Therapeutic Gases Oxygen

Oxygen
Oxygen, water, and food are of fundamental
importance to the animal organism. Of these
three basic essentials for the maintenance of
life, the deprivation of oxygen leads to death
most rapidly. Therapy with oxygen is useful or
necessary for life in several diseases and
intoxications that interfere with normal
oxygenation of the blood or tissues.

Normal Oxygenation
Oxygen moves down a stepwise series
of partial pressure gradients from the
inspired air to the body's cells and their
mitochondria. Air normally contains
20.9% oxygen, equivalent (at normal
barometric pressure) to a partial
pressure of 159 mm Hg

Normal Oxygenation
Blood Oxygen Content
Oxygen

in blood is carried primarily in

chemical combination with hemoglobin and
to a small extent in physical solution in
plasma.
When fully saturated, each gram of
hemoglobin binds about 1.3 ml of oxygen.
Hemoglobin is about 98% saturated when
air is breathed under normal circumstances

FIGURE 2-1 Anchor Points of the Oxygen Dissociation Curve. The curve is
shifted to the right by an increase in temperature, P CO2, H+, and 2,3-DPG. The
oxygen concentration scale is based on a hemoglobin concentration of 14.5
g/100 ml.

FIGURE 9-3 Response of the Arterial PO2 to Increased Inspired Oxygen

Concentrations in a Lung With Various Amounts of Shunt. Note that the
PO2 remains far below the normal level for 100% oxygen. Nevertheless,
useful gains in oxygenation occur even with severe degrees of shunting.
(This diagram shows typical values only; changes in cardiac output,
oxygen uptake, etc., affect the position of the lines.)

Oxygen Deprivation
Hypoxia is the term used to
denote insufficient oxygenation
of the tissues.

Causes of Hypoxia
Prepulmonary Hypoxia. Hypoxia can be
caused by inadequate delivery of oxygen to
the lung.

results from inadequate ventilation brought about

by airway obstruction (laryngospasm,
bronchospasm), muscular weakness (disease or
neuromuscular-blocking drugs), or impaired
respiratory drive [central nervous system (CNS)
disease, opioids, anesthetics].

Causes of Hypoxia
Pulmonary Hypoxia - abnormal
pulmonary function can impair
oxygenation of the blood.
mismatch

between ventilation and

perfusion- (e.g., adult respiratory distress
syndrome, asthma, emphysema).
thickened barrier to diffusion and
intrapulmonary shunting of venous blood
(fibrosis, pulmonary edema).

Causes of Hypoxia
Postpulmonary Hypoxia
inadequate delivery of oxygen to tissues
may be the result of low cardiac output
(shock), maldistribution of cardiac output
(sepsis, vascular occlusion)
an inadequate concentration of oxygen in
arterial blood (anemia, hemoglobinopathies,
carbon monoxide poisoning).

 the

tissues may be unable to extract or

utilize sufficient oxygen. This may result
from an unusually high metabolic demand
(thyrotoxicosis, hyperpyrexia) or to
malfunction of cellular enzyme systems
(cyanide poisoning).

Effects of Hypoxia
Respiration
Cardiovascular System
Central Nervous System
Cellular and Metabolic Effects

Respiration
Ventilatory rate and depth progressively
increase during hypoxia as a result of
stimulation of carotid and aortic
chemoreceptors; minute ventilation
almost doubles when normal individuals
inspire gas with a PO2 of 50 mm Hg

Cardiovascular System
Cardiac output increases with hypoxia
as a result of increased heart rate and
decreased peripheral vascular
resistance.
Severe hypoxia, however, can produce
bradycardia and, ultimately, circulatory
failure.

CNS
The CNS is least able to tolerate hypoxia.
Hypoxia is accompanied initially by
decreased intellectual capacity and
impaired judgment and psychomotor
ability; this state progresses to confusion
and restlessness and ultimately to stupor,
coma, and death as the PaO2 decreases
below 30 to 40 mm Hg.

Cellular and Metabolic Effects

Delivery of oxygen to mitochondria slows as
the partial pressure gradient from capillaries
to tissues decreases.
At a mitochondrial PO2 of less than about 1
mm Hg (130 Pa), aerobic metabolism stops,
and the less efficient anaerobic pathways of
glycolysis become responsible for the
production of cellular energy.
The cellular concentrations of Na+, Ca2+, and
H+ increase, leading to cell death.

Adaptation to Hypoxia
Long-term hypoxia results in adaptive
physiological changes
increased numbers of pulmonary alveoli,
increased concentrations of hemoglobin in
blood and myoglobin in muscle, and a
decreased ventilatory response to hypoxia
Short-term exposure to altitude produces
similar adaptive changes

Acute exposure - "mountain sickness

a syndrome characterized initially by headache,
nausea, dyspnea, and impaired judgment,
progressing to pulmonary and cerebral edema
Mountain sickness is treated by inhalation of
oxygen, descent to lower altitude, or by an
increase in ambient pressure. Treatment with
diuretics (carbonic anhydrase inhibitors) and
steroids also may be helpful.

Effects of Oxygen
Inhalation
The primary use for inhalation of
oxygen is to reverse the effects of
hypoxia; other consequences usually
are minor. However, when oxygen is
breathed in excessive amounts, toxic
effects can occur

Respiration
Inhalation of oxygen at 1 atmosphere or
above causes a small degree of respiratory
depression in normal subjects, presumably
as a result of loss of tonic chemoreceptor
activity.
Within a few minutes, ventilation increases
because of a paradoxical increase in the
tension of carbon dioxide in tissues.

Carbon dioxide is carried by blood in the form of bicarbonate.

This mechanism of carbon dioxide transfer operates more
readily when a hydrogen ion acceptor, such as
deoxyhemoglobin (a stronger base than oxyhemoglobin), is
available.
Oxygen at a high PO2, (e.g., during hyperbaric oxygenation), the
amount of physically dissolved oxygen may be sufficient to
satisfy the requirements of tissue.
little or no oxygen is extracted from oxyhemoglobin, and
deoxyhemoglobin is not formed.
Carbon dioxide is then buffered less efficiently, and the PCO2 of
the tissues rises by several mm Hg.

Oxygen Toxicity
Oxygen toxicity probably results from an
increased production of reactive species such
as superoxide anion, singlet oxygen,
hydroxyl radical, and hydrogen peroxide. The
oxidative damage initiated by these
substances is propagated by lipid
peroxidation and ultimately involves all
components of the cell. Cell injury and death
are presumed to result from loss of
membrane integrity.

Central Nervous System. CNS oxygen

toxicity does not occur when the partial
pressure of inspired oxygen is less than 2
atmospheres; its occurrence is thus limited to
a small number of hyperbaric applications.
CNS toxicity is observed before pulmonary
toxicity when oxygen is administered at
partial pressures above 2.5 atmospheres
characterized by convulsions, which may be
preceded by visual symptoms or muscular
twitching

Therapeutic Uses
Correction of Hypoxia
Reduction of the Partial Pressure of an
Inert Gas
Oxygen as a Diluent
Hyperbaric Oxygen Therapy

CONSERVATIVE MANAGEMENT
C

OXYGEN THERAPY
Clear benefit of long term o
2 TRIALS N O T T ( Nocturnal O2 Ttherapy trial )
MRC

( Medical Rsearch Council, UK )

Continuous O2 (24 hrs/day) better than

nocturnal O2 (12 hrs/day) which is better
than no O2

OXYGEN THERAPY
MODES OF OXYGEN DELIVERY
APPARATUS
(L / MIN)
NASAL CATHETER
SEMI RIGID MASK
VENTURI MASK

O2 FLOW
%

26
4 15
6 12
40, 50, 60
SOFT PLASTIC MASK4 15
VENTILATORS
VARYING
CPAP CIRCUITS
VARYING
OXYGEN TENT
7 10

CONC.

25 40
35 - 70
24, 28, 35,
40 80
21 100
21 100
60 - 80

Nasal kanul
1liter/mt
2 l/mt
3 l/mt
4 l/mt
5 l/mt
6 l/mt

--- FiO2 = 24%

--- FiO2 = 28%
--- FiO2 = 32%
--- FiO2 = 36%
--- FiO2 = 40%
--- FiO2 = 44%

mask
5 6 l/mt --- FiO2 = 40%
6 7 l/mt --- FiO2 = 50%
7 8 l/mt --- FiO2 = 60%

PATIENTS FOR HOME OXYGEN THERAPY

STABLE COURSE OF DISEASE

2 ABGs AT ROOM AIR AT REST FOR 20 MNTS

* RESTING PaO2 < 55 FOR > 3 WKS
OR PaO2 55 59 + CLINICALLY COR PULMONALE
AND / OR HAEMATOCRIT > 55 %
* NOCTURNAL HYPOXEMIA OR HAEMATOCRIT > 55 %
OR CLINICAL PULMONARY HYPERTENSION
* NORMOXIC PATIENT WITH LESS DYSPNOEA +
INCREASING EXERCISE CAPABILITY WITH O2

OXYGEN DOSE
#

CONTINUOUS O2 FLOW 1 2 L/MIN

WITH SINGLE / DOUBLE NASAL CANNULA
WITH ADEQUATE SaO2

LOWEST FLOW TO RAISE PaO2 TO 60-65 mm

OR SaO2 88-94 %

INCREASE BASE -LINE FLOW BY 1 L / MIN

DURING SLEEP AND EXERCISE

CONTROLLED O2 THERAPY
MODERATE TO SEVERE HYPOXIA
(PaO2 <55 mm Hg) IN COPD
CAN CAUSE MORTALITY
SHOULD BE CORRECTED IMMEDIATELY
INCREASE PaO2 TO 60 mmHg WHILE
MAINTAINING PH > 7.25
SEVERITY OF ACIDOSIS IS A BETTER
PROGNOSTIC GUIDE THAN ABSOLUTE
pCO2 LEVELS.
contd

CONTROLLED OXYGEN THERAPY

contd

NORMALLY 24% - 26% INSPIRED OXYGEN

UPTO 30% IF HYPOXIA UNRELIEVED.
RESPONSE --1. RELIEF OF HYPOXIA + REDUC. IN PCO2 + CLINICAL
IMPROVEMENT
2. RELIEF OF HYPOXIA + INITIAL RISE IN PCO2
AND pH /< 7.25 LATER CHANGING TO NORMAL
WITH
FALL IN PCO2
3. IF UNCONTROLLED OXYGEN THEN RAPID RISE IN
PCO2 AND DROP IN pH <7.25 . CAN BE LETHAL.

DOMESTIC OXYGEN SYSTEM

#

LIQUID PORTABLE DEVICE ..

LIGHT WEIGHT

LONG RANGE PORTABLE CANNISTER

PRACTICAL AMBULATORY SYSTEM

BUT

MORE EXPENSIVE THAN CONCENTRATOR

ALONE
NOT AVAILABLE IN SMALLER PLACES

.. contd

DOMESTIC OXYGEN SYSTEM .

#

OXYGEN CONCENTRATOR
- LOW COST
- CONVENIENT
- ATTRACTIVE EQUIPMENT
- WIDE-SPREAD AVAILABILITY

BUT
- ELECTRICITY REQUIRED
-

NOT PORTABLE

MAY NEED BACK-UP TANK

Contd

DOMESTIC OXYGEN SYSTEM

CONTD
#

COMPRESSED GAS

LOW COST IN GENERAL

WIDE-SPREAD AVAILABILITY

BUT

MULTIPLE TANK REQUIREMENT

FREQUENT DELIVERIES REQUIRED

HEAVY & UNSIGHTLY TANKS

= DIFFICULT AMBULATION.

FUTURE TRENDS IN OXYGEN THERAPY

1)

TRANS-TRACHEAL OXYGEN

Reduction in supplemental o2

Improved exercise tolerance

Reduced hospitalisation

Better patient compliance

Cosmetic value

Hypoxia & sleep disorders avoided

cont

FUTURE TRENDS IN OXYGEN THERAPY

OXYSPECS / OXYFRAMES

CONCEALED OXYGEN TUBINGS

SINGLE / DOUBLE NASAL CANNULA

COSMETICALLY MORE ACCEPTABLE

USES SMALLER BATTERY- POWERED

OXYGEN CONCENTRATORS

DEMAND CANNULA / DEMAND SYSTEMS

ALLOWS O2 FLOW DURING

INSPIRATION ONLY

SAVES 50 % OXYGEN