Pulmonary + Respiratory Physiology Flashcards

(445 cards)

1
Q

Major functions of respiration

A

Inflow and outflow of air between the atmosphere and the alveoli​

Diffusion of O2 and CO2 between air and blood​

Transport of oxygen and CO2 in the blood and body fluids to and from tissue

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2
Q

Airway Anatomy parts

A

Trachea​

Right and Left Main Bronchi​

Lobar Bronchi​

Segmental Bronchi​

Terminal Bronchioles​

Respiratory Bronchioles​

Alveolar Ducts

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3
Q

Characteristics of conducting airways

A

Have NO alveoli

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4
Q

Acinus is distal to

A

terminal bronchioles

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5
Q

Conducting airways

A

Trachea​

Right and Left Main Bronchi​

Lobar Bronchi​

Segmental Bronchi​

Terminal Bronchioles

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6
Q

The Respiratory Zone

A

The Acinus​

What is this comprised of?​

Makes up most of the volume of the lung​

2.5-3 liters at rest

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7
Q

Each RBC spends about how long in the capillary network?

A

0.75 seconds in the capillary network​

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8
Q

What MPAP is needed to generate 6L of Flow?

A

15 mm hg needed to generate 6 liters of flow

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9
Q

Surfactant is made by

A

TYPE II alveolar epithelial cells​

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10
Q

Surfactant is a made of

A

phospholipids, proteins and ions​

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11
Q

Muscles of expiration function

A

pull rib cage down

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12
Q

Muscles of inspiration function

A

Pull rib cage up

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13
Q

Muscles of inspiration

A

primarily external intercostals. Also SCM, Anterior serrati, scaleni– elevate rib cage– sternum moves outward from vert column and AP diameter inc 20%​

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14
Q

Muscles of expiration

A

primarily abdominal recti, internal intercostals​

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15
Q

Pleural pressure

A

Pressure of fluid between lung pleura and chest wall pleura. -5 cm h20 at rest

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16
Q

Alveolar pressure

A

Pressure of the air inside the alveolus. When airway open and no flow- 0 cm h20​

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17
Q

Transpulmonary pressure

A

Difference between alveolar pressure and pleural pressure. Really a measurement of the elastic recoil of the lung​

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18
Q

Pleural pressure function

A

fights lung tissue elastic recoil

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19
Q

Alveolar pressure

A

zero at airway rest, must get negative to get air in​

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20
Q

greater TPP illustrates

A

greater compliance of the system​

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21
Q

Lung compliance formula

A

the amount the lungs will expand for each unit of increase in transpulmonary pressure

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22
Q

How much air is needed to increase TPP by 1cm

A

Normally 200 ml air

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23
Q

Compliance is determined by

A

elastance of lung tissue and surface tension of alveoli. Also compliance of system involves chest wall compliance. ​

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24
Q

Elastic forces of lung tissue determined mainly from

A

elastin and collagen fibers. Alveoli forces moderated by surfactant.​

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25
Transpleural pressure elastance is mainly related to
surface tension btwn air and fluid​
26
The thoracic cage is what percentage of the total lung system?
50%
27
Anatomic Dead Space (Definition)
The volume of air in the conducting airways
28
Anatomic Dead Space (Amount)
~150mL
29
What factors can change the anatomic dead space amount?
posture, size of person, and at the extremes of physiology​
30
Physiologic Dead Space formula
(PacO-PeCo) /PaCo
31
Alveolar ventilation is
the rate at which new air enters the alveoli​
32
Dead Space Volume (Formula)
Va= RR (Vt-Vd) expressed in L/min
33
Which region of the lung ventilates better?
Lower regions of the lung ventilate better than upper regions​
34
Average tidal Volume
500mL
35
Average IRV
3100 mL
36
Average ERV
1200 mL
37
Average Residual volume
1200 mL
38
Tidal volume
Amount of air inhaled or exhaled with each breath under resting conditions
39
IRV
Inspiratory Reserve Volume Amount of air that can be forcefully inhaled after a normal tidal volume inhalation
40
ERV
Expiratory Reserve Volume Amount of air that can be forcefully exhaled after a normal tidal volume exhalation
41
RV
Residual Volume Amount of air remaining in the lungs after a forced exhalation
42
TLC
Total Lung Capacity Maximum Amount of air contained in lungs after a maximum inspiratory effort
43
TLC Formula
TLC= TV +IRV+ERV+RV
44
Vital capacity
Maximum amount of air that can be expired after a maximum inspiratory effort
45
Average Vital capacity
3100-4800 mL
46
Average TLC
4200-6000mL
47
AVerage inspiratory capacity
2400-3600 mL
48
Average Functional Residual Capacity
1800-2400 mL
49
Inspiratory capacity
Maximum amount of air that can be inspired after a normal expiration
50
inspiratory Capacity formula
IC= TV+IRV
51
Functional residual capacity
Volume of of air remaining in the lungs after a normal tidal volume expiration
52
FRC Formula
FRC=ERV+RV
52
Boyle's Law (Formula)
P1V1=P2V2
52
Charles' Law (Definition)
The volume of gas is directly proportional to its absolute temperature
52
Charles' Law formula
V1/T1=V2/T2
52
Boyle's Law (Definition)
As volume increases, the pressure of the gas decreases in proportion
53
Ideal Gas Law (formula)
PV=nRT
53
Diffusion Limited
The amount of gas that is taken up by the blood depends on the amount of blood and not all the blood-gas barrier
54
Perfusion Limited
the amount that gets into the blood is limited by the diffusion properties of the blood gas barrier and not by the amount of blood. ​
55
Shunting
blood entering the arterial system without going through ventilated areas of the lung.
56
Shunt Equation
Qs/Qt= (Cco2-Cao2)/(CcO2-cvO2)
57
Qs/Qt
Shunt fraction Shunt flow divided by Total Cardiac output
58
Dead Space Equation
VD/VT= (Paco-peCo)/(Paco)
59
FiO2
Fraction of inspired oxygen
60
Room air FiO2
0.21 in room air
61
PaO2
Partial pressure of Alveolar Oxygen
62
atmospheric pressure
760 mmHg at sea level
63
PH2O
H2O Vapor pressure in the alveolus : Usually 47 mmHg at 37C
64
West Zone 1
where alveolar pressure is higher than arterial or venous pressure
65
West Zone 2
where alveolar pressure is higher than arterial or venous pressure
66
West Zone 3
where both arterial and venous pressure is higher than alveolar​
67
West Zone 4
where the interstitial pressure is higher than alveolar or pulmonary venous pressure.​
68
West Zone 1 formula
PA > Pa > Pv
69
West Zone 2 Formula
Pa > PA > Pv
70
West Zone 3 Formula
Pa > Pv > PA
71
West Zone 4 Formula
Pa > Pi > Pv > PA
72
Respiratory system resistance
a combination of resistance to gas flow in the airways and resistance to deformation of tissues of both the lung and chest wall​
73
Airway Resistance Formula
RrS=Rt+K1+K2V
74
Rt (in airway resistance)
The resistance from deformation of the lungs and chest wall
75
K1 (in airway resistance)
empirical constant representing gas viscosity
76
K2 (in airway resistance)
An empirical constant representing gas density and airway geometry
77
V (in airway resistance)
the flow as volume per unit of time
78
Tissue resistance from lung parenchyma
~70%
79
Tissue resistance from chest wall
~30%
80
What contributes to the work of breathing
Elastic work Resistive work
81
Elastic work​
Work done to overcome elastic recoil of the lung​ Work done to overcome elastic recoil of the chest (which is subtracted from the work done to overcome the elastic recoil of the lung)​
82
Resistive work
Work done to overcome tissue resistance, otherwise referred to as viscous resistance​
83
Contributors to resistive work
Chest wall resistance​ Lung resistance
84
Work done to overcome airway resistance, which includes
Airway resistance​ Resistance of airway devices and circuits
85
Respiratory Control Centers (controllers)
Nucleus retroambiguous nucleus paraambigualis Nucleus ambiguous
86
nucleus retroambiguous role and efferents/effectors
Upper motor neuron axons to contralateral expiratory muscles
87
Nucleus paraambigualis Role and efferents/effectors
Upper Motor neuron axons to contralateral inspiratory muscles
88
Nucleus ambiguous Role and efferent/effectors
vagus nerve: to larynx, pharynx and muscularis uvulae Glossopharyngeus muscle to stylopharyngeus muscle
89
Pre-botzinger complex role and efferrent/effectors
Respiratory pacemaker (Central pattern generator) Interneurons connecting to other respiratory control regions
90
Botzinger Complex- role and efferent/effectors
Expiratory Function inhibitory interneurons to phrenic motor neurons and other respiratory control regions
91
Pontine respiratory group role and efferrent/effectors
Integrates descending control of respiration from the CNS Interneurons connecting to other respiratory control regions
92
Cerebral Cortex role and efferrent/effectors
Volitional and behavioral respiratory control Pontine respiratory group
93
mechanoreceptors in the bronchial and lung tissue (stimulus/Afferent nerve)
inflation/Deflation Vagus Nerve
94
Central chemoreceptors (Stimulus/afferent nerve)
ph No Nerve
95
Aortic Glomerulus Cells- in the aortic arch, subclavian arteries and pulmonary trunk (Stimulus/Afferent nerve)
Aortic nerve (branch of the vagus) PaO2 Changes in O2 delivery (anemia, carboxyhemoglobin, hypotension), PacO2
96
Carotid body glomus Type I cells- sited at the bifurcation of the common carotid (Stimulus/Afferent nerve)
Stimuli- PaO2, PaCo2, pH, temp, Glucose (hypoglycemia) Afferent nerve- Glossopharyngeal
97
Sniffing position
Helps to align Oral, Pharyngeal, and Laryngeal axes for optimal intubating conditions * Neck flexion (~35 deg) with head/AO extension (~85-90 deg)
98
FIBEROPTIC BRONCHOSCOPE (FOB)
Consists of an light source, handle, insertion cord (shaft), and sometimes a screen * Handle contains eyepiece (if no screen), working channel ports, control lever, and focusing ring
99
FOB uses
Diagnostic or therapeutic bronchoscopy * Placement tracheal tubes or gastric tubes * Advantageous in patients with difficult airways or where rigid laryngoscopy is not an option
100
Disadvantages of FOB
Fragile Difficult to use Difficult to clean Longer time to secure airway Difficult with blood/secretions Risk of laryngeal trauma
101
Nasopharynx can be obstructed by
choanal atresia, septal deviation, mucosal swelling or foreign material (blood, mucous, objects)
102
Oropharynx entry can be blocked by
the soft palate lying against the posterior pharyngeal wall
103
The pathway of gas can be restricted by the epiglottis in the
hypopharynx
104
Laryngeal obstruction related to spasm (laryngospasm) must be treated by
positive airway pressure, deeper anesthesia, muscle relaxants or endotracheal intubation
105
Laryngeal closure can occur from
intrinsic or extrinsic muscles of the larynx
106
Tight airway closure results from
Contraction of external laryngeal muscles, which force the mucosal folds of the quadrangular membrane into apposition
107
Stridor suggests
Glottic (laryngeal) obstruction or laryngospasm (most often on inspiration)
108
Williams Oral airway
 Was designed for blind orotracheal intubations  Can be used as an aid to fiberoptic intubations  If using for fiberoptic, the tracheal tube connector has to be removed during intubation
109
Contraindications of nasopharyngeal airways
 Hemorrhagic disorders  Anticoagulation therapy  Sepsis  Basilar skull fracture  History of epistaxis  Nasal packing in place
110
FiO2 of supplemental oxygen delivered is dependent on
flow rate and device used
111
In nasal cannula, what is max flow rate?
6L/min
112
simple mask flow rates
No less than 5 L/min to avoid CO2 rebreathing (usually 6-10 L/min
113
Reservoir masks Can deliver FiO2 up to
1.0 (15L/min)
114
Peak pressures > 20 cm h2O can cause
gastric distention
115
Pulmonary veins
Four pulmonary veins (RUPV, RLPV, LUPV, LLPV)  Empty into left atrium  Oxygenated blood from the lungs
116
Pulmonary artery
 Originates at the RV apex/pulmonic valve  Divides into right and left main branches  Very compliant system  Mixed venous blood pumped by the RV
117
Bronchial vessels
Bronchial arteries originate from the systemic circulatory system (1-2% CO)  Transport arterial blood (oxygenated)  Empties into pulmonary veins after passing through the tissues
118
High pressure, low flow circulation (Pulmonary) Source
Systemic arterial blood from bronchial arteries (branches of the thoracic aorta)
119
High pressure, low flow circulation (Pulmonary) Supplies
Trachea, bronchial tree, supporting tissues of the lung, adventitia of pulmonary arteries and veins
120
Low pressure, high flow circulation  Source
Venous blood from body  pulmonary artery  alveoli (gas exchange)
121
Low pressure, high flow circulation Supplies
Returns via pulmonary veins to the LA  LV and then pumped systemically
122
Pulmonary arterial system
 Low pressure system  Thin vessel walls  Relatively little smooth muscle
123
The lung is required to always be able to accept
the entire CO
124
Pulmonary Artery Circulation pressure
25/10 mmHg
125
Pulmonary artery cathether uses
Uses: assessment of patients with pulmonary hypertension, cardiogenic shock, and unexplained dyspnea
126
Pulmonary artery cathterization
an intravascular catheter is inserted through a central vein (femoral, jugular, antecubital or brachial) to connect to the right side of the heart and advance towards the pulmonary artery
127
The “extra-alveolar” vessels are exposed to lower pressure (than alveolar pressure). These can be pulled open by
the radial traction of the surrounding lung parenchyma
128
PVR is normally small but can reduce even further as
pressure within the vessels increases
129
Recruitment
Opening of previously closed vessels
130
Distension
 Increase in caliber of vessels  Change in shape from near flat to circular
131
Distension is the predominant mechanism for
decreased PVR at higher vascular pressures
132
PVR is highest at
very large lung volumes
133
Lung Volume affects
PVR
134
PVR is also high at
very low lung volumes
135
Resistance is the least when?
at normal TV breathing
136
If the lung is completely collapsed
Requires much more pressure to allow blood flow  Critical opening pressure
137
What else affects PVR
 Extra-alveolar vessels contain smooth muscle  Substances that cause contraction of smooth muscle will increase PVR
138
Substances that cause contraction of smooth muscle
 Serotonin  Histamine  Norepinephrine  Thromboxane A2  Endothelin  Nitrous oxide  (Hypoxia)
139
What are some vasodilators?
 Nitric oxide  Phosphodiesterase inhibitors  Calcium channel blockers  Prostacyclin
140
Calculation of pulmonary resistance
Resistance = Change in Pressure / Flow PVR = [(mPAP – PCWP)/CO] x 80
141
SVR Equation
SVR = [(MAP – CVP)/CO] x 80
142
Change in Pressure
 Mean Pulmonary Artery Pressure (mPAP)  Left atrial pressure (is approximated by Pulmonary Capillary Wedge Pressure (PCWP)
143
Qp = Qs =
Cardiac Output
144
Hypoxic Pulmonary Vasoconstriction (HPV)
 Decreased O2 concentration in alveoli  blood vessel constriction  This is the opposite of what happens in the systemic circulation
145
Gravity and positioning affect blood flow and therefore
gas exchange
146
When upright, what area of the lungs receives the least amount of bloodflow?
Apex receives least amount of blood
147
When Supine, how is blood distribution in the lungs allocated?
 Apex and base are now about equal  Posterior (or dependent) portion of the lung receives more blood flow than the anterior portion
148
When hanging upside down, what area of the lungs receives the most blood flow?
Apex receives most blood flow
149
how does exercise affect blood flow throughout the lungs
Exercise causes the blood flow in increase throughout and the differences between the areas becomes less
150
West Zone 1 doesn't occur under normal conditions. When might this occur?
 Reduced arterial pressure  Increased alveolar pressure
151
Which west zone mimics normal blood flow?
Zone 3
152
In hypoxic pulmonary vasoconstriction, Hypoxia (PO2 in the alveoli) causes
local action on the artery without requiring CNS connections
153
Hydrostatic pressure (formula)
Pc – Pi
154
Colloid osmotic pressure
𝜋c - 𝜋i
155
Starling’s equation
Net fluid out = K[(Pc – Pi)– 𝜎(𝜋c - 𝜋i)] K = filtration coefficient
156
Pulmonary edema
Fluid can leak into the interstitial space (perivascular/peribronchial space) and eventually get into the alveoli (obviously this is going to interfere with gas exchange)
157
Angiotensin I in pulmonary circulation
Converted to Angiotensin II by ACE
158
Angiotensin II in Pulmonary circulation
unaffected
159
Vasopressin in pulmonary circulation
Unaffected
160
bradykinin in pulmonary circulation
Up to 80% inactivated
161
Serotonin in pulmonary circulation
Almost completely removed
162
Norepinephrine in pulmonary circulation
Up to 30% removed
163
histamine in pulmonary circulation
not affected
164
Dopamine in pulmonary circulation
not affected
165
E2 and F2x in pulmonary circulation
Almost completely removed
166
A2 in Pulmonary circulation
not affected
167
PGI2 in pulmonary circulation
not affected
168
Leukotrienes in pulmonary circulation
Almost completely removed
169
What is a normal pressure in the right atrium?  A: 5  B: 10  C: 15  D : 20
A: 5
170
What is the normal pressure in the right ventricle?  A: 25/15  B: 10/0  C: 15/5  D: 25/0
 D: 25/0
171
When floating a pulmonary artery catheter, how can you tell that you’ve entered the main pulmonary artery?
C: The diastolic pressure will increase
172
Calculate the PVR for this patient: mPAP 20, PCWP 7, CO 5.5.  A: 166  B: 189  C: 275  D: 392
B: 189 PVR = [(mPAP – PCWP)/CO] x 80
173
Which of the following would be most consistent with West Zone 2?  A: Pa > Pv > PA  B: PA > Pa > Pv  C: Pa > PA > Pv
C: Pa > PA > Pv
174
At what lung volume would PVR be the highest?  A: TV end-exhalation  B: Vital capacity end-inhalation  C: Vital capacity end-exhalation  D: Total lung capacity
 B: Vital capacity end-inhalation
175
At what lung volume would PVR be the lowest?  A: TV end-exhalation  B: Vital capacity end-inhalation  C: Vital capacity end-exhalation  D: Total lung capacity
A: TV end-exhalation
176
Which of the following is most important in the HPV phenomenon?  A: PaO2  B: PvO2  C: PAO2  D: PACO2
C: PAO2
177
Which of the following would cause pulmonary edema by increased hydrostatic pressure?  A: TRALI  B: ARDS  C: CHF  D: Diffuse alveolar hemorrhage
C: CHF
178
Which of the following is metabolically unaffected by passing through the pulmonary circulation  A: Angiotensin I  B: Serotonin  C: Angiotensin II  D: Bradykinin
C: Angiotensin II
179
how is oxygen carried throughout the blood
Attached to hemoglobin Dissolved in blood
180
once o2 has diffused from alveoli, what happens?
It is transported to the peripheral tissue capillaries almost entirely in combination with hemoglobin
181
Oxygen carrying capacity formula
CaO2= (1.39 x Hgb x (sat/100))+ (0.003. x PaO2)
182
Henry’s Law
The amount of a gas that is dissolved in the blood is proportional to the partial pressure of that gas
183
Normal arterial blood with a PaO2 of 100mmHg contains
0.3ml O2/100ml (i.e. very little)
184
For every mmHg of PO2, there is 0.003 ml O2/100ml of
Blood
185
hemoglobin
An iron-porphorin compound attached to a protein globulin made of alpha and beta polypeptide chains
186
normal Adult hemoglobin
HgbA
187
normal fetal Hemoglobin
Hgb F
188
How does Hgb F compare to Hgb A?
higher affinity for o2 than HgbA
189
HgbF is for what age of people?
Newborn Gradually replaced over 1st 6-8 mo of post-natal life
190
Abnormal hemoglobin S=
Sickle Cell
191
Sickle Cell abnnormal Hgb
Contains Valine instead of Glutamic acid in Beta chains Decreased affinity for O2 and rightward shift in the hgb/o2 curve
192
Methemoglobinemia
Ferrous ion of Hgb A (Fe2+) is oxidized to the ferric form (Fe3+)
193
Elevated concentration of methemoglobin in RBCs
Methemoglobinemia
194
Methemoglobinemia results in
Overall reduced ability of RBC to release oxygen to tissues
195
Causes of methemoglobinemia
 Nitrites  Some local anesthetics (Benzocaine)  Congenital
196
Oxygen + hemoglobin =
HgbO2
197
hemoglobin in the oxygenated state is said to be
Relaxed or R State
198
hemoglobin in the deoxygenated state is said to be
tensed or T state
199
Oxygen rapidly binds to hemoglobin up to a PaO2 of
about 50 mmHg, then rate of binding slows
200
maximum amount of O2 that can be bound
O2 capacity
201
O2 Saturation
Percentage of available O2 binding sites that have o2 attached
202
O2 Saturation formula
Sat= (O2 combined with hemoglobin/ O2 capacity) x100
203
in strenuous exercise, o2 requirements
may increase by up to 20x normal
204
Diffusing capacity for O2 increases almost 3x during exercise due to
increased surface area of capillaries participating in diffusion
205
What primary mechanism allows your PVR to drop during exercise
206
shunt flow in o2 Transport
Blood from the lung will mix with blood that passed from the aorta through the bronchial circulation
207
Shunt blood has PO2 of
40 mmHg
208
Pulmonary venous blood has PO2 of
104 mmHg
209
Venous admixture --> PO2 of
95 mmHg
210
Tissue PO2 is determined by a balance between
Rate of O2 transport to the tissues from the blood * Rate at which O2 is used by the tissue
211
What partial pressure of O2 is needed to fulfill normal cellular function requirements???
212
P50
= PO2 at which 50% of hemoglobin is saturated  Normal is about 27 mmHg
213
Right Shift in oxygen dissociation curve
O2 bound to Hgb with less affinity
214
Right shift in Oxygen dissociation curve characteristics
 Increased H+ (Acidosis)  Increased PCO2 (Bohr Effect)  Increased Temperature  Increased 2,3-diphosphoglycerate Sickle Cell anemia
215
Left Shift in oxygen dissociation curve
Left Shift
216
right shift in Oxygen dissociation curve characteristics
 Alkalosis  Lowered PCO2 (redundant)  Hypothermia  Decreased 2,3-diphosphoglycerate  Carbon monoxide
217
CO2 is carried in blood in 3 different forms
 Dissolved  Bicarbonate  Combination with proteins as carbamino coumpounds (bound to hemoglobin)
218
Similar to O2, carbon dioxide obeys
Henry’s Law The amount of a gas that is dissolved in the blood is proportional to the partial pressure of that gas
219
Co2 vs o2 solubility
CO2 is about 20x more soluble than O2
220
Carbamino Compounds
Formed by combination of CO2 with terminal amine groups in blood proteins  Most importantly, globin of hemoglobin  Hgb -> carbaminohemoglobin
221
Carbamino synthesis
Reaction occurs rapidly without an enzyme and reduced Hgb can bind more CO2 as carbaminohemoglobin than HgbO2
222
Haldane effect
The lower the saturation of Hb with O2, the larger the CO2 concentration for a given PCO2  Reduced Hb has more ability to accept H+ ions produced when carbonic acid dissociates and forms carbaminohemoglobin  “Oxygenated blood carries less CO2 for the same PaCO2”  CO2 curve is steeper and more linear than O2 curve.  CO2 curve is right-shifted by increases in oxygen saturation.
223
Haldane effect
Basically, if the PaCO2 remains constant (x-axis) but the O2 saturation falls, the overall CO2 concentration is increased. This plot is loosely referred to as the “CO2 dissociation curve”  Essentially the curve shifts to the right with increasing SpO2
224
Respiratory Acidosis
Increase in PCO2  Decreases the HCO3-/PCO2 ratio and thus decreases the pH (acidosis)
225
Respiratory Alkalosis
Decrease in PCO2  Increases the HCO3-/PCO2 ratio and thus increases the pH (alkalosis)
226
Metabolic Acidosis
Decrease in HCO3-  Decreases the HCO3-/PCO2 ratio and thus decreases the pH (acidosis)
227
Metabolic Alkalosis
Increase in HCO3-  Increases the HCO3-/PCO2 ratio and thus increases the pH (alkalosis)
228
The presence of hemoglobin in normal arterial blood increases it’s oxygen concentration approximately how many times? A. 10 B. 30 C. 50 D. 70 E. 90
D. 70
229
Since O2 saturation of normal arterial blood is about 97%, the total O2 concentration is given by
(1.39 x Hb x .97) + 0.3 mL O2/100 mL blood
230
Therefore, presence of Hb increases O2 concentration by about
70 times
231
A patient with CO poisoning is treated with hyperbaric oxygen that increases the PaO2 to 2000mmHg. The amount of oxygen dissolved in the arterial blood (in ml/100ml) is: A. 2 B. 3 C. 4 D. 5 E. 6
E. 6
232
A patient with severe anemia has normal lungs. You would expect which of the following: A. Low arterial PO2 B. Low arterial O2 saturation C. Normal arterial O2 content D. Low oxygen content of mixed venous blood E. Normal tissue PO2
D. Low oxygen content of mixed venous blood
233
In CO poisoning, you would expect of which of the following to be true: A. Reduced arterial PO2 B. Normal O2 content of arterial blood C. Reduced oxygen content of mixed venous blood D. O2 dissociation curve shifted to the right E. Carbon monoxide has a distinct odor
C. Reduced oxygen content of mixed venous blood
234
If the patient has normal pulmonary function, the arterial PO2 will be normal, but the O2 content will be
Reduced
235
Most of the CO2 transported in the arterial blood is in which form: A. Dissolved B. Bicarbonate C. Attached to hemoglobin D. Carbamino compounds E. Carbonic acid
B. Bicarbonate
236
90% of CO2 transported in the arterial blood is in the form of
bicarbonate
237
A patient with chronic lung disease has arterial pH, PO2 and PCO2 values of 7.35, 50mmHg and 60mmHg. How would his acid-base status best be described? A. Normal B. Partially compensated respiratory alkalosis C. Partially compensated respiratory acidosis D. Metabolic acidosis E. Metabolic alkalosis
C. Partially compensated respiratory acidosis
238
A patient with chronic pulmonary disease undergoes emergency surgery. Postoperatively, the arterial pH, PO2, and PCO2 are 7.2, 50mmHg, 50mmHg respectively. How would you describe the patient’s acid/base status? A. Mixed respiratory and metabolic acidosis B. Uncompensated respiratory acidosis C. Fully compensated respiratory acidosis D. Uncompensated metabolic acidosis E. Fully compensated metabolic acidosis
A. Mixed respiratory and metabolic acidosis
239
The lab provides the following report on arterial blood from a patient: pH – 7.25, pCO2 – 32, HCO3 – 25. You conclude that there is: A. Respiratory alkalosis with metabolic compensation B. Acute respiratory acidosis C. Metabolic acidosis with respiratory compensation D. Metabolic alkalosis with respiratory compensation E. A lab error
E. A lab error
240
41yo patient on mechanical ventilation for several days develops a fever and sepsis. ABG shows PaO2 of 72mmHg, unchanged from the previous day. What physiologic changes would you expect? A. Decreased CO2 production B. Decreased shunt fraction C. Increased arterial O2 concentration D. Increased arterial O2 saturation E. Increased P50 for hemoglobin
E. Increased P50 for hemoglobin
241
Fever causes a ________ shift of the O2 hemoglobin dissociation curve
Rightward i.e. at any level of PaO2, there will be a lower O2 saturation and therefore a lower O2 concentration.  No effect on shunt fraction`
242
243
Recommendation: pressure on the lateral tracheal wall should be kept between
20-30 cm H20
244
What clinical situations are most appropriate for reinforced tubes?
in situations where the tube is likely to be bent or compressed as in head & neck surgery
245
Reinforced/armored tubes
have a metal or nylon spiral woven reinforcing wire covered both internally and externally by rubber, PVC or silicone
246
Disadvantages of reinforced tubes
 Tube may rotate on the stylet during intubation  Insertion through nose & intubating LMA is difficult (connector is bonded to tube)  Fixation of these tubes are more difficult  If the patient bites the tube it will cause permanent deformity resulting in obstruction of the tube
247
Advantages of reinforced tubes
 Resistance to kinking and compression  The portion of the tube outside the patient can be easily angled away from the surgical field without kinking  Can be used for patients with tracheostomies
248
RAE Tube/ pre-formed/ Ring-Adai-Elwyn
 Preformed bend that facilitates the head & neck surgeries  Available in cuffed, uncuffed ,nasal, and oral  Each tube has a rectangular mark at the center of the bend
249
Advantages of RAE tubes
 Easy to secure and reduce the risk of unintended extubation  Breathing system remains away from surgical field
250
Disadvantages of RAE tubes
 More resistance than conventional tubes  Difficult to suction
251
Advantage of MLT
The small diameter provides better surgical access
252
Disadvantages of MLTs
incomplete exhalation & occlusion (increased resistance)
253
NIM Tube
 Designed to monitor recurrent laryngeal nerve EMG activity during surgery  The tube is wire-reinforced & has 4 stainless steel electrodes above the cuff. The electrodes are connected to a monitor
254
RV + ERV =
FRC
255
TV + IRV
Inspiratory capacity
256
IRV+ TV+ ERV=
Vital Capacity
257
VC+ RV=
TLC
258
IC+ FRC=
TLC
259
IRV+ TV+ ERV+ RV=
TLC
260
Flow rate of expired air is greatly dependent on
lung volumes
261
Flow is limited by
airway compression
262
After a small amount of air is exhaled
the flow rate begins to drop quickly as the lung volume decreases
263
In restrictive diseases, what happens to flow rate and volume exhaled
They are REDUCED
264
In restrictive diseases, given the low lung volumes, the flow rate can be quite high when?
near the end of exhalation because of increased lung recoil
265
in obstructive diseases, how is the flow rate?
Flow rate is very low for a given lung volume
266
What does the flow volume curve look like in obstructive diseases?
A “scooped-out” appearance of the flow volume curve appears
267
In Restrictive diseases, inspiration is limited by
Reduced compliance of the lung or chest wall  Weakness of inspiration muscles
268
in obstructive diseases, ____is typically abnormally large, but _____ ends early
TLC Expiration
269
Early airway closure is secondary to
increased smooth muscle tone in the bronchi (asthma) or loss of radial traction (emphysema)
270
The FEV1 (or FEF 25-75%) is reduced by
an increase in airway resistance or reduction in elastic recoil of the lung.  Independent of airway expiratory effort
271
The flow rate is independent of the resistance of the airways downstream of the collapse point but instead is determined by
the elastic recoil pressure and the resistance of the airways upstream of the collapse point
272
Both the increase in airway resistance and the reduction of lung elastic recoil pressure can be important factors in reducing
FEV1
273
in dynamic compression, Flow is determined by alveolar pressure minus pleural pressure (not pressure at the mouth) and is therefore
Effort independent
274
Lung volumes are measured by
Spirometry
275
What Lung volumes cannot be measured by Spirometry?
FRC and RV
276
FRC can be measured by
helium dilution  Helium is virtually insoluble in blood  C1 = known concentration of helium body plethysmograph
277
How is a helium dilution test performed?
Subject takes several breaths and the helium concentration in the spirometer and the lung equilibrate
278
Formula for determining FRC
C1 x V1= C2 x (V1+ V2)
279
Body Plethysmograph
Subject makes respiratory efforts (↓P in lungs)  Expands the gas in the lungs (↑V in lungs) and increasing lung volume which will increase the pressure in the box because there is less gas volume in the box (↑P and ↓ in the box)
280
Formula for body Plesmythograph
P1xV1 = P2 (V1-△V) => Solve for △V
281
Diffusing capacity for carbon monoxide (DLCO) is measured by
Diffusing capacity for carbon monoxide (DLCO) is measured by
282
Diffusion capacity for O2 is measured
very difficult to measure (only done in research labs)
283
Regional variation in ventilation and blood flow can be measured using
radioactive xenon
284
blood preferentially flows to what part of the lung?
Lung bases
285
Measuring ventilation inequality
Single breath method – very similar to Fowler method for determining anatomic dead space
286
Multiple breath method
Patient breaths 100% O2 over multiple breaths, N2 is measured at the lips as a function of time
287
in the Multiple-breath method, If FRC = TV, then
N2 concentration should ”half” with each breath
288
in the Multiple-breath method, in a diseased lung, we see
a non- linear washout of N2 (due to non- uniform ventilation
289
PFT Test of flow
Forced Expiratory Spirometry  FEV and FEV1  FVC
290
When can a FEV/FEV1/ FVC test be done?
Can be done before or after a bronchodilator to determine bronchodilator responsiveness
291
Are Flow tests effort dependent or effort independent?
Effort independent
292
Diffusion Capacity (DLCO)
Measures the ability of the lungs to transfer a gas from the alveoli into the RBCs in the pulmonary capillaries * Reflects properties of the alveolar- capillary membrane
293
In DLCO, how is exhaled concentration measured?
Patient breathes in 0.3% CO and exhaled concentration is measured * The greater the DLCO, the lower the exhaled concentration
294
The greater the DLCO
the lower the exhaled concentration
295
Patient’s height, weight, sex and age have correlated
predicted “normal” values  Lung volumes  Flows
296
 FEV1 - Decreased  FVC – Decreased  FEV1/FVC Ratio – Decreased  DLCO – Decreased
Obstructive Disease
297
 FEV1 – Normal (to slightly low)  FVC – Decreased  FEV1/RVC ratio – Normal (to increased)  DLCO - Decreased
Restrictive Disease
298
 Asthma  COPD  Chronic bronchitis  Emphysema
Obstructive Disease (think difficulty exhaling)
299
 Interstitial lung disease  Pulmonary fibrosis  Chest wall and pleural diseases  Obesity  Scoliosis  Neuromuscular diseases  ALS
Restrictive Disease (think difficulty inhaling)
300
A fixed obstruction
will effect both exhalation and inhalation
301
OSA
Patient has respiratory efforts but cannot move air due to upper airway obstruction
302
How is OSA Diagnosed
Diagnosed via sleep study (measuring Apnea-Hypopnea Index = # of apneas and hypopneas per hour of sleep)
303
AHI 0-5
No Disease
304
AHI 21- 40
Moderate OSA
304
AHI 6-20
Mild OSA
305
AHI > 40
Severe OSA
306
FEV1
volume of air forcibly exhaled in 1 second
307
FVC
forced vital capacity
308
All "Capacities" are
SUmmation of other volumes
309
Closing Capacity
Closing Volume + Residual Volume
310
Closing Volume
the volume of air in the lungs at which the airways in the dependent portion of the lung begin to close/collapse
311
Residual Volume
the volume of air in the lungs following a maximum exhalation
312
Closing Capacity
313
Closing capacity > FRC
This is less than ideal
314
How is closing capacity measured
Single Breath N2 washout method
315
Single Breath N2 washout method
Patient is breathing room air (approximately 79% N2) Then we have the patient take a vital capacity breath of 100% O2 We measure the N2 concentration at the lips on the subsequent exhalation The concentration of N2 is measured and recognized in four phases
316
Closing Capacity Phase 1
Pure Dead space
317
Closing Capacity Phase 3
Pure alveolar gas
318
Closing Capacity Phase 2
Mixture of dead space & alveolar gas
319
Closing Capacity Phase 4
Occurs near the end of expiration, is signified by a sharp increase in N2 concentration
320
Why is phase 4 of closing capacity signified by a sharp increase in N2 concentration?
The apex of the lungs are almost certainly always “open” or expanded so during a vital capacity breath, they will not expand much more Therefore they don’t take in as much of the 100% O2 and they contain a lot of the N2 from the previous breaths
321
A young person will have a closing volume that is approximately what percent of their vital capacity?
10%
322
As you age, what happens to the closing volume
It increases I.e. closing capacity increases
323
At age 65, what happens to the closing capacity
is approximately the same as the FRC About 40% of vital capacity
324
Certain diseases increase closing capacity
COPD Asthma Pulmonary Edema
325
Does Obesity affect closing capacity
Actually, this does not increase the closing capacity, but does decrease the FRC (by decreasing the ERV) Closing volume can be greater than FRC --> V/Q mismatch, shunting, and hypoxia Because of this, closing capacity will approach FRC at a younger age than would be expected
326
Obstructive Lung Diseases (Inhale/exhale)
CAN’T EXHALE
327
Restrictive Lung Diseases
CAN’T INHALE
328
Obstructive Lung Diseases
Reduced elasticity or premature closure of small airways that results in increased lung volumes, but decreased ventilation
329
COPD
Emphysema Chronic bronchitis
330
Asthma
Usually a temporary obstruction that is reversible (due to inflammation of airways)
331
Restrictive Lung Diseases
Reduced lung volumes due to damage to the lung tissue itself or structural change/weakness of the thorax
332
Intrinsic Restrictive Lung Diseases
pathology within the lung parenchyma (i.e. pulmonary fibrosis)
333
Extrinsic Restrictive Lung Diseases
Chest wall or pleural dysfunction (i.e. severe scoliosis)
334
Pink Puffer
Emphysema
335
Blue Bloater
Chronic Bronchitis
336
Obstructive Lung Diseases (Examples)
COPD Emphysema (“pink puffer”) Chronic bronchitis (“blue bloater”) Asthma Bronchiectasis Cystic Fibrosis
337
Restrictive Lung Diseases
Obesity Pulmonary Fibrosis Scoliosis (severe) Neuromuscular Disease ALS Muscular Dystrophy Myasthenia Gravis Sarcoidosis (and other ILDs) Auto-immune diseases Truncal burns
338
FEV1 in obstructive lung disease
Low
339
FEV1 in Restricitve Lung disease
Normal or slightly low
340
FEV1/FVC in Obstructive Lung disease
Low
341
FEV1/FVC in Restrictive Lung Disease
Normal or high
342
Peak expiratory flow rate in Obstructive Lung disease
Low
343
Peak expiratory flow rate in restrictive lung disease
Normal
344
Residual volume in obstructive lung disease
High
345
Residual volume in restrictive lung disease
Low, Normal, or high
346
Vital Capacity in Obstructive lung disease
Low
347
Vital Capacity in Restrictive Lung disease
Low
348
Total Lung capacity in Obstructive lung disease
High
349
TLC in Restrictive lung disease
Low
350
DLCO in Restrictive Lung disease
Depends
351
DLCO in obstructive lung disease
Depends
352
DLCO
DLCO is really a function of how well a gas transitions from the alveoli to the blood stream
353
If you have less alveolar surface area (like in severe emphysema) less CO can be taken up by the blood, therefore DLCO would be
low in a patient with emphysema
354
Low DLCO
conditions that decrease effective alveolar surface area
355
COPD/emphysema effects on alveolar surface area
Less alveolar surface area
356
Restrictive lung disease effet on alveolar surface area
(less lung volume/area
357
Lung diseases that decrease effective blood supply to the lungs
CHF Anemia
358
Drugs that cause pulmonary toxicity
bleomycin, amiodarone
359
Diseases that cause normal to high DLCO
Asthma Polycythemia (increased Hgb)
360
L -> R intra-cardiac shunt effect on DLCO
Normal to high DLCO
361
Alveolar hemorrhage effect on DLCO
Normal to high DLCO
362
of the commonly tested “obstructive” diseases, which one has increased DLCO
Asthma
363
Carboxyhemoglobin effects on DLCO
Reduces
364
Anemia effects on DLCO
Reduces
365
Altitude effects on DLCO
Increases
366
Low DLCO with restriction
Interstitial lung disease Pneumonitis
367
Low DLCO with obstruction
Emphysema Cystic fibrosis Bronchiolitis Lymphangioleiomyomatosis
368
Increased DLCO thought to be increased lung/airway vascularity and pulmonary capillary blood volume in
Asthma
369
Low DLCO with normal spirometry
Anemia Pulmonary vascular disease Early interstitial lung disease
370
Anemia DLCO in normal spirometry
Mild decrease
371
Pulmonary vascular disease DLCO in normal spirometry
Mild to severe decrease
372
Early interstitial lung disease DLCO in normal spirometry
Mild to moderate decrease
373
Increased DLCO situations
Polycythemia Severe obesity Asthma Pulmonary hemorrhage Left to right intracardiac shunting Mild left heart failure Exercise just prior to the test
374
How would mild left heart failure affect DLCO
INcreased pulmonary capillary blood volume and increased DLCO
375
How would exercise just prior to the test affect DLCO
Increased cardiac output and increased DLCO
376
How would left-to-right intracardiac shunting affect DLCO
Increased DLCO
377
How does Severe Obesity affect DLCO
Increased DLCO
378
Polycythemia effects on DLCO
Increased DLCO
379
Perioperative management of obstructive lung diseases
Bronchodilator (albuterol) Anti-Cholinergic (Ipratropium) Steroids
380
Intraoperative management of obstructive lung disease
Warm and humidify air Increase I:E ratio (provide for longer exhalation) Avoid hyperventilation (allow some permissive hypercapnia)
381
Perioperative management of restrictive lung diseases
Avoid “elective procedures” in setting of acute respiratory events If smokers: should stop (even 24h of cessation will reduce carboxyhemoglobin) They have decreased compliance: many require increased PEEP, increased FiO2 and RR May require post-op ventilation Treat their pain (prevent splinting
382
What 3 cardiopulmonary function tests are important for thoracotomy patients
Predicted post-op FEV1 Predicted post-op DLCO Preoperative Vo2 Max assesses the interaction between cardiac and pulmonary function Need to know the patient’s preoperative PFTs and cardiopulmonary functional status * Additionally - need to know a little bit about pulmonary anatomy (i.e. how much are they planning to resect)
383
What does Preoperative Vo2 assess?
the interaction between cardiac and pulmonary function
384
How many lung segments do humans have
42
385
RUL has how many segments
6
386
RML has how many segments
4
387
RLL has how many segments
12
388
LUL has how many segments
10
389
LLL has how many segments
10
390
3-Legged stool of Pre-thoracotomy respiratory assessment
Respiratory mechanics Cardio-pulmonary reserve Lung Parenchyma function
391
If ppoFEV1 > 40%
Low risk for perioperative respiratory complications
392
If ppoFEV1 < 30%
High-Risk
393
VO2 max Pre-op > 20 ml/kg/min
Low Risk
394
VO2 max Pre-op < 15 ml/kg/min
High Risk
395
ppoDLCO > 40% of predicted
Low-Risk
396
Is ppoDLCO a good indicator of long-term survival?
No
397
Closing Capacity is defined as  A: TLC – RV  B: FRC + RV  C: Closing Volume + RV  D: Closing Volume – RV  E: Closing Volume/FRC
C: Closing Volume + RV
398
True or False: An increased closing capacity improves respiratory mechanics and efficiency?
FALSE
399
True or False: Obese patients will become hypoxic quicker than averaged sized patients (assuming no additional lung pathology) because they have increased closing capacity
FALSE
400
Which statement about the predictive power of pre-operative assessment of pulmonary function prior to a thoracotomy for lobectomy is MOST likely true?  A: A predicted post-operative FEV1 > 40% indicates a low risk for post- operative respiratory complications  B: A normal pre-operative maximal oxygen consumption (VO2 max) is a poor predictor of post-thoracotomy outcome  C: A DLCO = 50% of predicted suggests an unacceptable risk for pulmonary complications  D: The FEV1 is the most useful predictor for post-thoracotomy outcome
A: A predicted post-operative FEV1 > 40% indicates a low risk for post-operative respiratory complications
401
What would you expect to find in restrictive lung disease?  A: Increased FVC  B: Increased FEV1  C: Normal to increased FEV1/FVC ratio  D: Decreased FEV1/FVC ratio
C: Normal to increased FEV1/FVC ratio
402
What would you expect to find in obstructive lung disease?  A: Increased FVC  B: Increased FEV1  C: Normal to increased FEV1/FVC ratio  D: Decreased FEV1/FVC ratio
D: Decreased FEV1/FVC ratio
403
What lung volumes make up the Functional Residual Capacity?  A: TV + ERV + RV  B: TV + ERV  C: ERV + RV  D: TV + RV
C: ERV + RV
404
Hypoxic Pulmonary Vasoconstriction is also known as
AKA von Euler-Liljestand mechanism
405
Pulmonary Artery smooth muscle cells contract because of
increases in intracellular calcium L type calcium channels and nonspecific cation channels
406
in HPV, The hypoxia sensor is located in
the PASMC, thus it acts as sensor & effector
407
Is HPV Present in the transplanted lung?
Yes
408
When is HPV typically present in Anesthesia?
Most often during one-lung ventilation
409
One-Lung Ventilation absolute indications
Isolation of one lung from the other to avoid spillage Control of the distribution of ventilation Unilateral bronchopulmonary lavage
410
Is VATS an absolute indication for One-Lung Ventilation?
No, this is a relative indication
411
What circumstances would we one-lung ventilate to avoid spillage?
In cases of infection or hemorrhage
412
What circumstances would we one-lung ventilate to control the distribution of ventilation?
Bronchopleural fistula Bronchopleural Cutaneous Fistula Surgical opening of major conducting airway Giant unilateral lung cyst or bulla, Tracheobronchial tree disruption Hypoxemia due to unilateral lung disease
413
Relative indications for one-lung ventilation
High Priority surgical exposure Medium Priority surgical exposure Post-Cardiopulmonary bypass Severe Hypoxemia (unilateral lung disease)
414
What level of indication is one-lung ventilation in severe hypoxia due to unilateral lung disease
Absolute or Relative
415
What level of indication is one-lung ventilation in
416
What level of indication is one-lung ventilation in Isolation of one lung from the other to avoid spillage or contamination- infection, massive hemorrhage
Absolute
417
What level of indication is one-lung ventilation in Control of the distribution of ventilation- bronchopleural fistula/ Bronchopleural cutaneous fistula?
Absolute
418
What level of indication is one-lung ventilation in Surgical opening of a major conducting airway
absolute
419
What level of indication is one-lung ventilation in a giant unilateral lung cyst or bulla
Absolute
420
What level of indication is one-lung ventilation in life-threatening hypoxemia due to unilateral lung disease
Absolute
421
What level of indication is one-lung ventilation in tracheobronchial tree disruption
Absolute
422
What level of indication is one-lung ventilation in High-Priority Surgical exposure cases?
Relative
423
What level of indication is one-lung ventilation in Medium Priority Surgical exposure cases
Relative
424
What level of indication is one-lung ventilation in Post Cardiopulmonary bypass after removing totally occluding chronic unilateral pulmonary emboli
Relative
425
High-Priority Exposure surgical cases include
Thoracic Aortic aneurysms, pneumonectomy, upper lobectomy, mediastinal exposure, Thoracoscopy
426
Medium- Priority Exposure surgical cases include
Middle and lower lobectomies, subsegmental resections, esophageal resections, Procedures on the thoracic spine
427
What are the predictors for intra-op hypoxia?
Side of the operation Lung function abnormalities Distribution of Perfusion
428
PO2 low on 2 lungs is predictive of
PO2 on one lung
429
Is obstructive lung disease helpful or harmful in one-lung ventilation
Can be both. If have emphysema than may auto peepCan be both. If have emphysema than may auto peep
430
What diagnostic test can help determine the distribution of perfusion?
V/Q Scan
431
What does a V/Q Scan help determine?
Distribution of perfusion
432
What factors can alter distribution of perfusion
Central versus peripheral lesions Supine versus lateral Right versus left sided surgeries
433
Patients with large central tumors will likely already have
less perfusion to the operative side compared with folks who have peripheral tumors
434
Patients with large central tumors will have more hypoxia when in which position and why?
supine because less ability for gravity to move perfusion to the ventilated lung
435
PAO2 with right side down and ventilated vs Supine
may be as much as 100 mm Hg higher
436
2 Healthy women ascent to a mountain of 4500+ ft and after 12 hrs, PA Catheters are inserted. Subject A has a Pulmonary Capillary pressure of 18mmHg, compared to only 10mmHg in subject B. For which of the following is Subject A at higher risk than subject B? - Delayed Airway closure on Expiration -Decreased Alveolar Surface tension -Increased volume of Anatomic dead space -Decreased bronchial circulation blood flow -Leakage of plasma and RBCs into the alveolar space
Leakage of plasma and RBCs into the Alveolar space
437
Condition in which plasma and RBCs leak into the alveolar space
Pulmonary Edema
438
A Newborn is hospitalized for tachypnea and hypoxemia for several days following birth and is determined to have a genetic defect affecting the primary structural elements of the cilia. For which of the following problems is this newborn at risk as a result? -Decreased surfactant production - Increased diffusion distance across the blood-gas interface -Decreased pulmonary blood flow - thickening of the alveolar basement membrane -Decreased airway mucus clearance
Decreased airway mucous clearance Increased risk of recurrent infection
439