Focused monitoring
Our
goals in monitoring the patient under anesthesia are driven by two
consid-erations:
·
Are we ventilating the patient’s lungs optimally and giving just
the right amount of drugs and fluids? In other words, we monitor so that we can
titrate our ministrations to a conceptual optimum.
·
Do the data we gather from the patient and the equipment indicate
potential danger or trends that require our intervention? In other words, for
safety’s sake, we monitor variables that can indicate threatening problems, be
they the consequence of anesthetic or surgical actions or based on the
patient’s disease.
Many
signals we monitor subserve both titration and safety. For example, during
anesthesia, we observe the patient’s response to electrical stimulation of a
motor nerve (the “twitch monitor”) in order to titrate the administration of neuromus-cular blocking drugs (muscle
relaxants). At the end of anesthesia, we observe the same response in order to
make sure that the patient has adequate muscle power to breathe without help –
an important safety concern! Many,
perhaps even most, other signals fall only into the safety category. For
example, we monitor the ECG, oxygen saturation and inspired CO2 for
safety sake, not for titration.
All
monitoring builds on old-fashioned inspection, auscultation, and palpation.
Indeed, instruments do not tell all, and at times may even fail. The clinician
must still be able to assess the patient and the system without recourse to
instruments. Rarely will the instruments alone make a diagnosis for you. More
often than not, you will have to take into consideration facts not captured by
instruments. First comes inspection.
More
than any other monitoring activity in the operating room, inspection must be
practised and honed. In anesthesia, the pattern of breathing gives more
impor-tant information than any other observation.
During
spontaneous breathing, the patient’s chest should rise smoothly, with chest and
abdomen moving in harmony. We speak of “rocking the boat” when the abdomen
rises during inspiration and the upper chest lags behind, a sign of respir-atory
impairment because of upper airway obstruction, partial muscle paralysis, or
pulmonary disease such as emphysema. The next glance should be directed at the
larynx, which should be quiescent during breathing. With beginning res-piratory
insufficiency, the larynx moves downward a little with every inspiration, the
so-called tracheal tug. The greater the respiratory impairment, the greater the
laryngeal excursions with breathing, culminating in the agonal breathing
pat-tern where larynx, floor of mouth, and tongue move with every desperate
inspir-ation. Particularly in children, flaring nostrils indicate respiratory
weakness, often enough leading to respiratory failure when small children can
no longer muster the effort to overcome weakness or obstruction.
Don’t
forget to check the pupils. When the patient lies face-down or the surgeon
works in the face, we must tape the eyes shut to guard against corneal
abrasions. At other times, a look at the eyes can be helpful. During general
anesthesia, the eyes should be still, the pupils constricted – or at least not
dilated – and left should equal right. Light reflexes disappear under surgical
anesthesia. Widely dilated pupils – if not the result of mydriatic drugs –
indicate grave danger (the “open window to eternity”). The sclera may be
injected under light anesthesia as is also true for sleep. And while you are at
it, look at the palpebral conjunctiva of the lower lid. The conjunctiva should
be pink (not pale with anemia or bluish with hypoxemia or engorged with venous
obstruction).
At the
end of an anesthetic in which muscle relaxants were used, we need to make sure
that the patient has the muscle power to maintain normal ventilation. While the
nerve stimulator (see below) is helpful, a simple clinical test is even better:
ask the patient to lift his head off the pillow and keep it up for 5 seconds.
If he can do that, you can be reasonably assured that he will be able to
maintain normal ventilation. When the operative site (neck, upper chest) makes
that impossible, we must assess not only the response to the nerve stimulator
but also the pattern of breathing and SpO2.
Cool
clinicians wear a stethoscope slung around their necks. Even cooler clinicians
actually use the instrument to listen, for example, over the upper trachea: is
air escaping at the end of mechanical inspiration? We welcome this sign in
small children in whom we avoid compression of the tracheal mucosa with
uncuffed endotracheal tubes. In adults we like to inflate the cuff of the
endotracheal tube so that a little gas will escape only when we exceed by a few
cm H2O the chosen peak inspiratory pressure. That has two
advantages. For one, it assures us that the cuff is not compressing the
delicate, tracheal ciliated mucous membrane more than necessary. For another,
it provides an emergency escape valve should excessive pressure build up in the
breathing circuit. That is rare but has occurred when safety relief valves had
failed.
After
intubation of the trachea, we listen over both lung fields for breath sounds
and check the epigastrium to make sure that we are not delivering gas into the
stomach during manual inspiration.
The
lowly stethoscope (cheap, non-electronic, sturdy, time honored) often makes the
diagnosis for us. No electronic instrument identifies a pneumo-thorax, but
breath sounds on one side and not the other, and the chest rising more on one
side than the other spells pneumothorax or endobronchial intubation. Also,
consider a patient who becomes tachycardic, hypoxemic, and hypotensive, and
assume that pneumothorax ranks high on your list of differential diagnoses. If
breath sounds over the left chest equal those over the right and both sides of
the chest move equally, a significant pneumothorax moves to the bottom of the
differential diagnosis, and pulmonary embolism or cardiac tamponade move up.
Don’t abandon the stethoscope.
Remember
to listen to heart sounds, either through the chest wall or from behind with an
esophageal stethoscope. With cardiovascular depression from deep anesthesia,
the sounds become muffled. Cardiac tamponade will do the same. In either case,
blood pressure will be low and heart rate high. Air embolism may cause the
infamous mill wheel murmur produced by blood being beaten into foam in the
heart. That is a late sign of air embolism, usually too late to be helpful.
Therefore, when worried about the possibility of air embolism, we watch the
end-tidal CO2 (it decreases with pulmonary embolism), and we monitor
for air with a precordial Doppler instrument or with a transesophageal
echocardiograph. A pulmonary artery catheter will also show signs of increased
PA pressure when air bubbles impede blood flow through pulmonary artery
branches.
How
old-fashioned can you get? Putting a hand on the patient will give you all
sorts of information. More than just the presence of a pulse, we may assess its
quality. Is the patient warm or cold and clammy? (The latter with sympathetic
activity causing vasoconstriction and sweating.) Are his muscles fasciculating?
(With shivering or after the administration of succinylcholine.) Put the palms
of your hands on the clavicles, letting your fingers rest on the upper chest.
Does the upper chest rise during spontaneous inspiration? (See above for “rocking
the boat”.) What is the muscle tone? In spontaneously breathing infants, the
inter-costal spaces should not retract during inspiration. Infants will also
have flaccid fingers with muscle paralysis or deep anesthesia.
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