Captain Paramedic Gene McDaniel

Phoenix Fire Department

EMS Division
MECHANICS OF RESPIRATION

Understanding Airway
Management….or Not
 Goals of Respiration
Primary Goals Of The Respiration System

• Distribute air & blood flow for gas exchange

• Provide oxygen to cells in body tissues
• Remove carbon dioxide from body
• Maintain constant homeostasis for metabolic needs
 Functions of Respiration

Respiration divided into four functional events:

1.Mechanics of pulmonary ventilation

2.Diffusion of O2 & CO2 between alveoli and blood
3.Transport of O2 & CO2 to and from tissues
4.Regulation of ventilation & respiration
 External & Internal Respiration
External Respiration Internal Respiration
• Mechanics of breathing • Intracellular oxygen
• The movement of gases metabolism
into & out of body • Cellular transformation
• Gas transfer from lungs • Krebs cycle – aerobic
to tissues of body ATP generation
• Maintain body & • Mitochondria & O2
cellular homeostasis utilization
 Pulmonary Ventilation
The main purpose of ventilation is to maintain an
optimal composition of alveolar gas

• Alveolar gas acts a stabilizing buffer compartment between the

environment & pulmonary capillary blood
– Oxygen constantly removed from alveolar gas by blood
– Carbon dioxide continuously added to alveoli from blood
– O2 replenished & CO2 removed by process of ventilation, by simple diffusion.

• The two ventilation phases (inspiration & expiration) provide this

stable alveolar environment

• Breathing is the act of creating inflow & outflow of air between the
atmosphere and the lung alveoli
 Physiological Lung Structure
• Lung weighs 1.5% of body weight
– 1 kg in 70 kg adult
– Alveolar tissue is 60% of lung weight

• Alveoli have very large surface area

– 70 m2 internal surface area
– 40 x the external body surface area

• Short diffusion pathway for gases

– Permits rapid & efficient gas exchange into blood
– 1.5 µm between air & alveolar capillary RBC
– Blood volume in lung - 500ml (10% of total blood volume)
 Respiratory Mechanics
Multiple factors required
to alter lung volumes
• Respiratory muscles generate force to inflate &
deflate the lungs
• Tissue elastance & resistance impedes
ventilation
• Distribution of air movement within the lung,
resistance within the airway
• Overcoming surface tension within alveoli
 The Breathing Cycle
• Airflow requires a pressure gradient
• Air flow from higher to lower pressures
• During inspiration alveolar pressure is sub-
atmospheric allowing airflow into lungs
• Higher pressure in alveoli during expiration
than atmosphere allows airflow out of lung
• Changes in alveolar pressure are generated by
changes in pleural pressure
 Inspiration
Active Phase Of Breathing Cycle
• Motor impulses from brainstem activate muscle contraction
• Phrenic nerve (C 3,4,5) transmits motor stimulation to diaphragm
• Intercostal nerves (T 1-11) send signals to the external intercostal
muscles
• Thoracic cavity expands to lower pressure in pleural space
surrounding the lungs
• Pressure in alveolar ducts & alveoli decreases
• Fresh air flows through conducting airways into terminal air spaces
until pressures are equalized
• Lungs expand passively as pleural pressure falls
• The act of inhaling is negative-pressure ventilation
 Muscles of Inspiration: Diaphragm
Most Important Muscle Of Inspiration
• Responsible for 75% of inspiratory effort
• Thin dome-shaped muscle attached to the lower ribs, xiphoid process,
lumbar vertebra
• Innervated by Phrenic nerve (Cervical segments 3,4,5)
• During contraction of diaphragm
– Abdominal contents forced downward & forward causing increase in vertical
dimension of chest cavity
– Rib margins are lifted & moved outward causing increase in the transverse
diameter of thorax
– Diaphragm moves down 1cm during normal inspiration
– During forced inspiration diaphragm can move down 10cm
• Paradoxical movement of diaphragm when paralyzed
– Upward movement with inspiratory drop of intrathoracic pressure
– Occurs when the diaphragm muscle is denervated
Diaphragm
Movement of Thorax During
Breathing Cycle
Movement of Diaphragm
 Transdiaphragmatic Pressure
• Effect of abdominal pressure on chest wall mechanics is
transmitted across the diaphragm
– Abdominal pressure equal atmospheric pressure in supine position
when respiratory muscles are relaxed
– Increasing abdominal pressure pushes diaphragm cephalad into
thoracic cavity, decreasing FRC.
• (FRC=Functional Reserve Capacity)

• FRC reduced by increased intra-abdominal pressure

situations
Examples: Pregnancy, Obesity, Bowel obstruction, Laparoscopic
surgery, Ascites, Abdominal mass, Hepatomegaly, Trendelenburg
position, Valsalva maneuver
 Muscles of Inspiration
External Intercostal Muscles
• The external intercostal muscles connect to adjacent ribs
• Responsible for 25% of inspiratory effort
• Motor neurons to the intercostal muscles originate in the respiratory
centers of the brainstem and travel down the spinal cord. The motor
nerves leave the spinal cord via the intercostal nerves. These originate
from the ventral rami of T1 to T11, they then pass to the chest wall
under each rib along with the intercostal veins and arteries.
• Contraction of EIM pulls ribs upward & forward
– Thorax diameters increase in both lateral & anteroposterior directions
– Ribs move outward in “bucket-handle” fashion
– Intercostals nerves from spinal cord roots innervate EIMs
• Paralysis of EIM does not seriously alter inspiration because
diaphragm is so effective but sensation of inhalation is decreased
 Muscles of Inspiration
Accessory Muscles
These muscles assist with forced inspiration
during periods of stress or exercise

Scalene Muscle
• Attach cervical spine to apical rib
• Elevate the first two ribs during forced inspiration
Sternocleidomastoid Muscle
• Attach base of skull (mastoid process) to top of
sternum and clavicle medially
• Raise the sternum during forced inspiration
 Expiration
The Passive Phase Of Breathing Cycle

• Chest muscles & diaphragm relax contraction

• Elastic recoil of thorax & lungs return to equilibrium
• Pleural & alveolar pressures rise
• Gas flows passively out of the lung
• Expiration - active during hyperventilation & exercise
 Muscles of Active Expiration
Active expiration requires abdominal &
internal intercostals muscle contraction

• Rectus abdominus/abdominal oblique muscles

– Contraction raises intra-abdominal pressure to move diaphragm upward
– Intra-thoracic pressure raises and forces air out from lung
• Internal intercostals muscles
– Assist expiration by pulling ribs downward & inward
– Decrease the thoracic volume
– Stiffen intercostals spaces to prevent outward bulging during straining

These muscles also contract forcefully during coughing, vomiting, &

defecation
 Transpulmonary Pressure
• The pressure difference between the alveolar
pressure & pleural pressure on outside of lungs
• The alveoli tend to collapse together while the
pleural pressure attempts to pull outward
• The elastic forces which tend to collapse the
lung during respiration is Recoil Pressure
 The Pleura Space
• Two parts of the pleural membrane
– Visceral pleura is a thin serosal membrane that envelopes the lobes of the lungs
– Parietal pleura lines the inner surface of the chest wall, lateral mediastinum, and
most of the diaphragm
• Pleura space enclosed by a continuous membrane
– The two pleural membranes slide against each other
– The pleural membranes are difficult to separate apart
– Separated by a thin layer of serous fluid ( a large amount would be a pleural
effusion as seen in CHF, CA, infection)
• Pleura sac
– The continuous membranes fold to create a sac inferiorly
– Both pleura line this potential space inclosing a small amount of fluid
• Pleural fluid
– Functions as a lubricant between the membranes, prevents frictional irritation
– Causes the visceral & parietal pleura to adhere together, maintains surface
tension
– Lymphatic drainage maintains constant suction on pleura (-5cmH2O)
 Compliance of the Lungs
• Compliance is a measure of the distensibility of the lungs
• Compliance = change in lung volume/ change in lung pressure
• Cpulm = DVpulm / DPpulm
• The extent of lung expansion is dependant on increase of
transpulmonary pressure
• Normal static compliance is 70-100 ml of air/cm of H2O
transpulmonary pressure
• Different compliances for inspiration & expiration based on the
elastic forces of lungs
– Compliance reduced by higher or lower lung volumes, higher expansion
pressures, venous congestion, alveolar edema, atelectasis & fibrosis
– Compliance increased with age & emphysema secondary to alterations of
elastic fibers
 Elastic Forces of the Lung
Elastic Lung Tissue Surface Air-fluid Interface

• Elastin & Collagen fibers of lung • 2/3 of total elastic force in lung
parenchyma • Surface tension of H2O
• Natural state of these fibers is • Complex synergy between air &
contracted coils fluid holds alveoli open
• Elastic force generated by the • Without air in the alveoli a fluid
return to this coiled state after filled lung has only lung tissue
being stretched and elongated elastic forces to resist volume
• The recoil force assists to deflate changes
lungs • Surfactant in the alveoli fluid
reduces surface tension, keeps
alveoli from collapsing
 Surface Tension Elastic Forces
The net effect on the lung is to simultaneously
attempt to collapse alveoli by water tension
• Water-air interface creates tension on inner alveoli
surface
• Water has strong attraction to itself resulting in a tight
contraction of H2O molecules together
• Elastic force caused by water tension attempts to
force air out of alveoli
 Surfactant
• A synthesized fatty-acid product of Type II pneumocyte
• Surfactant lowers the surface tension of the alveoli fluid

DPPC-Dipalmitoyl phosphatidyl choline

• Hydrophobic & Hydrophilic opposing ends
• Alignment of intermolecular repulsive forces
• DPPC opposes water self-attractant elastic force to reduce
alveolar surface tension
• Reduction of surface tension greater when film compressed
closer as DPPC repel each other more
Multiple Functions of Surfactant
• Lowers surface tension of alveoli & lung
– Increases compliance of lung
– Reduces work of breathing

• Promotes stability of alveoli

– 300 million tiny alveoli have tendency to collapse
– Surfactant reduces forces causing atelectasis
– Assists lung parenchyma ‘interdependant’ support

• Prevents transudation of fluid into alveoli

– Reduces surface hydrostatic pressure effects
– Prevents surface tension forces from drawing fluid into alveoli from
capillary
 Total & Alveolar Ventilation
Total Ventilation or Minute Alveolar Ventilation
Ventilation
• Volume of fresh air entering
• Total volume of air conducted alveoli each minute (70% of total
into lungs per minute ventilation or minute ventilation)
• Single breath = Tidal Volume • Alveolar ventilation is always less
(VT) than total ventilation
• VT varies with age, sex, body • Anatomical dead space and its
position & activity portion of tidal volume (30%)
• Normal VT is 0.5 L affect amount of gas exchanged in
alveoli
• Minute ventilation = VT X freq
• Alveolar O2 concentration steady
• 6 L/min. = 0.5 L X 12 breaths/min. state achieved when supply
matches demand
 Anatomic Dead Space
• Dead Space = ventilated but not
perfused
• The portion of tidal volume
fresh air which does not go
directly to the terminal
respiratory units (30%)
• The conducting airways do not
participate in O2 & CO2
exchange
• Dead space roughly 2 ml/kg
ideal body weight or weight in
pounds
• Anatomical differs from
physiological dead space also
described as wasted ventilation
 Wasted Ventilation
• The concept of physiologic dead space (VPD)
describes a deviation from ideal ventilation relative to
blood flow

• Wasted ventilation includes anatomical dead space

plus any portion of alveolar ventilation that does not
exchange O2 or CO2 with pulmonary blood flow
(alveolar dead space)

• Ventilation/blood flow (V/Q) mismatch where blood

flow blocked ( clot or emboli)
 Features of Laminar Flow
• Laminar flow is parallel streams of flow
• Velocity in center of airway twice as fast than
at edges of tube
• Poiseuille Law describes resistance to flow
through a tube
– Pressure increases proportional to flow rate & gas
viscosity
– Smaller airway radius & longer distances increase
flow resistance
 Airflow through Tubes
• As air flows through a tube – a pressure
difference exists between the ends of tube
• This pressure difference depends on rate &
pattern of air flow
• Airflow at low flow rates is laminar
• Turbulence occurs at higher flow rates or
changes in air passageway (airway
branches/diameter/velocity/direction changes)
 Turbulent Flow
• Turbulence occurs at higher flow rates or air
velocity
• Local eddies form at sides of airway & stream
lines of flow become disorganized
• Pressure no longer proportional to flow
• Increases in density, velocity & airway
resistance make turbulence more probable
 Chief Site of Airway Resistance
*Major resistance is at the
medium-sized bronchi

• Most of pressure drop occurs

at seventh division
• Very small bronchioles have
very little resistance
– Less than 20% drop at airways
less than 2mm
– Paradox secondary to prodigious
number of small airways in
parallel
– Air velocity becomes low,
diffusion takes over
Factors Determining Airway Resistance

• Lung Volume
– Linear relationship between lung volumes & conductance
of airway resistance
– As lung volume is reduced - airway resistance increases
• Bronchial Smooth Muscle
– Contraction of airways increases resistance
– Bronchoconstriction caused by, acetylcholine, low Pco2,
direct stimulation, histamine, environmental, cold
• Density & Viscosity Of Inspired Gas
– Increased resistance to flow with elevated gas density
– Changes in density rather than viscosity have more
influence on resistance
 Work of Breathing
• Work is required to move the lung & chest
• Work represented as pressure X volume (W=PxV)
• Difficult to directly measure total work of breathing done by
movement of lung & chest wall
• Oxygen consumption measurements can be used to
determine work of breathing
– O2 cost of quiet breathing is 5% of total resting oxygen
consumption
– Hyperventilation increases O2 cost to 30%
– High O2 cost in obstructive lung disease limits exercise ability
A little pre-planning goes a long way…
“A mind once stretched by new
Ideas never regains it original
dimensions…”
 Why do we Intubate?
• Inability to protect and maintain patent airway.

• Failure of oxygenation or ventilation.

• Anticipated need based on clinical course

 Ideal conditions for intubation
• Ideal Lighting, positioning, etc.
• Plenty of assistance
• Time to prepare, plan, discuss
• Option to Abort
• Empty Stomach
• Back up available.
 Ideal Pt. for intubation
• Intact, clear airway
• Wide open mouth
• Pre-Oxygenated
• Intact respiratory drive
• Normal dentition/good oral hygiene
• Clearly identifiable and intact Neck and Face
• Big open Nostrils
• Good Neck Mobility
• Greater than 90 KG, Less than 110 kg.
If only they looked this good…
 In Reality Our patients are:
• Immobilized
• Traumatized
• Compromised
• Prioritized
• Beer-n-Pizza-ized
They Tend to look like This:
And This:
And This (after failed ETT attempt)
 OK , Here You Go!
• Mandibular Aplasia
 What does this mean to us?
• Well, many Anesthesiologist have the option to
“Abort” induction, or to work through a problem with
as much assistance as needed.
• In the REAL WORLD of EMS that is seldom the
case for Paramedics.
• However many of the BASIC principles are valid in
the clinical evaluation of Patients, and thus valuable
in our education as medics.
• Knowing these principles will improve our decision
making process and Patient Care;.
 Before intubation
• Is there another means of getting our desired
results BEFORE we attempt Direct Oral ETT?
(Especially if we RSI)
• CPAP ?
• PPV with BVM or Demand Valve?
• Nasal ETT?
• Do we have all the help we need, all Airway
equipment with us? (Suction?)
 What are we going to do if we
don’t get the Tube?

• Plans “A”, “B” and “C”

• Know this answer before you tube.

 Plan “A”: (ALTERNATE)

• Different Length of blade

• Different Type of Blade
• Different Position
 Plan “B”: (BVM and BLIND
INTUBATION Techniques )
• Can you Ventilate with a BVM? (Consider
two NPA’s and a OPA, gentile Ventilation)

• Multi-Luman Airway?

• LMA an Option?
What do we do when faced with a
Can’t Intubate Can’t Ventilate
situation?

• Plan “C”: (CRIC) Needle, Surgical, P/C

 Do YOU feel ready to enact Plans
A, B, C at a drop of a hat?
• Feel familiar with all those tools and
techniques?

• As Paramedics we should, After all we will

provide the only definitive care in these
patients.
 Thanks for Your Attention!!

Captain Paramedic Gene McDaniel

Phoenix Fire Department

EMS Division

[email protected]