Síguenos en Twitter     Síguenos en Facebook     Síguenos en Google+     Síguenos en YouTube     Siguenos en Linkedin     Correo Grupsagessa     Gmail     Yahoo Mail     Dropbox     Instagram     Pinterest     Slack     Google Drive     Reddit     StumbleUpon     Print

SOBRE EL AUTOR **

Mi foto
FACP. Colegio de médicos de Tarragona Nº 4305520 / fgcapriles@gmail.com

WORLD EMERGENCY MEDICINE SOCIETIES

Rapid IJ (aka Easy Internal Jugular Cannulation)

Buscar en contenido

Contenido:

lunes, 22 de julio de 2013

Oxígeno en hipercapnia

FreeUpToDate (subscription required - free)
Disclosures: All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Oct 2012. | This topic last updated: Apr 30, 2012.
"SUMMARY AND RECOMMENDATIONS
Overview
  • Hypercapnia generally results from an increase in carbon dioxide (CO2) production or a decrease in alveolar ventilation. Reduced alveolar ventilation, the most common cause of hypercapnia, is caused by decreased minute ventilation (VE) or poor matching of ventilation and perfusion of airspaces (V/Q mismatching), described physiologically as an increased ratio of dead space to tidal volume ventilation (VD/VT).
  • Acute hypercapnia may produce a depressed level of consciousness, increases in cerebral blood flow and intracranial pressure, and depression of myocardial contractility. 
  • Normal individuals do not exhibit a depressed level of consciousness until the arterial tension of carbon dioxide (PaCO2) is greater than 60 to 70 mmHg (8.0 to 9.3 kPa), while patients with chronic hypercapnia may not develop symptoms until the PaCO2 rises acutely to greater than 90 to 100 mmHg. 
  • In addition to decreased VE and V/Q mismatching, the increase in PaCO2 caused by administration of oxygen to hypercapnic COPD patients is felt to be due to the reduced capacity for oxygenated hemoglobin to carry carbon dioxide (ie, rightward displacement of the CO2-hemoglobin dissociation curve in the presence of increased oxygen concentration), known as the Haldane effect 
For hypercapnic patients with hypoxemia, safe administration of oxygen therapy can be achieved using the following approach:
  • The inspired concentration of oxygen (FIO2) is gradually increased by increments of 4 to 7 percent (eg, from 24 to 28 percent) with close monitoring of both PaO2 and PaCO2. Venturi masks may be used to permit tight regulation of the maximal FiO2 that is administered to the patient. When using nasal cannula, the oxygen flow rate is generally increased by 1 L per minute at a time. The goal is a pulse oxygen saturation (SpO2) of 90 to 93 percent or a PaO2 of 60 to 70 mmHg (8 to 9.3 kPa). 
  • Treat the underlying causes of acute respiratory failure (eg, COPD, heart failure, pneumonia) simultaneously.
  • The development of acute hypercapnia with significant acidemia (eg, pH<7.20) and/or a marked depression in the level of consciousness is an indication for intubation and mechanical ventilation. Oxygen should not be removed entirely from the patient in an effort to avert intubation.
  • Noninvasive positive pressure ventilation may help avoid the need for endotracheal intubation."