Saturación de oxígeno – sO2
El papel fisiológico y fisiopatológico, intervalos de referencia y las causas más probables de valores anormales
Saturación de oxígeno – sO2
La saturación de oxígeno (sO2) es la relación entre la concentración de oxihemoglobina y la concentración de hemoglobina funcional (es decir, oxihemoglobina (O2Hb) y desoxihemoglobina (HHb) capaz de transportar oxígeno. Es decir [24]:
La sO2 refleja la utilización de la capacidad de transporte de oxígeno disponible actualmente.
En la sangre arterial un 98–99% de oxígeno se transporta en eritrocitos unidos a la hemoglobina. El 1-2% restante del oxígeno transportado en sangre se disuelve en el plasma sanguíneo: esta es la porción notificada como presión parcial de oxígeno (pO2) [6]. (ver pO2).
Intervalo de referencia de la sO2 – ejemplos
Adultos/niños (ST, a): 94-98% Recién nacidos (ST, a): 40–90% [4] ST: sangre total; a: arterial
Una sO2 de menos del 80% en adultos se considera potencialmente mortal [25].
Antecedentes fisiológicos – sO2
Cada molécula de hemoglobina puede unir un máximo de cuatro moléculas de oxígeno para formar O2Hb (ver Hb, O2Hb). La función de aporte de oxígeno de la hemoglobina (es decir, su capacidad de "captar" oxígeno en la microvasculatura de los pulmones, transportarlo en la sangre arterial y "liberarlo" en la microvasculatura de las células de tejido) es posible gracias a un cambio reversible en la estructura de la hemoglobina que altera su afinidad por el oxígeno (ver Hb) [18]. Un factor significativo que determina la afinidad de la hemoglobina por el oxígeno es la pO2 de la sangre. La relación entre la pO2 y la sO2 se describe mediante la curva de disociación de oxihemoglobina (CDO) (Fig. 5), que revela, esencialmente, que cuanto más elevada es la pO2, mayor es la afinidad de la hemoglobina por el oxígeno; lo que se hace evidente mediante un aumento de la sO2 [21].
El nivel de pO2 alcanza su máximo en la sangre arterial en los pulmones debido a la difusión del oxígeno inspirado a través de la membrana alveolar desde los alvéolos hasta la sangre (Fig. 3). En consecuencia, la hemoglobina tiene en este caso la mayor afinidad por el oxígeno, y se une rápidamente al oxígeno dando como resultado ∼100% de hemoglobina saturada (sO2(a)) debido a la sangre de la vena tebesiana. Por el contrario, en los tejidos en los que la pO2 es menor, la hemoglobina presenta una disminución de la afinidad por el oxígeno, cuyo resultado es la liberación de oxígeno a las células de tejido. La sO2 de la sangre venosa (sO2(v)) que regresa desde los tejidos a los pulmones disminuye en consecuencia (∼75%) [21]. Esto se ilustra en la Figura 5.
FIG. 5: Curva de disociación de oxihemoglobina. Para obtener más información sobre la CDO, consulte p50. a: arterial; v: venosa
¿Por qué medir la sO2?
La sO2 junto con la pO2 proporciona los medios para evaluar la oxigenación de la sangre. Debido a la forma sigmoidea de la CDO, la sO2 es menos informativa que la pO2 cuando la sangre está adecuadamente oxigenada. En la parte plana superior de la curva, los grandes cambios en la pO2 se reflejan en cambios mucho más pequeños del sO2. De hecho, en casos de hiperoxemia (ver pO2) el sO2 puede alcanzar el 100%, y cualquier oxígeno adicional será únicamente el oxígeno disuelto en el plasma sanguíneo. En este caso, la pO2 seguirá siendo el único medio para evaluar la oxigenación de la sangre.
El sO2 es un factor determinante importante del contenido de oxígeno total (ver ctO2).
El sO2 es un parámetro útil para la monitorización de la terapia con oxígeno suplementario.
¿Cuándo debería medirse el sO2?
La medición del sO2 es clínicamente útil en el diagnóstico, la evaluación y la monitorización de pacientes con enfermedad respiratoria aguda o crónica grave o insuficiencia respiratoria debido a afecciones distintas de las enfermedades respiratorias (por ejemplo, traumatismo cerebral o torácico, sobredosis de drogas).
Las causas que conducen a un sO2 afectado son idénticas a las de la pO2, la ctHb o la ctO2 (ver pO2).
Causas de la disminución del sO2
La disminución del sO2 indica que la captación de oxígeno presenta dificultades y puede ser el resultado de [14]:
- Causas mecánicas (p. ej., obstrucción de las vías respiratorias, traumatismo torácico)
- Enfermedades neuromusculares (p. ej., síndrome de GuillainBarré, miastenia grave)
- Drogas que deprimen el centro respiratorio (p. ej., opioides, heroína, morfina)
- Neumonía grave
- Embolia pulmonar
- Edema pulmonar
- Asma agudo
- Síndrome de dificultad respiratoria aguda (SDRA)
- Enfermedad pulmonar obstructiva crónica (EPOC)
- Enfermedad pulmonar (ej. fibrosis)
- Neumotórax
- Cardiopatía congénita cianótica
Síntomas asociados a la disminución de la sO2
Entre los síntomas asociados a hipoxemia e insuficiencia respiratoria que pueden causar una medición de la sO2 se encuentran [14]:
- Disnea al mínimo esfuerzo
- Falta de aliento/dificultad para respirar/distrés respiratorio (disnea)
- Aumento de la frecuencia respiratoria (taquipnea)
- Cianosis
- Dilatación nasal
- Sibilancias/crepitaciones al auscultar
- Aumento de la sudoración (diaforesis)
- Confusión, desorientación, somnolencia
- Coma
- Aumento del recuento de glóbulos rojos (policitemia) con hipoxemia crónica prolongada
Tres formas de evaluar la sO2 en pacientes críticos
La sO2 se puede determinar de tres maneras: Oximetría de pulso (SpO2), calculando a partir de la pO2, o midiendo directamente en analizadores de gases en sangre. En el caso de pacientes críticos, diversos estudios han demostrado la importancia de utilizar sO2 medido en lugar de SpO2 o sO2 calculado para evitar tratar inadecuadamente a estos pacientes [26, 27, 28, 31]. Se prefiere el sO2 medido en los cálculos, como los de shunt y contenido de oxígeno, para limitar los errores críticamente importantes que pueden ser el resultado del sO2 calculado [29, 30]. Entre los pacientes de cuidados intensivos que presentan un alto riesgo de hipoxia tisular, ya sea por fallo pulmonar, descompensación cardíaca, transporte inadecuado de oxígeno o trastornos a nivel celular, una medición precisa del sO2 es esencial para la planificación de la terapia [32, 33]. La directriz del Clinical and Laboratory Standards Institute (CLSI) [24] establece con respecto al sO2 calculado con analizadores de gases en sangre:
"Pueden producirse errores clínicamente significativos al incorporar un valor calculado de este modo para sO2 en cálculos posteriores como la fracción de shunt o, por suponer que el valor obtenido es equivalente a la oxihemoglobina fraccionaria.”
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