Hypoxia and oxygen therapy

Historical considerations

Carl Wilhelm Scheele – 1773

Discovered O2

John Pristley – 1774

Was the first to publish

a paper on O2

Antoine Lavoisier – 1777

Coined the term “O2”

Oxygen:

Colourless

Odourless

Tasteless

Transparent gas

Slightly heavier than air

Constitues 20-21% of atmospheric air

Essential for life

Importance of O2 in cell chemistry

Required in aerobic metabolism for:

1. Production of high energy phosphate compounds (ATP)

2. Dehydrogenation of flavo proteins

3. Biotransformation of drugs

4. Oxidation of certain other substrates..

Definations:

Hypoxia: low level of oxygen at tissue level

Hypoxemia: low levels of oxygen in blood

Partial pressure: the pressure exerted on a surface by the molecules of individual gases.

The partial pressure of oxygen can be calculated for a given atmospheric pressure, by multiplying concentration of a gas by the atmospheric or barometric pressure.

Eg: 760 mm Hg 21% = 160 mm Hg

Oxygen cascade

Oxygen cascade refers to the progressive decrease in the partial pressure of oxygen from the ambient air to the cellular level.

PO2 in inspired air 150-160 mm Hg

PO2 in alveolar gas (PAO2) 100- 110 mm Hg

PO2 in arterial blood (PaO2) 98 mm Hg

PO2 in Capillary blood 50-80 mm Hg

PO2 in tissues 30- 50 mm Hg

PO2 in cell mitochondria 10- 20 mmHg

Factors affecting oxygenation at various levels in O2 cascade:

Partial pressure Affected by:

Inspired oxygenPiO2

Barometric pressurePB

Oxygen concentrationFiO2

Alveolar gas PAO2

Oxygen consumptionVO2

Alveolar ventilationVA

Arterial bloodPaO2

Dead space ventilationIncreased V/Q

ShuntDecreased V/Q

Cellular PO2 Cardiac outputCO

HemoglobinHb

Oxygen therapy

Goals of oxygen therapy:

1. Correcting Hypoxemia

By raising Alveolar & Blood levels of Oxygen

Easiest objective to attain & measure

2. Decreasing symptoms of Hypoxemia

Supplemental O2 can help relieve symptoms of hypoxia

Lessen dyspnoea/work of breathing

Improve mental function

3. Minimizing Cardiopulmonary workload

Cardiopulmonary system will compensate for Hypoxemia by:

Increasing ventilation to get more O2 in the lungs & to the Blood

Increased work of breathing

Increasing Cardiac Output to get more oxygenated blood to tissues

Hard on the heart, especially if diseased

Hypoxia causes Pulmonary vasoconstritcion & Pulmonary Hypertension

These cause an increased workload on the right side of heart

Over time the right heart will become more muscular & then eventually fail (Cor Pulmonale)

Supplemental o2 can relieve hypoxemia & relieve pulmonary vasoconstriction & Hypertension, reducing right ventricular workload!!

At our institution, minimal acceptable saturation for post surgical patients who are cared for in non critical setup is 92%

Assessing the need for oxygen therapy

3 basic ways:

Laboratory measures – invasive or noninvasive

PAO2, PaO2, SaO2, SpO2 monitoring

Clinical Problem or conditionpostoperative patients, pneumonia, atelectasis,

pulmonary edema, etc…

Symptoms of hypoxemia

Eg: tachycardia, tachypnoea, hypertension, cyanosis, dyspnoea, disorientation, clubbing, etc

Methods of oxygen administration

Method selection depends upon required concentration of oxygen.

However, during oxygen therapy the relative dangers of hypoxia and O2 toxicity should be kept in mind.

Criteria for selecting the method:

1. Patient’s GCS and patient’s comfort

2. Level & range of FiO2 required

3. Extent of humidification required

Classification of O2 therapy devices

Oxygen delivery systems

Low flow systems

High flow systems

Low flow O2 delivery system

Flow does not meet inspiratory demand

Oxygen is diluted with air on inspiration

These devices have limited reservoir to store oxygen and are unable to deliver consistent inspired oxygen concentrations in settings of varying respiratory rates & tidal volumes.

Nasal prongs:

Simple face masks:

High flow O2 delivery system:

Supplies given FiO2 at flow rates higher than inspiratory demand.

They are suitable for delivering consistent and predictable concentrations of oxygen.

Uses entrainment of air to maintain oxygen supply.

Eg: venturi mask, non rebreathing mask, puritan face mask.

Air Entrainment system

Amount of air entrained varies directly with:port size

Velocity

The more air

entrained:Higher flow

Lower FiO2

Venturi mask:

Non rebreathing mask with reservoir mask:

Indications for O2 therapy:

Arterial PO2 < 60 mmHg or SaO2 < 90%

Cardiac & respiratory arrest

Respiratory failure

Cardiac failure or myocardial infarction

Shock of any cause

Increased metabolic demands (eg. Burns, multiple injuries, severe sepsis)

Post operative state

Carbon monoxide poisoning.

Hypoxia

HYPOXIA: A condition in which the oxygen available is inadequate at the tissue level

Five types of hypoxia: Anemic

Hypoxemic

Histotoxic

Circulatory

Hypermetabolic

Anemic Hypoxia

Having a decreased carrying capacity for oxygen, the pt with decreased or abnormal Hb

Anemia Carbon monoxide poisoning Methemoglobinemia Sickle Cell Anemia

Treatment involves blood transfusions, hyperbaric chamber, bone marrow transplant

Hypoxemic Hypoxia

Low PAO2 due to the atmosphere

Hypoventilation – PCO2 is rising

Diffusion Defects

The PaO2 will be lower in all cases, but the PCO2 may or may not be increased.

Treatment: Compensatory actions to reduce inequalities, supplemental oxygen

Histotoxic Hypoxia

Inability for tissues to utilize oxygen available

Cyanide Poisoning will inhibit cellular metabolism from occuring; the cells can not process the O2

Treatment: Reversal of poisoning, supplemental oxygen and/or ventilation

Circulatory Hypoxia

A decrease in cardiac output results in a low BP and a prolonged systemic transit time

The PaO2 can be high, but because of the time it takes to get to the tissues, the pt is hypoxic

Cardiovascular instability or failure Shock Arrhythmias

Treatment include increasing cardiac output with use of cardiovascular drugs and therapy, supplemental oxygen

Hypermetabolic Hypoxia

In some disease states the body requires a slight increase in metabolism (i.e. – wound healing requires 5% increase)

Extensive burns and some cancers will cause large increases metabolism to the point that supplemental O2 is required

Treatment: Supplemental O2 or FiO2

Approach to selecting appropriate O2 delivery system:

Purpose (Objective)

Increase FiO2 to correct hypoxemia

minimize symptoms of hypoxemia

Minimize Cardiopulmonary workload

Patient

Cause & severity of hypoxemia

Age

Neuro status/orientation

Airway in place/protected

Regular rate & rhythm (minute Ventilation)

Equipment Performance

The more critical, the greater need for high stable FiO2

Becomes more difficult the more critical due to pt varying pattern

Pt Categories

Emergency

Highest FiO2 possible

Highest PaO2 possible

Critical Adult

>60% O2

PaO2 >60mmHg

SpO2 >90%

Stable adult, acute illness, mild hypoxemia

Low to moderate FiO2

Response to therapy, not precise concentrations

Chronic dz adult, acute on chronic illness

Ensure adequate oxygenation without depressing Ventilation

• SpO2 85-90%

• PaO2 50-60mmHg

• Use ventilating mask to control FiO2 precision

• Assess response to therapy!!

• If not maintainable on Cannula, use masks

Pt may remove mask frequently due to

• Discomfort

• Convenience

• Change in mental status

Encourage Cannula use between mask use if mask must come off for periods

Precautions & Hazards

O2 Toxicity

Primarily affects Lungs & CNS

2 determining factors of O2 toxicity

PO2

Time of exposure

i.e., higher the PO2 & exposure time the greater the toxicity.

CNS effects occur with Hyperbaric Pressures

Pulmonary effects can occur @ clinical PO2 levels

Patchy infiltrates on x-ray, prominent in lower lung fields

Major alveolar injury

Pathophysiology

High PO2 damages capillary endothelium

Followed by interstitial edema & AC membrane thickening

Type I cells are destroyed (cells that create new lung tissue, gas exchange cells)

Type II cells proliferate (trigger inflamatoryresponse)

Exudative phase

• Alveolar fluid buildup (from inflamatory response) leads to

low ventilation/perfusion ratio (shunting)

hypoxemia

Hyaline membranes form @ alveolar level

• Proteinaceous eosinophilic (basic) material

• Composed of cellular debris & condensed plasma proteins.

Pulmonary fibrosis develop

Pulmonary Hypertension develops

Treatment: Try to keep pt alive while reducing FiO2

Cause:

Overproduction of O2 free radicals

• Byproducts of cellular metabolism

• Toxic in excessive amounts

• Normally antioxidants & other special enzymes dispose of excess free radicals

• Neutrophils (WBC’s) & macrophages flood the infiltrate the tissue & mediate inflammation response, leading to more free radicals

How much is too much?

>50% for very extended times

>PO2 the less time it takes

Goal of ideal oxygen therapy:

Use the lowest FiO2 possible to maintain adequate tissue oxygenation

Other side effects

Growing lungs are more sensitive to O2

Retinopathy of Prematurity (ROP), more later

Bronchopulmonary Dysplasia (BPD), chronic lung dz, Absorption Atelectasis, Fire hazards, etc

Depression of Ventilation Hypercarbic drive is blunted

High PCO2 no longer stimulates pt to increase Ventilation

Suppression of hypoxic driveThe only stimulus left to increase Ventilation is due to hypoxia

When you add to much O2, (remove the hypoxia) you effectively remove the neurological stimulus to breathe. (peripheral chemoreceptor’s)

• Hypoventilation occurs

CO2 continues to elevate to sedative levels

• Pt stops breathing until hypoxic again

• If CO2 is too high, they will remain sedated & causes Cardiopulmonary arrest

• Never withhold O2 therapy from a Hypoxic pt (PaO2)

Take home message!!

Oxygen is a drug, prescribe it as other drugs, ie, amount, device and time should be specified.

If patient’s SpO2 is not good with nasal cannula, consider changing the device instead of increasing flow rate.

Overzealous use of oxygen is often without justification & consideration of toxic effects of oxygen therapy. So think before such unaccounted for use of oxygen.

Bibliography:

i. Anaesthesia for medical students .

ii. The ICU book ; by Paul Marino