1 Early elevation (within 3 hours) may
suggest myocardial injury, but less specific
Homocysteine 4–12 μmol/L 4–12 μmol/L 1 Damages vessel endothelial, which may
increase the risk for cardiac disease.
Associated with deficiencies in folate,
0.01667 High in heart, kidney, liver, and skeletal
muscle. Five isoenzymes: LD1 and LD2
mostly in heart, LD5 mostly in liver and
skeletal muscle, LD3 and LD4 are
nonspecific. ↑ in malignancy, extensive
BNP <100 pg/mL <100 ng/L 1 BNP >500 ng/L indicates congestive heart
failure. Released from ventricles with ↑
1 NT-proBNP has similar clinical utility to
CRP 0–1.6 mg/dL 0–16 mg/L 1 Nonspecific indicator of acute
inflammation. Similar to ESR, but more
rapid onset and greater elevation. CRP >3
mg/dL increases risk of cardiovascular
hs-CRP 0–2.0 mg/L 0–2.0 mg/L 1 More sensitive measure of CRP;
concentrations from 0.5 to 10 mg/L; hsCRP <1.0 mg/L low risk for cardiovascular
disease; 1.0–3.0 mg/L average risk; and
>3.0 mg/L high risk for cardiovascular
AST 0–35 units/L 0–0.58 μkat/L 0.01667 Large amounts in heart and liver; moderate
amounts in muscle, kidney, and pancreas. ↑
with MI and liver injury. Less liver specific
ALT 0–35 units/L 0–0.58 μkat/L 0.01667 From heart, liver, muscle, kidney, pancreas.
↑ negligible unless parenchymal liver
disease. More liver specific than AST
0.01667 Large amounts in bile ducts, placenta, bone.
↑ in bile duct obstruction, obstructive liver
disease, rapid bone growth (e.g., Paget
GGT Sensitive test reflecting hepatocellular
injury; not helpful in differentiating liver
disorders. Usually high in chronic alcoholics
Bilirubin—total 0.1–1 mg/dL 2–18 μmol/L 17.1 Breakdown product of hemoglobin, bound
to albumin, conjugated in liver. Total
bilirubin includes direct (conjugated) and
indirect bilirubin. ↑ with hemolysis,
Amylase 35–118 units/L 0.58–1.97
0.01667 Pancreatic enzyme; ↑ in pancreatitis or duct
Lipase 10–160 units/L 0–2.67 μ kat/L 0.01667 Pancreatic enzyme, ↑ acute pancreatitis,
elevated for longer period than amylase
PSA 0–4 ng/mL 0–4 mcg/L 1 ↑ in BPH and also in prostate cancer. PSA
levels of 4–10 ng/mL should be worked up.
Risk of prostate cancer increased if free
TSH 0.5–4.7 μ units/mL 0.5–4.7
1 ↑ TSH in primary hypothyroidism requires
exogenous thyroid supplementation; ↓ TSH
Procalcitonin <0.5 ng/mL <0.5 mcg/L 1 ↑ Bacterial infections—low risk of sepsis if
<0.5 ng/mL; high risk of severe sepsis if
<200 mg/dL <5.2 mmol/L 0.02586 Current guidelines do not recommend a
target level; consult current guidelines
LDL <100 mg/dL <2.58 mmol/L 0.02586 Current guidelines do not recommend a
target level, but rather starting moderate- to
high-intensity statin therapy based on
current risk factors; consult current
HDL Female: >50 mg/dL Female: >1.29 0.02586 Current guidelines do not recommend a
target level; consult current guidelines
<150 mg/dL <1.70 mmol/L 0.0113 ↑ by alcohol, saturated fats, drugs. Obtain
fasting level. Current guidelines do not
Hct ↓ with anemias, bleeding, hemolysis. ↑ with
Male 13.8–17.5 g/dL 138–175 g/L
Female 12.1–15.3 g/dL 121–153 g/L
a Describes average RBC size; ↑ MCV =
macrocytic, ↓ MCV = microcytic
MCH 27–33 pg 1.66–2.09 fmol/cell Measures average weight of Hgb in RBC
MCHC 33–36 g/dL 20.3–22 mmol/L More reliable index of RBC hemoglobin
Concentration will not change with weight
0.5%–1.5% 0.005–0.015 Indicator of RBC production; ↑ suggests ↑
number of immature erythrocytes released
in response to stimulus (e.g., iron in irondeficiency anemia)
ESR 0–30 mm/hour 0–30 mm/hour Nonspecific; ↑ with inflammation, infection,
neoplasms, connective tissue disorders,
pregnancy, nephritis. Useful monitor of
temporal arteritis and polymyalgia
/L Consists of neutrophils, lymphocytes,
monocytes, eosinophils, and basophils; ↑ in
ANC 2,000 cells/μ L ANC = WBC × (% neutrophils +%
bands)/100; if <500 ↑ risk infection, if
Neutrophils 40%–70% 0.4–0.7 ↑ in neutrophils suggests bacterial or fungal
infection. ↑ in bands suggests bacterial
Eosinophils 0%–8% 0–0.08 Eosinophils ↑ with allergies, parasitic
infections, and certain neoplasms
/μ L = thrombocytopenia; <20 ×
/μ L = ↑ risk for severe bleeding
Male 45–160 mcg/dL 8.1–31.3 μ mol/L Body stores two-thirds in Hgb; one-third in
bone marrow, spleen, liver; only small
amount present in plasma. Blood loss major
Female 30–160 mcg/dL 5.4–31.3 μ mol/L ↑ needs in pregnancy and lactation
TIBC 220–420 mcg/dL 39.4–75.2 μ mol/L ↑ capacity to bind iron with iron deficiency
Please refer to Chapter 27, Fluid and Electrolyte Disorders, for more detailed
Reference Range: 135–147 mEq/L or mmol/L
Sodium is the predominant cation of the extracellular fluid (ECF), and human cells
reside in salt water. Along with chloride, potassium, and water, sodium is important
in establishing serum osmolarity and osmotic pressure relationships between
intracellular fluid (ICF) and ECF. Osmoregulatory system regulates the plasma
sodium concentrations to remain in a normal range by controlling water intake and
6 An increase in the serum sodium concentration could suggest either
impaired sodium excretion or volume contraction. On the contrary, a decrease in the
serum sodium concentration to less-than-normal values could reflect hypervolemia,
abnormal sodium losses, or sodium starvation. Although healthy individuals are able
to maintain sodium homeostasis without difficulty, patients with kidney failure, heart
failure, or lung disease often encounter sodium and water imbalances. In adults,
changes in serum sodium concentrations most often represent water rather than
sodium imbalance. Therefore, serum sodium concentrations are more reflective of a
patient’s fluid status rather than sodium balance. Clinical manifestations of
hyponatremia or hypernatremia are mostly neurologic, and rapid changes in serum
sodium concentrations can lead to severe and sometimes fatal brain injury.
Hyponatremia can result from dilution of the sodium concentration in serum or from a
total body depletion of sodium. The finding of hyponatremia implies that sodium has
been diluted throughout all body fluids because water moves freely across cell
membranes in response to oncotic pressures. Hyponatremia can denote low, high, or
normal tonicity. Dilutional hyponatremia is the most common form and results from
7 Some clinical conditions such as cirrhosis, congestive heart failure
the syndrome of inappropriate antidiuretic hormone secretion (SIADH), and renal
impairment, as well as the administration of osmotically active solutes (e.g., albumin
and mannitol) are commonly associated with dilutional hyponatremia. Drugs that can
induce SIADH, thereby causing a reversible hyponatremia (especially in the elderly),
include cyclophosphamide, carbamazepine, desmopressin, oxcarbazepine, oxytocin,
serotonin selective reuptake inhibitors, and vincristine.
from sodium depletion presents as a low serum sodium concentration in the absence
of edema. Sodium-depletion hyponatremia can be caused by mineralocorticoid
deficiencies, sodium-wasting renal disease, or replacement of sodium-containing
fluid losses with nonsaline solutions.
7 Therapy with thiazide diuretics may also lead
to the development of severe hyponatremia. Hyponatremia can be frequently seen in
hospitalized patients; however, morbidity varies significantly in severity, and serious
complications can be due to the disorder itself or due to the inappropriate
management and rapid correction of the sodium levels.
Hypernatremia represents a state of relative water deficiency in relation to the
body’s sodium stores. Because sodium contributes to the cell’s tonicity,
hypernatremia denotes hypertonicity and at least transient cellular dehydration.
Some of the causes of hypernatremia are loss of free water, loss of hypotonic fluid,
or excessive sodium intake. Free water loss is uncommon, except in the presence of
diabetes insipidus. Diarrhea is the most common cause of hypotonic fluid loss in
infants and the elderly. Increased retention of sodium in patients with
hyperaldosteronism can also increase serum sodium concentrations. Excessive salt
intoxication is usually accidental or iatrogenic and most commonly results from
inappropriate intravenous administration of hypertonic salt solutions. Some β-lactam
antibiotics (e.g., ticarcillin) contain a modest sodium load and can cause fluid
overload when high dosages are administered.
The primary defense against hypertonicity is thirst and subsequent fluid intake.
Hypernatremic syndromes, therefore, usually occur in patients who are unable to
drink sufficient fluids. For example, demented elderly patients are at increased risk
because they depend on others for their water requirements. Similarly, patients who
are vomiting, comatose, or not allowed oral fluids are at risk for hypernatremia.
Reference Range: 3.5–5.0 mEq/L or mmol/L
Potassium is the most abundant intracellular cation in the body responsible for
regulating enzymatic function and neuromuscular tissue excitability. Approximately
90% of the total body potassium is found in the ICF, with the majority in muscle, and
only about 10% available in the ECF. The potassium ion in the ECF is filtered freely
at the glomerulus of the kidney, reabsorbed in the proximal tubule, and secreted into
the distal segments of the nephron. Because the majority of potassium is sequestered
within cells, a serum potassium concentration is not a good measure of total body
potassium. Intracellular potassium, however, cannot be measured easily. Fortunately,
the clinical manifestations of potassium deficiency (e.g., fatigue, drowsiness,
dizziness, confusion, electrocardiographic changes, muscle weakness, and muscle
pain) correlate well with serum concentrations. The serum potassium concentration
is buffered and can be within normal limits despite abnormalities in total body
potassium. During potassium depletion, potassium moves from the ICF into the ECF
to maintain the serum concentration. When the serum concentration decreases by a
mere 0.3 mEq/L, the total body potassium deficit is approximately 100 mEq. Serum
potassium concentrations, therefore, can be misleading when interpreted in isolation
from other considerations, and assumptions should not be made as to the status of
total body potassium concentration based solely on a serum concentration
measurement. Disorders of potassium are commonly the result of (1) alterations in
intake, (2) alterations with excretion, and/or (3) unbalanced transcellular shifting of
potassium (e.g., metabolic acidosis/alkalosis).
The kidneys are responsible for about 90% of daily potassium loss (~40–90
mEq/day), and the remaining 10% of potassium is excreted in the stool and a
negligible amount in sweat. The kidneys, however, have only a limited ability to
conserve potassium. Even when potassium intake has ceased, the urine will contain
at least 5 to 20 mEq of potassium per 24 hours. Therefore, prolonged intravenous
therapy with potassium-free solutions in a patient unable to obtain potassium in foods
(e.g., nothing by mouth) can result in hypokalemia. Hypokalemia can also be induced
by osmotic diuresis (e.g., mannitol and glucosuria), use of thiazide or loop diuretics
(e.g., hydrochlorothiazide, furosemide, respectively), excessive mineralocorticoid
activity, or protracted vomiting. Although the fluid secreted along most of the upper
gastrointestinal (GI) tract contains only a modest amount of potassium (i.e., 5–20
mEq/L), vomiting can induce hypokalemia because of the combined effect from
decreased food intake, loss of acid, alkalosis, and loss of sodium. The loss of large
amounts of colonic fluid through severe diarrhea and/or laxative abuse can cause
potassium depletion because fluid in the colon is high in potassium content (i.e., 30–
40 mEq/L). Insulin and stimulation of β2
-adrenergic receptors can also induce
hypokalemia because both increase the movement of potassium into cells from the
ECF. The magnitude of a potassium deficiency is difficult to establish because of the
limited presence of potassium in the ECF. Equation 2-1 can be used to estimate the
potassium deficit with hypokalemia:
It is also important to note that hypomagnesemia often accompanies hypokalemia,
because magnesium is necessary for the shifting of sodium, potassium, and calcium in
and out of cells. As a result, hypokalemic individuals not responding to potassium
therapy may be refractory to treatment until hypomagnesemia is corrected. Some
laboratories omit magnesium from the general electrolyte panel, so this test may need
Hyperkalemia most commonly results from decreased renal excretion of potassium
(e.g., renal failure, renal hypoperfusion, and hypoaldosteronism), excessive
exogenous potassium administration, or excessive cellular breakdown (e.g.,
hemolysis, burns, crush injuries, surgery, and infections). Drug-induced causes
include angiotensin converting enzyme inhibitors, angiotensin receptor blockers,
aldosterone antagonists, and nonsteroidal antiinflammatory drugs, to name a few.
Metabolic acidosis can also induce hyperkalemia because hydrogen ions move into
cells in exchange for potassium and sodium. Abnormal potassium concentrations in
the serum primarily affect excitability of nerve and muscle tissue (e.g., myocardial
tissue). As a result, arrhythmias can be induced by hyperkalemia or hypokalemia.
Potassium also affects some enzyme systems and acid–base balance, as well as
carbohydrate and protein metabolism.
Reference Range: 21–32 mEq/L or mmol/L
) content in the serum represents the sum of bicarbonate
) and dissolved CO2 concentrations. The dissolved CO2
relatively small component of total CO2 content, making CO2 essentially a measure of
the serum bicarbonate. Chloride and bicarbonate are the primary negatively charged
anions that offset the positively charged cations (i.e., sodium and potassium).
Although several buffer systems (e.g., hemoglobin [Hgb], phosphate, and protein)
participate in regulating pH within physiologic limits, the carbonic acid–bicarbonate
system is the most important. From a clinical standpoint, most disturbances of acid–
base balance result from imbalances of the carbonic acid–bicarbonate system. The
importance of bicarbonate in maintaining physiologic pH is presented in Chapter 26,
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