Bradypnea and Tachypnea: Differential and Treatment

CA-1 · draft

CA-1 Bootcamp day 14. Authored from cited abstracts; every claim carries a PMID.

Not reviewed. This deck cannot be opened, downloaded or sent until you approve it. Read every point and its source first — they were drafted from search results, not from clinical judgement.

Before induction

Volatile agents depress spontaneous ventilation dose-dependently and they do it mainly by shrinking the breath rather than slowing it - as desflurane rose from 0.5 to 1.5 MAC in children, tidal volume and minute ventilation fell significantly and end-tidal carbon dioxide rose - so a normal-looking respiratory rate is not evidence of adequate ventilation.
Opioid-induced respiratory depression complicates 0.5 per cent or fewer of opioid treatments and still produces regular fatalities, and naloxone is the only reversal available, which is why it is titrated to effect and then continued rather than given once and walked away from, since most opioids outlast a single dose of it.
Residual neuromuscular block has been reported in as many as 70 per cent of patients and it does more than weaken the diaphragm - it degrades respiratory control itself and the pharyngeal coordination that keeps the upper airway open - so the fast shallow breathing of a partially reversed patient is an airway problem as much as a ventilation problem.
A train-of-four ratio of at least 0.9 became the accepted threshold for protecting the airway against aspiration before tracheal extubation, and reaching it is established by quantitative monitoring rather than by a head lift or a hand squeeze.
A rising respiratory rate in a spontaneously breathing patient is the body attempting to clear carbon dioxide, and the finding that turns that from housekeeping into an emergency is end-tidal carbon dioxide that keeps climbing despite the increased minute ventilation - the early diagnostic clue to malignant hyperthermia.
About 1.3 per cent of patients given a general anaesthetic had an unanticipated critical respiratory event in recovery - hypoxaemia, a respiratory rate below 8 or a carbon dioxide above 50 mmHg, or upper airway obstruction - and the anaesthetic risk factors were choices the anaesthetist had made, including opioid premedication, higher fentanyl doses and higher relaxant doses.

Questions in the room

Her rate is 7 but the saturation is 99 per cent. Why does that not reassure me?
Give me four reasons a patient breathes fast in recovery, and tell me which one you can rule out from the end of the bed.
You suspect residual paralysis. What measurement, not what manoeuvre, would settle it?
When would you give naloxone here, how much, and what happens forty minutes later if you give it and walk away?

Oral boards stem

A 71-year-old woman is breathing spontaneously through a laryngeal mask for a knee arthroscopy. Over ten minutes her respiratory rate falls from 16 to 7, the end-tidal carbon dioxide climbs from 42 to 58 mmHg, and the saturation stays at 99 per cent on 50 per cent oxygen. Twenty minutes later, in recovery, she is breathing 32 times a minute, using her accessory muscles, and saturating 91 per cent on a face mask. Take both halves in turn: what is the differential for the low rate, what is the differential for the high one, and what do you do about each?

Sources

Behforouz et al., Anesthesia and Analgesia 1998 PMID 9806682
Dahan et al., Anesthesiology 2010 PMID 20010421
Fuchs-Buder et al., Current Opinion in Anaesthesiology 2016 PMID 27755128
Hunter, British Journal of Anaesthesia 2017 PMID 29161387
Rosenberg et al., Orphanet Journal of Rare Diseases 2015 PMID 26238698
Rose et al., Anesthesiology 1994 PMID 8053592
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