Clinical Measurement and Equipment

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Clinical measurement and equipment

Describe the physical principles of the pulse oximeter. What are


the limitations of the technique?
Most anaesthetists believe that continuous measurement of oxygen saturation
during anaesthesia is absolutely essential. Equally essential, therefore, is a
broad understanding c f how the technique works with particular reference to its
limitations and potential sources of error.
Introduction
Pulse oximetry has been widely available for only about 12 years but very
rapidly has become established as arguably the single most important form of
monitoring in anaesthetic practice.
Physical principles
 Oxygenated haemoglobin (HbO2) and deoxygenated haemoglobin (Hb)
have differential absorption spectra.
 At a wavelength of 660 nm (red light) HbO2, absorbs less than lib, hence
its red colour.
 At a wavelength of 940 run (infra-red light) this is reversed and Hb absorbs
more than Hb02. At 800 nm - the isobestic point - the absorption
coefficients are identical.
 The pulse oximeter uses two light emitting diodes which emit pulses of red
(660 nm) and infra-red (980 run) light every 5-10 μs from one side of the
probe. The light is transmitted through tissue to be sensed by a
photocell.
 The output is submitted to electronic processing during which the
absorption of the blood at the two different wavelengths is converted to a
ratio which is compared to an algorithm produced from experimental
data.
 Oximetry aims to measure the saturation in arterial blood, and so the
instrument detects the points of maximum and minimum absorption
(during cardiac systole and diastole). It measures the pulsatile component
and subtracts the non-arterial constant component before displaying a
pulse waveform and the percentage oxygen saturation. Hence, strictly
defined, it is measuring the Sao2 (plethysmographic) rather than the Sao2
(arterial).
Sources of error and limitations
 Pulse oximetry is calibrated against volunteers and so calibration against
dangerously hypoxic values is impossible. The instruments are less
accurate at Spo2 values <70%.
 Interference for ambient light. Can occur if light is bright and direct, but the
pulsed nature of the emissions is intended to allow detection of and
compensation for any ambient light.
 Loss of the pulsatile component. Occurs in conditions of hypoperfusion,
hypothermia, peripheral vasoconstriction, narrow pulse pressure, arrythmias
which distort the points of maximum and minimum absorption, venous
congestion.
 Movement artefact or electrical interference (neither are major problems).
 Infra-red absorption by other substances: nail varnish, staining from e.g. nicotine.
 More significant is absorption by abnormal haemoglobin and other substances:
— Heavy smokers or CO poisoning: carboxyhaemoglobin (COHb) has a similar
absorption coefficient to HbO, and will give abnormally high reading of -96%.
_ Jaundiced patients: bilirubin has a similar absorption coefficient to Hb and will
give abnormally low saturations.
- Meth4emoglobinaemia: MetHb has absorption similar at both wavelengths and
gives a reading of -84%.
— Dyes such as methylene or disuiphine blue give falsely low readings.

Problems in interpretation
· Pulse oximetry does not detect respiratory failure. A high F1o2, may mask
Ventilatory 'failure by ensuring high SPO2% readings.
· In very anaemic patients Spo2% readings may show high saturations although
oxygen delivery to the tissues may be impaired.
Describe the physical principles which underlie the function of a
'Rotameter' flowmeter. What factors may lead to inaccuracies in its use?
There are few anaesthetics given which do not involve the use of at least one
'Rotameter' flowmeter. ('Rotameter' is a tradename which continual use has
given the status of a generic object.) It is important, therefore, to be aware of how
they function as well as of potential sources of inaccuracy.
Introduction
it would be unusual to find many anaesthetics, either general or local, which do
not involve the administration of at least oxygen via a 'Rotameter'. 'Rotameter'
is the tradename for a variable-orifice, fixed-pressure-difference flowmeter,
which gives a continuous indication of the rate of gas flow.
Physical principles
· A bobbin floats within a vertical conical glass tube, supported by the gas

flow which is controlled by a needle valve.


· At low flows the orifice around the bobbin is an annular tube and the gas
flow is laminar. Flow rate through a tube is related to the viscosity of the
gas end the fourth power of the radius.
· At higher flows and further up the tube the area of the orifice is larger in

relation to the bobbin and the flow is turbulent. Flow rate is related to the
density of the gas and the square of the radius.
· These factors mean, therefore, that 'Rotameters' have to be calibrated for the

specific gases that they are measuring and are not interchangeable for
different gases.
· The pressure across the bobbin at any flow rate remains constant, because

the force to which it gives rise is exactly balanced by the force of gravity acting
on the bobbin.
Other features
· The bobbin is designed with small slots or fins in its upper part so that it will

rotate centrally within the gas stream. This is to prevent it sticking to the side
of the tube because of dirt or static electricity.
· To prevent the accumulation of static charge tubes have either a conductive

coating or have a conductive strip at the back.


· The flowmeter blocks are designed to ensure that the bobbin remains visible

at the top of the tubes.


Sources of inaccuracy
· Accumulation of dirt or static electricity not overcome by the design

features above.
· Flowmeter block that is not vertical: the bobbin must not impinge on the sides

of the tube.
· Back pressure on the gas flow may still be a problem on some anaesthetic

machines.
· Cracked seals or tubes may provide a source of error.
How does a capnometer or capnograph measure CO2 concentration?
What useful information is conveyed by the capnogram (the graph
of CO2 against time)?
Together with pulse oximetry, capnography is regarded by most anaesthetists to
be indispensable. Some believe it to be more useful than oximetry because of
the large amount of information that can be obtained from an end-tidal CO 2
reading and a capnograph trace. This question aims to explore whether you are
aware of the clinical information that can be obtained during routine CO 2
monitoring.
Introduction
Capnography has the potential to convey a large amount of vital clinical
information about both the respiratory and cardiovascular status of a patient,
and for this reason there are many anaesthetists who believe it to be the single
most useful form of monitoring in anaesthetic practice.
Physical principles
· Most capnographs measure CO2 by means of infra-red absorption. A molecule

will absorb infra-red radiation as long as it contains at least two different


atoms.
· The system comprises an infra-red source, a filter to ensure that only

radiation of the desired wavelength is transmitted, a crystal window (glass


absorbs infra-red), sample chamber and photodetector.
· The fraction of radiation absorbed is compared with a reference gas (so

regular calibration against zero and known CO2 concentrations is essential)


before the value is displayed.
· The infra-red wavelength absorbed varies with the gas, thereby allowing its

identification. There is some overlap between CO2 and N20 for which
modem instruments can compensate, collision broadening would otherwise
elevate falsely the CO2 readings.
Clinical information
 No CO2 trace:
- Oesophageal intubation. Its use is mandatory wherever tracheal
intubation is used.
- Disconnection of breathing system.
- Tracheal tube displacement.
- Cessation of CO2 production due to circulatory arrest.
 Low or falling end-tidal CO2:
- Hyperventilation. May be due e.g. to pain or inadequate anaesthesia in a
spontaneously breathing patient, or to over-ventilation in IPPV.
- Pulmonary embolism (gas or thrombus). Sudden fall of CO2 excretion due
to compromise of the pulmonary circulation.
- Decreased cardiac output, hypoperfusion, shock.
 Normal end-tidal CO2:
— Adequate ventilation.
 High or rising end-tidal CO2:
— Inadequate ventilation.
— Rebreathing (this may just increase the baseline which does not return to zero).
— Soda lime exhaustion.
— Malignant hyperpyrexia or other hypermetabolic state in which CO2
production increases.
 Abnormal capnography wave forms:
- Slow upstroke and slowly rising plateau: indicates chronic or acute
airway obstruction (this may be lower or upper airway as well as in the
breathing system).
- Inspiratory dips in the wave form: indicates partial recovery from
neuromuscular blockade.
- Raised baseline: rebreathing as above.
How can jugular venous bulb oxygen saturation be measured?
What is the purpose of this investigation? What factors cause it
to increase or decrease?
This is an area of specialist practice which you may not have encountered. If you
are struggling the answer is best developed from first principles.
Introduction
Jugular venous oxygen saturation (Sjvo2) provides a measure of global cerebral
oxygenation and finds uses in neurosurgery, in neurotrauma and in cerebral
monitoring during cardiac surgery.
Measurement
· Sjv 02 is usually measured via an intravascular catheter threaded retrogradely

up
the internal jugular vein as far as the jugular bulb. Normal value is 55-75%.
· A fibreoptic catheter uses reflectance oximetry (as in PA monitoring of mixed

venous saturation) to provide continuous Sjvo2monitoring. As with pulse


oximetry the apparatus uses the light absorption spectra of haemoglobin and
deoxyhaemoglobin.
· Catheter placement can be facilitated by locating the vessel using ultrasound,

and is verified by lateral skull X-ray which should confirm the tip lying at the
level of, and medial to, the mastoid process.
Alternatively a sample may be taken directly from the jugular bulb and the
oxygen saturation measured by co-oximetry.
Factors which change Sjvo2
· Sjvo2 is an indirect indicator of cerebral oxygen utilization: when o 2 demand
exceeds supply then extraction increases and Sjvo2 falls (desaturated at
<50%), conversely when supply exceeds demand it rises (luxuriant at >75%).
It is a specific measure of global cerebral oxygenation but is not sensitive to
smaller focal areas of ischaemia.
· The difference in oxygen content between arterial and jugular venous blood
(AjvDO2) is given by CMRO2 (cerebral metabolic rate for 02)/CBF (cerebral
blood flow). Normal is 4-8 ml 02/ 100 ml of blood.
· If AJVDo2 is <4 supply is luxuriant: if >8 it suggests ischaemia
· Increased oxygen demand or decrease in supply (fall in SJVo2 and rise in
Appo,) results from:
- Raised ICP.
- Systemic hypotension (severe).
- Hypocapnia (<3.75 kPa).
- Arterial hypoxia.
- Cerebral vasospasm.
— Increased metabolic demand: pyrexia, seizures.
· Decreased oxygen demand or increase in supply (rise in Soo, and fall in Afrood
results from:
- Decreased metabolic demand (hypothermia; sedation).
- Increased blood supply.
- Hypercapnia.
- Arterial hyperoxia.
- Brain death (minimal demand).
Explain the basic principles of surgical diathermy. What are its
potential problems?
Diathermy is used very widely in surgical practice but it does have
implications for the anaesthetist, who will be blamed, unfair though it may
seem, should a patient suffer a burn due to malpositioning of the plate.
Diathermy may also interfere with monitors and can disrupt pacemaker
function and so is a topic on which some basic knowledge is expected.
Introduction
Diathermy is used widely in surgical practice, both for coagulation and for
cutting, and relies on the heating generated as an electric current passes
through a resistance that is concentrated in the probe itself.
Principles of action
►Heat generation is proportional to the power that is developed: typically
50-400 W.
► high frequency sine waveform is used for cutting: typically 0.5 MHz.
► A damped waveform is used for coagulation: typically 1.0-4.5 MHz.
►High frequency is necessary because muscle is very sensitive to direct current
and to alternating current at frequencies less than –10 kHz. This is
particularly important in relation to myocardial muscle: low frequencies may
precipitate fibrillation.
►Burning and heating effects can occur at all frequencies.
Types of diathermy
· Unipolar. There are two connections to the patient: the neutral (or indifferent)

patient plate, and the active coagulation or cutting electrode. Current passes
through both but the current density at the active electrode is very high and
generates high temperatures. At the patient plate the current density is
dispersed over a wide area and heating does not occur. The patient plate and
hence the patient is kept at earth potential, which reduces the risks of
capacitor linkage (in which diathermy current may flow in the absence of
direct contact). Modern diathermy machines incorporate isolating capacitors
to minimise the problem. An alternative is to use an earth free or floating
circuit.
* Bipolar. Current is localised to the instrument: it passes only from one

blade of the forceps to the other. Bipolar diathermy uses low power, and
this limits its efficacy in the coagulation of all but small vessels. The circuit
is not earthed.
Problems
 Thermal injury at the site of the indifferent electrode (the diathermy
plate) which must be in close and even contact with a large area of skin,
ideally an area that is well perfused and which will dissipate heat.
Adhesive and conductive gels are useful. If the area of contact is small
the current density increases to the point at which a burn is probable.
 Thermal injury at metal contact site if plate is detached or malpositioned.
The diathermy current may flow to earth through any point at which the
patient is touching metal (operating table, lithotomy poles, ECG
electrodes, etc.) and cause a burn.
 Activation of instrument when it is not in contact with the tissue to be
cut or coagulated.
 Circuit may be completed via a route that does not include the
indifferent electrode: may result in a burn.
 Alcoholic skin preparation solutions have ignited after diathermy
activation.
 Interference with pacemaker function (indifferent electrode should be
sited as far distant as possible and bipolar should be used if possible).
 Diathermy may lead to ischaemia and infarction of structures supplied
by fine end-arteries. Classic examples include the penis (hence unipolar
must be avoided. in circumcision) and the testis which has a
vulnerable vascular pedicle.
Outline ways of measuring humidity and evaluate the methods by
which gases can be humidified in clinical practice. Why is this
important?
Anaesthesia frequently involves bypassing sites in the upper airway that are
responsible for the humidification of inspired gases. Artificial humidification is
important in the context both of anaesthesia and intensive care, and so you
will be expected to know about the different methods that are commonly
used.
Introduction
The mass of water vapour that is present in a given volume of air (the
absolute humidity) varies with temperature so that at 20°C fully saturated air
contains 17 g m-3. By the time that it reaches the alveoli at 37°C this air is
fully saturated and contains 44 g m-3. Anaesthetic and medical gases,
however, are dry and may bypass the normal humidification mechanisms.
Measurement
· Hair hygrometer. The hair, which is linked to a spring and pointer,

elongates as humidity increases. It is accurate between relative humidities of


-30% and 90%.
· Wet and dry bulb hygrometer. Cumbersome. Temperature difference

between two thermometers relates to evaporation of water round the wet


bulb which in turn relates to ambient humidity. Calculated from tables.
· Regnault's hygrometer. Accurate. Air is blown through ether within a silver

tube. The temperature at which condensation appears on the outer surface is


the dew point, the temperature at which ambient air is fully saturated. The
ratio of the s.v.p. at the dew point to the s.v.p. at ambient temperature gives
the relative humidity Determined from tables.
· Transducers. As a substance absorbs atmospheric water there is a change

either in capacitance or in electrical resistance.


· Mass spectrometer. Accurate. Expensive.

Methods of humidification
· HME (heat and moisture exchange) filter. This is a widely used method,

which is passive, and which cannot, therefore, attain 100% efficiency, but
which may reach 70-80%. The HME contains a hygroscopic material within a
sealed unit. As the warm expired gas cools so the water vapour condenses on
the element, which is warmed both by the specific heat of the exhaled gas and
the latent heat of the water. Inhaled, dry and cool gas is thus warmed during
inspiration, during which process the element cools down prior to the next
exhalation. Problems include moderate inefficiency in prolonged use,
increased dead space, infection risk.
· Water bath (cold). Passive, in that dry gases bubble through water at room

temperature. The system is inefficient (-30%) and becomes more so as the


loss of latent heat of vaporisation cools the water further.
· Water bath (warm). Active. Dry gases bubble through water which is

heated, usually to 60°C (to inhibit microbial contamination). Very efficient


>90%. More complex and risk of thermal injury to patient (minimised by
thermostats).
· Nebulisers. Active. Gas driven and ultrasonic. Not in common use. Can
deliver gas with >100% relative humidity and may overload pulmonary tree
with fluid.
Consequences of failure to humidify gases
· Drying and keratinisation of parts of the tracheobronchial tree.

· Reduction of ciliary activity and impairment of the mucociliary escalator.

· Inflammatory change in the dilated pulmonary epithelium, drying and

crusting of secretions.
· Mucus plugging, atelectasis, superimposed chest infection, impaired gas

exchange.
Patients at risk
· Those undergoing prolonged anaesthesia.

· Those with pre-existing respiratory disease in whom the impairment of

important pulmonary defence functions will be more significant.


· Those at the extremes of age: neonates, infants and the elderly.

· All intensive care patients.

Marking points: Detailed information about methods of measuring humidity


is Much less important than an awareness Of the advantages and limitations of the
devices that are in Use.. Commonsense alone should help you to identify which
patients are Particularly at .risk and you Will be expected to do so.
Describe the features of a modern anaesthetic machine that contribute
to the safety of a patient undergoing general anaesthesia.
This is a core topic. Your answer can readily be arranged by following the gas
flow through from cylinder or pipeline to the fresh gas outlet. The features are
numerous and you will have little time to do more than list them.
Introduction
The modern anaesthetic machine delivers accurate mixtures of anaesthetic gases
and inhalational agents at variable, controlled flow rates and at low pressure. It
accomplishes this via a number of features that are best described by tracing
the gas flow through the system from the cylinder or pipeline to the fresh gas
outlet.
Gas cylinders
· Colour coded for the UK (but no international consistency).

· Molybdenum steel: robust construction and rigorous regular hydraulic testing

(which also applies to the cylinder outlet valve).


· Pin-index system (unique to each gas) prevents connection to the wrong yoke,

and side guards on each yoke ensure that the cylinders are vertical.
· Bourdon pressure gauge indicates cylinder pressure.

· Pressure regulator/ reducing valve reduces pressure to 4 bar, and a relief valve

is located downstream in case of regulator failure.


Gas pipelines
· Colour coded for the UK (but no international consistency).

· Reducing valves lower pressures to 4 bar.

• Schrader coupling system ensures that connections are non-interchangeable.


· The hose connection to the anaesthetic machine should be permanent, the

threads are gas specific (NIST – non-interchangeable screw thread) and a one-
way valve ensures unidirectional flow.
Flow restrictors
 Placed upstream of the flowmeter block and protect the low-pressure part of
the system from damaging surges in gas pressure from the piped supply.
 May sometimes be used downstream of vaporiser back bar to minimise
back pressure associated with IPPV.
Oxygen failure devices
· Systems vary. In one example a pressure sensitive valve closes when 02 pressure

falls below 3 bar, and the gas mixture is vented, activating an audible warning
tone. The same valve opens an air-entrainment valve so that the patient cannot
be exposed to a hypoxic mixture resulting from failure of 0 2 delivery.
Flow control valves
 These govern the transition from the high to the low pressure system.
Reduce the pressure from 4 bar to just above atmospheric as gas enters the
flow Meter block.
 An interlock system between 02 and N20 control valves prevents N20
administration of >75%.
Flowmeters
 Constant pressure variable orifice flowmeters, calibrated for specific gas.
 Antistatic coating to prevent sticking, vanes in bobbin to ensure rotation
 Oxygen knob in UK is always on the left, is larger, is hexagonal in profile
and is more prominent than the others (this position risks hypoxic mixture
if there is damage to a downstream flow meter tube).
 CO2 has disappeared from many machines: where it is still delivered it is
usually governed to prevent a flow >500 ml min-1.
Vaporisers and back bar
· Most common is temperature-compensated variable bypass device to allow

accurate delivery of dialled concentrations.


· Locking mechanism on back bar prevents more than one vaporiser use at a

time.
· Non-return valve on back bar prevents retrograde flow (the pumping effect of

IPPV).
· Pressure relief valve on downstream end of back bar protects against increases

in the pressure within the circuit


Emergency oxygen flush
· 0 2 is supplied direct from the high pressure circuit upstream of the vaporiser

block and provides 35-75 L mirr' (if the 0, flowmeter needle valve is opened
fully it delivers - 40 L
· Both methods may cause barotrauma in vulnerable patients.

Common gas outlet ,


· Receives gases from the back bar and from the emergency 0 2 flush.
· Swivel outlet with standard 15 min female connection.
Classify the common types of hypoxia. What are the features of an
anaesthetic machine which are designed to minimise the risk of
delivering hypoxic gas mixtures?
The importance of these topics is obvious. The concept of oxygenation is
fundamental to anaesthetic practice, and machine safety is another core subject (is
similar to the previous question)
Introduction
The whole practice of anaesthesia itself is based on the avoidance of hypoxia,
the causes of which are classified as follows.
Causes of hypoxia
· Hypoxaemic hypoxia. Pao2 is low because of hypoxic inspired gas mixture,

severe alveolar hypoventilation or apnoea, ventilation/ perfusion mismatch


(endobronchial intubation, lung disease etc).
· Stagnant hypoxia. Pao2 , and haemoglobin oxygen-carrying capacity are

normal but the blood supply to tissues is inadequate due to diminished cardiac
output or occlusion of the peripheral vascular'system.
· Anaemic hypoxia. Pao2 is normal but low haemoglobin reduces 02 carriage

and delivery to tissues.


· Cytotoxic hypoxia. Pao2, and haemoglobin oxygen-carrying capacity are

normal but cellular poisons inhibit 02, utilisation. Examples are CN or CO


which poison cytochrome systems.
Anaesthetic machine features
· Gas cylinders

— These are colour coded for the UK (but no international consistency).


— Pin-index system (unique to each gas) prevents connection to the wrong
yoke, and side guards on each yoke ensure that the cylinders are vertical.
— Bourdon pressure gauge indicates cylinder pressure.
· Gas pipelines

- Colour coded for the UK (but no international consistency).


- Schrader coupling system ensures that connections are non-interchangeable.
- The hose connection to the anaesthetic machine should be permanent, the
threads are gas specific (NIST - non-interchangeable screw thread) and a
one-way valve ensures unidirectional flow.
· Oxygen failure devices

— Systems vary. In one example a pressure sensitive valve closes when 02


pressure falls below 3 bar, and the gas mixture is vented, activating an
audible warning tone. The same valve opens an air-entrainment valve so
that the patient cannot be exposed to a hypoxic mixture resulting from
failure of 02 delivery.
· Flow control valves
— An interlock system between 02 and N20 control valves prevents Is120
administration of >75%.
· Flowmeters

- Constant pressure variable orifice flowmeters, calibrated for specific gas.


- Antistatic coating to prevent sticking, vanes in bobbin to ensure rotation.
- Oxygen control knob in UK is always on the left, is larger, is hexagonal and is
more prominent than the others (however this position risks hypoxic
mixture if there is damage to a downstream flowmeter tube).
· Oxygen analyser
— Should be placed as near to the patient as possible, typically at the common
fresh gas outlet
What factors associated with the anaesthetic machine and patient breathing
system may cause barotrauma? How is the risk reduced? Why is a high airway
pressure alarm system important during general anaesthesia?
This is another variant on the machine safety theme but with a different
emphasis. You will see that familiarity with the basic features of the modern
anaesthetic machine can be very useful.
Introduction
High airway pressure (Paw) may indicate a direct problem with the patient or a
problem with the machine and breathing system that imminently may damage
a patient. High Paw alarms alert the anaesthetist to either possibility without
distinguishing between the two.
Equipment features
· Gas cylinders and pipelines

— Deliver very high and potentially lethal pressures.


— Pressure regulator/ reducing valve reduces pressure to 4 bar, and a relief
valve is located downstream in case of regulator failure.
— Reducing valves on pipelines lower pressures to 4 bar.
· Flow restrictors

— Placed upstream of the flowmeter block and protect the low-pressure part of
the system from damaging surges in gas pressure from the piped supply.
· Flow control valves
— These govern the transition from the high to the low pressure system.
Reduce the pressure from 4 bar to just above atmospheric as gas enters
the flowmeter block.
— Needle valves restrict flow.
· Vaporisers and back bar

— Pressure relief valve on downstream end of back bar protects against


increases in the pressure within the circuit
· Emergency oxygen flush

— 02 is supplied direct from the high-pressure circuit upstream of the vaporiser


block and can provides 35-75 L min-I (if the 0, flowmeter needle valve is
opened fully it delivers -40 min-').
— 02 flush may be jammed or held open. It should not be lockable.
— Both methods may cause barotrauma in vulnerable patients.
· Ventilator pressure relief valve

— Closes during inspiratory phase of IPPV and vents gas after bellows refills.
Should it stick in the dosed position the will increase.
· Scavenging system
— A pressure relief valve in system vents excess gas in reservoir to atmosphere. If
this valve fails then pressure is transmitted back to the breathing system.
· Breathing system and airway

- Kinks or obstruction in breathing system hoses will increase P aw.


- One-way PEEP valve will obstruct flow if placed in the inspiratory limb and
will obstruct expiratory flow if incorrectly orientated in the expiratory
limb.
- APL (adjustable pressure-limiting valve) will vent gas into the scavenging
system; if it is screwed shut the bag will distend with an increase in
pressure.
- Anaesthesia breathing bags are designed so that pressure will not exceed
-50-60 mmHg (behave according to the law of Laplace: P =2T/ R).
Problematic only in patients with lung disease (e.g. emphysema).
- ETT (or LMA) may kink or obstruct, may get cuff herniation.

Value of high airway pressure alarm


 Should be placed so that it senses pressure on the patient side of the
inspiratory and expiratory valves, not the machine side, so is as close to
the airway as possible.
 Warns of danger to the patient of barotrauma (factors described above).
 Warns of problems with the patient in whom high airway pressure may be
caused by:
— Bronchoconstriction.
— Pneumothorax.
— Expiratory efforts against ventilator (as muscle relaxants wear off).
Cardiac and thoracic anaesthesia

What are the main postoperative problems which occur in the first 24 hours
following a coronary artery bypass graft? Outline their management.
Coronary artery bypass grafting (CABG) is a common procedure in the developed
world, but although it has become routine there remain a large number of
potential complications, many of them related to cardiopulmonary bypass (CPB),
which can affect every organ system. The question is testing your appreciation of
the main principles rather than specifics. If you are struggling then it may help to
consider the worse case scenarios, given the huge array of complications of CPB
that have been described.
Introduction
Surgery for coronary artery disease involves the insertion of a vascular graft in
an organ which may have precarious function. The surgery may be prolonged
and is enabled by the use of cardiopulmonary bypass, which as a non-physiological
process has been associated with a large number of complications. There are,
therefore, several problems which may occur in the first postoperative day.
Cardiovascular
· Cardiac failure. Cardiac output may be compromised because of pre-existing

ischaemic damage or because the myocardium is stunned after CPB and


prolonged surgery.
— Deterioration is prevented by optimising oxygen supply in face of demand.
— Monitor function (PA catheter) and manage accordingly: inotropic support and
vasodilators may suffice. May need infra-aortic ballon pump counter-
pulsation or assist devices (depending on the centre).
· Tamponade. Cardiac output may be compromised by tamponade.

— High index of suspicion and early decompression.


· Arrhythmias. Cardiac output may be compromised by arrhythmias.

— Seek cause (e.g. IC' derangement) treat with anti-arrhythmics or pacing as


required.
• Bleeding. Cardiac output may be compromised by surgical bleeding or
coagulation problems.
— Check coagulation; discontinue drugs which may be contributing,
coagulation factors and platelets if indicated. Re-operation if bleeding
continues.
Systems problems
Many relate to CPB and potential effect of hypoperfusion and emboli on end-organs.
· Central nervous system. Failure to recover full consciousness.
Persistent drug effects? (particularly if hypothermic).
Micro-emboli during/after CPB: air, silicon, debris, fat, platelet aggregates. Cerebral
hypoperfusion.
Manage by maintaining cerebral perfusion pressure and oxygenation (but beware stressing
the graft by elevated systemic pressures).
· Renal. CPB reduces blood flow and GFR by 30%.
— Hypoperfusion and emboli may lead to acute renal failure.
— Appropriate renal support according to impairment.
· Pulmonary. May get 'pump lung': oedema due to overload with subsequent ARDS-like
picture.
— Supportive ventilatory and circulatory management.
· Gastrointestinal. Organ impairment may follow hypoperfusion and emboli.
— Pancreatitis, bowel ischaemia leading to acute abdomen.
— May need surgical intervention.
What are the principles of cardiopulmonary bypass in the adult? What are
the main complications of this technique?
Cardiopulmonary bypass (CPB) provides a substitute intact circulation while the
heart is isolated. It may make sense, therefore, for you to consider how the
normal circulation functions, because CPB is analogous. The technique is
complex and invasive and so there are complications associated with the
mechanics. It is non-physiological and yet perfuses every organ and system in the
body Many of the complications, therefore, are predictable, even if your
acquaintance with cardiac anaesthesia is slight.
Introduction
A patient who is on CPB has the temporary equivalent of an intact circulation.
The differences are that the heart is isolated, the flow is (usually) non-pulsatile,
and the circulation is exteriorised. Bypass is non-physiological and although it
enables complex cardiac surgery it has been associated with numerous
complications.
Principles of cardiopulmonary bypass
· CPB replaces the functions of the intact circulation by ensuring organ

perfusion with oxygen-enriched blood from which CO2 has been removed.
· Components include:

— Venous line (usually from vena cavae) drains into a reservoir for gas
exchange in which blood is oxygenated and CO2 is removed.
- Bubble oxygenator in which 02 is bubbled through the perfusate (cheap,
simple, but requires defoaming to reduce air emboli and damages formed
blood components).
Membrane oxygenator in which gas exchange takes place across a semi-
permeable membrane (fewer emboli form and less damage to RBCs).
- Arterial line (usually to ascending aorta) via a pump (roller or centrifugal):
flow may be non-pulsatile or pulsatile (no proven benefit).
_ Pump for cold cardioplegic solution (contains potassium for EMI) arrest,
energy substrate for metabolism).
_ Ventricular drain to vent heart: may get some aortic regurgitation if not
prevented by aortic cross-clamp, or flow through bronchial and thebesian
veins. May overdistend LV and cause critical ischaemia and post-bypass
dysfunction.
— Filters (27 micron) on both sides of the circulation to remove air and blood
micro-emboli (also reduce platelets).
- Heat exchanger is crucial part of the system to allow temperature control
(hypothermia reduces oxygen demand by 6-9% per °C fall in core
temperature).
- Priming: the system (volume 1.5-2.5 L) is primed either with crystalloid or
colloid/ crystalloid. Acute haemodilution is inevitable as soon as bypass is
established. Can prime with blood if necessary to maintain haematocrit at
20-25%.
- Anti-coagulation. Crucial. Coagulation within any part of the circuit (pump
or patient) is lethal. Synthetic surfaces of circuit cause diffuse thrombosis
and oxygenator failure if anticoagulation is inadequate.
· Complications of circuit;
— Arterial side: cannula may kink, block or fail to deliver adequate flow.

— Venous side: low return: bleeding, obstruction, air lock, aortic dissection.
— Oxygenator failure.
— Pump may cause aortic dissection.

— Coagulation may be inadequate.


— May react to prolamine reversal (anaphylactoid, histamine release,
hypotension, pulmonary hypertension).
— Inadequate LV venting: cardiac distension.
— Embolism: air, silicon, fat, platelet aggregates.

Complications associated with perfusion


· Hypothermia: coagulopathy, hyperglycaemia, drug metabolism reduced.
· Fluid overload (common).

· Coagulopathy: is related to CPB time (>2 hours is deleterious); decrease in

platelet number and function may deplete Factors V and VIII.


· Myocardial stunning after cardioplegia (temperature is crucial).

· Complement activation: may get 'post-perfusion lung' (ARDS).

· Central nervous system: potential ischaemia due to hypoperfusion,

problems with emboli: air, thrombus, debris, silicon (subtle post-bypass


deficits are -common).
· Renal function: bypass decreases renal blood flow and GFR by 30% (worse

if bypass time is prolonged).


· Gastrointestinal: hypoperfusion of splanchnic bed and potential for critical

gut ischaemia, pancreatic and liver dysfunction.


Marking points: If you can convey the basic principles of an artificial circulation you should
be able to outline the major complications which follow The complete hstwif not be expected
.
What are the anaesthetic implications of mitral stenosis?
Rheumatic heart disease is the commonest cause of mitral stenosis, but both
problems are increasingly rare. Valvular disease is of interest to anaesthetists
because of the risk that anaesthesia and surgery will cause perioperative
decompensation. It is a popular exam topic because it allows discussion of
physiology and pharmacology applied to a fixed cardiac output state.
Introduction
Mitral stenosis is almost always rheumatic in origin and is increasingly rare.
It is a progressive disease that leads to a fixed output state which is maintained
by compensatory mechanisms, and it is the propensity for anaesthesia to
disrupt these mechanisms that makes it such a significant condition.
Pathophysiology
►Narrowing (almost always rheumatic in origin) is slowly progressive
and symptoms appear relatively early. May suddenly deteriorate if there
is an increased demand for cardiac output as in pregnancy, or if atrial
fibrillation supervenes.
►Determination of the pressure gradient across the valve (LA : LV) is less
reliable than estimations of valvular area, which is the key factor which
determines flow, Normal mitral valve area is 4-6 cm' and stenosis may be
graded as revere (<I cm2), moderate (1.1-1.5 cm") and mild (1.6-2,5 ant)
(There is a gap between 2.5 and 4 cm2, which would be classified,
presumably, as 'very mild' or 'insign ficant'.)
►As narrowing progresses the contribution of atrial contraction to left
ventricular filling increases from 15% to 40%. This is why the onset of atrial
fibrillation may be so catastrophic. Atrial dilatation and hypertrophy results
from this compensation. In time the increased left atrial pressure (LAP) is
reflected in pulmonary hypertension and right ventricular overload.
►Relative bradycardia allows sufficient time for diastolic flow across the
stenosis.
Anaesthesia implications
► The main aim is to prevent decompensation.
►Bradycardia may allow an increased stroke volume but the cardiac output
may drop unacceptably as a result. Tachycardia may diminish stroke
volume to the point that cardiac output is even more impaired.
►Sudden onset of atrial fibrillation must be treated aggressively, with DC
cardioversion if necessary, otherwise pulmonary oedema may supervene. If
atrial fibrillation is already present the ventricular response rate must be
controlled. Patients may also be on oral anticoagulants which will need to be
changed to parenteral heparin during the perioperative period.
►Normovolaemia must be maintained. If LAP falls then cardiac output will
drop. Volume must be sufficient to allow flow across the stenotic valve.
Patients may also be very sensitive to any increase in venous return (as can
occur with the use of an arterial tourniquet or placing the patient in
lithotomy, as well as with infusions of fluid) which may precipitate pulmonary
oedema. Cardiac output cannot increase in response to enhanced venous
return.
► Effective myocardial contractility is important for the maintenance of
cardiac output in mitral stenosis (as in most valvular lesions), and undue
depression must be avoided.
•Must avoid increasing pulmonary vascular resistance (hypercapnia,
hypoxia, acidosis, nitrous oxide). Right heart failure, should it supervene,
must also be treated aggressively.
► Systemic vascular resistance must be maintained in order to allow
adequate coronary perfusion during diastole.
►Infective bacterial endocarditis potentially affects any abnormal valve
and antibiotic prophylaxis should be given.
What are the anaesthetic implications of aortic stenosis?
Aortic stenosis may be caused by rheumatic heart disease, but also occurs as a
consequence of degeneration and calcification in a congenitally abnormal
(usually bicuspid) valve. Anaesthetic management is based upon the need to
avoid perioperative decompensation. Like mitral stenosis, it is a popular exam
topic because it allows discussion of physiology and pharmacology applied to a
fixed cardiac output state.
introduction
Unlike mitral stenosis aortic stenosis may progress without symptoms so
that sudden death may even be the first presenting feature. Like mitral stenosis
it leads to a fixed output state which is maintained by compensatory
mechanisms, and it is the propensity for anaesthesia to disrupt these
mechanisms that makes it a significant condition. Decompensated mitral
stenosis manifests as heart failure; decompensated aortic stenosis may be
fatal.
Pathophysiology
►Determination of the pressure gradient across the valve (left ventricle :
ascending aorta) is less reliable than estimations of valvular area, which is the
key factor that determines flow. Normal aortic valve area is 2.5-3.5 cm2 and an
area ,1 .-r11.2 is an indication for immediate surgical valve replacement. At
areas <0.7 cm; any demand for increased cardiac output (exercise, pyrexia,
pregnancy, etc.; is associated with angina pectoris, syncope and sudden death.
Clinical signs include narrowec pulse pressure (<30 mmHg suggests severe
disease). Systolic blood pressure may be lower than expected because of the
reduced cardiac output (SBP = CO x SVR).
►As narrowing progresses there is increased pressure loading on the LV,
which undergoes concentric hypertrophy. The less compliant hypertrophic LV
has increased 02 demand and reduced 02 supply (systole through the
stenosed valve is prolonged and so diastolic time during the cardiac cycle is
proportionately reduced).
►Atrial contraction makes a significant contribution to left ventricular
filling, which must be maintained. Atrial fibrillation may lead to
decompensation.
Anaesthesia implications
►The main aim is to prevent decompensation, in particular by
maintaining coronary perfusion during diastole.
►Effective myocardial contractility is important for maintenance of cardiac
output in aortic stenosis (as in most valvular lesions), and undue depression
must be avoided. Increasing myocardial drive will increase myocardial work
and 02 demand, and may precipitate subendocardial ischaemia.
►Systemic diastolic blood pressure must be maintained. If SVR falls then
coronary diastolic perfusion may fail with disastrous consequences.
Vasodilatation must be avoided and preload maintained to allow flow across
the stenotic valve. This has obvious implications for the use of the many
anaesthetic agents which decrease SVR, including local anaesthetics used in
subarachnoid and extradural block. Cardiopulmonary resuscitation in the
presence of aortic stenosis and LV hypertrophy is rarely successful.
►Bradycardia will decrease cardiac output but tachycardia is even
more detrimental because it limits diastolic coronary perfusion. Arrhythmias,
including atrial fibrillation, require urgent treatment, but myocardial
depressants such as beta-adrenoceptor blockers are better avoided.
►Infective bacterial endocarditis potentially affects arty abnormal valve
and antibiotic prophylaxis should be given.
►These patients can be very difficult to manage. Anaesthesia should include
invasive monitoring of intra-arterial and central venous pressure, and it may
be
necessary to run a continuous infusion of vasopressor such as norepinephrine
(noradrenaline) to ensure that SVR is maintained.
How do you confirm that a double-lumen endobronchial tube has been
placed correctly? Outline the possible complications associated with this
procedure.
Some argue that clinical confima don of double-lumen tube placement should
largely be historical, although clinical assessment may have a place in conjunction
with other techniques. Most of the complications are linked to malposition and
this is the area on which your answer should concentrate.
Introduction
Double-lumen bronchial tubes, which allow separation and isolation of the lungs,
have an important role in thoracic, aortic, spinal and gastro-oesophageal surgery.
The surgical procedures are generally complex and prolonged and the hazards of
one-lung anaesthesia itself mandate that tube positioning must be optimal.
Clinical confirmation
· Double-lumen endobronchial tubes (DLEBT) are bulky when compared to a

conventional tracheal tube, and are more complex to insert. Different tubes
require different insertion techniques but in all cases there is rotation within
the airway of between 90° and 180°.
· Length of tube. Correct insertion defines the situation in which the upper

surface of the bronchial cuff is immediately distal to the bifurcation of the cw:na.
The distance can be measured. The average depth of insertion for a patient of
height 170 cm 's 29 cm, and the distance alters by 1 cm for every 10 cm change
in height. This distance from the incisors can therefore be used as a guide.
· Auscultation (both lung fields). With both tracheal and endobronchial cuffs

inflated, check bilateral and equal air entry (allowing for pulmonary pathology).
· Auscultation (alternate lung fields). Clamp one side and check that breath

sounds disappear on the ipsilateral, and remain on the contralateral side.


Reverse the orocess.
· Palpation. During all three stages above, manual ventilation using the reservoir

bag will reveal whether it has normal compliance (again allowing for pulmonary
pathology).
· Monitoring: oximetry and, particularly, capnography when compared from

both lumina, may indicate placement problems.


· Malpositioning. If the above signs indicate that the tube is in the wrong place a

combination of manoeuvres (unilateral clamping and bronchial cuff inflation-


deflation with repeated auscultation) can in theory identify the site and nature of
malposition. In practice this can be difficult, particularly if the tube moves during
surgery when access to the chest wall is limited.
Fibreoptic bronchoscopy
· It is evident, however, that clinical confirmation is insufficient. NCEPOD's 1998

examination of oesophagogastrectomy implicated problems with double lumen


tubes in 30% of deaths. Studies have confirmed that critical malpositioning
occurs in over 25% of cases and general misplacements complicate over 80% of
uses.
· Variations in anatomy are common, particularly if distorted by tumour or

effusion.
· Routine use of ftbreoptic bronchoscopy is the only way of avoiding these
problems and ensuring accurate positioning as well as intraoperative checking if
indicated. It also minimises the complications of DLEBT placement as outlined
below.

Complications of double-lumen tubes


· Malposition

Occlusion of major bronchus with lobar collapse and secondary infection.


Failure to achieve adequate lung separation and one-lung ventilation. This
may necessitate prolonged surgical retraction with associated trauma.
- Failure to protect dependent lung from infected secretions from non-
dependent lung (catastrophic in e.g. case of bronchopleural fistula).
· Trauma during insertion and rotation

— Disruption of the tracheobronchial tree, may be associated with excessive


endobronchial cuff pressures.
Trauma to larynx and supraglottic structures.
What physiological changes are associated with one-lung anaesthesia?
Describe the management of a patient in this situation who becomes
hypoxic.
One lung anaesthesia is a technique that is used for complex and specialist
procedures, but the physiological changes that ensue are of particular
anaesthetic relevance and so make it an attractive science-based clinical topic.
You will be expected to understand the basic principles rather than (as used to be
the case) details of the many and varied double lumen devices and bronchial
blockers that historically were used.
Indications
The indications for anaesthesia during which one lung is deliberately collapsed
to facilitate surgical exposure include pulmonary, aortic, spinal and oesophageal
surgery. Patients undergoing such procedures are commonly high risk and the
physiological changes imposed by one lung anaesthesia can present a
significant challenge.
Physiological changes
· The surgical side is uppermost and the non-ventilated upper lung is usually

described as the non-dependent lung.


· When ventilation is interrupted the remaining blood flow takes no part in gas

exchange and this shunt contributes to hypoxia.


· The shunt is reduced because gravity favours flow to the dependent lung, and
becaus€ surgical compression and lung retraction may further decrease blood
flow.
§ Surgical ligation of non-dependent vessels (in their entirety if a pneumonectomy

is being performed) will also reduce shunt.


· Hypoxic vasoconstriction decreases flow by -50% to the non-dependent lung and

may reduce shunt from -50% down to 30% (which is still significant).
· The dependent lung loses volume because of compression, and hypoxic

vasoconstriction, should it occur, may divert some blood to the non-dependent


lung.
· Secretions may pool in the dependent lung and suction removal via a double-

lumen tube may be difficult.


Ventilatory management
· Ventilator settings: same as for double-lung ventilation with tidal volume of -10

ml kg-': higher volumes increase Paw and vascular resistance so more blood
may flow to the non-ventilated lung and increase shunt. Lower volumes may
cause atelectasis.
• Although shunt is not substantially improved by supplemental 02 the F1o2 is
usually increased to 0.8-1.0.
· The respiratory rate is adjusted to keep Paco 2 at -40 mmHg (5.3 kPa).

Management of hypoxia
· Check F1o2, and increase if necessary (but may not help if substantial shunt is

the problem).
• Check tidal volume and ventilator indices.
• Check double-lumen tube position with fibreoptic bronchoscope (displacement to
a suboptimal position is common).
•Maintain at -5.3 kPa as hypocapnia may decrease hypoxic pulmonary
vasoconstriction.
•Add CPAP to upper lung (-5 cmH2O) and warn surgeon that lung may partially
re-expand.
• Add PEEP to lower lung (-5 cm1-120) to increase volume in potentially
atelectatic areas — but note that this may increase vascular resistance and
divert blood to upper lung.
•Increase both CPA? and PEEP in small increments.
•If none of these manoeuvres works it may be necessary to revert to full
double-lung ventilation (with retraction to allow surgery to continue

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