Oxygen Therapy

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Oxygen Therapy Pulmonary Medicine
Department Ain Shams University http//telemed.sha
ms.edu.eg/moodle5
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At the end of this lecture the student should be
able to

1. Know the basic principles of oxygen transport.
2. Identify the common methods of oxygen
   administration.
3. Compare the different oxygen delivery devices.
4. Discuss the tools of monitoring tissue
   oxygenation.
5. Recommend oxygen therapy in different specific
   situations.

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• BASIC PRINCIPLES OF OXYGEN TRANSPORT
• Gas exchange in the lungs concerns ventilation,
  perfusion and diffusion.
• Arterial hypoxemia may occur because of
• A decrease in PIO2.
• Alveolar hypoventilation.
• Ventilation/perfusion disturbance.
• Impaired diffusion at the alveolar capillary
  barrier.

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One measure of the ability of the lung to
transfer O2 to the capillary bed is P (A-a)
O2. PAO2 FIO2 (PB-PH2O) - PaCO2/R. Neither
alveolar hypoventilation nor low PIO2 causes
increased P (A-a) O2. Impaired diffusion, V/Q
mismatch, shunting of blood past alveolar
capillaries venous admixture, all increase P
(A-a)O2.
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Po2 mmHg
Graphical representation of sequential steps in
the drop in oxygen tension (PO2) at various
stages of oxygen transport from atmosphere to
peripheral tissues. Values depicted are
calculated using the alveolar gas equation.
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• Oxygen Delivery and Utilization
• DO2 CO x CaO2
• DO2 O2 delivery, ml/min.
• CO Cardiac output L/min.
• CaO2 O2 content of arterial blood ml/dl.
• CaO2 (Hb x 1.34 x SaO2) (PaO2 x 0.003)
• Hb Hemoglobin conc. gm/dl.
• 1.34 O2 carrying capacity of Hb at 37?C ml/gm.
• Sat. O2 Percentage saturation of Hb with O2.
• 0.003 Solubility coefficient for O2.

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ml/min/m2
MOF
Delivery Dependent
OXYGEN UPTAKE VO2
Normal
110
Delivery Independent
330
OXYGEN DELIVERY DO2 ml/min/m2
Relationship between oxygen supply and
consumption in normal and critically ill
patients. MOF, multiple organ failure syndrome.
DO2 crit, 330 ml/min/ m2.
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METHODS OF OXYGEN ADMINISTRATION AND ADJUNCTS TO
IMPROVE OXYGENATION
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Oxygen Delivery Devices and FIO2 Capabilities
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Oxygen Delivery Devices and FIO2 Capabilities
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Oxygen Delivery Devices and FIO2 Capabilities
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Oxygen Delivery Devices and FIO2 Capabilities
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• MONITORING OF TISSUE OXYGENATION
• Arterial Blood Gases Analysis
• Intermittent sampling
• For laboratory analysis.
• On-demand (extravascular) fluorescent sensors
• Placed in the A.B.P monitoring line.
• (Adv. reduces errors, blood loss, risk of
  infection).
• Continuous (intravascular) ABG analysis
• Through intravascular blood gas sensors
  (technically difficult).

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• Pulse oximetry
• Principle differential absorption of red of
  infrared light by oxyhemoglobin and reduced
  hemoglobin in the pulsatile fraction of blood
  under the sensor probe. The Sat. is calculated
  from nomogram obtained from studies of healthy
  volunteers.
• Advantage
• Simple, self calibrating, continuous non invasive
  measurement of saturation in healthy and
  critically ill patients with adequate arterial
  profusion.
• Accurate at sat. gt90 and less accurate at sat.
  gt80 in spont. breathing healthy subjects and lt
  90 in mechanically ventilated patients.

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Factors affecting the accuracy of pulse oximetry
saturation.
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• Transcutaneous PO2
• TcPO2 measures local O2 across the dermal
  surface, allows cont. assessment unlike pulse
  oximeter it also measures hyperoxia.
• In neonates it is accurate and strongly
  correlates with PaO2. It needs heated electrode
  which can cause thermal burns and blisters.
• TcPO2 is inaccurate in adults because skin
  surface is thick, uneven and subject to changes
  in local blood flow.

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• Patients who need oxygen
• Respiratory arrest
• Fluid in the alveoli
• Pulmonary edema.
• Pneumonia.
• Near drowning.
• Chest trauma.
• Collapsed alveoli (atelectasis)
• a. Airway obstruction.
• Any unconscious patient.
• Choking.
• b. Failure to take deep breaths
• Pain (rib fracture).
• Paralysis of the respiratory muscles (spine
  injury).
• Depression of the respiratory center (head
  injury, drug overdose).
• c. Collapse of an entire lung (pneumothorax).

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• Other gases in the alveoli
• a. Smoke inhalation.
• b. Toxic inhalations.
• c. Carbon monoxide poisoning.
• Any patient in cardiac arrest.
• Any patient in shock.
• Any patient complaining of shortness of breath.
• Any patient with signs of respiratory
  insufficiency.
• Any patient breathing fewer than 10 times/
  minute.
• Any patient complaining of chest pain.
• Any patient suspected to be suffering a stroke.
• (Caroline, 1995).

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OXYGEN THERAPY IN SPECIFIC SITUATIONS Acute
exacerbation of COPD Rationale low flow O2 by
nasal cannula or ventura mask is given during
acute vent. failure to achieve PaO2 of 60 Hg and
SaO2 of 92. Intubation is indicated on the
basis of objective undersirable effects of
respiratory acidosis (PH lt7.20), consciousness
level deterioration or development of
arrhythmias. O2 induced hypercapnia is related
to an increase in (VD/VT) or (V/Q) mismatch. NPPV
significantly decreased the rate of intubation.
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• In Acute Asthma
• The worsened V/Q with parentral bronchodilators
  is due to the substantial increase in cardiac
  output. Because of absence of appreciable shunt,
  these patients respond to modest O2 suppl. with
  correction of hypoxemia.
• O2 therapy need not be controlled unlike the
  situation in COPD.
• O2 attenuates bronchoconstriction in EIA.

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• O2 Therapy in Cardiovascular Diseases
• In cardiogenic pulmonary edema O2 suppl. is part
  of the standard therapy.
• CPAP of 12.5 cm H2O O2 suppl. improved
  oxygenation and cardiac function.
• O2 is recommended in patients with CAD or CHF
  with associated hypoxemia.

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• Oxygen in Liver Disease
• The intrapulmonary shunt and diffusion-perfusion
  defect characteristic of the hepato pulmonary
  syndrome result in increased P (A-a)O2.
• The high C.O aggravates hypoxemia.
• O2 is required to correct severe hypoxemia but
  resolution of the H.P.S. associated hypoxemia
  occurred only after liver transplantation.

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• Sickle Cell Crisis
• The pathophysiologic process of acute vaso
  occlusive crisis is due to presence of diskotic
  cells in the microcirculation where PO2 is
  decreased.
• O2 is a potent antisickling agent. Oxygenated
  RBCs can't sickle, and cells sickled at low PO2
  return to normal when oxygenated.
• Monitoring O2 therapy should be by ABG and not by
  pulse oximetry.

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• O2 Therapy in Sleep Breathing Disorders
• N.CPAP is the most effective treatment of OSA in
  terms of reducing RDI and DEF.
• TTO2 is superior to nasal O2, allowing O2 flow
  below the site of obstruction. Also may increase
  mean airway pressure and reduce OSA. It can be
  used alternatively in patients who can't tolerate
  CPAP.

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• Oxygen During Air Travel
• The risks of hypobaric exposure during air
  travel are related to
• Decrease in PaO2.
• Expansion of gases within trapped spaces (e.g
  bulla or pneumothorax). Within the range of (7000
  - 8000 feet) the TPO2 (150 mmHg) falls by 5 mmHg
  per 1000 feet ascended.

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• Prediction of in-flight PaO2
• Direct measurement of PaO2
• At simulated cabin altitude,
• Under hypobaric conditions (e.g. unpressurized
  air craft).
• PaO2 at 8000 feet 0.238 x (PaO2 sea level)
  20.098 x (FEV1/FVC) 22.258.
• This formula is used to predict a fall if
  in-flight PaO2 lt 50 mmHg for normal and stable
  COPD patients.
• PaO2 at sea level gt72 mmHg ? No need for
  in-flight O2.
• No guidelines currently exist for patients
  already receiving O2 at sea level and for those
  with hypoxemia caused by restrictive chest
  diseases and/or decreased ventilatory drive.

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Sequence of pulmonary changes during hyperoxic
exposure in humans
Beers, 1998
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Advantages and disadvantages of oxygen sources
Kampelmacher and Lammers, 1994
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• Domiciliary O2 LTOT
• Indications of LTOT
• Chronic airflow obstruction specially if PaCO2 gt
  45 mmHg.
• Advanced interstitial pulmonary disease.
• Advanced pulmonary malignancy.
• Advanced cystic fibrosis.
• Severe congestive heart failure.
• Cong. cyanotic heart disease.
• (Breslin et al., 1991).

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• Physiological Criteria for LTOT in COPD
• PaO2 lt 55 mmHg indicates immediate treatment.
• PaO2 56-60 mmHg when
• PaO2 lt55 mmHg daily at rest.
• PaO2 56-60 mmHg daily at rest and polycythemia
  (HCT gt55) or P (mPAP gt 20 mmHg) or clinical
  corpulmonale or other manifestations of tissue
  hypoxia e.g. neuropsychiatric symptoms.
• PaO2 gt 60 mmHg troubled by nocturnal or E.I
  hypoxemia. No need for LTOT.
• (Herwaarden et al., 1996).

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• Patient should be non smoker, properly treated,
  clinically and functionally evaluated after a
  stabilization period of 6-12 weeks.
• The rationale for LTOT is to improve survival
  and give better quality of life.
• The goal is to achieve PaO2 60-80 mmHg and SaO2
  gt90.
• Prescription O2 should be continuous for at
  least 15 hs/day. Increasing the hours gives
  better results. Sudden breaks result in severe
  hypoxemia.
• Dose
• Daytime at rest 1-3 L/min.
• At night additional 0.5-1 L/min.
• During exercise up to 4-6 L/min.

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• Adverse Effects of O2 Therapy
• These may be related to the device used e.g.
  nasal irritation, epistaxis, conjunctivitis
  inspissated secretions or barotrauma and
  volutrauma associated with mech. ventilation.
• O2 induced hypercopnia in COPD is due to V/Q
  mismatch.
• Hyperoxia produces pulmonary toxicity through
  production of O2 free radicals (O2-, OH-, O1,
  H2O2) at a rate that overwhelmes the antioxidant
  defences.
• O2F.R damage cell membranes, enzymes and nucleic
  acids leading eventually to cell death.

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• Management Strategies to Improve Oxygenation in
  ARDS
• Low VT PEEP.
• Inverse ratio ventilation (IRV).
• Permissive hypercapnia with low VT approach.
• Extrapulmonary Gas Exchange Techniques
• Extracorporeal membrane oxygenation (ECMO).
• Intravena caval oxygenation (IVOX).
• Extracorporeal CO2 removal (ECCO2R).
• Prone positioning.
• Partial liquid ventilation (PLV) and (PAGE).
• Surfactant (survanta, alveofact, curosurf or
  exosurf).
• Nitric oxide (NO).
• Prostacyclin.

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• Hyperbaric Oxygen Therapy
• HBO therapy involves intermittent inhalation of
  100 O2 under a pressure gt1 atm (IATA 1 kg/cm2
  or 735.5 mmHg).

• Mechanisms of Action
• Pressure
• Mechanical reduction in the bubble size by an
  increase in the ambient pressure. At 5 atm. the
  bubble is reduced to 20 of its original volume
  and 60 of its original diameter.

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• Hyperoxia
• The amount of O2 in plasma is 0.3 ml. An
  increase in PO2 has a negligible impact on total
  HbO2 content, however it increases the amount of
  O2 dissolved in plasma.
• CaO2 (Hb x 1.34 x Sa O2) (PaO2 x 0.003)
• with 100 FIO2, plasma O2 increases to 2 ml. At
  3 ATA plasma O2 increases to 6.8 ml (the average
  tissue requirements for O2). Thus, HBO could
  sustain life without Hb.
• (Hyperoxia Life without blood).

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The immune system, antimicrobial and phagocytic
activity, wound healing, vascular tone are all in
need for O2. The antimicrobial activity ceases
under conditions of hypoxia (tissue PO2 lt 30
mmHg). HBO produces generalized vasoconstriction
and small ? C.O but the ? in plasma O2 result in
an overall ? DO2 to tissues. In conditions such
as burns, cerebral edema crush injuries, this
HBO induced (v.c) reduces edema and swelling
while keeping adequate tissue oxygenation.
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• Indications for HBO
• Acute conditions
• Decompression sickness.
• HBO at 3-6 ATA reduces bubble size, ? N2
  gradient and ? DO2 to ischemic tissues.
• Air or gas embolism.
• Immediate descent to 6 ATA for 15 - 30 min. Then
  to 3 ATA with prolonged O2 therapy.
• CO poisoning
• HBO at 3 ATA decreases COHb half life from 320
  min. to 20 min.
• Acute traumatic ischemia, crush injury and
  compartment syndrome.
• Clostridial gangrene.
• Necrotizing soft tissue infection.

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• Chronic conditions
• Osteomylitis (refractory).
• Radiation necrosis
• Osteo-radionecrosis and soft tissue
  radionecrosis.
• Caries in radiated bones.
• Skin grafts or flaps (compromised).
• Enhancement of healing in selected problem wounds.

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• Major Complications of HBO
• Barotrauma
• Pneumothorax, pneumomediastinum and air embolism.
• Ear trauma, tympanic membrane rupture and sinus
  trauma.
• Oxygen toxicity
• Pulmonary O2 toxicity.
• CNS toxic reactions.
• Others
• Claustrophobia.
• Reversible visual changes.

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Extracorporeal Membrane Oxygenation "ECMO" Blood
passes from the ivc (via a femoral vein catheter)
through a gas exchanging membrane, the oxygenated
blood being returned to the aorta (via a femoral
artery catheter). ECMO requires high blood flows
up to 80 of C.O which may lead to blood trauma
and ? pulmonary perfusion. This may compromise
lung repair.
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ECCO2 R is a veno-venous technique (femoral vein
- ivc). Low flow rates (1-2 L/min) with high gas
flow 40 L/min) reduce blood trauma and provide
50 of total O2 requirement. ECCO2 R combined
with low PPV improved ventilation and perfusion
and consequently lung repair in ARDS. IVOX
technique a device placed in the ivc to allow
gas exchange through microbore tubes to supply
90 of O2 requirement.
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Heliox, a premixed gas (80 or 70 He and 20
or 30 O2) is one third the density of air.
Hence, it decreases the driving pressure required
to move gas across narrowed airways. In upper
airway obstruction, Heliox alters gas flow from
tubulent to laminar and decreases airway
resistance. Heliox proved to be effective in
diffuse airway obstruction associated with acute
asthma and COPD.
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PFCs have low surface tension, high density,
slow evaporortion, and homogenous
distribution. PFCs decrease surface tension by
coating the alveolar lining, maintaining alveolar
stability. Being non compressible fluid, they
distend alveoli abolish the alveolar lining air
interface. This results in improvement of V/Q
mismatch and oxygenation by recruiting
atelectatic alveoli, redirecting blood flow to
better ventilated non dependent areas.
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Sorougi and Masoud on 1982 studied the
difference in PaCO2, as an index of ventilatory
response in COPD patients, between breathing room
air, 40 and 100 oxygen. All patients completed
the test with 40 O2 with little effect on PaCO2.
With 100 O2 only 5 patients completed the test
because of rise of PaCO2. The only parameter
that can depend on giving FIO2 gt40 to a COPD
patient is the initial PaCO2 while breathing room
air.
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Khalil Y, 1985 studied the role of controlled
O2 therapy in acute respiratory failure of COPD
through ABG, spirometric and hemodynamic
parameters. There was sig. improvement in
cardiac index, ? PCWP, ? PVR and ? A.R. with
observed improvement in ABG. In the study of
Goda, 1989 stable COPD patients were assessed
(pulmonary physiologic and hemodynamics) before
and 2 months after controlled low flow O2 for 18
hrs through the whole night and most of
daytime. The results showed sig. improvement in
PaO2 which correlated with the improved PAP, PVR,
FEV1, FVC, Ti, VT/Ti, P0.1, Pdi and
HCT. Correction of hypoxemia was the most
determinant factor in these studies.
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Khalil Y and Atta M.S., 1997 compared the acute
effects of n. BiPAP vs Almitrine bismesylate (AB
100 mg) on ABG, pulmonary hemodynamics, LVEF, DO2
in stable COPD patients. BiPAP appeared to be
highly effective and superior to AB in improving
gas exchange and hemodynamic parameters, LVEF as
well as DO2 response.
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Hassanein et al., 1998 studied BiPAP in patients
with acute R.F due to COPD exacerbation with
special emphasis on reducing the rate of
intubation. Though BiPAP reduced the need for
intubation, it didn't reduce PaCO2 to the
baseline level which is a golden target in the
management of acute exacerbation of COPD.
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El-Kholy et al., 1998 investigated the effects
of oxidative stress on plasma F.A. profile in
(mech. vent.) and (non vent.) COPD patients with
acute infective exacerbation and acute resp.
failure. With the oxidative stress, there was
loss of "PUFA" with adaptive rise in "SFA" and
mono USFA "Oleic acid". a pattern aggravated by
mech. ventil. hence, the need for antioxidants as
adjuvant therapy.
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Assessment of tissue oxygenation in patients
with chronic hypoxemia. Khater, 1995 demonstrated
that Oxygen ectraction index, concentration of
Extractable O2 and compensation factor were
closely correlated to each other and to PVO2,
reflecting the state of tissue oxygenation in
these patient, with ch. hypoxemia.
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O2 extraction tension is a better index to the
overall O2 status than PaO2, to be used in
different clinical situations. In these patients
with ch. stable P.F., VO2 is independent of DO2
and they react to exercise with ? DO2 and tissue
O2 extraction.
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Abdel Maguid et al., 1983 recommended
supplemental O2 during thoraconcnetesis
particularly when large volumes (800 ml) are
aspirated. Abd El Sabour et al., 1999 showed
that suppl. O2 is important during and after
injection sclerotherapy specially in patients
with Pugh Child B and C lec. of hepato pulmonary
susped.
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Arafa et al., 2000 demonstrated that hypoxemia
that might develop during F.O.B. should be
corrected by suppl. O2 to prevent the potential
and serious cardiac complications.
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In sleep breathing disorders Abd El Aty N, 1993
showed that monitoring nocturnal O2 sat. by pulse
oximetry is a simple screening test for O.S.a.
for COPD with OSA full P.S.G. is
indicated. Tagel Din, 1994 studied 8.5 patients
with OSA by fall PSG. management included and for
home treatment. Domiciliary O2 at 2-4 L/min. was
prescribed for patients who didn't use CPAP with
25 recorded improvement.
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Oral oxygen therapy Salah El Din, 2000 studied
oral liquid O2 in COPD and I.P.F patients with
hypoxemia. Thirty drops t.d.s. /8 hrs for 7
days. There was sig. improvement in PaO2 in both
V.P.F. and COPD groups and PaCO2 showed sig.
decrease in both groups by the end of the study.
No remarkable effects on P.F.T. could be detected.
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Hyperbaric oxygen therapy El-Shahawy, 1997
studied the effect of HBO on H. pylori induced
gastric and duodenal levious. He demonstrated
that eradication of H. pylori by HBO is more
rapid in gastritis than due gastritis and again
better than in peptic ulcer disease.
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Khalaf, 1998 studied the early effects of HBO on
the cellular and biochemical profile of BAL of 20
divers from the Egyptian Naval Rescue Unit
(E.N.R.U). BAL was done before and 2 hs. after
exposure to 100 O2 at 3 ATA. The results showed
that in BAL, neutrophils and macrophages,
albumin, phospholipids, fibronectin and n.
elastase could be considered an early markers for
O2 toxicity.
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FUTURE PERSPECTIVES ARTIFICIAL OXYGEN
CARRIERS Hb-based O2 carriers With genetic
engineering (using recombinant DNA technology)
fucntional human Hb could be produced in
bacteria, yeast and plants. Fucntional
characteristics can be achieved by specific amino
acid substitutions to reduce O2 affinity and ?
DO2 to tissues.
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Artificial blood cells The O2 dissociation curve
of encapsulated Hb is similar to that of RBCs, an
artificial membrane protects the cell from
enzymatic activity and released
haem. Liposomes Microencapsulation of Hb in
bilayered phospholipids and sterols with the
formation of artificial RBC (enohemocyte or
pseudo hemocyte) with variable oxygen affinity.
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Nanocapsules Micro encapsulation of polymer Hb
and enzymes in "n. caps." decreases effects of
lipids on RES, avoids peroxidation and increases
stability. Also reduce methemoglobin and radical
scavengers e.g. SOD and catalase (Change and Yu,
1998).
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• Adverse effects of artificial oxygen carriers
• Immune suppression.
• Nephrotoxicity.
• Free radical production.
• Vasoconstriction.
• Neurotoxicity.
• Interference with lab. chemistry.

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Perfluorocarbons "PFCs" Synthetic hydrocarbons
able to dissolve large quantities of gases
including O2 and rank in the order CO2
gtO2gtN2. The O2 solubility for PFCs is 40-50
(when equilibrated with 100 O2 at 37?C at atm.
pressure) compared to 3 for plasma. The O2 E.R
for PFCs is much higher than that of blood or Hb
soentions, thus increasing O2 diffusion to
tissues even at low PO2 (Ma et al., 1997).
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• Possible biomedical applications for artificial
  oxygen carriers
• Oxygen delivery to ischemic tissues.
• Fluid resuscitation and perioperative blood loss.
  Wound healing.
• Organ preservation for transplantation.
• Cell culture.
• Cancer therapy.
• Imaging and diagnostics.
• Liquid ventilation.
• Prevention of air embolism.
• Ophthalmic surgery.
• (Adams and Cashman, 2000).

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Fouda E, 1991 compared arterial vs venous
samples for PO2, PCO2 and PH. in acute severe
asthma. A sig. difference was observed in PO2
and PCO2 but not in PH. There was ve correlation
among the values of PO2, PCO2 and pH in the
arterial and venous samples during the course of
treatment.
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Arterio-venous differences in PO2 and PCO2 were
smaller during acute attacks increasing
progressively after relief of the acute hypoxic
state and further increase after complete
improvement.
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In the study of Khalil M and Hosny M, 1994
changes in ABG were traced following the use of
nebulized salbutamol in patients with acute
asthmatic exacerbations. A fall in PaO2
following the use of nebulized B2 agonists is
unpredictable and it is wise to use O2 supplement
only when there is initial hypoxemia.
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Sharaf El Din et al., 1998 studied the local
antioxidant defences is bronchial asthma. They
demonstrated that there's an increase in local
production of glutathione and selenium is much
reduced in serum and BAL of those asthmatics.
This deficiency may be a contributing factor in
the pathogenesis of asthma.
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