Ch. 15 Airway Management
*Terms highlighted are on FISDAP Airway
Study Term sheet*
*Body can survive up to 6 mins w/ out oxygen
Upper Airway:
All structures above glottic opening or the space
between the vocal cords
Lower Airway: Extends from glottis to the pulmonary Ventilation-Perfusion Ratio & Mismatch (V/Q
capillary membrane Mismatch)
*Cricoid Ring-lies inferior to thyroid cartilage and forms *A failure to match ventilation & perfusion contributes
lower portion of larynx / only circumferential ring of to most O2 & CO2 exchange abnormalities
trachea *Normal resting min ventilation: 6 L/min
*Cricoid Membrane-located between thyroid and
cricoid cartilages / site of cricothyrotomy Factors Affecting Ventilation
*Epiglottis-structure that closes over trachea during Intrinsic (Internal) factors: infection, allergic reaction,
swallowing
unresponsiveness
*Glottis-narrowest portion of the airway
*Must visualize: Epiglottis, Glottis, & Vocal Cords
before intubation Factors Affecting Ventilation cont’d:
Extrinsic Factors: trauma and foreign body airway
*Surfactant- obstruction
Surfactant lubes the lungs and decreases surface
tension in the alveoli *Meds that depress CNS (in excess) lower resp. rate &
reduce Tidal Volume = decrease alveolar volume &
Oxygenation-process of loading oxygen molecules onto overall minute volume = increased CO2 in resp. &
hemoglobin molecules in bloodstream circulatory system = increased CO2 in blood (acidotic)
-for oxygenation to occur: the % of O2 inhaled during
ventilation, the fraction of inspired oxygen (FIO2), must *Neuro muscular disorders (muscular dystrophy &
be adequate polio) can affect ability of nervous system to control
-oxygenation cannot occur without ventilation but breathing 🡪 muscular dystrophy causes degeneration of
ventilation can occur without oxygenation muscle fibers, slowing muscle development and loss of
*External Respiration- muscle contractility
is the gas exchange inside of the lung,
*Internal respiration- *Blunt/penetrating trauma and burns can disrupt
is the gas exchange inside of the body in metabolizing airflow into the lungs /Trauma to the chest wall can lead
tissues to inadequate pulmonary ventilation
Hypoxia S/S Respiratory splinting-example: when a pt. w/ a flail
Early signs: Restlessness, irritability, tachycardia, and chest breathes shallow to alleviate pain
anxiety
Late signs: Mental status changes, a weak pulse, and Angioedema-edema of the deep dermis and
cyanosis subcutaneous tissue (usually due to allergic reaction)
*Responsive patients will present w/ dyspnea (SOB)
Hypoventilation- Carbon dioxide production exceeds
elimination.
,-Can occur in two ways: *Closed environments may have decrease in ambient
1. CO2 production can exceed the body’s ability to oxygen
eliminate it *CO (Carbon Monoxide) has high affinity for attaching
2. CO2 elimination can be depressed to the extent it no to hemoglobin (250%)
longer keeps up w/ normal metabolism
Internal Factors: conditions that reduce surface area for
Hyperventilation- Carbon Dioxide (Co2) elimination gas exchange also decrease body’s oxygen supply (COPD
exceeds Co2 production / Pneumonia / Pulmonary Edema)
-Co2 levels drop in blood causing: dizziness, tingling,
etc. Intrapulmonary Shunting- the presence of pulmonary
surfactant causes a decrease in alveolar surface tension,
Blood CO2 too low (Alkalosis) thus impairing the exchange of gases in the lungs.
patient’s breathing may be slow/shallow to retain CO2 nonfunctional alveoli create a barrier to the diffusion of
in attempt to decrease pH Oxygen and CO2 resulting in blood entering the lungs
Resp Alkalosis: increased resp from the rt. Side of the heart and bypassing the alveoli
Metabolic Alkalosis: decreased resp and returning deoxygenated to the left side of heart
unoxygenated
Blood CO2 too high (Acidosis)
patient’s breathing may increase to eliminate high levels *Excess lactic acid in blood 🡪 lowers pH
of CO2 from blood (Ketoacidosis / Aspirin OD)
Resp Acidosis: decreases resp *If levels of insulin decrease in body, then cellular
Metabolic Acidosis: increases resp uptake glucose decreases -without enough glucose,
cells will metabolize fatty acids resulting in Ketoacidosis
(form of metabolic acidosis)
Circulatory Compromise
When circulatory system is compromised 🡪 perfusion
becomes inadequate and the body’s oxygen demands
will not be met
*A decrease in Minute Volume = buildup of CO2 in *Obstruction of blood flow to individual cells & tissues
blood is typically related to trauma emergencies (hemothorax
*An increase in Minute Volume = decreases CO2 in / sucking chest wound / etc.) – all these conditions
blood inhibit gas exchange at the tissue level as a result of
their effects on the resp. and circulatory system
Hypercapnia or Hypercarbia-increased levels of CO2 in
blood *Cardiac tamponade, heart failure 🡪 inhibit ability of
Hypocapnia or Hypocarbia-decreased levels of CO2 in heart to effectively pump oxygenated blood to tissues
blood
*Blood loss & anemia-reduce the oxygen-carrying
Factors Affecting Oxygenation & Respiration ability of the blood-without enough circulating red
blood cells, not enough hemoglobin molecules are
External Factors: partial pressure of Oxygen (PaO2) in available to bind w/ O2
air have key role in respiration Hemorrhagic Shock (form of hypovolemic
shock)-decrease in blood volume due to severe blood
*High altitudes-% of O2 stays same, partial pressure loss which leads to inadequate oxygen delivery at the
decreases because atmospheric pressure decreases cellular level
, Vasodilatory Shock-vasodilation of blood vessels -Metabolic Alkalosis
without loss of blood volume
Metabolic Acidosis/Alkalosis
Effects of Ventilation on Cardiac Output (Words of *Fluctuations in pH due to available bicarb in body =
Wisdom) metabolic acidosis or alkalosis
*Normal breathing 🡪 negative pressure created by
breath increases venous return of blood to heart Respiratory Acidosis/Alkalosis
*Fluctuations in pH due to respiratory disorders that
*Negative intrathoracic pressure draws air into chest result in excess CO2 retention or elimination = resp.
cavity (negative pressure ventilation)-same pressure acidosis or alkalosis
draws venous blood back to heart from the head (via
superior vena cava) and abdomen (via inferior vena *Metabolic acidosis may create resp. alkalosis as a
cava) compensatory response!
*When pts transfer from negative pressure ventilation Corrective Action for Low or High etCO2 Measurement
to positive pressure ventilation (forcing of air into lungs) When Ventilating -
they lose this stimulus of venous return resulting in If etco2 is too high then do better chest compressions
decreased cardiac output or ventilate more often. If etco2 is too low then
ventilate less often
*Because positive pressure ventilation causes an Assessing Airway Patency
increase in intrathoracic pressure it creates a pressure *An unresponsive pt. has a compromised airway until
gradient which the heart must pump against 🡪 increases ruled out!
the afterload (amount of resistance against which a Gag Reflex-spastic pharyngeal and esophageal reflex
ventricle must contract) caused by stimulating the posterior pharynx to prevent
foreign bodies from entering the trachea
*The greater the pressure used to ventilate a pt. =
decreased preload (volume of blood that returns to Words of Wisdom
heart) Hypoxemia-low level of oxygen in arterial blood (can be
>The BEST way to minimize this complication is to reversed w/ supplemental oxygen)
ventilate the pt. for ONE SECOND-just enough
for chest rise-and avoid ventilating pt. too fast! Hypoxia-part of body or whole body is deprived of
adequate oxygen supply at the tissue level (requires
Acid-Base Balance more aggressive oxygen treatment-ventilation support
*Respiratory system 🡪 fastest way to eliminate excess of at times)
acid in body (CO2 blown off by lungs)
Anoxia-lack of oxygen that results in tissue & cellular
*Renal system regulates pH by filtering out or retaining death (untreated hypoxia leads to anoxia)
more Hydrogen ions and retaining or filtering out bicarb
when needed Normal Respiratory Ranges
Adults: 12-20
*Anything that inhibits resp. function can lead to acid Children: 12-37
retention and acidosis! (1 to 18 yrs.)
Infants: 30-53
Four main clinicals of presentations of acid-based (1 month-1 year)
disorders:
-Resp. Acidosis Recognizing Inadequate Breathing
-Resp. Alkalosis
-Metabolic Acidosis
*Terms highlighted are on FISDAP Airway
Study Term sheet*
*Body can survive up to 6 mins w/ out oxygen
Upper Airway:
All structures above glottic opening or the space
between the vocal cords
Lower Airway: Extends from glottis to the pulmonary Ventilation-Perfusion Ratio & Mismatch (V/Q
capillary membrane Mismatch)
*Cricoid Ring-lies inferior to thyroid cartilage and forms *A failure to match ventilation & perfusion contributes
lower portion of larynx / only circumferential ring of to most O2 & CO2 exchange abnormalities
trachea *Normal resting min ventilation: 6 L/min
*Cricoid Membrane-located between thyroid and
cricoid cartilages / site of cricothyrotomy Factors Affecting Ventilation
*Epiglottis-structure that closes over trachea during Intrinsic (Internal) factors: infection, allergic reaction,
swallowing
unresponsiveness
*Glottis-narrowest portion of the airway
*Must visualize: Epiglottis, Glottis, & Vocal Cords
before intubation Factors Affecting Ventilation cont’d:
Extrinsic Factors: trauma and foreign body airway
*Surfactant- obstruction
Surfactant lubes the lungs and decreases surface
tension in the alveoli *Meds that depress CNS (in excess) lower resp. rate &
reduce Tidal Volume = decrease alveolar volume &
Oxygenation-process of loading oxygen molecules onto overall minute volume = increased CO2 in resp. &
hemoglobin molecules in bloodstream circulatory system = increased CO2 in blood (acidotic)
-for oxygenation to occur: the % of O2 inhaled during
ventilation, the fraction of inspired oxygen (FIO2), must *Neuro muscular disorders (muscular dystrophy &
be adequate polio) can affect ability of nervous system to control
-oxygenation cannot occur without ventilation but breathing 🡪 muscular dystrophy causes degeneration of
ventilation can occur without oxygenation muscle fibers, slowing muscle development and loss of
*External Respiration- muscle contractility
is the gas exchange inside of the lung,
*Internal respiration- *Blunt/penetrating trauma and burns can disrupt
is the gas exchange inside of the body in metabolizing airflow into the lungs /Trauma to the chest wall can lead
tissues to inadequate pulmonary ventilation
Hypoxia S/S Respiratory splinting-example: when a pt. w/ a flail
Early signs: Restlessness, irritability, tachycardia, and chest breathes shallow to alleviate pain
anxiety
Late signs: Mental status changes, a weak pulse, and Angioedema-edema of the deep dermis and
cyanosis subcutaneous tissue (usually due to allergic reaction)
*Responsive patients will present w/ dyspnea (SOB)
Hypoventilation- Carbon dioxide production exceeds
elimination.
,-Can occur in two ways: *Closed environments may have decrease in ambient
1. CO2 production can exceed the body’s ability to oxygen
eliminate it *CO (Carbon Monoxide) has high affinity for attaching
2. CO2 elimination can be depressed to the extent it no to hemoglobin (250%)
longer keeps up w/ normal metabolism
Internal Factors: conditions that reduce surface area for
Hyperventilation- Carbon Dioxide (Co2) elimination gas exchange also decrease body’s oxygen supply (COPD
exceeds Co2 production / Pneumonia / Pulmonary Edema)
-Co2 levels drop in blood causing: dizziness, tingling,
etc. Intrapulmonary Shunting- the presence of pulmonary
surfactant causes a decrease in alveolar surface tension,
Blood CO2 too low (Alkalosis) thus impairing the exchange of gases in the lungs.
patient’s breathing may be slow/shallow to retain CO2 nonfunctional alveoli create a barrier to the diffusion of
in attempt to decrease pH Oxygen and CO2 resulting in blood entering the lungs
Resp Alkalosis: increased resp from the rt. Side of the heart and bypassing the alveoli
Metabolic Alkalosis: decreased resp and returning deoxygenated to the left side of heart
unoxygenated
Blood CO2 too high (Acidosis)
patient’s breathing may increase to eliminate high levels *Excess lactic acid in blood 🡪 lowers pH
of CO2 from blood (Ketoacidosis / Aspirin OD)
Resp Acidosis: decreases resp *If levels of insulin decrease in body, then cellular
Metabolic Acidosis: increases resp uptake glucose decreases -without enough glucose,
cells will metabolize fatty acids resulting in Ketoacidosis
(form of metabolic acidosis)
Circulatory Compromise
When circulatory system is compromised 🡪 perfusion
becomes inadequate and the body’s oxygen demands
will not be met
*A decrease in Minute Volume = buildup of CO2 in *Obstruction of blood flow to individual cells & tissues
blood is typically related to trauma emergencies (hemothorax
*An increase in Minute Volume = decreases CO2 in / sucking chest wound / etc.) – all these conditions
blood inhibit gas exchange at the tissue level as a result of
their effects on the resp. and circulatory system
Hypercapnia or Hypercarbia-increased levels of CO2 in
blood *Cardiac tamponade, heart failure 🡪 inhibit ability of
Hypocapnia or Hypocarbia-decreased levels of CO2 in heart to effectively pump oxygenated blood to tissues
blood
*Blood loss & anemia-reduce the oxygen-carrying
Factors Affecting Oxygenation & Respiration ability of the blood-without enough circulating red
blood cells, not enough hemoglobin molecules are
External Factors: partial pressure of Oxygen (PaO2) in available to bind w/ O2
air have key role in respiration Hemorrhagic Shock (form of hypovolemic
shock)-decrease in blood volume due to severe blood
*High altitudes-% of O2 stays same, partial pressure loss which leads to inadequate oxygen delivery at the
decreases because atmospheric pressure decreases cellular level
, Vasodilatory Shock-vasodilation of blood vessels -Metabolic Alkalosis
without loss of blood volume
Metabolic Acidosis/Alkalosis
Effects of Ventilation on Cardiac Output (Words of *Fluctuations in pH due to available bicarb in body =
Wisdom) metabolic acidosis or alkalosis
*Normal breathing 🡪 negative pressure created by
breath increases venous return of blood to heart Respiratory Acidosis/Alkalosis
*Fluctuations in pH due to respiratory disorders that
*Negative intrathoracic pressure draws air into chest result in excess CO2 retention or elimination = resp.
cavity (negative pressure ventilation)-same pressure acidosis or alkalosis
draws venous blood back to heart from the head (via
superior vena cava) and abdomen (via inferior vena *Metabolic acidosis may create resp. alkalosis as a
cava) compensatory response!
*When pts transfer from negative pressure ventilation Corrective Action for Low or High etCO2 Measurement
to positive pressure ventilation (forcing of air into lungs) When Ventilating -
they lose this stimulus of venous return resulting in If etco2 is too high then do better chest compressions
decreased cardiac output or ventilate more often. If etco2 is too low then
ventilate less often
*Because positive pressure ventilation causes an Assessing Airway Patency
increase in intrathoracic pressure it creates a pressure *An unresponsive pt. has a compromised airway until
gradient which the heart must pump against 🡪 increases ruled out!
the afterload (amount of resistance against which a Gag Reflex-spastic pharyngeal and esophageal reflex
ventricle must contract) caused by stimulating the posterior pharynx to prevent
foreign bodies from entering the trachea
*The greater the pressure used to ventilate a pt. =
decreased preload (volume of blood that returns to Words of Wisdom
heart) Hypoxemia-low level of oxygen in arterial blood (can be
>The BEST way to minimize this complication is to reversed w/ supplemental oxygen)
ventilate the pt. for ONE SECOND-just enough
for chest rise-and avoid ventilating pt. too fast! Hypoxia-part of body or whole body is deprived of
adequate oxygen supply at the tissue level (requires
Acid-Base Balance more aggressive oxygen treatment-ventilation support
*Respiratory system 🡪 fastest way to eliminate excess of at times)
acid in body (CO2 blown off by lungs)
Anoxia-lack of oxygen that results in tissue & cellular
*Renal system regulates pH by filtering out or retaining death (untreated hypoxia leads to anoxia)
more Hydrogen ions and retaining or filtering out bicarb
when needed Normal Respiratory Ranges
Adults: 12-20
*Anything that inhibits resp. function can lead to acid Children: 12-37
retention and acidosis! (1 to 18 yrs.)
Infants: 30-53
Four main clinicals of presentations of acid-based (1 month-1 year)
disorders:
-Resp. Acidosis Recognizing Inadequate Breathing
-Resp. Alkalosis
-Metabolic Acidosis
