Pump prime for cpb

Mohammed Elmasry asked 11 months ago
1 Answers
Alessio Moretto answered 11 months ago

The limitation of any volume replacement therapy is reached when the ability of the blood to transport O2 is insufficient to supply the tissues. This limit is currently thought to be reached at a hemoglobin concentration of about 7 g / dL in patients without apparent cardiac disease.
50 to 70% crystalloids go into the extravascular space, so the hemodilution is actually much lower. In the order of 1 ml every 3.2 infusions (so with a priming of 1150 actually the intravascular dilution is 360 ml)
If we put Albumin 5% 100 ml, the hemodilution will increase. We will have 1050 diluting 330 ml, + 100 of albumin that draws liquids 3.5: 1 and then another 350, so the intravascular dilution will be 680 ml. No study has shown a better outcome using colloids.
Mannitol is distributed exclusively in the extracellular space, causing cellular desiccation and hypervolemia; it is rapidly excreted by the kidney, causing osmotic diuresis. It is indicated in the prevention and / or treatment of the oliguric phase in acute renal failure, before it becomes irreversible and stabilized; in the treatment of intracranial and spinal hypertension and brain masses, to reduce intraocular pressure; to increase renal excretion of toxic substances; for measuring the glomerular filtrate. A particular advantage of mannitol and its protective effect on renal function. During cardiopulmonary bypass in adults, fluid priming containing 10 g, this is good for priming osmolarity.
 1000 ml contain:
Sodium chloride 6.0 g
Potassium chloride 0.3 g Calcium chloride dihydrate 0.2 g Sodium acetate 4.0 g mEq / liter: Na + 132
K + 4 Ca ++ 3
Cl- 110
Acetate as HCO – 29
Theoretical osmolarity: mOsm / l 277 pH: 6.0-7.0 – SID 29
Acetate and oxidized in the form of acetic acid (assumption H +) with two moles of O2
So for each mole of oxidized acetate, one mole of bicarbonate is produced and for every two moles of O2 consumed only one mole of CO2 is produced. RQ of 0.5, compared to glucose (dextrose), which has an RQ of 1.0, this means that the acetate metabolism consumes only inhaled and exhaled meta O2 as CO2.
Acetate is normally produced in the intestine, it is a by-product of tissue metabolism. The normal value for acetate in the blood is between 0.01-0.07 mmol / L and is rapidly transformed into acetyl coenzyme A (fundamental molecule in the metabolism of all living organisms), and possibly oxidized in the liver in CO2 and water . It prevents the development of acidosis at the beginning of bypass and does not require the addition of a swab such as bicarbonate. An mEq of acetate is equivalent to a mEq of bicarbonate.
Acetate plays a fundamental role in the metabolism of carbohydrates and lipids. Its effect can therefore be summarized as follows:
• “Acetate replaces fat as oxidative fuel, without carrying out glucose oxidation”;
• all tissues have the enzymes necessary for acetate metabolism, especially the liver, muscle, myocardium, and renal cortex;
• acetate rarely produces a slight increase in glucose concentration (use in diabetics; lactate> glucose).
• The heart (300 g) as a whole oxidizes about 2 mmol / min of acetate.
• The alkalizing effect of acetate is very rapid. The HCO3- concentration increased already after 15 minutes and 60% to 80% is eliminated as CO2 through the lungs within 1-12 hours.
• Acetate is metabolised significantly faster than lactate.
• Acetate metabolism is unchanged in patients with diabetes.
• Myocardial metabolism shows an oxidation of free fatty acids (FFA) decreased from 50% to about 25%.
• Acetate is a fuel delivered 209 kcal / mol.
Even if used in hemodialysis, acetate (but not lactate or HCO3-) has been associated with vasodilatory effects, depending on the dose (it is likely to occur only with rapid administration of high doses from 50 to 100 mmoles of acetate within one hour), presumably mediated by the release of adenosine from tissues.
Acetate is a common additive to IV solutions. It is used as a bicarbonate substitute because it is stable in solution and is converted to bicarbonate in the liver. In adults, the conversion of acetate to bicarbonate takes 5-10 minutes, in normothermia (in a child it can take 6 hours). There are no side effects except hypernatremia.


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