Labs report hematocrit or PCV as a percent (e.g., 45%), and you’ll often see “hematocrit/PCV” used interchangeably on the same report. Typical adult reference ranges vary by laboratory and context (including sex, altitude, and pregnancy). [1][2]

How it’s measured

Most analyzers calculate hematocrit from the red blood cell count and average size of red blood cells (RBC × MCV); some labs still use the microhematocrit method (centrifuging blood to separate RBCs from plasma and measuring the height of the packed RBC layer) as a cross-check. Either way, the result reflects the proportion of red blood cells relative to plasma, not an absolute cell count in isolation. [1]

Why does a “hematocrit/PCV high” result happen?

There are two broad reasons:

• Relative (hemoconcentration): Plasma volume is reduced (e.g., dehydration, diuretics), so the red-cell percentage looks higher even if red-cell mass hasn’t changed. [2]
• True erythrocytosis: The total red blood cell mass has increased (bone marrow making too many cells or secondary drivers, such as hypoxia, smoking/carbon monoxide attaching to blood cells, high altitude, or renal/EPO-related causes). Clinicians separate these with history, repeat testing, and a few targeted checks. [2][3]

First read of a high result

Re-evaluate hydration and recent illness, review medications and exposures (e.g., androgens, smoking/CO), and consider a quick oxygen check. If the elevation persists, physicians may administer erythropoietin or EPO (a hormone that controls red blood cell production) and conduct other targeted tests to determine whether the rise reflects hemoconcentration or an actual increase in red blood cell mass. [3]

Need help after a high PCV result?

Consult your healthcare professional (HCP) for the best next steps.

A high hematocrit/PCV indicates that red blood cells occupy a larger fraction of the blood, but this occurs for two distinct reasons. Relative (spurious) erythrocytosis reflects reduced plasma volume (e.g., dehydration), whereas true (absolute) erythrocytosis reflects an increased red-cell mass. Distinguishing the two drives the next steps and risk assessment. [3][4]

Relative erythrocytosis (hemoconcentration)

Typical scenarios include fluid loss from vomiting or diarrhea, the use of diuretics, significant burns, or acute stress states; in these settings, the hematocrit is elevated because plasma volume is reduced rather than because red-cell mass has increased. Practical clues include a recent history of dehydration and improvement after rehydration. EPO is typically normal, and repeat CBCs tend to return to baseline as volume normalizes. [2][3]

True erythrocytosis (increased red-cell mass)

Causes are primary (bone-marrow–driven, e.g., polycythemia vera) or secondary (hypoxia, smoking/carboxyhemoglobin, high altitude, cyanotic heart disease, renal disease/EPO-secreting lesions, exogenous androgens or EPO, high-affinity hemoglobin).

Patterns help: a low EPO suggests a primary process, while a normal/high EPO favors secondary causes. Screening often includes pulse oximetry (± sleep study), carboxyhemoglobin testing if smoking/CO exposure is possible, a medication review, and targeted imaging when EPO is inappropriately elevated. [3][4]

Common causes of a high PCV blood test

Secondary (more common) drivers:

Many cases of high hematocrit/PCV reflect a physiologic response to reduced oxygen delivery or external signals that stimulate the production of red blood cells. Typical causes include:

• Chronic lung disease (COPD, interstitial lung disease)
• Obstructive sleep apnea
• High altitude
• Smoking/carboxyhemoglobin
• Cyanotic heart disease
• Renal hypoxia
• EPO-secreting tumors (e.g., renal cell carcinoma)

Exogenous agents such as androgens or EPO can also raise PCV. Congenital causes include high-affinity hemoglobin variants and rare defects in enzymes or oxygen-sensing pathways. Clinicians screen patients with a comprehensive history, pulse oximetry (plus sleep study), carboxyhemoglobin testing when appropriate, medication review, EPO level assessment, and targeted imaging when EPO levels are inappropriately high. [3][4]

Primary marrow causes:

Polycythemia vera (PV), a myeloproliferative neoplasm (a blood cancer in which the marrow produces too many cells), is almost always associated with JAK2 mutations and is the prototypical primary erythrocytosis. In PV, erythroid precursors proliferate independently of physiologic need, so EPO levels are typically low. The diagnosis relies on meeting international rules for diagnosis by WHO/ICC thresholds (hemoglobin/hematocrit cut points) together with JAK2 positivity and supportive marrow morphology. [5][6][7]

Why cause matters:

Secondary erythrocytosis is managed by treating the driver (e.g., hypoxia, smoking cessation, medication adjustments), whereas PV follows disease-specific pathways once confirmed. That’s why “high PCV blood test” triggers a structured, cause-first evaluation before any long-term plan is set.[3][4]

A simple decision path

• Rehydrate and repeat the CBC
• Check oxygenation and exposures
• Add serum EPO

Option A: If EPO is low or the phenotype fits PV, test JAK2 V617F (then exon 12 if needed) and consider marrow per WHO/ICC guidance;

Option B: If EPO is normal/high, pursue secondary drivers first. Red-cell mass studies, which confirm absolute erythrocytosis using nuclear isotope dilution,are rarely needed today and are reserved for select dilemmas. [3]

Start by confirming the result and context. Re-evaluate hydration status and intercurrent illness, then repeat the CBC to see whether the elevation persists after rehydration and recovery. This helps distinguish relative hemoconcentration from an actual rise in red-cell mass. [3]

Assess oxygenation and exposures next. A bedside pulse oximetry reading (and overnight oximetry or a sleep study when obstructive sleep apnea is suspected) screens for hypoxic drivers. In smokers or those with potential carbon monoxide exposure, a carboxyhemoglobin level can help clarify whether impaired oxygen delivery is contributing to the issue. Review medications and substances that may raise PCV (e.g., androgens, therapeutic EPO) and note altitude or recent travel that could shift baseline values. [3][4]

Order a serum EPO level early and interpret it in conjunction with the clinical picture. Low EPO supports a primary marrow process (e.g., polycythemia vera), warranting JAK2 V617F testing (followed by exon 12 testing if needed) and consideration of bone marrow evaluation according to the WHO/ICC frameworks. Normal or high EPO points toward secondary erythrocytosis and should trigger a focused search for hypoxia, renal/EPO-secreting causes, or exogenous agents. Red-cell mass studies are rarely necessary and reserved for select diagnostic dilemmas. [3][5][7]

Check iron status (ferritin, transferrin saturation) because iron deficiency can mask the presence of PV. Hematocrit may appear “normal” while the RBC count is elevated. Replete iron when indicated and reassess; persistent erythrocytosis after correction strengthens the case for a primary process. [3][5][6]

Start with the cutoffs used in modern criteria

Sustained hemoglobin/hematocrit >16.5 g/dL / 49% in men or >16.0 g/dL / 48% in women raises concern for polycythemia vera (PV), especially when the RBC count trends high across serial CBCs. These thresholds originate from WHO/ICC frameworks and are applied in conjunction with the rest of the ruleset, rather than in isolation. [5][7]

Pair the CBC with targeted tests that anchor PV biology

A subnormal EPO level supports a primary erythrocytosis, and JAK2 V617F is the first-line mutation assay; if V617F is negative and suspicion remains, test JAK2 exon 12. Bone-marrow examination looks for panmyelosis (trilineage overgrowth with characteristic megakaryocytes). A diagnosis is made when the WHO/ICC rule is met, all three major criteria, or the first two major plus the minor (low EPO). [5][7]

In practice, clinicians may establish a working diagnosis when JAK2 positivity accompanies sustained Hgb/Hct above thresholds and a low EPO, then proceed to marrow for confirmation and to exclude look-alikes. Red-cell mass studies have become uncommon and are reserved for select dilemmas when CBC/EPO/marrow do not align. [3][7]

Watch for pitfalls that blur the picture

Iron deficiency can lower average red blood cell size and mask erythrocytosis; hematocrit may appear “normal” while RBC count is elevated, so iron studies and repletion (when indicated) should precede a final label. Reassessing after hydration or iron correction reduces the likelihood of misclassification. [3][5][6]

A markedly elevated Hct or PCV with acute symptoms warrants urgent evaluation to rule out thrombosis, severe hypoxia, or hyperviscosity. Red-flag symptoms include new neurologic deficits or confusion, sudden severe headache or vision loss, chest pain, shortness of breath, unilateral leg swelling, or syncope. These presentations may signal stroke/TIA, myocardial ischemia, pulmonary embolism, or other thrombotic events and should not wait for routine follow-up. [3][4][6]

Urgency also increases when oxygen saturation is low, when the Hct remains persistently high despite rehydration, or when there is a known or suspected myeloproliferative neoplasm such as PV. In these settings, clinicians prioritize stabilization (oxygenation, anticoagulation when indicated, and targeted investigations) while determining whether the elevation reflects secondary drivers (e.g., hypoxia, carboxyhemoglobin, exogenous agents) or a primary marrow process. [3][4][6]

If a secondary cause is identified, correct the driver and re-trend the data. After treating hypoxia (e.g., using continuous positive airway pressure [CPAP] for sleep apnea), stopping carbon monoxide exposure, adjusting exogenous androgens/EPO, or addressing dehydration, clinicians repeat the CBC to confirm that the hematocrit/PCV normalizes. An EPO level and oxygen assessment may be rechecked if the clinical picture changes or if erythrocytosis persists despite intervention. [3][4]

If polycythemia vera is confirmed, monitoring is structured and ongoing. Follow-up typically includes a hematocrit (and a broader CBC), a review of the thrombotic/bleeding history, symptom assessment, and spleen findings. Targets and visit cadence are individualized, but the emphasis is on maintaining safe hemoglobin/hematocrit levels over time while monitoring platelets, white blood cells, and tolerance to any interventions. Marrow or abdominal-pelvic imaging is used selectively when the course is atypical. [3][6][7]

When results don’t reconcile, the process may step back and re-classify based on the physician’s discretion. Persistently high hematocrit/PCV after hydration and iron repletion, discordant indices (e.g., microcytosis with a high RBC count), or an EPO level that does not fit the clinical context should prompt a second look at differentials and, when appropriate, JAK2 testing and bone-marrow evaluation per WHO/ICC guidance. The label follows the pattern over time, not a single draw. [3][5]

1. Is hematocrit the same as packed cell volume (PCV)?

Yes, hematocrit and PCV both describe the percentage of blood composed of red cells; most laboratories use the terms interchangeably. [1][2]

2. What level counts as “high”?

Reference ranges vary by lab and context (sex, altitude). For diagnosing PV, frameworks use sustained thresholds around Hgb/Hct > 16.5 g/dL / 49% (men) and > 16.0 g/dL / 48% (women), interpreted in conjunction with EPO, mutation testing, and marrow examination, not in isolation. [5][7]

3. Can dehydration alone raise hematocrit/PCV?

Yes, reduced plasma volume (hemoconcentration) can temporarily elevate hematocrit/PCV; rehydration and a repeat CBC typically normalize it if red-cell mass is unchanged. [3]

4. Which medicines or exposures commonly increase hematocrit?

Exogenous androgens and therapeutic erythropoietin (EPO) can raise hematocrit/PCV; smoking/carbon monoxide and hypoxia from sleep apnea or lung disease are frequent non-drug drivers. [3][4]

5. Do I need a red blood cell mass test?

Though contemporary evaluations rely on CBC trends, EPO, hypoxia/exposure assessment, JAK2 testing (when indicated), and marrow, red-cell mass studies are reserved for select dilemmas. However, it’s best to consult your HCP if this test is needed. [3]

6. When should JAK2 testing be considered?

Please consult your HCP if this test is needed. JAK2 V617F (then exon 12 if needed) when hematocrit/PCV is persistently elevated, EPO is low, and the overall picture suggests a primary process rather than secondary causes; marrow confirmation follows current frameworks. [5][7]

1. Mondal H, Zubair M. Hematocrit. [Updated 2024 Oct 6]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan. Available on https://www.ncbi.nlm.nih.gov/books/NBK542276/
2. Billett HH. Hemoglobin and Hematocrit. In: Walker HK, Hall WD, Hurst JW, editors. Clinical Methods: The History, Physical, and Laboratory Examinations. 3rd edition. Boston: Butterworths; 1990. Chapter 151. Available on https://www.ncbi.nlm.nih.gov/books/NBK259/
3. Mithoowani, S., Laureano, M., Crowther, M. A., & Hillis, C. M. Investigation and management of erythrocytosis. Cmaj. 2020;192(32):E913-E918.
4. Pillai AA, Fazal S, Mukkamalla SKR, et al. Polycythemia. [Updated 2023 May 20]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Available on https://www.ncbi.nlm.nih.gov/books/NBK526081/
5. Silver, R. T., Chow, W., Orazi, A., Arles, S. P., & Goldsmith, S. J. Evaluation of WHO criteria for diagnosis of polycythemia vera: a prospective analysis. Blood, The Journal of the American Society of Hematology 2013;122(11):1881–6.
6. Fox, S., Griffin, L., & Robinson Harris, D. Polycythemia Vera: Rapid Evidence Review. American family physician 2021;103(11):680–7.
7. Tefferi, A., & Barbui, T. Polycythemia vera: 2024 update on diagnosis, risk-stratification, and management. American Journal of Hematology 2023;98(9):1465–87.