Low hematocrit and hemoglobin



Anemia reflects blood loss that exceeds replacement by physiological marrow erythropoiesis and/or red cell transfusions. In many cases the location of hemorrhage may be obvious–or easily deduced–from the patient’s history and physical exam: trauma, surgical sites, extensive hematoma, melana, hematemesis, menorrhagia, epistaxis, third-space hemorrhage (Cullen’s sign, Turner’s sign).

In other cases the site of blood loss may be difficult to determine, requiring endoscopic examinations and/or imaging studies of the retroperitoneum, peritoneum, and soft tissue. Hemorrhagic anemia can be complicated by qualitative or quantitative platelet defects, and by congenital, acquired, or therapeutic changes in the quantity or activity of blood coagulation proteins.


Destructive defects can be broadly classified as inherited, mechanical, acquired non-immune, and acquired immune.

Inherited anemias of this type can result from congenital defects in hemoglobin, metabolic enzymes, and/or red cell membranes. These defects, which result in increased clearance of red cells through a number of different mechanisms, generally result in accelerated destruction of red blood cell progenitors in the marrow (ineffective erythropoiesis) and shortened half-life of mature erythrocytes in the peripheral circulation (hemolysis).

As a group, these disorders are characterized by markers of hemolysis (increased LDH and bilirubin, reduced haptoglobin) with normal Coombs studies, as well as a compensatory elevation in erythropoiesis (can manifest as a reticulocytosis).

Mechanical anemias of this type can be traced to defects in normal vascular flow by therapeutic devices (artificial heart valves, extracorporeal circulation), structural defects (aortic stenosis, renal artery stenosis), or several conditions that result in microvascular occlusion. This last group of disorders includes the microangiopathies, which are characterized by fragmented red cells (schistocytes), including DIC, TTP, HUS, eclampsia, carcinomatosis, allograft rejection, and malignant hypertension.

Non-immune conditions that result in red cell destruction include malaria, chemical agents that are directly toxic to red cells, and thermal injury (burns).

Immune processes that cause red cell destruction typically result from the deposition of antibodies on the red cell membrane. The specific clinical manifestation may depend upon the antibody class: IgG antibodies are directed against red cell membrane proteins, while IgM antibodies typically target membrane polysaccharides. Auto-antibodies may occur spontaneously, or in response to an inciting factor (e.g., infection or drug).

IgG (‘warm-reacting’) antibodies generally adhere to red cell membranes at or near core body temperature, while IgM (‘cold-reacting’) antibodies may display a lower thermal amplitude. Blood-bank studies based upon the Coombs principles can generally distinguish autoimmune from non-immune causes of hemolysis.

Production defect

In healthy individuals, red blood cells survive in the peripheral circulation for approximately 100-120 days. Senescent cells are continuously removed by the reticuloendothelial system and are replaced by maturing red blood cells that are released from the bone marrow into the peripheral circulation (generally at the reticulocyte stage of development). Conditions that reduce marrow erythropoiesis–even in the absence of hemorrhage or pathological destruction–can result in significant anemia.

Nutritional deficiencies (iron, vitamin B12, folate) are common causes of reticulocytopenic (hypoproliferative) anemias, as are a several infections, including parvovirus. Toxic, malignant, and other conditions can produce hypoproliferative anemias, while inflammatory conditions can produce defects in iron trafficking and a corresponding “anemia of chronic disease.”


The wide variability in the reported prevalence of anemia results, in part, from the lack of standard universal definitions. As a general rule, anemias can be defined as hemoglobin values <13 g/dL in men, and <12 g/dL in women (World Health Organization). A high prevalence of anemia is observed in elderly inpatients and in nursing-home residents.

Anemia in this elderly population has been associated with increased morbidity and mortality, and is commonly attributed to nutritional deficiencies (iron, vitamin B12, and folate), chronic medical conditions, myelodysplasia, and/or other etiologies, including MDS.


The prognosis for a patient with anemia is generally determined by the underlying disorder, but can also depend upon the speed and accuracy with which the pathophysiology of the anemia is identified; this is particularly true for hemorrhagic and destructive causes of anemia.

Special considerations for nursing and allied health professionals.


Description of the Problem:

Jeffrey, McCullough. Transfusion Medicine. 2005.

Emergency Management:

Greer, JP, Foerster, J, Lukens, JN, Rodgers, GM, Paraskevas, F, Glader, B. Wintrobe’s Clinical Hematology. 2004.

Adamson, JW. “The erythropoietin/hematocrit relationship in normal and polycythemic man: Implications of marrow regulation”. Blood. vol. 32. 1968. pp. 597-609.

Erslev, AJ. N Engl J Med. vol. 324. 1991. pp. 1339-44.

Goodnough, LT, Price, TH, Parvin, CA. “Erythropoietin response to anaemia is not altered by surgery or recombinant human erythropoietin therapy”. Br J Haematol. vol. 87. 1994. pp. 695-9.

Specific Treatment:

Herbert, PC, Wells, G, Blajchman, MA. “A multicenter, randomized, controlled clinical trial of transfusion requirements in critical care. Transfusion Requirements in Critical Care Investigators, Canadian Critical Care Trials Group”. N Engl J Med. vol. 340. 1999. pp. 409

Herbert, PC, Yetisir, E, Martin, C. “Transfusion Requirements in Critical Care Investigators for the Canadian Critical Care Trials Group”. Crit Care Med. vol. 29. 2001 Feb. pp. 227-234.

Pritchard, JA, Hunt, CF. “A comparison of the hematologic responses following the routine prenatal administration of intramuscular and oral iron”. Surg Gynecol Obstet. vol. 106. 1958. pp. 516

Auerbach, M, Rodgers, GM. “Intravenous iron”. N Engl J Med. vol. 357. 2007. pp. 93

Faich, G, Strobos, J. “Sodium ferric gluconate complex in sucrose: safer intravenous iron therapy than iron dextrans”. Am J Kidney Dis. vol. 33. 1999. pp. 464

Miller, HJ, Hu, J, Valentine, JK, Gable, PS. “Efficacy and tolerability of intravenous ferric gluconate in the treatment of iron deficiency anemia in patients without kidney disease”. Arch Intern Med. vol. 167. 2007. pp. 1327

Goodnough, LT, Skikne, B, Brugnara, C. “Erythropoietin, iron, and erythropoiesis”. Blood. vol. 96. 2000. pp. 823

Disease Monitoring, Follow-up and Disposition:

World Health Organ Tech Rep Ser. vol. 405. 1968. pp. 5

Low Hemoglobin: Possible Causes

What happens when someone has low hemoglobin?

If a disease or condition affects the body’s production of red blood cells, the hemoglobin levels may drop. Fewer red blood cells and lower hemoglobin levels may cause the person to develop anemia.

What is anemia?

Anemia is a blood disorder that occurs when there is not enough hemoglobin in a person’s blood. When a person develops anemia, he or she is said to be “anemic.” There are several different types of anemia. Some types cause only mild health problems, while others are much more severe. Each type of anemia comes from one of these factors:

  • The body cannot make enough hemoglobin.
  • The body makes hemoglobin, but the hemoglobin doesn’t work right.
  • The body does not make enough red blood cells.
  • The body breaks down red blood cells too fast.

What causes anemia?

Your body uses iron to make hemoglobin. A lack of iron in the body is the most common cause of anemia. This is called iron-deficiency anemia. If you don’t get enough iron, your body cannot make hemoglobin. Factors that can lower your body’s stores of iron include the following:

  • Blood loss (caused by ulcers, trauma, some cancers, and other conditions; and, in women, during monthly periods)
  • An iron-poor diet
  • An increase in the body’s need for iron (in women during pregnancy)

What are the symptoms of anemia?

There are a number of symptoms that occur in all types of anemia, including:

  • Feeling tired
  • Trouble breathing
  • Dizziness
  • Headache
  • Feeling cold
  • Weakness
  • Pale skin

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High Hemoglobin Count

What is a high hemoglobin count?

Hemoglobin is a protein in red blood cells that helps blood carry oxygen throughout the body. (Hemoglobin contains iron, which gives blood its red color.) The hemoglobin count is an indirect measurement of the number of red blood cells in your body. When the hemoglobin count is higher than normal, it may be a sign of a health problem.

Normal hemoglobin counts are 14 to 17 gm/dL (grams per deciliter) for men and 12 to 15 gm/dL for women. Hemoglobin levels depend on many factors, including age, race, gender and the general health of the person.

Hemoglobin is usually measured as part of a complete blood count (a routine blood test), along with hematocrit (the percentage of the blood that is made up of red blood cells), to help diagnose medical conditions and learn more about the person’s health.

What can cause a high hemoglobin count?

Many factors can affect the hemoglobin level. Sometimes a high hemoglobin count is the result of lifestyle or a side effect of taking medication.

Medical conditions that can cause high hemoglobin levels include:

  • Polycythemia vera (the bone marrow produces too many red blood cells)
  • Lung diseases such as COPD, emphysema or pulmonary fibrosis (lung tissue becomes scarred)
  • Heart disease, especially congenital heart disease (the baby is born with it)
  • Kidney tumors
  • Dehydration (from diarrhea or lack of fluids)
  • Hypoxia (low blood oxygen levels)
  • Carbon monoxide exposure (usually related to smoking)

Lifestyle factors that can cause a high hemoglobin count include:

  • Smoking cigarettes
  • Living at a high altitude
  • Taking performance-enhancing drugs such as anabolic steroids (for example, synthetic testosterone) or erythropoietin

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Several small studies have associated anemia due to vitamin B12 deficiency,1,2 thalassemia,3 and sickle cell anemia4 with low heart rate variability (HRV). However, no study has examined whether anemia is associated with HRV in patients who have heart disease. Several studies have shown that low HRV independently predicts sudden cardiac death and overall mortality in patients who have heart disease,5–10 suggesting that low HRV may contribute to the adverse cardiac outcomes associated with anemia. We hypothesized that anemia is associated with an imbalance of cardiac autonomic tone as measured by low HRV in patients who have coronary heart disease (CHD). To determine whether anemia is associated with HRV, we measured hemoglobin and HRV in a cross-sectional study of 874 ambulatory patients who had stable CHD.

The Heart and Soul Study is a prospective cohort study of psychosocial factors and health outcomes in patients who have CHD. Details regarding our methods have been previously published.11 Outpatients who had documented CHD were recruited from 2 veterans affairs medical centers (San Francisco VA Medical Center, San Francisco, California, and the VA Palo Alto Health Care System, Palo Alto, California), 1 university medical center (University of California, San Francisco, California), and 9 public health clinics in the Community Health Network of San Francisco. Patients were eligible to participate if they had ≥1 of the following: a history of myocardial infarction, angiographic evidence of ≥50% stenosis in ≥1 coronary vessel, previous evidence of exercise-induced ischemia by treadmill or nuclear testing, a history of coronary revascularization, or a diagnosis of CHD by an internist or cardiologist (based on a positive angiographic or exercise treadmill test result in >98% of cases). Patients were excluded if they were unable to walk 1 block or were planning to move from the local area within 3 years.

Between September 2000 and December 2002, 1,024 participants were enrolled and completed a day-long study appointment at the San Francisco VA Medical Center. A total of 150 participants was excluded from HRV analysis because they were not in sinus rhythm (n = 76) or had missing Holter data (n = 74), leaving 874 participants for this cross-sectional study. During their day-long appointment, all participants completed a comprehensive medical health interview and questionnaire and underwent exercise treadmill stress testing with echocardiographic imaging. Participants then underwent 24-hour ambulatory Holter electrocardiography for measurement of HRV. The protocol was approved by the appropriate institutional review boards, and all participants provided written informed consent.

After an overnight fast, venous blood samples were drawn into tubes that contained ethylenediaminetetraacetic acid. Hemoglobin values were obtained with the Beckman Coulter LH 750 (Fullerton, California); interassay coefficient of variation was 0.4%. The laboratory technicians who measured these values were blinded to the results of the stress echocardiogram. We defined anemia as a hemoglobin level ≤12 g/dl in accordance with previous studies.12–14 Hemoglobin was also examined as a continuous predictor variable.

We measured HRV indexes obtained by 3-channel, 24-hour, ambulatory Holter electrocardiographic recording as recommended by the Task Force of the European Society of Cardiology and the North American Society of Pacing and Electrophysiology.15 Holter recordings were scanned 500 times in real time, and electrocardiographic data were digitized at a frequency of 128 Hz. Software (GE Healthcare, Waukesha, Wisconsin) was used to detect and label each QRS complex. The software measures all cycles in which beats have normal morphologic characteristics and cycle lengths within 20% duration of the preceding cycle length. The processed electrocardiograms were carefully reviewed and modified as necessary by an editor who was blinded to hemoglobin levels.

Annotated QRS data were processed by other software (GE Healthcare) to compute time-domain variables, including SD of NN intervals in milliseconds and SD of 5-minute mean NN intervals in milliseconds. The software also computed frequency-domain variables using a fast-Fourier transformation over the 24-hour period, including very-low-frequency power (0.0033 to 0.04 Hz), low-frequency power (0.04 to 0.15 Hz), high-frequency power (0.15 to 0.4 Hz), and wideband frequency power (0.0033 to 0.4 Hz) in square milliseconds.12,16,17 Very-low-frequency power and wideband frequency power were available for only 478 participants because the software was upgraded during the study. In a quality control check, we performed blinded repeat measurements of 20 tapes and found >99% concordance in readings between the 2 software programs.

Age, gender, ethnicity, marital status, smoking status, alcohol use, and medical history were determined by questionnaire. Participants were instructed to bring their medication bottles to the study appointment, and study personnel recorded all current medications. Participants were considered to be physically active if they answered fairly, quite, very, or extremely active (vs not at all or a little active) to the following multiple-choice question: “Which of the following statements best describes how physically active you have been during the last month, that is, done activities such as 15 to 20 minutes of brisk walking, swimming, general conditioning, or recreational sports?” We measured weight and height and calculated body mass index (kilograms per square meters).

Systolic and diastolic blood pressures were measured with a standard sphygmomanometer. We assessed left ventricular (LV) ejection fraction (systolic function) and diastolic pulmonary vein flow (diastolic function) on echocardiograms obtained at rest. Presence of ischemia was assessed by a symptom-limited, graded exercise treadmill test according to a standard Bruce’s protocol, and wall motion score index at peak exercise using stress echocardiography was calculated.18 We also assessed the presence of inducible ischemia, defined as the presence of ≥1 new wall motion abnormality, at peak exercise. LV mass was determined by echocardiography, and LV mass index was calculated by dividing LV mass by body surface area. Creatinine clearance was assessed by 24-hour urine collection.

Differences in baseline characteristics between participants who had anemia and those who did not were compared with 2-tailed Student’s t tests for continuous variables and chi-square tests for dichotomous variables. The frequency-domain HRV measurements were log-transformed to produce normal distributions. We used analysis of covariance to compare mean HRV values in participants who had anemia and those who did not after adjusting for potential confounding variables using a backward elimination procedure (p <0.05 for retention). We used logistic regression to determine the association of anemia with low HRV (defined as lowest quartile of each HRV index). All analyses were performed with SAS version 8 (SAS Institute, Cary, North Carolina).

Ninety of the 874 participants (10.3%) had anemia (hemoglobin ≤12 g/dl). Compared with participants who did not have anemia, those who did were less likely to be men, to be white, to drink alcohol, and to be physically active (Table 1). Participants who had anemia were more likely to have diabetes mellitus and congestive heart failure and to take diuretics. Compared with those who did not have anemia, participants who had anemia had higher LV mass index values, greater likelihood of diastolic pulmonary vein flow, lower diastolic blood pressure, and lower creatinine clearance.

Table 1

Characteristics of 874 Participants, Stratified by Presence of Anemia

Values are mean ± SD or numbers of patients (percentages).

In age-adjusted analyses, time- and frequency-domain measurements of mean HRV were lower in participants who had anemia (Table 2). In multivariable analyses, anemia remained associated with lower mean HRV, but this association was statistically significant only for very-low-frequency and wideband frequency power measurements (Table 2).


Heart Rate Variability in 873 Participants, Stratified by the Presence of Anemia (hemoglobin ≤12 g/dl)

*Values for VLF and WBF were available for only 478 participants. †All variables listed in Table 1 were entered into the multivariable models. Other variables associated with SDNN (at p <0.05) were smoking, diabetes, angina, CABG, asthma/COPD, β-blocker use, renin-angiotensin system inhibitor use, diuretic use, and heart rate at rest. Other variables associated with SDANN were smoking, diabetes, angina, CABG, asthma/COPD, β-blocker use, renin-angiotensin system inhibitor use, diuretic use, and heart rate at rest. Other variables associated with VLF were gender, current smoking, history of stroke, history of diabetes, heart rate at rest, and systolic blood pressure. Other variables associated with LF were current smoking, history of hypertension, history of diabetes, CABG, and heart rate at rest. Other variables associated with HF were age, history of diabetes, angina, previous CABG, heart rate at rest, and diastolic dominant pulmonary vein flow. Other variables associated with WBF were gender, current smoking, history of diabetes, history of stroke, renin-angiotensin system inhibitor use, previous CABG, heart rate at rest, systolic blood pressure, and diastolic dominant pulmonary vein flow.

When HRV was examined as a dichotomous outcome (defined as the lowest quartile of each HRV index), the presence of anemia remained associated with low HRV (Figure 1). Of the 90 participants who had anemia, 29% to 41% had low HRV compared with 23% to 25% of the 784 participants who did not have anemia (p values <0.05 for all HRV indexes except high-frequency power). With the exception of high-frequency power, each decrease in hemoglobin of 1 g/dl was associated with increased odds of being in the lowest quartile of HRV, and this association remained strong after adjusting for potential confounding variables (Table 3).

Proportion of participants who had HRV in the lowest quartile according to presence (hemoglobin ≤ 12 g/dl, n = 90) (dark gray bars) and absence (n = 784) (light gray bars) of anemia. p <0.05 for association of anemia with all HRV indexes except high frequency. LnHF = natural-log high-frequency power; LnLF = natural-log low-frequency power; LnVLF = natural-log very-low-frequency power; LnWBF = natural-log wideband frequency power; SDANN = SD of 5-minute mean NN intervals; SDNN = SD of NN intervals.


Association of Each Gram-per-Deciliter Decrease in Hemoglobin With Low Heart Rate Variability in Older Adults with Coronary Heart Disease*

*Two hundred eighteen of 873 participants were in the lowest quartile of SDNN, SDANN, LF, and HF, 120 of 478 participants were in the lowest quartile of VLF and WBF. †Adjusted for all variables listed in Table 1.

OR = odds ratio; other abbreviations as in Table 2.

This is the first reported association of anemia and low HRV in patients who have CHD. Several small studies have found decreased HRV in selected patients who have anemia.1–4 However, no study has examined the association between anemia and HRV in a broad spectrum of outpatients, nor has a study demonstrated an association between anemia and low HRV in patients who have CHD.

In this study, anemia was associated with depressed very-low-frequency, low-frequency, and wideband frequency power but not with depressed high-frequency power. This finding is in accordance with previous studies that have shown depressed very-low frequency, low-frequency, and wideband frequency power but not high-frequency power to be predictive of ventricular tachycardia and cardiac events.8,9,19 Low-frequency power is believed to reflect the modulation of sympathetic and parasympathetic tones,16 whereas high-frequency power is believed to reflect pure parasympathetic tone.17 Although the precise physiologic meaning of very-low-frequency power is not completely understood, it has been suggested that very-low-frequency power is influenced by thermoregulation, fluctuation in the renin-angiotensin axis, function of peripheral chemoreceptors, and physical activity,9 all of which may be associated with adverse cardiovascular outcomes.

Iron Deficiency


Iron deficiency is the most common nutrient deficiency in the world. Three levels of iron deficiency are generally identified (3):

  • Iron stores are depleted, but the functional iron supply is not limited.
  • The supply of iron is low enough to impair red blood cell formation, but not low enough to cause measurable anemia.
  • There is inadequate iron to support normal red blood cell formation, resulting in anemia.

Individuals at increased risk of iron deficiency include:

  • Infants and children between the ages of 6 months and 4 years due to the rapid growth rates sustained during this period (4).
  • Early adolescence is another period of rapid growth. In females, the blood loss that occurs with menstruation results in additional iron requirement (4).
  • In pregnant women, the developing fetus and placenta as well as blood volume expansion, increase the iron requirement (4).
  • Individuals with chronic blood loss (e.g., intestinal parasitic infection) (1).
  • People who donate blood frequently, especially menstruating women, may need to increase their iron intake to prevent deficiency (1).
  • Individuals with celiac disease, an autoimmune disorder.
  • Individuals with Helicobacter pylori infection (24).
  • Individuals who have had gastric bypass surgery may suffer from poor absorption of iron from food.
  • People consuming only vegetarian diets, because iron from plant sources is less efficiently absorbed than that from animal sources (11).
  • Individuals who engage in regular intense endurance training, which may be due to increased microscopic bleeding from the gastrointestinal tract or increased fragility and rupture (‘hemolysis’) of red blood cells(11).


Most of the symptoms of iron deficiency are a result of the associated anemia, and may include fatigue, rapid heart rate, and rapid breathing on exertion.

Iron deficiency also impairs the ability to maintain a normal body temperature on exposure to cold.

Severe iron deficiency anemia may result in brittle and spoon-shaped nails, sores at the corners of the mouth, and a sore tongue. In some cases, advanced iron-deficiency anemia may cause difficulty in swallowing due to the formation of webs of tissue in the throat and gullet (25).

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