L’ipercapnia da iperossigenazione nel paziente con insufficienza respiratoria ipercapnica (tipo 2)

31 Ott

Fin dagli inizi della pratica clinica il messaggio che tutti abbiamo ricevuto sulla somministrazione di O2 nel paziente BPCO era: bassi flussi basse FiO2, rischio di ipercapnia e di carbonarcosi.

Alla richiesta di spiegazioni fisiopatologiche la risposta era (ed è scommetterei): è colpa del drive ipossico che stimola i centri respiratori del BPCO e che, quando viene alterato con la somministrazione “selvaggia” di O2, induce ipoventilazione e quindi ipercapnia.

Approfondendo, da grande, ho scoperto che il famoso “drive ipossico” è in gran parte una leggenda metropolitana, e soprattutto non è assolutamente responsabile dell’ipercapnia nell’insufficiente repiratorio cronico.

Possiamo imputare tale condizione a due meccanismi fisiopatologici:

  1. Vasocostrizione ipossica polmonare
  2. Effetto Haldane

L’iperossigenazione rende meno “efficiente” la normale vasocostrizione ipossica che, escludendo le zone meno ventilate del polmone, permette il mantenimento di  un rapporto ventilazione perfusione ottimale. E’ quindi il mismatch tra ventilazione e perfusione il maggior responsabile dell’ipercapnia da iperossigenzaione del paziente con IR ipercapnica.

Take home point per la pratica clinica: Nel paziente con IR cronica tipo 2 (ipercapnica)FiO2 massimo del 35% per raggiungere target di saturazione tra 88 e 92%.

References
Oxygen_induced hypercapnia in COPD myths and facts
Guideline for Emergency Oxygen Use in Adult Patients: Executive Summary

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