Oxygen
PHYsical Properties
Oxygen is:
tasteless,
colourless
and odourless,
with a specific gravity of 1.105
and a molecular weight of 32.
At atmospheric pressure, it liquefies at 183 C (B.P.)
(but at 50 ata the liquefaction temperature increases to 119 C.)
Oxygen supports combustion
although the gas itself is not flammable.
Manufacture.
Medical grade oxygen (99% or 99.5% pure)
manufactured by fractional distillation of liquefi ed air.
Before liquefaction of air, carbon dioxide is removed
and liquid oxygen and nitrogen separated by means of their
different boiling points
(oxygen, 183 C; nitrogen,195 C).
Oxygen Bulk Store
A reliable supply of oxygen is a critical requirement in any surgical area.
Oxygen is stored as a compressed gas at room temperature or refrigerated as a liquid.
Many institutions use piped oxygen
and this is supplied either by
o a bank of oxygen cylinders, ensuring a continuous supply,
o or from liquid oxygen
Small hospitals: store oxygen in two separate
Banks (groups) of several high-pressure O2 cylinders (H-cylinders) connected
by a manifold
All cylinders are of size J / large cylinders
The two groups alternate in supplying oxygen to the pipelines
Only one bank is utilized at a time.
In both groups, all cylinder valves are open so that they empty simultaneously
All cylinders have non-return valves.
The supply automatically changes from one group to the other when the first group of cylinders is
nearly empty.
The changeover also activates an electrical signaling system, which alerts staff to change the empty
cylinders
The number of cylinders in each bank depends on anticipated daily demand.
Manifold: contains valves that reduce the cylinder pressure (approximately 2000 pounds per
square inch [psig]) to line pressure (55 5 psig)
and automatically switch banks when one group of cylinders is exhausted.
.
.
large hospitals : liquid oxygen storage system
more economical in premises using in excess of 150,000 L of oxygen per week
o however even when a hospital possesses a liquid oxygen plant, it is still necessary to hold, an
additional reserve banks of oxygen cylinders that can provide one days oxygen requirements
in case of supply failure.
Liquid oxygen must be stored well below its critical temperature of 119C
{because gases can be liquefi ed by pressure only if stored below their critical temperature}.
Liquid oxygen is stored at a temperature of approximately 165 C at 10.5 bar in what is in effect a giant
Thermos flask a vacuum insulated evaporator (VIE).
Some heat passes from the environment through the insulating layer between the two shells of the flask,
increasing the tendency to evaporation and pressure increase within the chamber.
Pressure is maintained constant by transfer of gaseous oxygen into the pipeline system (via a warming
device).
However, if the pressure increases above 17 bar (1700 kPa), a safety valve opens and oxygen runs to
waste.
When the supply of oxygen resulting from the slow evaporation from the surface in the VIE is inadequate,
the pressure decreases and a valve opens to allow liquid oxygen to pass into an evaporator, from which gas
passes into the pipeline system.
The pressure of oxygen in a hospital pipeline is approximately 4 bar (60 lb in2),
which is the same as the pressure distal to the reducing valves of gas cylinders attached to anaesthetic
machines.
Liquid oxygen plants are housed some distance away from hospital buildings because of the risk of
fire.
Oxygen Concentrators. The oxygen concentrator depends upon the ability of an artificial zeolite to entrap molecules
of nitrogen
Oxygen concentrators produce oxygen from ambient air by absorption of nitrogen onto some types of alumina
silicates.
These devices cannot produce pure oxygen, but the concentration usually exceeds 90%; the remainder
comprises nitrogen, argon and other harmless inert gases.
Oxygen concentrators are useful both in hospitals and in long-term domestic use in remote areas, in developing
countries and in military surgery.
emergency (E-cylinder):
To guard against a hospital gas-system failure, the anesthesiologist must always have an
emergency (E-cylinder) supply of oxygen available during anesthesia.
Most anesthesia machines accommodate E-cylinders of oxygen
Oxygen is supplied in cylinders at a pressure of 137 bar (approximately 2000 lb in2) at 15 C.
In the UK, the cylinders are painted black with a white shoulder.
As oxygen is expended, the cylinders pressure falls in proportion
to its content
A pressure of 1000 psig indicates an E-cylinder that is approximately half full and represents 330
L of oxygen at atmospheric pressure and a temperature of 20C
If the oxygen is exhausted at a rate of 3 L/min, a cylinder that is half full will be empty in 110 min.
Oxygen cylinder pressure should be monitored before use and periodically during use.
Anesthesia machines usually also accommodate E-cylinders for medical air and nitrous oxide,
and may accept cylinders of
helium.
Compressed medical gases utilize a pin index safety system for these cylinders to prevent
inadvertent crossover and connections for different gas types.
As a safety feature of oxygen E-cylinders, the yoke has integral components made from Woods
metal.
This metallurgic alloy has a low melting point, which allows dissipation of pressure that might
otherwise heat the bottle to the point of ballistic explosion.
This pressure-relief valve is designed to rupture at 3300 psig, well below the pressure E-
cylinder walls should be able to withstand (more than 5000 psig).
Adverse Effects of Oxygen.
1. Fire. Oxygen supports combustion of fuels. An increase
in the concentration of oxygen from 21% up to
100% causes a progressive increase in the rate of combustion
with the production of either conflagrations
or explosions with appropriate fuels.
2. Cardiovascular depression. An increase in PaO2
leads to direct vasoconstriction, which occurs in peripheral
vasculature and also in the cerebral, coronary,
hepatic and renal circulations. This effect is not manifest
at a PaO2 of less than 30 kPa and assumes clinical
importance only at hyperbaric pressures of oxygen.
Hyperbaric pressures of oxygen also cause direct
myocardial depression. In patients with severe cardiovascular
disease, elevation of PaO2 from the normal
physiological range to 80 kPa may produce clinically
evident cardiovascular depression.
Absorption atelectasis. Because oxygen is highly
soluble in blood, the use of 100% oxygen as the inspired
gas may lead to absorption atelectasis in lung units distal
to the site of airway closure. Absorption
collapse may occur in as short a time as 6 min with
100% oxygen, and 60 min with 85% oxygen. Thus, even
small concentrations of nitrogen exert an important
splinting effect and this accounts for current avoidance
of 100% oxygen in estimation of pulmonary shunt
ratio (Qs /Qt )
ii
in patients with lung pathology, in
whom a greater degree of airway closure would result
in greater areas of alveolar atelectasis. Absorption atelectasis
has been demonstrated in volunteers breathing
100% oxygen
at FRC; atelectasis is evident on chest
radiography for a period of at least 24 h after exposure.
Pulmonary oxygen toxicity. Chronic inhalation
of a high inspired concentration of oxygen may
result in the condition termed pulmonary oxygen
toxicity (Lorrain-Smith effect), which is manifest by
hyaline membranes, thickening of the interlobular
and alveolar septa by oedema and fibroplastic proliferation.
The clinical and radiological appearance
of these changes is almost identical to that of the
acute respiratory distress syndrome. The biochemical
mechanisms underlying pulmonary oxygen toxicity
probably include:
oxidation of SH groups on essential enzymes
such as coenzyme A
peroxidation of lipids; the resulting lipid peroxides
inhibit the function of the cell
inhibition of the pathway of reversed electron
transport, possibly by inhibition of iron and SHcontaining
flavoproteins.
These changes lead to loss of synthesis of pulmonary
surfactant, encouraging the development of absorption
collapse and alveolar oedema. The onset of
oxygen-induced lung pathology occurs after approximately
30 h exposure to a Pio2 of 100 kPa.
Central nervous system oxygen toxicity.
Convulsions, similar to those of grand mal epilepsy,
occur during exposure to hyperbaric pressures of
oxygen.
Retrolental fibroplasia. Retrolental fibroplasia
(RLF) is the result of oxygen-induced retinal vasoconstriction,
with obliteration of the most immature retinal
vessels and subsequent new vessel formation at the
site of damage in the form of a proliferative retinopathy.
Leakage of intravascular fluid leads to vitreoretinal
adhesions and even retinal detachment. Retrolental
fibroplasia occurs in infants exposed to hyperoxia in
the paediatric intensive care unit and is related not to
the FiO2 per se, but to an elevated retinal artery PO2.
It is not known what the threshold of PaO2 is for the
development
of retinal damage, but an umbilical
arterial PO2 of 812 kPa (6090 mmHg) is associated
with a very low incidence of RLF and no signs of systemic
hypoxia. It should be stressed, however, that
there are many factors involved in the development of
RLF in addition to arterial hyperoxia.
Depressed haemopoiesis. Long-term exposure to
elevated FiO2 leads to depression of haemopoiesis and
anaemia.
Emergence and tracheal extubation after inhalational anesthesia carries high risk of cardiovascular
complications. It often provokes significant early postoperative arterial hypertension and
tachycardia in patients, which is thought to be mediated by increase in adrenaline concentration at
the time of emergence [1]. These hemodynamic responses are often worrisome for an anesthetist as
it causes increases in intra cranial pressure (ICP), myocardial afterload and oxygen demand and
peripheral vascular resistance; which may lead to increased chances of; intracranial bleeding,
myocardial infarction (MI), arrhythmia, postoperative bleeding form the site of surgery and
prolonged duration in the post-anesthesia care unit (PACU).
Recently, this problem has started to be addressed and studies are being conducted on exchange
extubation with laryngeal mask airway (LMA) [2] or on drugs which may blunt these hemodynamic
changes. Since, exchange extubation may risk losing the patients airway, prolong emergence time
and requires skill which may need experience and learning, it is safe to assume that most anesthetist
would prefer using a drug, then get themselves in a complex position at the time of patient
emergence and recovery. Various drugs have been used to attenuate these hemodynamic changes
and their efficacies compared. To name a few, remifentanil[3] (opioid), dexmedetomide[4] ( 2
agonist), verapamil[5], nicardipine[6], diltiazem[7] (calcium channel blockers), and esmolol[8] (1
antagonist) have all been used, in different groups of patients.
Lidocaine is a sodium channel blocker and a local anesthetic, it has long been known to help
reduce hemodynamic changes and has come under study in a number of trails to compare the
hemodynamic stability provided by various pharmacological interventions. It has been given in
intravenous (I/V) form at extubation, applied topically as gel on endotracheal tube (ETT) or as
spray directly on the vocal cords [9] and even used to fill ETT cuff [10].With a central neural
blockade mechanism of action, these changes may be attributable to the blocking of autonomic
fibers and a direct depressant effect on various components of the cardiovascular system.
Labetalol is a combined selective 1 -adrenergic receptor blocker and non-selective adrenergic
receptor blocker. It has come under study in neurosurgery patients [6-8] in whom hemodynamic
changes had to be avoided, as it would otherwise have led to catastrophic rises in intracranial
pressures. Since, labetalol lowers the blood pressure primarily by blocking peripheral arteriolar
alpha-adrenoceptors thus reducing peripheral resistance and, by concurrent beta-blockade, it also
protects the heart from reflex sympathetic drive that would otherwise occur. All these effects
would be expected to attenuate the hemodynamic response at the time of emergence and benefit a
patient undergoing elective non-cardiac surgeries.
In a study conducted in 50 American Society of Anesthesiologist (ASA) I and II patients, who
received no pharmacological intervention at emergence; in whom extubation was done when their
breathing was considered to be sufficient and were able to obey simple commands, Bindu et al
demonstrated, an increase of greater than 30% in heart rate (HR) and more than 20% rise in blood
pressure (BP), mean arterial pressure (MAP) from the preoperative baseline [11].The aim of this
trial will be to study the effectiveness of labetalol and lidocaine, in attenuating theses
hemodynamic responses, where the placebo group will act as a control. Effectiveness will
measured by comparing the decreases in HR, BP and MAP, in both the treated groups, as these
would lead to less workload and oxygen consumption by the heart, which would result in a smooth
recovery of the patients from General Endotracheal tube Anesthesia (GETA) and shorter stay in
the PACU.
