SEPT 10 Built from the handwritten pages you uploaded on 10 September 2026.

Massive transfusion & electrolyte ECG

Which complication the vignette is describing, and the ECG changes of every electrolyte disturbance.

Definition and targets

Massive transfusion: replacement of one whole blood volume in 24 hours · or 50% within 4 hours · or 4 units within 1 hour.
Resuscitation targets: MAP 60–65 mmHg · Hb 7–9 g/dL · platelets > 50 (>100 with head injury) · fibrinogen > 1.5–2 g/L · PT and APTT < 1.5 × normal · ionised calcium > 1.1 mmol/L · temperature > 35 °C · pH > 7.2.
The lethal triad: hypothermia · acidosis · coagulopathy. Each worsens the others.

The scenario	The answer	Why
4 units of PRBC given, now oozing	Dilutional thrombocytopenia	Stored red cells contain no functional platelets
10–12 units given, surgeon says oozy	DIC	Consumption of factors and platelets with fibrinolysis
Oozing in the MRI or CT suite after coiling	Hypothermic coagulopathy	The radiology suite is cold and the patient is uncovered — enzymatic clotting is temperature dependent
Liver surgery / transplant / liver failure, given whole blood or FFP: narrow pulse pressure, ↑ CVP, hypotension	Citrate toxicity → hypocalcaemia	The failing liver cannot metabolise citrate, which chelates calcium
Tall T waves, prolonged PR, widened QRS after massive transfusion	Hyperkalaemia	Potassium leaks from stored red cells

Commonest with FFP and platelets, not with red cells — plasma products carry far more citrate per unit.
Risk rises when transfusing faster than about 1 unit every 5 minutes, or above roughly 150 ml/min, and in liver failure or during the anhepatic phase.
Signs: hypotension with a narrow pulse pressure, raised CVP and end-diastolic pressure, reduced contractility, tremor, and QT prolongation.
Treatment: calcium chloride or gluconate, guided by ionised calcium — not total calcium, which is misleading.
Citrate is metabolised to bicarbonate, so a late metabolic alkalosis is common after large volume transfusion.

Disturbance	ECG changes	Hook
Hypokalaemia	ST depression · flat or inverted T · U wave · long QU	"No K, no T — U instead"
Hyperkalaemia	Tall peaked T → flat P → prolonged PR → QRS widening → sine wave → arrest	T first, QRS last — QRS widening means act now
Hypocalcaemia	Prolonged ST segment → prolonged QT	Low Ca stretches the ST
Hypercalcaemia	Shortened ST · short QT · widened T	The mirror image
Hypomagnesaemia	Tall T · ST depression · long QT · torsades	Looks like hyperkalaemia and hypokalaemia at once
Hypermagnesaemia	Prolonged PR · QRS widening · AV block	Same picture as hyperkalaemia

Calcium acts on the ST segment and QT. Low calcium lengthens, high calcium shortens.
Potassium acts on the T wave. High peaks it, low flattens it and adds a U wave.
Both hyperkalaemia and hypermagnesaemia widen the QRS and prolong the PR — conduction slowing is the shared final pathway, and it is the sign that arrest is near.
Calcium does not lower potassium — it stabilises the myocardial membrane. It buys time; insulin–dextrose, salbutamol and dialysis remove the potassium.

The commonest inherited bleeding disorder is von Willebrand disease — not haemophilia.
Bacterial infection is commonest with PLATELETS, because they are stored at room temperature (20–24 °C) rather than refrigerated.
Platelets must never be frozen — freezing destroys their function.
Tranexamic acid within 3 hours of traumatic haemorrhage reduces death from bleeding; given later it may be harmful.

4 units oozing dilutional

10–12 units DIC

Cold room hypothermic

Liver + FFP citrate

↑K peaked T, wide QRS

↓K flat T, U wave

↓Ca long QT

Platelets room temp → infection

Built from your massive transfusion and ECG changes pages. See also Coagulation & transfusion.