basics of anaesthesia monitoring

1. Oxygen and associated gasses
Dr.Pradeep Charan
Dr.Rakesh Kumawat

2. HISTORY:
Oxygen was officialy
discovered by
Joseph Pristley
in August 1774.
Lavoisier & Colleagues
1780 – 1789
Demonstration
of significance

3. Preparation :Large scale commercial preparation is
done by fractional distillation of air
In some conditions, Electrolysis of
water and other chemical reactions
are used to prepare O2.
Storage : O2 is stored in Liquid form in insulated
tanks.
or as Gas form in cylinders at high
pressures (102783.8 mm Hg. or 2000
psig or 13700 kpa)
A Pressure regulator maintain a
constant supply pressure of 400 kpa
(60 psi or 3001mmHg) in hospital pipe
sytem

4. Oxygen :
Properties:
Molecular Weight 32.00
Relative Density 1.105
Boiling Point -1830C
Critical Temperature - 1180C
Melting Point -2180C
Abundance Atmosphere 20.95%
Human body 65%
Solubility in water at 370C 2.4 ml O2 / 100 ml of H2O
Solubility in Blood at 370C 0.003 ml/ 100 ml blood

5. Oxygen Lack (Hypoxia)
• Failure of the tissue to receive adequate
quantities of Oxygen is variously described as
anoxia, hypoxia or oxygen lack
• Anoxia means total lack of oxygen

6. OXYGEN THERAPY ….. WHAT?
Administration of O2 in concentration more than in
ambient air
↑Partial Pr of O2 in insp. Gas (Pi o2)
↑Partial Pr of O2 in alveoli (PAo2)
↑Partial Pr of O2 in arterial blood (Pao2)

7. What is the Oxygen Cascade?
The process of declining oxygen tension from atmosphere to
mitochondria
Atmosphere air (dry) (159 mm Hg)
↓ humidification
Lower resp tract (moist) (150 mm Hg)
↓ O2 consumption and alveolar ventilation
Alveoli PAO2 (104 mm Hg)
↓ venous admixture
Arterial blood PaO2 (100 mm Hg)
↓ tissue extraction
Venous blood PV O2 (40 mm Hg)
↓
Mitochondria PO2 (7 – 37 mmHg)

8. OXYGEN CASCADE
• PO2 drop in stages from
158mmHg (21KPa) in dry
air to the low levels in the
mitochondria
• Pasteur point- level of
PO2 fall in the
mitochondria to 1-2mm
Hg (0.2 Kpa)where
aerobic metabolism
stops, anaerobic
metabolism will start and
acidosis will occur.

9. METABOLISM

10. O2Hb dissociation curve
0 20 40 60 80 100 120 140 160
0
20
40
60
80
100
%
Hb
Sat
with
O
2
PO2 mmHg

11. Classification of Hypoxia
1. Hypoxic Hypoxia: defective mechanism of oxygenation in
the lungs due to
a Reduced PiO2 • Decrease FIO2 Rebreathers.
Hypoxic gas supply
• Decrease Barometric pressure High altitude
b Fink effect / diffusion
Hypoxia
•Solubility N2O more than N2
c Reduced alveolar
ventilation
• Absolute
• Relative – Fever, Seizures, Halothane shakes
d Reduced diffusing
capacity
• Due to thickening of alveolar capillary membrane
e Venous admixture • True shunt – Rt to Lt shunt
• Intrapulmonary shunting in Zones of Low V/Q ratio
e.g. atelectasis etc.

12.  2. Stagnant hypoxia –type of hypoxia which is
caused by inadequate blood flow ,which
results in less oxygen available to the tissues
Decrease tissue perfusion
General – Decrease Cardiac output
Local – Arterial or venous occlusion e.g.
atheroma,
embolism,
trauma,
Vasoconstriction.

13. 3. Histotoxic hypoxia– adequate amount of oxygen
is inhaled through the
lungs and delivered to
tissues,but the tissues are
unable to use the oxygen
sodium nitroprusside contains a cyanide radical,
so overdose of this drug can cause histotoxic
hypoxia
Low P5O - Partial pressure of O2 at which Hb is 50%
saturated. normally 27mm Hg (3.6 kpa).
Low P50 – Shift to Left of Hb dissociation
curve. In this way, low P50 can produce
tissue hypoxia
Cause of shift to left is alkalosis,redused 2,3
DPG,hypothermia

14. 4. Anaemic hypoxia - due to
Decrease concentration of functional hemoglobin
PaO2 is normal
(a)Anemia – Increase 2,3 DPG Synthesis – shift to Rt – unloading
O2 blood to tissue.

15. (b) CO Poisoning –affinity of Hb for CO is about 250
times higher then O2
 Coal gas is common cause of co poisoning
 Commercial paint remover contain methyl chloride
has caused sever co poisoning

16. Methaemoglobinaemia - Methemoglobin lacks the
electron that is needed to form a bond with oxygen
and, thus, is incapable of oxygen transport.
Sulphhaemoglobinaemia- rare blood condition that
occurs when a sulfur atom is incorporated into the
hemoglobin molecule.

17. Post operative Hypoxia –
i. Fink effect
ii. Increase V / Q mismatch due to decrease
FRC.
iii.Stagnant Hypoxia
iv.Hypoventilation
(a) Drugs
(b) Obstruction
(c) Pain
(d) Intra operative Hyperventilation.

18. Effects of Hypoxia –
Depends on :
Duration, degree of hypoxia
Idiosyncracy of individual
Other factors such as drugs, disease & temperature.
CVS Systemic vascular resistance reduced
Cardiac output increased
Peripheral chemoreceptor stimulation – increase in
sympathetic activity
CNS Cerebral vasodilation
RS Ventilation increased
Pulmonary vascular resistance increased
METABOLISM Aerobic metabolism reduced
Anaerobic metabolism – metabolic acidosis
ORGAN FAILURE
Haemoglobin Cyanosis
Reduced haemoglobin is a better buffer
Reduced solubility of haemoglobin S in chronic hypoxia

19. Goal :
To maintain
adequate tissue
oxygenation while
minimizing cardio
pulmonary work.

20. Objectives:
To correct documented or suspected acute
Hypoxemia.
To Decrease symptoms associated with chronic
Hypoxemia.
To Decrease workload that hypoxemia imposes
on the cardiopulmonary system.

21. Indications
• Documented hypoxemia
• Adults, children, and infants : PaO2 < 60 mm
Hg or SaO2 < 90%
• Neonates, PaO2 < 50, SaO2 < 88%, or capillary
PO2 < 40mm Hg
• Acute care situations in which hypoxemia is
suspected
• Acute myocardial infarction.
• Cardiogenic pulmonary edema
• Acute Lung injury
• Acute respiratory distress syndrome
• Pulmonary fibrosis
• Cyanide poisioning

22. ASSESSMENT
• The need for oxygen therapy should be
assessed by
1. monitoring of ABG - PaO2, SpO2
2. clinical assessment findings.

23. PaO2 as an indicator for Oxygen
therapy
• PaO2 : 80 – 100 mm Hg : Normal
60 – 80 mm Hg : cold, clammy
extremities
< 60 mm Hg : cyanosis
< 40 mm Hg : mental deficiency
memory loss
< 30 mm Hg : bradycardia
cardiac arrest
PaO2 < 60 mm Hg is a strong indicator for
oxygen therapy

24. Clinical Signs of Hypoxia
Finding Mild to Moderate Severe
Respiratory Tachypnea Tachypnea
Dyspnea Dyspnea
paleness Cynosis
Cardiovascular Tachycardia Tachycardia, eventual bradycardia,
arrhythmia
Mild hypertension,
peripheral
vasoconstriction
Hypertension and eventual Hypotension
c.n.s Restlessness Somnolence
Disorientation Confusion Distressed appearance
Headache Blurred vision
Lassitude Tunnel vision, Loss of coordination,
impaired judgment, Slow reaction time,
Manic-depressive activity, Coma,
Clubbing.

25. MONITORING
• Physical examination for clinical findings of
hypoxemia
• Pulse oximetry
• ABG analysis
– pH
– pO2
– pCO2
• Mixed venous blood oxygenation

26. Oxygen Delivery Equipments
Classification
Category Device FiO2 Stability
Low Flow Nasal Cannula Variable
Nasal Catheter Variable
Transtracheal Catheter Variable
Reservoir Reservoir Cannula Variable
Simple mask Variable
Partial rebreathing mask Variable
Nonrebreathing mask Variable
Nonrebreathing Circuit (closed) Fixed
High Flow Air-entrainment mask Fixed
Air-entrainment nebulizer Fixed
Blending system (Open) Fixed
Enclosure Oxyhood Fixed
Isolette Variable
Tent Variable

27. Oxygen Content (Co2)
Amount of O2 carried by 100 ml of blood
Co2 =Dissolved O2 + O2 Bound to hemoglobin
Co2 = Po2 × 0.0031 + So2 × Hb × 1.34
(Normal Cao2 = 20 ml/100ml blood
Normal Cvo2 = 15 ml/100ml blood)
Co2 = arterial oxygen content (vol%)
Hb = hemoglobin (g%)
1.34 = oxygen-carrying capacity of hemoglobin
Po2 = arterial partial pressure of oxygen (mmHg)
0.0031 = solubility coefficient of oxygen in plasma

28. Oxygen Flux
Amount of of O2 leaving left ventricle per minute.
= CO × Hb sat x Hb conc x 1.34
100 100
= 5000 x 97 x 15.4 x 1.34
100 100
= 1000 ml/min
CO = cardiac output in ml per minute.
Do2 = oxygen flux

29. Complications of Oxygen therapy
1. Oxygen toxicity
2. Depression of ventilation
3. Retinopathy of Prematurity
4. Absorption atelectasis
5. Fire hazard

30. 1. O2 Toxicity
• Primarily affects lung and CNS.
• 2 factors: PaO2 & exposure time
• CNS O2 toxicity (Paul Bert effect)
– occurs on breathing O2 at pressure > 1 atm
– tremors, twitching, convulsions

31. Pulmonary Oxygen toxicity(Lorrain-Smith
effect)
C/F
 acute tracheobronchitis
• Cough and substernal pain
• ARDS like state

32. Pulmonary O2 Toxicity (Lorrain-Smith
effect)
Mechanism: High pO2 for a prolonged period of time
↓
intracellular generation of free radicals e.g.:
superoxide,H2O2 , singlet oxygen
↓
react with cellular DNA, sulphydryl proteins &lipids
↓
cytotoxicity
↓
damages capillary endothelium,
↓

33. Interstitial edema
Thickened alveolar capillary membrane.
↓
Pulmonary fibrosis and hypertension

34. A Vicious Cycle

35. How much O2 is safe?
100% - not more than 12hrs
80% - not more than 24hrs
60% - not more than 36hrs
Goal should be to use lowest possible FiO2
compatible with adequate tissue oxygenation

36. Indications for 70% - 100% oxygen
therapy
1. Resuscitation
2. Periods of acute cardiopulmonary instability
3. Patient transport

37. 2. Depression of Ventilation
• Seen in COPD patients with chronic hypercapnia
• Mechanism
↑PaO2
suppresses peripheral V/Q mismatch
chemoreceptors
depresses ventilatory drive ↑ dead space/tidal volume ratio
↑PaCO2

38. 3. Retinopathy of prematurity (ROP)
• Premature or low-birth-weight infants who receive
supplemental O2
• Mechanism
↑PaO2
↓
retinal vasoconstriction
↓
necrosis of blood vessels
↓
new vessels formation
↓
Hemorrhage → retinal detachment and blindness
To minimize the risk of ROP - PaO2 below 80 mmHg

39. 4. Absorption atelectasis
100% O2
oxygen
nitrogen
PO2 =673
PCO2 = 40
PH2O = 47
A B
A – UNDERVENTILATED
B – NORMAL VENTILATED

40. Denitrogenation Absorption
atelectasis
The “denitrogenation” absorption atelectasis is
because of collapse of underventilated alveoli
(which depends on nitrogen volume to remain
above critical volume )
↓
Increased physiological shunt

41. 5. Fire hazard
• High FiO2 increases the risk of fire
• Preventive measures
– Lowest effective FiO2 should be used
– Use of scavenging systems
– Avoid use of outdated equipment such as
aluminium gas regulators
– Fire prevention protocols should be followed for
hyperbaric O2 therapy

42. Oxygen challenge concept
↑ FiO2 by 0.2
↑ PaO2 > 10 mmHg ↑ PaO2 < 10 mmHg
↑ PaO2 < 10 mmHg in response to an oxygen challenge of 0.2 –
refractory hypoxemia

43. Implications of Oxygen challenge
concept
To identify refractory hpoxemia (as it does not
respond to increased FiO2)
Refractory hpoxemia depends on increased
cardiac output to maintain acceptable FiO2
Potentially deleterious effect of increased
FiO2 can be avoided

44. Carbon dioxide(CO2)
• First isolated by Black in
1757
• Physiological
significance was
appreciated by Yandell
Henderson & J.S.
Haldane

45. Properties of CO2
• Colourless
• Irritant to mucosa when inhaled in high
concentration
• CO2 found in atmosphere at a conc of 0.03 vol
percent
• CO2 stored in grey cylinder in liquid form

46. Preparation
 –by product in manufacture of hydrogen and
process of fermentation
 in laboratory
NaHCO3 +HCl --- NaCl+H2O+Co2

47. Use of CO2 in anaesthesia
• To rise the PCO2 when discontinuing IPPV so
that spontaneous respiration is established
more quickly
• To stimulate respiration after induction of
anaesthesia. So patient breath
N2O/O2/halothane mixture spontaneously
• Co2 is sometimes used to stimulate
respiration to facilitate blind nasal intubation

48. Helium(He)
• It was isolated by
Ramsay & Lockyer in
1895

49. Properties of He
• Inert, colourless,odourless gas
• Apart from hydrogen Helium is the lightest
known gas
• Molecular weight = 4
• Relative density= 0.14 (air= 1)
• Diffuse through skin and rubber

50. Preparation of Helium
• Main source: Natural gas is found in United
States in Texas and Kansas
• Other gases which are found in natural gas are
removed by absorption, liquefaction or
scrubbing with water and sodium hydroxide

51. Clinical uses of helium
• Partial respiratory obstruction
• for example in tracheal stenosis patient:-
80percent helium and 20 percent oxygen
having a relative density of 0.33 (air=1)is
administered
• It is important that it should be administered
via a well fitted face mask because if it is
diluted with air , the advantage of low relative
density is lost

52. Principles of gas analysis
• In anaesthesia practice, knowledge of the
concentration of a gas like O2, CO2 or N2O is
often required for the satisfactory
management of the patient

53. Classification of gas
analyser
1)Chemical analysis:- by
haldane apparatus that is
modified over the years in
various ways

54. 2) Physical analysis:-
• Magnetic analyser
• Infrared analyser
• Oxymeter
• Fuel cell
• Gas chromatography
• Mass spectrometer
3) Specific electrodes:-
For O2, CO2, N2O, N2 etc

55. References
Benumof’s Airway management
Morgan’s clinical anaesthesiology
Paul L. Marino The ICU Book.
churchill's