TARev - Respiratory Review

Pulmonary Physiology 2018
TA Review
March 8th 2018
Dan Leisman, Emily Markovic, Benjamin Asriel and Jimmitti Teysir

Respiratory Mechanics
Emily Schlussel Markovic

Adapted from slides by Dennis Dacarett-Galeano
Respiratory Mechanics
Inhalation has to overcome 2 forces:
1. Elastic Forces – think of the intrinsic property of a rubber band to snap back
2. Resistive Forces -- Flow-dependent (air viscosity, diameter of the airway, etc)
Forces that determine the respiratory system:

1. Chest wall (Expansive force)
2. Lung elastic force (Collapsing force)
-tissue elastic recoil and surface tension in alveoli
3. Frictional resistance
-combination of tissue and airway resistance
-determines lung compliance
(functional residual capacity)

Respiratory Mechanics: Pneumothorax
The intrapleural pressure equilibrates with the atm → Expansive and collapsing
forces can no longer oppose each other → The lungs collapse and the chest expands
Intrapleural Pressure < 0

Lung Structure and Compliance
C = Compliance (mL/mm Hg)
C = ΔV/ΔP V = Volume (mL)
P = Pressure (mm Hg)
• Compliance describes how distensible the system is (inversely related to elastance)

• High compliance = easy to expand, won’t snap back (low elastance)
• Low compliance = stiff, hard to expand (high elastance)
• The lung is more compliant during expiration (hysteresis)
• Inflation of the lungs follows a different curve than deflation
At very high and low volumes, compliance is small.
(You can apply a lot of pressure but the volume
will change minimally).
At middle volumes, compliance is larger → lung is

easier to expand.
It’s more energy efficient to stay in this range.
Surfactant
• Synthesized by type II alveolar cells, starting at 24 wks gestation
• Promotes compliance (reduces work of breathing)
• Reduces the surface tension - lines the alveoli and disrupts the intermolecular forces
between liquid molecules
• Prevents collapse
• Effect is greater in smaller alveoli - compensates for the differences in alveolar size
Law of Laplace: P = 2T/r

P= collapsing pressure on alveolus
T= surface tension
r= radius of alveolus
Inspiration
• Diaphragm contracts →abdominal
contents pushed downward → ribs
lifted up and out
• Increase in intra-thoracic volume →
lowers intra-thoracic pressure → air
rushes in (P1V1=P2V2)
• During exercise: inspiration assisted
by external intercostals and
accessory muscles
Expiration
• Normally passive: diaphragm
relaxes → ribs move down and in
(forces reverse)
• During exercise/disease state

(asthma): expiration assisted by
internal intercostals and
abdominals
The Breathing Cycle
(functional
residual
capacity)
Lung Volumes
Disease States
• Emphysema: loss of elastic fibers → increased
compliance → barrel chest
– Obstructive (can’t breath OUT)
• Pulmonary fibrosis → excessive fibrotic tissue →

decreased compliance
– Restrictive (can’t breath IN)
• Asthma: airway SM constriction → decreased

resistance (resistance = 8ηl/πr4)
– Obstructive
RESPIRATORY MECHANICS
1. In a maximal expiration, the total volume expired is
A. tidal volume (TV)
B. vital capacity (VC)
C. expiratory reserve volume (ERV)
D. residual volume (RV)
E. functional residual capacity (FRC)
F. inspiratory capacity
G. total lung capacity
1. In a maximal expiration, the total volume expired is
A. tidal volume (TV)
B. vital capacity (VC)
C. expiratory reserve volume (ERV)
D. residual volume (RV)
E. functional residual capacity (FRC)
F. inspiratory capacity
G. total lung capacity
2. During pulmonary function testing, a 52-year-old smoker inspires a normal breath and
then expires completely into the spirometer, expelling a measured volume of air. In a second
test, the patient inspires maximally and then expires completely into the spirometer,
expelling a second measured volume of air.
By subtracting the volume of air obtained in the first test from the volume obtained in the
second test, it is possible to determine which of the following?
A. Expiratory Reserve Volume

B. Functional Residual Capacity
C. Inspiratory Capacity
D. Inspiratory Reserve Volume
E. Vital Capacity
F. Tidal Volume
3. During pulmonary function testing, a 52-year-old smoker inspires a normal breath and
then expires completely into the spirometer, expelling a measured volume of air. In a second
test, the patient inspires maximally and then expires completely into the spirometer,
expelling a second measured volume of air.
By subtracting the volume of air obtained in the first test from the volume obtained in the
second test, it is possible to determine which of the following?
A. Expiratory Reserve Volume

B. Functional Residual Capacity
C. Inspiratory Capacity
D. Inspiratory Reserve Volume
E. Vital Capacity
3. A woman at 30 weeks gestation has been diagnosed with diabetes mellitus. She is
rushed to delivery because of signs of preeclampsia. After a cesarean section delivery,
the newborn baby is noted to have signs of cyanosis, tachypnea, and dyspnea. Which of
the following is a characteristic of the substance that likely to be insufficient in the
baby?
A. It decreases compliance of small alveoli

B. It increases the surface tension of alveoli
C. It disrupts liquid intermolecular forces in alveoli
D. It is produced by type 1 pneumocytes in alveoli
E. It consists primarily of sphingomyelin.
3. A primigravida woman at 30 week’s gestation has been diagnosed with diabetes
mellitus. She is rushed to delivery because of signs of preeclampsia. After a cesarean
section delivery, the newborn baby is noted to have signs of cyanosis, tachypnea, and
dyspnea. Which of the following is a characteristic of the substance that is likely to be
insufficient in the baby?
A. It decreases compliance of small alveoli

B. It increases the surface tension of alveoli
C. It disrupts liquid intermolecular forces in alveoli
D. It is produced by type 1 pneumocytes in alveoli
E. It consists primarily of sphingomyelin
Pulmonary Circulation
Emily Schlussel Markovic
Adapted from slides by Sharely Fred Torres
Pulmonary Vessels
● Pulmonary Capillaries: great for gas exchange
○ Extensive capillary network → large surface area
○ Low pressure (RV < LV) → low resistance
○ Thin walled: small diffusion barrier
● Pulmonary Arterioles: carry deoxy blood to lungs

○ Constrict/relax SM to alter resistance and control blood flow
○ Optimize oxygenation - decrease perfusion (Q) to poorly ventilated (V) areas
■ Hypoxic vasoconstriction: mediated by low PAO2 (<70 mmHg)
● Local - disease
● Global
○ High altitude - increase PVR
○ Fetal circulation (reverses at birth)
○ Other mediators
■ Nitric Oxide activates cGMP → relaxes SM (decreased NO → constrict)
■ Increased endothelin
Pulmonary Circulation: Distribution & Zones
Zone 1 – apex of lung – PA > Pa > Pv
● High Alveolar pressure compresses arterioles → less perfusion → no gas exchange →

physiologic dead space
● Can cause physiologic dead space (no ventilation) with blood loss (decreased P a) or
mechanical ventilator (increased PA)
Zone 2 – middle of lung – Pa > PA > Pv
● Blood flow driven by arterial-alveolar pressure differences
Zone 3 – base of lung – Pa > Pv > PA
● Capillaries most open (gravity) → blood flow is highest

● Blood flow driven by arterial-venous pressure differences
Pulmonary Circulation – Shunting
● Physiologic shunts: 2% of CO bypasses the alveoli; (PaO2 < PAO2)
○ bronchial blood flow
○ coronary blood flow
● Right to Left Shunt: Deoxygenated blood from R heart reaches L heart without
passing through lungs → hypoxemia
○ Increasing PiO2 will not help (shunted blood always dilutes)
○ PaCO2 generally not increased; O2 chemoreceptors less sensitive
● Left to Right Shunt: Oxygenated blood from L heart re-circulates through lungs
(ASD, VSD, PDA) → increased pulmonary blood flow
○ Po2 of right heart will be elevated
○ No hypoxemia
1. A patient in the Emergency Department is found to have decreased arterial PO2
and an increased A-a gradient. Which of the following could explain these
findings?
a) Hypoventilation
b) Right to left cardiac shunt
c) Anemia
d) CO poisoning
e) Ascent to high altitude

#1- Answer
B. Right to left cardiac shunt.
Hypoventilation, R-L cardiac shunt, and ascent to high altitude will all
cause hypoxia by decreasing PO2.
However, only the R-L cardiac shunt has an increased A-a gradient
because a portion of the pulmonary cardiac output is never oxygenated.
2. You are a pulmonary TA teaching the Mount Sinai class of 2021. A very wise
student ask you to explain the difference between pulmonary and systemic
circulation. In response to her question you answer that compared with the
systemic circulation, pulmonary circulation has:
a) higher blood flow
b) lower resistance
c) higher arterial pressure
d) higher capillary pressure
e) higher cardiac output

#2- Answer
B. Lower resistance. The pulmonary circulation is

characterized by both lower pressures and lower resistance
than the systemic circulation.
Blood flow in both the systemic and pulmonary systems are

nearly equal (flow = pressure/resistance).
3. When a person is standing, blood flow in the lungs is:
a. equal at the apex and the base
b. highest at the apex owing to the effects of gravity on arterial pressure
c. highest at the base because that is where the difference between arterial and
venous pressure is greatest
d. lowest at the base because that is where alveolar pressure is greater than
arterial pressure
#3- Answer
C. highest at the base because that is where the difference between arterial and
venous pressure is greatest
VQ Concepts
Jimmitti Teysir
Questions Adapted from slides by Shareley Fred Torres
Defining the Terms
Ventilation (V): The amount of air that reaches the alveoli (~ 4L/min)
Perfusion (Q): the amount of blood that reaches the alveoli (~ 5L/min)
Ideally, ventilation and perfusion are equal, such that V/Q =1.
In other words, there is just enough oxygen to saturate the blood.

Both V and Q are greatest at the lung base
However, Q >>V because of

increased hydrostatic
pressure at the lung base
(gravity).
Therefore, the ratio V/Q is

lowest at the lung base.
V/Q is lowest at the lung base!
Figure from: Cross, M., & Plunkett, E. (2014). Ventilation/perfusion mismatch. In

Physics, Pharmacology and Physiology for Anaesthetists: Key Concepts for the FRCA
(p. 218). Cambridge: Cambridge University Press.
doi:10.1017/CBO9781107326200.090
V/Q ratio varies throughout the upright lung
V/Q is greatest at the apex

● “Wasted ventilation”
● PAO2 is also greatest here
V/Q is lowest at the base

● “Wasted perfusion”
● PACO2 is greatest here
Figure from First Aid 2018, pg. 651

What is a pulmonary shunt?
Shunt: airway obstruction
● Example: choking on a peanut
● Alveoli unable to oxygenate blood
● “Perfusion without Ventilation”
● V/Q = 0
This represents a R→ L shunt:

blood does not get oxygenated by the
lungs and deoxygenated (venous)
blood enters the L atrium. PaO2 and PaCO2 approach mixed venous blood
Figure from:
https://www.pharmacology2000.com/Anesthesia2000_2014/physics/Chemistry
_Physics/physics11.htm
Implications of shunting
Increased A-a gradient
● Oxygen is not getting to the arteries from the alveoli, thus increasing the
O2 difference between them.
Hypoxic vasoconstriction
● In the lungs, pulmonary arteries uniquely vasoconstrict in response to low
oxygen. This is to ensure that blood is diverted to alveoli that can
participate in gas exchange.
What is dead space?
Dead space: ventilation w/o perfusion
● Example: Pulmonary Embolism
● V/Q = ∞
Alveolar gases approach inspired

humidified air
● PAO2 approaches PIO2 (150 mmHg)

Figure from: https://clinicalgate.com/pulmonary-embolism-6/
● PACO2 approaches PICO2 (0 mmHg)
Review
Arterial blood
resembles inspired
concentrations
Shunt and Dead Space

Arterial blood approaches represent the extreme
venous concentrations
ends of V/Q mismatch!
Ventilation Equations
Key Equations Normal Values

Minute ventilation rate (L/min) VT = 450 ml
V̇E = VT x RR VD = 150 ml
RR = 14 /min
Alveolar Ventilation rate (L/min) V̇E = 6.3 L/min
V̇A = (VT – VD) x RR V̇A = 4.2 L/min
Patm = 760 mmHg
Physiologic Dead Space (L) PH2O = 47 mmHg
VD = VT x [(PaCO2 – PECO2)/PaCO2] FIO2 = 0.21
R = respiratory quotient = CO2 / O2 ≈ 0.8
Alveolar gas equation Q = cardiac output = 5-6 L/min
PAO2 = FIO2(Patm – PH2O) – PaCO2/R V/Q ≈ 0.8
PaCO2 = 40 mmHg
A-a gradient A-a < 10 mmHg
A-a gradient = PAO2 – PaO2
1. A pulmonary physiologist is working on an experiment and he decides to apply a small
amount of positive pressure ventilation to lungs to assess changes in pulmonary blood
flow. Which of the following will be noted in this experiment, assuming the patients are
standing?
a. Regional differences between blood flow will not be as great as ventilation differences
b. When standing, blood flow will remain even throughout the lung zones
c. Blood flow will be reduced in zone 1
d. Blood flow will be increased in zone 2
e. Blood flow in zone 3 will be driven by the difference in alveolar and venous pressures
1. A pulmonary physiologist is working on an experiment and he decides to apply a small
amount of positive pressure ventilation to lungs to assess changes in pulmonary blood
flow. Which of the following will be noted in this experiment, assuming the patients are
standing?
a. Regional differences between blood flow will not be as great as ventilation differences
b. When standing, blood flow will remain even throughout the lung zones
c. Blood flow will be reduced in zone 1
d. Blood flow will be increased in zone 2
e. Blood flow in zone 3 will be driven by the difference in alveolar and venous pressures
2. A 60 year old patient comes in for a physical exam and you want to be thorough so you
decide to perform pulmonary function testing. The patient has a 50-pack-year history of
smoking. Laboratory testing reveals an arterial CO2 pressure of 40 mm Hg and an expired
CO2 pressure of 30 mm Hg. His physiologic dead space is 125 mL. What is the patient’s
tidal volume?
a. 50 mL
b. 100 mL
c. 500 mL
d. 1000 mL
e. 2500 mL
2. A 60 year old patient comes in for a physical exam and you want to be thorough so you
decide to perform pulmonary function testing. The patient has a 50-pack-year history of
smoking. Laboratory testing reveals an arterial CO2 pressure of 40 mm Hg and an expired
CO2 pressure of 30 mm Hg. His physiologic dead space is 125 mL. What is the patient’s
tidal volume?
a. 50 mL
b. 100 mL
VD = VT × ([PaCO2 – PECO2] / PaCO2)
c. 500 mL 125 = VT × (40-30/40)
d. 1000 mL 500 ml = VT
e. 2500 mL
3. A 7-year-old boy was playing with his toys and he accidentally swallowed one of his
marbles. His parents rush him to the Emergency Department for immediate care. On
bronchoscopy, the ED team finds an area of the lung is not being ventilated due to bronchial
obstruction. The pulmonary capillary blood serving that area would have had a PO2 that is
a. equal to atmospheric PO2
b. equal to mixed venous PO2
c. equal to normal systemic arterial PO2
d. higher than inspired PO2
e. lower than mixed venous PO2

3. A 7-year-old boy was playing with his toys and he accidentally swallowed one of his
marbles. His parents rush him to the Emergency Department for immediate care. On
bronchoscopy, the ED team finds an area of the lung is not being ventilated due to bronchial
obstruction. The pulmonary capillary blood serving that area would have had a PO2 that is
a. equal to atmospheric PO2
b. equal to mixed venous PO2
c. equal to normal systemic arterial PO2
d. higher than inspired PO2
e. lower than mixed venous PO2

4. You are on your last week of Internal Medicine rotation and since you are a
thorough medical student, you decide to calculate a patient’s A-a gradient who
comes in for shortness of breath to narrow your differential diagnosis. You are
given the measurement of PO2= 43 and PCO2= 50. What is the A-a gradient?
a. 7 mm Hg
b. 20 mm Hg
c. 47 mm Hg
d. 93 mm Hg
4. You are on your last week of Internal Medicine rotation and since you are a
thorough medical student, you decide to calculate a patient’s A-a gradient who
comes in for shortness of breath to narrow your differential diagnosis. You are
given the measurement of PO2= 43 and PCO2= 50. What is the A-a gradient?
a. 7 mm Hg
PAO2= PiO2 – PaCO2/R = 150 mmHg- 50/0.8 ~ 63
b. 20 mm Hg
PAO2 - PaO2 = 63 -42 = 20 mm Hg
c. 47 mm Hg
d. 93 mm Hg
Gas Diffusion; O2 Transport and Delivery
Dan Leisman
Important Numbers
• Body Temp = 37C PO2 160 Dry inspired
• Standard Pressure = 760 mmHg PCO2 0 air
• % of gases in dry air at barometric

PO2 150
pressure of 760 mmHg : O2 (21%), PCO2 0
Humidified
tracheal air
N2 (79%), CO2 (0%)
• Water vapor pressure in trachea: PAO2 100 Alveolar
47 mmHg PACO2 40 air
• Solubility of O2 in blood: 0.003 mL O2 CO2
O2 / 100 mL blood / mmHg

PVO2 40 PaO2 100
PVCO2 46 PaCO2 40
Mixed venous Systemic
blood arterial blood
46
Important Equations
• General Gas Law PV = nRT
– How much space and pressure does a gas take?
• Boyle: P1V1 = P2V2
– How does a change in pressure change the volume of a gas, or vice versa
• Dalton: Px = (PB – PH2O) X F
– Partial pressure of a gas when it is part of a mixture (ignore PH2O if air is dry)
• Henry: Cx = Px X Solubility
– What is the concentration of dissolved gas in solution, if you know its partial pressure
(Px in liquid/capillary same as Px in gas/air)
• Diffusion(Fick): Vx dAΔP / T
Vx=volume gas transferred per unit-time d=coefficient(gas specific) A=surface area T=membrane thickness
– More surface area for diffusion, larger pressure gradient/driving force, higher diffusion
coefficient: faster diffusion. Thicker surface through which gas diffuses: slower diffusion
Gases in blood
• Nitrogen: dissolved
• Oxygen: almost all on hemoglobin
• Carbon dioxide: 90% as bicarb (converted in RBC), 7% dissolved, 2-
3% as carboxyhemoglobin (different binding site vs. O2)
• Diffusion of Gases across capillaries: simple diffusion. Rate
affected by:
1. Driving force (partial pressure difference)
2. Diffusion coefficient (D)
3. Surface area available (larger is faster)
4. Thickness of barrier (thicker = slower)
CO2 Transport
• CO2 is transported in 3 forms:
o Dissolved CO2 (small amount)
o CO2-Hb (small amount)
o HCO3- (90%)
• Carbonic anhydrase converts

CO2 into HCO3- and H+.
o In the lungs, this reaction is
reversed.
Diffusion-Limited Gas Exchange
• total amount of gas transported
across the alveolar-capillary barrier
is limited by the diffusion process
– as long as the partial pressure
gradient for the gas is maintained,
diffusion will continue along the
length of the capillary
– PaCO rises only slightly along capillary
length because in capillary blood, CO
is avidly bound to Hgb
– This is why we can use CO to
measure diffusion capacity.
Slide Adapted from lecture by Hooman Poor, MD

Perfusion-Limited Gas Exchange
• total amount of gas transported
across the alveolar-capillary barrier is
limited by blood flow (perfusion)
– partial pressure gradient is not
maintained, and in this case, the only
way to increase the amount of gas
transported is by increasing blood flow
– N2O exists completely in solution (not
bound to Hgb); all N2O in capillary
causes partial pressure
– O2 (under normal conditions) and CO2
are perfusion limited
Slide Adapted from lecture by Hooman Poor, MD

Gas Exchange
1. Carbon Dioxide is found predominantly in what
form in the blood?
a) A polysaccharide-bound molecule
b) A dissolved gas
c) A protein-bound molecule
d) A negative ion
e) A diprotic acid
Gas Exchange
1. Carbon Dioxide is found predominantly in what
form in the blood?
a) A free gas
b) A dissolved Gas
c) A protein-bound molecule
d) A negative ion
e) A diprotic acid
Gas Exchange
2. Which of the following patients would most likely
experience diffusion-limited alveolar exchange of
oxygen?
a) A long-time smoker with chronic bronchitis
b) A child experiencing an asthma attack
c) A coal miner who develops pulmonary fibrosis
d) An Olympic athlete while running the 1,000 meter dash
e) A med student running on 2 hours of sleep and 8 cups of coffee.
Gas Exchange
2. Which of the following patients would most likely
experience diffusion-limited alveolar exchange of
oxygen?
a) A long-time smoker with chronic bronchitis
b) A child experiencing an asthma attack
c) A coal miner who develops pulmonary fibrosis
d) An Olympic athlete while running the 1,000 meter dash
e) A med student running on 2 hours of sleep and 8 cups of coffee.
Arterial Oxygen Content (CaO2)
• Oxygen found in two forms in the blood FiO2 – outside air
– dissolved → 2% of oxygen
– bound to hemoglobin → 98% of oxygen
• CaO2 = (1.34 x Hgb x O2 saturation) + (0.003 x PaO2)

PAO2 – alveoli
• CaO2 expressed as mL of O2 per 100 mL of blood
• 1 g of Hgb can bind 1.34 mL of O2 when fully saturated (Hgb PaO2 – arterial blood
expressed in g/dL)
• 0.003 mL of dissolved O2 per mmHg of partial pressure of O2

SaO2 – Hb Saturation
Hb Structure
Hb = Heme + Globin
Fe2+ + Porphyrin
● Hb is made up of 4 globin chains, each

complexed with a Heme subunit that can bind
one molecule of oxygen.
○ (So, one Hb molecule can bind four
molecules of oxygen.)
Hb-bound O2: 1.34 x [Hb] x % sat
● HbA = α2β2
● HbF = α2γ2
● HbA2 = α 2δ2
● Pathologic forms: HbS, HbC
O2 Dissociation Curve
• Hb binds oxygen cooperatively -- that is, each bound
molecule of oxygen increases Hb’s affinity for O2.
• Some PO2’s to be familiar with (rough numbers):

o 100 mm Hg → arterial PO2, Hb is 100%
saturated.
o 40 mm Hg → venous PO2, Hb is 75%
saturated.
o 25 mm Hg → Hb is 50% saturated. This is the
P50 of Hb.
• In metabolically active tissues, there is: ↑ CO2, Temp, 2,3-BPG and ↓ pH

• These factors combine to shift the curve rightward, decreasing Hb’s affinity for oxygen ...and thereby
increasing oxygen release to the tissues that need it most.
Hypoxia vs. Hypoxemia
● Hypoxia = Low oxygen delivery (or utilization) by the tissues.
● Hypoxemia = Low PaO2 → a possible cause of hypoxia
O2 delivery = O2 content x Cardiac Output

Oxygen Delivery
Hypoxia vs. Hypoxemia
Hypoxia = Low oxygen delivery, or utilization, by the tissues.
Hypoxemia = Low PaO2 → a possible cause of hypoxia
DO2 = CO x [(1.34 x Hgb x O2 sat) + (0.003 x PaO2)]
O2 Delivery = Cardiac Output x O2 Content
Shock = cellular/tissue hypoxia due to reduced DO2 and/or increased O2 consumption or inadequate O2
utilization
Causes of Hypoxia:
1. Low arterial O2 tension (Hypoxemia)
2. Low O2 saturation (carbon monoxide poisoning, methemoglobinemia)
3. Low O2 unloading = High affinity (carbon monoxide)
4. Low O2 reservoir = Low Hemoglobin (anemia)
5. Low Cardiac Output (hypovolemic shock, cardiogenic shock)
6. Low oxygen utilization (sepsis, cyanide)
7. Extremely High O2 demand
Mechanisms of Hypoxemia (5)
Remember: Hypoxemia = Low PaO2 FiO2 – outside air
The 5 Causes of Hypoxemia:

PAO2 – alveoli
1. Low FiO2 = Not enough oxygen in the air
2. Hypoventilation
PaO2 – arterial blood
3. Diffusion Impairment
4. V/Q mismatch (with low V/Q units)*
5. Shunt (Q = 0 → V/Q = not a number) SaO2 – hemoglobin
V/Q mismatch with high V/Q units does NOT cause hypoxemia*
“But wait, what about a Pulmonary Embolism? Doesn’t that have high V/Q units?”
Yes, but this isn’t why patients w/ PE become hypoxemic. Don’t worry about it for your test, but if you’re interested, ask/email one of us.
CO Poisoning
• CO binds to Hb at the same site as O2,
but with 250 times greater affinity.
o Note that the CO-Hb dissociation curve looks
the same as the O2-dissociation curve, but
that the PCO values are 1/250th of the PO2 Pulse oximetry will
values for the same % saturation.
be NORMAL!!!
• CO essentially beats O2 to the Hb
binding sites, and it causes a left-shift
of the curve as well, impairing O2
release.
o (It does some other stuff too, but nothing
really relevant to pulmonary physiology.)
O2 Content & Delivery
1. Which of the following would you expect to shift
the O2 dissociation curve to the left?
a) A skin infection that decreased tissue pH
b) Spending 3 months in a Colorado Ski-Town
c) A thyroid disease that increased a patients overall metabolism
d) A viral infection that caused a fever
e) A drug that causes the kidneys to excrete more H+
1. Which of the following would you expect to shift
the O2 dissociation curve to the left?
a) A skin infection that decreased tissue pH
b) Spending 3 months in a Colorado Ski-Town
c) A thyroid disease that increased a patients overall metabolism
d) A viral infection that caused a fever
e) A drug that causes the kidneys to excrete more H+
2. Which of the following could be a cause
hypoxemia?
a) Iron deficiency → decreased hemoglobin content
b) Anaphylaxis (severe allergic reaction) → complete airway
occlusion
c) Carbon monoxide poisoning
d) A left-to-right ventricular shunt
e) Hyperventilation
2. Which of the following could be a cause
hypoxemia?
a) Iron deficiency → decreased hemoglobin content
b) Anaphylaxis (a severe allergic reaction) → complete airway
occlusion
c) Carbon monoxide poisoning
d) A left-to-right ventricular shunt
e) Hyperventilation
3. A 26 y/o woman presents to the ER c/o SOB. Her labs reveal the following:
RBC = 3.5 x 106/uL
Hb = 10 gm%
PaO2 = 95 mm Hg
Hb saturation = 100%
PaCO2 = 40 mm Hg
What is the O2 content of her arterial blood?

3. A 26 y/o woman presents to the ER c/o SOB. Her labs reveal the following:
RBC = 3.5 x 106/uL
Hgb = 10 gm%
PaO2 = 95 mm Hg
Hgb saturation = 100%
PaCO2 = 40 mm Hg
What is the O2 content of her arterial blood?
13.9 mL O2/dL
O2 content = Hb-bound O2 + Dissolved O2.
O2 content = (1.34 x [Hb] x %sat) + (0.003 x PaO2)
O2 content = (1.34 x 10 g/dL x 1.0) + (0.003 x 95 mm Hg) = 13.69 mL O2/dL
O2 content = (13.4) + (0.29) = 13.69 mL O2/dL
*Notice how little oxygen is dissolved vs. bound to Hb (0.29 vs. 13.4)*
4. A 56 y.o M is admitted for a gastrointestinal bleed. He stabilizes after IV fluids
and endoscopic intervention. His Hgb is 9.1 (normal >13.5). While in the
hospital he contracts pneumonia. He is found to be in acute respiratory
distress and rapid response is called. His SaO2 is 68%. Despite quick action, it
takes more than an hour to bring his SaO2 back to > 90%. Brain tissue
normally dies within 10 minutes of ischemia, but this patient had no
neurologic consequences.
How is this possible?
What is a comorbid condition that would likely have prohibited this favorable
outcome?
This patient was anemic and profoundly hypoxemic, and probably “should” not have survived, much less
without permanent brain damage. However, the amount of oxygen delivery is equal to the total arterial
oxygen content x the cardiac output. The only way a patient could have survived over an hour of such
low oxygen content would be to compensate by dramatically increasing his HR and stroke volume. If a
sufficient elevation were achieved, it could mitigate the hypoxemia and anemia to maintain O2 delivery
and prevent cerebral hypoxia. This patient luckily had a very healthy heart.
What might have prohibited this good outcome?

This patient was anemic and profoundly hypoxemic, and probably “should” not have survived, much less
without permanent brain damage. However, the amount of oxygen delivery is equal to the total arterial
oxygen content x the cardiac output. The only way a patient could have survived over an hour of such low
oxygen content would be to compensate by dramatically increasing his HR and stroke volume. If a sufficient
elevation were achieved, it could counter the hypoxemia and anemia to maintain O2 delivery and prevent
cerebral hypoxia. This patient luckily had a very healthy heart.
What might have prohibited this good outcome?

The patient would almost certainly have died if he had a history of significant
heart disease, such as congestive heart failure.
Control of Breathing
Jimmitti Teysir
Questions Adapted from slides by Dennis Dacarett-Galeano
Overview
Voluntary Control: cerebral cortex
Involuntary Control
● Brainstem: medulla (main respiratory center); pons (provides additional
regulation to control rate of breathing)
● Chemoreceptors: detect PaO2 and PaCO2 in blood
● Mechanoreceptors: in lungs and joints
Respiratory Muscles: diaphragm, intercostals, accessory muscles

Brainstem Control
Medulla Pons
● Dorsal Respiratory Group: ● Apneustic Center (lower pons):

inspiratory center excites inspiratory center
● Ventral Respiratory Group: ● Pneumotaxic Center (upper

expiratory center; only active pons): inhibits inspiration; not
during exercise necessary for normal breathing
Just for Reference
Central Chemoreceptors
● Located in the ventral medulla
● Detect PCO2, which is the main stimulus for breathing

○ Goal: maintain PCO2 ~ 40 mm Hg
● How?
○ Central chemoreceptors are sensitive to the pH of CSF
○ CO2 is able to cross the BBB into CSF, and is converted to H+ and HCO3-
via carbonic anhydrase
○ H+ stimulates chemoreceptors, which stimulate medullary inspiratory center
● Decrease in pH (aka lots of CO2) → signal to breathe

Peripheral Chemoreceptors
● Located in the carotid and aortic bodies
○ Relay to inspiratory center va CN IX and X, respectively
● Primarily responsive to low PO2 (< 60 mm Hg)

○ Also detect PCO2, H+
● Take home: the body is more responsive to changes in CO2 than O2

○ It is possible to be hypoxic and not have shortness of breath!
Other Receptors
● Juxtacapillary (J) Receptors: in alveolar walls next to pulmonary capillaries
○ Fire when they sense that capillaries are congested; i.e.: congestive heart failure
○ Cause rapid shallow breathing (SOB sensation)
● Joint/Muscle Receptors: stimulate breathing during exercise
● Irritant Receptors: in the epithelial lining of airways

○ Cause bronchioles to constrict & increase RR
● Lung Stretch Receptors: Hering-Breuer reflex

○ Prevents the lung from over-distending by inhibiting the apneustic center (pons)
Breathing while asleep
● Sleep normally reduces the ventilatory drive
○ PCO2 increases by 2-6 mm Hg
○ NREM Stage 3: deep sleep, regular breathing
○ REM: brain is active, most cardiac/respiratory instability
● Sleep apnea: cessation of breathing

○ Central: loose central effort to breathe
○ Obstructive (more common): airway blocked or collapsed
● Ondine’s curse: drive to breathe when sleeping is completely lost

○ Congenital Central Hypoventilation Syndrome
1. Hypoxemia produces hyperventilation by a direct effect on the
A. Phrenic nerve
B. J receptors
C. Lung stretch receptors
D. Medullary chemoreceptors
E. Carotid and aortic body chemoreceptors

1. Hypoxemia produces hyperventilation by a direct effect on the
A. Phrenic nerve
B. J receptors
C. Lung stretch receptors
D. Medullary chemoreceptors
E. Carotid and aortic body chemoreceptors

2. A stroke that destroyed the respiratory center of the medulla would be expected
to lead to
A. immediate cessation of breathing
B. apneustic breathing
C. ataxic breathing
D. rapid breathing (hyperpnea)
E. none of the above, since breathing would remain normal

2. A stroke that destroyed the respiratory center of the medulla would be expected
to lead to
A. immediate cessation of breathing
B. apneustic breathing
C. ataxic breathing
D. rapid breathing (hyperpnea)
E. none of the above, since breathing would remain normal

3. The afferent (sensory) endings for the Hering-Breuer reflex are stretch
receptors (mechanoreceptors) in the
A. aorta and carotid arteries
B. arteries in the cerebral circulation
C. lungs
D. heart
E. diaphragm and intercostal muscles

3. The afferent (sensory) endings for the Hering-Breuer reflex are stretch
receptors (mechanoreceptors) in the
A. aorta and carotid arteries
B. arteries in the cerebral circulation
C. lungs
D. heart
E. diaphragm and intercostal muscles

4. Hyperventilating allows one to hold one’s breath for a longer period of time,
because hyperventilation
A. increases the oxygen reserve of systemic arterial blood
B. decreases the PCO2 of systemic arterial blood
C. decreases the pH of systemic arterial blood
D. increases brain blood flow
E. none of the above, since hyperventilation reduces the time one can
voluntarily stop breathing
5. The most important afferent (sensory) receptors for the respiratory response to
systemic arterial carbon dioxide (PaCO2) are the:
A. CO2 receptors of the aortic and carotid bodies
B. H+ receptors of the aortic and carotid bodies
C. CO2 receptors in the medulla of the brain
D. H+ receptors in the medulla of the brain
E. CO2 receptors in the airways and lungs

5. The most important afferent (sensory) receptors for the respiratory response to
systemic arterial carbon dioxide (PaCO2) are the:
A. CO2 receptors of the aortic and carotid bodies
B. H+ receptors of the aortic and carotid bodies
C. CO2 receptors in the medulla of the brain
D. H+ receptors in the medulla of the brain
E. CO2 receptors in the airways and lungs

Pulmonary Function Testing
Benjamin Asriel
adapted from slides created by Caroline Eden
Lung Volumes and Capacities
lungs at rest (birth/death) = Zero Point = non-forced exhale
lungs at rest (birth/death) = Zero Point = non-forced exhale
lungs at rest (birth/death) = Zero Point = non-forced exhale = exhale of tidal volume
Tidal Volume (TV) = involuntary breath
TV
TV
Inspiratory Reserve Volume (IRV) = amount that can be inhaled past tidal volume
IRV
TV
IRV
TV
Expiratory Reserve Volume (ERV) = amount that can be exhaled past tidal volume
IRV
TV
ERV
IRV
TV
ERV
Residual Volume (RV) = what’s left in lungs after fullest possible exhale
IRV
TV
ERV
RV
“Volumes” combine to make “Capacities:”
IRV
TV
ERV
RV

Inspiratory Capacity = TV + IRV = amount inspired from zero point
IRV
IC =
TV TV + IRV
ERV
RV

Functional Residual Capacity = ERV + RV = amount left in lungs at zero point
IRV
IC =
TV TV + IRV
ERV
FRV =
RV ERV + RV

Vital Capacity = TV + IRV + ERV = total largest breath a living thing can make
IRV
IC = VC =
TV TV + IRV TV + IRV
ERV + ERV
FRV =
RV ERV + RV

Vital Capacity = TV + IRV + ERV = total largest breath a living thing can make
Total Lung Capacity = VC + RV IRV
= sum of everything, IC = VC =
including residual volume (dead space) TV TV + IRV TV + IRV
ERV + ERV TLC
FRV =
RV ERV + RV
Basics
● TV=volume of air inhaled and exhaled during quiet breathing (500 ml)
● IRV=Additional volume that can be inspired above TV (3000 ml)
● ERV=Additional volume that can be expired below TV (1200 ml)
● RV=Volume of gas in the lungs after a maximal forced expiration (1200 ml)
● VC=The volume of air a subject is able to exhale after a maximal inspiration to total lung
capacity
● FEV1 = The volume of air exhaled in the first second of expiration
● FRC = Equilibrium volume of the lungs
Important Equations:
IC= TV +IRV
VC= TV+IRV+ERV
TLC= TV+IRV+ERV+RV
FRC= RV+ERV
VD= TV × (PaCO2-PeCO2)/PaCO2
Minute Ventilation(VE)= TV × RR
Alveolar Ventilation(VA)=(TV-VD) × RR
Spirometry (“spirare” = latin meaning breathe, “metron” = greek meaning measure)
- Measurements from perspective of the
spirometer
Flow
(y-axis)
Volume
(x-axis)
- Measurements from perspective of the
spirometer
normal
Flow
(y-axis)
Volume
(x-axis)
- Measurements from perspective of the spirometer
- increased volume = more volume in the machine, less in the patient’s
lungs
normal
Flow
(y-axis)
Volume
(x-axis)
- increased volume = more volume in the machine, less in the patient’s
lungs
normal
full expiration
Flow
(y-axis)
Volume
(x-axis)
- increased volume = more volume in the machine, less in the patient’s lungs
- decreased volume = less volume in the machine, more in the patient’s
lungs
normal
full expiration
Flow
(y-axis)
Volume
(x-axis)
- decreased volume = less volume in the machine, more in the patient’s
lungs
normal
full expiration
Flow
(y-axis)
full inspiration
Volume
(x-axis)
- decreased volume = less volume in the machine, more in the patient’s lungs
- positive flow = flow into machine (out of lungs)
normal
full expiration
Flow
(y-axis)
full inspiration
Volume
(x-axis)
normal
expiration
full expiration
Flow
(y-axis)
full inspiration
Volume
(x-axis)
- negative flow = flow out of machine (into lungs) normal
expiration
full expiration
Flow
(y-axis)
full inspiration
Volume
(x-axis)
expiration
full expiration
Flow
(y-axis)
inspiration
full inspiration
Volume
(x-axis)
More Volumes/Capacities expiration
FVC = Forced Vital Capacity = max air full expiration

Flow
exhaled after full inspiration
(y-axis)
inspiration
FEV1 = Forced Expiratory Volume in 1
full inspiration
second = volume of air exhaled in first
second of expiration Volume
(x-axis)
REPRESENTATIVE SPIROGRAMS
IN HEALTH AND DISEASE
RESTRICTION NORMAL OBSTRUCTION
hard to inhale hard to exhale

Flow
Volume
FEV1 FEV1: Normal FEV1
FVC FVC: Normal FVC

COMMON PATTERNS OF PULMONARY
FUNCTION ABNORMALITIES
RESTRICTION OBSTRUCTION
MEASUREMENT hard to inhale hard to exhale
FEV1
FVC
FEV1/FVC WNL or
RV
TLC
Ex: Interstitial lung disease, Ex: Asthma, Emphysema,

Obesity, neurologic disease, Chronic bronchitis
muscle weakness
Other Types of Testing/Graphs
These spirometry graphs are a good way to look at FVC, FEV1. On the left that the y axis is flow(When you start a forceful exhale,
you can blow a lot out quickly at the beginning, and as you continue to exhale there’s less coming out). If you’re math oriented,
think of the expiration section as the derivative of the first 2 seconds of the graph on the right.
Diffusing Capacity of CO = DLCO =

measurement of status of the alveolocapillary membrane
Expiratory Pressure
(Pe) and Inspiratory
Pressure (Pi)
measure respiratory
lung volume! muscle strength
Q. Which are the three volumes/capacities that cannot be measured by spirometry alone?
A) Expiratory Reserve Volume, Vital Capacity, Forced Vital Capacity

B) Residual Volume, Functional Residual Capacity, Total Lung Capacity
C) Inspiratory Reserve Volume, Expiratory Reserve Volume, Functional Residual Capacity
D) Residual Volume, Tidal Volume, Functional Residual Capacity
E) Functional Residual Capacity, Inspiratory Capacity, Total Lung Capacity
Q. Which are the three volumes/capacities that cannot be measured by spirometry alone?
A) Expiratory Reserve Volume, Vital Capacity, Forced Vital Capacity

B) Residual Volume, Functional Residual Capacity, Total Lung Capacity
C) Inspiratory Reserve Volume, Expiratory Reserve Volume, Functional Residual Capacity
D) Residual Volume, Tidal Volume, Functional Residual Capacity
E) Functional Residual Capacity, Inspiratory Capacity, Total Lung Capacity
Q: A patient’s vitals are as follows: HR = 65, Temp = 98.6, RR
= 12, BP = 110/70. They also have the following lung
volumes/capacities:
IRV=2.5 L, ERV = 1.5L VC = 4.0 L TLC = 5500
What is the patient’s minute ventilation?
A)4L/min
B)6 L/min
C)9 L/min
D)12 L/min
E)18 L/min
F) 24 L/min
Q: A patient’s vitals are as follows: HR = 65, Temp = 98.6, RR
= 12, BP = 110/70. They also have the following lung
volumes/capacities:
IRV=2.5 L, ERV = 1.0 L VC = 4.0 L TLC = 5500
What is the patient’s minute ventilation?
A)4L/min
B)6 L/min
C)9 L/min
D)12 L/min
E)18 L/min
F) 24 L/min
Q: A 7 year old girl with juvenile idiopathic scoliosis with a 30 degree
spinal curve presents to your pediatrics practice for a physical.
Thought she has no difficulty breathing at the moment, you know that
this condition is likely to progress in this patient, and so you decide to
send her for pulmonary function tests to understand her pulmonary
baseline. Compared to normal PFTs for her age, how do you expect
this patient’s PFTs to compare?
A)increased FEV1, increased FVC, increased FEV1/FVC

B)decreased FEV1, decreasedFVC, decreased FEV1/FVC
C)increased FEV1, increased FVC, decreased FEV1/FVC
D)decreased FEV1, decreased FVC, increased FEV1/FVC
E)decreased FEV1, decreased FVC, no difference in FEV1/FVC
Q: A 7 year old girl with juvenile idiopathic scoliosis with a 30 degree
spinal curve presents to your pediatrics practice for a physical.
Thought she has no difficulty breathing at the moment, you know that
this condition is likely to progress in this patient, and so you decide to
send her for pulmonary function tests to understand her pulmonary
baseline. Compared to normal PFTs for her age, how do you expect
this patient’s PFTs to compare?
A)increased FEV1, increased FVC, increased FEV1/FVC

B)decreased FEV1, decreasedFVC, decreased FEV1/FVC
C)increased FEV1, increased FVC, decreased FEV1/FVC
D)decreased FEV1, decreased FVC, increased FEV1/FVC
E)decreased FEV1, decreased FVC, no difference in FEV1/FVC
Extreme Breathing
Benjamin Asriel
adapted from slides created by Caroline Eden
Extreme Breathing – Exercise
Parameter Response to Exercise
O2 consumption Increase
CO2 production Increase
Ventilation rate Increase
Arterial PO2 and PCO2 No change
Arterial pH Decrease during strenuous exercise, past the
“anaerobic threshold”
Venous PCO2 Increase
Pulmonary blood flow and cardiac output Increase (exercise in a normal individual is mostly
limited by CO, specifically SV)
V/Q ratio More evenly distributed throughout the lung (more
‘ideal’)
Physiologic dead space Decrease
O2 – hemoglobin dissociation curve Shifts to the right; increased P50 and decreased
affinity for O2
Blood flow distribution Increase in working muscle, decrease in skin,

viscera, and non-working muscle
Extreme Breathing – High Altitudes
Parameter Response to High Altitude
Alveolar PO2 Decrease (due to decreased barometric pressure)
Arterial PO2 Decrease (hypoxemia)
Consequences: CNS complaints
Ventilation rate Increase (hyperventilation response to hypoxemia)
Note: hypoxic drive is weaker and more variable than
hypercapnic drive
Arterial pH Increase (respiratory alkalosis due to hyperventilation)
Hemoglobin concentration Increase (increase RBC concentration; polycythemia
compensation can also increase blood viscosity)
2,3-DPG concentration Increase (shifts dissociation curve to increase unloading at
tissue but lose loading at lung)
O2 – hemoglobin dissociation curve Shifts to the right; increased P50 and decreased affinity for O2
Pulmonary vascular resistance (PVR) Increase (hypoxic vasoconstriction!)
Consequences: pulmonary edema, RV overload
Pulmonary arterial pressure Increase (secondary to increased resistance)
Extreme Breathing – Diving
• Whereas the problem with high altitude is low

pressure, with diving the problem is increased
pressure (1 atm per 33 feet)
• Nitrogen diffuses into tissues → nitrogen narcosis
(anesthetic effect)
• Rapid ascent: comes out of solution and causes
bubbles in circulation → decompression sickness
• “Nitrox” gas mixtures: higher O2 fractions but risk of
oxygen toxicity in CNS (Maximum Operating Depth)
Q. A friend who is into biohacking calls to tell you that they read that elite athletes who train
at high altitude have higher levels of serum 2,3 DPG. They are thinking of starting a business
marketing 2,3 DPG to the public as an exercise supplement. Assuming it is possible to
formulate a supplement that increases serum 2,3, DPG, why might this be a bad idea?
A) It will lower DLCO

B) it will decreased the total blood oxygen content
C) levels of 2,3 DPG are unrelated to exercise states
D) high levels of 2,3, DPG will prevent O2 unloading in the tissues
Q. A friend who is into biohacking calls to tell you that they read that elite athletes who train
at high altitude have higher levels of serum 2,3 DPG. They are thinking of starting a business
marketing 2,3 DPG to the public as an exercise supplement. Assuming it is possible to
formulate a supplement that increases serum 2,3, DPG, why might this be a bad idea?
A) It will lower DLCO

B) it will decrease the total blood oxygen content
C) levels of 2,3 DPG are unrelated to exercise states
D) high levels of 2,3, DPG will prevent O2 unloading in the tissues
Which of these increase during peak exercise?
A) hemoglobin O2 affinity
B) lung zone 1 V/Q ratio
C) venous O2
D) venous pH
E) venous CO2
F) arterial CO2
Which of these increase during peak exercise?
A) Hemoglobin O2 affinity
B) Lung Zone 1 V/Q ratio
C) venous O2
D) Venous pH
E) venous CO2
F) Arterial CO2
Q: Which of these combinations is most likely to cause acute CNS toxicity?
A) deep scuba dive with nitrox; O2 content 64%, N2 36%

B) shallow scuba dive with nitrox: O2 content 64%, N2 36%
C) deep scuba dive with nitrox: O2 content 21%, N2 content 79%
D) shallow scuba dive with nitrox: O2 content 21%, N2 content 79%
Q: Which of these combinations is most likely to cause acute CNS toxicity?
A) deep scuba dive with nitrox; O2 content 64%, N2 36%

B) shallow scuba dive with nitrox: O2 content 64%, N2 36%
C) deep scuba dive with nitrox: O2 content 21%, N2 content 79%
D) shallow scuba dive with nitrox: O2 content 21%, N2 content 79%

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Pulmonary Physiology 2018

Dan Leisman, Emily Markovic, Benjamin Asriel and Jimmitti Teysir

Emily Schlussel Markovic

Forces that determine the respiratory system:

(functional residual capacity)

Intrapleural Pressure < 0

• Compliance describes how distensible the system is (inversely related to elastance)

At middle volumes, compliance is larger → lung is

Law of Laplace: P = 2T/r

• During exercise/disease state

• Pulmonary fibrosis → excessive fibrotic tissue →

• Asthma: airway SM constriction → decreased

A. Expiratory Reserve Volume

A. Expiratory Reserve Volume

A. It decreases compliance of small alveoli

A. It decreases compliance of small alveoli

● Pulmonary Arterioles: carry deoxy blood to lungs

● High Alveolar pressure compresses arterioles → less perfusion → no gas exchange →

Zone 2 – middle of lung – Pa > PA > Pv

● Blood flow driven by arterial-alveolar pressure differences

Zone 3 – base of lung – Pa > Pv > PA

● Capillaries most open (gravity) → blood flow is highest

b) Right to left cardiac shunt

e) Ascent to high altitude

a) higher blood flow

c) higher arterial pressure

d) higher capillary pressure

e) higher cardiac output

B. Lower resistance. The pulmonary circulation is

Blood flow in both the systemic and pulmonary systems are

a. equal at the apex and the base

b. highest at the apex owing to the effects of gravity on arterial pressure

In other words, there is just enough oxygen to saturate the blood.

However, Q >>V because of

Therefore, the ratio V/Q is

Figure from: Cross, M., & Plunkett, E. (2014). Ventilation/perfusion mismatch. In

V/Q is greatest at the apex

V/Q is lowest at the base

Figure from First Aid 2018, pg. 651

This represents a R→ L shunt:

Alveolar gases approach inspired

● PAO2 approaches PIO2 (150 mmHg)

Shunt and Dead Space

Key Equations Normal Values

c. Blood flow will be reduced in zone 1

d. Blood flow will be increased in zone 2

c. Blood flow will be reduced in zone 1

d. Blood flow will be increased in zone 2

c. 500 mL 125 = VT × (40-30/40)

a. equal to atmospheric PO2

b. equal to mixed venous PO2

c. equal to normal systemic arterial PO2

d. higher than inspired PO2

e. lower than mixed venous PO2

a. equal to atmospheric PO2

b. equal to mixed venous PO2

c. equal to normal systemic arterial PO2

d. higher than inspired PO2

e. lower than mixed venous PO2

• % of gases in dry air at barometric

• Solubility of O2 in blood: 0.003 mL O2 CO2

O2 / 100 mL blood / mmHg

• Carbonic anhydrase converts