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:

ColourlessOdourlessTastelessTransparent gasSlightly heavier than airConstitues 20-21% of atmospheric airEssential 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 proteins3. Biotransformation of drugs4. Oxidation of certain other substrates..

Definations:

Hypoxia: low level of oxygen at tissue levelHypoxemia: low levels of oxygen in bloodPartial 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 & measure2. Decreasing symptoms of Hypoxemia

Supplemental O2 can help relieve symptoms of hypoxiaLessen dyspnoea/work of breathingImprove 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 condition postoperative 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 required3. 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 arrestRespiratory failureCardiac failure or myocardial infarctionShock of any causeIncreased metabolic demands (eg. Burns,

multiple injuries, severe sepsis)Post operative stateCarbon 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

AnemiaCarbon monoxide poisoningMethemoglobinemiaSickle Cell Anemia

Treatment involves blood transfusions, hyperbaric chamber, bone marrow transplant

Hypoxemic Hypoxia

Low PAO2 due to the atmosphereHypoventilation – PCO2 is risingDiffusion 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 failureShockArrhythmias

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 possibleHighest PaO2 possible

Critical Adult>60% O2PaO2 >60mmHgSpO2 >90%

Stable adult, acute illness, mild hypoxemiaLow to moderate FiO2Response to therapy, not precise concentrations

Chronic dz adult, acute on chronic illnessEnsure 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

PO2Time 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

levelsPatchy infiltrates on x-ray, prominent in lower

lung fieldsMajor 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 inflamatory response)

Exudative phase• Alveolar fluid buildup (from inflamatory

response) leads tolow ventilation/perfusion ratio (shunting)hypoxemiaHyaline membranes form @ alveolar level

• Proteinaceous eosinophilic (basic) material• Composed of cellular debris & condensed

plasma proteins.Pulmonary fibrosis developPulmonary 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 O2Retinopathy of Prematurity (ROP), more

laterBronchopulmonary 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

THANK YOU!!