Pulmonary + Respiratory Physiology Flashcards
Major functions of respiration
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
Airway Anatomy parts
Trachea
Right and Left Main Bronchi
Lobar Bronchi
Segmental Bronchi
Terminal Bronchioles
Respiratory Bronchioles
Alveolar Ducts
Characteristics of conducting airways
Have NO alveoli
Acinus is distal to
terminal bronchioles
Conducting airways
Trachea
Right and Left Main Bronchi
Lobar Bronchi
Segmental Bronchi
Terminal Bronchioles
The Respiratory Zone
The Acinus
What is this comprised of?
Makes up most of the volume of the lung
2.5-3 liters at rest
Each RBC spends about how long in the capillary network?
0.75 seconds in the capillary network
What MPAP is needed to generate 6L of Flow?
15 mm hg needed to generate 6 liters of flow
Surfactant is made by
TYPE II alveolar epithelial cells
Surfactant is a made of
phospholipids, proteins and ions
Muscles of expiration function
pull rib cage down
Muscles of inspiration function
Pull rib cage up
Muscles of inspiration
primarily external intercostals. Also SCM, Anterior serrati, scaleni– elevate rib cage– sternum moves outward from vert column and AP diameter inc 20%
Muscles of expiration
primarily abdominal recti, internal intercostals
Pleural pressure
Pressure of fluid between lung pleura and chest wall pleura. -5 cm h20 at rest
Alveolar pressure
Pressure of the air inside the alveolus. When airway open and no flow- 0 cm h20
Transpulmonary pressure
Difference between alveolar pressure and pleural pressure. Really a measurement of the elastic recoil of the lung
Pleural pressure function
fights lung tissue elastic recoil
Alveolar pressure
zero at airway rest, must get negative to get air in
greater TPP illustrates
greater compliance of the system
Lung compliance formula
the amount the lungs will expand for each unit of increase in transpulmonary pressure
How much air is needed to increase TPP by 1cm
Normally 200 ml air
Compliance is determined by
elastance of lung tissue and surface tension of alveoli. Also compliance of system involves chest wall compliance.
Elastic forces of lung tissue determined mainly from
elastin and collagen fibers. Alveoli forces moderated by surfactant.
Transpleural pressure elastance is mainly related to
surface tension btwn air and fluid
The thoracic cage is what percentage of the total lung system?
50%
Anatomic Dead Space (Definition)
The volume of air in the conducting airways
Anatomic Dead Space (Amount)
~150mL
What factors can change the anatomic dead space amount?
posture, size of person, and at the extremes of physiology
Physiologic Dead Space formula
(PacO-PeCo)
/PaCo
Alveolar ventilation is
the rate at which new air enters the alveoli
Dead Space Volume (Formula)
Va= RR (Vt-Vd)
expressed in L/min
Which region of the lung ventilates better?
Lower regions of the lung ventilate better than upper regions
Average tidal Volume
500mL
Average IRV
3100 mL
Average ERV
1200 mL
Average Residual volume
1200 mL
Tidal volume
Amount of air inhaled or exhaled with each breath under resting conditions
IRV
Inspiratory Reserve Volume
Amount of air that can be forcefully inhaled after a normal tidal volume inhalation
ERV
Expiratory Reserve Volume
Amount of air that can be forcefully exhaled after a normal tidal volume exhalation
RV
Residual Volume
Amount of air remaining in the lungs after a forced exhalation
TLC
Total Lung Capacity
Maximum Amount of air contained in lungs after a maximum inspiratory effort
TLC Formula
TLC= TV +IRV+ERV+RV
Vital capacity
Maximum amount of air that can be expired after a maximum inspiratory effort
Average Vital capacity
3100-4800 mL
Average TLC
4200-6000mL
AVerage inspiratory capacity
2400-3600 mL
Average Functional Residual Capacity
1800-2400 mL
Inspiratory capacity
Maximum amount of air that can be inspired after a normal expiration
inspiratory Capacity formula
IC= TV+IRV
Functional residual capacity
Volume of of air remaining in the lungs after a normal tidal volume expiration
FRC Formula
FRC=ERV+RV
Boyle’s Law (Formula)
P1V1=P2V2
Charles’ Law (Definition)
The volume of gas is directly proportional to its absolute temperature
Charles’ Law formula
V1/T1=V2/T2
Boyle’s Law (Definition)
As volume increases, the pressure of the gas decreases in proportion
Ideal Gas Law (formula)
PV=nRT
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
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.
Shunting
blood entering the arterial system without going through ventilated areas of the lung.
Shunt Equation
Qs/Qt= (Cco2-Cao2)/(CcO2-cvO2)
Qs/Qt
Shunt fraction
Shunt flow divided by Total Cardiac output
Dead Space Equation
VD/VT= (Paco-peCo)/(Paco)
FiO2
Fraction of inspired oxygen
Room air FiO2
0.21 in room air
PaO2
Partial pressure of Alveolar Oxygen
atmospheric pressure
760 mmHg at sea level
PH2O
H2O Vapor pressure in the alveolus :
Usually 47 mmHg at 37C
West Zone 1
where alveolar pressure is higher than arterial or venous pressure
West Zone 2
where alveolar pressure is higher than arterial or venous pressure
West Zone 3
where both arterial and venous pressure is higher than alveolar
West Zone 4
where the interstitial pressure is higher than alveolar or pulmonary venous pressure.
West Zone 1 formula
PA > Pa > Pv
West Zone 2 Formula
Pa > PA > Pv
West Zone 3 Formula
Pa > Pv > PA
West Zone 4 Formula
Pa > Pi > Pv > PA
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
Airway Resistance Formula
RrS=Rt+K1+K2V
Rt (in airway resistance)
The resistance from deformation of the lungs and chest wall
K1 (in airway resistance)
empirical constant representing gas viscosity
K2 (in airway resistance)
An empirical constant representing gas density and airway geometry
V (in airway resistance)
the flow as volume per unit of time
Tissue resistance from lung parenchyma
~70%
Tissue resistance from chest wall
~30%
What contributes to the work of breathing
Elastic work
Resistive work
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)
Resistive work
Work done to overcome tissue resistance, otherwise referred to as viscous resistance
Contributors to resistive work
Chest wall resistance
Lung resistance
Work done to overcomeairway resistance,which includes
Airway resistance
Resistance of airway devices and circuits
Respiratory Control Centers (controllers)
Nucleus retroambiguous
nucleus paraambigualis
Nucleus ambiguous
nucleus retroambiguous role and efferents/effectors
Upper motor neuron axons to contralateral expiratory muscles
Nucleus paraambigualis Role and efferents/effectors
Upper Motor neuron axons to contralateral inspiratory muscles
Nucleus ambiguous Role and efferent/effectors
vagus nerve: to larynx, pharynx and muscularis uvulae
Glossopharyngeus muscle to stylopharyngeus muscle
Pre-botzinger complex role and efferrent/effectors
Respiratory pacemaker (Central pattern generator)
Interneurons connecting to other respiratory control regions
Botzinger Complex- role and efferent/effectors
Expiratory Function
inhibitory interneurons to phrenic motor neurons and other respiratory control regions
Pontine respiratory group role and efferrent/effectors
Integrates descending control of respiration from the CNS
Interneurons connecting to other respiratory control regions
Cerebral Cortex role and efferrent/effectors
Volitional and behavioral respiratory control
Pontine respiratory group
mechanoreceptors in the bronchial and lung tissue (stimulus/Afferent nerve)
inflation/Deflation
Vagus Nerve
Central chemoreceptors (Stimulus/afferent nerve)
ph
No Nerve
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
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
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)
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
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
Disadvantages of FOB
Fragile
Difficult to use
Difficult to clean
Longer time to secure airway
Difficult with blood/secretions
Risk of laryngeal trauma
Nasopharynx can be obstructed by
choanal atresia, septal
deviation, mucosal swelling or foreign material (blood,
mucous, objects)
Oropharynx entry can be blocked by
the soft palate lying
against the posterior pharyngeal wall
The pathway of gas can be restricted by the epiglottis in the
hypopharynx
Laryngeal obstruction related to spasm (laryngospasm) must
be treated by
positive airway pressure, deeper anesthesia,
muscle relaxants or endotracheal intubation
Laryngeal closure can occur from
intrinsic or extrinsic muscles of the larynx
Tight airway closure results from
Contraction of external laryngeal muscles, which force the mucosal folds of the quadrangular membrane into apposition
Stridor suggests
Glottic (laryngeal) obstruction or
laryngospasm (most often on inspiration)
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
Contraindications of nasopharyngeal airways
Hemorrhagic disorders
Anticoagulation therapy
Sepsis
Basilar skull fracture
History of epistaxis
Nasal packing in place
FiO2 of supplemental oxygen delivered is dependent on
flow rate and device used
In nasal cannula, what is max flow rate?
6L/min
simple mask flow rates
No less than 5 L/min to
avoid CO2 rebreathing
(usually 6-10 L/min
Reservoir masks Can deliver FiO2 up to
1.0
(15L/min)
Peak pressures > 20 cm h2O can cause
gastric distention
Pulmonary veins
Four pulmonary veins (RUPV, RLPV, LUPV, LLPV)
Empty into left atrium
Oxygenated blood from the lungs
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
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
High pressure, low flow circulation (Pulmonary) Source
Systemic arterial blood from bronchial arteries (branches of the
thoracic aorta)
High pressure, low flow circulation (Pulmonary) Supplies
Trachea, bronchial tree, supporting tissues of the lung, adventitia of
pulmonary arteries and veins
Low pressure, high flow circulation
Source
Venous blood from body pulmonary artery alveoli (gas
exchange)
Low pressure, high flow circulation Supplies
Returns via pulmonary veins to the LA LV and then pumped
systemically
Pulmonary arterial system
Low pressure system
Thin vessel walls
Relatively little smooth muscle
The lung is required to always be able to accept
the entire CO
Pulmonary Artery Circulation pressure
25/10 mmHg
Pulmonary artery cathether uses
Uses: assessment of patients with pulmonary hypertension, cardiogenic shock, and unexplained dyspnea
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
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
PVR is normally small but can reduce even further as
pressure within the vessels increases
Recruitment
Opening of previously closed vessels
Distension
Increase in caliber of vessels
Change in shape from near flat to circular
Distension is the predominant mechanism for
decreased PVR at higher vascular pressures
PVR is highest at
very large lung volumes
Lung Volume affects
PVR
PVR is also high at
very low lung volumes
Resistance is the least when?
at normal TV breathing
If the lung is completely collapsed
Requires much more pressure to
allow blood flow
Critical opening pressure
What else affects PVR
Extra-alveolar vessels contain smooth muscle
Substances that cause contraction of smooth muscle will increase PVR
Substances that cause contraction of smooth muscle
Serotonin
Histamine
Norepinephrine
Thromboxane A2
Endothelin
Nitrous oxide
(Hypoxia)
What are some vasodilators?
Nitric oxide
Phosphodiesterase inhibitors
Calcium channel blockers
Prostacyclin
Calculation of pulmonary resistance
Resistance = Change in Pressure / Flow
PVR = [(mPAP – PCWP)/CO] x 80
SVR Equation
SVR = [(MAP – CVP)/CO] x 80
Change in Pressure
Mean Pulmonary Artery Pressure (mPAP)
Left atrial pressure (is approximated by Pulmonary Capillary Wedge Pressure
(PCWP)
Qp = Qs =
Cardiac Output
Hypoxic Pulmonary Vasoconstriction (HPV)
Decreased O2 concentration in alveoli blood vessel constriction
This is the opposite of what happens in the systemic circulation
Gravity and positioning affect blood flow and
therefore
gas exchange
When upright, what area of the lungs receives the least amount of bloodflow?
Apex receives least amount of blood
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
When hanging upside down, what area of the lungs receives the most blood flow?
Apex receives most blood flow
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
West Zone 1 doesn’t occur under normal conditions. When might this occur?
Reduced arterial pressure
Increased alveolar pressure
Which west zone mimics normal blood flow?
Zone 3
In hypoxic pulmonary vasoconstriction, Hypoxia (PO2 in the
alveoli) causes
local action on the artery without requiring CNS connections
Hydrostatic pressure (formula)
Pc – Pi
Colloid osmotic pressure
𝜋c - 𝜋i
Starling’s equation
Net fluid out = K[(Pc – Pi)– 𝜎(𝜋c - 𝜋i)]
K = filtration coefficient
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)
Angiotensin I in pulmonary circulation
Converted to Angiotensin II by ACE
Angiotensin II in Pulmonary circulation
unaffected
Vasopressin in pulmonary circulation
Unaffected
bradykinin in pulmonary circulation
Up to 80% inactivated
Serotonin in pulmonary circulation
Almost completely removed
Norepinephrine in pulmonary circulation
Up to 30% removed
histamine in pulmonary circulation
not affected
Dopamine in pulmonary circulation
not affected
E2 and F2x in pulmonary circulation
Almost completely removed
A2 in Pulmonary circulation
not affected
PGI2 in pulmonary circulation
not affected
Leukotrienes in pulmonary circulation
Almost completely removed
What is a normal pressure in the right atrium?
A: 5
B: 10
C: 15
D : 20
A: 5
What is the normal pressure in the right ventricle?
A: 25/15
B: 10/0
C: 15/5
D: 25/0
D: 25/0
When floating a pulmonary artery catheter, how can you tell that
you’ve entered the main pulmonary artery?
C: The diastolic pressure will increase
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
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
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
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
Which of the following is most important in the HPV phenomenon?
A: PaO2
B: PvO2
C: PAO2
D: PACO2
C: PAO2
Which of the following would cause pulmonary edema by
increased hydrostatic pressure?
A: TRALI
B: ARDS
C: CHF
D: Diffuse alveolar hemorrhage
C: CHF
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
how is oxygen carried throughout the blood
Attached to hemoglobin
Dissolved in blood
once o2 has diffused from alveoli, what happens?
It is transported to the peripheral tissue capillaries almost entirely in combination with hemoglobin
Oxygen carrying capacity formula
CaO2= (1.39 x Hgb x (sat/100))+ (0.003. x PaO2)
Henry’s Law
The amount of a gas that is dissolved in the blood is proportional to
the partial pressure of that gas
Normal arterial blood with a PaO2 of 100mmHg
contains
0.3ml O2/100ml (i.e. very little)
For every mmHg of PO2, there is 0.003 ml O2/100ml of
Blood
hemoglobin
An iron-porphorin compound attached to a protein globulin made of alpha and beta polypeptide chains
normal Adult hemoglobin
HgbA
normal fetal Hemoglobin
Hgb F
How does Hgb F compare to Hgb A?
higher affinity for o2 than HgbA
HgbF is for what age of people?
Newborn
Gradually replaced over 1st 6-8 mo of post-natal life
Abnormal hemoglobin S=
Sickle Cell
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
Methemoglobinemia
Ferrous ion of Hgb A (Fe2+) is oxidized to the ferric form (Fe3+)
Elevated concentration of methemoglobin in RBCs
Methemoglobinemia
Methemoglobinemia results in
Overall reduced ability of RBC to release oxygen to tissues
Causes of methemoglobinemia
Nitrites
Some local anesthetics (Benzocaine)
Congenital
Oxygen + hemoglobin =
HgbO2
hemoglobin in the oxygenated state is said to be
Relaxed or R State
hemoglobin in the deoxygenated state is said to be
tensed or T state
Oxygen rapidly binds to hemoglobin up to a PaO2 of
about 50 mmHg, then rate of binding slows
maximum amount of O2 that can be bound
O2 capacity
O2 Saturation
Percentage of available O2 binding sites that have o2 attached
O2 Saturation formula
Sat= (O2 combined with hemoglobin/ O2 capacity) x100
in strenuous exercise, o2 requirements
may increase by up to 20x normal
Diffusing capacity for O2 increases almost 3x during exercise due
to
increased surface area of capillaries participating in diffusion
What primary mechanism allows your PVR to drop during exercise
shunt flow in o2 Transport
Blood from the lung will mix with
blood that passed from the aorta
through the bronchial circulation
Shunt blood has PO2 of
40 mmHg
Pulmonary venous blood has PO2
of
104 mmHg
Venous admixture –> PO2 of
95
mmHg
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
What partial pressure of O2 is needed to fulfill normal cellular function
requirements???
P50
= PO2 at which 50% of
hemoglobin is saturated
Normal is about 27 mmHg
Right Shift in oxygen dissociation curve
O2 bound to Hgb with less affinity
Right shift in Oxygen dissociation curve characteristics
Increased H+ (Acidosis)
Increased PCO2 (Bohr Effect)
Increased Temperature
Increased 2,3-diphosphoglycerate
Sickle Cell anemia
Left Shift in oxygen dissociation curve
Left Shift
right shift in Oxygen dissociation curve characteristics
Alkalosis
Lowered PCO2 (redundant)
Hypothermia
Decreased 2,3-diphosphoglycerate
Carbon monoxide
CO2 is carried in blood in 3 different forms
Dissolved
Bicarbonate
Combination with proteins as carbamino coumpounds (bound to hemoglobin)
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
Co2 vs o2 solubility
CO2 is about 20x more soluble than O2
Carbamino Compounds
Formed by combination of CO2 with terminal amine groups in blood proteins
Most importantly, globin of hemoglobin
Hgb -> carbaminohemoglobin
Carbamino synthesis
Reaction occurs rapidly without an enzyme and reduced Hgb can bind more
CO2 as carbaminohemoglobin than HgbO2
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.
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
Respiratory Acidosis
Increase in PCO2
Decreases the HCO3-/PCO2 ratio and thus decreases the pH (acidosis)
Respiratory Alkalosis
Decrease in PCO2
Increases the HCO3-/PCO2 ratio and thus increases the pH (alkalosis)
Metabolic Acidosis
Decrease in HCO3-
Decreases the HCO3-/PCO2 ratio and thus decreases the pH (acidosis)
Metabolic Alkalosis
Increase in HCO3-
Increases the HCO3-/PCO2 ratio and thus increases the pH (alkalosis)
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
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
Therefore, presence of Hb increases O2 concentration by about
70
times
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
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
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
If the patient has normal pulmonary function, the arterial PO2 will
be normal, but the O2 content will be
Reduced
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
90% of CO2 transported in the arterial blood is in the form of
bicarbonate
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
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
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
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
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`
Recommendation: pressure on the lateral tracheal wall should be kept between
20-30 cm H20
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
Reinforced/armored tubes
have a metal or nylon spiral woven reinforcing wire
covered both internally and externally by rubber, PVC or
silicone
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
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
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
Advantages of RAE tubes
Easy to secure and reduce the risk of unintended extubation
Breathing system remains away from surgical field
Disadvantages of RAE tubes
More resistance than conventional tubes
Difficult to suction
Advantage of MLT
The small diameter provides better
surgical access
Disadvantages of MLTs
incomplete exhalation & occlusion (increased resistance)
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
RV + ERV =
FRC
TV + IRV
Inspiratory capacity
IRV+ TV+ ERV=
Vital Capacity
VC+ RV=
TLC
IC+ FRC=
TLC
IRV+ TV+ ERV+ RV=
TLC
Flow rate of expired air is greatly
dependent on
lung volumes
Flow is limited by
airway
compression
After a small amount of air is exhaled
the flow rate begins to drop quickly as the lung volume decreases
In restrictive diseases, what happens to flow rate and volume exhaled
They are REDUCED
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
in obstructive diseases, how is the flow rate?
Flow rate is very low for a given
lung volume
What does the flow volume curve look like in obstructive diseases?
A “scooped-out” appearance of the
flow volume curve appears
In Restrictive diseases, inspiration is limited by
Reduced compliance of the lung or chest wall
Weakness of inspiration muscles
in obstructive diseases, ____is typically
abnormally large, but _____ ends
early
TLC
Expiration
Early airway closure is secondary to
increased smooth muscle tone in the bronchi (asthma) or loss of radial traction (emphysema)
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
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
Both the increase in airway resistance and
the reduction of lung elastic recoil pressure
can be important factors in reducing
FEV1
in dynamic compression, Flow is determined by alveolar pressure
minus pleural pressure (not pressure at
the mouth) and is therefore
Effort independent
Lung volumes are measured by
Spirometry
What Lung volumes cannot be measured by Spirometry?
FRC and RV
FRC can be measured by
helium dilution
Helium is virtually insoluble in blood
C1 = known concentration of helium
body plethysmograph
How is a helium dilution test performed?
Subject takes several breaths and the helium concentration in the spirometer and the lung equilibrate
Formula for determining FRC
C1 x V1= C2 x (V1+ V2)
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)
Formula for body Plesmythograph
P1xV1 = P2 (V1-△V) => Solve for △V
Diffusing capacity for carbon monoxide (DLCO) is measured by
Diffusing capacity for carbon monoxide (DLCO) is measured by
Diffusion capacity for O2 is measured
very difficult to measure (only done in research labs)
Regional variation in ventilation and blood flow can be measured using
radioactive xenon
blood preferentially flows to what part of the lung?
Lung bases
Measuring ventilation inequality
Single breath method – very similar to Fowler method for determining anatomic dead space
Multiple breath method
Patient breaths 100% O2 over multiple breaths, N2 is measured at
the lips as a function of time
in the Multiple-breath method, If FRC = TV, then
N2 concentration should ”half” with each breath
in the Multiple-breath method, in a diseased lung, we see
a non- linear washout of N2 (due to non- uniform ventilation
PFT Test of flow
Forced Expiratory Spirometry
FEV and FEV1
FVC
When can a FEV/FEV1/ FVC test be done?
Can be done before or after a bronchodilator to determine bronchodilator responsiveness
Are Flow tests effort dependent or effort independent?
Effort independent
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
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
The greater the DLCO
the lower the exhaled concentration
Patient’s height, weight, sex and age have correlated
predicted “normal” values
Lung volumes
Flows
FEV1 - Decreased
FVC – Decreased
FEV1/FVC Ratio – Decreased
DLCO – Decreased
Obstructive Disease
FEV1 – Normal (to slightly low)
FVC – Decreased
FEV1/RVC ratio – Normal (to increased)
DLCO - Decreased
Restrictive Disease
Asthma
COPD
Chronic bronchitis
Emphysema
Obstructive Disease (think difficulty exhaling)
Interstitial lung disease
Pulmonary fibrosis
Chest wall and pleural diseases
Obesity
Scoliosis
Neuromuscular diseases
ALS
Restrictive Disease (think difficulty inhaling)
A fixed obstruction
will effect both exhalation and inhalation
OSA
Patient has respiratory efforts but cannot move air due to upper airway obstruction
How is OSA Diagnosed
Diagnosed via sleep study (measuring Apnea-Hypopnea Index = # of apneas and hypopneas per hour of sleep)
AHI 0-5
No Disease
AHI 21- 40
Moderate OSA
AHI 6-20
Mild OSA
AHI > 40
Severe OSA
FEV1
volume of air forcibly exhaled in 1 second
FVC
forced vital capacity
All “Capacities” are
SUmmation of other volumes
Closing Capacity
Closing Volume + Residual Volume
Closing Volume
the volume of air in the lungs at which the airways in the dependent portion of the lung begin to close/collapse
Residual Volume
the volume of air in the lungs following a maximum exhalation
Closing Capacity
Closing capacity > FRC
This is less than ideal
How is closing capacity measured
Single Breath N2 washout method
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
Closing Capacity Phase 1
Pure Dead space
Closing Capacity Phase 3
Pure alveolar gas
Closing Capacity Phase 2
Mixture of dead space & alveolar gas
Closing Capacity Phase 4
Occurs near the end of expiration, is signified by a sharp increase in N2 concentration
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
A young person will have a closing volume that is approximately what percent of their vital capacity?
10%
As you age, what happens to the closing volume
It increases
I.e. closing capacity increases
At age 65, what happens to the closing capacity
is approximately the same as the FRC
About 40% of vital capacity
Certain diseases increase closing capacity
COPD
Asthma
Pulmonary Edema
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
Obstructive Lung Diseases (Inhale/exhale)
CAN’T EXHALE
Restrictive Lung Diseases
CAN’T INHALE
Obstructive Lung Diseases
Reduced elasticity or premature closure of small airways that results in increased lung volumes, but decreased ventilation
COPD
Emphysema
Chronic bronchitis
Asthma
Usually a temporary obstruction that is reversible (due to inflammation of airways)
Restrictive Lung Diseases
Reduced lung volumes due to damage to the lung tissue itself or structural change/weakness of the thorax
Intrinsic Restrictive Lung Diseases
pathology within the lung parenchyma (i.e. pulmonary fibrosis)
Extrinsic Restrictive Lung Diseases
Chest wall or pleural dysfunction (i.e. severe scoliosis)
Pink Puffer
Emphysema
Blue Bloater
Chronic Bronchitis
Obstructive Lung Diseases (Examples)
COPD
Emphysema (“pink puffer”)
Chronic bronchitis (“blue bloater”)
Asthma
Bronchiectasis
Cystic Fibrosis
Restrictive Lung Diseases
Obesity
Pulmonary Fibrosis
Scoliosis (severe)
Neuromuscular Disease
ALS
Muscular Dystrophy
Myasthenia Gravis
Sarcoidosis (and other ILDs)
Auto-immune diseases
Truncal burns
FEV1 in obstructive lung disease
Low
FEV1 in Restricitve Lung disease
Normal or slightly low
FEV1/FVC in Obstructive Lung disease
Low
FEV1/FVC in Restrictive Lung Disease
Normal or high
Peak expiratory flow rate in Obstructive Lung disease
Low
Peak expiratory flow rate in restrictive lung disease
Normal
Residual volume in obstructive lung disease
High
Residual volume in restrictive lung disease
Low, Normal, or high
Vital Capacity in Obstructive lung disease
Low
Vital Capacity in Restrictive Lung disease
Low
Total Lung capacity in Obstructive lung disease
High
TLC in Restrictive lung disease
Low
DLCO in Restrictive Lung disease
Depends
DLCO in obstructive lung disease
Depends
DLCO
DLCO is really a function of how well a gas transitions from the alveoli to the blood stream
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
Low DLCO
conditions that decrease effective alveolar surface area
COPD/emphysema effects on alveolar surface area
Less alveolar surface area
Restrictive lung disease effet on alveolar surface area
(less lung volume/area
Lung diseases that decrease effective blood supply to the lungs
CHF
Anemia
Drugs that cause pulmonary toxicity
bleomycin, amiodarone
Diseases that cause normal to high DLCO
Asthma
Polycythemia (increased Hgb)
L -> R intra-cardiac shunt
effect on DLCO
Normal to high DLCO
Alveolar hemorrhage effect on DLCO
Normal to high DLCO
of the commonly tested “obstructive” diseases, which one has increased DLCO
Asthma
Carboxyhemoglobin effects on DLCO
Reduces
Anemia effects on DLCO
Reduces
Altitude effects on DLCO
Increases
Low DLCO with restriction
Interstitial lung disease
Pneumonitis
Low DLCO with obstruction
Emphysema
Cystic fibrosis
Bronchiolitis
Lymphangioleiomyomatosis
Increased DLCO thought to be increased lung/airway vascularity and pulmonary capillary blood volume in
Asthma
Low DLCO with normal spirometry
Anemia
Pulmonary vascular disease
Early interstitial lung disease
Anemia DLCO in normal spirometry
Mild decrease
Pulmonary vascular disease DLCO in normal spirometry
Mild to severe decrease
Early interstitial lung disease DLCO in normal spirometry
Mild to moderate decrease
Increased DLCO situations
Polycythemia
Severe obesity
Asthma
Pulmonary hemorrhage
Left to right intracardiac shunting
Mild left heart failure
Exercise just prior to the test
How would mild left heart failure affect DLCO
INcreased pulmonary capillary blood volume
and increased DLCO
How would exercise just prior to the test affect DLCO
Increased cardiac output and increased DLCO
How would left-to-right intracardiac shunting affect DLCO
Increased DLCO
How does Severe Obesity affect DLCO
Increased DLCO
Polycythemia effects on DLCO
Increased DLCO
Perioperative management of obstructive lung diseases
Bronchodilator (albuterol)
Anti-Cholinergic (Ipratropium)
Steroids
Intraoperative management of obstructive lung disease
Warm and humidify air
Increase I:E ratio (provide for longer exhalation)
Avoid hyperventilation (allow some permissive hypercapnia)
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
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)
What does Preoperative Vo2 assess?
the interaction between cardiac and pulmonary
function
How many lung segments do humans have
42
RUL has how many segments
6
RML has how many segments
4
RLL has how many segments
12
LUL has how many segments
10
LLL has how many segments
10
3-Legged stool of Pre-thoracotomy respiratory assessment
Respiratory mechanics
Cardio-pulmonary reserve
Lung Parenchyma function
If ppoFEV1 > 40%
Low risk for perioperative respiratory complications
If ppoFEV1 < 30%
High-Risk
VO2 max Pre-op > 20 ml/kg/min
Low Risk
VO2 max Pre-op < 15 ml/kg/min
High Risk
ppoDLCO > 40% of predicted
Low-Risk
Is ppoDLCO a good indicator of long-term survival?
No
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
True or False: An increased closing capacity improves respiratory mechanics and efficiency?
FALSE
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
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
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
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
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
Hypoxic Pulmonary Vasoconstriction is also known as
AKA von Euler-Liljestand mechanism
Pulmonary Artery smooth muscle cells contract because of
increases in intracellular calcium
L type calcium channels and nonspecific cation channels
in HPV, The hypoxia sensor is located in
the PASMC, thus it acts as sensor & effector
Is HPV Present in the transplanted lung?
Yes
When is HPV typically present in Anesthesia?
Most often during one-lung ventilation
One-Lung Ventilation absolute indications
Isolation of one lung from the other to avoid spillage
Control of the distribution of ventilation
Unilateral bronchopulmonary lavage
Is VATS an absolute indication for One-Lung Ventilation?
No, this is a relative indication
What circumstances would we one-lung ventilate to avoid spillage?
In cases of infection or hemorrhage
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
Relative indications for one-lung ventilation
High Priority surgical exposure
Medium Priority surgical exposure
Post-Cardiopulmonary bypass
Severe Hypoxemia (unilateral lung disease)
What level of indication is one-lung ventilation in severe hypoxia due to unilateral lung disease
Absolute or Relative
What level of indication is one-lung ventilation in
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
What level of indication is one-lung ventilation in Control of the distribution of ventilation- bronchopleural fistula/ Bronchopleural cutaneous fistula?
Absolute
What level of indication is one-lung ventilation in Surgical opening of a major conducting airway
absolute
What level of indication is one-lung ventilation in a giant unilateral lung cyst or bulla
Absolute
What level of indication is one-lung ventilation in life-threatening hypoxemia due to unilateral lung disease
Absolute
What level of indication is one-lung ventilation in tracheobronchial tree disruption
Absolute
What level of indication is one-lung ventilation in High-Priority Surgical exposure cases?
Relative
What level of indication is one-lung ventilation in Medium Priority Surgical exposure cases
Relative
What level of indication is one-lung ventilation in Post Cardiopulmonary bypass after removing totally occluding chronic unilateral pulmonary emboli
Relative
High-Priority Exposure surgical cases include
Thoracic Aortic aneurysms, pneumonectomy, upper lobectomy, mediastinal exposure, Thoracoscopy
Medium- Priority Exposure surgical cases include
Middle and lower lobectomies, subsegmental resections, esophageal resections, Procedures on the thoracic spine
What are the predictors for intra-op hypoxia?
Side of the operation
Lung function abnormalities
Distribution of Perfusion
PO2 low on 2 lungs is predictive of
PO2 on one lung
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
What diagnostic test can help determine the distribution of perfusion?
V/Q Scan
What does a V/Q Scan help determine?
Distribution of perfusion
What factors can alter distribution of perfusion
Central versus peripheral lesions
Supine versus lateral
Right versus left sided surgeries
Patients with large central tumors will likely already have
less perfusion to the operative side compared with folks who have peripheral tumors
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
PAO2 with right side down and ventilated vs Supine
may be as much as 100 mm Hg higher
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
Condition in which plasma and RBCs leak into the alveolar space
Pulmonary Edema
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