Case report

Camilla Tozzetti

A 48-year-old woman hospitalized in the hematologic clinic because of chronic myeloid leukemia, during the night required the attention of the on-call physician for dyspnea associated with tachycardia. General physical examination revealed pallor and rhythmic tachycardia (145 beats/min). Her temperature was 98.6°F (37°C), respiratory rate was 32 breaths/min, blood pressure was 104/54 mmHg, and oxygen saturation was 95%. A complete blood count performed in the afternoon demonstrated an Hb of 9 g/dL, but the patient reported she had hematemesis in the late evening. “Did you give oxygen?”, asked the physician to the nurse. “No doctor, oxygen saturation is 95%. She called me for tachycardia, should I ask for the cardiologist?” Blood withdrawn was performed again, showing a further decrease in the Hb level (6 g/dL). Blood was requested and in the meantime colloid infusion started. The reluctance of the nurse was finally overcome and oxygen was added at 10 L/min. Tachycardia and dyspnea gradually relapsed.

Comment

Chiara Adembri, Pietro Amedeo Modesti

Oxygen saturation (SaO2), together with measurements of heart rate, blood pressure, respiratory rate and temperature, is now included among the essential vital sign assessment in patients care [1]. The routine monitoring of this parameter has increased the recognition of hypoxic episodes occurring in different clinical settings or during various procedures. However, while a low SaO2 (<90–92%) always alarm care givers, there is also the risk of a false assumption, that is “normal” saturation (SaO2 ≥ 94) means no hypoxia. When speaking with students, a misconception about the relationship between arterial oxygen partial pressure (PaO2) and hemoglobin saturation is not rarely encountered [2] because oxygen delivered (DO2) to tissue is perceived normal only on the basis of SaO2 and PaO2 [3]. Although the primary factor that determines how much oxygen is actually bound to hemoglobin is the partial pressure of oxygen (pO2) in the hemoglobin solution, SaO2 and PaO2 cannot be considered alone without considering blood hemoglobin content nor cardiac output (CO) because DO2 = CO × CaO2 where CaO2 is the oxygen content of blood. An anemic patient (Hb = 7 g/dL) may have an O2 saturation of Hb of 100% with a pO2 of 95 mmHg, thus looking deceptively non-hypoxic, although the total DO2 of arterial blood is reduced by an half. With very low Hb values, DO2 may even become inadequate to meet the tissue oxygen requirements (VO2) for aerobic metabolism, a failure defining circulatory shock. Clinicians challenged to support DO2 to avoid tissue hypoxia have to rapidly consider all the different components because CaO2 is derived from hemoglobin content (Hb), SaO2, and a constant K (the coefficient for hemoglobin–oxygen binding capacity) (CaO2 = Hb × SaO2 × K) [4]. Respiratory failure and inadequate DO2 can thus result from malfunction of any aspect of the “ventilatory apparatus”, oxygen uptake in the lung via inspiration, passive oxygen diffusion into arterial blood, hemoglobin content and dissociation kinetics or from low CO. Each of these parameters taken alone can fail to detect the presence of tissue hypoxia [4].

Marked dyspnea of BC, with the increased ventilatory rate and depth, was mainly due to the hypoxic stimulus of chemoceptors. Carbon dioxide is the main stimulus to ventilation. However, an arterial PaO2 of <60 mmHg also acts as an important stimulus. In particular carotid body senses soluble O2 and signals the respiratory center to increase respiratory rate and depth (hypoxix ventilator response) [5]. Although O2 solubility in blood is very low (0.003 mL/dL per mmHg, a constant independent of prevailing pO2), O2 content in plasma is a variable dependent on prevailing pO2 (0.3 mL O2/dL). In conclusion, a FiO2 increase cannot further enhance the oxygen Hb transport so that DO2 cannot be significantly enhanced; however, soluble O2 in plasma may increase thus reducing the stimulus at the chemoceptors level. Oxygen administration might thus reduce the hypoxic ventilator response even if only rapid plasma expansion with consequent CO increase may have increased DO2.