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Oxygen Therapy

Oxygen was discovered independently by the Swedish apothecary Karl W.Scheele, in
1772, and by the English amateur chemist Joseph Priestly,in August 1774.

Priestley first liberated oxygen by intensely heating 'mercurius calcinatus' (mercuric
oxide) placed over liquid mercury in a closed vessel. He called this new gas
"dephlogisticated air, "oxygenated."

Joseph Priestley and Carl Wilhelm Scheele both independently discovered oxygen,
but Priestly is usually given credit for the discovery.

Priestley called the gas produced in his experiments 'dephlogisticated air' and
Scheele called his 'fire air'.

The name oxygen was created by Antoine Lavoisier who incorrectly believed that
oxygen was necessary to form all acids.

The Element Oxygen

•  Atomic Number: 8
•  Atomic Weight: 15.9994
•  Melting Point: 54.36 K (-218.79°C or -361.82°F)
•  Boiling Point: 90.20 K (-182.95°C or -297.31°F)
•  Density: 0.001429 grams per cubic centimeter
•  Phase at Room Temperature: Gas
•  Element Classification: Non-metal
•  Period Number: 2
•  Group Number: 16   Group Name: Chalcoge

Oxygen is a drug

Colorless, odorless, tasteless gas, makes up 21% of room air .It is NOT flammable but
does support combustion.

•  should be regarded as a drug .
•  Has a Drug Identification Number (DIN)
•  Oxygen  must  be  prescribed  in  all  situations  (except  for  the  immediate

management of critical illness).

• Oxygen should be prescribed to achieve a target saturation (Sp02), which

should be written on the drug chart .

Basic Concepts of Oxygen

• Composition of Room Air Nitrogen 78.08% ~78% Oxygen 20.946% ~21% Trace

gases ~1%

• Normal PO2 in arterial blood (PaO2) ≥ 95mmHg: decrease with age.
• PO2 in mitochondria ≥ 18 mmHg required to generate high energy phosphate

bonds e.x ATP

•  At rest the average adult male consumes about 225-250 ml of O2/min.
•  This can increase up to 10 folds during exercise.
•  There’s very small O2 reserve that can be consumed within 4-6  minutes of

cessation of spontaneous ventilation.

Oxygen content of blood

The theoretical maximum oxygen carrying capacity is 1.39 ml O2/g Hb, but direct
measurement gives a capacity of 1.34 ml O2/g Hb.1.34 is also known as Hüfner’s
constant.

The oxygen content of blood is the volume of oxygen carried in each 100 ml blood.
It is calculated by: (O2 carried by Hb) + (O2 in solution) = (1.34 x Hb x SpO2 x 0.01) +
(0.023 x PaO2)

Basic Concepts of Oxygen

Oxygen Cascade:

Inspired = 150 mmHg at Sea Level

↓ Alveolar PO

= 103

↓ Arterial=100

↓ Capillary= 51

↓ Mitochondrial= 1-10

(FiO

expressed as 0.21-1.0 or 21- 100%)

Clinical Conditions With Increased Risk of Hypoxia

1.  Myocardial infarction
2.  Acute pulmonary disorders
3.  Sepsis
4.  Drug overdose
5.  Liver failure
6.  Head trauma
7.  CHF
8.  Hypovolemic shock
9.  Blunt chest trauma
10. Acute neuromuscular disease
11. Acute abdomen (splinting)
12. Acute pancreatitis
13. Spinal cord injury

Indications for Oxygen Therapy

1.  Tachypnea
2.  Cyanosis
3.  Restlessness
4.  Disorientation
5.  Cardiac arrhythmias
6.  Slow bounding pulse
7.  Tachycardia
8.  Hypertension
9.  Dyspnea
10. Coma
11. Labored breathing (use of accessory muscles, nasal flaring)
12. Lethargy
13. Tremors/seizure activity

“Generally speaking”, a patient who is breathing less than 12 and more than 24 times
a minute needs oxygen of some kind

Oxygen therapy To ensure safe and effective treatment

Oxygen is required for the functioning and survival of all body tissues and deprivation
for more than a few minutes is fatal.

In immediately life threatening situations oxygen should be administered.

Hypoxaemia. Acute hypotension. Breathing inadequacy. Trauma. Acute illness. CO
poisoning. Severe anaemia. During the peri-operative period.

Oxygen therapy Humidification Is recommended if more than 4 litres/min is delivered.

Helps prevent drying of mucous membranes.

Helps prevent the formation of tenacious sputum.

Oxygen concentrations will be affected with all delivery systems if not fitted correctly
or tubing becomes kinked and ports obstructed.

The oxyhaemoglobin dissociation curve showing the relation between partial
pressure of oxygen and haemoglobin saturation

Methods of Oxygen Delivery

Most common methods of oxygen delivery include

1.  Nasal Cannula
2.  Venturi Mask
3.  100% Non-Rebreather Mask
4.  Mechanical Ventilation

1. Nasal Cannula

Comfortable, convenient, mouth breathing will not effect % of O2 delivered

Liters/min = %

•  2 l/m = 24-28%
•  3 l/m = 28-30%
•  4 l/m = 32-36%
•  5 l/m = 36-40%
•  6 l/m = 40-44%

Cannot administer > 6 liters/minute (44%)

Provides limited oxygen concentration

Used when patients cannot tolerate mask

Prongs and other uses

Concentration of 24 to 44%

Flow rate set between 1 to 6 liters

For every liter per minute of flow delivered, the oxygen concentration the
patient inhales increases by 4%

2. Venturi Mask

FiO2 Delivery

•  Blue 24% Yellow 28%
•  White 31% Green 35%
•  Pink 40%

Concerns

Tight seal is a must Interferes with eating/drinking

Condensation collection

Provides precise concentrations of oxygen

Entrainment valve to adjust oxygen delivery

Mostly used in the hospital setting for COPD patients

3. 100% Non-Rebreather

Delivery percentages

•  6 l/min = 55 – 60 %
•  8 l/min = 60 – 80 %
•  10 l/min = 80 – 90 %
•  >12 l/min = 90 + %

Benefit: Has a one way expiratory valve that prevents re-breathing expired
gases

Concern

May lead to O2 toxicity

100% Non-Rebreather Mask partial rebreather Mask

4. Mechanical Ventilation

Allows administration of 100% oxygen

Controls breathing pattern for patients who are unable to maintain adequate
ventilation

Is a temporary support that “buys time” for correcting the primary pathologic
process

Indications for Mechanical Ventilation

1.  Mechanical Failure
2.  Ventilatory Failure
3.  Oxygenation Failure
4.  General Anesthesia
5.  Post-Cardiac Arrest

Two categories of ventilators

1. Negative pressure ventilators

• Iron lung
• Cuirass ventilator

2. Positive pressure ventilators

Two categories

• Volume-cycled (volume-preset)
• Pressure-cycled (pressure-preset)

Mechanical Ventilation PEEP

• Description

Maintains a preset positive airway pressure at the end of expiration

Increases PaO2 so that FiO2 can be decreased

Increases DO2 (amt of delivered O2 to tissue)

Maximizes pulmonary compliance

Minimized pulmonary shunting

• Indications

1. PaO2 < 60 on FiO2 > 60% by recruiting dysfunctional alveoli
2. Increases intrapulmonary pressure after cardiac surgery to decrease

intrathoracic bleeding (research does not support this idea)

• Advantages

1.  Improves PaO2 and SaO2 while allowing FiO2 to be decreased
2.  Decreases the work of breathing
3.  Keeps airways from closing at end expiration (esp. in pts with surfactant

deficiency)

• Disadvantages

1. Increased functional residual capacity (increases risk for barotrauma)

2.  Can cause increased dead space and increased ICP
3.  In pts with increased ICP, must assure CO2 elimination
4.  Contraindicated:  hypovolemia,  drug  induced  low  cardiac  output,

unilateral lung disease, COPD

Mechanical Ventilation CPAP

• Description

Constant positive pressure is applied throughout the respiratory cycle
to keep alveoli open

• Indications

1. To wean without having to remove the ventilator and having to connect

to additional equipment

2. Mechanical Ventilation CPAP

• Advantages

Takes advantage of the ventilator alarm systems providing
psychological security of the ventilator being there

• Disadvantages

Patient may sense resistance as he breathes through the ventilator
tubing

Mechanical Ventilation Complications

1.  Respiratory arrest from disconnection
2.  Respiratory infection (VAP)
3.  Acid-base imbalances
4.  Oxygen toxicity
5.  Pneumothorax
6.  GI bleeding
7.  Barotrauma
8.  Decreased cardiac output

Ventilator Weaning

•  Vital Capacity at least 10 – 15 ml/kg
•  Tidal Volume > 5 ml/kg
•  Resting minute volume > 10 L per minute
•  ABG’s adequate on < 40% FiO2
•  Stable vital signs
•  Intact airway protective reflexes (strong cough)
•  Absence of dyspnea, neuromuscular fatigue, pain, diaphoresis, restlessness,

use of accessory muscles

Primary Acid-base Disorders:

1. Respiratory alkalosis - A primary disorder where the first change is a lowering of

PaCO

, resulting in an elevated pH. Compensation (bringing the pH back down

toward normal) is a secondary lowering of bicarbonate (HCO

) by the kidneys; this

reduction in HCO

is not metabolic acidosis, since it is not a primary process.

Primary Event

Compensatory Event

HCO

↓HCO

↑ pH ~ ------- ↑ pH ~ --------

↓ PaCO

↓

PaCO

2. Respiratory acidosis - A primary disorder where the first change is an elevation of

PaCO

, resulting in decreased pH. Compensation (bringing pH back up toward

normal) is a secondary retention of bicarbonate by the kidneys; this elevation of
HCO

is not metabolic alkalosis since it is not a primary process.

Primary Event Compensatory Event

HCO

↑

HCO

↓ pH ~ ---------

↑PaCO

↑

PaCO

3. Metabolic acidosis - A primary acid-base disorder where the first change is a

lowering of HCO

, resulting in decreased pH. Compensation (bringing pH back up

toward normal) is a secondary hyperventilation; this lowering of PaCO

is not

respiratory alkalosis since it is not a primary process.

Primary Event

Compensatory Event

↓ HCO

↓HCO

↓ pH ~ ------------ ↓ pH ~ ------------

PaCO

↓

PaCO

4. Metabolic alkalosis - A primary acid-base disorder where the first change is an

elevation of HCO

, resulting in increased pH. Compensation is a secondary

hypoventilation (increased PaCO

), which is not respiratory acidosis since it is not

a primary process. Compensation for metabolic alkalosis (attempting to bring pH
back down toward normal) is less predictable than for the other three acid-base
disorders.

Primary Event Compensatory Event

↑

HCO

↑HCO

↑ pH ~------------ ↑ pH ~ ---------

PaCO

↑PaCO

Some Clinical Causes

METABOLIC ACIDOSIS

↓HCO

& ↓

a. Increased anion gap

• lactic acidosis; ketoacidosis; drug poisonings

(e.g., aspirin, ethylene glycol, methanol)

b. Normal anion gap

• diarrhea; some kidney problems (e.g., renal

tubular acidosis, interstitial nephritis)

METABOLIC ALKALOSIS

↑ HCO

& ↑

a. Chloride responsive (responds to NaCl or KCl therapy): contraction

alkalosis, diuretics, corticosteroids, gastric suctioning, vomiting

b. Chloride resistant: any hyperaldosterone state (e.g., Cushing’s

syndrome, Bartter’s syndrome, severe K

depletion)

RESPIRATORY ACIDOSIS

↑PaCO

& ↓

a. Central nervous system depression (e.g., drug overdose)
b. Chest

bellows

dysfunction

(e.g.,

Guillain-Barré

syndrome,

myasthenia gravis)

c. Disease of lungs and/or upper airway (e.g., chronic obstructive lung

disease, severe asthma attack, severe pulmonary edema)

RESPIRATORY ALKALOSIS ↓PaCO

↑

a.  Hypoxemia (includes altitude)
b.  Anxiety
c.  Sepsis
d.  Any acute pulmonary insult (e.g., pneumonia, mild asthma attack, early

pulmonary edema, pulmonary embolism)