2025 Airway Management Exam 1 Flashcards
Anatomy and Physiology of Airway
Upper Respiratory System
Nose
Mouth
Sinuses
Pharynx
Larynx
Frontal Sinus
Sphenoid Sinus
Nasal conchae: Superior, Middle, Inferior
Nasal Cavity
External Nares
Internal Nares
Entrance to Auditory Tubes
Oral Cavity
Hard Palate
Soft Palate
Pharynx: Naso, Oro, Laryngo (Hypo)
Epiglottis
Glottis
Vocal Fold
Framework of Nose
Bony: Frontal Bone, Nasal Bones, Maxilla
Cartilaginous: Lateral nasal cartilages, Septal cartilage, Alar cartilage
Dense Fibrous Connective Adipose Tissue
Upper Airway Functions
Heat
Respiratory
Humidification
Filtration
Olfaction
Reservoir for secretions: Paranasal sinuses, Nasolacrimal ducts
Phonation: Modification of speech
Nose Anatomy
Nasal Septum: R and L nasal cavities
Turbinates aka Conchea
Nose Blood Supply
Anterior Ethmoid Artery
Posterior Ethmoid Artery
Sphenopalatine Artery
Greater Palatine Artery
Superior Labial Artery
… all flow into Kiesselbach’s Plexus
Kiesselbach’s Plexus
Aka Little’s Area
Most common source of clinically significant epistaxis
Pharynx
The pharynx is the part of the digestive system situated posterior to the nasal and oral cavities and posterior to the larynx.
12-15 cm long
Extends from the base of the skull down to the inferior border of the cricoid cartilage (around the C6 vertebral level), where it becomes continuous with the esophagus
It is therefore divisible into nasal, oral, and laryngeal parts:
(1) nasopharynx
(2) oropharynx
(3) laryngopharynx
Pharynx Function
The pharynx is the common channel for:
Deglutition (swallowing)
Respiration
Food and air pathways cross each other in the pharynx
In the anesthetized patient, the passage of air through the pharynx is facilitated by extension of the neck.
Swallowing Process
BEGINNING DEGLUTITION
Pharynx ascent
Dilation with tensing of soft palate
Tongue moves upward
No air enters nasopharynx
Larynx ascends
Elevation of hyoid-laryngeal complex
BOLUS ENTERS PHARYNX
Pharynx descends
Constrictors contract from to top to bottom to transport bolus towards UES
BOLUS ENTERS ESOPHAGUS
Nasopharynx
Posterior portion of the nasal cavity, with which it has a common function as part of the respiratory system.
Primarily of respiratory function
Eustachian tubes open into the nasopharynx
Oropharynx
Extends inferiorly from the soft palate to the superior border of the epiglottis
Primarily of digestive function
Laryngopharynx (Hypopharynx)
Extends from the superior border of the epiglottis to the inferior border of the cricoid cartilage, where it becomes continuous with the esophagus
Lies between C4-C6
Oral Cavity
Tooth Numbering
Top Back Right to Top Back Left (1-16)
Bottom Back Left to Bottom Back Right (17-32)
Type of Teeth (Top and Bottom)
Central Incisor
Lateral Incisor
Cuspid or Canine
First Premolar
Second Premolar
First Molar
Second Molar
Third Molar or Wisdom Teeth (17-21yo)
Peds = 20 teeth
Adults = 32 teeth (28 if wisdom teeth removed)
Tongue Nerve Supply
SENSORY NERVES
Anterior 2/3 of tongue
Lingual nerve (CN V Trigeminal – sensation)
Facial nerve (CN VII Facial – mostly taste)
Posterior 1/3 of tongue
Glossopharyngeal nerve (CN IX)
MOTOR NERVES
Hypoglossal nerve (CN XII) – mostly
Superior Laryngeal nerve (CN X Vagus) – minimal
Cranial Nerves
Olfactory nerve (CN I): The nerve that carries smell information from the nose to the brain
Optic nerve (CN II): The nerve that carries visual information from the retina to the brain
Oculomotor nerve (CN III): The nerve that controls four of the six eye muscles
Trochlear nerve (CN IV): The nerve that helps move the eye down and out
Trigeminal nerve (CN V): The largest cranial nerve that provides sensory information to the face and controls the muscles used for chewing
Abducens nerve (CN VI): The nerve that controls the lateral rectus muscle of the eye
Facial nerve (CN VII): The nerve that extends from the brain stem
Vestibulocochlear nerve (CN VIII): The nerve that carries information about sound and balance from the inner ear to the brain
Glossopharyngeal (IX): Primarily responsible for sensory functions in the pharynx and posterior tongue, including taste
Vagus (X): A mixed nerve that controls various involuntary functions in the body including heart rate, digestion, and breathing
Accessory (XI): Primarily motor, controlling the muscles of the neck.
Hypoglossal (XII): Responsible for controlling the muscles of the tongue
Larynx
The larynx is the organ that connects the lower part of the pharynx with the trachea
Begins at C4-C6
It serves as a:
Valve to guard the air passages
especially during swallowing
Maintenance of a patent airway
Vocalization
Laryngeal Functions
Air passage into and out of the lungs
Protection of lungs from liquids and solids
Phonation
Effort closure: Coughing, Lifting, Defecation
Larynx Cartilages
The larynx possesses:
3 paired cartilages
Arytenoid
Corniculate
Cuneiform
3 single cartilages
Thyroid
Cricoid
Epiglottic
Types of Larynx Cartilage
Types of Cartilage
Hyaline
Calcifies - beginning in middle life
Ossifies - as age advances
If become calcified, become viable radiographically
Cricoid, Arytenoid, Thyroid
Elastic
Neither calcifies nor ossifies
Maintains functional form throughout life
Epiglottic, Corniculate, Cuneiform
Epiglottic Cartilage
TYPE
Elastic cartilage
GENERAL SHAPE
Leaf
ARTICULATIONS
None
ATTACHMENTS
Hyoepiglottic ligament
Thyroepiglottic ligament
FUNCTIONS
Protects against food entering the larynx
Thyroid Cartilage
STRUCTURE - OTHER
Superior cornu (horns) – suspend thyroid cartilage from hyoid bone
Inferior cornu (horns) – suspend cricoid cartilage from thyroid cartilage
ARTICULATIONS
Inferior cornu & cricoid cartilage
ATTACHMENTS
Thyrohyoid membrane cephalad
Cricothyroid membrane caudad
Vocal cords – midline, interior
FUNCTIONS
Protects larynx
Suspends 7 (of 8) laryngeal folds
TYPE
Hyaline cartilage
GENERAL SHAPE
Shield
UNIQUE ASPECT
Largest laryngeal cartilage
STRUCTURE – PHYSICAL EXAM
Alae (wings) - 2
Prominentia laryngis (Adam’s apple); midline fusion of alae
Thyroid notch
Cricoid Cartilage
STRUCTURE – PHYSICAL EXAM
Midline, rounded prominence below prominentia laryngis
Can be depressed into esophagus
Only Complete Ring
C5-C6
ARTICULATIONS
Thyroid cartilage’s inferior cornu
Arytenoid cartilage’s bases
ATTACHMENTS
Cricothyroid membrane – cephalad
Trachea - caudad
TYPE
Hyaline cartilage
GENERAL SHAPE
Signet ring
UNIQUE ASPECT
Only circumferential laryngeal structure
STRUCTURE – PHYSICAL EXAM
Midline, rounded prominence below prominentia laryngis
Can be depressed into esophagus
FUNCTIONS
Supports arytenoid cartilages
Must be able to identify for cricothyrotomy
Pressure on this structure for Rapid Sequence Induction (RSI) – Sellick’s maneuver
Corniculate Cartilages (horn-like)
GENERAL SHAPE
Conical nodules
UNIQUE ASPECT
Cartilages of Santorini (Italian
anatomist, 1700s)
STRUCTURE – PHYSICAL EXAM
Tubercles appear beside interarytenoid incisure
STRUCTURE – OTHER
Located in aryepiglottic folds
FUNCTIONS
Spring-like action (stressed by adduction of arytenoid cartilages) produces recoil assistance with mediolateral separation of arytenoids and reopening of glottis
Cuneiform Cartilages (wedge-shaped)
GENERAL SHAPE
Small, elongated STRUCTURE –
PHYSICAL EXAM
Tubercles appear lateral to
corniculate tubercles
STRUCTURE – OTHER
Located in aryepiglottic folds
ATTACHMENTS
Arytenoid cartilages
FUNCTIONS
Stiffens aryepiglottic folds
Spring-like action facilitates reopening of glottis
Innervation of the Airway
Superior laryngeal nerve (SLN) – Internal Branch
Pierces thyrohyoid membrane
Sensory
Supraglottic region
SLN – External Branch
Motor
Cricothyroid muscles
Recurrent Laryngeal Nerve (RLN)
Motor: All intrinsic laryngeal muscles except cricothyroids
Sensory: Infraglottic
Lecture 1, Slide 40, 41, 42
Larynx Cartilages
Know how to identify
Lecture 1, Slides Throughout
Innervation Complications
SLN damage occurs (thyroidectomy, neoplasm, or trauma) and contraction of cricothyroid muscle bilaterally – results in acute airway obstruction
Complete paralysis of RLN and SLN – midway position of vocal cords – seen after NMB given (cadaveric position, seen with administration of NMB)
A contraction of ALL the laryngeal muscles – Laryngospasm (cords close)
Lower Airway
Trachea
Also known as the windpipe, this tube carries air from the upper respiratory system to the lungs. The trachea is made of cartilage rings that keep it from collapsing or over-expanding.
Bronchi
These passageways carry air to the lungs. The left bronchus carries air to the left lung, and the right bronchus carries air to the right lung. (Primary, Secondary, Tertiary)
Bronchioles
These are smaller branches of the bronchi that clean, warm, and moisten the air that’s inhaled.
Alveoli
These tiny air sacs in the lungs are where oxygen is absorbed and carbon dioxide is released.
Lungs
These spongy organs are where the exchange of gases between the blood and air takes place.
Trachea
~12-15 cm long, 1.5-2cm internal diameter
Extends from the cricoid cartilage to the bronchial bifurcation (Carina)
Carina: T5 at expiration, T6 at inspiration
16 to 20 C- shaped cartilages
Trachealis muscle runs vertically for the posterior aspect
5th thoracic vertebra – trachea bifurcates into R & L mainstem bronchi
R mainstem bronchus and tracheal axis is more acute
R mainstem bronchus intubation
Greater risk for aspiration of food liquids
Adult Angle of R Bronchus: 20 degrees; L Bronchus 40 male/50 female
Pediatric Airway
Head
Very large (in relation to body)
Occiput elevates head
Little muscle tone
Tendency for cervical flexion
Tendency for airway obstruction
Nose
Obligate nasal breathing
Nasal passages smaller
Tongue
Larger (in relation to oral cavity)
Larynx
Is situated at a higher level than in adults, infant it is funnel shaped
Epiglottis
Omega shaped
Horizontally oriented
Longer
Stiffer
Vocal cords
Antero-inferior plane
C3-C4 Glottic Opening, in adults C4-C5, Premature Infant C3
Narrowest part in pediatrics:
cricoid cartilage
Narrowest part in adult:
rima glottidis
Trachea and Mainstem Bronchi
Shorter and narrower
Right mainstem has less acute angle
Diameter of larynx affected more by edema
Airway Length and Purposes
Airway extends from the nose and mouth to the alveoli
Upper = filter/humidify/warm
Lower = ventilation/oxygenation
Bronchi
1st bifurcation at carina leads to R & L lung
R main bronchus less angled than L
Easier to R mainstem intubate
RUL of lung only 2.5cm from carina
Walls in larger airways contain:
smooth muscle
elastic tissue
cartilage
Lungs
Right
3 lobes
10 broncho-pulmonary segments
Left
2 lobes
9 broncho-pulmonary segments
23 airway divisions between trachea and alveoli
Gas movement
Tidal flow – larger airways
Diffusion – smaller airways (division 17 and smaller)
Tracheobronchial Tree
23 divisions/generations
Cartilaginous support lost at bronchioles (becomes only smooth muscle)
Gas exchange begins on pulmonary bronchioles (generations 17-19)
Trachea - 0
Primary Bronchus - 1
Secondary Bronchus - 2
Tertiary Bronchus - 3
Bronchiole - 4
Terminal Bronchiole - 5-16
Respiratory Bronchiole - 17-19
Alveolar Duct - 20-22
Alveolar Sac - 23
Pleura
Pleura
Double layer surrounding the lungs
Visceral (defined as relating to organ) pleura – lung
Parietal (defined as relating to cavity) pleura – lines thoracic cavity
Intrapleural space
Small amount of lubricating fluid
Location of Lungs and Pleura
Clavicle to 8th rib anteriorly
10th rib laterally
T12 posteriorly
Pneumothorax
Air in Pleural Space
Alveoli
Size is a function of both gravity and lung volume
Average diameter ~0.05-
0.33mm
Largest at apex of lung (more negative intrapleural pressure) & smallest at base of lung
Gas exchange on thin side (no intestitium and few organelles) (~0.4μm thick)
Thick side provides support (interstitial space) (1-
2 μm)
50-100m2 surface area for gas exchange
Laplace’s Law
Tension within wall of sphere filled to a particular pressure depends on the radius of the sphere
P = 2T/R
Formula that describes why small alveoli tend to collapse (atelectasis)
Lecture 2, Slide 13
Pulmonary Epithelium
Type I pneumocytes
Flat cells, form tight junctions with one another
Prevent passage of large oncotically active molecules into alveolus
Type II pneumocytes
More numerous
Occupy <10% of alveolar space
Cuboidal cells
Produce and secrete surfactant
Able to undergo cell division
Produce type I pneumocytes
Resistant to hypoxia
Interstitial Space
The space between cells in the body
Pulmonary Circulation
Gas exchange with alveoli
Low pressure (25/10mmHg)
Can accommodate large increase in blood flow with no change in pressure
Does so by vascular distension and recruitment of unperfused capillaries
Hypoxia is the main stimulus for an increase in pulmonary vascular resistance via hypoxic pulmonary vasoconstriction
Only vascular bed where hypoxia/hypercarbia lead to vasoconstriction; everywhere else in the body hypercarbia and hypoxia causes vasodilation to occur.
Bronchial Circulation
Supplies parenchyma of the lung itself
Drains to L heart with pulmonary vein
Deoxygenated blood = physiological shunt
Descending thoracic aorta gives rise to the L and R bronchial arteries
Supply oxygenated blood to lungs (connective tissue, septa, bronchi) and after joins pulmonary veins without oxygenation
Control of Ventilation In Brain
Located in Brain Stem
MEDULLA
Breathing Regulation
Dorsal respiratory group (DRG)
Inspiratory center
“pacemaker” for respiratory system
Ventral respiratory group (VRG)
Expiratory coordinating center
PONTINE CENTERS
Apneustic center
Sends impulse to DRG, designed to sustain inspiration
Pneumotaxic center
Limit depth of inspiration
Chemical Control of Ventilation
Peripheral chemoreceptors
Composed of carotid and aortic bodies
Respond to:
lack of oxygen
↑ CO2
↑ H+
Central chemoreceptors
Located in medulla
Respond to CO2, H+
Mechanism of Breathing
INSPIRATION
Initiated by creating sub-atmospheric pressure (-5 cm H2O) in alveoli by increasing volume of thoracic cavity by action of inspiratory muscles
Diaphragm generates the negative intrathoracic pressure
Primary ventilatory muscle
Innervation from C3-5
(“C3-4-5 keeps the diaphragm alive”)
External intercostal muscles
Innervation by intercostal nerves (T1-T12)
EXPIRATION
Initiated by creating intra-alveolar pressure that is higher than atmospheric pressure & flow to mouth results
During relaxed breathing, initiated by relaxation of diaphragm and external intercostals
Normally passive process
Accessory Muscles of Breathing
CERVICAL STRAP MUSCLES
Most important inspiratory accessory muscles
Primary inspiratory muscles when diaphragm is impaired
Omohyoid
Sternohyoid
Thyrohyoid
ABDOMINAL MUSCLES
Most powerful muscles of active expiration
Important for expulsive efforts (i.e. coughing)
Other muscles with less contribution:
Sternocleidomastoid
Intercostals
Large back and intervertebral muscles of shoulder girdle
Lung Volumes and Capacities
Tidal Volume (VT)
Each normal breath
~500mL (~ 6-8mL/kg)
Inspiratory Reserve Volume (IRV)
Maximal additional volume that can be inspired above tidal volume
~3000mL
Expiratory Reserve Volume (ERV)
Maximal volume that can be expired below tidal volume
~1100mL
Residual Volume (RV)
Volume remaining after maximal exhalation
~1200mL
Total lung capacity (TLC)
RV+ERV+VT+IRV
~5800mL
Functional Residual Capacity (FRC)
RV+ERV
~2300mL
Lecture 2, Slide 25
Functional Residual Capacity (FRC)
Lung volume at end of a normal exhalation
Measured by nitrogen wash-out, helium wash-in, or total body plethysmography
During apnea this is the reservoir of O2
GA ↓ FRC ≈ 400mL, supine position ≈ 800mL
Factors that alter FRC
Body habitus – directly proportional to height
Obesity dec FRC, 2° reduced chest compliance
Posture – decr. when moved from upright to supine/prone
2° reduced chest compliance
Lung disease – decr. Restrictive disorders
Diaphragmatic tone – contributes either way
Ascites, abdominal surgery, & pregnancy
FRC and O2 Stores
When apneic, existing O2 stores consumed by cellular metabolism
Rate of O2 consumption at rest is 1 MET (Metabolic equivalent)
Approximately 3.5ml/min/kg of O2
Average 70kg adult ~ 250ml of O2/min
If 21% FIO2
->0.21 x 2300mL = 483mL of O2 in lungs
Time to consumption of O2 stores: 483/250 = 1.9 mins
If 100% FIO2
-> 1.0 x 2300mL = 2300mL of O2 in lungs
Time to consumption of O2 stores: 2300/250 = 9.2 mins
Closing Capacity
Closing Capacity(CC)
Volume at which small collapsible airways begin to close in dependent parts of the lung
Alveoli continue to be perfused, but no longer ventilated
intrapulmonary shunting
hypoxia
Measured using tracer gas (Xenon-133) which is inhaled near residual volume and then exhaled from total lung capacity
Normally well below FRC
Inc. with age
44yo CC=FRC in supine position
66yo CC=FRC in most upright individuals
Increased by smoking, obesity, aging, and supine position
Vital Capacity
Maximum volume of gas that can be exhaled following maximal inspiration
Dependent on respiratory muscle strength and chest- lung compliance
Normal ~60-70mL/kg
Forced Vital Capacity
Measuring vital capacity as an exhalation that is hard and as rapid as possible
Forced Expiratory Volume (FEV1)
Forced volume in 1 second (can go to 2 or 3s)
COPDers have a lower FEV1 than normal
Less than 50% of normal indicates greatest risk of complications
Ratio of FEV1/FVC
Ratio of FEV1/FVC ≥80% in normal adults is proportional to degree of airway obstruction
Lecture 2, Slide 31
Flow-Volume Loop
A “flow volume loop” is a graphical representation of airflow (measured in liters per second) plotted against lung volume (in liters) during a forced breath in and out, essentially showing how quickly air can be moved at different lung volumes, which is used to diagnose and localize airway obstructions in the lungs by analyzing the shape of the loop produced during a test; a normal loop has a characteristic shape, while abnormalities like “dips” or flattened sections indicate potential issues like asthma or upper airway obstruction depending on where the abnormality occurs on the loop.
Lecture 2, Slides 32, 33
Restrictive Lung Disease
Decreased lung compliance or increase in lung resistance
FEV1/FVC normal
Volume is the problem
Static lung compliance
Ventilator Management:
Increase O2, PEEP, RR
Decrease TV
Extrinsic Pulmonary Disorders
Pleura, chest wall, diaphragm
Pleural Effusions
Pneumothorax
Masses
Intrinsic Pulmonary Disorders
Pulmonary Edema
Pneumonia
Pneumonitis-(aspiration)
ARDS
Obstructive Lung Disease
Most common
Increased resistance to airflow
Results in air trapping (can’t breathe out)
FEV1/FVC decreased
Flow is the problem
Associated with Dynamic Compliance
Ventilator Management:
Increase I:E Ratio and decrease RR to allow more time to exhale
Allow higher EtCO2 because of dead space volume gradient
Asthma
Emphysema
Bronchitis
Cystic Fibrosis
Pulmonary Compliance
The relationship between the ∆P and the resultant volume increase ∆V of the lungs and thorax
Compliance = change in volume (V)/ change in pressure (P)
Either dynamic (peak) or static (plateau)
Static Compliance
Volume/(Plateau Pressure – PEEP)
Reflects elastic resistance of lung and chest wall
Plateau pressure is when air flow stops
Alveoli only
Pneumonia, effusion, atelectasis
Dynamic Compliance
Volume/(Peak Inspiratory Pressure-PEEP)
Reflects static compliance and airway resistance
Always lower than static compliance because PIP is always higher than plateau pressure
Peak pressure is generated when air flows
Airways AND alveoli
Asthma, bronchospasm, obstruction
AND Pneumonia, effusion, atelectasis
Airway Resistance
Poiseuille’s Law… Lecture 2, Slide 40
Force through orifice is
Proportional
to change in pressure
to radius of orifice to 4th power
Inversely proportional
to viscosity
to length
Laminar Flow
Occurs when gas passes down parallel-sided tubes at less than a certain critical velocity
Airways below main bronchi
Orifice Flow
Occurs at severe constrictions such as a nearly closed larynx or a kinked ET
Turbulent Flow
When flow exceeds the critical velocity it becomes turbulent (i.e. flow in the trachea)
Four conditions change laminar flow to turbulent
high gas flows
sharp angles within the tube
branching in the tube
a change in tube diameter
Alveolar Ventilation in Lungs
R lung > L (53% vs. 47%)
Lower < upper
Pleural pressure ↓ 1 cmH2O for every 3 cm decrease in lung height
Distribution of Ventilation and Perfusion
5 L/min blood flow to lungs
~70-100mL in pulmonary capillaries undergoing gas exchange
Capillaries perfuse more than 1 alveolus
Hypoxic pulmonary vasoconstriction
Blood flow to an unventilated area is shut down and diverted
Decreases perfusion to non-functioning areas to overcome ventilation perfusion mismatch
Anesthesia can alter this compensatory mechanism
Hypoxia and acidosis
-> pulm. vasoconstriction
Hypocapnia
-> pulmonary vasodilation
Systemic circulation has opposite effect
Zones of West
3 zones of perfusion – regardless of position
Lower portions
more blood flow
less ventilation pressure
Higher portions
less blood flow
more ventilation pressure
Zone 1 – upper = PA>Pa>Pv
Alveolar pressure continually occludes pulm. capillaries
Zone 2 – middle = Pa>PA>Pv
Pulm. capillary flow is intermittent and varies with respiration
Zone 3 – lower = Pa>Pv>PA
Pulm. capillary flow is continuous
Ventilation and Perfusion Ratios
V = Alveolar ventilation ~4L/min
Q = Pulmonary capillary perfusion ~5L/min
V/Q ratio relates to the efficiency with which lung units resaturate venous blood with O2 and eliminate CO2
Overall 0.8 for individual lung units
Can range from
1:1 = Normal, 0.3 to 3.0, most ~1.0
1:0 = Dead Space
0:1 = Shunt
0 = no ventilation, absolute shunt
∞ = no perfusion, absolute dead space
Dead Space
The portion of VT that does not participate in gas exchange
Anatomic dead space
The gas that ventilates the conducting airways (oro-nasopharynx to terminal bronchioles)
Alveolar dead space
Alveolar gas that doesn’t take part in gas exchange b/c of
underperfused alveoli (West zone 1)
“wasted ventilation”
Can be caused by large tidal volumes/PEEP
Physiologic dead space
Sum of anatomic and alveolar dead space
Normally ~33%
Calculate Dead Space
PaCO2- etCO2 gradient
Normally 3-5 mmHg
Bohr Equation=Physiological dead space
Alveolar Gas Equation
At sea level
PAO2 = 0.21(760-47) – 40/.8
PAO2 = 99.7 mmHg
Lecture 2, Slide 51
Arterial Oxygen Tension
PaO2 = 120 – (Age/3)
Normally 60-100 mmHg
A-a gradient
PAO2-PaO2
Normally ~15
Increases w/ age
A-a Gradient Example
A 40 year old patient comes in with signs of hypoxia due to a narcotic overdose. ABG show 7.3 ph, co2 of 55, Pao2 of 65, pulse ox is reading 88% and RR is 5 on room air. Calculate the A-a gradient.
A-a oxygen gradient = [(FiO2x [Patm - PH2O]) - (PaCO2÷ R)] - PaO2
[(0.21) x (760-47) – (55 ÷ 0.8)] – 65=15.98
Normal A-a gradient, we can then conclude, is due to hypoventilation and not a gas exchange issue.
A-a Gradient Example
A patient with pulmonary edema is on 80% oxygen (intubated) and their abg shows ph 7.31/ co2 55/pao2 65/86% pulse ox reading.
-a oxygen gradient = [(FiO2x [Patm - PH2O]) - (PaCO2÷ R)] - PaO2A-a gradient = [(0.80) x (760-47) – (55 ÷ 0.8)] – 65=436.65
This proves the patient is not being hypoventilated but instead has an issue with gas exchange. The pulmonary edema must be treated to see their pulse ox reading increase.
R to L Shunts
Desaturated mixed venous blood from the right heart returns to the left heart without being resaturated with O2 in the lungs
CAN produce hypoxia (cannot be overcome by increasing FIO2)
Areas where V/Q = 0
(blood shunted away from ventilated areas)
2-5% of cardiac output is normally shunted through postpulmonary shunts which include:
Thebesian
Bronchial
Mediastinal
Pleural veins
L to R Shunts
Cannot produce hypoxia
Septal defect (SD)
Blood Oxygen Content
CaO2 = (1.39 x Hgb x SaO2) + (PaO2 x .003)
Expressed in units of mL/dL or mL/100mL
Important aspect of equation reflects that simply increasing dissolved O2 is 1000x less effective than binding O2 to hemoglobin (Hgb)
In other words, increasing blood carrying capacity more effective to improve oxygenation than increasing amount of dissolved blood (ie, Increasing FiO2)
