Dr SURENDRA

FNB-CCM

RTIICS KOLKATA

Oxygen is a colorless, odorless, tasteless gas that is

essential for the body to function properly and to survive.

Oxygen should be regarded as a drug. It is prescribed

to prevent/treat hypoxaemia, but not hypercapnia or

breathlessness. (Oxygen has not been shown to have

any effect on the sensation of breathlessness in non-

hypoxaemic patients.)

Oxygen saturation is considered as ‘‘the fifth vital

sign’’,

Oxygen therapy is the administration of oxygen

at a concentration greater than room air (

20.946%)

Oxygen may be necessary for life, but it doesn’t

prevent death.

there are no direct measurements of the oxygen

tension in tissues but indirect measures of tissue

oxygenation are used to guide aerobic support

The oxygenation of hemoglobin is evaluated by

the fraction of the hemoglobin in blood that is fully

saturated with O2. This is called the O2 saturation

(SO2) and can be measured using

spectrophotometry

Oxygen therapy is a key treatment in

respiratory care.

Used at cellular level as the final electron

acceptor in the electron transport chain in the

mitochondria of cell

the heart relies on oxygen to pump blood

at the alveolus the PAO2 is 100 mmHg (13.3

kPa).

The transfer of a gas across a membrane relies on

physical principles and is summarized by Fick’s

first law of diffusion:

O2 diffusion = K × A/T × P

Transport of oxygen to the cells can thus be

divided into six simple steps reliant only on the

laws of physics:

(1) convection of oxygen from the environment

into the body (ventilation);

(2) diffusion of oxygen into the blood (oxygen

uptake):

(3) reversible chemical bonding with haemoglobin;

(4) convective transport of oxygen to the tissues

(cardiac output):

(5) diffusion into the cellsand organelles;

(6) the redox state of the cell.

Oxygen source

Inspired Oxygen (Fio2)

Alveolar Oxygen (PAO2)

Arterial Oxygen (PaO2)

Caplillary Oxygen (PcO2)

Tissue Oxygen Mitochondrial

Oxygen

Venous Oxygen

(PvO2)

Atmospheric Oxygen (21%)

Oxygen Cylinders

Liquid Oxygen

Oxygen Concentrator

Inspired Air: 150

Alveolar : 100

Arterial :95

Capillary: 50

Tissue: 20

Mitochondria:

1-20

Mitochondrial function is jeopardized at PO2<30mmHg or SPO2 of

30%

Diffusion Capacity

•Property of the alveolar-capillary

membrane

•Ease with which oxygen moves

from inhaled air to the red blood

cells in the pulmonary capillaries

The arterial PaO2 is less than PAO2 due to presence of:

Intrapulmonary Shunts Deep true bronchial veins Thebesian veins

Normal venous admixture <5%

Blood through low V/Q units

Total shunt because of the above factors is 2% of CO.

Focal Hypoventilation

Shunt Effect

Wasted Perfusion

HYPOXEMIA

Hypoxemia without hypercarbia

(Type 1 RF)

Dead Space Effect

Wasted Ventilation

INCREASED WORK OF BREATHING

Minute Ventilation-

PaCO2 Disparity

( Type II RF )

V/Q <1

Low V/Q UnitsV/Q >1

High V/Q Units

V/Q=1.0V/Q=0 V/Q= infinity

Type I or Hypoxemic (PaO2 <60 at sea level): Failure of oxygen

exchange

Increased shunt fraction (Q S /QT )

Due to alveolar flooding

Hypoxemia refractory to supplemental oxygen.

Type II or Hypercapnic (PaCO2 >45): Failure to exchange or remove

CO2

Decreased alveolar minute ventilation (V A )

Often accompanied by hypoxemia that corrects with supplemental

oxygen

Type III Respiratory Failure: Perioperative RF

Type IV Respiratory Failure: Shock

Alveolar arterial oxygen difference P(A-a)O2

Normal is 5-15 mm Hg because oxygenated blood is

mixed with deoxygenated blood.

Affected by:

Age : Increases with age

FiO2: Increases with increasing FiO2.

Indicator of pulmonary parenchymal dysfunction.

Normal P/F > 400; Maximum P/F = 700

Relation between PaO2 and FiO2 is non linear and influenced by:

- Denitrogenation Absorption Atelectesis

-PEEP

Advantage: Simple - bypasses need to calculate PAO2

Disadvantage: Cannot distinguish between Type 1 and Type II RF

S/F = 64+ 0.84 X (P/F)

Thickened interface between air and blood:

Collagen deposition

Cellular infiltration

Reduced surface area for diffusion: Low V/Q due to partially collapsed alveoli

Decreased Delivery with Normal Oxygen Extraction:

Reduced Hb

Reduced SaO2

Reduced Blood Volume

Reduced CO

Normal delivery with increased O2 consumption or extraction

desolved : 0.003 X PaO2 ( Normal is 0.3-0.5ml )

At a normal body temperature (37°C), each increment in PO2 of 1 mm Hg will increase the concentration of dissolved O2 by 0.03 mL/L [0.003ml/dl]

Bound to Hb (19.5 ml) --% of heme binding sites saturated with oxygen is the Hb oxygen saturation %.

CaO2 = (1.34 X Hb X SaO2) + 0.003 X PaO2

Eg at 100% SaO2, Hb 15g%, PaO2 120 mm Hg

CaO2= (1.34 X 15 X 100/100)+(0.003 X 120)

=20.46ml

The

relationshi

p

between

SO2 and

PO2 is

describe

d by

ODC

Depends on oxygen content and cardiac output

= CO X CaO2

= 5000 X 20/100

= 1000ml/min

: Oxygen consumption by tissue per min.

250ml/min at rest

: Oxygen Extraction Ratio

VO2/DO2 = 0.25 (Normal range is 0.22-0.32)

Indicates balance b/w delivery and uptake

Low Values: Flow Maldistribution

Metabolic Poison

High Values: Compensatory increase in extraction for reduced

delivery.

Since oxygen is not stored in tissues, the VO2 is also a

global measure of the oxygen consumption of

metabolizing tissues

This equation is a modified version of the Fick equation

for cardiac output (CO = VO2/CaO2 –CvO2); using

this equation to calculate the VO2 is called the

reverse Fick method

the VO2 that is calculated from the modified Fick

equation must change by at least 18% for the change

to be considered significant.

The calculated VO2 from the modified Fick equation is not the whole body VO2 because it does not include the O2 consumption of the lungs. Normally, the VO2 of the lungs accounts for less than 5% of the whole body VO2 , but it can make up 20% of the whole body VO2 when there is inflammation in the lungs (which is common in ICU patients).

The whole body VO2 is measured by monitoring the O2 concentration in inhaled and exhaled gas-- needs an oxygen analyzer

it records the VO2 as the product of minute ventilation (VE) and the fractional concentration of O2 in inhaled and exhaled gas (FIO2 and FEO2).

Oxygen Flux and RequirementsThe supply of oxygen is dependent upon the hemoglobin

(Hb), O2 saturation % (SaO2) and cardiac output (Q).

"Oxygen flux" denotes the total amount of oxygen delivered to the body per minute and is given by the equation:

Oxygen flux = 1.34 x Hb in g/dL x (SaO2/100) x (Q in mL/min)/100 = 1000 mL/min

A 50% reduction in [Hb] (from 15 to 7.5 g/dL) results in an equivalent 50% reduction in CaO2 (from 20 to 10 mL/dL), while a 50% reduction in the PaO2 (from 90 to 45 mm Hg, which corresponds to a decrease in SaO2 from 98% to 78%) results in only a 20% decrease in CaO2 (from 20 to 16 mL/dL). This demonstrates that anemia has a much greater influence on arterial oxygenation than hypoxemia.

The cumulative deficit in tissue oxygenation is called

the oxygen debt,

and clinical studies have shown a direct relationship

between the size of the oxygen debt and the risk of

multiorgan failure

Low VO2 due to a decreased metabolic rate

(hypometabolism) and inadequate tissue oxygenation

resulting in anaerobic metabolism.[ common in icu]

Breathing pattern regular and at normal

rate.

pink color in nail beds, lips, conjunctiva

of eyes.

No confusion, disorientation, difficulty

with cognition.

Arterial oxygen concentration or

hemoglobin

Oxygen saturation within normal limits.

Date and time oxygen started.

Method of delivery.

Oxygen concentration and flow rate.

Patient observation.

Add oronasal care to the nursing care

plan

Need is determined by measurement of inadequate oxygen

tensions and/or saturations, by invasive or noninvasive

methods, and/or the presence of clinical indicators as

previously described.

Arterial blood gases

Pulse oximetry

Clinical presentation

Documented hypoxemia: Pa02 <60 mm Hg or Sa02 <90%

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 (e.g., postanesthesia recovery)

Should be determined through evaluation of the patient

(clinical assessment and blood gas result)

In general the indication are:-

1. Hypoxemia/hypoxia

2. Excessive work of breathing

3. Excessive myocardial work

4. Improvement of oxygenation in patient with decreased

O2 carrying capacity ( anaemia)

5. Promotion of absorption of air in the body cavity

Goal directed approach

- post operative (thoracic/abdominal

surgery)

- post extubation

- conscious state/coughing

- redistribution of fluid

- positioning

Three clinical goals of O2 therapy

1. Treat hypoxemia

2. Decrease work of breathing (WOB)

3. Decrease myocardial Work

FACTORS THAT DETERMINE

WHICH SYSTEM TO USE

1. Patient comfort / acceptance by the Pt

2. The level of FiO2 that is needed

3. The requirement that the FiO2 be

controlled within a certain range

4. The level of humidification and /or

nebulization

5. Minimal resistance to breathing

6. Efficient & economical use of oxygen

Low Flow Devices [Patient's inspiratory flow > flow delivered by the

device]

Nasal cannula Nasal catheter

Transtracheal catheter

Reservoir[Reserve volume (flow x time) ≥

patient's tidal volume ,, Fixed flow devices if RV > Inspiratory flow]

Simple mask

Partial rebreathing mask Nonbreathing mask

High Flow Devices[The High-flow system always exceeds

the patient's flow ,Provide fixed FIO2 ]

Air-entrainment mask Air-entrainment nebulizer T-piece with a venturi device

Breathing circuits with reservoir bags

Enclosure

Oxyhood Tent Isolette

EQUIPMENT FLOW FIO2 SPECIAL NOTES

NASAL CANNULA 1 - 6 L/M .24 – 44 6 L/M MAX.

SIMPLE O2 MASK 6 - 10 L/M .35 – 55 USE 5 L/M (WITHOUT BAG) MINIMUM

RESERVOIR MASK 10-15 L/M .60 -80 (MASK WITH BAG) (BAG TO NOT

COLLAPSE)

VENTI MASK 3 L/M .24, 26, 31, READ ENCLOSED6 L/M .35, .40, .50 INSTRUCTIONS

NEBULIZER 8 L/M OR > .28, .30, .35 MIST MUST BE .40, .50, 70 VISIBLE

*** SHOWS THAT FIO2 VARIES WITH DIFFERENTF, VT, INSPIRATORY FLOW RATES.

Partial Rebreathing System Non Rebreathing System

.

Flow: Varies

FiO2: 24%-60%

Advantages: Easy to apply;

disposable,

inexpensive;

stable,

precise Fio2

Disadvantages: Limited to adult use,

Use: Patients in unstable condition who need precise Fio2.

Flow: 10-15 L/min input,

Should provide output flow of atleast 60 lit/min

FiO2: 28%-100%

Advantages: Provide temperature control and humidification

Disadvantage: FiO2<0.28 and >0.40 not ensured

FiO2 varies with back pressure

High infection risk

T-piece:

Attaches to ETT or tracheostomy tubes

Can be variable performance or fixed performance.

Breathing Circuits:

Consist of inspiratory and expiratory limb with reservoir bag.

Two limbs are connected through a Y-connector to either a tight

fitting mask or an endotracheal tube.

Weaning should be considered when the patient becomes comfortable, his underlying disease is stabilized, BP, pulse rate, respiratory rate, skin color, and oxymetry are within normal range.

weaning can be gradually attempted by discontinuing oxygen or lowering its concentration for a fixed period for e.g., 30 min. and reevaluating the clinical parameters and SpO2 periodically.

Patients with chronic respiratory disease may require oxygen at lower concentrations for prolonged periods.

Monitoring oxygen therapy Oxygen therapy should be given continuously and should

not be stopped abruptly until the patient has recovered, since sudden discontinuation can wash-out small body stores of oxygen resulting in fall of alveolar oxygen tension.

The dose of oxygen should be calculated carefully.

Partial pressure of oxygen can be measured in the arterial blood.

Complete saturation of hemoglobin in arterial blood should not be attempted.

Arterial PO2 of 60 mmHg can provide 90% saturation of arterial blood, but if acidosis is present, PaO2 more than 80 mmHg is required.

In a patient with respiratory failure, anaemia should be corrected for proper oxygen transport to the tissue.

A small increment in arterial oxygen tension results in a significant rise in the saturation of hemoglobin.

Under normal situations, no additional benefit is secured by raising PaO2 level to greater than 60 to 80 mmHg.

An increase of 1% oxygen concentration elevates oxygen tension by 7 mmHg.

Measurement of arterial blood gases repeatedly is difficult so a simple and non-invasive technique like pulse oximetermay be used to assess oxygen therapy.

Rivers, Emmanual

◦ NEJM 2001; 345: 1368-1377

◦ Early goal-directed therapy in severe sepsis

and septic shock during the first 6 hours after

presentation

◦ Significant reductions in mortality, morbidity in

experimental group that optimized oxygen

delivery and consumption variables

Oxygen toxicity is cellular injury of the lung parenchyma and airway epithelium due to release of cytoxicfree oxygen radicals.

There is no exact threshold at which O2 toxicity occurs, however signs of gas exchange abnormalities occur within 24-48 hours if on 100% oxygen. Atelectasis leading to drop in PO2, decreased lung compliance, infiltrates on x-ray.

Breathing FiO2 up to 50 % for 2-7 days usually does NOT result in toxicity.

12/10/2014 59

Inhibition of Hypoxic pulmonary vasoconstriction

Increased SVR with reduced coronary, cerebral and renal blood flows. [cause vasoconstriction] reducing DO2 when an increase demand, may worsen outcome from CVA and AMI..

Reduced cardiac output & haemodynamic instability.

Increased production of reactive oxygen species.

Paradoxical decrease in O2 consumption due to maldistribution of blood flow due to peripheral shunts which open up to protect the

vital organs from non-physiological effects of hyperoxia.

CO2 Narcosis: In COPD patients, high FiO2 removes the hypoxic drive & causes hypoventilation and narcosis.

Denitrogenation Adsorption AtelectasisFire ( airway fires)

Mucosal damage due to lack of humidity

O2 Toxicity:

Respiratory: ARDS Like syndrome

LUNG TOXICITY (LORRIANE SMITH EFFECT)

Neurological: Seizures (Hyperbaric)

CNS TOXICITY (PAUL BERT EFFECT)

Children: Bronchopulmonary dysplasia

Retrolental fibroplasia

Hypoventilation and Carbon Dioxide

Narcosis

- the increased PO2 decreased and eliminates the

hypoxic drive ( esp. in pt. with chronic CO2 retention

)

- Under this circumstances O2 must be given at low

concentration <30% Ventilatory drive:

Absorption Atelectasis

- Nitrogen a relatively insoluble and exists 80% by

volume of the alveolar gas.N2 assists in maintaining

alveolar stability.O2 therapy replaced N2. Once O2

absorb into the blood the alveolar will collapse esp. in

alveolar distal to the obstruction.

Pulmonary Oxygen Toxicity- The exposure of the high O2 and for prolonged

period

can lead to parenchymal changes

- In general FiO2 > 50% for prolonged period shows increased O2 toxicity

- Pulmonary changes mimic ARDS (Exudativechanges and proliferative changes.)

Sx –cough, burning discomfort, nausea and vomiting,

headache, malaise and etc

Haldane effect: increasing FiO2 decreases the CO2

buffering capacity of haemoglobin, thus potentially

leading to an increase in PaCO2 and acidaemia.

Higher density of oxygen compared with air:

increased viscosity increases the work of breathing in

high conc.

Fire

O2 support combustion

Do not smoke while receiving O2 therapy

Patient on Chemotherapy

Patient on chemotherapy especially

bleomycin will develop pulmonary fibrosis

if get excessive O2 therapy

Carban monoxide

poisoning[100% O2

at 3 atmp]

Tt of cluster

headache, reduction

in oxidative stress in

colonic surgery and

prevention of

desaturation during

Endoscopy.

The use of

hyperoxia to treat

postoperative

nausea and vomiting

and prevent

postoperative

wound infections

lacks high-quality

evidence

Hyperbaric oxygen therapy is the

therapeutic use of oxygen at

pressures greater than 1 atm.

Indications:

hypoxemia should be verified with pulse oximetry and /or ABG’s when situation more stable.

Oxygen is a drug and should be administered keeping

following things in mind: mode of administration, flow

rate, FiO2 (venturi), treatment goal, monitoring, when to

stop.

Oxygen should be prescribed to achieve a target

saturation of 94–98% for most acutely ill patients or 88–

92% for those at risk of hypercapnic respiratory failure

as very high levels will not offer any clinical advantage in

most conditions.

The PaO2 measurement is useful for evaluating gas

exchange in the lungs, not for evaluating the

oxygenation of blood.

Nursing Guidelines Oxygen updated Jan 2013Nottingham University Hospitals NHS Trust

Thorax 2008;63(Suppl VI) BTS guideline for emergency oxygen use

in adult patients

Oh,z manual

The icu book