Acute cardiac dilatation
This complication occurs when stored blood is infused into the vascular bed too quickly. Rapid (jet) infusion or pumping under excess pressure is most dangerous. The myocardium physically cannot keep up with pumping the incoming volume of fluid.
Clinically, the condition manifests as cyanosis of the skin and the patient's complaints of severe pain in the right upper quadrant. The hemodynamic picture is very characteristic: there is a decrease in blood pressure (BP) against the background of an increase in central venous pressure (CVP). The pulse becomes small, rapid, and loses its regular rhythm (arrhythmia).
Management requires immediate action:
- Stop the blood infusion completely.
- Perform a phlebotomy of 200 to 300 ml to unload the right heart chambers.
- Administer cardiac glycosides (e.g., strophanthin-K) and vasopressors.
- Inject 10 ml of a 10% calcium chloride solution.
Citrate intoxication
The main cause of this condition is the entry of a large amount of preservative into the bloodstream. The toxic dose of citrate for humans is 0.3 g per kilogram of body weight.
The pathogenesis is due to the fact that citrate actively binds free calcium ions (Ca²⁺), leading to acute hypocalcemia. In addition, the preservative itself has a direct toxic effect on organs and tissues. The patient begins to experience muscle tremor, progressing to convulsions. Heart rate increases, blood pressure drops, and arrhythmia is recorded. In extremely severe cases, pupillary dilation, pulmonary edema, and cerebral edema are observed.
Prevention: to prevent this complication, 5 ml of a 10% calcium chloride or calcium gluconate solution must be administered prophylactically for every 500 ml of transfused stored blood.
Potassium intoxication
This type of intoxication is directly related to the expiration dates of transfusion media. Transfusion of large doses of blood that has been stored for a long time (more than 10 days) carries a huge risk of excessive potassium entering the recipient's body. Laboratory tests reveal hyperkalemia.
Excess potassium has a catastrophic effect on the myocardium, causing myocardial atony, bradycardia, and various arrhythmias. The most formidable consequence is ventricular fibrillation followed by complete cardiac arrest.
To avoid this complication, it is recommended to use fresh blood with a short shelf life (3 to 5 days), as well as washed or thawed red blood cells. If intoxication has already developed, specific treatment includes:
- Infusions of 10% calcium chloride solution, which acts as a direct potassium antagonist.
- Administration of isotonic sodium chloride solution.
- Injections of 40% dextrose solution combined with insulin.
- Use of cardiotonic and cardiac medications.
Homologous blood syndrome
This syndrome develops during massive transfusions from many different donors. It is important to understand that the complication occurs even if all transfused blood is perfectly compatible in terms of ABO and Rh blood groups. The cause is individual incompatibility of plasma proteins from different people.
The clinical picture develops rapidly:
- The recipient's skin pales and acquires a pronounced bluish tint.
- The pulse becomes weak and rapid, blood pressure drops, while CVP paradoxically increases.
- Severe pulmonary symptoms develop: initially, multiple fine moist rales are auscultated in the lungs, which, as pulmonary edema progresses, are replaced by coarse rales and gurgling respiration.
An interesting feature is the laboratory picture: despite active and adequate replacement of blood loss, the patient exhibits a drop in hematocrit and a sharp decrease in circulating blood volume (CBV).
Briefly: answers to topical questions
What specific ECG changes are recorded during potassium intoxication?
Specific ECG changes during potassium intoxication depend on the blood potassium concentration and manifest as repolarization and conduction disorders. ECG changes dynamics:
- $K^+$ level 6–7 mmol/L — appearance of tall, narrow, and peaked positive T waves (tented T wave), shortening of the QT interval.
- $K^+$ level 7–8 mmol/L — widening or disappearance of the P wave, widening of the QRS complex.
- $K^+$ level 8–9 mmol/L — fusion of the QRS complex with the T wave, giving the QRST complex a sinusoidal appearance.
- $K^+$ level >9 mmol/L — development of atrioventricular block, ventricular tachycardia, or ventricular fibrillation.
What is the pathophysiological mechanism of pulmonary edema development in homologous blood syndrome?
In homologous blood syndrome, the causes are individual incompatibility of plasma proteins during blood transfusion from multiple donors and microcirculatory disorders. The pathogenesis is based on erythrocyte stasis, microthrombosis, blood pooling, and altered blood clotting time. Pulmonary manifestations include multiple fine moist rales with progressive pulmonary edema, the appearance of coarse rales, and gurgling respiration.
To prevent citrate intoxication, use the "5 for 500" rule: for every 500 ml of stored blood, always add 5 ml of 10% calcium solution.
Class and exam questions
What does the prevention of potassium intoxication consist of?
It consists of refusing to use donor blood stored for more than 10 days. Instead, fresh blood with a short shelf life (3–5 days) should be used, or washed and thawed red blood cells.
How does hemodynamics change in acute cardiac dilatation?
Due to the heart's inability to pump the rapidly arriving volume of fluid, blood pressure (BP) decreases, while central venous pressure (CVP), on the contrary, increases. The pulse becomes small, rapid, and arrhythmic.
What happens to the circulating blood volume in homologous blood syndrome?
Paradoxically, despite continuous replacement of blood loss via blood transfusion, circulating blood volume (CBV) and hematocrit sharply decrease due to the immune conflict of plasma proteins.
What else to study on this topic
- Pathophysiology of pulmonary edema development in homologous blood syndrome
- Mechanism of calcium ion binding by sodium citrate
- Pharmacodynamics of calcium chloride as a physiological potassium antagonist
- Clinical evaluation of hemodynamics: the relationship between BP and CVP during blood transfusions
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