Abstract Introduction Arterial oxygen content (CaO2) is the primary determinant of systemic oxygen delivery (DO2), calculated as: DO2 = CO × (1.34 × Hb × SaO2 + 0.003 × PaO2) If CaO2 falls below a critical threshold, oxygen extraction becomes inadequate, anaerobic metabolism predominates, and circulatory shock occurs. Profound anemia even in the absence of sepsis, haemorrhage or cardiac dysfunction can critically reduce CaO2 and trigger this cascade. We present a case of severe anemia leading to circulatory shock that rapidly resolved with red blood cell transfusion. Case Description A 59-year-old woman with anemia due to chronic occult gastrointestinal blood loss and heart failure with mildly reduced ejection fraction (45%) presented with 2 days of diffuse myalgias and thirst. Initially, patient was ambulatory and vital signs were stable, however, she rapidly developed encephalopathy, bradycardia to 30bpm, and hypotension requiring intubation and high-dose norepinephrine and vasopressin. Laboratory evaluation showed hemoglobin 1.4 g/dL, lactate 15 mmol/L, pH 6.8 with bicarbonate 6 mEqL, and creatinine 2.0 mg/dL. Arterial oxygen content (CaO2) was approximately 2.1 mL O2/dL (normal: 16-20).Whole body CT did not show any signs of an active hemorrhage. Transthoracic Echocardiography ruled out cardiogenic shock and tamponade. Chest CT did not show pulmonary embolism or pneumothorax. Sepsis was ruled out as patient was afebrile with normal WBC count and negative urine and blood cultures. Normal glucose, absent ketones, normal cortisol and thyroid function tests ruled out endocrine and metabolic causes of shock. No evidence of hemolysis as patient had normal haptoglobin and lactate dehydrogenase. Profound anemia was thus identified as the primary driver of impaired DO2 and subsequent acidosis and shock. After transfusion of four units of red blood cells, her mentation improved alongside rapid hemodynamic recovery. Discussion An experimental study in healthy volunteers demonstrated that hemoglobin as low as 5 g/dL can be tolerated if euvolemia is maintained, and compensatory increase in cardiac output and decrease in systemic vascular resistance occurs. Weiskopf RB et al. JAMA. 1998;279:217-221. Profound anemia can precipitate circulatory shock when compensatory mechanisms are inadequate. The patient’s critically low hemoglobin resulted in severely reduced CaO2 (2.1) and impaired DO2. This was further compounded by bradycardia, vasoplegia, and likely myocardial dysfunction. Patients ability to increase cardiac output was limited producing tissue hypoxia, lactic acidosis, and refractory shock. Amongst a plethora of things on the differential in a patient with circulatory shock, profound anemia should also be considered. This abstract is funded by: None
Wahaj et al. (Fri,) studied this question.