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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