, which promotes alveolar collapse

126
Q

According to the law of Laplace, the tendency of an alveolus to collapse is

A

directly proportional to surface tension and inversely proportional to alveolar radius.

127
Q

Each alveolus contains the same amount of surfactant. Difference between smaller and larger surfactant.

A

Larger alveoli have a relatively smaller concentration of surfactant.
Smaller alveoli have a relatively large concentration of surfactant.

128
Q

What types of pneumocytes begin producing surfactant between

A

Type 2 pneumocytes22 – 26 weeks with peak production occurring at 35 – 36 weeks.

129
Q

Fetal lung maturity can be hastened by

A

corticosteroids (betamethasone).

130
Q

Type 2 pneumocytes produce surfactant, which has 2 main functions :

A

Lowers surface tension and prevents alveolar collapse.

131
Q

In zone 1 there is

A

no pulmonary blood flow.

132
Q

In zone 3 pulmonary blood flow is

A

proportional to the arterial-to venous pressure gradient.

133
Q

In zone 1 alveolar pressure is higher than

A

arterial pressure

134
Q

In zone 2 ventilation is

A

matched to perfusion (not V > Q).

135
Q

Zone IV ​ = ​ Pulmonary Edema:

A

Pa > Pist > Pv > PA (aivA)

136
Q

In each alveolar unit, the ventilation to perfusion ratio is determined by the relative pressures between the:

​

A
  1. ​ Alveolus: PA
  2. ​ Arterial capillary: Pa
  3. ​ Venous capillary: Pv
  4. ​ Interstitial space: Pist
137
Q

Originally, gravity was believed to be the

​

A

most significant influence on the distribution of perfusion throughout the lung. This hypothesis stated that the base received more blood flow than the apex.

138
Q

Is there perfusion is zone 1

A

NO its dead space : PA>Pa>Pv

139
Q

This zone usually does not occur in normal lung?

A

Zone I

140
Q

What 3 conditions can increase Zone 1:

A

Hypotension

PE and Excessive airway pressures.

141
Q

What happens to the bronchioles to combat zone I?

A

To combat zone I, the bronchioles of unperfused alveoli constrict to reduce dead space.

142
Q

Zone II is known as the waterfall

A

Pa> PA> Pv

143
Q

Is there ventilation /perfusion or both in zone II?

A

There are ventilation and perfusion (V/Q = 1).

144
Q

In zone II, blood flow is directional proportion to the

A

blood flow is directly proportional to the difference in Pa - PA. The greater the difference between Pa - PA, the greater the blood flow. Because pulmonary capillary pressure and alveolar pressure change throughout the respiratory cycle, it is possible for a zone II unit to transiently change to zone I or zone III.

145
Q

Zone III ​ =

​

A

Shunt: ​ Pa > Pv > PA. Blood flow is a function of the pulmonary arteriovenous pressure difference (Pa - Pv).

146
Q

To combat zone III, hypoxic pulmonary vasoconstriction reduces

A

pulmonary blood flow to underventilated units.
Since the pressure in the capillary is always higher than the alveolus, the vessel is always open, and blood is always moving through it. This is why the tip of the pulmonary artery catheter should be placed in zone III.

147
Q

In the absolute sense, shunt occurs when there is

A

blood flow in the absence of ventilation (V/Q = 0).

148
Q

Most zone III units are

A

“shunt-like” - they are better perfused than they are ventilated (V < Q).
​

149
Q

Not All Shunt Occurs in the Lungs

Anatomic shunt describes any

A

venous blood that empties directly into the left side of the heart. Since this blood bypasses the lungs, it never has the opportunity to saturate with oxygen

150
Q

Sites that contribute to the normal anatomic shunt include: 3 ( TPB)

A 
Thebesian veins (drain left heart)
Bronchiolar veins (drain bronchial circulation)
Pleural veins (drain bronchial circulation)
151
Q

The pressure in the interstitial space exceeds the pressure in the pulmonary capillaries and the alveolus.

A

Exceeds the pressure in the pulmonary capillaries and the alveolus.
Pulmonary edema is a classic example of zone IV. It occurs when the rate of fluid entry into the pulmonary interstitium exceeds the rate of fluid removal by the

152
Q

Pulmonary edema : It is usually the result of 1 of 2 phenomena:

A
  1. Fluid is pushed across the capillary membrane by a significant increase in capillary hydrostatic pressure
  2. ​ Fluid is pulled across the capillary membrane by a profound reduction in pleural pressure.
153
Q

What is the classic examples of Pulmonary Edema ?

A

Pulmonary edema is a classic example of zone IV. It occurs when the rate of fluid entry into the pulmonary interstitium exceeds the rate of fluid removal by the lymphatic system.

154
Q

Fluid is pushed across the capillary membrane by a significant increase in capillary hydrostatic pressure. examples are

A

Fluid overload, mitral stenosis, and severe pulmonary vasoconstriction.

155
Q

Fluid is pulled across the capillary membrane by a profound reduction in pleural pressure.
Examples are ​

A

Laryngospasm or inhalation against a closed glottis leading to negative pressure pulmonary edema.

156
Q

A patient is breathing room air at sea level. The arterial blood gas reveals a PaO2 of 60 mmHg and a PaCO2 of 70 mmHg. Calculate the patient’s alveolar oxygen concentration. ​

A

62 mmHg

157
Q

The alveolar gas equation tells us the

A

partial pressure of oxygen in the alveolus.

158
Q

Alveolar oxygen ​ = ​

A

FiO2 ​ x ​ (Pb ​ - ​ PH2O) ​ - ​ (PaCO2 ​ / ​ RQ)

0.21 ​ x ​ ( 760 ​ - ​ 47 ) ​ - ​ (70 ​ / ​ 0.8) ​ = ​ 62.23 ​ ~ ​ 62 mmHg

159
Q

FiO2 is always higher than the partial pressure of oxygen in the alveolus (PAO2). Why?

​
​

A

Inspired air becomes 100% humidified as it moves towards the alveoli. This water takes up space and dilutes the oxygen concentration. ​
Furthermore, inspired air (lots of oxygen and no carbon dioxide) mixes with expired air (a little oxygen and lots of carbon dioxide). This dilutes the concentration of oxygen going towards the alveoli.

160
Q

The alveolar gas equation illustrates several 3 very important points.

​

A
  1. ​ Hypoventilation can cause hypercarbia and hypoxemia.
  2. ​ Supplemental oxygen can easily reverse hypoxemia, however it does nothing to reverse hypercarbia.
  3. ​ Hypercarbia can go undetected in the patient breathing supplemental oxygen. ​
161
Q

For example, hypoventilation increases PaCO2. The increased PaCO2 competes with

A

oxygen for space inside the alveolus and dilutes the concentration of oxygen. In this situation, supplemental oxygen can increase PAO2 as well as PaO2. You should understand that this only masks hypoventilation and will not treat the cause.

162
Q

Normal PAO2 ​calculation :

The patient’s PaO2 is ___mmHg . What is the most appropriate intervention

A

PAO2= 0.21 ​ x ​ ( 760 ​ - ​ 47 ) ​ - ​ 35 ​ = ​ 105.98 mmHg
​This patient’s PaO2 is 60 mmHg, so he has a normal A-a gradient (more on this in the next question). If we increase the FiO2 to 40% then
0.40 ​ x ​ ( 760 ​ - ​ 47 ) ​ - ​ 70 ​ = ​ 197.7 mmHg
​By increasing the FiO2 to 40%, we fixed the hypoxemia but not the hypercarbia. The most appropriate intervention is to increase his alveolar ventilation, which would remedy both the hypoxemia and hypercarbia.

163
Q

How is the respiratory quotient calculated (RQ)=

A

Respiratory Quotient = Carbon dioxide production/ oxygen consumption => 200ml/min/250ml/min = 0.8

164
Q

An RQ > 1 suggests_____which occurs with ______

A

lipogenesis. This occurs with overfeeding.

165
Q

An RQ of 0.7 suggests_____This occurs with

​

A

lipolysis; starvation.

166
Q

The A-a gradient is the difference between

A

PAO2 and PaO2.

167
Q

There are 5 causes of hypoxemia:

A

​hypoxic mixture, hypoventilation, diffusion limitation, V/Q mismatch, and shunt.

168
Q

The A-a gradient is normal in

A

hypoxic mixture and hypoventilation.

169
Q

The A-a gradient is increased by

A

diffusion limitation, V/Q mismatch, and shunt.

170
Q

By relating partial pressure of oxygen inside the alveolus to the partial pressure of oxygen in the arterial circulation, it helps us diagnose the cause of hypoxemia by indicating the

A

amount of venous admixture.

171
Q

2 main causes of hypoxemia related to the A-a Gradient?

A

Normal A-a Gradient

Increased A-a Gradient

172
Q

Normal A-a Gradient cause of hypoxemia include

A

reduced FiO2 and hypoventilation

173
Q

Increased A-a Gradient cause of hypoxemia include

A

Diffusion limitation
V/Q mismatch
Shunt

174
Q

Increased A-a Gradient cause of hypoxemia include: Diffusion limitation explanation

A

Capillary thickening hinders O2 diffusion

175
Q

Increased A-a Gradient cause of hypoxemia include:

V/Q mismatch

A

Poor matching of V and Q

176
Q

Increased A-a Gradient cause of hypoxemia include:

Shunt

A

Pulmonary blood bypasses alveoli

177
Q

When the Increased in A-a Gradient cause of hypoxemia include: Shunt, can it be treated with O2? why or why not?

A

No ; because there is no way for O2 to access the pulmonary capillary.

178
Q

When breathing room air, the normal A-a difference is ________why?

​

A

< than 15 mmHg. Why is this? The Thebesian, bronchiolar, and pleural veins bypass the alveolar-capillary interface and deliver deoxygenated blood to the left heart. This accounts for a very small physiologic shunt. ​

179
Q

The A-a gradient is increased by:

​
​

A 
Aging (closing capacity increases relative to FRC)
Vasodilators (decreased hypoxic pulmonary vasoconstriction)
Right-to-left shunt (atelectasis, pneumonia, bronchial intubation, intracardiac defect)
Diffusion limitation (alveolocapillary thickening hinders O2 diffusion)
180
Q

Why does aging increases the A-a gradient?

A

Closing capacity increases relative to FRC

181
Q

**Estimation of % Shunt

A

Shunt increases 1% for every 20 mmHg of A-a gradient

In our example, the A-a gradient is 218 mmHg, so this roughly translates into a shunt of 11% ​ (218 / 20 = 11)

182
Q

Tidal volume is

Spirometry cannot measure residual volume, therefore it also can’t measure total lung capacity or functional residual capacity. These are drawn in blue in the image.
Closing volume and capacity are dynamic measurements that assess small airway closure. They also can’t be measured with spirometry.

A

6 - 8 mL/kg.

183
Q

Vital capacity is.

A

65 - 75 mL/kg

184
Q

Functional residual capacity is

A

35 mL/kg.

185
Q

TV , VC, and FRC are all values calculated based on

A

All of these values are calculated on ideal body weight (not total body weight).

186
Q

Lung volumes males vs females.

A

are ~ 25% smaller in females

187
Q

Lung volumes tend to change with body position - they are

A

larger when sitting and smaller when supine.

188
Q

Obstructive lung disease tends to cause air trapping. Patients with (3 conditions) have increased RV, CC, and TLC

A

Asthma, emphysema, and bronchitis have an increased residual volume, closing capacity, and total lung capacity.

189
Q

Spirometry cannot measure

A

residual volume, therefore it also can’t measure total lung capacity or functional residual capacity.

190
Q

They also can’t be measured with spirometry.

A

Closing volume and capacity are dynamic measurements that assess small airway closure.

191
Q

Gas that can be forcibly inhaled after tidal inhalation is

A

IRV

192
Q

Gas that enters and exits the lungs during tidal breathing?

A

TV

193
Q

Gas the can be forcibly exhaled after tidal exhalation

A

ERV

194
Q

Volume of gas that remains in the lungs after complete exhalation and cannot be exhaled from the lungs

A

RV

195
Q

IRV volume

A

3000ml

196
Q

Tidal volume in mL is

A

500 ml

197
Q

ERV volume is___ml

A

1100ml

198
Q

The volume above residual volume where the small airways begin to close?

A

Closing volume

199
Q

Closing volume _ml

A

Variable.

200
Q

IRV + TV+ERV+ RV

A

TLC

201
Q

IRV + TV + ERV

A

VC

202
Q

IRV + TV

A

IC

203
Q

RV + ERV

A

FRC

204
Q

Closing capacity is

A

RV + CV

205
Q

A lung capacity includes

A

2 or more lung volumes.

206
Q

2 conditions that can reduce FRC

A

Obesity

Pulmonary edema

207
Q

The FRC is the lung volume where the

​

A

inward elastic recoil of the lungs is balanced by the outward elastic recoil of the chest wall (FRC = RV + ERV).

208
Q

Patients with COPD and advanced age on FRC

A

increased FRC. Air trapping increases RV, and this increases FRC.

209
Q

FRC is reduced (2)

A

by obesity and pulmonary edema.

210
Q

Patients with COPD and advanced age have an _____FRC.

A

increased

211
Q

Air trapping on RV and FRC

A

Air trapping increases RV, and this increases FRC.

212
Q

Functional residual capacity is the

​
Diaphragmatic tone and position also affect FRC.
Normal FRC = 35 mL/kg.

A

volume of air in the lungs at end-expiration.

213
Q

What is the reservoir of oxygen that prevents hypoxemia during apnea?

A

FRC

214
Q

At FRC, What happens with the recoil of the lungs?

A

the inward elastic recoil of the lungs is balanced by the outward elastic recoil of the chest wall – this is called static equilibrium.

215
Q

The inward elastic recoil of the lungs is balanced by the outward elastic recoil of the chest wall – this is called

A

static equilibrium.

216
Q

How to Measure FRC

A

FRC can be measured indirectly by nitrogen washout, helium wash-in, or body plethysmography.

217
Q

Can FRC be measured by Spirometry?

A

FRC cannot be measured with spirometry, because the residual volume cannot be exhaled and RV is a component of the FRC.

218
Q

Conditions that reduce FRC have several things in common. Name 3

A

they reduce outward lung expansion and or reduce lung compliance.

219
Q

When FRC is reduced, intrapulmonary shunt (zone 3)

A

increases. PEEP acts to restore FRC by reducing zone III.

220
Q

How does general anesthesia affect FRC?

A

GA decreases FRC because it ships the diaphragm up (cephalad) about 4 cm and result in decreased muscle tone and increased expiratory muscle tone.

221
Q

How does obesity affect FRC?

A

Decreases FRC because it decreases chest wall compliance and increase airway collapsibility .

222
Q

How does pregnancy affect FRC?

A

Pregnancy shift diaphragm up as a result of the gravid uterus , decreases chest wall compliance.

223
Q

How is neonate FRC affected?

A

Decrease FRC because less alveoli leads to decrease lung compliance. Cartilaginous ribcage that is prone to collapse

224
Q

How does advanced age affect FRC?

A

Increase FRC, decrease elastic lung tissue leads to air trapping leading to increase RV and increase FRC.

225
Q

Name 3 positions that decrease FRC?

A

Supine, Lithotomy and Trendelenburg

226
Q

Name 3 positions that increase FRC?

A

Prone, sitting and lateral

227
Q

What is the cause of the decrease in FRC when in the lithotomy position?

A

Gravity alters the distribution of pulmonary blood flow.

228
Q

4 other things that can decrease FRC other than positions ?

A 
Paralysis
Inadequate anesthesia
Excessive IV fluids
HIgh FiO2
Reduced pulmonary compliance.
229
Q

3 things that can increase FRC other than positions ?

A

Obstructive lung disease
PEEP
Sigh breaths

230
Q

How does obstructive lung disease increase FRC

A

Air trapping–> increase RV and increase FRC

231
Q

How does PEEP increase FRC?

A

Recruits collapsed alveoli
partially overcomes effects of GA
decrease venous admixture –> Increase PaO2

232
Q

Closing capacity is the sum of closing volume and:

A

Residual volume

233
Q

As a person exhales, there is a point where pleural pressure exceeds airway pressure.
​

A

This external force collapses the small airways that lack cartilage and traps gas distally in the alveoli. Since pleural pressure is higher in the dependent region of the lung, the airways in this region close first.

234
Q

Closing Volume is the point at which

A

dynamic compression of the airways begins. Said another way, it is the volume above residual volume where the small airways begin to close during expiration.

235
Q

Factors that increase closing volume (CLOSE-P):

​

A 
COPD
Left ventricular failure
Obesity
Supine position
Extremes of age
Pregnancy
236
Q

Factors that Affect Closing Volume & Capacity

​

A

While closing volume is very important, the relationship between functional residual capacity and closing capacity is of much greater importance, because this will determine if the airways collapse during tidal breathing.

237
Q

Under normal circumstances, FRC relationship to CC?
Anything that decreases FRC relative to CC or anything that increases CC relative to FRC will convert normal V/Q units to low V/Q units or shunt units.
PEEP can reverse this process by increasing the FRC relative to CC.

A

the FRC is greater than CC (airways do not collapse during tidal breathing).

238
Q

When CC is greater than FRC, airway closure occurs when? What 2 things does it contribute to?

A

occurs during tidal breathing. This contributes to intrapulmonary shunting and hypoxemia.

239
Q

Anything that decreases FRC relative to CC or anything that increases CC relative to FRC will

A

convert normal V/Q units to low V/Q units or shunt units.

PEEP can reverse this process by increasing the FRC relative to CC.

240
Q

How Does Age Affect Closing Capacity?

​

A

In a young, healthy patient, airway closure occurs just above residual volume. As we age, pleural pressure becomes progressively higher such that the small airways begin to close sooner and at higher lung volumes. This explains the progressive reduction in PaO2 that occurs with aging.

241
Q

Consequences of Aging:

​

A

Increased FRC
Increased closing capacity
Increased residual volume
Decreased vital capacity

242
Q

How Do Anesthesia & Age Affect Closing Capacity?

​

A

By age 30, CC ~ FRC when under general anesthesia.
By age 44, CC ~ FRC when supine. some say 45
By age 66, CC ~ FRC when standing so say 65

243
Q

How Do We Measure Closing Volume & Closing Capacity?

A

Closing capacity is best measured by washout of a tracer gas, such as nitrogen or xenon-133. This gas is inhaled at residual volume, and the measurement is taken as the patient exhales from total lung capacity.

244
Q 
Oxygen content (CaO2) tells us what much?
​

Most oxygen forms a reversible bond with hgb, while the remainder dissolves into the blood according to Henry’s law.

A

how much oxygen is present in 1 deciliter of blood.

245
Q 
Calculate the patient's arterial oxygen content from the data set:
Hgb 9 g/dL
Heart rate 100 bpm
Stroke volume 70 mL
SaO2 90%
PaO2 60 mmHg
A

11

Formula is (1.34 x Hgb xSaO2/100) + (PaO2 x 0.003)

246
Q

DO2 ​ =

A

​ CaO2 ​ x ​ CO ​ x ​ 10

247
Q

Most oxygen forms a

A

reversible bond with hgb, while the remainder dissolves into the blood according to Henry’s law.

248
Q

Note that________ is needed for oxygen delivery (DO2) but not oxygen carrying capacity (CaO2).

A

CO (HR x SV)

249
Q

After oxygen diffuses through the alveolar capillary membrane, it is transported by the blood in 2 ways:

A

Reversibly binds with hemoglobin (97%)

Dissolves in the plasma (3%)

250
Q

Oxygen Bound to Hemoglobin ​

A

(1.34 ​ x ​ Hgb ​ x ​ SaO2)

251
Q

Most of the oxygen in the blood reversibly binds with hemoglobin. What describes the characteristics of this bond?

A

The oxyhemoglobin dissociation curve

252
Q

Each gram of hemoglobin molecule can carry a theoretical maximum of

A

1.39 mL of molecular oxygen.

253
Q

Normal Hgb and Hct values: for male and female

A

Male: ​ ​ ​ ​ 15 g/dL ​ and ​ 45%
Female: ​ 13 g/dL ​ and ​ 39%

254
Q

Oxygen Dissolved in the Plasma ​

A

(PaO2 ​ x ​ 0.003)

255
Q

Dissolved O2 is measured by PaO2.

A

PaO2 should be used to determine gas exchange in the lungs and not as a measure of oxygen content in the blood

256
Q

Oxygen dissolves in the plasma according to_____ law. ​

A

Henry’s

257
Q

The concentration of gas in a solution is___________ above the solution.

A

directly proportional to the partial pressure of the gas

258
Q

The solubility coefficient for oxygen is

A

0.003 mL/dL/mmHg.

259
Q

Oxygen and. solubility compared Co

A

Oxygen is 20 times less soluble than CO2.

260
Q

PaO2 should be used to determine

A

gas exchange in the lungs and not as a measure of oxygen content in the blood

261
Q

Again, CaO2 only tells us how much

A

O2 is contained in the blood (bound to hgb + dissolved).

262
Q

Oxygen delivery (DO2) tells us how fast a

A

quantity of O2 is delivered to the tissues. The cardiac output is the deriving mechanism of DO2.

263
Q

DO2 =

A

CaO2 x CO x 10 = 1000 ml/min
Since hemoglobin is measured as g/dL and cardiac output is measured as L/min, we need to convert all of the units to liters. The number 10 is a conversion factor that accomplishes this goal.

264
Q

Oxygen Consumption (VO2): We can use the______principle to calculate oxygen consumption.

A

Fick It assumes that VO2 is the difference between the amount of O2 that leaves the lungs and the amount of O2 that returns to the lungs. The difference between these values is the amount of O2 that was consumed by the body. The conversion factor of 10 is used for the same reason as DO2.

265
Q

Numbers you must know for VO2

A

VO2 = 3.5 mL/kg/min

VO2 ~ 250 mL/min (assumes 70-kg male)

266
Q

P50 is the PaO2 where

A

hemoglobin is 50% saturated with oxygen.

267
Q

Decreased P50 (left shift):

A

Hgb has a stronger hold on oxygen.

Examples: ​ Hgb F, hypocarbia, and carboxyhemoglobin

268
Q

Increased P50 (right shift):

A

Hgb is more willing to release oxygen.

Examples: ​ acidosis, hyperthermia, and increased 2,3 DPG

269
Q

2,3-DPG is produced during

A 
RBC glycolysis (Rapoport-Luebering pathway).
It maintains the curve in a slightly right shifted position at all times.
270
Q

What does hypoxia increases and what does it facilitates?

A

Hypoxia increases 2,3-DPG production. This facilitates O2 offloading. ​

271
Q

2,3 DPG is an important compensation mechanism during

A

chronic anemia

272
Q

In banked blood, the concentration of 2,3-DPG______ What does that mean?

A

falls. This shifts the oxyhemoglobin dissociation curve to the left and reduces the amount of O2 available at the tissue level.

273
Q

Other Hgb and OxyHgb curves

A

Hgb F doesn’t respond to 2,3-DPG, which explains why Hgb F has a left shift (P50 =19 mmHg).

274
Q

Bohr Effect

​

A

CO2 and hydrogen ions cause a conformational change in the hemoglobin molecule; this facilitates the release of oxygen. Said another way, CO2 and H+ cause Hgb to release oxygen.

275
Q

The oxyhemoglobin dissociation curve tells us the tendency of -_______

A

hemoglobin to bind oxygen.

276
Q

The P50 is the

A

PaO2 where hgb is 50% saturated by oxygen. A lower P50 reflects a left shift, and a higher P50 reflects a right shift.

277
Q

Maximum O2 loading occurs at a

A

PaO2 of ~ 100 mmHg. A PaO2 above this cannot improve O2 loading, but it does increase the amount of O2 that is dissolved in the plasma.

278
Q

Many of the conditions that shift the curve are related to

A

metabolic rate.

279
Q

Tissues with a high metabolic rate consume

A

more O2 and produce more CO2, hydrogen ions, and heat. This causes a right shift (right = rise in temp, 2,3-DPG, CO2, and H+).
Most hemoglobinopathies cause a left shift.

280
Q

Tissues with a high metabolic rate consume

A

more O2 and produce more CO2, hydrogen ions, and heat. This causes a right shift (right = rise in temp, 2,3-DPG, CO2, and H+).

281
Q

Most hemoglobinopathies cause a ____shift.

A

Left

282
Q

1 molecule of glucose converts to

A

38 molecules ATP.

283
Q

What is the energy currency in the body?

A

Adenosine triphosphate (ATP)

284
Q

ATP It is produced by

A

oxidation of proteins, carbohydrates, and fats (ADP + Pi → ATP).
It is consumed by reactions necessary for life (ATP → ADP + Pi).
The phosphate bond is a high energy bond.
ATP can’t be stored, so the supply must be continuously replenished.

285
Q

What is primary substrate used for ATP synthesis.

A

Glucose

286
Q

Aerobic metabolism produces much

​

A

more ATP than anaerobic metabolism.

287
Q

There are 3 key processes involved in aerobic glucose metabolism:

A

glycolysis, Krebs cycle, and electron transport.

288
Q

Glycolysis ​ (Glucose ​ → ​ Pyruvic Acid)

The primary goal of glycolysis is

A

to convert 1 glucose to 2 pyruvic acid molecules. The fate of pyruvic acid depends on whether or not oxygen is available.

289
Q

In the absence of oxygen, pyruvic acid is converted to

A

lactate in the cytoplasm. ​
If oxygen is available, pyruvic acid is transported into mitochondria.
​

290
Q

Next, 2 molecules of pyruvic acid are converted into

A

2 molecules of Acetyl Coenzyme A.

291
Q

2,3 DPG is produced in the Rapoport-Luebering pathway about halfway through glycolysis. The more glucose molecules that go through glycolysis, the more

A

2,3 DPG is produced.

292
Q 
Krebs Cycle (Citric Acid Cycle)
Krebs cycle takes place in the
A

matrix of the mitochondria.

293
Q

Krebs cycle The reaction begins when

A

oxaloacetic acid and Acetyl coenzyme A react to produce citric acid.

294
Q

The reaction ends with the production of

A

oxaloacetic acid (which is reused at the beginning of the next cycle), NADH, and CO2.

295
Q

Krebs cycle: The primary goal of this reaction is to

A

produce a large quantity of H+ ions in the form of NADH. These are used in electron transport.
Products of protein and lipid metabolism can also enter Krebs cycle.

296
Q

Krebs cycle NET ATP gain is

A

2

297
Q

Glycolysis ​ is the conversion of

A

(Glucose ​ → ​ Pyruvic Acid)

298
Q

Oxidative Phosphorylation Pathway

A

The primary goals of glycolysis and Krebs cycle is to liberate hydrogen from glucose. Up to this point, there has only been a net gain of 4 molecules of ATP for 1 molecule of glucose, so we haven’t produced very much ATP…yet…

299
Q

NADH is split into

A

NAD+, H+, and 2 electrons. A proton gradient is generated across a membrane, which drives ATP synthesis with the help of ATP synthase. ​

300
Q

Oxidative Phosphorylation: The electrons are fed into the _______mechanism.

A

chemiosmotic

301
Q

ATP is used to carry out

A

energy-dependent processes in the body.

302
Q

The end products of oxidative phosphorylation are

A

water and 34 ATP molecules.

303
Q

Serves as the final electron acceptor.

A

Oxygen; Oxidative Phosphorylation

304
Q

Net Gain Oxidative Phosphorylation

A

34 ATP

305
Q

Lactic Acid Pathway
Remember that_______is the final electron acceptor in electron transport, so if there is no oxygen, this reaction backs up.

The accumulation of lactic acid creates a lactic acidosis, which is an anion gap metabolic acidosis. ​
The body’s enzymes tend not to function properly in an acidic environment and serves as the basis of the altered homeostasis during times of acidosis. ​
When the oxygen supply is re-established, intracellular lactate is converted back to pyruvic acid inside the cell, and aerobic metabolism starts again. ​ Serum lactate is cleared primarily by the liver.

A

oxygen. Since pyruvic acid isn’t used, its concentration increases.

306
Q

The lactic acid pathway provides an

A

alternative mechanism to convert pyruvic acid to ATP, albeit a very small amount of it - just 2 molecules. In addition to producing less ATP, there is also another problem - lactic acid is the end product of this pathway. So, the lactic acid pathway doesn’t back up, lactate is released into the extracellular space and the circulation. If oxygenation isn’t restored, complications of lactic acidosis ensue.

307
Q

The accumulation of lactic acid

A

creates a lactic acidosis, which is an anion gap metabolic acidosis. ​ The body’s enzymes tend not to function properly in an acidic environment and serves as the basis of the altered homeostasis during times of acidosis. ​ When the oxygen supply is re-established, intracellular lactate is converted back to pyruvic acid inside the cell, and aerobic metabolism starts again. ​

308
Q

Serum lactate is cleared primarily by the

A

liver

309
Q

CO2 is the by-product of______. It diffuses from the cells into the venous circulation and then diffuses into erythrocytes. ​

A

aerobic respiration

310
Q

In the presence of carbonic anhydrase (inside the RBC),

A

CO2 and H2O react to form H2CO3. Carbonic acid rapidly dissociates into H+ and HCO3-. The H+ is buffered by hemoglobin, and the HCO3- is transported to theplasma to function as a buffer. ​
Cl- is transported into the erythrocyte to maintain electroneutrality. This is known as the chloride or Hamburger shift.

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