oxygen and oxygen therapy

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OXYGEN AND OXYGEN THERAPY PADMAJA PALLAVI PANDEY

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Page 1: Oxygen and oxygen therapy

OXYGEN AND OXYGEN THERAPY

PADMAJA PALLAVI PANDEY

Page 2: Oxygen and oxygen therapy

CONTENTS Oxygen The Fick Principle Oxygen Electrode Oxygen Transport Oxyhemoglobin Dissociation Curve (ODC) Transport of carbon Dioxide Carbon Dioxide Dissociation Curve Oxygen Content Oxygen Delivery Postoperative Hypoxemia Oxygen Flux Oxygen Cascade CO Poisoning

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CONTENTS Hypoxia Oxygen Therapy and devices Peak Inspiratory Flow Rate Low Flow Systems High flow systems Performance devices Venturi effect Medium Dependency System Neonates and Infants Clean and Sterilization Choice of Devices Hazards of oxygen therapy Oxygen Toxicity

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OXYGEN Oxygen is a drug. It must be used meticulously & diligently. If abused it can cause complications. The major reason for O2 therapy is hypoxia. Hypoxia is deficiency of O2 at tissue levels. Hypoxemia refers to reduced O2 tension in arterial blood. A gas with chemical formula of O2 Colourless, odorless, tasteless Boiling point -183 C Melting point –216.6C Critical temp. –118.4C , Critical pressure 736.9psi Constitutes about 20.95% of atmosphere

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THE FICK PRINCIPLE Used to measure widely differing physiological flow parameters. A substance is added or subtracted from the flow that it is desired

to measure. Flow of liquid in a given period of time = the amount of

substance entering or leaving the stream in the same period of time, divided by the concentration difference before and after the point of entry or exit.

Two forms of indicator dilution technique can be used to measure blood flow :-

1. An indicator is injected at a constant rate upstream and its concentration is measured from a downstream sample after mixing has taken place.

Flow = rate of infusion of indicator/concentration of indicator in blood

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THE FICK PRINCIPLE Nontoxic dyes such as Indocyanine green have been used for

physiological measurements of blood flow. Radioactive tracers may also be used.

The direct Fick principle is the basis of the calculation of cardiac output from measurements of the steady-state oxygen consumption of the body as follows :-

CO = Oxygen consumption/Arteriovenous oxygen content difference

Oxygen consumption is measured over a fixed period of time using a volumetric method or indirectly by measuring the inspired and expired volumes & oxygen concentrations.

Arteriovenous oxygen content difference = Arterial oxygen content - the mixed venous (Pulmonary artery) oxygen content

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THE FICK PRINCIPLE2. A slug of indicator is injected and the concentration of the

indicator is sampled continuously downstream. In the thermodilution measurement of cardiac output, a bolus of

saline is injected into the right atrium and a thermistor continuously measures the temperature of the blood downstream in the pulmonary artery.

The CO is inversely proportional to the area under the plot of temperature with time and is calculated using a modified Stewart-Hamilton equation, the denominator of which is the integral of the change in blood temperature.

A modification of this technique uses a special catheter that pulse-heats blood in the right side of the heart and detects the rise in temperature in the pulmonary artery, which estimates the continuous estimation of CO.

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OXYGEN ELECTRODE The principle of the Clark-type, polarographic electrode for the

measurement of the partial pressure of oxygen (Po2) in a blood sample involves the electrolytic reduction of oxygen at a cathode constructed of glass-coated platinum.

The platinum electrode is charged negatively w.r.t. a suitable reference electrode, (Ag/AgCl2) in a solution containing oxygen.

At the cathode, the oxygen combines with water and the additional electrons to give hydroxyl ions in a reduction process :-

O2 + 2H2O + 4ē →2H2O + 4ē → 4OHˉ

The hydroxyl ions are buffered by the electrolyte (e.g. potassium chloride) :-

4OHˉ + 4KCl → 4KOH = 4Clˉ

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OXYGEN ELECTRODE At the anode of the PO2, oxidation or loss of electrons occurs.

The electrons in the process are provided by the silver anode and chloride ions, which form silver chloride :-

4Ag + 4Clˉ → 4AgCl + 4eˉ

The clark electrode has an oxygen-permeable, plastic membrane covering the tip of the cathode.

As the polarizing voltage increases, the current flow reaches a plateau at about 0.6 to 0.8V, minimizes interference due to electrochemical reactions with other gases and provides sufficient voltage to drive the reaction.

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OXYGEN ELECTRODE There is a linear relation between the current generated and the

concentration of oxygen in the solution.

The dependence on temperature is controlled by using a precise operating temperature, such as with an electronic heat source.

The system is calibrated with two gases :-1. Containing no oxygen and 2. Containing a known amount of oxygen

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OXYGEN TRANSPORT At breathing air, oxygen reserve in a 3-L FRC is about 500 ml. The blood stores about 850 ml of Oxygen.

Increasing the Inspired Oxygen Fraction (FiO2), increases oxygen stores in the FRC to nearly 3 L which increases dissolved oxygen but has less effect on the volume bound to hemoglobin, as it is nearly fully saturated at breathing air.

Oxygen is carried to the tissues by means of being dissolved in the plasma and bound to hemoglobin.

The amount dissolved depends on the partial pressure and Solubility, giving 0.003 ml per 100 ml blood for each mmHg of Po2.

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OXYGEN TRANSPORT (CONT.) Blood substitues such as Perfluoronated hydrocarbons have a

high oxygen solubility & can carry as much oxygen as blood, at high oxygen tensions.

In theory, 1 gm of Hb can combine with 1.39 ml of oxygen i.e. Hoffman coefficient but in reality, this amount is less i.e. 1.34-1.36 ml because in vivo the heme group of a small fraction of hemoglobin is oxidized to methemoglobin , which is unable to release its oxygen to the tissues.

Nitrites & Sulfonamides oxidize hemoglobin, as can a congenital deficiency in the enzyme methemoglobin reductase.

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OXYGEN TRANSPORT (CONT.) If the oxygen capacity of hemoglobin is 1.36 ml/gm, 15 gm of

hemoglobin can combine with 20.4 ml of oxygen – the oxygen content.

The oxygen saturation of Hb (SaO2) is expressed as a percentage of the oxygen capacity :

1. O2 content = (1.36×Hb×So2/100) + (0.003×Po2)2. O2 content= O2 bound to Hb+O2 dissolved in plasma

Where the O2 content is given as ml O2 per 100 ml blood, Hb is given as g per 100 ml and Po2 is given as mmHg

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ODC The shape of the curve have important physiologic advantages :-

1. The flat upper portion implies that small changes in alveolar oxygen (breath holding, moderate altitude) have harmful effect on full oxygen saturation of blood.

2. At alveolar oxygen tensions of less than 70 mmHg(9.3kPa), small reductions in capillary oxygen tension result in large reductions in hemoglobin oxygen content, which facilitates the unloading of oxygen from hemoglobin to supply the tissues.

3. The position of the ODC is described by the term P50, which is the oxygen tension required for 50% saturation of hemoglobin and is normally 27 mmHg(3.6kPa). P50 may shift to the right or left under certain physiologic conditions.

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Oxygen Hemoglobin Dissociation Curve

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Normal Oxyhemoglobin Dissociation Curve

97% saturation = 97 PaO2 (normal)90% saturation = 60 PaO2 (danger)80% saturation = 45 PaO2 (severe hypoxia)

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SHIFT TO LEFT• Increase in pH• Decrease in CO2• Decrease in 2.3-DPG • Decrease in temperature

SHIFT TO RIGHT• Decrease in pH• Increase in CO2• Increase in 2,3-DPG• Increase in temperature

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ODC A right shift means that more oxygen is unloaded at a given Po2. BOHR EFFECT :- The effect of altering Pco2 is mainly

associated with change in the hydrogen ion concentration. Conditions associated with a right shift in the ODC are found in

active tissues, so that hemoglobin gives up its oxygen more easily where it is needed most.

The compound 2,3-DPG is an endproduct of red cell metabolism and is increased :-

1. Anemia2. Thyrotoxicosis3. Chronic Hypoxia – Lung disease & High altitude Stored blood has depleted 2,3-DPG and is less effective at

oxygen delivery.

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Bohr Effect : ↑pCO2 will facilitate offloading of O2 and formation of deoxy Hb Right shift

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TRANSPORT OF CARBONDIOXIDE

Tension of CO2 in venous blood is 46mmHg and in alveoli the tension is 40mmHg .

CO2 is distributed in the following manner-

1.In solution in plasma (5%) : This quantity is responsible for determining the tension of gas in the blood and also acts as an intermediate between the air in alveoli and inside the red cell .

2.As carbamino compound (25%) : CO2 can combine with amino group of Hb. - 3.5 times greater affinity to CO2 as compared to oxy hemoglobin

3.As carbonic acid: CO2+H20↔H2CO3

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TRANSPORT OF CARBONDIOXIDE

4.As Bicarbonate(90)% : Most of CO2 passes to red cells where enzyme carbonic anhydrase aids its rapid hydration to form carbonic acid . Carbonic Anhydrase is not found in plasma.

-Hamburger shift

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Carbon di oxide dissociation curve The CO2 dissociation curve relates to CO2 content of blood to

PCO2 to which it is exposed .The position of this curve depends on the degree of O2 of the blood.

HALDANE EFFECT: The more deoxygenated , the blood becomes the more CO2 it

carries at given PCO2 .

Deoxygenation of blood in peripheral capillaries facilitates loading of CO2 while oxygenation in pulmonary capillaries facilitates unloading of CO2.

Hence, Venous blood carries more CO2 as compared to arterial blood.

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Carbon dioxide dissociation curveCO2 stores are large : approx120L and primarily dissolved as CO2 and bicarbonate.

Equilibrium requires 20 to 30 mins, as compared to O2 which requires 4 – 5 mins.

Due to large capacity of intermediate + slow compartments , change in CO2 tension is slower than its fall, following acute ventilation.

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Carbon dioxide Diffusion rate of CO2 – 20 times greater than oxygen

PACO2 ( Alveolar CO2 Tension) = VCO2(total CO2 production ) / VA( alveolar ventilation )

Pulmonary End Capillary tension ( Pc’CO2 )= PACO2 End Tidal CO2 Tension ( PET CO2 ): clinical estimate of CO2. Normally, PA CO2 – PET CO2 < 5mm

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OXYGEN CONTENT The oxygen content of the blood is that quantity of oxygen contained

in the red cell , added to the quantity , dissolved in the plasma and is defined as the volume of oxygen in milliliters carried in 1 dL of blood.

Normally calculated from the equation :- CaO2 = Hb × 1.37 × SaO2 + 0.023 × PaO2 kPa (CaO2 = Hb × 1.37 × SaO2 + 0.0034 × PaO2 mmHg)a = An arterial blood sampleCaO2 = The arterial oxygen content in ml/dL of bloodHb = The hemoglobin concentration in g/dL of blood1.37 = The volume of oxygen in milliliters carried by 1g of fully

saturated hemoglobinSaO2 = The fractional hemoglobin saturationPaO2 = Arterial oxygen tension measured in kPa or mmHg

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OXYGEN CONTENT0.023 and 0.0034 = The solubility coefficients of oxygen in plasma (mL

of oxygen per dL plasma, in kPa or mmHg respectively)

The red cells’ contribution to oxygen content is controlled by the concentration of active hemoglobin and by the ability of hemoglobin to combine with oxygen i.e. the Saturation.

The saturation depends on the partial pressure of oxygen and the position of the oxygen dissociation curve.

Fractional hemoglobin saturation (SaO2) is defined as the ratio of oxyhemoglobin to total hemoglobin :-

SaO2 = HbO2/(HbO2 + Hb + metHb + COHb)Where HbO2 = OxyhemoglobinHb = Reduced hemoglobinmetHb = MethemoglobinCOHb = Carboxyhemoglobin

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OXYGEN CONTENT Multiwavelength co-oximeters are required to measure the

saturation.

Functional Saturation is used to describe hemoglobin saturation, which ignores the presence of methemoglobin and carboxyhemoglobin :-

fnSaO2 = HbO2/(HbO2 + Hb)

SaO2 is provided by blood gas analysis and measures saturation from PaO2 and the oxyhemoglobin dissociation curve.

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OXYGEN CONTENT Because methemoglobin and carboxyhemoglobin do not carry

oxygen, only SaO2 should be used when accurately calculating oxygen content.

With a hemoglobin level of 15g and normal values of PaO2 and SaO2, the arterial oxygen content is 20 ml/dL blood, 20 vol% or 9 mmol/L.

Normal oxygen content of blood is very similar to that of room air at sea level.

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OXYGEN DELIVERY The total quantity of oxygen delivered to the tissues per minute is a

function of the oxygen content and the Cardiac output. The overall flow rate of oxygen to the tissues is called the “O2 Delivery”.

With a normal Cardiac Output of 5L/min for a 70 kg adult, there will be a normal O2 delivery of 44.5mmol/min O2 or 1000 ml/min O2.

Since the normal Cardiac Output depends on the size of the patient , cardiac output is commonly indexed to body surface area (BSA) , using a normal cardiac index(CI) of 3L/min/m2 of O2 delivery.

CI = CO/BSA L/min/m2O2 Delivery = CaO2 × CI × 10 ml/min/m2 O2

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OXYGEN DELIVERY In an adult patient with a normal CI of 3L/min/m2, the oxygen

delivery index would be 600 ml/min/m2 O2 or approximately 27 mmol/min/m2 O2.

This measure of the oxygen delivery index is a value of total oxygen transport but it does not take into consideration of the regional variations in oxygen transport to specific organ systems.

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POSTOPERATIVE HYPOXEMIA The most important cause is the combination of :-

1. A reduced VA/Q intraoperatively2. Impaired postoperative ventilatory control induced by opioids. A reduced VA/Q shifts the PiO2 vs. SpO2 curve to the right so

that the steep part of the curve becomes a tangent to the inspired oxygen pressure.

Opioid administration causes a further shift to the right and this causes a profound fall in oxygen saturation.

So, postoperative oxygen saturation was measured continuously overnight with patients breathing air.

A fall in VA/Q causing a shift in the PiO2 vs. SpO2 curve to the right, is an important factor in predisposing patients to sleep-related hypoxemia.

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OXYGEN FLUX DEFINITION: The amount of oxygen leaving left ventricle per

minute in the arterial blood has been termed as oxygen flux .

It is expressed as : Cardiac Output ×Arterial oxygen saturation × Hemoglobin concentration ×1.31(vol of O2 combining with 1 gm of Hb )

5000ml/min × 98/100 ×15.6/100g/ml ×1.31

so, oxygen flux = 1000ml/min

250ml of this Oxygen is used in cellular metabolism & rest returns to lungs in mixed venous blood (75% saturated with oxygen).

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OXYGEN FLUXARTERIAL OXYGEN CONTENT: It is predominantly in combination with Hb. Cao2= Sao2×Hb×1.31

OXYGEN UPTAKE: When blood reaches the systemic capillaries, oxygen dissociates

from Hb & moves into tissues. rate at which this occurs is called oxygen uptake. normal range of Vo2 in healthy adults at rest is: 200-300ml/min

or 110-160 ml/min/m2 when adjusted for body size.

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OXYGEN UPTAKE Oxygen binds with hemoglobin but much less avidly than with

CO.

The oxygen partial pressure of mixed venous blood entering pulmonary capillaries is about 5.3 kPa (40 mmHg) compared with the alveolar tension of about 13.3 kPa (100mmHg).

Under normal conditions, the transfer of oxygen is perfusion limited.

If diffusion properties of the blood-gas barrier are impaired, for example in ARDS, then diffusion equilibrium may not occur by the end of the capillary.

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OXYGEN-EXTRACTION RATIO The fraction of oxygen delivered to the capillaries that is taken

up into the tissues is an index of efficiency of oxygen transport. Monitored with a parameter called oxygen-extraction

ratio(O2ER) Normally about 0.25 (range=0.2-0.3) So only 25% of oxygen delivered to systemic capillaries is taken

up into tissues. Though O2 extraction is low it is adjustable & can be increased

when oxygen delivery is impaired.

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OXYGEN CASCADE PO2 of dry air at sea level is 21.2kpa(159mmhg)

O2 moves down the partial pressure gradient from air through respiratory tract, alveolar gas, arterial blood, systemic capillaries, tissues & cell.

It reaches its lowest level in the mitochondria where it is consumed . Here PO2 is 0.5-3kpa(3.8-22.5mmhg)

The steps by which PO2 decreases from air to mitochondria are known as O2 cascade.

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OXYGEN CASCADE

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OXYGEN CASCADEDilution of inspired oxygen by water vapour: Concentration of atmospheric oxygen is 20.94%

As gas is inhaled through the respiratory tract, it becomes humidified at body temperature & added water vapour dilutes the O2 & ↓ PO2 below its level in ambient air.

PO2 = fractional conc’n of O2 in dry gas phase × (barometric pressure - saturated water vapour pressure)

PO2=0.2094(760-47) =149mmhg.

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CARBON MONOXIDE POISONING CO exposure produces cerebral hypoxia secondary to its

reversible combination with hemoglobin to form Carboxyhemoglobin.

Symptoms are related to the blood carboxyhemoglobin content, which depends on the duration of exposure, time since exposure and the treatment given.

In the early stages :-1. Throbbing headache2. Vomiting without Diarrhea3. Lethargy4. Hyperventilation

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CARBON MONOXIDE POISONING Symptoms may progress to :-1. Convulsions2. Coma3. Hypoventilation4. Bradycardia5. Cardiovascular collapse In the elderly, CO toxicity may present as a cerebrovascular

accident or myocardial infarction.

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SOURCES OF CO POISONING Inhalation of products of combustion. Faulty appliance Blocked flue Motor exhaust gas inhalation.

Because of the high affinity of CO for hemoglobin, a few breaths at high concentrations can be fatal; 1% CO in air can kill within a few minutes

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PATHOPHYSIOLOGY

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PATHOPHYSIOLOGY CO is colourless, odourless, nonirritant toxic gas CO toxicity due to

Cellular hypoxia Direct cellular injury

Cellular hypoxia CO competes with O2 for binding to Hb Affinity of Hb for CO x 200-250 > affinity for O2 O2-Hb dissociation curve shift to the left Impaired tissue release of O2 and cellular hypoxia

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PATHOPHYSIOLOGY Direct cellular injury

CNS reoxygenation injury Lipid peroxygenation Free radical formation

CO toxicity in pregnancy Risk of fetal injury

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Oxygen-Hemoglobin Dissociation Curve

Curve – shifted to left hyperbolic curve , decreases oxygen carying capacity

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DIAGNOSIS High level of clinical suspicion Serum COHb level Exhaled breath COHb level Measured by spectrophotometry Pulse oximetry cannot distinguish between HbO2 and COHb Comprehensive neurological and neuropsychological

assessment CO Neuropsychological Screening Battery CT brain to exclude other conditions

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CARBON MONOXIDE POISONINGTREATMENT :- Removal from the source of exposure Administration of 100% Oxygen immediately, after taking an

anticoagulated whole blood sample for carboxyhemoglobin estimation.

The pregnant patient or any patient who has had symptoms s/o. severe poisoning (including any degree of neurologic impairment) should be treated with Hyperbaric Oxygen.

Hyperbaric oxygen is effective in :-A. Reducing long-term mental impairment following CO poisoningB. Shortening the half-life of CarboxyhemoglobinC. Preventing late neurologic sequelae

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QUICK DEFINITION OF HYPOXIA

INADEQUATE O2 SUPPLY TO THE BODY TISSUES (ENTIRE BODY) OR (LOCALIZED REGION)

HYPOXIA MEANS

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SYMPTOMS OF HYPOXIA

DEPEND ON:

RAPIDITY AND SEVERITY

OF THE

DECREASE OF ARTERIAL Po2

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HYPOXIACAUSES :-Hypoxia could be due to arterial hypoxemia or failure of the

oxygen hemoglobin transport system :-

1. Arterial Hypoxemia – Low inspired oxygen partial pressure (high altitude) Alveolar hypoventilation (Sleep apnea, Narcotic overdose,

neuromuscular disorders, anesthetics and sedatives) Ventilation-perfusion mismatch (atelectasis , pneumonia, Acute

Asthma) Right to left shunts (Pneumonia, pulmonary embolism,

Arteriovenous malformation)

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HYPOXIA2. Failure of oxygen hemoglobin transport system :- Inadequate tissue perfusion (Cardiac failure, myocardial

infarction, hypovolemic shock) Low hemoglobin concentration (anemia, trauma) Abnormal oxygen dissociation curve (hemoglobinopathies, high

carboxyhemoglobin) Increased oxygen requirements in hypermetabolic states Histotoxic poisoning of intracellular enzymes (cyanide

poisoning, septicemia)

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HYPOXIACLASSIFICATION :-

1. Ischemic hypoxia - ↓ blood flow, normal CaO22. Hypoxemic hypoxia – CaO23. Hypoxic hypoxemia - ↓ PaO2, SaO2, Normal Hb4. Anemic hypoxemia - ↓ Hb , Normal PaO2, SaO25. Toxic hypoxemia - ↓ SaO2, Normal PaO2 (i.e. MetHb or COHb)

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TYPES OF HYPOXIA

1.HYPOXIC HYPOXIA:

- Dec. in O2 saturation of Hb like alveolar hypoventilation& low FiO2.

- O2 therapy fruitful results.

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2.STAGNANT HYPOXIA

- Due to low cardiac output states & vascular occlusion.

- O2 therapy helps to less extent.

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3.ANEMIC HYPOXIA

- O2 carrying capacity is reduced like anemia,hemodilution,CO poisoning.

- O2 therapy useful to some extent.

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4.HISTOTOXIC HYPOXIA

- Due to cyanide poisoning.- Cells cannot utilise O2.- O2 therapy least likely useful.

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OXYGEN THERAPYWHICH PATIENTS NEED :-American College of Chest Physicians and National Heart Lung and

Blood Institute recommendations for instituting oxygen therapy are :-

1. Cardiac and respiratory arrest2. Hypoxemia (PaO2 < 60mmHg, SaO2<90%)3. Hypotension (Systolic BP<100mmHg)4. Low Cardiac Output and metabolic acidosis5. Respiratory distress (RR>24/min)

While providing oxygen therapy, attempts must be made to find the underlying pathology and treat it.

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OXYGEN THERAPYTYPES :-Depending on the cause and severity, oxygen can be supplemented

from a range of oxygen therapy devices.1. Normobaric oxygen therapy :- When devices deliver oxygen at or just above atmospheric

pressure.

2. Hyperbaric oxygen therapy :- Patients in whom, either the oxygen carrying capacity of

hemoglobin is compromised e.g. CO Poisoning or extra tissue oxygen is required (in severe burns and tissue infections).

Supplemental oxygen may be delivered by dissolving it under pressure, in plasma.

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OXYGEN THERAPYINDICATIONS :- Patient factors – Cardiorespiratory disease, elderly, shivering , obesity

Surgical factors – Thoracic surgery, upper abdominal surgery

Physiological factors – Hypovolemia , hypotension, anemia

Postoperative analgesic technique – Patient controlled analgesia, IV Opioid infusion

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OXYGEN THERAPY DEVICESCLASSIFICATION :-

1. Performance of the device – Fixed – Venturi mask Variable – Nasal prong, Face mask2. Flows delivered by the device – Low flow – Nasal prongs, Face mask High flow – Venturi mask3. Patient – Dependent – Face mask, Nasal prongs, CPAP Device Independent – Ventilators4. Degree of dependency – Low dependency – Face mask, Nasal prongs Medium dependency – CPAP Mask and equipment High dependency – Noninvasive or IPPV

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NASAL CANNULA

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SIMPLE FACE MASK

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SIMPLE FACE MASK Open ports for exhaled

gas

Air entrained through ports if O2 flow through does not meet peak inspiratory flow

O2 inlet

Exhalation ports

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NON-REBREATHING BAG

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PEAK INSPIRATORY FLOW RATE If a patient is breathing spontaneously from a T-Piece with no

reservoir and zero FGF, then all the inspired gas would be room air.

FGF is ↑ to 100 L/min, then all the inspired gas would be taken from the FGF & FiO2 will be the same as the Fresh gas.

FGF are ↓ from 100L/min, there will be a point at which the FGF will not meet the patient’s requirements.

FGF < peak inspiratory flow, the patient will entrain room air which will dilute the FiO2 of the fresh gas.

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LOW-FLOW SYSTEMS Deliver oxygen at flows that are less than the patient’s inspiratory

flow rate leading to air entrainment.

The inhaled oxygen concentration (FiO2) may be low or high, depending on the specific device and the patient’s inspiratory flow rate.

Oxygen delivery varies with the patient’s inspiratory flow i.e. variable performance oxygen delivery systems.

An anesthetic breathing system having a tight fitting mask and a reservoir, can deliver a known FiO2.

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LOW-FLOW SYSTEMS Examples :-

1. No capacity system – Nasal cannula , Nasopharyngeal catheters2. Low capacity system (Capacity < 100 ml) – Simple and nebuliser face mask for children, Tracheostomy

mask3. Medium capacity system (Capacity 100-250 ml) – Simple and nebulizer face mask for adults4. High Capacity system (Capacity 250-1500 ml) – Face mask with reservoir bag5. Very high capacity system (Capacity > 1500 ml) – Incubators, Oxygen hood, Oxygen tents

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VENTURI VALVE

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HIGH FLOW SYSTEM Fixed-performance oxygen delivery systems as they can provide

a specific FiO2 at flows that meet or exceed the patient’s inspiratory flow requirement.

No defined cut-off point between low and high flow, about 10-15 L/min.

A constant proportion of air-oxygen mixture is created in excess of patient inspiratory flow rate and are independent of patient factors or fit to the face.

There is no rebreathing , as the CO2 gets washed out by the gas flow , which constantly exceeds the patients demand.

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HIGH FLOW SYSTEM When the flow is less than the peak inspiratory flow, the high

flow devices become patient-dependent

To work efficiently and to prevent air dilution, a fixed performance device should incorporate :-

1. A large volume face piece (not < 280 ml)2. Gas mixture flowing directly towards the nose and mouth3. Vents positioned well away from the patient airway. e.g.

Ventimask

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PERFORMANCE DEVICES Supplemental oxygen can be supplied by a variety of devices. The effectiveness of each device is determined by the capacity

of each device to deliver sufficient oxygen at high enough flow rate to match the patients spontaneous inspiratory flow rate.

In a non-intubated patient, breathing in an “open” system, the capacity of the oxygen therapy device to meet the patient’s inspiratory flow will determine how much room air will be entrained.

The FiO2 delivered from the oxygen source will be diluted by the entrained room air. Therefore, the oxygen delivery systems are categorized as :-

1. Variable Performance2. High-flow fixed performance

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PERFORMANCE DEVICES1. Variable performance systems :- No control on FiO2 Patient-dependent because the FiO2 that the patient receives will

change with changes in the respiratory parameters. For example, nasal catheters, nasal cannulae and masks with or

without a rebreathing bag.

2. High-flow fixed performance systems :- Controlled FiO2 Patient-independent because regardless of changes in respiratory

parameters, the patient will receive a constant predetermined inspired oxygen concentration (FiO2).

For example, Ventimask

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VENTURI EFFECT If the diameter of a tube is made smaller at some point in its

length and the flow through the tube is held constant, the velocity of the gas in the narrowed segment must increases.

The increase in kinetic energy that enables the gas to flow faster can only be achieved by converting some of its potential energy, which can only be derived from the pressure within the tube.

In the narrowed segment, the gas flows faster and the pressure is reduced.

Bernouille’s equation relates the pressure gradient across a tube and the velocity of the gas flowing through it :-

P + ρgH + 1/2ρv2 = constantWhere ρ = Density of the gasP = PressureH = Height measured from a fixed point

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VENTURI EFFECT The pressure is approximately proportional to the square of the

flow rate.

The most common application is found in the fixed-performance Venturi oxygen mask.

High-pressure oxygen from a cylinder or pipeline is acclerated through a small-diameter tube in the base of the mask.

At the point at which the tube emerges inside the mask, the pressure is reduced to below atmospheric and air is entrained which is mixed with the oxygen feed in the body of the mask.

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Venturi mask

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VENTURI EFFECT The concentration of oxygen received by the patient, depends on

the flow of oxygen and the diameter of the Venturi.

The Venturi principle can also be used as a generally applicable device to calculate the flow of gas by measuring the pressure drop in a narrowed segment in a specially constructed and calibrated tube.

Other devices that are used to measure the flow of gases include :-

1. Thermistor flowmeter (Cooled by the flow of gas)2. Moveable-pointer peak flowmeter (a variable-orifice flowmeter)

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MEDIUM DEPENDENCY SYSTEM Used when the patient needs some amount of respiratory

assistance along with oxygen supplementation.

It can only be used in spontaneously breathing patients. Example, CPAP Mask.

The CPAP device consists of a face mask with head strap, O2-CPAP Valve, flow generator and wide bore tubings.

The masks are available in various sizes and cover the mouth and nose. The mask is secured with a harness.

O2-CPAP Valves provide CPAP from 2.5-20 cm of water.

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MEDIUM DEPENDENCY SYSTEM The flow generator can be plugged into wall outlet for oxygen.

Has an ON switch, as well as a switch for adjusting the oxygen flow and oxygen concentration.

Wide bore tubing connects the flow generator to the mask.

There are 2 one way valves present in the body of the face mask :-

1. The inlet valve2. The outlet valve to which the CPAP valve is attached.

The facemask, CPAP valve and the wide bore tubings are for single use only.

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Estimating FiO2O2 Flow rate FiO2 O2 Flow rate FiO2 O2 Flow rate FiO2

Nasal cannula Oxygen mask Mask with reservoir1 0.24 5-6 0.4 6 0.62 0.28 6-7 0.5 7 0.73 0.32 7-8 0.6 8 0.84 0.36 9 0.80+5 0.4 10 0.80+6 0.44

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NEONATES AND INFANTS Enclosure systems are used to provide oxygen therapy to

neonates and small infants :-

1. Oxygen hoods :- Transparent enclosures designed to surround the head of the

neonate or small infant. It has an opening for the neck and comes in different sizes. Hoods are well-tolerated by infants and allow easy access to

chest, trunk, and extremities. Due limitation of the size, these hoods can be used only in

children below 1 year of age. A continuous flow of humidified oxygen is supplied to the hood. The hoods deliver 80-90% at a flow rate of 10-15L/min.

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OXYGEN HOODS

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NEONATES AND INFANTS2. Oxygen Tents :- Transparent enclosures in larger sizes (so-called tent houses or

huts) are available for patients who are too big for the hoods. The subject lies in the tent and CO2 is removed by soda lime

and water vapour by calcium chloride. The temperature in the tent is regulated by flowing oxygen and

air over ice chunks (to prevent accumulation of heat of exothermic reaction).

The tents are designed for children. FiO2 of 0.6-0.7 can be achieved with flow rates of 10-12

L/min. The air changes 20 times/hr. High output nebulizers can circulate cooled mist in the tent.

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Oxygen tent

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LIMITATIONS As the oxygen concentrations may vary within the hood, it

should be measured as near the nose and mouth as possible. There is a decrease in oxygen concentration whenever the

enclosure is opened. Nasal oxygen may need to be supplied during feeding and

nursing care of patients who are confined to hoods.

Flows > 7 L/min are required to wash out CO2 :-1. Devices can be confining and isolating2. FiO2 can vary from 0.21 to 1.0

Temperature of the gases in the hood should be maintained to provide a neutral thermal environment.

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NEONATES AND INFANTS3. Closed Incubators :- Transparent enclosures that provide a warm environment for

small infants with temperature instability. Supplemental oxygen can be added to incubators but may result

in an increased oxygen concentration. The primary purpose of an incubator is to provide a temperature-

controlled environment. FiO2 is maintained at 0.4 Humidified oxygen can be provided.

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EQUIPMENT RELATED POTENTIAL HARM

Prolonged exposure to humidified oxygen may increase risk for cutaneous fungal infection

Hypoxia or hypercapnia can result from inadequate or loss of gas flow.

Temperature within enclosures should be closely monitored to reduce the potential for cold stress or apnea from overheating in neonates.

Use of an improperly sized hood can result in irritation of the infant’s skin.

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CLEAN & STERILIZATION1. Low-flow systems :- Under normal circumstances, do not present clinically important

risk of infections and do not require routine replacement on the same patient.

Nasopharyngeal catheters should be changed every 24 hours. Transtracheal catheters should be changed every 3 months. Reservoir system – Under normal circumstances, reservoir

systems do not present clinically important risk of infection and do not require routine replacement on the same patient.

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CLEAN & STERILIZATION2. High-flow systems :- Large-volume nebulizers should be changed every 24 hours

when applied to patients with an artificial airway.

3. Enclosure Systems :- No recommendation regarding the frequency of changing

oxygen hoods and reservoirs while in use on the same patient.

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CHOICE OF DEVICES Need is determined by :-

1. Measurements of inadequate oxygen tensions.2. Saturations by invasive or noninvasive methods.3. The presence of clinical indicators.

Supplemental oxygen flow should be titrated to maintain adequate oxygen saturation as indicated by pulse oximetry SpO2 or appropriate arterial or venous blood gas values.

Nasal cannulae and nasopharyngeal catheters are used to provide low level supplemental oxygen. Also used to supplement oxygen in patients who are being fed so that there is no interruption in oxygen supplementation.

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CHOICE OF DEVICES Simple oxygen masks are used to provide supplemental oxygen

in the moderate range (0.35-0.50, depending on size & minute ventilation) for short periods of time (e.g., during procedures, for transport, in emergency situations).

Air-entrainment nebulizers, can be used when high levels of humidity or aerosol are desired.

Partial rebreathing masks are used to conserve the oxygen supply when higher concentrations (FiO2 > 0.4, < 0.6) are required (e.g., during transport).

Non-rebreathing masks are used to deliver concentrations > 0.60

Venturi mask are used when precise FiO2 has to be delivered e.g., COPD

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HOODS

Used to provide :- Controlled FiO2 in infants and small children. Controlled FiO2 and or increased heated humidity to patients

who cannot tolerate other devices. Controlled FiO2 when the chest, abdomen and extremities

must be accessible to caregivers.

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Oxygen hood

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HAZARDS OF O2 THERAPY

1.Drying of mucous membrane.2.Depression of ventilation in COPD.3.Reversal of compensatory hypoxic vasoconstriction.4.Atelectasis due to absorption collapse.5.O2 toxicity.

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OXYGEN TOXICITY 1.Pulmonary oxygen toxicity (Lorrain-Smith effect):- 100%O2 given for 12 hours or more.- 80% O2 for more than 24hrs.- 60%O2 more than 36hrs.

- Symptoms: substernal pain , irresistable cough , dyspnoea , ↓ compliance, pulmonary interstitial edema leading to fibrosis.

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OXYGEN TOXICITY

2.Retrolental fibroplasia :

- Occurs when PaO2 more than 80mmhg for more than 3 hrs in new born.

- Very premature babies are more susceptible.- O2 saturation must be around 90-92 %.

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OXYGEN TOXICITY

3.C.N.S O2 toxicity (Paul-Bert effect):

- O2 is given in hyperbaric chambers.

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PATHOGENESIS OF O2 TOXICITY

Exposure to ↑ Po2 damages capillary endothelium

Interstitial oedema & alveolar thickening follows

Type-1 alveolar cells are destroyed & Type-2 cells proliferate

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Exudative phase follows

Low V/Q ratio , Physiologic shunting & hypoxemia

Hyaline membrane forms in alveolar regions

Pulmonary fibrosis & hypertension develops

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AS LUNG INJURY WORSENS BLOOD OXYGENATION DETERIORATES

If this progressive hypoxemia is managed with additional oxygen, the toxic effect worsens

A vicious cycle sets in

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OXYGEN TOXICITY

INCREASED FiO2

LOW PaO2

INCREASED

SHUNTING

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THANK YOU.