Blood Physiology
Clinical Overview
Start with one idea that holds the whole chapter together: blood is a liquid organ that has to do two opposite jobs at once — stay fluid so it can flow and deliver oxygen, yet clot in milliseconds the instant a vessel is breached. Almost everything in this chapter is a way of keeping that balance, and almost every obstetric haematology emergency is the balance tipping one way (uncontrolled bleeding) or the other (unwanted clotting). Pregnancy deliberately shifts the set-point towards clotting, because the single most dangerous moment in a woman's reproductive life — placental separation — is a planned, massive wound.
From that one principle the rest follows. Blood is a transport, defence and haemostatic tissue. In O&G it explains anaemia, fetal oxygenation, haemorrhage, thrombosis, sepsis, thrombocytopenia, pre-eclampsia, HELLP, disseminated intravascular coagulation, red-cell alloimmunisation and transfusion. A Primary FCOG candidate must be able to move from a full blood count or coagulation panel back to the physiology of oxygen delivery, clot formation, clot breakdown and immune incompatibility — and to read every result as a statement about that fluid-versus-clot balance.
Pregnancy modifies nearly every part of blood physiology, and the changes are coherent once you see them as preparation for that planned wound. Plasma volume rises more than red-cell mass, producing physiological haemodilution (a buffer of spare volume to lose). Iron requirement rises to build the extra red cells. White-cell count, especially neutrophils, may rise. Platelets may fall slightly. Fibrinogen, factor VIII, von Willebrand factor and other clotting factors rise, while the natural anticoagulant protein S falls. Fibrinolysis is relatively suppressed. Venous stasis and endothelial injury at delivery complete Virchow's triad. These changes help a woman survive placental separation, but the same shift towards clotting increases VTE risk and makes obstetric haemorrhage coagulopathy behave differently from non-pregnant bleeding.
High-yield chains:
Iron deficiency -> reduced haem synthesis -> microcytic hypochromic red cells -> reduced oxygen reserve -> poor tolerance of postpartum haemorrhage.
Endothelial injury -> platelet adhesion through von Willebrand factor -> platelet activation -> thromboxane/ADP release -> platelet aggregation -> primary haemostatic plug.
Tissue factor exposure -> thrombin generation -> fibrinogen to fibrin -> factor XIII cross-linking -> stable clot.
Abruption/sepsis/amniotic fluid embolism -> systemic coagulation activation -> fibrinogen and platelet consumption -> DIC -> bleeding from uterus and puncture sites.
RhD-negative mother exposed to RhD-positive fetal red cells -> maternal IgG anti-D -> crosses placenta in later pregnancy -> fetal haemolysis -> anaemia, hydrops and jaundice.
Core Knowledge
Blood as a Tissue
Blood consists of cells suspended in plasma. Plasma carries water, electrolytes, proteins, hormones, nutrients, waste products and clotting factors. Red cells carry oxygen and carbon dioxide. White cells defend against infection and coordinate inflammation. Platelets maintain vascular integrity and start haemostasis. The endothelium is part of the blood system because it regulates tone, permeability, platelet adhesion, coagulation and fibrinolysis.
| Component | Main function | O&G relevance |
|---|---|---|
| Red cells | Oxygen and carbon dioxide transport | Anaemia, fetal oxygenation, transfusion thresholds |
| White cells | Innate and adaptive defence | Chorioamnionitis, puerperal sepsis, HIV, wound infection |
| Platelets | Primary haemostasis and endothelial maintenance | Gestational thrombocytopenia, ITP, HELLP, PPH |
| Plasma proteins | Oncotic pressure, transport, coagulation | Albumin, fibrinogen, clotting factors, drug binding |
| Endothelium | Antithrombotic surface, vascular tone and permeability | Pre-eclampsia, VTE, DIC, capillary leak |
The exam clue is that blood results must be interpreted as physiology. A low haemoglobin asks about oxygen delivery. A low platelet count asks about primary haemostasis and the cause of consumption or destruction. A prolonged PT/aPTT asks about factor deficiency, dilution, liver disease, anticoagulant effect or DIC. A "normal" fibrinogen in major obstetric bleeding can be dangerous because pregnancy fibrinogen should be high.
Red Cells, Haemoglobin and Oxygen Delivery
Red cells are biconcave, anucleate cells designed for gas transport. They contain haemoglobin, depend on glycolysis for energy, and survive about 120 days before removal by the reticuloendothelial system. Their membrane deformability allows passage through capillaries; loss of deformability contributes to haemolysis and splenic clearance.
Most ageing red cells are removed by macrophages in the spleen, with liver and marrow also contributing. Haem is broken down to bilirubin for hepatic handling, while iron is recycled. This is why haemolysis produces a linked pattern: anaemia, reticulocytosis if marrow can respond, raised LDH, low haptoglobin and increased unconjugated bilirubin.
Oxygen delivery is not equal to haemoglobin alone:
Arterial oxygen content depends mainly on haemoglobin concentration and oxygen saturation. Dissolved oxygen contributes little under normal conditions. This is why severe anaemia can cause tissue hypoxia despite a normal oxygen saturation, and why shock can cause tissue hypoxia despite an acceptable haemoglobin.
| Determinant | Physiology | Clinical implication |
|---|---|---|
| Haemoglobin concentration | Amount of oxygen carrier | Anaemia reduces reserve for labour, surgery and haemorrhage |
| Oxygen saturation | Percentage of Hb binding sites occupied | Hypoxia rapidly reduces oxygen content |
| Cardiac output | Flow delivering oxygen | Shock and heart disease reduce delivery |
| Tissue extraction | Local unloading and microcirculation | Sepsis can impair use of delivered oxygen |
| 2,3-BPG, pH, CO2, temperature | Shift Hb-oxygen affinity | Acidosis and heat shift right, increasing unloading |
Haemoglobin does not bind oxygen linearly: the relationship between the partial pressure of oxygen and how saturated haemoglobin becomes is the sigmoid oxygen dissociation curve. Its position is summarised by the P50 — the oxygen tension at which haemoglobin is half-saturated. A higher P50 means lower affinity (haemoglobin gives up oxygen more readily, a right shift); a lower P50 means higher affinity (it holds oxygen more tightly, a left shift). The curve's steep middle is what lets large amounts of oxygen be released for a small fall in tissue oxygen tension.
Three things shift the curve, and each matters obstetrically:
- The Bohr effect links acid-base physiology to oxygen delivery. Rising CO2 and falling pH (more hydrogen ions) shift the curve to the right, promoting oxygen unloading exactly where metabolism is highest. Maternal alkalosis (for example from over-breathing) shifts the curve left and reduces tissue unloading; severe maternal acidosis impairs cardiac function and fetal oxygenation through several pathways.
- 2,3-bisphosphoglycerate (2,3-BPG), a product of red-cell glycolysis, binds deoxyhaemoglobin and lowers oxygen affinity (right shift). It rises with chronic hypoxia, anaemia and altitude, helping tissues extract more oxygen. Crucially, it is depleted in stored (banked) red cells, which therefore have a left-shifted curve and release oxygen poorly until 2,3-BPG regenerates over hours after transfusion — a reason massive transfusion does not instantly restore tissue oxygenation.
- Temperature: heat shifts the curve right (more unloading in active or febrile tissue), cold shifts it left.