VENTILATION Minute volumen or minute ventilation

: Volumen of air entering/leaving the mouth or nose per minute

: Tidal volumen
: Respiration rate
=
Normal resting values
: 500mL : 500mL x 15/min = 7.5L/min
: 15 : 7.5L/min
 DEAD SPACE
During respiration theres a
gas exchange only in one place 2 : 150 m
the ALVEOLI 2 : 0

Dead space are the regions of

respiratory that dont
participate in gas Exchange

Anything that has air but

doesnt have alveoli would be
anatomic dead space
 Regions of the respiratory system that contain
DEAD SPACE air but dont participate in gas exchange

2 = 100
End Expiration
End
2 = 40 Tidal
Dead space

Anatomic Anatomic
Airway
2 = 150
No Flow = No End Inspiration
Alveolar
CO2
2 = 0
Physiologic +

Alveolar gases can measured with End - Tidal

 Gaseous composition End tidal respiration
2 = 100
2 = 40
At the end of expiration Dead space
(Blowing air out)
Air Will be the same as the alveoli
2 = 100
2 = 40
We can measured the alveoli
concentration at the mouth as
END TIDAL gases
End tidal its a way to 2 = 100
measured of alveolar gases 2 = 40
End tidal = 40 Will be
the same as arterial 2

Small a stand for parcial pressure in arterial blood

 Atmosphere
Gaseous composition 2 = 150
2 = 0

END OF INSPIRATION (Before

expiration)
Coming from atmosphere
At the end inspiration, gases are Alveolar
similar to inspired gases 2 = 150
2 = 0

Atmosphere End . Inspiration

2 = 150 2 = 100
2 = 0 2 = 40
DEAD SPACE
ALVEOLAR DEAD SPACE
Alveoli that are ventilated but not perfused
Theres no gas exchange
No blood flow
= 0
All 2 in the lung comes from blood FLOW
It doesnt exist in the normal lung
 : Represents air delivered to the alveolar zone per breath
: 500mL per inspiration
: 150mL per inspiration

=
Dead space

Alveolar Ventilation = Respiratory rate

= 500 150 15 = 5250

Tidal Ventilation
 ALVEOLAR VENTILATION

If is not greater than

or
Then you have 0 Alvelar
ventilation
= = 0 (Dead space)
 LUNG RESPIRATION
Diaphragm

Expiration
External intercostal Doesnt required
Passive
muscle
Inspiration Sternocleidomastoid Internal
intercostal
Forced Expiration
Accesories
Scalene Abdominal
Sternocleidomastoid
Scalene
Pecs Pecs
FORCE ACTING on the Lung
Recoil
Respiratory System

Transmural
IPP
presssure

Chest
Recoil
 At LOW lung volume complaince is HIGH Highr complaince LOW Recoil
If its easier to get air into so complaince is HIGH

Complaince
HIGH
Lung Vol
LUNGS

Recoil LOW

Complaince
LOW
Lung Vol air
Recoil HIGH
At HIGH lung volume complaince is LOW

LOW complaince HIGH Recoil

 LUNG RECOIL
HIGH Lung volumen
LOW complaince
Lung Recoil
HIGH Lung Recoil
Represents inward force created by
the elastic recoil properties of alveoli
As the lung expands Recoil
increases because alveoli wants to
get back to the previous shape
As the lung gets smaller Recoil LOW Lung volumen
decreases
HIGH Complaince
RECOIL, as a force, always acts to
collapse the lung LOW Lung Recoil
 CHEST WALL RECOIL
Represents outward force created by the FRC
chest wall
Chest is pullng OUT
Lungs are pulling IN
FRC (Functional Residual Capacity)
Represents the point where this outward
recoil of the chest wall is
counterbalanced by inward recoil of the
lung
FRC: they opposite but igual CHEST PULLS OUT
FRC: Inward (Lung) = outward (chest)
FRC is equilibrium
 INTRAPLEURAL PRESSURE
IPP Negative
Outward (chest) and inward (lung)
create a negative IPP because is
IPP Subatmospheric
Represents the pressure inside the thin film
of fluid between the visceral pleura, which
is attached to the lung, and the parietal Outward recoil
pleura, which is attached to the chest wall
where this outward recoil (Chest) IPP
Inward recoil
TRANSMURAL PRESSURE
Represents the pressure gradient across any tuve or
sphere
Calculatedas inside pressure minus outside pressure
: Pi Po

Pi
Po
 Recoil Lungs Pushing IN : Pi Po
Recoil Chest pushing OUT
: - IPP

Lung (inward
force)
FORCE ACTING ON
THE LUNG System

Recoil
Chest Wall
(outward force)
Intrapleural Negative
pressure (IPP) subatmosphere
IPP
Transmural
Pressure ( )

( )
 TRANSMURAL PRESSURE
The air flows inside the lung because Pi ( ) > Po = (+)
theres a pressure gradient
Alveolar pressure is Positive
Intrapleural pressure is Negative
It prevents the alveolar to
represents the pressure gradient
collapse
across the chest wall (Atelectasia)
: Pi Po Po (IPP) > Pi = (-)
= (Transpulmonar pressure)
 RESPIRATION
Before inspiration
FRC Neutral equilibrium
No Air FLOW
During inspiration
IPP more negative
increases (+) Net force
pushing out
Cause EXPANSION of the lungs
Alveolar volume ( )
Alveolar pressure ( )
End of Inspiration
Lungs expands until alveolar pressure
equlibrates with atmospheric pressure
=
Expiration
At resting condition is produced by
RELAXATION
IPP
alveolar volume ( )
Alveolar pressure ( )
RESPIRATION
 = 0
= 0 ; = 0

Lungs are at FRC inward and outward are equal

NO FLOW of air
IPP Negative (- 5)
: - IPP
: Positive Net force pushing out
= 0

: Pi Po
Po
IPP = - 5
: 0 (-5) Lungs pulling in
= +5 mm Chest pulling out
 = 0 = 0 ; = 0

Contraction of diaphragm and external

intercostal muscle pulls chest wall go up and
out
Chest pulls out IPP goes down
IPP decreases Increases
= 0

Po POSITIVE More force Pushing OUT

: 0 (-8)
IPP
Volume goes up ( )
= +8
Pressure goes down ( )
 = 0 = 0 ; = 0

Tidal Volume ( ) = 500 mL

= 150 Hgmm
Dead space ( ) = 150 mL = 0 mmHg
Alveolar volume ( ) = 350 mL
Volume goes Down ( )
Pressure goes UP ( )
= 0 : 0 (-8)
= +8
(Po)
IPP
Less POSITIVE Less force Pushing OUT, air is going to
come out
 = 0 = -5

= -8
EXPIRATION
Expiration is passive
Muscles relax
Chest wall is not longer pulling
is LESS
LESS force pushing OUT
Alveoli is trying to collapse
= 0

Po
Volume goes down ( )
IPP = - 5 Pressure goes up ( ) Lungs pulling in
Air FLOWS OUT
PRELOAD CVP = 0
It doenst collapse because IPP is negative so its positive keeping it open
Inspiration
Thats why INTRAVASCULAR PRESSURE can be ZERO (0)
During Inspiration = 0 (-5) = +5
Chest wall expands
IPP becomes more negative, thats
going to EXPAND the great VEINS
and Right Atrium Becomes more
When right atrium expand intravascular Negative

pressure goes down

Intravascular pressure VR Veins here are
(increasing pressure gradient driving VR to unaffected
the right heart)
Because theres is more blood
Increased output of the right heart delays
closing the pulmonic valve creating
Veins outside the chest are unaffected MAP = CO x TPR
 This also increased the across
all the vasculature of the lung,
Inspiration
for pulmonary
increasing their volumen. RA in chest expands vessel; their volume
During inspiration theres an increases pressure so Q (VR) increases
pulmonary vascular resistance
(PVR) Flow to LH
Pulmonary vessel expand and the
volumen of the blood in the pulmanary
circuit increases Becomes more
PVC is lowest at FRC Negative
VR
If Pulm Vasc Resistance in turn VR
to the LH and cardiac output of the Veins here are
left heart decreased, causing unaffected
systemic arterial pressure (drop in
systolic most prominent)
This will reduce vagal outflow to the
heart, thus HR increases (respiratory
sines arrhythmia)
MAP = CO x TPR
RA in chest expands
Inspiration Natural change
associated with
for pulmonary vessel; breathing
pressure so Q (VR)
their volume increases

Flow to LH

Becomes more Negative

VR to the right VR to the left

Veins here are
unaffected
Causes sytolic
BP to fall

MAP = CO x TPR
 returns to its
original level EXPIRATION Natural change associated
with breathing

Pulmonary vessel are compressed and

blood volume in the circuit decreased
Pressure gradiente
for VR decreased Blood Flow and
output Left ventricle
Becomes more
POSITIVE
Systemic venous
return and output of VR to the left
the right ventricule
are decreased Causes sytolic BP to
RISE (primary systolic)

MAP = CO x TPR
Vagal outflow increases reducing HR
Cardiac temponade; respiratory distress
 POSITIVE PRESSURE VENTILATION
PEEP
Positive End Expiratory
pressure CPAP
Lungs do NOT return to FRC
Makes IPP positive Continuous positive airway
Increase pulmonary vascular pressure (CPAP) is similar
resistance: Decreased cardiac Commonly used for
output obstructive sleep apnea
Helps prevents atelectasia:
ARDS, pneumothorax
 Inspiration
Pushing air into the lung
Positive pressure

ARDS
Prevents
Respiration

PEEP
atelectasia
Pneumothorax
Obstructive sleep
CPAP
apnea

Expiration
Take away the positive pressure
It goes back to FRC
 PNEUMOTHORAX
Air in the intrapleural space
Ar goes in because theres a negative pressure into
intrapeural space
IPP becomes positive
: Pi Po
: - IPP
: 0 0
= 0
If is 0 theres no force pushing out so the alveoli
collapse
When the LUNGS collapse the chest is going to come
OUT
Because Chest Recoil is pushing out
TENSION PNEUMOTHORAX
Positive pressure in the intrapleural space
Theres an opening between intrapleural space
and alveoli
Because theres a pressure gradient air can
blow in from the alveoli to the intrapleural
space
IPP becomes positive
Positive IPP will decreased VR and CO
Clinical signs
Respiratory distress
Distended neck veins
Contralateral tracheal shift
Asymmetry of breath sounds
Restrictive
Fibrosis

Sarcoidosis
PATHOLOGY
Asbestosis

Increase airway
resistence

Emphysema
Obstructive
Chonic
Bronquitis

Asthma
 Compliance
Pathology

FIBROSIS
Recoil

Compliance
Emphysema
Recoil
LUNG RECOIL Surfactant

Components of Lung recoil

1. Tissue
2. Surface tensin (predominant
component)
Inward force Surfactant
Its made by pneumocytes Type II Pathology
Lowers Surface tension more in
smaller alveoli Infant Respiratory Distress Syndrome
Dont have functional surfactant
Compliance Adult Respiratory Distress Syndrome
Reduces Surface Destroy the surfactant
tensin Sepsis: Cytokines (TNF alpha;
Recoil interleukins) infiltrations of Neutrophils
Gastric aspirations
 AIRWAY RESISTANCE Turbulance cause Resistance

Branching airway of the lung

First and second bronchi that
represent most of the airway Catecholamines produces
resistance bronchodilation
Epinephrine 2 receptor
Airway resistance
Present in Obstructive disease Other broncoconstriction are
Parasympathetic nerve stimulation Histamine Mast cells
produces bronchoconstriction Leukotrienes Anaphylaxis
Mediated by 3 receptors
Activation of 3 increases airway
secretions
 As lung volumen ; Airway Resistence Mechanical effect of lung
volume

Airway resistance depend

upon two factors:
1.
2. Radial traction

As lung volumen ; Airway Resistence

 As lung volumen ; Airway Resistence Mechanical effect of lung
volume
Airway resistance is
inversely related to lung
volumen

Inspiration IPP becomes
more negative so
increases
The more negative IPP the
greater the lung volumen
A reduce IPP opens big and
small airway to reduce the
resistance As lung volumen ; Airway Resistence
 As lung volumen ; Airway Resistence
Mechanical effect of lung
volume
Radia traction
Physical connection of alveoli
and small airways
1
=
4
In patients with obstructive
resistance is increases
Obstructive patients have
problems getting air out
Residual volumen As lung volumen ; Airway Resistence
 Pulmonary Function Test Forced Vital Capacity
Highly diagnostic
Restrictive disease
Characterized by reduce compliance
Decreased volumen
Obstructive disease
Characterized by increased resistance to
airflow
Decreased FLOW
 Pulmonary Function Test Forced Vital Capacity
In a forced expiration Lung recoil is driving force
Lung volume falls RECOIL falls FLOW falls
The Dynamic compression is going to trap air in the
alveoli creating the RESIDUAL volumen

+20 +20

+40
+20

NORMAL Obstructive disease Restrictive disease

OBSTRUCTIVE DISEASE REDUCED FLOW

Fundamentals pathologic
changes
1. Bronchoconstriction
2. Hypersecretion
3. Inflamation
4. Destruction of lung
parenchyma (emphysema)

5.
< %
OBSTRUCTIVE DISEASE REDUCED FLOW
1. Asthma
Administer a broncodilator (BD) B

If Flow gets better Dx Asthma

2. Chronic Bronquitis
DLCO Normal
3. Emphysema
VERY LOW RECOIL
LOW FLOW
DLCO Decreased
Reduce Surface area
4. Cystic Fibrosis
 Albuterol
Short 2

PHARMACOLOGY
agonists
Terbutaline

Salmeterol
Long acting 2
agonists
Formoterol

Cromolyn sodium
Mast Cell
stabilizer
Nedocromil
 Anti
Ipatropium
Pharmacology cholinergics
Phosphodiestere
Theophylline
Inhibitors

Montelukast
Anti
Leukotrienes
Zarfirlukast
Steroids
RESTRICTIVE DISEASE REDUCED VOLUMEN

Normal Flow
Reduce Volume
Lungs are restrictive from
expanding
All volumes are gonna fall

= % or Normal

Flow Volume Loops Lung recoil is
driving the flow

Inicially theres a very HIGH

FLOW
In expiration
Theres a stady decline in Flow until
it gets to RESIDUAL VOLUME
As Lung volumen Falls Flow
falss Recoil falls
Lung recoil is driving the FLOW
 At any given
lung volumen
theres gonna
be less flow Scalloping
Inward
Scalloping
Inward
 Restrictive
LOW LUNG RECOIL

Residual Volume
Flow Volume Loops
Total lung capacity
Obstructive

Scalloping

Total lung capacity

Residual Volume
 Water vapor
ALVEOLAR BLOOD GAS EXCHANGE pressure

2 = F ( Patm 47)
F: Fractional concentration of
oxygen in atmophere air is
21%
21/100 = 0.21
F: 0.21
Patm: 760
2 = 0.21 (760 47)
2 = 0.21 (713)
2 = 150 mmHg
ALVEOLAR BLOOD GAS EXCHANGE
2 = F ( Patm 47)
End Tidal is alveolar gases
Alveolar gases = Arterial gases
Theres a pressure gradient for 2
to diffuse into the alveoli
Blood coming in from venous
2 = 40 mmHg
2 = 47 mmHg
Theres a pressure gradiente for
Oxygen to diffuse into the
blood
2 = 100 mmHg
A a gradient 2 = 40 mmHg
ALVEOLAR BLOOD GAS EXCHANGE
If the gas in the blood

Diffusing capacity
equilibrates with alveolar
gases its perfussion limited

Perfusion-limited

Diffusion-limited
ALVEOLAR BLOOD GAS EXCHANGE

Alveolar gases determines

arterial gases

determine alveolar gases

Anatomic shunt
Drop the 2 in the arterial
blood
ALVEOLAR BLOOD GAS EXCHANGE
Factors affecting 2
1. Alveolar ventilation ( )
2. 2 production ( 2) Exercise & Hyperthermia
2 = 2

2
Increased in
Exercise
2
Hyperthemia
 Can use arterial or end tidal
ALVEOLAR BLOOD GAS EXCHANGE Increases in 2
Decreases in 2

Alveolar Air Equation

Factors affecting 2
2 = 47 2 ( 2 /)
1. Alveolar ventilation ( )
2. 2 production ( 2) 760 mmHg at sea level; 21% for room air;
decreased as one increasing this
ascends to high altitud, increases 2
Increased in which decreases 2 2

Exercise =
2
Hyperthemia
2 = 760 74 0.21 40/0.8 = 100 mmHg
2

2
Exercise & Hyperthermia
2 = 2

 FICKS LAW DIFFUSION
Exercise 2 is much more soluble
Emphysema

is rhe
rate of gas
diffusion

= 1 2

Fibrosis Important factor here is 2
Pulmonary edema Supplemental 2
(ARDS) Altitud
 DIFFUSING CAPACITY ( )
Clinical measure Area
of overall diffusion of
gases in the lungs


=

CO is the prototypical
Diffusion limited gas
Thickness
TRANSPORT OF 2 and 2
Hemoglobin 2 Content
Transport
Alveoli (Warehouse) Oxygen
If 2 = 100 mmHg
If 2 = 100 mmHg
Loading
Dissolved (loading zone) zone
0.3
0.4
Hb (Truck) Truck
19.4
19.4
Total content ( ) Tissue
19.7 vol%
19.8 vol%
2 delivery = Flow x Arterial 2 content (2 )
 OXYGEN Hb Dissociation curves
The more 2 its in the
loading zone the more gets
50 into the truck
Reduce affinity
Favor unlaoding
the 2 2 (loading zone)
The more 2 in
50 the blood the more
50 its gets onto the HB
Increased affiny
Favors loading 100
Loading zone

50 describe overall affinity of Hb for 2 2 in plasma is 0.3%
 Right shift the
Left shift the curve
curve
Left shift the
curve 50 increases
decreases Less affinity
Favors unlaoding
More affinity Right shift the curve
2 content
Favors laoding Easier for tissue to
2 content extract oxygen
More difficult Increased tissue
for tissue to metabolism
extract oxygen 2,3 BPG
(glycolisis)
stimulated by
hypoxia
Fetal Hb has a LOW 50 - VERY HIGH affinity favors loading
Policythemia
HB CONCENTRATION EFFECTS
More thucks
More Ca2 (2 Anemia
content) Less trucks
will be Less Ca2 (2
normal content)
VISCOSITY 50 will be
RESISTANCES normal

HIGH altitud
Red blood cells
NORMAL

Increased potential for turbulent Flow in the Aorta

 EFFECTS OF CARBON MONOXIDE
Carbon
monoxide Sat Reading
Hb2 content (2 ) will be
because it's normal
gonna displace is
it
Hb has much
greater affinity
for CO than 2
Hb will bind CO
over the 2
 If Venous oxygen goes down
Hb concentration & CO effects Two posibilities:
1. Comsuption went UP
1. Delivery went DOWN

The loading zone is normal Anemia & CO

Reduce delivery
2 delivery = Flow x Arterial 2 content (2 ) Venous O2 decreases
Infer based upon
venous 2
 2 Transport 3

Carbonic Anhydrase

2 + 2 0 2 3 + + 3 Carbamino Physically
compounds dissolved

Chloride Shift
Carbon dioxide (CO2) is generated in tissues as a byproduct of normal
metabolism.
It dissolves in blood plasma to form carbonic acid (H2CO3); red blood
cell (RBC) carbonic anhydrase catalyzes this reaction.
 2 Transport

Taking away the 3
it will drive
the reaction in this direction
Carbonic At tissue: moves into RBC
Anhydrase

2 + 2 0 2 3 + + 3

At the lungs its gonna reverse

everything
2 is gonna leave
The reaction will go this way
3 will go in and will go out At lungs: moves out of RBC
 ADAPT to
chronic changes
Chemoreceptors
Central (BRAIN)
Stimulated by
+

Stimulated by arterial +
Peripheral
DO NOT
2
ADAPT
 CENTRAL CHEMORECEPTORS
Chemoreceptors located in the brain
Chemoreceptors stimulate
ventilation
Stimulate by and +
If 2 stimulate VENTILATION
to maintain 2 constant (getting rid of
2 )
2 is soluble thats why 2 can
cross the blood-brain barrier easily and
stimulate central chemoreceptors
Stimulate ventilation
 CENTRAL CHEMORECEPTORS
+ will not getting into the
brain quickly to stimulate
central chemoreceptors
Chemoreceptores
Adapt to chronic changes
Not responsive to changes in
oxygen 2

Stimulate ventilation
 PERIPHERAL CHEMORECEPTORS
Located coratid bodies and aortic
bodies
Afferent neurons are IX and X
Monitor the blood
Stimuated by
2
arterial +
2 (not strong stimulus until 2
falls below 60 torr
DO NOT ADAPT
Phatology Integration

2 drive to breath
supressed by
COPD

Narcotics

General anesthetics
 CENTRAL RESPIRATORY CENTERS
C1 C2 transaction
Medullary centers Interrupt the phrenic nerve so
patients cant breath of their
Site of the inherent own C3

rhythm for
respiration.
The phrenic nerve
to the diaphram
comes out from C3 C5 C6 transaction
to C5 Preserve the connection to the
diaphragm
Patient can breath or their own
RESPIRATORY STRESS UNUSUAL

High altitud
Peripheral
Chemoreceptors
2 2 Stimulate ventilation
ENVIROMENTS
alveolar ventilation
High pressure enviroment

Carbon monoxide
poisoning

Compromised tissue
Hyperbaric Oxygen Clinical uses Costridium perfingrens
grafts

Rapture of the Deep Gas gangrena Staphylococcus aureus

Nitrogen
Caissons disease or
Vibrio vulnificu
decompression sickness
HIGH ALTITUD Hypoxic vasocontriction in pulmonary Upstream pressure

Stress is total pressure

total pressure = 2 = 2 = HYPOXEMIA
2 stimulates ventilation so 2 Pulmonary hypertension
(ACID)

+ Resistance Respiratory alkalosis

VISCORITY

% saturation of HB Erythropoietin Acute mountain

sickness
Reduce the amount of 2
RED BLOOD CELLS +
2
alleviate Kidney 3
POLYCYTHEMIA
Reduce 2 content Resolve the alkalosis
HIGH ALTITUD Oxygen radicals
Stress is total pressure
total pressure = 2 = 2 2 Toxicity

Total pressure = 2 = Hyperbaric Oxygen

Dissolved gases
coming out of NITROGEN
solution into
bubbles inside
the body on Clinical uses
Gets into the brain
depressurisation
in causes EUPHORIA

CO poisonin
Bends Rapture of the deep Gas gangrena
Caissons disease (Costridium perfingrens)
 IPP: -10
REGIONAL DIFFERENCES IN
VENTILATION
Apex PTM: +10 Less compliance APEX
Ventilation > Blood Flow
More distended Less ventilation
LUNG

IPP: -5 Blood Flow

Mean
PTM: +5

IPP: - 2.5

Base PTM: +2.5 More complaince

Less distended More ventilation

BASE
Blood Flow > Ventilation
Pressure = height x gravity x densidty Blood FLow Compared to one another
 REGIONAL DIFFERENCES IN VENTILATION
Less ventilation
at the Apex
Less blood flow

More Flow at
the bottom
More ventilation
at the bottom 2

2

 Ventilation and Blood Flow are equal 2 40 APEX
More ventilation than
blood Flow
/Q 1.0 2 100 Q V
VENTILATION PERFUSION

V/Q is
pH 7.4 Its over ventilated
2 increases, 2
2 = 40 decreases
MATCHING

/Q
/Q Normal 1.0 2 =100

pH = 7.4
BASE
More Flow than
2 40 ventilation
Q V
/Q 1.0 2 100 V/Q is
Its under ventilated
2
pH 7.4 Increases 2
2 decreases 2

VENTILATION PERFUSION MATCHING DEAD SPACE

V/Q determines the EXTREME

alveolar gases V/Q is
Ventilation with
V = ventilation NO BLOOD
FLOW
Q = Flow
All CO2 in the lung
comes from blood
Flow
BASE APEX
EXTREME More Flow than ventilation More ventilation than blood
V/Q = 0 Q V Flow (compared to one
V/Q is another)
Theres blood Flow but NO
Ventilation Its under ventilated so 2 Q V
So this is a SHUNT Increases and 2 decreases V/Q is
RIGHT TO LEFT SHUNT Its over ventilated
2 2 increases, 2 decreases
VENTILATION PERFUSION RELATIONSHIP
LOW V/Q
Under Ventilated
MORE FLOW M. Tb - Apex
of the lung
Because theres
more 2
V/Q is High

HIGHT V/Q
Over Ventilated
NO FLOW

Bug that likes oxygen and attacks the lungs: Mycobacterium tuberculosis
 Alveolar 2

Diffusion
impairment
Cause of
Hypoxemia
Severe V/Q
mismatch

Pulmanry Shunt
Hypoxic vasoconstriction pulmonary Normal A a 2 gradient
Pulmonay artery pressure COPD
Alveolar 2 Drug overdose
Increasing 2 helpful
(Hipoventilation) Inhalation anesthesia
CAUSES OF HIPOXEMIA Chest restriction
2 (hypoventilation
Respiratory acidosis)

Pulmonary edema
A a 2 gradient
(ARDS, left heart failure)
Diffusion impairment Restrictive disease
Increasing 2 helpful (pulmonary fibrosis)

A a 2 gradient Severe OBSTRUCTION

(Status asthmaticus, Cystic
Severe V/Q mismatch fibrosis, Anaphylaxis)
Increasing 2 helpful Infection (pneumonia); mucus
plugs (partial oclusin)
PULMONARY SHUNT
Low 2 blood
Reduces 2
Dignostic signs
Increases A a 2 gradient
Increasing NOT helpful
CAUSES
Atelactasis (pneumothorax; ARDS)
Complete oclusin of an airway
(mucus plug, foreing object
Tetralogy of fallot (TOF)
 LOW 2
DIFFERENTIAL FOR CAUSES OF
A a 2
gradiente
HYPOXEMIA

Normal Elevated

Cause is Increase
2 2

2 Corrects Doesnt
corrects 2 correct 2

Cause is
2 likely Diffussion /Q
right-to-left
elevated impairment mismatch
shunts
CORRECT ANSWER IS C
= 45 torr; = 27
27
2 = 150 ( ) = 116 Increased
0.8
A a 2 gradient = 116 45 = 71 = () 95 torr; = 39 ()
Elevated A a gradient
Pt is in hypovolemic shock with
the decreased cardiac output
Patient is not hypoventilation
(CO)
2 corrected the hypoxemia so is
PEEP is use to reduce cardiac
not a SHUNT
output
PEEP is not needed because the
In a patient with CO the PEEP
hypoxemia is already CORRECTED
is gonna make it worse
 Congenital heart
defects Shunting of Blood in the heart
Atrial septal Ventricular septal Patent ductus LEFT-TO-RIGHT SHUNT
defects (ASD) defects (VSD) arteriosis (PDA)

RA 2 RV 2 RA 2

RV 2 ; RV 2 RV 2

Pulmonary Pulmonary Pulmonary

arterial 2 arterial 2 arterial 2

Pulmonary blood Pulmonary blood Pulmonary blood

Flow Flow Flow

Pulmonary artery Pulmonary artery Pulmonary artery

pressure pressure pressure