Three functions of the blood demand attention: its volume, its oxygen-carrying capacity, and its ability or propensity to clot.
Blood volume varies with age, weight, and sex (see Vascular access and fluid management). As we know from donating blood, the average adult can easily lose 500 mL without conspicuous consequences. Indeed, healthy patients can tolerate a blood loss of 20% of their total blood volume. The body compensates for such loss by mobilizing interstitial and eventually even intracellular water to replenish the decreased intravascular volume. In the process, the hematocrit will fall gradually over a couple of days.
With a loss of blood volume, the patient also loses oxygen carrying capacity. Compensatory increases in cardiac output can insure uninterrupted delivery of oxygen, even in the anemic patient. As hematocrit decreases to about 30%, fluidity of blood increases, which improves flow and thus aids in the delivery of a higher cardiac output. There are limits to how much anemia can be toler-ated. If the anemia develops over weeks or months, astonishingly low hema-tocrit values can be compatible with an active life, though the patient will deal with easy fatigability. Thus, we cannot with confidence identify a cer-tain hematocrit value that compels us to administer red cells. The idea that a hematocrit below 30% would lead us to administer packed cells has long been abandoned; even 18% is now often accepted. Instead of picking a threshold at which we would call for a transfusion, we take many factors into account. We might merely watch an anemic patient with a good cardiovascular system and normal CNS and renal function, while the same hematocrit in a patient with congestive failure and arrhythmias or confusion signals an urgent need to increase oxygen carrying capacity. Generally, we expect a single transfusion (450 mL packed cells) to increase the hematocrit by 3 volume % in the average adult.
Like everything in life, too much of a good thing can be as bad as not enough. Thus, we find ourselves time and again in the position of interfering with the clotting mechanism to prevent thrombosis, or stimulating the system when the patient is at risk of bleeding into vital organs. In order to approach this problem in a rational manner, we need to recapitulate the normal clotting cascade. We will not delve into the details that fascinate hematologists and instead focus on specific points of common interest to anesthesiologists.
The normal clotting mechanism prevents uncounted (and unnoticed) bleeding opportunities in everyday life. This normal clotting mechanism is extraordinarily complex with a dizzying array of factors and steps, the most important to anes-thesia being the following:
Normally we have 150 000 to 450 000 platelets/µL. Surgical bleeding becomes a problem with counts below 50 000/µL, and spontaneous bleeding occurs below 20 000/µL. In patients with thrombocytopenia, we can increase the platelet count by 5000 to 10 000/µL with every platelet “pack,” necessitating multiple units in most patients (order 1 unit/10 kg body weight). Platelets have a limited survival of up to 5 days if properly stored. Note that, unless specifically requested, platelets are “random donor pooled” meaning the patient is exposed to MANY donors at once with platelet transfusions. In contrast, one single donor unit is equivalent to about 6 units of pooled platelets.
It plays a crucial role in the clotting cascade (where it is honored as factor IV). In stored blood, the calcium is bound up and deactivated by citrate. With massive (equivalent to an entire blood volume or more) and rapid blood transfusion, the liver may not be able to keep up the metabolism of calcium citrate, at which point plasma citrate can rise to the point where it will interfere with calcium’s function as a coagulation factor. Citrate intoxication will also cause hypotension, cardiac depression, and prolonged QT intervals.
· Von Willebrand’s disease is the most common inherited bleeding disorder. It comes in different degrees of severity and is associated with a decreased or qualitatively abnormal von Willebrand’s factor (VIII:vWF).
· Classic hemophilia (A), a genetic disease affecting males, is a factor VIII defi-ciency. Patients often suffer hemarthroses and have hematuria.
· Hemophilia B or Christmas Disease clinically resembles hemophilia A but is caused by a deficiency of factor IX.
Before anesthesia, these patients are treated with specific drugs, e.g., desmo-pressin (DDAVP3®) for von Willebrand’s disease, or factor transfusion.
The drug exhibits a medley of effects resulting in the inhibition of thrombin. Heparin is frequently given in the OR when coagulation must be stopped – as in vascular and cardiovascular procedures. In small doses, it is given to patients at risk for post-operative thrombosis. The effect of heparin is measured by the activated partial thromboplastin time (aPTT) and can be reversed by the admin-istration of protamine, a highly positively charged molecule that binds the highly negatively charged heparin. Of note, the effect of low molecular weight heparins (LMWH, e.g., enoxaparin) cannot be assayed by aPTT (requires an anti-Factor Xa activity assay), and is not completely reversed by protamine.
These oral anticoagulants inhibit vitamin K-dependent factors (II, VII, IX, and X). Their activity is assayed by the prothrombin time (PT), with a therapeutic range of 1.5–4 times normal. These agents can be reversed by the administration of vitamin K, or acutely by transfusing fresh frozen plasma (FFP).
The coagulation status of a patient can be assessed clinically: is there evidence of bleeding (bloody urine, black stools (blood in upper GI tract), bleeding gums and/or easy bruising)? There are several laboratory tests to evaluate the clotting cascade.
This tests the extrinsic coagulation cascade and is prolonged when tissue fac-tors are involved. Because there are differences between labs, an international normalized ratio (INR) has been adopted, with a normal value of 1.0.
This tests the intrinsic pathway of coagulation and almost all the factors except VII and XIII. We use this test to monitor heparin activity.
This is commonly used in the OR to test therapeutic heparin anticoagulation, e.g., during cardiopulmonary bypass or vascular surgery. We mix 2 mL of the patient’s blood in a test tube containing an activator of coagulation, such as celite (diatomaceous earth), kaolin, or glass particles. We then stir the blood and monitor the time to clot formation. An ACT>200 s indicates adequate anticoagulation for these procedures. Note ACT is not a good monitor for lesser levels of heparin anticoagulation, e.g., deep venous thrombosis (DVT) prophylaxis.
This is used much less frequently. A clever machine scrutinizes the whole clotting process by analyzing the patient’s blood in an oscillating cup as it clots around a piston. Developing fibrin between cup and piston transmits the oscillations, which are then recorded. As the clot forms, the device records the transmitted oscillations and, when normal, assume the shape of a bomb (no fins!). Abnormal clotting because of the presence of anticoagulants or thrombocytopenia or fib-rinolysis causes the bomb to look spindly or skinny, or leaf-shaped. Cognoscenti can read these shapes like a book.
We detail replacement of clotting factors in Vascular access and fluid manage-ment.
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