Moments with Morgan and Mickhail - Chapter 6, Part 1

Continue your journey to mastering anaesthesia—one chapter at a time. In this episode, Dr. J.R. Decker reads and discusses Chapter 6 (part 1) of Morgan & Mikhail’s Clinical Anesthesiology (7th Edition). Follow as you read along to strengthen your foundations in anaesthesia, one clear and engaging session at a time. Perfect for trainees, revision, or daily listening.

Episode Transcript

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Morgan and Mikhail's Clinical Anesthesiology, 7th Edition,
Chapter 6 Non cardiovascular monitoring Key concepts One

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carpinographs rapidly and reliably detect esophagal
intubation, A cause of anaesthetic catastrophe, but do
not reliably detect mainstream main stem bronchial intubation.

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2 Post operative residual paralysis remains a problem in
post anaesthesia care, producingpotentially injurious airway and
respiratory function compromise and increasing length of stay

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and cost in the post anaesthesiacare unit pack you.
The previous chapter reviewed the routine hemodynamic
monitoring used in anaesthesia practise.
This chapter examines the vast array of techniques and devices

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used perioperatively to monitor neuromuscular transmission,
neurological condition, respiratory gas exchange, and
body temperature. Respiratory gas exchange

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monitors Precordial and esophagal stethoscopes
Indications Prior to the routineavailability of gas exchange
monitors, anesthesiologists use the precordial or esophagal

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stethoscope to ensure that the lungs were being ventilated, to
monitor for circuit disconnections, and to
auscultate heart tones to confirm a beating heart.
Although largely supplanted by other modalities, the finger on

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the pulse and auscultation remain frontline monitors,
especially when technology fails.
Chest auscultation remains the primary method to confirm
bilateral lung ventilation in the operating room, even though

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detection of an end tidal carbondioxide waveform is definitive
to exclude esophageal intubationContra indications.
Esophageal stethoscopes and esophageal temperature probes

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should be avoided in patients with esophageal viruses or
strictures. Techniques and complications.
A precordial stethoscope, also known as the Wenger chest piece,

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is a heavy bell shaped piece of metal placed over the chest of
suprasternal notch. Although its weight tends to
maintain its position, double sided adhesive discs maintain an

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acoustic seal to the patient's skin.
Various chess pieces are available, but the child's size
works well for most patients. The bell is connected to the
anaesthesia provider's earpiece by extension tubing.

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The oesophagus stereoscope is a soft plastic catheter that is 8
to 24 F with balloon covered distal openings.
Although the quality of breath and breath sounds is much better

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than with a precordial stethoscope, it is.
Its use is limited to intubated patients.
Temperature probes, electrocardiogram, that is ECG
leads, ultrasound probes, and even atrial pacemaker electrodes

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have been incorporated into esophageal stethoscopes.
Placement through the mouth or nose can occasionally cause
mucosal irritation and bleeding.Rarely, the stethoscopes slides
into the trachea instead of the oesophagus, resulting in a gas

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leak around the tracheal tube curve.
Next Next we get to figure 6-1 talking about the esophageal
stethoscope showing the thermocouple connection to the

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monoral earpiece and connection to the temperature monitor.
Clinical considerations. The information provided by
precordial or esophageal steloscope includes confirming

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of ventilation, quality of breath sounds, EG, strider or
wheezing, regularity of heart rates, and quality of heart
tones. That is, muffle tones are
associated with decreased cardiac output.

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The confirmation of bilateral breath sounds after tracheal
intubation, however, is best made with a binaural
stethoscope. Pulse oximetry indications and

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contraindications Pulse oximeters are mandatory monitors
for any anaesthetic, including cases of moderate sedation.
There are no contraindications. Techniques and complications

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Pulse oximeters combine the principles of oximetry and
plethysmography to non invasively measure oxygen
saturation in arterial blood. A sensor containing light
sources, that is two or three light emitting diodes and a

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light detector, that is a photodiode is placed across a
finger, toe, earlobe or any other perfused tissue that can
be trans illuminated. When the light source and

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detector are opposite one another across the perfused
tissue, transmittance oximetry is used.
When the light source and detector are placed on the same
side of the patient, for examplethe forehead, the back scatter,

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that is reflectance of light is recorded by the detector.
Oximetry depends on the observation that oxygenated and
reduced haemoglobin differ in their absorption of red and
infrared light. This is the Lambert beer law,

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specifically oxyhemoglobin. HBO 2 absorbs more infrared
light that is 940 nanometers, whereas deoxyhemoglobin absorbs
absorbs more red light that is 660 nanometers and thus appears

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blue or cyanotic to the naked eye.
The change in light absorption during arterial pulsations is
the basis of oxymetric determinations.
The ratio of the absorptions of the red and infrared wavelengths

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is analysed by a microprocessor to provide the oxygen saturation
that is Spo 2 of arterial blood.Based on established norms, the
greater the ratio of red to infrared absorption, the lower

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the arterial haemoglobin oxygen saturation.
Arterial pulsations are identified by plethysmography
allowing corrections for light absorption by non pulsating
venous blood and tissue. The heat from the light source

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or sensor pressure may, in extraordinarily rare
circumstances, cause tissue damage.
No user calibration is required.Next we get to Figure 6-2,

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explaining the oxyhemoglobin anddeoxyhemoglobin differ in their
absorption of red and infrared light.
Kindly go through the figure fora few moments.

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Clinical considerations In addition to SPO 2, pulse
oximeters provide an indication of tissue perfusion, that is,
pulse amplitude and measure heart rate.

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Depending on a particular patient's oxygen.
Haemoglobin concentration curve Dissociation curve A 90%
saturation may indicate APAO 2 of less than 65 millimetres of
mercury. Clinically detectable cyanosis

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usually corresponds to SPO 2 of less than 80%.
Mainstream bronchial intubation will usually go undetected by
pulse oximetry in the absence oflung disease or low fraction of

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inspired oxygen that is FIO 2 concentrations.
Because carboxyhemoglobin that is, COHB and HBO to absorb light
at 660 nanometers. Pulse oximeters that compare

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only two wavelengths of light will register a falsely high
reading in patients with carbon monoxide poisoning.
Meth haemoglobin has the same absorption coefficient at both
red and infrared wavelengths. The resulting 1 to 1 absorption

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ratio corresponds to a saturation reading of 85%.
Thus, Meth haemoglobin anaemia causes a falsely low saturation
reading when Sao 2 is actually greater than 85%, and a falsely

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high reading if Sao 2 is actually less than 85%.
Most pulse oximeters are inaccurate at low SPO 2 and all
demonstrate a delay between changes in SA, O2 and Spo 2.

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Other causes of pulse oximetry artefacts include excessive
ambient light motion, methylene blue dye, venous pulsations in a
different limb, low perfusion for example, low cardiac output,

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profound anaemia, hypothermia, increased systemic vascular
resistance, a malposition sensorand leakage of light from the
light emitting diode to the photodiode by passing the
arterial bed that is optical shunting.

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Nevertheless, pulse oximetry canbe an invaluable aid to the
rapid diagnosis of hypoxia, which may occur in unrecognised
esophageal intubation, and it furthers the goal of monitoring
oxygen delivery to vital organs in the recovery room.

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Pulse oximetry helps identify post operative pulmonary
problems such as hyperventilation, bronchospasm
and actoelectasis. Advanced examination of the

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photoplethismographic waveform can aid in the assessment of
volume responsiveness in mechanically ventilated
patients. Two extensions of pulse oximetry
technology are mixed venous blood oxygen saturation, that is

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SVO 2 and non invasive brain oximetry.
The former requires the placement of a pulmonary artery
catheter containing fibre optic sensors that continuously

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determine SVO two in a manner analogous to pulse oximetry.
Because SVO two, that is venous blood oxygen saturation over
central venous oxygen saturation, that is SCVO 2,

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varies with changes in haemoglobin concentration,
cardiac output, arterial oxygen saturation and whole body oxygen
consumption, its reinterpretation is somewhat
complex. Impaired oxygen delivery to the

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tissues, that is reduced arterial oxygen saturation,
reduced cardiac output. Increased tissue oxygen demand
results in lower venous oxygen saturation.

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Higher venous oxygen concentrations occur when tissue
oxygen delivery exceeds tissue demand or arterial venous
shunting occurs. Measurement of central venous
oxygen saturation. SCVO 2 is frequently used as a

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surrogate for SVO 2, which is venous blood oxygen saturation.
SVO 2 measures the saturation ofvenous blood returning from the
upper body, the cardiac circulation, and the lower body.

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Normally, SVO 2 is approximately70% SCV.
O2 is usually a few percentage points higher as it does not
reflect venous return from the cardiac circulation.

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Noninvasive brain oximetry monitors regional oxygen
saturation, that is RSO 2 of haemoglobin in the brain.
A sensor placed on the forehead emits light of specific

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wavelengths and measures the light reflected back to the
sensor, that is near infrared optical spectroscopy.
Unlike pulse oximetry, brain oximetry measures venous and

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capillary blood oxygen saturation in addition to
arterial blood saturation. Thus, its oxygen saturation
readings represent the average oxygen saturation of all

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regional microvascular haemoglobin, which is
approximately 70%. Cardiac arrest.
Cerebral embolization and severehypoxia cause a dramatic

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decrease in regional oxygen saturation.
Cerebral oximetry is routinely employed in the perioperative
management of patients undergoing cardio pulmonary
bypass. Cartonography indications and

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contraindications. Determination of end tidal CO2,
that is, ET CO2 concentration toconfirm adequate ventilation is
mandatory during all anaestheticprocedures.

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Increases in alveolar dead speeds, ventilation, for
example, pulmonary thromboembolism, venous air
embolism, decreased pulmonary perfusion produce a decrease in
end tidal CO2 compared with arterial CO2 concentration.

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PA CO2, generally entitled CO2 and arterial or carbon dioxide
concentration increase or decrease depending upon balance
of carbon dioxide production andcarbon dioxide elimination, that

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is, ventilation. A rapid fall of north tidal
carbon dioxide is a sensitive indicator of air embolism in
which both an increase in Dead Space ventilation and a decrease

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in cardiac output may occur. Carpinography is also used to
gauge the success of ongoing resuscitation, where
improvements in perfusion will be heralded by increases in end
tidal carbon dioxide. There are no contraindications,

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techniques and complications. Carpinography is a valuable
monitor of the pulmonary, cardiovascular and anaesthetic
breathing systems. Carbinographs in common use rely

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on the absorption of infrared light by carbon dioxide.
As with oximetry, absorption of infrared light by carbon dioxide
is governed by the Beer Lambert Law.

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Diverting, that is, side stream carpinographs continuously
suction gas from the breathing circuits into a sample cell
within the bedside monitor. Carbon dioxide concentration is
determined by comparing infraredlight absorption in the sample

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cell with a chamber free of carbon dioxide.
Continuous aspiration of anaesthetic gas essentially
represents a leak in the breathing circuit that will
contaminate the operation room unless it is scavenged or

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returned to the breathing system.
High aspiration rates, that is up to 250 mils per minute and
low Dead Space. Sampling tubing usually
increases sensitivity and decrease lag time.

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However, if tidal volumes, that is Vt, are small, for example in
paediatric patients, a high rateof aspiration may entrain fresh
gas from the circuit and dilute end tidal CO2 measurements.

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Low aspiration rates, that is less than 50 miles per minute,
can retard end tidal carbon dioxide measurements and
underestimate it. During rapid ventilation,
diverting units are prone to water precipitation in the

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aspiration tube and sampling cell that can cause obstruction
of the sampling line and erroneous readings.
Expiratory valve malfunction anddepleted carbon dioxide
absorbent media are detected by the presence of carbon dioxide

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in inspired gas. Although inspiratory valve
failure also results in rebreathing carbon dioxide, this
is not as rapidly apparent because part of the inspiratory
volume will still be free carbondioxide, causing the monitor to

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read 0 during parts of the inspiratory phase.
Clinical considerations 1. Carpinographs rapidly and

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reliably detect esophageal intubation, A cause of
anaesthetic catastrophy, but do not reliably detect mainstream
bronchial intubation. Although there may be some

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carbon dioxide in the stomach from swallowed expired air, this
should be washed out within a few breaths.
Sodium cessation of carbon dioxide during the expiratory
phase may indicate a circuit disconnection.

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The increased metabolic rates caused by malignant hypothermia
causes a marked rise in end tidal CO2.
The gradient between the gradients between arterial

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carbon dioxide concentration andend tidal carbon.
Carbon dioxide concentration, which is normally 2 to 5
millimetres of mercury, reflectsalveolar Dead Space that is
alveolar, that are ventilated but not perfused.

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Any significant reduction in lung perfusion, for example air
embolism, decrease cardiac output or decrease blood
pressure, increases alveolar Dead Space, dilutes expired
carbon dioxide, and lessens end tidal carbon dioxide.

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Carbon graphs display a waveformof carbon dioxide concentration
that allows recognition of a variety of conditions.
Next we get to Figure 6-3, explaining the carbon graph,

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demonstrating phases of exploration and the order
parameters. Kindly pause this recording and
take your time to go through this very important figure.

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An aesthetic gas analysis Indications Analysis of
anaesthetic gases is essential during any procedure requiring
inhalation anaesthesia. There are no contraindications

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to analysing these gases. Techniques Techniques for
analysing multiple anaesthetic gases include mass spectrometry,
ramen spectrometry, infrared spectrometry, spectrophotometry

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or piezoelectric crystal, that is, quartz oscillation.
Most of these methods are primarily of historical
interest, as most anaesthetic gases are now measured by
infrared absorption analysis. Infrared units use a variety of

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techniques similar to that described for cartography.
These devices are all based on the Beer Lambert law, which
provides a formula for measuringan unknown gas within inspired

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gas. Because the absorption of
infrared lights passing through a solvent that is inspired or
expired gas is proportional to the amount of the unknown gas.
Oxygen and nitrogen do not absorb infrared light.

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There are a number of commercially available devices
that use a single or dual beam infrared light source and
positive or negative filtering. Because oxygen molecules do not
absorb infrared light, their concentration cannot be measured

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with monitors that rely on infrared technology, and hence
oxygen concentration must be measured by other means, which
we will see below. Clinical considerations.

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A oxygen analysis to measure theFIO 2 of inhaled gas.
Manufacturers of anaesthesia machines have relied on various
technologies. B Galvanic cell.

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Galvanic cell of fuel cell contains a lead anode and gold
cathode bathed in potassium chloride.
At the gold terminal, hydroxyl ions are formed that reacts with

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the lead electrode, thereby gradually consuming it to
produce lead oxide causing current which is proportional to
the amount of oxygen being measured to flow.

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Because the lead, the lead electrode is consumed.
Monitor life can be prolonged byexposing it to room air when not
in use. These are the oxygen monitors
used on many anaesthesia machines in the inspiratory limb

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C paramagnetic analysis. Oxygen is a non polar gas, but
it is paramagnetic and when placed in a magnetic field the

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gas will expand, constructing when the magnet is turned off.
By switching the field on and off and comparing the resulting
change in volume or pressure or flow to a known standard, the

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amount of oxygen can be measured.
D Polarographic Electrode A polarographic electrode has a
gold or platinum cathode and a silver anode, both bathed in an

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electrolyte separated from the gas to be measured by a semi
permeable membrane. Unlike the galvanic cell, a
polarographic electrode works only if a small voltage is

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applied to two electrodes. When voltage is applied to the
cathode, electrons combine with oxygen to form hydroxide ions.
The amount of current that flowsbetween the anode and the

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cathode is proportional to the amount of oxygen present E
Spirometry and pressure measurements Contemporary

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anaesthesia machines measure airway pressures, volume and
flow to calculate resistance andcompliance.
Measurements of flow and volume are made by mechanical devices
that are usually fairly lightweight and are often placed

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in the inspiratory limb of the anaesthesia circuit.
The most fundamental detected abnormalities include low peak
inspiratory pressure and High Peak inspiratory pressure, which

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indicates either a ventilator orcircuit disconnect or an airway
obstruction, respectively. By measuring the tidal volume
and breathing frequency, exhaledminute ventilation can be
calculated, providing some senseof security that ventilation

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requirements are being met. Spirometric loops are usually
displayed as flow versus volume and volume versus pressure.
There are characteristic changeswith obstruction, bronchial

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intubation, reactive Airways disease and so forth.
If a normal loop is observed shortly after induction of
anaesthesia and the subsequent loop is different, the observant

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anaesthesia provider is alerted to the fact that pulmonary or
airway compliance or both may have changed.
Mechanical ventilation and ventilators are discussed more
completely in Chapter 57, and Chapter 23 reviews respiratory

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Physiology. We get to Figure 6-4, explaining
a normal volume pressure loop and a normal flow volume loop.