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In volume-controlled ventilation a widening gap between peak and plateau pressure points at resistance somewhere between the ventilator and the alveolus, and the same obstruction under pressure control hides from you, because bench and modelling work showed delivered tidal volume did not fall until the tube was nearly completely occluded.
A capnograph that goes flat is a disconnection or a displaced tube until you have proved otherwise, and you should treat it that way: breathing-circuit disconnection was among the most frequently reported preventable critical incidents when anaesthetists were interviewed about their own near-misses, and international consensus guidance makes removal of the tube the default action when sustained exhaled carbon dioxide cannot be restored.
Trust the depth mark before you trust your stethoscope when you are new, because first-year residents in a randomised blinded trial missed endobronchial intubation on auscultation in 55 per cent of cases while insertion depth detected it with 88 per cent sensitivity, and that trial's own recommendation was to site tubes at 20 to 21 cm at the teeth in women and 22 to 23 cm in men.
Patient-ventilator dyssynchrony is not one thing but three - a problem with triggering the breath, with the flow delivered during it, or with cycling out of it - and each is identified by looking at the pressure, flow and volume waveforms rather than at the patient's chest.
Bronchospasm under anaesthesia usually shows itself as falling compliance and a falling saturation alongside the wheeze, and in the Australian incident reports the leading causes were airway irritation, a problem with the tracheal tube itself and aspiration of gastric contents - which is why you check the tube before you reach for the salbutamol.
Laryngospasm is treated first with your hands on the airway and only then with drugs, and if there is no intravenous line, suxamethonium can be given by the intramuscular, intraosseous or intralingual route - the delay you are racing is not hypoxaemia alone but the negative-pressure pulmonary oedema that intense inspiratory effort against a closed glottis produces.
The capnograph trace has gone flat and the airway pressure has dropped to nothing - what is your first action, and what is your second?
Peak pressure has risen and plateau pressure has not. What does that tell you, and where is the problem?
How would you distinguish endobronchial intubation from a right-sided mucus plug at the head of this bed, without a chest X-ray?
The patient is biting the tube and the pressure trace is chaotic - is this dyssynchrony, laryngospasm or light anaesthesia, and how does your answer change what you give?