More flexible RBCs result in less viscous blood, and young RBCs are more flexible than older RBCs. Hematocrit accounts for about 50% of the difference between normal blood viscosity and high blood viscosity.Įrythrocyte deformability refers to the ability of RBCs to elongate at high velocity and to bend and fold themselves to pass through the slender passageways of the capillaries. A higher percentage of red blood cells (RBCs) results in thicker blood. Hematocrit is the most obvious determinant of WBV. These include hematocrit, erythrocyte deformability, plasma viscosity, erythrocyte aggregation, and temperature. To do so, one must know something about how the physics of blood flow works and about what affects blood viscosity.įive primary factors determine blood viscosity.
It is important to understand the role of blood viscosity as a clinical marker. 6 In the Edinburgh Artery Study, elevated blood viscosity was the strongest predictor of stroke risk, after controlling all other major risk factors. 1-5 Elevated blood viscosity is a strong independent predictor of cardiovascular events. Blood viscosity is correlated with all known risk factors for cardiovascular disease, including age, sex, smoking, obesity, inflammation, insulin resistance, high blood pressure, low high-density lipoprotein cholesterol, high low-density lipoprotein cholesterol, and others. It is a direct measure of the “flow ability” of blood and is modifiable with existing naturopathic therapies. This important hemodynamic biomarker determines the amount of friction against the blood vessels, the degree to which the heart must work, and the quantity of oxygen delivery to the tissues and organs. I learned early on that a therapeutic international normalized ratio was not to be trusted.”īlood viscosity is a measurement of the thickness and stickiness of a patient’s blood. Only then, after lowering his WBV to a safe range, would I have discharged this patient safely to home to his loved ones. Dr Holsworth later became one of the world’s leading experts in the use of blood viscosity in a clinical setting and asked: “I wonder if this patient would be alive had I been able to evaluate his likely elevated WBV and treat him with antiviscogenic agents. Dr Holsworth recalled that his aforementioned patient had been discharged with normal vital signs and laboratory test results that provided no indication of the evolving danger. It was not until several years later that Dr Holsworth learned of the role of whole blood viscosity (WBV) in the formation of thrombi.
A mandatory autopsy revealed that the patient had a major pulmonary embolism, resulting in his sudden death. The patient was pronounced dead after several attempts at resuscitation. He rushed down to the emergency department, where cardiopulmonary resuscitation was in progress and assisted in the code. His patient had just collapsed in the parking lot. A few minutes later, Dr Holsworth’s pager buzzed. When the patient’s prothrombin time–international normalized ratio exceeded 2.0, Dr Holsworth was instructed by hematology-oncology to discharge the patient. He worked the patient up for congenital thrombophilias, cancer, hypothyroidism, and other conditions, and consulted with hematology-oncology on the case. Dr Holsworth started him on low-molecular-weight heparin subcutaneous injections concurrently with warfarin sodium. He was an intern in a Denver hospital when he admitted a patient diagnosed as having a blood clot in his leg. Ralph Holsworth, DO, recently shared a story with me about a patient he had in Colorado many years ago. Earlier, More Accurate Prediction of Cardiovascular Event Risk
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