ICU · Physiology / haematology immunology
Blood & Immunology Physiology
Also known as Blood physiology · Immunology physiology · Hematopoiesis · Innate immunity · Adaptive immunity · Complement cascade · Coagulation cascade · Inflammation · Red blood cell physiology · Oxygen-haemoglobin dissociation curve · 2,3-diphosphoglycerate · Bohr effect · Haldane effect · Fibrinolysis · Platelet function · Immunoparalysis · SIRS CARS MARS
Blood and immunology physiology: the hematopoiesis (the pluripotent stem cell → RBC, WBC, platelets). The red blood cell physiology (2,3-DPG, oxygen dissociation curve, Bohr effect, Haldane effect). The innate immunity (the neutrophils, the macrophages, the complement, the natural killer). The adaptive immunity (the T cells — the cellular; the B cells — the humoral antibodies). The complement cascade (the classical, the alternative, the lectin). The coagulation cascade (the intrinsic, the extrinsic, the common — the PT/aPTT/TT). The platelet function (the adhesion — vWF/GPIb; the activation; the aggregation — GPIIb/IIIa/fibrinogen). The fibrinolysis (the plasmin, the D-dimer). The inflammation (the cytokines, the acute-phase response). The immunoparalysis and the SIRS → CARS → MARS paradigm in the critical illness.
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A 62-year-old with pneumococcal sepsis is on day 1 in the ICU: febrile, acidotic, climbing lactate, on noradrenaline. Her oxygen–haemoglobin dissociation curve has shifted right — fever, acidosis and a rising 2,3-DPG all favour unloading, the tissue's own demand-driven rescue. Then she is transfused two units of stored blood for a haemoglobin of 68 g/L, and the curve snaps left: banked red cells are 2,3-DPG-depleted (their P50 falls from 26.6 toward 20 mmHg during storage) and hold their oxygen tightly, so tissue unloading transiently worsens even as the haemoglobin number climbs.[7][11][20][21]
Day 12 of the same admission. She "looks better" — afebrile, off vasopressors, CRP falling — then spikes again: purulent secretions and new infiltrates (ventilator-associated pneumonia), blood cultures growing Candida, CMV PCR newly positive. The monocyte HLA-DR has fallen below 8000 molecules per cell. The immune system that fought the infection on day 1 is now functionally silent.[12][10][17][30]
That is the single question this whole topic answers: why does the same patient die of too much inflammation on day 1 and too little immunity on day 12? Hold that question and every section below — the red cell, the complement, the clotting cascade, the SIRS–CARS swing — falls into place.[10]
References32ShowHide
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