Relative polycythemia
Relative polycythemia is an apparent rise of the erythrocyte level in the blood; however, the underlying cause is reduced blood plasma (hypovolemia, cf. dehydration). Relative polycythemia is often caused by loss of body fluids, such as through burns, dehydration, and stress. A specific type of relative polycythemia is Gaisböck syndrome. In this syndrome, primarily occurring in obese men, hypertension causes a reduction in plasma volume, resulting in (amongst other changes) a relative increase in red blood cell count. Symptoms
Doctors say that patients may not experience in any notable symptom of PV until the late stages. Although vague, these symptoms might help patients get help in the early years of the progression. Severe headache
Dizziness, fatigue, and tiredness
Unusual bleeding, nosebleeds
Pain
Itchiness
Numbness or tingling in different body parts

Notable people
Polycythemia is linked to increased performance in endurance sports due to the blood being able to store more oxygen. It can also be linked to damage from smoking. Eero Mäntyranta, Finnish cross-country skier
Bob Newhart, American comedian

See also
Cytopenia, a decrease in blood cell count
Capillary leak syndrome, another cause of hemoconcentration

References


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The fact that WPW patients are young and do not have structural heart disease, lead to using catheter ablation of the APs with the elimination of the atrial fibrillation as well as the episodes of re-entrant ventricular tachycardia. This elimination of the atrial fibrillation with ablation implies APs have some pathophysiologic role in the development of a-fib in the WPW patient.Functionally defined re-entry does not require the alternative anatomically defined circuit accessory pathways and it may not reside in just one location. Ventricular fibrillation (VF) following ventricular tachycardia (VT) may be described as a functionally defined re-entry problem caused by multiple mini re-entrant circuits spontaneously created within the ventricular myocardium. The original re-entrant circuit breaks down into multiple mini reentrant circuits. (VF becoming the grand finale of a single prolonged VT larger circus movement, propagating change in the "functional core" of the ventricular myocardium, dissipating mini reentrant circuits, exhibited as ventricular fibrillation.) Ischemia, electrolyte, pH abnormalities, or bradycardia are potential causes of functionally defined re-entry due to changes in the properties of the cardiac tissues functional core. (No accessory pathway required). For reentry to occur, the path length of circuit should be greater than the wave length (ERP × conduction velocity) of impulse. See also
AV reentrant tachycardia
AV nodal reentrant tachycardia

References


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