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Pathophysiology I > Respiratory Physiology > Flashcards

Respiratory Physiology Flashcards

1
Q

What are the principle functions of respiratory physiology?

A

Exchange gas between lung and blood
Regulate the blood hydrogen ion concentration
Immunologic function

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2
Q

Where does the electron transport chain take effect within the mitochondria?

A

Cristae, O2 accepts an electron and creates a gradient

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3
Q

When glucose is taken into the mitochondria what does it break down and form?

A

Pyruvate, a three carbon chain

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4
Q

What is pyruvate broken down to for during oxidative phosphorylation?

A

Acetyl CoA

CO2

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5
Q

What product of pyruvate enters the citric acid cycle?

A

Acetyl CoA

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6
Q

What occurs during the critic acid cycle?

A

Reduction of NAD/FADH

Production of CO2

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7
Q

How does phosphorylation of ADP to ATP occur?

A

It is a product of a proton gradient

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8
Q

How many ATP are formed by the electron transport chain?

A

36 (Total 38 created but two are used for the process)

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9
Q

At the end of the electron transport chain what can stop the gradient?

A

Not removing electrons

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10
Q

What transports the hydrogen into to the electron transport chain?

A

NAD

FADH

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11
Q

What are the products when NAD and FADH combine with a hydrogen and an electron?

A

NADH

FADH2

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12
Q

What process occurs when NADH and FADH2 enter the electron transport chain?

A

Oxidation

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13
Q

What is the electron used for in the electron transport chain?

A

Move hydrogen ion against its concentration gradient into the intermembrane space

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14
Q

What does the intermembrane have a lower pH?

A

Accumulation of hydrogen ions

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15
Q

What is the importance of oxygen in the electron transport chain?

A

Removes electrons in order to keep the gradient

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16
Q

What equation is representative of the electron transport chain?

A

2Protons + 2Electrons + 1/2O2 –> H2O

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17
Q

Where does the H2O go once it is formed at the end of the electron transport chain?

A

It diffuses along its concentration gradient out of the cell

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18
Q

How is ATP formed in the electron transport chain?

A

Hydrogen passes by last protein to create ADP which is then phosphorylated into ATP, a stored form of energy

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19
Q

Where is CO2 predominately formed during oxidative phosphorylation?

A

During the citric acid cycle and when pyruvate is converted to Acetyl CoA

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20
Q

What is pyruvate converted to if O2 is not present?

A

Lactate in the liver = Lactic acidic

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21
Q

How many ATP are created from one glucose molecule in anaerobic metabolism?

A

2 Molecules of ATP

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22
Q

If O2 is introduced back into metabolism what happens to the lactic acid that was created?

A

It is converted back to pyruvate

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23
Q

About how much oxygen is consumed by oxidative phosphorylation?

A

90%

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24
Q

How is lactic acid formed in the liver?

A

A hydrogen ion is added to a carboxycilic acid

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25
Q

Define pressure.

A

The force exerted by the collection of particles (browning motion)

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26
Q

What law states the total pressure of a gas is equal to the sum of the pressure of the individual gases in a mixture?

A

Dalton’s Law

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27
Q

According to boyle’s law how is pressure and volume affected by inspiration?

A

As volume increases pressure decreases

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28
Q

According to boyle’s law how is pressure and volume affected by expiration?

A

As volume decreases pressure increases

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29
Q

What gas law states the amount of gas dissolved in a liquid is directly proportional to the pressure applied to the gas as it overlies the liquid?

A

Henry’s Law

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30
Q

For every 1mmHg of O2 how much O2 is dissolved in the blood?

A

0.003mL O2/100mL of blood

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31
Q

For every 1mmHg of CO2 how much is dissolved in the blood?

A

0.067mL of CO2/100mL of blood

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32
Q

How is CO2 predominately carried in the blood?

A

HCO3

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33
Q

What is the driving force for O2 to bind to Hgb?

A

The partial pressure of dissolved O2 in the blood

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34
Q

What is the normal venous CO2?

A

About 46mmHg

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35
Q

Why is it beneficial to have majority of the CO2 as bicarbonate in the blood?

A

Modest changes in CO2 do not drastically impact the acid base balance

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36
Q

How does the rib cage move on inspiration?

A

Up and out, increasing the AP diameter and long axis by the diaphragm moving down

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37
Q

What portion of ventilation is made up of the diaphragm contracting downward?

A

75%, other 25% from the external intercostal muscles

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38
Q

What accessory muscles are used for inspiration in a patient with respiratory distress?

A

Sternocleidomastoid muscle
Scalene muscles
Pectoralis muscles

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39
Q

How does exhalation occur?

A

Passive, relaxing of muscles and elastic forces of the lungs take over

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40
Q

What muscles are used to actively exhale?

A 
Diaphragm
Internal intercostals (pull rib cage down)
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41
Q

Where do the conducting airways extend?

A

Trachea to the Terminal bronchioles

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42
Q

About how many branches are thought to be in the conducting airways?

A

60,000

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43
Q

What augments radial traction in the lungs?

A

Volume-directly related

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44
Q

What type of gas flow is in the trachea and bronchus?

A

Turbulent gas flow

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45
Q

Why isn’t there turbulent flow in the small airways of the lung?

A

Collectively they have a large surface area

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46
Q

What type of tissue do the larger airways have that help to keep them patent?

A

Cartilage

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47
Q

What type of cells generate mucus?

A

Goblet cells

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48
Q

What causes mucus secretion from goblet cells?

A

Direct irritants and particulate

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49
Q

What cause mucus secretion from mucus glands in the parenchyma?

A

Neuronal-Ach

Hormonal

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50
Q

Since cartilage isn’t present in the smaller airways what keeps them open?

A

Volume and radial traction

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51
Q

What type of cells form the epithelial wall in the alveoli?

A

Type I cells

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52
Q

What is the function of the type two cells?

A

Secrete surfactant

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53
Q

Other than producing surfactant, what is an additional skin of type II cells in the alveoli?

A

They can differentiate and form type one cells

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54
Q

What is the purpose of having a separate blood flow going to the conducting airways?

A

Provide blood flow and nutrients, down to the respiratory bronchioles

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55
Q

Why is the O2 in the pulmonary circulation decreased after the bronchial connection is made?

A

The bronchial connection brings venous blood from oxygenating the tracheobronchial tree

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56
Q

What type of resistance is in the pulmonary circulation?

A

Low resistance, high capacitance

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57
Q

Why is it beneficial for the diameter of the capillary membrane to be small making the RBCs flatten out?

A

Shorter distance for O2 to be dissolved into the blood and diffusion into the tissues

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58
Q

Why is it significant that the endothelial cells have large junctions?

A

Walls of capillary have a good chance of leaking fluid

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59
Q

What is the purpose of the lymphatic system?

A

Drains leakage from the capillaries and returns back to the right side of the heart

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60
Q

What is basically the only way leakage occurs in the alveoli?

A

When damage to the alveoli occurs

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61
Q

Whats the difference between transudate and exudate?

A 
Transudate = serum part of the blood
Exudate = liquid plus cellular debris
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62
Q

What nerve controls PSNS activity to the small airways?

A

Vagus nerve

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63
Q

What effect does the PSNS have on the small airways?

A

Bronchoconstriction

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64
Q

What autonomic system has predominately humoral control of the small airways?

A

SNS

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65
Q

What hormone effect the small airways and was is the result?

A

Epinephrine –> B2 receptors = bronchodilation

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66
Q

What physical and chemical effect control airway smooth muscle tone?

A

Airway protection, cillia, mucus

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67
Q

What cellular mechanisms control airway smooth muscle tone?

A

Activation of inflammatory cells

Cytokine production

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68
Q

What autonomic innervation is to the diaphragm?

A

Phrenic nerves (bilateral)

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69
Q

Where is the origin of the phrenic nerve?

A

C3-C5, injury above C5 = no spontaneous ventilation

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70
Q

What peripheral nerve block has a high incidence of blocking the phrenic nerve?

A

Interscalene block

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71
Q

What can be seen on a chest x-ray is unilateral phrenic nerve block has occurred?

A

Elevated hemidiaphragm

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72
Q

How much is pulmonary function decreased with a unilateral phrenic nerve block?

A

25% decreased pulmonary function

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73
Q

What is the most resistant respiratory muscle to neuromuscular blockade?

A

Diaphragm

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74
Q

Why is the diaphragm the hardest muscle to block and the fast muscle to recover for neuromuscular blockade?

A

Increased Ach receptor density
Increased Ach release
Decreased AchE activity

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75
Q

What is the Ach doing at the NMJ when a neuromuscular blocking agent is present?

A

Competing for the Ach receptor

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76
Q

Why is the onset of the block relatively rapid at the diaphragm?

A

It receives high blood flow

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77
Q

What autonomic innervation occurs the tracheobronchial tree?

A

Parasympathetic and Sympathetic (poorly represented)

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78
Q

What is the predominant source of resting smooth muscle tone?

A

The vagus nerve

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79
Q

What are the effects of the vagal nerve on the tracheobronchial tree?

A

Bronchoconstriction and increased secretions

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80
Q

Describe the Hering-Breuer Reflex?

A

Deep inspiration inhibits parasympathetic output and reduces bronchomotor tone

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81
Q

How does parasympathetic activity affect the pulmonary vasculature?

A

Vasodilation via nitric oxide

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82
Q

What type of muscarinic receptors are located in the pulmonary smooth muscle?

A

M3

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83
Q

Once Ach has agonized the M3 receptors in the smooth muscle of the lungs, how does contraction occur?

A

G-protein mediated response –>causes calcium release resulting in muscle contraction –> bronchoconstriction

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84
Q

Where is the sympathetic nerve origin to the tracheobronchial tree?

A

T1-T4 (cardio-acclerator center)

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85
Q

What has a more significant sympathetic effect on the tracheobronchial than neural innervation?

A

Circulating catecholamines
B2 = bronchodilation and decreased secretions
A1 = may result in bronchoconstriction and decreased secretions

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86
Q

What type of adrenergic receptors are present in the pulmonary vasculature?

A

B2 and A1

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87
Q

What is the mechanism that occurs when a B2 receptor is activated by epinephrine?

A

G-protein–>cAMP–> produces both protein kinase A (relaxation) and decreased Ca

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88
Q

What is the neurotransmitter for non-cholinergic parasympathetic nerves?

A

Vasoactive intestinal peptide

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89
Q

What is the effect of the VIP?

A

Binds to receptor and releases NO resulting in relaxation

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90
Q

What is the outer layer of the pleura?

A

Parietal pleura

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91
Q

What is the inner layer of the pleura?

A

Visceral pleura

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92
Q

According to boils law what occurs on inspiration?

A

Decreased pressure causes and increase in volume

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93
Q

How does air come into the lungs?

A

When ambient pressure is greater than that in the alveoli pressure

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94
Q

What is the formula for flow into the lungs?

A

F = Patm-Palv

Resistance

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95
Q

What occurs on expirations?

A

Relations of diaphragm and external intercostals and elasticity of the lungs resulting in an greater pressure in the alveoli compared to the atmosphere

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96
Q

Why do we consider atmospheric pressure 0?

A

Because we all live at atmospheric pressure 760mmHg

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97
Q

Why is the tendency of the chest wall to expand?

A

Due to the musculature

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98
Q

Define transpulmonary pressure?

A

The pressure across the alveoli and the interpleural space

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99
Q

What is the formula for transpulmoanry pressure?

A

Ptrans = Palveolar - Pintrapleural

Ptp - Palv - Pip

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100
Q

Why can the concept of transpulmonary pressure be confusing?

A

Talking about positive numbers (minus a negative) the pleura is a negative value

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101
Q

What is the formula for transthroacic pressure?

A

Ptt = Palv - Body surface

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102
Q

How does the supine position affect the respiratory pattern?

A

Decreases rib cage excursion

Abdominal breathing dominates, diaphragm holds a higher position (abdominal contents shift cephalad)

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103
Q

How does the lateral position affect respiratory pattern?

A

Dependent hemidiaphragm assumes higher position

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104
Q

How does altering sarcomeres of the diaphragm affect breathing?

A

According to frank starling, diaphragm contracts more profoundly increased ventilation until falling off the curve

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105
Q

How does light anesthesia impact respirations?

A

Irregular breathing and breath holding

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106
Q

How much MAC produces rapid shallow breathing?

A

1.2

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107
Q

What effect does N2O and narcotics have on respirations?

A

Slow, deep breathing

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108
Q

What lung volume cannot be measured with spiromety?

A

Residual Volume

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109
Q

Why can’t residual volume be recorded on spirometry?

A

It is the amount of gas left in the lungs after maximal exhalation

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110
Q

What gas is used to measure residual volume?

A

Xenon

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111
Q

About how much volume is in a typical persons total lung capacity?

A

5800mL

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112
Q

About how much volume is in a typical persons tidal volume?

A

500mL

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113
Q

About how much volume is in a typical persons inspiratory capacity?

A

3500mL

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114
Q

About how much volume is in a typical persons inspiratory reserve volume?

A

3000mL

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115
Q

About how much volume is in a typical persons functional residual capacity?

A

2300mL

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116
Q

About how much volume is in a typical persons expiratory reserve volume?

A

1100mL

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117
Q

About how much volume is in a typical persons vital capacity?

A

4600mL

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118
Q

About how much volume is in a typical persons residual volume?

A

1200mL

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119
Q

What two volumes make up the functional residual capacity?

A

Residual volume

Expiratory reserve volume

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120
Q

What volumes make up the total lung capacity?

A

Inspiratory reserve volume
Tidal volume
Expiratory reserve volume
Residual volume

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121
Q

What volumes make up the vital capacity?

A

Inspiratory reserve volume
Tidal volume
Expiratory reserve volume

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122
Q

What two volumes make up the inspiratory capacity?

A

Inspiratory reserve volume

Tidal volume

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123
Q

Define inspiratory reserve volume?

A

Everything you can inhale above your tidal volume

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124
Q

What is it called when two or more volumes are being discussed?

A

Capacity

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125
Q

What is the average vital capacity?

A

6-7mL/kg

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126
Q

What is the importance of vital capacity when ventilating a patient?

A

It sets the limits on your ventilation because it is the most gas a person can exchange:
How much gas you can bring in
How much gas you can exhale

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127
Q

What is the importance of the FRC?

A

It is predominately where gas exchange takes place

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128
Q

When does the best gas exchange occur?

A

When the pause occurs between inspiration and expiration

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129
Q

What are the effects to the FRC when applying a anesthetic to a patient?

A

Decreased FRC which is responsible for gas exchange

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130
Q

What components decrease the FRC with anesthesia?

A

Decrease in AP diameter

Focused shift in abdominal contents

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131
Q

Define closing volume.

A

The volume in the lungs at which small airways start to close

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132
Q

When volume is loss why do the small airways begin to close?

A

Loss in radial traction

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133
Q

What is the difference between closing volume and closing capacity?

A

The capacity includes the residual volume in addition to the volume at which small airways close

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134
Q

In a normal healthy person, where should their closing volumes be?

A

Below FRC so small airways shouldn’t close during normal tidal breathing

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135
Q

How does aging affect closing volumes?

A

It causes the line to move up meaning some small airways are closed during normal tidal breathing

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136
Q

How does disease processes affect closing volumes?

A

The line can be above TV meaning they may be walking around with a lower PaO2

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137
Q

At what age does your closing volume start to impinge on your tidal volume?

A

65 y/o

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138
Q

At what age does your closing volume start to impinge on your tidal volume when placed in the supine position?

A

44 y/o

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139
Q

Define resistance.

A

The decline in pressure which results when a gas flows through a tube

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140
Q

What is the formula for resistance?

A

R = p1 - p2

Flow

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141
Q

What factors determine the degree of resistance in the airways?

A

If the flow is laminar or turbulent
The dimensions of the airway (diameter)
Viscosity of the gas (this doesn’t really change)

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142
Q

Define friction.

A

Resistance to flow in a tube caused by adhesive and cohesive forces

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143
Q

What are cohesive forces?

A

Attraction of the molecules for one another (Internal friction)

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144
Q

What are adhesive forces?

A

Attractive force for the side of the tube (external friction)

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145
Q

What causes the natural elasticity of the lungs?

A

High content of elastin fibers

Surface tension

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146
Q

How is surface tension created?

A

At the interface between a liquid and a gas where the liquid molecules are pulled together by cohesive forces

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147
Q

What does the Law of Leplace define?

A

The pressure gradient across the wall of a sphere

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148
Q

What is the formula for the Law of Leplace?

A

Pressure = 2 x tension

Radius

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149
Q

What alters the surface tension?

A

Surfactant

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150
Q

In the absence of surfactant what occurs when the radius decline?

A

Pressure increases because tension stays the same

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151
Q

How does surfactant impact surface tension?

A

Surface tension declines when the radius declines so that pressure remains constant regardless of size of the alveoli

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152
Q

What is the purpose of having nitrogen in the lungs?

A

It keeps the alveoli inflated

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153
Q

What does compliance measure in the respiratory system?

A

Measurement of elastic recoil (think distensibility)

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154
Q

What is the formula for compliance?

A

Change in volume

Change in pressure

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155
Q

What is the normal compliance of the lungs?

A

100mL/1cmH2O

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156
Q

When is static compliance measured?

A

At equilibrium, when ventilating a patient there is a pause before between inspiration and expiration, measured here

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157
Q

When is dynamic compliance measured?

A

Measured volume and pressure during an entire breath (rhythmic breathing)

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158
Q

What is the only factor taken into account when measuring static compliance?

A

Elasticity of the lung

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159
Q

What two factors are taken into account when measuring dynamic compliance?

A

Elasticity of the lung and Airway resistance

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160
Q

What is the formula for compliance?

A

1/Resistance

It is the opposite of resistance

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161
Q

Define total compliance in the respiratory system?

A

It is the sum of lung compliance and chest wall compliance

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162
Q

What is the formula for lung compliance?

A

Ptp = Palv-Pint

Transpulmonary pressure = alveolar pressure - intrapleural pressure

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163
Q

What is the typical amount of lung compliance?

A

200mL/1cmH2O

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164
Q

What is the formula for chest wall compliance?

A

Transthoracic pressure = alveolar pressure = body surface

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165
Q

What is the typical amount of chest wall compliance?

A

200mL/1cmH2O

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166
Q

What is the non-elastic resistance component in the lungs?

A

Airway resistance to gas flow

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167
Q

What is poiseuille’s law law?

A

F = pi x radius to the fourth x delta p

viscosity x length

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168
Q

How does airway resistance relate to poiseuille’s law?

A

It is the opposite, directly related to viscosity and the distance of the tube

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169
Q

What is the most important factor regarding airway resistance?

A

Diameter or the caliber of the airway (to the fourth power)

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170
Q

What are the two forms of non-elastic resistance?

A

Volume-related airway collapse

Flow-Related airway collapse

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171
Q

What is the radius dependent on in the small airways of the lungs?

A

Volume = radial traction since no cartilage or smooth muscle is present

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172
Q

How is airway resistance related to lung volume?

A

Inversely proportional

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173
Q

How does PEEP effect resistance?

A

PEEP increases end expiratory volume and therefore can reduce resistance

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174
Q

Why is flow-related airway collapse called non-physiologic?

A

We don’t typically forcefully exhale

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175
Q

What is flow related airway collapse?

A

Forceful expiration produces the reversal of the normal trans-pulmonary pressure and results in airway collapse

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176
Q

What causes dynamic airway compression in flow-related airway collapse?

A

Generation of positive interpleural pressure

Pressure drop across intrathoracic airways due to increased airway resistance

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177
Q

What are the two points of the respiratory cycle where atmospheric pressure and alveolar pressure have equilibrated?

A

End expiration

End inspiration

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178
Q

Define effort dependent expiration.

A

The more effort by the patient the greater the flow

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179
Q

What occurs when pressure in the airway is less than intrapleural pressure?

A

Restriction of the airway occurs

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180
Q

Define effort independent expiration.

A

No matter how hard a patient tries to exhale they cannot increase their flow

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181
Q

What is the equal pressure point?

A

The point at which the pressure in the airway is equal to the pressure in the intrapleural pressure

182
Q

How does pathology affect the equal pressure point?

A

It moves down farther into the lungs causing more areas to collapse

183
Q

What is tissue resistance?

A

Frictional resistance of lung tissue to gas flow

184
Q

What are the three elastic resistance factors?

A

Natural elasticity of the lugs
Surface tension
Measured by compliance

185
Q

What are the three non-elastic resistance factors?

A

Volume-related resistance to gas flow
Flow related resistance to gas flow
Tissue resistance

186
Q

What makes up the vast majority of resistance to air flow?

A

Elastic forces

187
Q

When is the work of breathing exerted during normal inspiration?

A

During inspiration

188
Q

When is work of breathing exerted during active expiration?

A

WOB performed by both inspiratory and expiratory muscles

189
Q

What forces have to be overcome for active expiration to occur?

A

Overcome the elastic recoil of the lungs and chest
Frictional resistance to gas flow in the airways
Tissue frictional resistance

190
Q

If an increase in resistance in the airways occurs, how does that affect muscle effort?

A

Increased inspiratory muscle effort

191
Q

What type of breathing pattern occurs in patients with fibrotic lung disease in order to compensate for the decrease in lung compliance?

A

Rapid shallow breathing in order to decrease the work of breathing

192
Q

What type of breathing pattern occurs in patients with obstructive lung disease in order to compensate for the increase in airway resistance?

A

Slow deep breathing

193
Q

Induction of anesthesia decrease the FRC by what percentage?

A

15-20%

194
Q

What is a common fallacy regarding muscle relaxation and a reduction in FRC?

A

FRC is not made significantly worse by muscle relaxation

195
Q

At what degree of trandelburg will further decrease a patients FRC?

A

> 30 degrees

196
Q

How do volatile anesthetics impact the FRC?

A

The increase in airway resistance as a product of decrease in FRC is not apparent due to a bronchodilatory effect of the volatile anesthetics

197
Q

What are some common anesthesia related causes of increased airway resistance?

A

Laryngospasm
Bronchospasm
Airway tumor
ETT

198
Q

How does the anesthetic provider avoid the issue of increased WOB during a procedure?

A

Mechanical ventilation

199
Q

What is a normal vital capacity?

A

60-70mL/kg

200
Q

Define Fick’s Law?

A

Diffusion is directly proportional to the surface area, the pressure gradient between the two and the diffusion coefficient
Inversely proportional to the thickness of the membrane

201
Q

How can the anesthetic provider alter delta p in fick’s equation?

A

Increasing the FiO2

202
Q

What is the alveolar gas equation?

A

PAO2 = FiO2 (Barometric-H2O) - (PaCO2/RQ)

203
Q

What is the typical respiratory quotient we use to calculate PAO2?

A

0.8 for a combined diet

204
Q

What is a quick way in the clinical setting to calculate PAO2?

A

FiO2 x 6

205
Q

How do you calculate the inspired O2 partial pressure?

A

PO2 = FiO2 (barometric - H2O) in mmHg

206
Q

What components make up the oxygen tension in the lungs?

A

Inspired gas mixed with dead space gas
O2 taken into the blood
CO2 added to the blood

207
Q

What is the oxygen content equation?

A

CaO2 = (1.34 x HgB x SaO2) + (PaO2 x 0.003) per 100mL of blood

208
Q

What is the formula for the amount of O2 delivered to the tissues?

A 
DO2 = CO x O2 content     OR
DO2 = CaO2 x QT
209
Q

What part of the arterial O2 content equation could be changed to represent venous content?

A

% Saturation (around .75%)

PaO2 (about 40mmHg)

210
Q

What part of the arterial O2 content equation could be changed to represent capillary content?

A

% Saturation (100%)

PaO2 will be higher than arterial

211
Q

Why is the pulmonary capillary O2 content greater than the arterial O2 content?

A

The capillaries come into direct contact with alveolus however, shunt or V/Q mismatch can dilute arterial blood making its content less than capillary blood

212
Q

How does temperature affect dissolved gases?

A

The colder the temperature, the more a gas is dissolved

213
Q

What is the typical arterial and venous oxygen content?

A 
CaO2 = 20
CvO2 = 15
214
Q

If you subtract the venous O2 content from the arterial O2 content what does that tell you?

A

O2 consumption

215
Q

At resting metabolic rate about how much O2 does a typical patient consume?

A

About 25%, leaving a large reserve

216
Q

About how much does oxygen consumption increase for a 1 degree centigrade increase in body temperature?

A

About 7% increase

217
Q

What is the lifespan of a RBC?

A

120 days

218
Q

What makes up the structure of hemoglobin?

A

Four protein subunits
2 alpha chains
2 beta chains
4 Heme subunits (iron porphyrin compounds)

219
Q

Why isn’t the globin considered a protein?

A

Its a polypeptide because it has less than amino acids

220
Q

What four subunits make up porphyrin?

A

Pyrollic subunits

221
Q

What is the significance of the four porphyrin molecules that are bound to the iron core?

A

Oxygen binds to the iron core

222
Q

What occurs to the iron molecule when the oxygen binds to it?

A

Fe2 –> Fe3 and a structural change occurs

223
Q

What is the significance of the structural change that occurs when oxygen binds to the iron molecule?

A

It opens up the structure and allows additional O2 to bind more readily

224
Q

How many O2 molecules bind to a Hgb molecule?

A

Four (for each Heme sites)

225
Q

Where does CO2 bind to the Hgb molecule?

A

At the nitrogen molecule that links the heme molecule to the amino acid on the globular protein

226
Q

What is the advantage of the confirmation change that occurs when CO2 binds to the Hgb molecule?

A

It facilitates O2 to move off of the Hgb this is known as the Bohr effect (tissue level)

227
Q

What occurs to O2 once it leave the Hgb molecule?

A

It is dissolved and contributes to the partial pressure that drives the O2 in the tissue

228
Q

Where does CO bind to on the Hgb molecule?

A

The same place as O2, the iron molecule

Will knock O2 off of the iron molecule

229
Q

How do you get the CO off of the Fe molecule?

A

Have to increase the partial pressure of O2 to compete for the site – will need hyperbaric chamber

230
Q

How much O2 is bound to each gram of Hgb?

A

1.31mL (1.34 in clinical setting)

231
Q

What is the Hgb saturation?

A

It is the amount of O2 bound to Hgb as a percent of total O2 binding capacity

232
Q

What is responsible for the S shape of the OxyHgb dissociation curve?

A

The increased affinity for O2 to bind as the confirmation change with each O2 occurs

233
Q

What is the value of the OxyHgb dissociation curve?

A

It allows us to predict what is happening to our patient

234
Q

What is the name of the point in the OxyHgb dissociation curve at 50% saturation?

A

P50 is the partial pressure of O2 at which 50% of the Hgb is saturated

235
Q

What is the typical P50?

A

27mmHg

236
Q

What causes a right shift in the OxyHgb dissociation curve?

A 
Acidosis (increased CO2)
Increased temperature 
Increased DPG (byproduct of metabolism)
237
Q

What is the purpose of a right shift in the OxyHgb dissociation curve?

A

It illustrates that oxygen is more readily available at a higher partial pressure, don’t have to wait for it to drop as low to get the O2

238
Q

What is the P50 if the OxyHgb dissociation is shifted to the right?

A

40, meaning at a higher partial pressure more O2 is released

239
Q

What factors cause a left shift in the OxyHgb dissociation curve?

A

Alkalosis (decreased CO2)
Decreased Temperature
Decreased DPG

240
Q

What is the P50 if a left shift in the OxyHgb dissociation curve has occurred?

A

About 17, partial pressure would have to drop more significantly in order to release O2

241
Q

What is the P50 in fetal circulation?

A

About 17, the fetus wants to hold on to that oxygen

242
Q

What substances can bind to Hgb at the O2 sites, displacing it and causing a left shift?

A

CO
Cyanide
Nitric Acid
Ammonia (N3)

243
Q

How can abnormal substances binding to Hgb affect oxygenation.

A

Decreases O2 carrying capacity

Impairs O2 release because of left shift

244
Q

How can drugs impair O2 carrying capacity?

A

Oxidizes iron to the ferric state (F3)

245
Q

What drugs cause a decrease in O2 carrying capacity?

A

Sulfonamides
Nitrates
Nitrites
Prilocaine

246
Q

Why isn’t Prilocaine used in practice any more?

A

It caused methemoglobinemia, converts Fe2–>Fe3 which does not allow to bind O2

247
Q

What are some variations in Hgb?

A

Fetal Hgb (2 Alpha, 2 gamma) –> left shift bind O2 tighter
Hgb A2
Sickle Hgb (one amino acid substitution)
Beta Thalasemia

248
Q

How do you calculate the alveolar arterial gradient?

A

PAO2-PaO2

249
Q

What is the normal gradient between the alveoli and the arterial blood concentration?

A
250
Q

How much does the A-a gradient increase as a person ages?

A

20-30mmHg

251
Q

Why do we see an increase in the A-a gradient as a patient ages?

A

The closing volume elevated into the tidal volume with age

252
Q

What is the normal a/A ratio?

A

Normal >75%

253
Q

What is a clinical trick to estimate arterial O2?

A

PaO2 = 102 - (Age)

(3)

254
Q

What is the most common mechanism of hypoxia?

A 
Increase in the (A-a)DO
Caused by:
     R-->L shunt
     Amount of V/Q mismatch
     Mixed venous O2 tension
255
Q

Define mixed venous.

A

Venous return to the right side of the heart coming from all different tissue beds throughout the body
All beds have a little bit different metabolic rate and collectively contribute a different O2 content (40mmHg)

256
Q

How is the (A-a)DO2 related to shunt?

A

It is directly proportional (shunt increase, gradient increases)

257
Q

How is (A-a)DO2 related to PvO2?

A

It is inversely proportional (PvO2 decreases gradient increases)

258
Q

What factors decrease Mixed venous O2 (PvO2)?

A

Decreased CO
Increased consumption
Decreased Hgb concentration

259
Q

What is the normal level of shunt naturally occurring in a human?

A

2-5%

260
Q

What two factors cause a severe decrease in the transfer of O2 from the alveolar blood to the arterial blood?

A

Combination of a low CO and increased shunt

261
Q

What factors is the DO2 dependent on?

A

CO
Hgb
PaO2

262
Q

How would you measure O2 consumption in regard to cardiac output?

A

VO2 = Qt (flow per minute) x (CaO2 x CvO2)

263
Q

Why is O2 consumption said to be independent of O2 delivery?

A

Resting we only use 25% thus a large reservoir is present to use if metabolic needs increase

264
Q

At what point does O2 consumption become dependent on O2 delivery?

A

When the reservoir reaches 250mL or below

265
Q

Where are the body’s oxygen stores?

A

Includes what is in the lungs (FRC)
Bound to Hgb
Dissolved in the body fluids

266
Q

What is the most important body oxygen store in the body?

A

O2 in the lungs at FRC

its about 480mL lasting about 115 seconds

267
Q

Why is it so important to pre oxygenate our patients?

A

It creates a larger store 2300mL of O2 delaying hypoxemia

About 4-5minutes

268
Q

What is considered hypoxemia?

A
269
Q

What determines alveolar CO2 tension?

A

Production and alveolar ventilation

270
Q

In the clinical setting, what change is most likely to occur that will increase CO2 tension?

A

Whatever my alveolar CO2 is, its dependent alveolar ventilation

271
Q

How do we calculate alveolar ventilation?

A

Rate x (tidal volume - dead space)

272
Q

What is the formula for alveolar CO2?

A

PACO2 = production x 0.863
ventilation

Knowing that ventilation is inversely proportional to the CO2 content and the production is directly proportional

273
Q

Why is it assumed that alveolar CO2 is almost identical t arterial CO2?

A

Because CO2 is so soluble

274
Q

Why don’t modest changes to CO2 change the content very much?

A

The body has a large capacity to store and buffer CO2

275
Q

What is the normal range of CO2 dissolved in the blood at any given time?

A

2600-2800mL compared to O2 at 1000mL

276
Q

What is the only reason for an elevation in PCO2?

A

The level of ventilation is not adequate for the amount of CO2 produced and delivered to the lungs

277
Q

What factors can always explain hypercapnia?

A

Not enough total ventilation
Too much of the total ventilation ends up as dead space
Combination of the two listed above

278
Q

What is pulmonary end capillary CO2 tension?

A

Virtually identical to PACO2

279
Q

What factors determine the PcCO2?

A

Rate of diffusion across the alveolar capillary membrane
Pulmonary capillary blood volume (70-100mL)
Transit time of blood in capillaries

280
Q

How does CO2 diffusion across the Alv-Cap membrane compare to O2?

A

CO2 is 20x faster than O2

281
Q

What measurements are virtually identical to the arterial CO2 tension?

A

PACO2

PcCO2

282
Q

What is the relationship between PaCO2 and V/Q?

A

Low V/Q tends to increase CO2 (not good ventilation thus a rise in CO2)
High V/Q tends to decrease CO2 (high ventilation gets rid of CO2 faster)

283
Q

What has to occur in order to see significant gradients between arterial and alveolar CO2?

A

Marked V/Q abnormalities

284
Q

Why do severe disturbances in V/Q usually fail to alter arterial CO2?

A

Reflex increases in ventilation occur due to hypoxia

285
Q

What is the normal PaCO2 to ETCO2 gradient?

A

2-5mmHg

286
Q

How does the normal range of PaCO2 compare to the normal range of ETCO2?

A

PaCO2 35-45mmHg

ETCO2 3-42mmHg

287
Q

What are the three main reasons why elevated CO2 is dangerous?

A 
Fall in pH (acidosis)
Decreased PaO2 (hypoxia) --> unless FiO2 is increased
Less well defended the patient is against a further decrease in ventilation
288
Q

What are the three forms of CO2 in the body?

A

Bicarbonate HCO3
Carbamino compounds
Dissolved CO2

289
Q

About how much of the CO2 in our body is in the HCO3 form?

A

90%

290
Q

Why are RBCs crucial for production of HCO3 from CO2?

A

Presence of carbonic anhydrase

291
Q

How is CO@ carries as a carbamino compound?

A

Primarily on the amino groups of Hgb

Reversibly with amino groups NH2 of blood proteins

292
Q

How much CO2 is dissolved in the blood?

A

0.067mL CO2/ 100mL of blood

293
Q

In order to avoid accumulating too much HCO3 in the cell, how does it leave while maintaining electroneurtrality?

A

Switches with Cl also know as the chloride shift

Hamburger shift

294
Q

What is the name of the process where both the H ion and CO2 bump oxygen off of the Hgb molecule at the tissue level?

A

Bohr effect

295
Q

What is the name of the process that occurs in pulmonary capillaries that drives off H ion and CO2 from the Hgb due to high partial pressure of O2?

A

Haldane effect

296
Q

How does CPR work even though you are exhaling CO2?

A

Also exhaling O2 which can be delivered to the patient

297
Q

What determines the respiratory quotient?

A

Based on the types of energy source consumed:
Fats 0.7
Carbohydrates 1
Proteins: 0.8

298
Q

Defines venous admixture?

A

When blood bypasses the pulmonary circulation and enters the arterial circulation
Also known as a shunt

299
Q

Why does end capillary blood look slightly different than arterial blood?

A

Some degree of venous admixture is added to the arterial blood

300
Q

What is the PO2 and PCO2 of atmospheric air?

A

PO2 =160mmHg

PCO2 = 0.3mmHg

301
Q

Why is the PO2 reduced after passing the upper airways?

A

Water vapor pressure is subtracted after humidification occurs

302
Q

What is the PO2 and the PCO2 in the dead space of the lungs?

A

PO2 150mmHg

PCO2 0.3mmHg

303
Q

After the new gas mixes with the mixed venous gas at the capillary, what is the new PO2 and PCO2 in the alveoli?

A 
PO2= 105mmHg
PCO2 = 40mmHg
304
Q

What is the PaO2 and the PaCO2 in the mixed venous blood?

A 
PaO2 = 40mmHg
PaCO2 = 46mmHg
305
Q

What values should end capillary PCO2 and PO2 resemble?

A

Those in the alveoli
PO2 105
PCO2 40

306
Q

What are the normal values of PO2 and PCO2 after venous admixture has been added to the arterial blood?

A

PO2 100mmHg

PCO2 40mmHg

307
Q

Define minute ventilation?

A

The sum of all exhaled gas volume in one minute

RR x TV

308
Q

What is the difference between alveolar ventilation and minute ventilation?

A

Alveolar ventilation is just gas exchange each one minute and does not include the conduction airways

309
Q

How do you calculate alveolar ventilation?

A

RR x (TV-dead space)

310
Q

What two components make up physiologic deadspace?

A 
Anatomical deadspace  (conducting airways)
Alveolar deadspace (non-perfused alveoli)
311
Q

How can we roughly calculate a patient’s deadspace in the clinical setting?

A

2mL/kg OR

Use their weight in pounds

312
Q

What is the ratio of dead space to total tidal volume in the average adult?

A

About 30%

313
Q

What is Bohr’s equation?

A

Vd =(TV) x (PaCO2 - PetCO2) / PaCO2

314
Q

How does posture affect dead space?

A

Upright increase dead space

Supine postion decreases dead space

315
Q

What effect does gravity have on dead space?

A

When standing gravity causes more distention of the lung opening more up more airways allowing more volume to enter

316
Q

How does the position of the airway influence deadspace?

A

Neck extension causes an increase in dead space

Neck flexion causes a decrease in dead space

317
Q

How does age affect dead space?

A

As we age, dead space increases

318
Q

How does an ETT impact dead space?

A

Decrease dead space since it is bypassing the conduction airways

319
Q

How does positive pressure ventilation impact dead space?

A

Increase dead space, ventilating independent airways where circulation is worse

320
Q

What drugs specifically impact dead space?

A

Anticholinergics –> bronchodilation which increases volume in the airways

321
Q

How does pulmonary perfusion impact dead space?

A

Decreased perfusion increases dead space
PE
HoTN

322
Q

How does pulmonary vascular disease affect dead space?

A

Poor capillary circulation increases the amount of dead space

323
Q

What is one of the first major signs that a patient may have a PE?

A

Initially end tidal CO2 drops greatly in a short amount of time: 40 –> 20

324
Q

Why is a high rate low TV mode of ventilation not always the most effective?

A

At a certain point, the volume is so low that you might only be ventilating the dead space

325
Q

Why is alveolar ventilation uneven in any body position?

A

We do not have perfect V/Q matching

326
Q

What regions of the lungs are ventilated the best?

A

Lower dependent lung units better ventilated than upper independent lung units

327
Q

Progressing down the lung, for every 3cm decrease of lung height, how much does the intrapleural pressure change?

A

Intrapleural pressure becomes less negative by 1cmH2O

328
Q

Why does ventilation steadily increase as you move down the lung and then get worse?

A

The alveoli are so compressed in the very dependent lung regions, not good ventilation

329
Q

How much blood flow through the pulmonary vasculature in one minute?

A

The same as CO about 5L/min

330
Q

About how much blood is in the capillaries at one time?

A

70-100mL

331
Q

Why does a change in CO or blood volume produce a change in pressure in the pulmonary vasculature?

A

It is a high capacitance low pressure system

332
Q

How much does pulmonary volume change when shifting a patient from the supine to the upright position?

A

Decrease pulmonary volume by 27%

333
Q

What two normal processes increase pulmonary blood volume?

A

Systole and Inspiration

334
Q

How does tone in the vasculature affect pulmonary blood volume?

A

Vasoconstriction increase pulmonary blood volume
Vasodilation decreases pulmonary blood volume
Lungs considered a reservoir

335
Q

What factors have the most influence on the pulmonary vasculature tone?

A

Local tissue factors (autoregulation)

336
Q

How does hypoxia impact the pulmonary vasculature?

A

Vasoconstriction –> HPV

337
Q

What is the most significant driving factor in causing vasoconstriction in the pulmonary vasculature?

A

Decrease in PAO2

PvO2 does play a small role

338
Q

What is the importance of HPV?

A

Reduces intrapulmonary shunt and prevents hypoxia

339
Q

How does the concentration of CO2 affect pulmonary vasculature?

A

Increased CO2 causes vasoconstriction
Decreased CO2 causes vasodilation
Opposite to the rest of the body’s response

340
Q

Which is worse at the top of the lung ventilation or perfusion?

A

Perfusion

341
Q

Which is worse in the bottom of the lung, ventilation or perfusion?

A

Ventilation

342
Q

What occurs in the apices of the lung that causes V/Q mismatch?

A

Dead space, volume compresses the capillaries

343
Q

At what point in the lungs do you have the best V/Q matching?

A

The middle of the lung about rib 3

344
Q

What is the overall V/Q ratio?

A

0.8

345
Q

What is thought to be the norma range of V/Q throughout the lung?

A

0.3-3

346
Q

What is an absolute shunt?

A

Perfusion with no ventilation
Anatomic shunt (conducting airways)
Non-ventilated alveoli

347
Q

What is the overall effect of a shunt?

A

Decrease in PaO2

348
Q

Can hypoxia cause by an absolute shunt be treated with an increase in FiO2?

A

No, the O2 content isn’t the issue its the lack of ventilation

349
Q

If a problem isn’t considered an absolute shunt what is it classified as?

A

V/Q mismatch, there is not such thing as a relative shunt

350
Q

Will an increase in FiO2 help a V/Q mismatch when hypoxia is present?

A

Yes, because there is some degree of perfusion and some degree of ventilation

351
Q

What is the normal shunt flow to total flow ration?

A
352
Q

What three sources contribute to venous admixture?

A

Venous Admixture is considered an ABSOLUTE shunt:
Bronchial circulation
Thesbian veins
Low V/Q areas

353
Q

What is the shunt equation?

A

QT(CaO2) = Qs (CvO2) + (QT -Qs) x CcO2
Delivery times the O2 content equals shunt flow times venous concentration (shunt bypassing the lungs) plus the total flow minus the shunt flow times the capillary O2

354
Q

What is the equation for the shunt flow as a percentage of total flow?

A

Qs/QT (shunt divided by total flow)
CcO2 - CaO2
CcO2-CvO2

355
Q

What two components make up the mixed venous O2?

A

How well blood is oxygenated

How much O2 is consumed at the cellular level

356
Q

In a normal lung, what should the PaO2 and the CO2 be?

A

PaO2 104

CO2 40

357
Q

If dead space occurs what will the PaO2 and the CO2 look like?

A

PaO2 150
CO2 0
No exchange has occurred because there is no perfusion to exchange with

358
Q

If a shunt occurs what will the PaO2 and the CO2 look like?

A

PaO2 40
CO2 45
No gas exchange so it will equilibrate to what appears to be venous blood

359
Q

What is considered a significant shunt?

A

> 35% and the patient will still be hypoxic no matter how much the FiO2 is increased

360
Q

How does anesthesia cause abnormal gas exchange?

A

Increased dead space with controlled ventilation (ventilation follows path of least resistance into independent lung zones)
Increased intrapulmonary shunting and V/Q mismatching

361
Q

How does anesthesia increase venous admixture?

A

Atelectasis

Airway collapse in dependent regions of the lung

362
Q

At what ED50 do volatile agents inhibit HPV?

A

ED50 2 MAC

363
Q

What is the normal gradient between PaCO2 and ETCO2 and how does that change in a diseased lung?

A

Normal 2-5mmHg

Diseased: gradient increases 5-10mmHg

364
Q

What disease processes could cause physiologic shunt?

A

Mucus Plug
Pneumonia/ Pulmonary Edema
Right/Left Mainstem
Atelectasis

365
Q

How does headspace affect the PaCO2-ETCO2 gradient?

A

The gradient increases to a very large number

366
Q

What disease processes cause dead space?

A

PE
Hypovolemia
Shock
Cardiac Arrest

367
Q

What are the five categories of hypoxia?

A

Anemia Hypoxia –> Minimal effect with FiO2
Respiratory hypoxia –> increased FiO2 will help
Circulatory Hypoxia –> minimal improvement with FiO2
Histotoxic hypoxia –> minimal improvement with FiO2
Increased O2 requirement –> Improved with FiO2

368
Q

What is the cause of about 95% of all URIs?

A

Infectious nasopharyngitis (viral or bacterial)

369
Q

What are the symptoms of nasopharyngitis?

A

History of fever
Purulent nasal drainage
Productive cough
Malaise

370
Q

How might the provider tell the difference between nasalpharyngitis and allergy related symptoms?

A

Allergy related symptoms usually don’t report fevers or cough and have a history of sneezing and runny nose

371
Q

About how long does it take for airway hyperactivity to heal?

A

6 weeks

372
Q

How long should the provider wait to administer anesthesia after a URI has occurred?

A

4 weeks

373
Q

How does anesthesia affect the immune system?

A

Causes a reduction of B-lymphocyte numbers and T-lymphocyte responsiveness and antibody production

374
Q

How can positive pressure ventilation make a URI worse?

A

It can spread the infection to the lower respiratory tract

375
Q

What are the primary characteristics of asthma?

A

Airway inflammation (primary) and airway hyperreactivity

376
Q

Wha are the clinical manifestations of asthma?

A

Cough, wheezing dyspnea

This is reversible airway obstruction

377
Q

What are the chemical mediators in asthma?

A 
Histamine
Leukotrienes
Platelet activating factors
Prostaglandins
Bradykinins
378
Q

How does ASA and NSAIDs cause an asthma attach?

A

Inhibit COX thus the Lipoxxygenase enzyme pathway is activated

379
Q

What leukotriene is most detrimental to a patient with asthma?

A

Leukotriene B, it causes bronchoconstriction in the lungs

380
Q

What is the difference between respiratory insufficiency and respiratory failure?

A

Insufficiency PaCO2 is maintained with accessory muscle use

Failure PaCO2 rises even with accessory muscle use

381
Q

What are signs of serious airway obstruction?

A 
Pulsus paradoxus (heart heart beat but may not feel pulse due to significant b/p drop)
Right ventricular strain pattern (ST changes, BBB on right side of the heart)
382
Q

What is the mechanism of action of bronchodilators?

A

Increased cAMP via stimulation of adenyl cyclase = bronchodilation

383
Q

What is the mechanism of action of Xanthines?

A

Increased cAMP via inhibition of phosphodiesterase (inhibits enzyme from breaking cAMP down) = bronchodilation

384
Q

What is the mechanism of action of the anticholinergics when used for asthma?

A

Inhibits Ach which reduces the amount of bronchconstriction

385
Q

What is the mechanism of action of mast cell stabilizers?

A

Inhibition of mediator release from the mast cells

386
Q

What is usually the first line of treatment for asthma currently?

A

Anti-inflammatory drugs such as corticosteroids

387
Q

What is the mechanism of action of the anti-inflammatory corticosteroids?

A

Decreases the inflammatory response in the airways

388
Q

What is the mechanism of action of leukotriene receptor antagonists?

A

Antagonist of leukotriene receptor inhibiting the inflammatory cascade

389
Q

What adverse effects are associated with long acting bronchodilators?

A

Polymorphism of the B2 receptors, mostly seen in the african american population causing down regulation of the b2 receptor

390
Q

When is the most critical period in the OR with an asthmatic patient?

A

Instrumentation of the airway

391
Q

What drugs should be avoided in an asthmatic patient?

A

Those that cause histamine release:
Morphine
Atracurium
Meperidine

392
Q

How can using a MAC blade causes less manipulation in the airway than a miller?

A

The miller blade is inserted deeper into the airway, lifting the epiglottis is much more stimulating

393
Q

What is a good manner to ventilate asthmatic patients?

A

Minimize tidal volumes with prolonged expiratory times

394
Q

What may be occurring is a delay is seen in the rise of the capnograph waveform?

A

Suggests increasing obstruction

395
Q

What is the treatment for an intraoperative bronchospasm?

A

Deepen the anesthetic
B2 agonist
Hydrocortisone

396
Q

What is the most common pulmonary disorder?

A

COPD

397
Q

What are the two classifications of COPD?

A 
Emphysema (Type A)
Chronic Bronchitis (Type B)
398
Q

What is the definition of chronic bronchitis?

A

You must have a productive cough most days over the course of three months for at least a two month period

399
Q

What might a chest radiograph show in a patient with chronic bronchitis?

A

Increased lung markings from higher pressures in the pulmonary vasculature

400
Q

What abnormality is seen in the blood if a patient has chronic bronchitis?

A

Polycythemia

401
Q

When does Cor pulmonale typically develop in chronic bronchitis?

A

Early

402
Q

Why isn’t PaCO2 typically elevated in a patient with Emphysema?

A

They learn a way to ventilate that allows for reasonable gas exchange
Purse lip breathing (auto peep)

403
Q

What is the primary pathology in emphysema?

A

Not a disease of the airways, disease caused by destruction of the alveoli
Large alveoli that causes loss of radial traction

404
Q

What is one of the main reasons people get emphysema?

A

They have an alpha1 antitrypsin deficiency.

405
Q

What is the mechanism of trypsin and how does it affect the lung tissues?

A

Trypsin causes remodeling of the airway and the antitrypsin keeps it under control

406
Q

What is another name for people with chronic bronchitis?

A

Blue bloater

407
Q

What is another name for the people with emphysema?

A

Pink puffer, emaciated look

May develop barrel chest from air trapping

408
Q

How does a normal patients hemidiaphragm compare to a patients with emphysema?

A

Normal patient has a curved hemidiaphragm the right side a little higher than the left compared to the emphysemic patient that has a flat hemidiaphragm

409
Q

What is the treatment for COPD?

A

Supportive care

410
Q

Why does the anesthetic provider need to use caution when administering supplemental O2 to a patient with COPD?

A

O2 content is their primary drive to breathe

411
Q

What determines the degree of COPD?

A

Defined by the patient’s pulmonary function tests

412
Q

When should smoking be stopped prior to surgery?

A

6-8weeks

Even if you can get them to stop smoking 24hr prior to surgery shown some benefits (decreased carboxyHgb)

413
Q

Why is it so important to get a chest Xray in patients with COPD prior to surgery?

A

Look for presence of Bullae, known to rupture with positive pressure ventilation = pneumothorax

414
Q

What scale can be used to assess a patient’s COPD?

A

Modified dyspnea scale

415
Q

What is a good indicator we use in the pre op assessment that determines a patient’s ability to respond to and challenge their ventilation?

A

If they are able to climb up two flights of stairs without becoming short of breath

416
Q

What type of surgeries contribute to high risk perioperative pulmonary complications?

A

Thoracic
Vascular
Upper abdominal

417
Q

What isn’t a good indicator of fluid status in a patient with pulmonary HTN?

A

CVP, it reflects right ventricular function not fluid status

418
Q

What does a tension pneumothorax look like under general anesthesia in the OR?

A

HoTN, Hypoxemia, increased peak airway pressures, decreased tidal volumes, deviated trachea, absent chest movement or breath sounds

419
Q

Define restrictive airway disease?

A

Characterized by decreased lung compliance and lung volumes typically reduced

420
Q

What is the difference between intrinsic and extrinsic fibrotic disease?

A

Intrinsic is at the level of the alveoli and extrinsic that are outside the alveoli and the parenchyma

421
Q

What lung volumes are decreased in restrictive lung disease?

A

RV and ERV = decreased FRC, may become hypoxic quickly on induction

422
Q

At what O2 concentration can cause fibrosis if a patient has had bleomycin therapy?

A

> 30%

423
Q

How can O2 toxicity develop into pulmonary fibrosis?

A

Damaged tissues becomes fibrotic if the tissue survives the assault

424
Q

What is the desired PaO2 and why doesn’t it matter once you exceed that limit?

A

60-80mmHg if you go above that you aren’t oxygenating anymore the Hgb is already saturated

425
Q

What autoimmune disease is closely associated with pulmonary fibrosis?

A

Rheumatoid arthritis

426
Q

What type of ventilation is best for patients with fibrotic lung disease?

A

Decreased tidal volumes and increased rate

427
Q

What is the SpO2 goal to maintain in the OR in patients with fibrotic lung disease?

A

88-92%

428
Q

How much can a healthy person forcibly exhale in one second?

A

Most can exhale most of their forced vital capacity 75-80%

429
Q

What is the percent predicted when referring to pulmonary function test?

A

It compares how the patient actually did compared to a group of people that are the same gender, body habits and age –> compared to what the normal patient can do

430
Q

What is a diagnostic measurement that is used to determine if lung disease is present?

A

FEV1
FVc
This is the amount exhaled in one minute compared to the total amount exhaled

431
Q

What is the importance of the mid maximal flow test (MMF)?

A

It focuses in on the small airway disease

Normal: 25-75%

432
Q

What section of the PFTs are we looking at to assess MMF?

A

After the first 25% is exhaled and before the last 25% is exhaled

433
Q

What is a normal FEV3?

A

Most normal healthy people can get their entire forced vital capacity out within 3 seconds

434
Q

What is the normal minimum expiratory flow rate?

A

200mL/min

435
Q

Why is it possible that a person with restrictive lung disease may have normal looking pulmonary function tests?

A

Their FEV1 and FVC are both reduced proportionally thus they may still have a percentage of 75-80%
Make sure to look at the actual volumes compared to those of a normal healthy person

436
Q

How is FEV1, FVC and FEV1/FVC going to look like in obstructive lung disease?

A

FEV1: Decreased
FVC: Normal when given enough time to exhale
FEV1/FVC: Decreased

437
Q

How is FEV1, FVC and FEV1/FVC going to look like in restrictive lung disease?

A

FEV1: Decreased
FVC: Decreased
FEV1/FVC: Normal

438
Q

How is FEV1, FVC and FEV1/FVC going to look like in mixed pulmonary disease?

A

Everything is decreased

439
Q

What patients have the greatest risk for postoperative complications due to respiratory sequelae?

A

Those that have pulmonary function measurements

440
Q

At what vital capacity is indicative of severe pulmonary dysfunction?

A
441
Q

What is the value of maximal voluntary ventilation?

A

It measures the patents ability to meet an increase in O2 demand that may occur after an insult such as surgy

442
Q

What is the FEV1 absolute in a male and female?

A

Male: 3L
Female: >2L

443
Q

What is the normal FEV1/FVC ratio?

A

> 75-80%

444
Q

What is the normal PEFR absolute?

A

> 200L/min

445
Q

How does asthma impact the FEV1/FVC ratio and PEFR?

A
446
Q

What is the benefit to using a flow volume loop?

A

It can help determine the location of an obstruction
Intrathoracic
Extrathoracic

447
Q

What will a flow volume loop show if an extra thoracic lesion is present?

A

A flattened inspiratory loop, the negative pressure created causes the lesion to collapse in on the airway causing a decrease in flow
Normal exhalation loop due to positive pressure pushing the lesion out of the airway

448
Q

What will a flow volume loop show if an intra thoracic lesion is present?

A

Normal inhalation radial traction is able to pull the airway open
Flattened expiratory loop due to positive pressure forcing the lesion into the airways

449
Q

What does a flattened flow volume loop on both inspiration and expiration indicate?

A

Fixed large airway obstruction

Consider that this loop could also indicate poor effort

450
Q

What is type one acute respiratory failure?

A

Hypoxemia, PaO2

451
Q

What is type two acute respiratory failure?

A

Hypercapnea: PaCO2 >50mmHg

Commonly caused by severe airflow obstruction

Pathophysiology I (4 decks)

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