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Respiratory Therapy Fundamentals

The document provides an overview of respiratory therapy, defining it as a healthcare discipline focused on optimizing cardiopulmonary function. It traces the history of respiratory medicine from ancient times to the present, highlighting key developments and figures in the field. Additionally, it discusses the principles of respiratory care, including oxygen therapy, its objectives, and the physical properties of oxygen.

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0% found this document useful (0 votes)
47 views139 pages

Respiratory Therapy Fundamentals

The document provides an overview of respiratory therapy, defining it as a healthcare discipline focused on optimizing cardiopulmonary function. It traces the history of respiratory medicine from ancient times to the present, highlighting key developments and figures in the field. Additionally, it discusses the principles of respiratory care, including oxygen therapy, its objectives, and the physical properties of oxygen.

Uploaded by

David Martinez
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd

FUNDAMENTALS

OF RESPIRATORY
THERAPY
YVANNA DANNIELLEE DE JESUS- LABORERA, RTRP, MPA-HM ©

B.S. Respiratory Therapy


Foundations of Respiratory Care
Definitions:
• Respiratory Care – defined as the health care discipline that
specializes in the promotion of optimal cardiopulmonary
function and health.
• Respiratory Therapists – apply scientific principles to prevent,
identify and treat acute or chronic dysfunction of the
cardiopulmonary system.
Definitions:
• Respiratory care includes the assessment,
treatment, management, control, diagnostic
evaluation, education, and care of patients with
deficiencies and abnormalities of the
cardiopulmonary system.
HISTORY OF
RESPIRATORY
MEDICINE AND
SCIENCES
Ancient Period
• 1550 BC - world's oldest medical document, known as Ebers
Papyrus, describes an ancient Egyptian inhalational treatment for
Asthma.
• 800 BC - Biblical reference to what may be the first recorded
episode of mouth to mouth resuscitation.
• 500 to 300 BC - Hippocrates describes diseases as "humoral
disorders" and speculates that an essential substance in air enters
the heart and is then distributed throughout the body.
• 304 BC - Erasistratus of Alexandria describes the pneumatic theory
of respiration, in which air travel through the lungs to the heart then
through the air-filled arteries to the tissues of the body.
• 100 to 200 AD - Galen, in Asia Minor identifies "pneuma" as the vital
substance in inspired air that enters the heart and then the blood.
Middle Ages (500-1500 AD) and
Renaissance (1450-1600)
• 500 to 1500 AD - brings a period of little scientific
progress in the West; however, this period coincides
with the Golden Age of Arabian Medicine (850-1050 AD)
• 1400 to 1500s - Leonardo Da Vinci performs human
dissections and physiologic experiments on animals,
learning that sub-atmospheric intrapleural pressures
inflates the lungs and that there is a vital substance in air
that supports combustion.
• 1542 - Andreas Vesalius, one of the great early pioneers
in human anatomy, performs a thoracotomy on a pig,
placing a reed tracheostomy tube for ventilation of the
animal, and resuscitates an apparently dead person.
Seventeenth Century
(1600's)
• 1628 - William Harvey describes arterial and venous
circulatory systems.
• 1643 - Evangelista Torricelli builds the world's first
barometer for measurement of atmospheric pressure.
• 1648 - Blaise Pascal describes the relationship between
altitude and barometric pressure.
• 1662; 1666 - Robert Boyle explains the inverse
relationship between gas pressure and volume (Boyle's
Law). Also describes a mysterious substance in air that
supports combustion.
• 1683 - Anton Van Leewenhoek improves the microscope
and begins the science of microbiology.
Eighteenth Century (1700's)
• 1738 - Daniel Bernoulli determines that as the velocity of a liquid or
gas increases, the pressure decreases. He also proposed that gases
composed of tiny particles in rapid, random motion. This idea
became the basis of modern kinetic theory of gases, which was
further developed by James Clark Maxwell in 1860.
• 1744 - John Fothergill reports successful resuscitation methods.
• 1754 - Joseph Black rediscovers CO2, which he calls "fixed air"
(prior work had been done by Jean Baptiste van Helmot in the
1600's).
• 1771 - Carl Scheele makes "fire air" (oxygen) by heating magnesium
oxide; Scheele's findings are published in June, 1774.
• 1774 - John Priestly, usually credited with the discovery of oxygen,
publishes his work on "dephlogisticated air" O2 3 months after
Scheele's report.
Eighteenth Century (1700's)
• 1775 - Antoine Lavosier renames "dephlogisticated air" "oxygen," or
"acid maker," and demonstrates that Oxygen is absorbed by the
lungs and consumed by the body, producing carbon dioxide and
water, which are exhaled.
• 1776 - John Hunter recommends use of fireplace bellows for
artificial ventilation.
• 1787 - Jacques Alexandre Cesar Charles describes the relationship
between gas temperature and volume (Charle's Law)
• 1794 - Antoine Lavosier describes oxygen absorption by the lungs
and carbon dioxide production.
• 1798 - Thomas Beddoes establishes the Pneumatic Institute in
Bristol and uses oxygen to treat a variety of disorders.
Nineteenth Century (1800's)
• 1800 - William Henry determines that the amount of gas dissolved
in liquid is directly proportioned to its partial pressure (Henry's Law).
• Adolf Fick describes a method to calculate cardiac output based on
oxygen consumption and arterial and venous oxygen content. QT =
(VO2)/(CaO2-CVO2)
• 1801 to 1808 - John Dalton describes his atomic theory and the
relationship between the partial pressures and total pressure of a
gas mixture. (Dalton's Law)
• 1806 - Simon de La Place describes relationship between pressure
and surface tension in fluid droplets.
• 1808 - Joseph Louis Gay-Lussac describes relationship between gas
pressure and temperature (Gay-Lussac's Law).
• 1811 - Amedeo Avogradro describes "Avogadro's Principle," where
equal volumes of all gases (at the same time temperature and
pressure) contain the same number of molecules.
Nineteenth Century (1800's)
• 1816 - Rene T. H. Laennec invents the stethoscope for
chest auscultation and lays the foundation for modern
pulmonology with his book, Disease of the Chest.
• 1831 - Thomas Graham describes diffusion of gases
(Graham's Law).
• 1837 - Heinrich Magnus measures arterial and venous
blood oxygen and carbon dioxide content.
• 1846 - John Hutchinson develops the spirometer a d
measures the vital capacity of over 2000 human
subjects.
• 1865 - Louis Pasteur describes his "germ theory" of
disease.
Nineteenth Century (1800's)
• 1864 - Alfred F. Jones patents a negative pressure device
to support ventilation.
• 1876 - E. J. Woillez develops the spirophore negative
pressure ventilator.
• 1878 - Paul Bert demonstrates that low inspired oxygen
levels cause hyperventilation.
• 1880 - William Mac Ewan reports success with oral
intubation.
• 1885 - Johann Friedrich Miescher-Rusch demonstrates
that CO2 is the major stimulus for breathing.
• 1886; 1904 Christian Bohr describes the oxygen
hemoglobin curve.
Nineteenth Century (1800's)
• 1888 - The Fell-O'Dwyer device combines a foot-operated
bellows with laryngeal tube for ventilatory support.
• 1895 - William Roentgen discovers the "x-ray." A direct vision
laryngoscope is introduced by Chevalier Jackson in the United
States and Alfred Kirstein i Germany.
Twentieth Century
• Early 1900's - Christian Bohr, K.A. Hasselbach, August Krogh, John
Scott Haldane, Joseph Barcroft, John Gillies Priestly, Yandell
Henderson, Lawrence J. Henderson, Wallace O. Fenn, Herman Rahn,
and others make great strides in respiratory physiology and the
understanding of oxygenation, ventilation, and acid-base balance.
• 1904 - Christian Bohr, K.A. Hasselbach, and August Krogh describes
the relationships between oxygen and carbon dioxide transport.
Ernst Sauerbruch uses a negative pressure operating chamber for
surgery in Europe.
• 1907 - Karl von Linde begins large scale commercial preparation of
oxygen.
• 1909 - Samuel James Melltzer introduces oral endotracheal
intubation.
• 1910 - O2 tents are in use, and the clinical use of aerosolized
epinephrine is introduced.
Twentieth Century
• 1911 - Heinrich Drager develops the Pulmotor ventilator for use in
resuscitation.
• 1913 - Chevalier Jackson develops a laryngoscope to insert
endotracheal tubes.
• 1918 - Oxygen mask is used to treat combat-induced pulmonary
edema.
• 1919 - Andre Strohl suggests the use of forced vital capacity (FVC) as
a measure of pulmonary function.
• 1920 - Sir Leonard Hill develops an oxygen tent to treat leg ulcers.
• 1926 - Alvan Barach develops an oxygen tent with cooling and
carbon dioxide removal.
• 1928 - Phillip Drinker develops his "iron lung" negative pressure
ventilator.
Twentieth Century
• 1938 - Barach develops the meter mask for administering dilute
oxygen. Walter Boothby, Randy Lovelace, and Arthur Bulbulian
devise the BLB mask at the Mayo Clinic for delivering high
concentrations of oxygen.
• 1940 - Isoproterenol a potent beta1 and beta2 bronchodilator
administered via aerosol, is introduced. Most common side effects
are cardiac (beta1)
• 1945 - Hurley Motley, Andre Cournand, and L. Werko use IPPB to
treat a variety of respiratory disorders.
• 1947 - The ITA is formed in Chicago, Illinois. The ITA later becomes
American Association for Respiratory Care.
• 1948 - Bennett introduces the TV-2P positive pressure ventilator.
• 1948 - FEV1 is introduced as a pulmonary function measure of
obstructive lung disease.
Twentieth Century
• 1951 - Isoetherine (Bronkosol), a preferential beta2 aersol
bronchodilator, is introduced with fewer cardiac side effects.
• 1952 - Ernst Morch introduces the piston ventilator.
• 1954 - The ITA becomes AAIT.
• 1958 - Bird introduces the Bird Mark 7 positive pressure ventilator.
• 1960 - The Campbell Ventimask for delivering dilute concentrations
of oxygen is introduced.
• 1961 - Sister Mary Yvonne Jenn becomes the first registered
respiratory therapist. Also, metaproterenol, a preferential beta2
bronchodilator, is introduced.
• 1963 - Board of School is formed to accredit inhalation therapy
educational programs.
• 1964 - The Emerson Postoperative Ventilator (3-PV) positive
pressure ventilator is introduced.
Twentieth Century
• 1967 - The Bennett MA-1 volume ventilator is introduced, ushering in the modern age
of mechanical ventilatory support for routine use in critical care units.
• 1967 - Combined pH-Clark-Severinghaus electrode is developed for rapid blood gas
analysis.
• 1968 - Fiberoptic bronchoscope becomes available for clinical use. The Engstrom 300
and Ohio 560 positive pressure volume ventilators are introduced.
• 1969 - ARDS and PEEP are describes by Thomas Petty, D.G. Ashblaugh, and D.B.
Bigelow.
• 1970 - Swan-Ganz catheter developed for measurement of pulmonary artery
pressures. American Respiratory Care Foundation is incorporated. Joint Review
Committee for Inhabitation Therapy Education is incorporated to accredit respiratory
therapy educational programs.
• 1971 - Continuous Positive Airway Pressure is introduced by Gregory. Respiratory
Care Journal is named.
• 1972 - Siemens Servo 900 is introduced.
• 1973 - IMV is described by Robert Kirby and John Downs. The AAIT becomes AART.
Twentieth Century
• 1974 - IMV Emerson ventilator is introduced.
• 1974 - National Board of Respiratory Therapy is formed.
• 1975 - Bourns Bear 1 ventilator is introduced.
• 1977 - The JRCITE becomes JRCRTE.
• 1978 - Puritan Bennett introduces the MA-2 volume ventilator. The AAR
Times magazine is introduced.
• 1979 - AIDS is recognized by the Centers for Disease Control, later Centers
for Disease Control and Prevention.
• 1982 - Siemens Servo 900C and Bourns Bear II are introduced.
• 1983 - NBRT becomes NBRC.
• 1984 - Bennett 7200 mircoprocessor controlled ventilator is introduced.
• 1984 - The AART is renamed to AARC.
• 1991 - Servo 300 ventilator is introduced.
• 1992, 1993 - AARC holds national respiratory care education consensus
conferences.
• 1998 - The CoARC is formed, replacing JRCRTE.
Twenty-First Century
• 2002 - NBRC adopts a continuing competency program for respiratory
therapists to maintain their credentials.
• 2002 - The Tripartite Statements of Support are adopted by the AARC, NBRC
and CoARC to advance respiratory care education and credentialing.
• 2003 - The AARC publishes its white paper on the development of
baccalaureate and graduate education in respiratory care. Asian Bird Flu
appears in South Korea.
• 2004 - The 50th AARC International Congress is held in New Orleans.
• 2005 - Number of working respiratory therapists in the U.S. reaches
132,651.
• 2006 - The National Heart, Lung, and Blood Institute of the U.S. Department
of Health and Human Services begins national awareness and education
campaign for COPD. AARC works with government officials to recruit and
train respiratory therapists for disaster response.
• 2007 - First AARC president to serve a 2 year term begins term of office.
• 2008 – First of three conferences held for 2015 and beyond strategic
initiative of the AARC.
Principles of
Respiratory Care
States of Matter
• Solids – have a fixed volume and shape. The molecules that made
up the solid can have the shortest distance to travel until they
collide with each other.
• Liquids – have a fixed volume, but adapt to the shape of the
container. Similar to solids, liquids are dense and cannot be
compressed easily.
• Gas – molecular attractive forces are very weak. Gas molecules
exhibit rapid, random motion with frequent collisions. Gases have
no inherent boundaries and are easily compressed and expanded.
Similar to liquids, gases can flow.
• Plasma – referred to as a fourth state of matter. It is a combination
of neutral atoms, free electrons and atomic nuclei. They can react to
electromagnetic forces and flow freely similar to a liquid or gas.
Internal Energy of Matter
Two types:
1. Potential energy – energy at rest
2. Kinetic energy – energy in motion
Heat and the first Law of
Thermodynamics
• Thermodynamics – either the science studying the properties
of matter at various temperatures or the kinetics (speed) of
reactions of matter at various temperatures.
Oxygen Therapy
Overview
• Oxygen is vital to sustain life.
• Is essential for normal cell metabolism, as tissue oxygenation is
essential for all normal physiological.
• High levels of O2 in the blood and tissue can be helpful or damaging
depending on circumstances.
• Oxygen therapy is the administration of oxygen-enriched air to a
patient as a medical intervention, which can be for a variety of
purposes in both chronic and acute patient care.
• It should be benefit the patient by increasing the supply of oxygen
to the lungs and thereby increasing the availability of O2 to the
body tissues, especially when the patient is suffering from hypoxia
and/or hypoxemia.
Overview
• RT must remember that O2 is a drug and should be
administered according to prescription as in any other
potentially-dangerous medication.
• RT must be technically competent to make patient
rounds and determine the effectiveness of the O2
therapy to satisfy expected treatment plans.
Objectives
 To recognize the physical and chemical properties of
oxygen.
 To define oxygen therapy and define the basic goals of
oxygen therapy.
 To discuss the indications, contraindications and
hazards of oxygen therapy.
 To define hypoxemia and identify the different causes
of hypoxemia.
 To recognize hypoxia and the different types of hypoxia.
 To identify the different devices used in oxygen delivery
and administration.
Physical Properties of Oxygen
• Colorless, tasteless and odorless gas that comprises of 20.95%
of the atmosphere.
• The density of O2 at 0 Celsius and 1 atm pressure is 1.429
gm/liter
• Slight solubility of 3.3/100 volumes of H2O at STP.
• Oxygen does not burn but supports combustion.
• Production of O2 is by “fractional distillation” which is the
most widely used method.
Chemical Properties of
Oxygen
• Atomic Number: 8
• Atomic Weight: 16
• Molecular Weight: 32 @ 25 Celsius
• Specific Gravity: 1.11 gm/liter
• Boiling Point: -182.96 C
• Melting Point: -218.40 C
• Critical Pressure: 715.87 psi
Definition:
• Is the administration of oxygen-enriched air to a patient as a
medical intervention, which can be for a variety of purposes in
both chronic and acute patient care.
• Oxygen therapy is administered to treat hypoxemia, of which
the immediate effect is increasing the patient’s FiO2 which
increases the alveolar O2 tension (PaO2).
Goals of Oxygen Therapy
A. To help treat hypoxemia and hypoxia
1. Hypoxemia is the diminished oxygen levels in the blood.
2. Hypoxia is the deficiency of O2 at the cellular level.
3. Hypoxemia is determined by performing blood gas
analysis.
Goals of Oxygen Therapy
B. To decrease the work of breathing.
1. When a patient is hypoxemic, the body responds by
increasing respiratory rate and/or depth of breathing.
2. To increase O2 levels, the body through the stimulation
of the peripheral chemoreceptors begins to increase the
amount of ventilation to supply more O2 to the body.
3. Supplemental O2 to treat this cause and relieves the
symptoms.
Goals of Oxygen Therapy
C. To decrease myocardial work.
1. When hypoxemia is present, the heart tries to
compensate by increasing its output to supply O2 to tissue
faster and more efficiently.
2. Supplemental O2 should alleviate the hypoxemia and
decrease myocardial work.
Clinical Indications
of Oxygen Therapy
A. Hypoventilation
1. Drug overdose
2. Neuromuscular disease
3. Shock
4. Cerebral vascular accident (CVA)
B. Cardiac Diseases
1. Myocardial infarction
2. Angina Pectoris
3. Pulmonary Edema
4. Left heart failure
5. Cardiac Arrest
C. Hypoxemia due to Respiratory Diseases
1. Emphysema
2. Bronchitis
3. Asthma
4. Pneumonia
5. Pulmonary Fibrosis
D. Shock
1. Resulting in decrease blood flow and blood pressure.
E. Noxious gas poisoning
1. Smoke inhalation
2. Chlorine
3. Carbon monoxide poisoning
4. Gasoline fumes
F. Anesthesia
1. Reaction to anesthetic gases
Hazards and
Precautions in Oxygen
Therapy
A. Oxygen-induced Hypoventilation
- this condition occurs primarily with COPD patient who has
a chronic history of hypoventilation.
1. In normal people:
a. the normal stimulus for respiration is the amount of CO2
in the blood, or more appropriately in the CSF surrounding
the pons and medulla area.
b. as the CO2 level rises in the blood, it stimulates the
respiratory system centers in the CNS and causes the
patient to breathe faster and deeper so that this excess
CO2 levels can be eliminated by ventilation.
c. as CO2 levels fall, the rate and depth of ventilation return
to their normal state.
2. In COPD patients:
a. the regulation of breathing by CO2 levels is altered in
COPD patients.
b. as the disease progresses, alveolar destruction makes
elimination of CO2 more difficult.
c. the body becomes insensitive to the normal breathing
stimulus of CO2 and become dependent on a “hypoxic
drive” with blood O2 levels serving to regulate breathing
rates.
d. high levels of O2 in the blood may now seriously retard
the patient’s respiratory rate by taking away the hypoxic
respiratory drive or may lose stimulus to breathe.
e. oxygen toxicity can be avoided by giving only enough O2
to keep PaO2 between 50-60 mmHg and by using nasal
cannula or venturi mask to give precise O2.
B. Absorption Atelectasis
1. Normally, a man breathes room air, with 20.95% oxygen and
78% nitrogen (N2) which is the bulk of gas in the lungs or alveoli.
2. This N2 is inert in the body, but it does keep the alveoli open
because it does not exert a pressure.
3. If a patient is given 100% O2, the N2 slowly washed-out of the
lungs and the body, this is what we called “nitrogen wash-out.”
4. With the N2 no longer in the alveoli, the O2 may diffuse into
the blood faster than it can be replaced by ventilation
(breathing).
5. As O2 is being diffused into the blood, the volume
of gas in the alveoli will be reduced thus
lowering the pressure, which is needed to keep it open.
6. This reduction of gas pressure may get low
enough to allow the alveoli to collapse.
7. Along with the reduction of pressures in the
alveoli, high levels of O2 cause destruction of
surfactant which also leads to alveolar collapse.
8. This can be avoided by watching your patients
vigilantly and checking the chest x-ray, blood gases
and breath sounds.
C. Oxygen toxicity
1. Oxygen, although essential to life, is considered a drug and in high
concentrations is toxic to tissue.
2. Generally, FiO2 below 40-50% will not cause any problem.
3. As the FiO2 rises from 50-100%, the faster one may see toxic effects
of O2.
4. Some toxic manifestations of O2 are:
a. Pulmonary edema
b. Intra-alveolar hemorrhage
c. Hyaline-membrane formation
d. Surfactant depletion
e. Atelectasis
f. Decreased compliance
g. Reduced muco-ciliary mobility
h. Impaired gas transfer
i. Bronchopulmonary dysplasia
j. Hypercapnia
k. Refractory hypoxemia
l. Damage to capillary epithelium
5. Effects are seen in 2 phases:
a. 1st phase – occurs after 1-4 days and is called
exudative stage. Is usually marked by endothelial
swellings, interstitial edema and loss of surfactant
to hyperplasia of Type II cells.
b. 2nd phase – occurs after 4 days and is called
the proliferative stage. This includes cellular
swelling and continued loss of surfactant along with
the development of a hyaline membrane and
thickened alveolar-capillary membrane.
6. O2 toxicity can be avoided by giving the lowest
possible FiO2 that will produce satisfactory blood
gas levels.
D. Retonipathy of Prematurity (ROP)
1. Formerly known as retrolental fibroplasia (RLF), it occurs
primarily in patients in whom the retinal arteries have not
fully developed yet.
2. PaO2 above 145-155 mmHg for as little as 4-5 hours
causes the arterioles to constrict that leads to blindness.
3. It must be remembered that it is not the FiO2 exposed to
the external eyes that causes the problem, but the PaO2
level in the blood which supplies the eye.
4. Generally keep the FiO2 under 40% and keep the PaO2
below 100 mmHg.
Hypoxemia
Definition:
• Is the low oxygen level in the blood.
• Hypoxemia can be determined by blood gas analysis.
Signs and Symptoms:
• Tachycardia
• Agitation and anxiety
• Progressive irritability
• Depression
• Headache
• Muscle weakness
• Double vision
• Difficulty with coordination
• Judgmental errors
• Loss of consciousness
• Cardiac arrhythmias
• Diaphoresis
• Cyanosis
• Drowsiness
Effect of Hypoxemia:
• Increase cardiac output
• Dilates peripheral blood vessels including cerebral vessels
• Constricts pulmonary blood vessels
• Causes proliferation of the capillary network in the skeletal
muscle.
Causes of
Hypoxemia
1. Hypoventilation
• Is caused by a decreased rate and/or decreased depth of
respirations.
• This results in a lower than normal amount of O2 in the alveoli
and decreased PaO2.
• Hypoxemia due to hypoventilation will respond to O2 therapy
by the cause of hypoventilation should also be treated.
2. Shunt
• A condition in which blood is circulated without being
oxygenated.
• Shunts do not respond to O2 therapy because a portion of the
deoxygenated blood never reaches the lungs.
• If hypoxemia does not respond to O2 therapy, it may be due
to shunt disorder.
3. Ventilation/Perfusion
Mismatch
• V/Q mismatch is the most common cause of hypoxemia.
• A low V/Q area is an area of the lung that is under ventilated
in comparison to the amount of perfusion to that area.
• This type of disorder is similar to a shunt and is often called
“shunt effect.”
• Anything that decreases the amount of ventilation to an area
of the lung will cause a V/Q mismatch. Examples are:
bronchospasms, atelectasis, pneumonia, pulmonary edema,
emphysema and other obstructive disease.
4. Diffusion Defect
• The alveolar-capillary (a-c) membrane is thickened enough to
impair diffusion of O2 across the membrane into the capillary
membrane.
• This is a rare condition because by the time the blood is 1/3 of
the way past the alveolus, it is already saturated.
Determine the cause
of Hypoxemia
A. Determine the “Partial pressure of
Inspired Oxygen”
• Formula: PiO2 = FiO2 (PB – H20)
• Where:
PB = Barometric pressure (760 mmHg)
PH20 = water vapor pressure at body
temperature, 37 C (47 mmHg)
Example :PiO2 = 0.21 (760 – 47)
= 0.21 X 713 mmHg
= 149.73 mmHg
B. Calculate “Alveolar Oxygen Tension”

• Formula: PAO2 = PiO2 – (PaCO2) X 1.25


• Where: PaCO2 = 40 mmHg
1.25 = respiratory quotient (RQ)
= normal is 0.8

Example: PAO2 = 149.73 mmHg – (40 mmHg x 1.25)


= 149.73 – 50 mmHg
= 99.73 mmHg
C. Use of “Alveolar-arterial PO2
Gradient”
• Formula: P (A – a) O2 = PAO2 – PaO2
= 99.73 mmHg – 70 mmHg
= 29.73 mmHg

Normal values:
- increases with age due to the increase in V/Q
encountered with increasing age:
- For: 30 years old = 11 mmHg
50 years old = 21 mmHg
70 years old = 30 mmHg
Interpretation:
• Normal P(A-a)O2 – in a hypoxemic patient, the sole cause of
hypoxemia is alveolar hypoventilation.
• > Normal P(A-a)O2 – the cause of hypoxemia is either due to
shunt, V/Q mismatch or diffusion defect.
Hypoxia
Definition:
• Is the deficiency of oxygen at the cellular level.
• It is not practical to measure cellular O2 levels, as values vary
from tissue to tissue and system to system and would not be
representative of the whole body.
Types of Hypoxia
1. Hypoxemic Hypoxia
• There’s an inadequate O2 in the blood for normal cellular
demand due to low FiO2.
• Causes are:
• Alveolar hypoventilation
• Low inspired PO2
• Altered V/Q ratios
• Impaired alveolar-capillary diffusion
• True venous admixture or a combination of these disturbances
2. Anemic Hypoxia
• Blood cannot carry the O2 delivered even if the PaO2 was
adequate.
• Caused by:
• Anemia, there’s not enough Hb to carry O2
• Carbon monoxide poisoning, the Hb is combined with carbon
monoxide so it cannot bind with enough O2
• Bleeding
• Sickle cell anemia
3. Ischemic or Stagnant Hypoxia
• PaO2 and Hb are adequate but blood is not moving fast
enough or perfusion is inadequate.
• The PaO2 in the blood is normal, yet the tissues suffer
from hypoxia.
• An example of hypoxia without hypoxemia.
• Caused by:
• Shock
• Cardiovascular insufficiency
• Vasoconstriction
• Venous or arterial obstruction
• Cardiac arrest
4. Histotoxic Hypoxia
• The PaO2 and circulatory time are adequate but there is a
problem at the tissue level whereby the tissue cannot utilize
the O2.
• Examples are:
• Cyanide poisoning
• Alcohol poisoning
Color coding of gas
cylinders
Color Coding of Cylinders
A. Therapeutic
1. Air Yellow
2. Oxygen Green; White (WHO)
3. O2/CO2 – Carbogen Green w/ gray cylinder
4. O2/He – Helium Green w/ brown shoulder
5. Carbon dioxide Gray
B. Anesthetic
1. Cyclopropane (CH2) Orange
2. Nitrous Oxide (N2O) Light Blue
3. Ethylene (C2H4) Red
Safety in Handling Cylinders
1. Gases Flammability Information: whenever handling
medical gas cylinders, the following information about
the flammability of gases should be observed:
a. Non-flammable – Nitrogen (N2), Carbon dioxide
(CO2), Helium (He)
b. Supports combustion – Oxygen (O2), Air, N2O,
O2/N2, O2/He
c. Flammable – Cyclopropane and Ethylene
Safety Signs
• To ensure the safety in the workplace, appropriate signs
should be posted in the patient’s room to ensure and where it
is appropriate.
• Since O2 supports combustion, a “No Smoking” sign should be
posted whenever O2 is in use.
Storage of Cylinders
• The RT is responsible for maintaining a safe environment
around gas cylinders by properly securing and/or mounting
cylinders.
Transport
• The RT should ensure safe transport off cylinders.
• Large cylinders should be transported by means of a sturdy
vehicle with the cylinders properly secured.
Volume and pressure in Medical Gas
Cylinders
• The volume of gas in a cylinder is directly related to the
cylinder pressure at a constant temperature. A tank that
is full at 2,400 psi and will be half-full at 1,200 psi.
• The pressure of a cylinder containing gas will not have a
direct relationship to volume because the pressure is
that of the gas vapor in balance with the liquid at a given
temperature.
Note: To convert cubic feet to liters:
1 cubic feet = 28.3 liters
FULL
CYLINDER CUBIC FEET OF GAS
GAS
PRESSURE
D E G H&K
O2 2,200 12.7 22.0 187 244

O2/H2 1,800 12.7 22.0 187 244

He/O2 2,200 10.8 17.7 150 194

O2/N2 2,200 187 244

AIR 2,200 187 244


Oxygen Delivery
Systems
Definition:
• Is a device that is used to administer, regulate and
supplement oxygen to a patient to increase the oxygen level in
the blood.
• The system entrains O2 and air to deliver the required FiO2 to
the patient.
Classifications of
Oxygen Delivery
Systems
High-flow or Fixed performance
• Provides a constant FiO2 by delivering gas at flow rates
exceeding the patient’s peak inspiratory flow rate.
• Uses device that entrain a fixed proportions of room air.
• One which the entire minute volume is provided to the
patient.
• Provides adequate minute ventilation to the patient in the
face of changing ventilatory patterns.
• Provides the patient with gas flow which exceeds the required
minute volume.
Low-Flow or Variable
performance
• Provide O2 at flow rates that are lower than patient’s
inspiratory demands; thus, when total ventilation exceeds the
capacity of the O2 reservoir, room air is entrained.
• The final FiO2 delivered depends on the ventilatory demands
of the patient, the size of the O2 reservoir, and the rate at
which the reservoir is filled.
• At a constant flow, the larger the tidal volume, the lower the
FiO2 and vice-versa.
High Flow Oxygen
Delivery System
A. Non-Rebreather Mask
• Delivers high O2 concentrations (95% - 100%)
• Its structure is very similar to a partial rebreather mask,
except that it has the addition of three one-way valves:
one on each exhalation port and the 3rd one lies between
the patient and the reservoir bag.
• One-way valves prevent re-breathing and prevent
entrainment of room air.
• Liter flow should be adjusted so that the reservoir bag is
inflated at 2/3 during inhalation and should not collapse
on inspiration.
• If the minute volume, flow rates and reservoir are
adequate to meet the ventilatory demands of the
patient, the mask is called a high-flow system.
B. Venturi Mask
• Utilizes the venturi principle to deliver precise FiO2 concentrations.
• Ideal for patients with irregular VT rates and breathing patterns.
• The FiO2 remains the same with increases or decreases in the flow
through O2 inlet.
• The FiO2 will increase as the internal diameter of the gas injector
increases and with increased resistance or obstruction downstream.
• The FiO2 decreases as the size of the air entrainment ports are
increased.
• Total flow increases as the size of the air entrainment ports are
increased.
• Venturi masks can deliver fixed FiO2 from 24% - 50%
C. Aerosol Face Masks
• These masks are used to deliver aerosolized air to the patient
requiring long-term oxygen therapy.
• They are used with mask that has large exhalation ports to
allow exhaled air and excess aerosol to escape and large-bore
corrugated tubings to the large volume nebulizer.
• Indicated for patients with viscous secretions or an inability to
mobilize secretions with coughing or chest physiotherapy.
D. Aerosol Tracheostomy Mask/Collar

• Is used to deliver high flow aerosolized O2 for patients with


tracheostomy tube.
E. Oxygen Hood/Head Box
• Is a device placed over the head of an infant to deliver high
concentrations of O2.
• Flow ranges between 7-14 l/min should be used to prevent
CO2 build-up and maintain FiO2 without sealing the infant’s
neck around the hood.
F. Oxygen Mist Tent/Croupette
• Is used for pediatric patients requiring a controlled environment.
• Set flow between 12-15 l/min to prevent CO2 build-up inside the
tent.
• Variable FiO2 at 40-50% and difficult to control.
Low Flow Oxygen Delivery
Devices
A. Nasal Cannula
• Used to administer O2 via the nasal pharynx via two short
prongs inserted into the nares and through which gas flow
enters.
• It can deliver FiO2 between 24-45% though the exact FiO2 will
depend on the patient’s respiratory rate, VT and inspiratory
flow.
• Liter flow should not exceed more than 6 l/min as this will
cause headache and dryness of the nasal mucosa.
• To approximate FiO2, for every 1 l/min increase in flow, FiO2
increases by 4%.
B. Simple Face Mask
• Is an oxygen delivery device designed to deliver an FiO2
between 40-50% using flow of 6-10 l/min.
• Flow should be not less than 5 l/min to flush-out exhaled CO2.
C. Partial Re-breather Mask
• Is an oxygen deliver device similar to the simple face mask,
except that it incorporates a reservoir bag.
• It can deliver an FiO2 using flow from 6-10 l/min.
• Adjust flow to keep the reservoir bag inflated at least 2/3
during inhalation.
Administration Flow rate (L/min) Approximate
Device FiO2

Nasal Cannula 1 0.24

2 0.28

3 0.31

4 0.34

5 0.37

6 0.40
Administration Flow rate (L/min) Approximate
Device FiO2

Venturi Mask (24%) 4 0.24

(28%) 4 0.28

(35%) 8 0.35

(40%) 8 0.40
Administration Flow rate (L/min) Approximate
Device FiO2

Simple Mask 6 0.35

7 0.40

8 0.45

9 0.50

10 0.55
Administration Flow rate (L/min) Approximate
Device FiO2

Partial rebreathing 6 0.35


mask
7 0.40

8 0.45

9 0.50

10 0.60
Administration Flow rate (L/min) Approximate
Device FiO2

Face Tent 15 0.30-0.40


(40%)

(70%) 15 0.45-0.55

(100%) 15 0.45-0.55
Administration Flow rate (L/min) Approximate
Device FiO2

Aerosol/Tracheal 15 0.35-0.40
mask (40%)

(70%) 15 0.45-0.60

(100%) 15 0.45-0.60
Venturi ratios and gas flows
FiO2 O2 Flow rate Air entrainment Total gas flow
ratio (L/min)
0.24 4 25:1 97

0.28 4 10:1 44

0.35 8 5:1 48

0.40 8 3:1 32

0.70 10 0.6:1 16

1.0 10 0:1 10
Conditions resulting in Hypoxemia that can be improved
by supplemental oxygen administration

Medical condition FiO2

Acute cerebral vascular accident 0.60-1.0

Acute cor pulmonale 0.60-1.0

Anaphylactic shock 1.0

Acute sepsis 0.50-1.0

Asphyxia neonatorium 0.60-1.0

Asphyxia 1.0

Asthma 0.40-0.60
Conditions resulting in Hypoxemia that can be
improved by supplemental oxygen administration

Medical condition FiO2

Bullar polio 0.60

Bronchiolitis 0.40-0.60

Burn shock 0.60-1.0

Bronchial obstruction 0.80-1.0

Congestive heart failure 0.40-0.60

Carbon monoxide poisoning 0.90-1.0

Chronic cor pulmonale 0.60-1.0

Caesarian delivery 0.25-0.40


Conditions resulting in Hypoxemia that can be
improved by supplemental oxygen administration

Medical condition FiO2

Ecclampsia 1.0

Electroshock 1.0

Fetal bradycardia 0.40-1.0

Gas poisoning (other than monoxide) 0.60-1.0

Hemorrhagic shock 0.60-1.0

Laryngotracheobronchitis 0.60-1.0

Myocardial infarction 0.60-1.0

Neurosurgery 0.40-0.60
Conditions resulting in Hypoxemia that can be improved
by supplemental oxygen administration

Medical condition FiO2

Pulmonary emphysema 0.40-1.0

Pulmonary embolism 1.0

Pulmonary edema 0.60-1.0

Pneumonia 0.40-1.0

Premature infants 0.21-0.40

Postoperative surgery 0.30-0.40

Postoperative atelectasis 0.40

Tetanus 0.60-1.0

Traumatic shock 0.60-1.0


Contraindications for Oxygen
Therapy
Oxygen toxicity
1. Early symptoms
a. retrosternal discomfort and/or tracheobronchitic
pain
b. restlessness
c. cough
d. lethargy
e. vomiting
f. dyspnea
Oxygen toxicity
2. Late signs
a. respiratory insufficiency
b. cyanosis
c. frothy or bloody sputum
d. asphyxia
Oxygen toxicity
• Healthy individuals will begin to develop symptoms after 4-12
hours of breathing 100% oxygen at 1 atmosphere.
• Oxygen toxicity is a trap that may cause the unaware clinician
to continue to increase inspired FiO2 in an attempt to treat
the obvious increased hypoxia.
Conditions that may increase a patient’s
susceptibility to oxygen toxicity
• Viral and bacterial infections
• Extremes in humidity
• Hypercapnia
• Acidosis
• Hyperthermia
• Corticosteroids
• Catecholamines
• Hyperthyroidism
• Pulmonary edema
TO SUMMARIZE:
Indications for Oxygen Therapy
• Evidence of Hypoxemia
• PaO2 of < 60 mmHg
• SpO2 of less than 90%
• Severe trauma
• Known or suspected MI or acute coronary syndrome
• Short term
• Surgery or post-anesthesia
Cautions/Hazards of Oxygen Therapy

• Oxygen induced Hypercapnia


• Chronic CO2 retainers
• Adjust saturation requirements
• Absorption atelectasis
• Oxygen toxicity
• Oxygen supports combustion and
increases fire risks
Terminologies
• High flow device vs. Low flow device
• High concentration vs. Low
concentration
• Pulse oximeter
• Titration protocols
High Flow vs. Low Flow
• Low flow adds oxygen to patients
inspiratory flow
• High flow provides all inspiratory flow
• 40-60 liters per minute
High Concentration vs. Low Concentration

• Low concentration
• 21% to 50%
• High concentration
• 50% to 100%
• Either can be high flow or low flow
Pulse Oximeter
• Inaccurate in presence of:
• Dark pigmentation
• Poor perfusion
• Some nail polishes
• Ambient light
• Movement
• Correlate with pulse
Oxygen Titration
• Protocols are written to allow staff to increase or decrease
flows or FiO2
• Usually done by one department for consistency
• Keeps SpO2 > 92% for most patients
• Keeps SpO2 between 88% and 92% for patients with COPD
• Greatly reduce the use of oxygen
Oxygen Flowmeters
• Read center of float (ball)
Oxygen Delivery Devices
• Nasal cannula
• Simple mask
• High flow/Low flow mask
• Air entrainment or Venturi mask
• Partial/Non-rebreather mask
• High flow blender
Nasal Cannula
• Two nasal prongs
• 6 to 25 ft. tubing
• Low flow
• Low concentration
Nasal Cannula
• FiO2 estimation (normal respiratory rate, rhythm and volume)
• 1 = 24%
• 2 = 28%
• 3 = 32%
• 4 = 36%
• 5 = 40%
• 6 = 44%
• Humidify > 4 liters
• Cannot exceed 6 liters unless specialty system used
Simple Oxygen Mask
• 5-10 liters per minute
• < 5 liters will not flush CO2 from
mask
• 35-50% FiO2
• Switch to cannula for meals, etc.
Air Entrainment/Venturi Mask
• High flow device
• Entrains air through side ports to
achieve high flows
• Variable entrainment ports and/or
jets adjust FiO2
• Manufacturer recommends liter flows
for each FiO2
Partial Re-breather Mask
• Low flow, medium concentration
• 40-70%
• 6-10 liters per minute
• Bag should remain at least 1/3 full
during inspiration
Non Re-breather Mask
• Low flow, high concentration
• Valves added
• 60-80%
• 10 liters per minute
• Commonly (wrongly) referred to as
100% NRB
Blender System
• Delivers both high and low
concentration at high flows
• Requires heated humidification
• High concentration mask or T-
piece
• Costly
Aerosol Generators
• Main purpose is to provide
aerosol
• Provide oxygen or air depending
on the gas source
• Require higher flows to get
aerosol output
Bag-Valve/Mask System
• With reservoir and 10-15 liters
will deliver up to 100%
• 40-60% with oxygen and no
reservoir
Oxygen Cylinders
• Changing regulators
• Identify/check cylinder contents
• “Crack” cylinders
• Attach the regulator
• Assure regulator is tight
• Open cylinder valve and read pressure
• Adjust appropriate flow
Cylinder safety
• Cylinders must be chained, or be
secured in a cart or stand at all times
• Keep cylinders away from extreme
heat or open flames
• Close valves when not in use
• Use no oil
• Do not lay cylinders on the floor
Calculation of Cylinder Duration
• D, E and H cylinders are most common
• Others may also be used
• Cylinders are considered empty at < 500psi
• Each cylinder has a tank factor for estimating contents of a full
or partially full cylinder using pressure
• H cylinder = 3.14
• E cylinder = 0.28
• D cylinder = 0.16
Calculation of Cylinder Duration

• Cylinder pressure x tank factor = duration


liter flow

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