OXYGEN THERAPY

MD SEMINARDr IRAPPA

JOSEPH PRIESTLEY•Joseph Priestley’s discovered molecular oxygen.• Lavoisier’s demonstrated the respiratory gasexchange, use of inhaled oxygen in treatment of a variety of clinical disorders accelerated rapidly during the late eighteenthcentury.

•Joseph Priestley discovered molecular oxygen in 1890.• Lavoisier’s demonstrated the respiratory gasexchange, use of inhaled oxygen in treatment of a variety of clinical disorders in the late eighteenthcentury.

INTRODUCTION Oxygen is an odorless, tasteless, colorless, and

transparent gas .

Oxygen is slightly heavier than air.

Because oxygen supports combustion, there is always danger of fire, when oxygen is being used.

Oxygen can be dispensed from a cylinder, piped in system, liquid oxygen reservoir or oxygen concentrated .

Mammalian energy is provided by anaerobic and aerobic respiration.

Aerobic respiration renders most efficient ATP production

Substantial part of critical care is targeted at treating and / or preventing hypoxia

>50% of hospitalized patients were receiving oxygen without a written order.

In a retrospective study of 90 consecutive hospitalized patients, oxygen therapy was

-prescribed inappropriately in 21 percent; -monitoring was inadequate in 85 percent; -and documentation of physiological

criteria for termination of therapy was lacking in 88 percent of all patients.

Small D, Duha A, Wieskopf B, et al. Uses and misuses of oxygen in hospitalized patients. Am J Med 1992;92:591–595.

OXYGEN CARRYING CAPACITY OF BLOOD Chemical combination with

hemoglobin30‐100 fold increase in O2 transport15‐20 fold increase in CO2 transport

97-98% Carried in Combination With Hb and 2-3% dissolved in Plasma

O2 CONTENT = 1.34 x Hb x Sat of Hb + 0.0031 x PO2

Oxygen delivery (Do2) volume of oxygen (in milliliters) that reaches the

systemic capillaries each minute DO2 = Q X CaO2 X10 Q=Cardiac output CaO2=oxygen content of arterial blood

Oxygen uptake (VO2) volume of oxygen (in mL) that leaves the capillary

blood and moves into the tissues each minute VO2 = Q X (CaO2 – CvO2) x 10

Oxygen extraction ratio (O2ER) fraction of the oxygen delivered to the capillaries that

is taken up into the tissues O2ER = VO2/DO2

Rate of oxygen uptake (VO2) from the microcirculation

Normal O2 extraction ratio – 25%Maximum O2 extraction – 50-60%

Maintaining a DO2:VO2 ratio of 4:1 or higher has been recommended as a management strategy to avoid the anaerobic threshold in critically ill patients

•Relationship between oxygen consumption (˙VO2 ) and oxygen transport (DO2 ). •The critical DO2 , indicative of the transition from supply dependent to supply-independent conditions, is denoted by the arrow. •Anaerobic metabolism existsunder supply-dependent conditions and ensueswhen oxygen consumption exceeds oxygen supply.

•Relationship between oxygen consumption (˙VO2 ) and oxygen transport (DO2 ). •The critical DO2 , indicative of the transition from supply dependent to supply-independent conditions, is denoted by the arrow. •Anaerobic metabolism existsunder supply-dependent conditions and ensueswhen oxygen consumption exceeds oxygen supply.

PAO2 = FIO2 × (PB – PH2O) – PaCO2/R FIO2 = fractional concentration of inspired O2

(0.21 when breathing room air); PB = barometric pressure (~760 mmHg at

sealevel) PH2O = water vapor pressure (47 mmHg when air

is fully saturated at 37°C) R = respiratory quotient (the ratio of CO2

production to O2 consumption, usually assumed to be 0.8)

alveolar-arterial O2 difference(PAO2 – PaO2) Normal 10-15 mm Hg Gradient increases 3 mm every decade after 30

yrs of age

FACTORS AFFECTING OXY-HEMOGLOBIN DISSOCIATION CURVE

Hyperventilation due to carotid chemo receptor stimulation becomes pronounced when the arterial partial pressure of oxygen (Pao2) falls to 40mmHg

Peripheral vasodilation with consequent systemic hypotension and eventually coma occurs if the Pao2 falls below 30mmHg

OXYGEN UPTAKE IN LUNGS Inspired O2 concentration Barometric pressure Alveolar ventilation V/Q distribution & matching O2 diffusion from alveoli to pul

capillaries

SOURCE OF OXYGEN

Oxygen concentratorsFilter the gas using a chemical sieve

material zeolite (synthetic aluminium silicate) and a

gas separation method known as pressure swing adsorption(PSA)

Nitrogen molecules are captured by the zeoliteDeliver oxygen at concentrations of 85% or greaterFlow rate upto5 L/min ( new 10 L/min)

Liquid oxygen systemsmaintain an oxygen temperature of

approximately -297°FPressure – 1.5 atm to 3.4 atmGenerate flow of 0.25 to 15 L/minMinor loss of 0.5 kg/day – stored properly to

avoid fire hazard

Compressed gas cylinders Full cylinders contain O2 at pressure – 137 atmosphere Pressure falls below 8 atm – cylinder is empty Sizes

C – 137 L/ 2.5 Kg ; D – 340 L/3.9 Kg E – 680 L/ 6.5 Kg : J – 6800 L/78 Kg

How many hours the contents last = V/F/60 V=number of litres remaining in cylinder F=flow of oxygen per minute( 60 being minutes in

hour)

Large oxygen cylinders holding 6,800 litres (230 cu ft) can last about two days at a flow rate of 2 litres per minute

OXYGEN CONCENTRATIO

N

FiO2 depends onVentilatory minute volume ( RR X TV)Flow rate of supplemental o2

For a fixed flow rate of oxygenThe greater the ventilation, the lower the

Fio2 Fixed Fio2 to a patient with varying

ventilatory requirement can be provided only if total ventilatory volume is provided at required Fio2

If entire minute ventilatory volume requirement of patient is delivered by system – high flow/fixed performance system

If proportion of minute ventilatory volume requirement is delivered by system – low flow/ variable performance

High flow systems deliver about 40 l/min of gas through the mask, which is usually sufficient to meet the total respiratory demand.

High flow system provideFixed fio2 independent of patients MV (RR X TV)

Masks contain venturi valves, which use the principle of jetmixing (Bernoulli effect)

Bernoulli's principle states that for an inviscid fluid, an increase in the speed of the fluid occurs simultaneously with a decrease in pressure

When oxygen passes through a narrow orifice it produces a high velocity stream that draws a constant proportion of room air through the base of the venturi valve causing air entrainment

Air entrainment depends onVelocity of the jet (the size of orifice and

oxygen flow rate)size of the valve ports

FiO2 depends on MVV & oxygen flow

DETERMINING REQUIRED FIO2 FOR PATIENT PaO2/PAO2 = Constant PAO2 = FiO2 x (Patm – PH20) - PaCO2/RQ

Abg drawn at room air (FiO2-0.21) gives Pa02 & PaC02

Calculate PAO2 for minimum PaO2 of 60 mmHg

Substituting PAO2 in alveolar gas equation gives FiO2

A patient of COPD has PaO2 of 35 mm Hg and PaCO2 of 58 mm Hg 0n room air; what should be the FiO2 requirement to bring PaO2 to 60mm Hg? PAO2 = FiO2 x (Patm – PH20) - PaCO2/RQ PAO2 =0.21 x (760-47) – 58/0.8 PAO2 =77 PaO2/PAO2 = Constant 35/77=60/PAO2 PAO2 = 132

Desired FiO2 for PaO2 of 60 mm Hg can be determined by substituting above PAO2 in alveolar gas equation 132=FiO2 X (760-47) – 58/0.8 FiO2 = 28.8

OXYGEN DELIVERY DEVICES

Low-flow/Variable performance devices Nasal cannula Simple masks Partial rebreathing masks Non-rebreathing masks Endotracheal & tracheostomy tubes with T-piece

High-flow/Fixed performance devices Venti-masks (air entrainment masks) Mechanical aerosol systems High-flow humidifier systems Endotracheal & tracheostomy tubes with

mechanical ventilation

NASAL CANULAS Delivers about 24 to 44% FiO2 For every 1 litre litre for minute flow of Oxygen FiO2

increases by 4 %. Flows above 6 L/min do not significantly increase Fio2

above 44 percent; these higher flows may result in drying of mucous membranes.

FiO2 varies with patient respiratory rate and tidal volumeReservoir capacity- 50 ml1l/min 24% oxygen2l/min 28% oxygen3l/min 32% oxygen4l/min 36% oxygen5l/min 40% oxygen6l/min 44% oxygen

SIMPLE MASK Reservoir capacity – 150 to 200 ml Minimum flow rate – 6 L/min (clear

exhaled gases) FiO2 – 0.4 to 0.6

PARTIAL REBREATHING MASKS Only one valve at expiration port Lacks valve between mask and reservoir First 1/3 of expired gas fills reservoir FiO2 – 0.35 to 0.8 Flow rate of O2 – 8 to 10 L/min

NON REBREATHING MASKS 2 sets of valves One at exhalation port Other between mask and reservoir FiO2 –0.4 to 1 Flow rate of O2 8 to 10 L/min Precaution – prevent Reservoir collapse in inspiration by minimum flow

PULSE-DOSE OXYGEN DELIVERY DEVICES (PDOD), DEMAND OXYGEN DELIVERY SYSTEMS (DODS)

PDOD/DODS have varying performance characteristics,which include bolusvolume, trigger sensitivity and trigger response time.

VENTI-MASKS (AIR ENTRAINMENT MASKS) Exceeds patient inspiratory demand (>30

LPM) Become variable performance device if flow

< 30 L/minFiO2 Air:Oxyge

nRecommended O2 L/min

Total gas flow

24 25:1 3 7926 15:1 3 4728 10:1 6 6830 8:1 6 5335 5:1 9 5040 3:1 12 5050 1.7:1 15 41

COLOUR CODED VENTURI MASKS

Colour of Mask attachment

Oxygen (%) Rate of OxygenL/Min (LPM)

Blue 24 2

White 28 4

Yellow 35 8

Red 40 10

Green 60 15

Copyright ©1998 BMJ Publishing Group Ltd.Bateman, N T et al. BMJ 1998;317:798-801

TRANS TRACHEAL CATHETERS Save oxygen by efficiency of 2:1 to 3:1 Risk of infection & subcutaneous

emphysema

HUMIDIFIERS Glass bottle containing water through

which oxygen is passed before being delivered to patient

Cascade humidifierUses bubble diffusionUsed with mechanical ventilators

NEBULIZERS Jet nebulizers

Based on bernoullis effect Ultrasonic nebulizers

electronic oscillator generate a high frequency ultrasonic wave, which causes the mechanical vibration of a piezoelectric element

vibrating element is in contact with a liquid reservoir and its high frequency vibration produce a vapor mist

Flow rate – 10 to 15 L/min fiO2 0.28 - 1

OXYGEN THERAPY FOR

PULMONARY DISORDERS

Hypoxemia: low levels of oxygen in the blood

Hypoxia: decreased tissue oxygenation Goal of oxygen therapy: to use the

lowest fraction of inspired oxygen for an acceptable blood oxygen level without causing harmful side effects.

SYSTEM SIGNS AND SYMPTOMS

Respiratory -Tachypnea, breathlessness, dyspnea,cyanosis

Cardiovascular- Increased cardiac output, palpitations, tachycardia, arrhythmias, hypotension, angina, vasodilatation, diaphoresis, and shock

Central nervous -Headache, impaired judgment, inappropriate behavior, confusion, euphoria, delierium, restlessness, papilledema, seizures, obtundation, coma

Neuromuscular -Weakness, tremor, asterixis, hyper-reflexia, incoordination

Metabolic -Sodium and water retention, lactic acidosis

INDICATIONS FOR OXYGEN THERAPY

American College of Chest Physicians and NHLBI

American College of Chest Physicians and NHLBI

Accepted Indications

Acute hypoxemia (Pao2 < 60 mmHg; Sao2 < 90%)

Cardiac and respiratory arrest Hypotension (systolic blood

pressure < 100 mmHg) Low cardiac output and

metabolic acidosis (bicarbonate < 18 mmol/L) Respiratory distress

(respiratory rate > 24/min)

Questionable Indications

Uncomplicated myocardial infarction

Dyspnea without hypoxemia

Sickle cell crisis Angina Severe trauma Short-term therapy or

surgical intervention.eg, post-anesthesia recovery, hip surgery

OXYGEN THERAPY IN THE HOME OR ALTERNATE SITE HEALTH CARE FACILITY Long-term oxygen therapy (LTOT) in the home or

alternate site health care facility is normally indicated for the treatment of hypoxemia. LTOT has been shown to significantly improve survival in hypoxemic patients with COPD. LTOT has been shown to reduce hospitalizations and lengths of stay

Laboratory indications: Documented hypoxemia in adults, children, and infants older than 28 days as evidenced by PaO2≤ 55 mmHg or SaO2≤ 88% in subjects breathing

room air PaO2 of 56-59 mm Hg or SaO2 or SpO2 ≤ 89% in

association with specific clinical conditions (eg, cor pulmonale, congestive heart failure, or erythrocythemia with hematocrit >56%

NONCONTINUOUS OXYGEN∗ Some patients may not demonstrate a

need for oxygen therapy at rest (normoxic) but will be hypoxemic during ambulation, sleep, or exercise.

During exercise: Pao2 < 55 mmHg or SaO2 < 88% with a low level of exertion

During sleep: Pao2 < 55 mmHg or SaO2 <88% with associated complications, such as

pulmonary hypertension, daytime sommolence, and cardiac arrhythmias

RESPIRATORY CARE •AUGUST 2007 VOL 52 NO 1

DURATION OF ADMINISTRATION Oxygen therapy use in COPD for the

treatment of chronic hypoxemia should be administered continuously (ie, 24 hours per day) atleast >15 hrs/day

During periods of sleep, activity flow may be increase by 1-2 L/min

Copyright ©2006 BMJ Publishing Group Ltd.

Currie, G. P et al. BMJ 2006;333:34-36

Long term oxygen therapy prolongs survival in hypoxaemic patients with

COPD when used for &ge;15 hours/day. (Results from the nocturnal oxygen

therapy trial (NOTT) and the MRC trial)

HYPERBARIC OXYGEN THERAPY ----------------------INDICATIONS• CO poisoning • Gas embolism • Decompression

sickness• Cyanide poisoning• Adjunct to treatment

of cancers

• Crush injury and other acute traumatic ischemia

• Blood loss anemia that refused transfusion

• Selected refractory anaerobic infections (gas gangrene, necrotizing soft tissue infections, refractory osteomyelitis)

• Radiation Necrosis

• Dermatological: compromised grafts or flaps, burns, enhancement of healing in selected problem wounds

Generally used as an adjunctive therapy

COMPLICATIONS OF OXYGEN THERAPY Supression of hypoxic ventilatory drive Effects on circulation

Vagally mediated bradycardiaMild increase in peripheral vascular resistanceSlight decrease in cardiac outputSlight decrease in pulmonary vascular

resistance Effects on respiration

1oo % o2 inhalation cause 10% decline in MV95% O2 over 3 hrs – marginally decrease

diffusion capacity

TOXIC EFECTS OF OXYGEN Generation of Oxygen free radicalse − e− + 2H e− e− + H O2 → O2·− → H2O2 → OH· → H2O. Initiate lipid peroxidation – membrane

defects Activate complement and coagulation

cascade Depletion of cellular ATP levels Denaturing of enzymes Imbalance in protease – antiprotease levels Damage to DNA

Tracheo-bronchitis Acute lung injury Bronchopulmonary dysplasiae Seizures Retrolental fibroplasia Risk of injury less at FiO2 of <0.5 even

for prolonged periods Keep FiO2 <0.6 – saturation 90%

Toxicity dose and time dependent Considerable variability in susceptibility CNS (>3ATM) Pulmonary (>2ATM)

Primary Morphologic and Cellular Changes The first three phases—initiation, inflammation,

and destruction—occur during exposure to both lethal and sublethal doses of hyperoxia.

The fourth phase—proliferation and fibrosis—occurs if there is re-exposure to sublethal oxygen levels.

PULMONARY OXYGEN TOXICITY

Lorrain Smith effect Threshold: 0.5-0.75ATM Airway collapse due to lack of other non-

respiratory gases Pulmonary physiological effects of

hyperoxia include depression of hypoxic ventilatory drive, pulmonary vasodilation, and absorption atelectasis.

Irritation (cough, burning) on deep inspiration, SOB

Progressive reduction in compliance, interstitial edema and fibrosis

FiO2<0.5 if possible Safe period of FiO2>0.5 vary from 16-

30hrs

Safe upper limit of FiO2 for chronic oxygen therapy in ambulatory setting is largely undefined

ABSORPTION ATELECTASIS

A B A B

100% O2

oxygen nitrogen

PO2 =673PCO2 = 40PH2O = 47

A BAfter ~15 minutes,blood N2 is depleted.Poorly ventilated &well perfused units (A)become atelectactic.

CNS OXYGEN TOXICITY Paul Bert effect Classically in diving Symptoms non-specific

Tunnel vision Tinnitus Irritability Tonic-clonic seizure (exposure time

before onset unpredictable)

Mx: stop O2, benzodiazepines for convulsion

Anti-oxidant enzymesSuperoxide dismutaseCatalase

Free radical scavengersVitamin EBeta carotene

Prescriptions should include 1. Source of Oxygen.2. Delivery system.3. Oxygen concentration & Flow rate.4. Duration of Administration.5. Instructions for monitoring

OXYGEN ALERT CARDOXYGEN ALERT CARD

Name: ______________________________

I am at risk of type II respiratory failure with a raised CO2 level.

Please use my % Venturi mask to achieve an

oxygen saturation of _____ % to _____ % during exacerbations

Use compressed air to drive nebulisers (with nasal oxygen a 2 l/min).If compressed air not available, limit oxygen-driven nebulisers to 6 minutes.

DRUG OXYGEN (Refer To Trust Oxygen Policy)

 

Circle target oxygen saturation88-92% 94-98% Other___

STOP DATE

Starting device/flow rate________ PRN / Continuous

PHARM

(Saturation is indicated in almost all cases except for palliative terminal care)  

SIGNATURE / PRINT NAME DATEddmmyy

Oxygen prescriptionModel for oxygen section in hospital

prescription charts

Tick if saturation not indicated

Respiratory Rate, Oxygen saturation and oxygen therapy Clinical review required if saturation is outside target rangeContinuous Oxygen / PRN / Not on oxygen therapy Target range: 88-92% 94-98% Other_____

Respiratory Rate

Respiratory Rate

Oxygen Saturation %

OxygenSaturation %

OxygenDevice or Air

OxygenDevice or Air

Oxygen flow rate L/min

Oxygen flow rate L/min

Your Initials*

Your Initials*

Model for respiratory section of observation chart

Codes for recording oxygen delivery on observation chartA Air. (Patient not requiring oxygen therapy)AX Measurement on air for a patient who is on PRN Oxygen therapyAW Measurement on air for a patient who is being weaned off oxygen but not yet discontinued on chartN Nasal CannulaeSM Simple maskV24 Venturi 24% V28 Venturi 28% V35 Venturi 35% V40 Venturi 40% V60 Venturi 60%H28 Humidified oxygen at 28% (“Quatro” or similar device) (also H 35, H40, H60)RM Reservoir MaskTM Tracheostomy MaskCP Patient on CPAP systemNIV Patient on NIV systemOTH Other device

*All changes to oxygen delivery systems must be initialled by a registered nurse or equivalent

If the patient is medically stable and in the target range on two consecutive rounds, report to a registered nurse to consider weaning off oxygen (unless the oxygen prescription is part of a timed protocol

Copyright ©2000 BMJ Publishing Group Ltd.

Dodd, M E et al. BMJ 2000;321:864-865

Charting Oxygen treatment

Critical Illness

Requiring High Levels of Oxygen

Supplementation

Serious Illness Requiring Moderate Levels of Oxygen if the Patient is HypoxaemicCOPD and Other Conditions Requiring Controlled or low-dose Oxygen TherapyConditions for which patients should be monitored closely but oxygen therapy is not required unless the patient is hypoxaemic Pres

crib

e to

targ

et

BTS RECOMMENDATIONS

Is the patient critically ill*?

Yes – treat with reservoir or bag-

valve mask

NoIs the patient at risk of hypercapnic respiratory

failure?

Yes – aim for SpO2 88-92% or level on alert

card pending ABGNo – aim for SpO2 94-98%

No – is SpO2< 85%?

Start with 24 or 28%Venturi mask

Start withnasal cannulae (2-6 l/min)or face mask (5-10 l/min)

*Critical illness is defined as cardiopulmonary arrest, shock, major trauma & head injury, near-drowning, anaphylaxis, major pulmonary haemorrhage and carbon monoxide poisoning.

Prior to Blood Gas Analysis

Yes – aim for SpO2 88-92% or level on alert

card pending ABGReduce FiO2 if SpO2 >

92%

pH < 7.35 and PaCO2 > 6.0 kPa or patient tiring

Consider NIV or IPPV

Perform Arterial Blood Gases

Yes – aim for SpO2 88-92% or level on alert

card pending ABGReduce FiO2 if SpO2 >

92%

pH < 7.35 and PaCO2 > 6.0 kPa or patient tiring

pH > 7.35 and PaCO2 > 6.0 kPa

Maintain SpO2 88-92% with lowest FiO2

Repeat ABG in 30-60 mins

Consider NIV or IPPV

Perform Arterial Blood Gases

Yes – aim for SpO2 88-92% or level on alert

card pending ABGReduce FiO2 if SpO2 >

92%

PaCO2 < 6.0 kPa

pH < 7.35 and PaCO2 > 6.0 kPa or patient tiring

pH > 7.35 and PaCO2 > 6.0 kPa

Maintain SpO2 94-98% with lowest FiO2 unless

previous NIV or IPPV

Maintain SpO2 88-92% with lowest FiO2

Repeat ABG in 30-60 mins

Consider NIV or IPPV

Perform Arterial Blood Gases

THANKS

Devices Suggested flow rate(L/min)

O2% Advantages

Disadvantages

Cannula 1liter2liter3liter4liter5liter6liter

24%28%32%36%40%44%

Light weight ,comfortable ,inexpensive , continuous use with meals and activities.

Nasal mucosa ,drying , variable fio2

Catheter 1-6liter 23-40% Inexpensive

Variable fio2,requires frequent change ,gastric distension can occur

Simple mask

5liter6liter8liter 

40%45-50%55-60%

Simple to use , inexpensive

Poor fitting,variable fio2,must remove to feeding .

Mask partial re-breather

6-15liter 70-90% Moderate O2 concentration

Warm,poor fitting ,must be removed to feeding

Mask non-breather NRM

12liter 82-100% High o2 concentration

Poor fitting

Mask nonbrather NRM

12liter 82-100% High o2 concentration

Poor fitting

Mask venturi

4 -6liter   6-8liter

24,26,28   30,35,40

Provide low levels of supplemental o2. Precise fio2 additional humidity availabe

Must be removed to eat

Mask aerosal

8-10 30-100% Good humidity,accurate fio2

Uncomfortable some.

Trachestomy colar

8-10liter 30-100% Good humidity,accurate fio2

`uncomfortable some

T-piece briggs

8-10 liter 30-100% Same as trachestomy colar

Heavy with tubing

Face tent 8-10 liter 30-100% Fairly accurate fio2

Bulky compresom

NIV - INDICATIONS Acute Type I and II Respiratory failure Chronic Type II RF / Sleep apnoea Patients who are deemed not for intubation Acidosis (pH 7.10 - 7.35 – although the lower limit is

not strictly adhered to in practice) Hypercapnia where PaCO2 ≤12KPa Tachypnoea [RR>30]

The patient should be Co-operative (i.e. not too confused) Able to maintain own airway with a good cough

reflex Haemodynamically stable

They should show clinical +/or ABG improvement within 2 hours

NIV - CONTRAINDICATIONS Competent patient declines or refuses Previously documented wish not for further

NIV (End of life decision in terminal disease)

Unco-operative or very confused patient Haemodynamic instability Respiratory arrest Patients at high risk of aspiration Facial trauma or surgery

NONINVASIVE POSITIVE-PRESSURE VENTILATION

BiPAP cycling machine delivers a set inspiratory positive airway pressure each time the client begins to inspire. At exhalation, it delivers a lower set end-expiratory pressure. Together the two pressures improve tidal volume.

Technique uses positive pressure to keep alveoli open and improve gas exchange without airway intubation.

CONTINUOUS NASAL POSITIVE AIRWAY PRESSURE

Technique delivers a set positive airway pressure throughout each cycle of inhalation and exhalation.

Effect is to open collapsed alveoli. Clients who may benefit include those with

atelectasis after surgery or cardiac-induced pulmonary edema; it may be used for sleep apnea.

NORMAL RANGE FOR OXYGEN SATURATION Normal range for healthy young adults is

approximately 96-98% (Crapo AJRCCM, 1999;160:1525) Slight Fall With Advancing Age -A study of 871 subjects

showed that age > 60 was associated with minor SpO2 reduction of 0.4% {Witting MD et al Am J Emerg Med 2008: 26: 131-136}

WHAT IS THE MINIMUM ARTERIAL OXYGEN LEVEL RECOMMENDED IN ACUTE ILLNESS

Target SaO2Critical care consensus guidelines Minimum 90%

Surviving sepsis campaign Aim at 88-95%

But these patients have intensive levels of nursing & monitoring

This guideline recommends a minimum of 94% for most patients – combines what is near normal and what is safe

EXPOSURE TO HIGH CONCENTRATIONS OF OXYGEN MAY BE HARMFUL Absorption Atelectasis even at FIO2 30-50% Intrapulmonary shunting Post-operative hypoxaemia Risk to COPD patients Coronary vasoconstriction Increased Systemic Vascular Resistance Reduced Cardiac Index Possible reperfusion injury post MI Worsens systolic myocardial performance Oxygen therapy INCREASED mortality in non-hypoxic patients with

mild-moderate stroke This guideline recommends an upper

limit of 98% for most patients. Combination of what is normal and safeHarten JM et al J Cardiothoracic Vasc Anaesth 2005; 19: 173-5

Kaneda T et al. Jpn Circ J 2001; 213-8Frobert O et al. Cardiovasc Ultrasound 2004; 2: 22Haque WA et al. J Am Coll Cardiol 1996; 2: 353-7Thomaon aj ET AL. BMJ 2002; 1406-7Ronning OM et al. Stroke 1999; 30

SOME PATIENTS ARE AT RISK OF CO2 RETENTION AND ACIDOSIS IF GIVEN HIGH DOSE OXYGEN Chronic hypoxic lung disease

COPDSevere Chronic AsthmaBronchiectasis / CF

Chest wall diseaseKyphoscoliosisThoracoplasty

Neuromuscular disease Obesity hypoventilation

WHAT IS A SAFE LOWER OXYGEN LEVEL IN ACUTE COPD?

In acute COPD pO2 above 6.7

kPa or 50 mm Hg will prevent death PaO2 above about

85%(Keep SpO2 ≥88% to allow for

oximeter error and ensure PaO2 >85% )

SaO 2

mmHg

PaO2

OxyHaemoglobin Dissociation Curve

This guideline recommends a minimum saturation of 88% for most COPD patients

Murphy R, Driscoll P, O’Driscoll R Emerg Med J 2001; 18:333-9

WHAT IS A SAFE UPPER LIMIT OF OXYGEN TARGET RANGE IN ACUTE COPD ? 47% of 982 patients with exacerbation of COPD were hypercapnic on

arrival in hospital

20% had Respiratory Acidosis (pH < 7.35)

5% had pH < 7.25 (and were likely to need ICU care)

Most hypercapnic patients with pO2 > 10 kPa were acidotic (equivalent to oxygen saturation of above ~ 92%)

i.e. They had been given too much oxygen

RECOMMENDED UPPER LIMITS Keep PaO2 below 10 kPa and

keep SpO2 ≤ 92% in acute COPD Plant et al Thorax 2000; 55:550

RECOMMENDED TARGET SATURATIONS Most patients====94 - 98% Risk of hypercapnic respiratory failure

==88 – 92%* *Or patient specific saturation on Alert Card

The molecular and cellular bases for tissue injury in oxygen toxicity are thought to be mediated biochemically by reactive free radicals, the formation of which directly depends on the oxygen concentration. Since oxygen concentration is directly proportional to partial pressure, breathing 100 percent O2 at an altitude of 5000 feet (0.8 ata), 80 percent O2 at sea level (1 ata), or 40 percent O2 in a hyperbaric chamber (2 ata) for the same duration results in a similar toxicity profile.

Extrapulmonary physiological effects of hyperoxia include suppression of erythropoiesis, systemic vasoconstriction, and depression of cardiac output.

FACTORS INFLUENCING HB DISSOCIATION CURVE

Alteration of PCO2 or pH will therefore affect oxygen availability

TYPES OF HYPOXIA

COMPLICATIONS OF HYPERBARIC THERAPY Barotrauma (middle ear and sinuses),

gas embolism on decompression Oxygen toxicity Visual problem (myopia, cataract)

O2 IN ACUTE MI For example, in patients with low oxygen-carrying capacity

(e.g., severe anemia), or in flowlimited states (e.g., acute angina pectoris), increases in Pao2 beyond 60 mmHg (yielding increases in Sao2 from 90 to 100 percent) may result in marginal, but potentially important,increases in tissue oxygen delivery.

AcuteMyocardial Infarction; Hypoxemia is extremely common in acute myocardial infarction.In such patients, oxygen administration is of unquestioned benefit. Data supporting use of oxygen therapy in nonhypoxemic patients with acute myocardial infarction is controversial. Double-blinded studies of the value of oxygen in uncomplicated myocardial infarction demonstrate nosignificant effects on morbidity or mortality.

Inadequate Cardiac Output (Low-Flow States) Oxygen has been recommended for temporary treatment of inadequate systemic perfusion resulting from cardiac failure.Although this practice seems reasonable, no clinical studies to date have proved the value of oxygen therapy in this setting. Oxygen therapy is used in conjunction with inotropic agents and other devices to assist cardiac output as definitivetreatment is undertaken.

Trauma and Hypovolemic Shock Oxygen has been advocated as adjunctive therapy in the setting of acute trauma. The low-flow state induced by acute hemorrhage is best treated by increasing the supply of circulating hemoglobin.However, supplemental oxygen as supportive therapy seems warranted until red blood cells become available for transfusion.

CARBON MONOXIDE INTOXICATION

In carbon monoxide poisoning, the Pao2 is a poor guide to the need for oxygen therapy. Despite a normal or “supranormal” Pao2 , a state of significant tissue hypoxia exists, as often indicated by a severe metabolic acidosis. Because of the high concentration of carbon monoxide–bound hemoglobin (carboxyhemoglobin), administration of supplemental oxygen does not increase tissue oxygen delivery.However, administration of pure oxygen markedly shortens the half-life of circulating carbon monoxide (80 min vs. 320 min on room air). Thus, oxygen administration for carbonmonoxide poisoning constitutes an accepted therapy. Hyperbaric oxygen administration represents the current standard of care for those patients with high carboxyhemoglobin levels and evidence of end-organ ischemia-reperfusion damage

Bernoulli principle of fluid physics for gaseous jet-mixing.As forward flowof inspired gas increases, the lateral pressure adjacent and perpendicular to the vector of flow decreases, resulting in entrainment of gas.

INDICATIONS FOR OXYGEN THERAPY Cardiac and respiratory arrest Hypoxemia ( pO2 < 58.5 mmHg,

Sat<90%) Hypotension ( Systolic BP < 100 mmHg) Low Cardiac Output and Metabolic

Acidosis ( bicarbonate <18 mmol/l) Respiratory distress ( RR>24/minute)American College of Chest Physicians and NHLBI

OXYGEN THERAPY FOR ADULTS IN THE ACUTE CARE FACILITY Indications

Documented hypoxemia. PaO2 of < 60 mm Hg or SaO2 of < 90% in subjects

breathing room air An acute care situation in which hypoxemia is

suspected, substantiation of hypoxemia is required within an appropriate period of time following initiation of therapy

Severe trauma Acute myocardial infarction Short-term therapy or surgical intervention eg, post-anesthesia recovery, hip surgery

RESPIRATORY CARE • JUNE 2002 VOL 47 NO 6

GRAPH SHOWING THE EFFECTS OF EQUIVALENT (50%) REDUCTIONS IN HEMOGLOBIN CONCENTRATION (HB) AND ARTERIAL PO2 (PAO2) ON THE OXYGEN CONCENTRATION IN ARTERIAL BLOOD (CAO2).