alkalosis

DEFINITION of alkalosis

Alkalosis is the overarching term for any pathological process that drives blood pH upward toward or beyond normal, with the resulting state of elevated arterial pH above 7.45 more precisely termed alkalemia (“alkaline blood”) — the same process-vs-state distinction that separates acidosis from acidemia. The two primary physiological mechanisms produce the major clinical divisions: metabolic alkalosis results from either a primary gain of bicarbonate (HCO₃⁻) or a primary loss of hydrogen ions (H⁺) from the body, most commonly through loss of hydrochloric acid (HCl) via vomiting or nasogastric suctioning, diuretic-induced chloride depletion (contraction alkalosis), or mineralocorticoid excess; it is characterized by elevated serum bicarbonate above 26 mEq/L and compensatory hypoventilation (CO₂ retention). Respiratory alkalosis results from primary alveolar hyperventilation causing excessive CO₂ elimination, driving PaCO₂ below 35 mmHg and pH upward; it is the most common acid-base disturbance in hospitalized patients, triggered by anxiety, pain, fever, sepsis, hypoxia, salicylate toxicity, or iatrogenic mechanical ventilator over-breathing. A critical clinical classification for metabolic alkalosis is the urine chloride test: chloride-responsive alkalosis (uCl < 25 mEq/L) indicates volume depletion driving renal bicarbonate retention — responds to normal saline and KCl replacement; chloride-resistant alkalosis (uCl > 40 mEq/L) indicates mineralocorticoid excess or severe hypokalemia — does not respond to saline and requires treatment of the underlying hormonal or electrolyte cause.

Clinical Indicators: In ICD-10-CM, E87.3 is the single billable code for all forms of alkalosis — metabolic, respiratory, and NOS are all captured under this one code, with NO subcategory expansion (unlike acidosis, which was expanded toE87.20/21/22 in FY2023). Coders must code the underlying cause as an additional diagnosis to fully reflect the clinical picture and support medical necessity. The note under E87.3 explicitly includes metabolic alkalosis, respiratory alkalosis, and alkalosis NOS — all route here.

ETYMOLOGY of alkalosis

arabic medieval-latin greek newlatin

Component Origin Meaning
alkali- Arabic al-qaliy → Medieval Latin alkali ”The ashes; burned ashes (of saltwort)” — from Arabic al (“the”) + qaliy (“plant ash, calcined ashes”), from qala (“to roast in a pan”); the saltwort plant (Salsola kali) was burned to produce soda ash, a highly alkaline substance used in soap and glassmaking since antiquity; the word entered Medieval Latin as alkali circa the late 14th century and later defined the modern chemistry concept of a base by Humphry Davy in 1813; appears in alkalosis, alkalemia, alkaline, alkylation
-osis Ancient Greek -ωσις (-ōsis) “Process, condition, abnormal or pathological state” — the highly productive Greek suffix indicating an ongoing pathological or physiological process; appears in alkalosis, acidosis, stenosis, fibrosis

Literally: “A condition of excess alkali/base” — a hybrid compound coined in New Latin circa 1900-1910, combining the Arabic-origin chemistry term alkali with the Greek pathological suffix -osis. Alkalosis and its counterpart acidosis were formalized as a paired clinical taxonomy at the dawn of twentieth-century biochemistry as blood pH measurement became possible. The antonym pair acidosis / alkalosis represents one of the rare Arabic-Latin-Greek hybrid compound constructions in medical terminology — alkali traveling through Arabic → Medieval Latin → modern chemistry → New Latin medical nomenclature before joining the Greek -osis suffix. The precursor term alkali itself is etymologically traceable to the saltwort plant burned by Arab chemists in medieval glassmaking, giving medicine a base-descriptor rooted in both botany and industrial chemistry.

Component	Origin	Meaning
alkali-	Arabic al-qaliy → Medieval Latin alkali	”The ashes; burned ashes (of saltwort)” — from Arabic al (“the”) + qaliy (“plant ash, calcined ashes”), from qala (“to roast in a pan”); the saltwort plant (Salsola kali) was burned to produce soda ash, a highly alkaline substance used in soap and glassmaking since antiquity; the word entered Medieval Latin as alkali circa the late 14th century and later defined the modern chemistry concept of a base by Humphry Davy in 1813; appears in alkalosis, alkalemia, alkaline, alkylation
-osis	Ancient Greek -ωσις (-ōsis)	“Process, condition, abnormal or pathological state” — the highly productive Greek suffix indicating an ongoing pathological or physiological process; appears in alkalosis, acidosis, stenosis, fibrosis

🔀 ALIASES / ALTERNATE TERMS

Term Context
Alkalemia The technically precise term for the state of elevated blood pH (arterial pH > 7.45); alkalosis is the process generating excess base, alkalemia is the result in the blood; ICD-10-CM uses “alkalosis” as the coded entity but both map to E87.3.
Metabolic alkalosis The subtype driven by bicarbonate excess or hydrogen ion loss; explicitly included under E87.3; the most clinically common subtype in hospitalized patients (diuretics, vomiting, NG suction).
Respiratory alkalosis The subtype driven by hypocapnia from hyperventilation; also included under E87.3; the most common acid-base disorder in hospitalized patients overall.
Contraction alkalosis A specific subtype of metabolic alkalosis caused by ECF volume contraction around a fixed bicarbonate pool, concentrating the bicarbonate — classically from over-diuresis or NG suctioning with inadequate saline replacement.
Hypochloremic alkalosis A metabolic alkalosis characterized by low serum chloride — from vomiting, NG suction, or diuretics losing HCl — maintaining the alkalosis through chloride depletion; indexes to E87.3 with E87.8 (hypochloremia) as additional code when documented.
Hypokalemic alkalosis Metabolic alkalosis driven by or maintaining severe potassium depletion — hypokalemia causes H⁺ to move intracellularly to compensate for K⁺ loss, generating alkalosis; code E87.3 + E87.6 (hypokalemia).

Term	Context
Alkalemia	The technically precise term for the state of elevated blood pH (arterial pH > 7.45); alkalosis is the process generating excess base, alkalemia is the result in the blood; ICD-10-CM uses “alkalosis” as the coded entity but both map to E87.3.
Metabolic alkalosis	The subtype driven by bicarbonate excess or hydrogen ion loss; explicitly included under E87.3; the most clinically common subtype in hospitalized patients (diuretics, vomiting, NG suction).
Respiratory alkalosis	The subtype driven by hypocapnia from hyperventilation; also included under E87.3; the most common acid-base disorder in hospitalized patients overall.
Contraction alkalosis	A specific subtype of metabolic alkalosis caused by ECF volume contraction around a fixed bicarbonate pool, concentrating the bicarbonate — classically from over-diuresis or NG suctioning with inadequate saline replacement.
Hypochloremic alkalosis	A metabolic alkalosis characterized by low serum chloride — from vomiting, NG suction, or diuretics losing HCl — maintaining the alkalosis through chloride depletion; indexes to E87.3 with E87.8 (hypochloremia) as additional code when documented.
Hypokalemic alkalosis	Metabolic alkalosis driven by or maintaining severe potassium depletion — hypokalemia causes H⁺ to move intracellularly to compensate for K⁺ loss, generating alkalosis; code E87.3 + E87.6 (hypokalemia).

🔗 RELATED TERMS

acidosis — E87.2 / E87.20 / E87.21 / E87.22 / E87.29; the opposing acid-base disorder driving pH below 7.35 via acid accumulation or base loss; frequently coexists with alkalosis in mixed disorders.

Mixed disorder of acid-base balance — E87.4; simultaneous acidotic and alkalotic processes (e.g., metabolic alkalosis from diuretics + respiratory alkalosis from sepsis-driven hyperventilation); physician must explicitly document the mixed disorder — never infer from ABG values alone without physician attestation.

hypokalemia — E87.6; profoundly interconnected with metabolic alkalosis — hypokalemia drives renal H⁺ loss to spare K⁺, perpetuating alkalosis; and alkalosis itself shifts K⁺ intracellularly, worsening hypokalemia; always code separately as an additional diagnosis when documented.

Hypochloremia — E87.8 (other disorders of electrolyte and fluid balance, NEC); chloride depletion from vomiting, NG suctioning, or loop/thiazide diuretics is the central maintenance factor in chloride-responsive metabolic alkalosis; code additionally when documented.

Hyperaldosteronism — E26.01 (Conn’s syndrome, primary) / E26.09 (other primary) / E26.1 (secondary); excess aldosterone drives renal H⁺ and K⁺ secretion, producing chloride-resistant metabolic alkalosis with hypertension and hypokalemia; must be coded as the primary etiology when documented.

Bartter syndrome — E26.81; a rare hereditary renal tubular disorder of chloride reabsorption failure in the loop of Henle producing severe hypokalemic metabolic alkalosis, hyperreninemia, and hyperaldosteronism without hypertension; must be specifically documented by the physician.

Acute respiratory failure — J96.01 (with hypoxia) / J96.02 (with hypercapnia); respiratory alkalosis from hypoxia-driven hyperventilation is a common early finding in ARDS, pulmonary embolism, and pneumonia — code the underlying respiratory failure as primary, with E87.3 additionally when documented.

Nausea with vomiting — R11.2; prolonged vomiting is among the most common precipitants of metabolic alkalosis in both inpatient and outpatient settings; code additionally as the clinical trigger when documented.

CODING CORNER

🏥 ICD-10-CM CODES

Primary Diagnosis — Alkalosis (E87.3)

⚠️ ICD-10-CM / Chapter Nuances: E87.3 is the single billable code for ALL forms of alkalosis — metabolic, respiratory, hypochloremic, hypokalemic, contraction, and NOS are all captured here with NO further subcategory expansion (unlike acidosis which was expanded in FY2023). This is a critical distinction — do NOT create a non-existent E87.30/E87.31/E87.32 structure. Sequencing depends on the clinical scenario: if alkalosis is the primary reason for the encounter, E87.3 leads; if a primary condition (e.g., hyperaldosteronism, respiratory failure, vomiting) generated the alkalosis as a manifestation, the primary condition should lead and E87.3 follows. Always code the underlying cause as an additional diagnosis. The Excludes1 note under E87 (parent category) excludes electrolyte imbalance in hyperemesis gravidarum (O21.1) — do NOT use E87.3 for alkalosis in the context of severe pregnancy vomiting; O21.1 captures it.

Code Description
E87.3 Alkalosis (The single, definitive, fully billable code for all forms of alkalosis — metabolic, respiratory, NOS; no subcategories exist; always add underlying cause as additional code)
E87.4 Mixed disorder of acid-base balance (Use when physician explicitly documents a mixed disorder; requires co-existing acidotic and alkalotic processes with physician documentation — never infer from lab values alone)

Commonly Associated / Co-Diagnosis Codes (Code Additionally)

Code Description
E87.6 Hypokalemia (Code additionally when hypokalemia co-exists with or perpetuates alkalosis — one of the most critical co-codes; alkalosis and hypokalemia are interdependent and both must be coded when documented)
E87.8 Other disorders of electrolyte and fluid balance, not elsewhere classified (Code additionally for hypochloremia when explicitly documented as a co-existing finding in metabolic alkalosis from vomiting or NG suctioning)
E87.1 Hypo-osmolality and hyponatremia (Code additionally when hyponatremia accompanies the alkalosis, as seen in severe volume-depleted contraction alkalosis)
E26.01 Primary hyperaldosteronism due to adenoma (Conn’s syndrome; code as primary etiology for chloride-resistant metabolic alkalosis with hypertension and hypokalemia)
E26.09 Other primary hyperaldosteronism (Bilateral adrenal hyperplasia or other non-adenoma primary hyperaldosteronism causing chloride-resistant metabolic alkalosis)
E26.1 Secondary hyperaldosteronism (Renal artery stenosis or other secondary aldosterone excess driving chloride-resistant alkalosis)
E26.81 Bartter’s syndrome (Hereditary renal tubular chloride-wasting disorder producing severe hypokalemic metabolic alkalosis without hypertension — must be physician-documented)
R11.2 Nausea with vomiting, unspecified (Code additionally when protracted vomiting is the documented precipitant of metabolic alkalosis)
J96.01 Acute respiratory failure with hypoxia (Primary code when respiratory alkalosis develops secondary to hypoxia-driven hyperventilation in acute respiratory failure)
F41.0 Panic disorder without agoraphobia (Code when anxiety/panic attack is the documented driver of hyperventilation-induced respiratory alkalosis)
T50.901A Poisoning by unspecified drugs, initial encounter (When salicylate toxicity or other drug-induced hyperventilation causes respiratory alkalosis — use appropriate T-code for the specific agent when identified)
O21.1 Hyperemesis gravidarum with metabolic disturbance (⚠️ Excludes1 note: alkalosis in hyperemesis gravidarum codes exclusively to O21.1 — do NOT additionally report E87.3 in this context)

🔧 COMMON CPT CODES (Evaluation & Laboratory Diagnostics)

Arterial Blood Gas (ABG) — Primary Diagnostic Tool

⚠️ CPT Nuance: 82803 and 82805 are mutually exclusive — never report both for the same specimen. 82805 (includes measured co-oximetry O₂ saturation) is reported instead of 82803, not in addition to it. For serial ABGs monitoring alkalosis treatment response, append modifier -91 to each repeat same-day draw. Do NOT separately bill individual gas components (pH, CO₂, O₂) when the panel code covers them.

CPT Code Description
82803 Gases, blood, any combination of pH, pCO₂, pO₂, CO₂, HCO₃ (including calculated O₂ saturation) (The core ABG code; report ONCE per arterial specimen regardless of how many parameters are measured; critical for alkalosis diagnosis — confirms elevated pH, low pCO₂ in respiratory alkalosis or elevated HCO₃ in metabolic alkalosis)
82805 Gases, blood, any combination of pH, pCO₂, pO₂, CO₂, HCO₃ (including calculated O₂ saturation); with O₂ saturation by co-oximetry, when performed (Report in place of 82803 — NOT in addition — when measured O₂ saturation via co-oximetry is included in the same specimen)
82374 Carbon dioxide (bicarbonate) (Serum CO₂/bicarbonate; report separately when a standalone venous bicarbonate is drawn to monitor metabolic alkalosis or to document elevated HCO₃ for coding support — do NOT separately report if a BMP/CMP was already billed that includes CO₂)
82435 Chloride; blood (Serum chloride critical for alkalosis workup — hypochloremia confirms chloride-responsive alkalosis; also used in anion gap calculation for co-existing metabolic acidosis evaluation)
84295 Sodium (Serum sodium; required for anion gap calculation and assessment of volume status in contraction alkalosis)
84132 Potassium; serum, plasma or whole blood (Serum potassium; essential in every alkalosis workup — hypokalemia perpetuates metabolic alkalosis and must be identified for targeted treatment)
80048 Basic metabolic panel (Calcium, total) (Includes CO₂/bicarbonate, sodium, potassium, chloride, BUN, creatinine, glucose — the most commonly ordered panel in alkalosis evaluation; if BMP is billed, do NOT separately report the individual component codes 82374, 82435, 84295, 84132 included within it)
83735 Magnesium (Report separately when hypomagnesemia is evaluated as a co-contributor to refractory alkalosis — magnesium depletion impairs potassium repletion and perpetuates both hypokalemia and alkalosis)

Urine Studies

CPT Code Description
82435 Chloride; urine (Urine chloride — the critical differentiating test between chloride-responsive [uCl < 25 mEq/L] and chloride-resistant [uCl > 40 mEq/L] metabolic alkalosis; report with -QW modifier if performed on a waived analyzer; bill the urine specimen separately from the serum specimen)

Treatment-Related CPT Codes

CPT Code Description
96365 Intravenous infusion, for therapy, prophylaxis, or diagnosis; initial, up to 1 hour (Report for IV normal saline (0.9% NaCl) infusion in chloride-responsive metabolic alkalosis — volume and chloride replacement is the primary treatment; also report for IV potassium chloride (KCl) infusion when IV route is required for hypokalemia treatment)
96366 +Intravenous infusion, each additional hour (Add-on; report for each additional hour of IV saline or IV potassium infusion beyond the first hour; list separately in addition to 96365; never alone)
96374 Therapeutic, prophylactic, or diagnostic injection (specify substance or drug); intravenous push, single or initial substance/drug (Report for IV push potassium chloride bolus or acetazolamide administration for severe metabolic alkalosis resistant to conventional therapy)
94002 Ventilation assist and management, initiation of pressure or volume preset ventilators for assisted or controlled breathing; hospital inpatient/observation, initial day (Report when mechanical ventilator rate is adjusted to manage iatrogenic hyperventilation-induced respiratory alkalosis in an intubated patient — requires documentation of ventilator setting changes targeting PaCO₂ normalization)
94003 …each subsequent inpatient/observation day (Report for each subsequent day of active ventilator management; requires daily documentation of respiratory alkalosis management in ventilator-dependent patients)

Modifiers Commonly Used

Modifier Usage
-91 Repeat clinical diagnostic laboratory test — Append to 82803 or 82805 when the same ABG is repeated on the same calendar day for serial monitoring of alkalosis treatment response (do NOT use -91 for equipment repeat/malfunction — use -QW or rerun under appropriate modifier in waived testing context)
-59 Distinct procedural service — Append to a separately identifiable laboratory code (e.g., urine 82435 for chloride) when it could be bundled with serum 82435 billed on the same date; distinguishes the separate clinical rationale for urine vs. serum chloride measurement
-25 Significant, separately identifiable E/M service — Append to 99213 / 99214 / 99223 when the physician performs a significant, separately documented E/M on the same day as a procedure such as IV infusion initiation (96365) or ventilator management (94002)
-QW CLIA waived test — Append when point-of-care electrolyte or basic metabolic testing is performed on a CLIA-waived analyzer at the bedside in the context of alkalosis monitoring; verify specific payer QW policies

⚠️ Coding Note: The single most important compliance fact in alkalosis coding is that E87.3 has NO subcategories — unlike acidosis which was expanded in FY2023, alkalosis remains a single undivided billable code. Attempting to report E87.30 (metabolic), E87.31 (respiratory), or any other sub-digit simply does not exist in ICD-10-CM and will result in an unrecognized code rejection. The second most critical rule is the O21.1 Excludes1 boundary — alkalosis in the context of hyperemesis gravidarum in a pregnant patient codes exclusively to O21.1; appending E87.3 alongside O21.1 is a direct Excludes1 violation. For chloride-resistant metabolic alkalosis, always query the physician for documentation of the underlying mineralocorticoid driver (primary or secondary hyperaldosteronism, Bartter syndrome, Cushing’s) — those diagnoses dramatically affect risk adjustment, DRG assignment, and medical necessity for workup procedures. When billing serial ABGs for alkalosis monitoring in the ICU, modifier -91 is mandatory for every repeat same-day draw — billing multiple units of 82803 without -91 will be denied as duplicate claims. For BMP vs. individual component billing: if 80048 is billed, do NOT additionally bill 82374, 82435, 84295, or 84132 for the same blood draw — those components are bundled into the panel and separate billing constitutes unbundling.

Code	Description
E87.3	Alkalosis (The single, definitive, fully billable code for all forms of alkalosis — metabolic, respiratory, NOS; no subcategories exist; always add underlying cause as additional code)
E87.4	Mixed disorder of acid-base balance (Use when physician explicitly documents a mixed disorder; requires co-existing acidotic and alkalotic processes with physician documentation — never infer from lab values alone)

Code	Description
E87.6	Hypokalemia (Code additionally when hypokalemia co-exists with or perpetuates alkalosis — one of the most critical co-codes; alkalosis and hypokalemia are interdependent and both must be coded when documented)
E87.8	Other disorders of electrolyte and fluid balance, not elsewhere classified (Code additionally for hypochloremia when explicitly documented as a co-existing finding in metabolic alkalosis from vomiting or NG suctioning)
E87.1	Hypo-osmolality and hyponatremia (Code additionally when hyponatremia accompanies the alkalosis, as seen in severe volume-depleted contraction alkalosis)
E26.01	Primary hyperaldosteronism due to adenoma (Conn’s syndrome; code as primary etiology for chloride-resistant metabolic alkalosis with hypertension and hypokalemia)
E26.09	Other primary hyperaldosteronism (Bilateral adrenal hyperplasia or other non-adenoma primary hyperaldosteronism causing chloride-resistant metabolic alkalosis)
E26.1	Secondary hyperaldosteronism (Renal artery stenosis or other secondary aldosterone excess driving chloride-resistant alkalosis)
E26.81	Bartter’s syndrome (Hereditary renal tubular chloride-wasting disorder producing severe hypokalemic metabolic alkalosis without hypertension — must be physician-documented)
R11.2	Nausea with vomiting, unspecified (Code additionally when protracted vomiting is the documented precipitant of metabolic alkalosis)
J96.01	Acute respiratory failure with hypoxia (Primary code when respiratory alkalosis develops secondary to hypoxia-driven hyperventilation in acute respiratory failure)
F41.0	Panic disorder without agoraphobia (Code when anxiety/panic attack is the documented driver of hyperventilation-induced respiratory alkalosis)
T50.901A	Poisoning by unspecified drugs, initial encounter (When salicylate toxicity or other drug-induced hyperventilation causes respiratory alkalosis — use appropriate T-code for the specific agent when identified)
O21.1	Hyperemesis gravidarum with metabolic disturbance (⚠️ Excludes1 note: alkalosis in hyperemesis gravidarum codes exclusively to O21.1 — do NOT additionally report E87.3 in this context)

CPT Code	Description
82803	Gases, blood, any combination of pH, pCO₂, pO₂, CO₂, HCO₃ (including calculated O₂ saturation) (The core ABG code; report ONCE per arterial specimen regardless of how many parameters are measured; critical for alkalosis diagnosis — confirms elevated pH, low pCO₂ in respiratory alkalosis or elevated HCO₃ in metabolic alkalosis)
82805	Gases, blood, any combination of pH, pCO₂, pO₂, CO₂, HCO₃ (including calculated O₂ saturation); with O₂ saturation by co-oximetry, when performed (Report in place of 82803* — NOT in addition — when measured O₂ saturation via co-oximetry is included in the same specimen)*
82374	Carbon dioxide (bicarbonate) (Serum CO₂/bicarbonate; report separately when a standalone venous bicarbonate is drawn to monitor metabolic alkalosis or to document elevated HCO₃ for coding support — do NOT separately report if a BMP/CMP was already billed that includes CO₂)
82435	Chloride; blood (Serum chloride critical for alkalosis workup — hypochloremia confirms chloride-responsive alkalosis; also used in anion gap calculation for co-existing metabolic acidosis evaluation)
84295	Sodium (Serum sodium; required for anion gap calculation and assessment of volume status in contraction alkalosis)
84132	Potassium; serum, plasma or whole blood (Serum potassium; essential in every alkalosis workup — hypokalemia perpetuates metabolic alkalosis and must be identified for targeted treatment)
80048	Basic metabolic panel (Calcium, total) (Includes CO₂/bicarbonate, sodium, potassium, chloride, BUN, creatinine, glucose — the most commonly ordered panel in alkalosis evaluation; if BMP is billed, do NOT separately report the individual component codes 82374, 82435, 84295, 84132 included within it)
83735	Magnesium (Report separately when hypomagnesemia is evaluated as a co-contributor to refractory alkalosis — magnesium depletion impairs potassium repletion and perpetuates both hypokalemia and alkalosis)

CPT Code	Description
82435	Chloride; urine (Urine chloride — the critical differentiating test between chloride-responsive [uCl < 25 mEq/L] and chloride-resistant [uCl > 40 mEq/L] metabolic alkalosis; report with -QW modifier if performed on a waived analyzer; bill the urine specimen separately from the serum specimen)

CPT Code	Description
96365	Intravenous infusion, for therapy, prophylaxis, or diagnosis; initial, up to 1 hour (Report for IV normal saline (0.9% NaCl) infusion in chloride-responsive metabolic alkalosis — volume and chloride replacement is the primary treatment; also report for IV potassium chloride (KCl) infusion when IV route is required for hypokalemia treatment)
96366	+Intravenous infusion, each additional hour (Add-on; report for each additional hour of IV saline or IV potassium infusion beyond the first hour; list separately in addition to 96365; never alone)
96374	Therapeutic, prophylactic, or diagnostic injection (specify substance or drug); intravenous push, single or initial substance/drug (Report for IV push potassium chloride bolus or acetazolamide administration for severe metabolic alkalosis resistant to conventional therapy)
94002	Ventilation assist and management, initiation of pressure or volume preset ventilators for assisted or controlled breathing; hospital inpatient/observation, initial day (Report when mechanical ventilator rate is adjusted to manage iatrogenic hyperventilation-induced respiratory alkalosis in an intubated patient — requires documentation of ventilator setting changes targeting PaCO₂ normalization)
94003	…each subsequent inpatient/observation day (Report for each subsequent day of active ventilator management; requires daily documentation of respiratory alkalosis management in ventilator-dependent patients)

Modifier	Usage
-91	Repeat clinical diagnostic laboratory test — Append to 82803 or 82805 when the same ABG is repeated on the same calendar day for serial monitoring of alkalosis treatment response (do NOT use -91 for equipment repeat/malfunction — use -QW or rerun under appropriate modifier in waived testing context)
-59	Distinct procedural service — Append to a separately identifiable laboratory code (e.g., urine 82435 for chloride) when it could be bundled with serum 82435 billed on the same date; distinguishes the separate clinical rationale for urine vs. serum chloride measurement
-25	Significant, separately identifiable E/M service — Append to 99213 / 99214 / 99223 when the physician performs a significant, separately documented E/M on the same day as a procedure such as IV infusion initiation (96365) or ventilator management (94002)
-QW	CLIA waived test — Append when point-of-care electrolyte or basic metabolic testing is performed on a CLIA-waived analyzer at the bedside in the context of alkalosis monitoring; verify specific payer QW policies

A Word from MedlinePlus

Alkalosis is a condition in which the body fluids have excess base (alkali). This is the opposite of excess acid (acidosis).

Causes

The kidneys and lungs maintain the proper balance (proper pH level) of chemicals called acids and bases in the body. Decreased carbon dioxide (an acid) level or increased bicarbonate (a base) level makes the body too alkaline, a condition called alkalosis. There are different types of alkalosis. These are described below.

Respiratory alkalosis means too much carbon dioxide is breathed causing a low carbon dioxide level in the blood. This can be due to:

Fever

Being at a high altitude

Hyperventilation

Lack of oxygen

Liver disease

Lung disease, which causes you to breathe faster (hyperventilate)

Aspirin poisoning

Metabolic alkalosis means there is too much bicarbonate in the blood. It can occur due to certain kidney diseases. Two forms of metabolic alkalosis are:

Hypochloremic alkalosis — It is caused by an extreme lack or loss of chloride, such as from prolonged vomiting.

Hypokalemic alkalosis — It may also be caused by the kidneys’ response to an extreme lack or loss of potassium. This can occur from taking certain water pills (diuretics).

Compensated alkalosis occurs when the body returns the acid-base balance and blood pH to near normal in cases of alkalosis, but bicarbonate and carbon dioxide levels remain abnormal.

Exams and Tests

Your health care provider will perform a physical exam and ask about your symptoms.

Lab tests that may be ordered include:

Arterial or venous blood gas analysis.

Basic metabolic panel (group of blood tests that measure sodium and potassium levels, kidney function, and other chemicals and functions) to show whether the type of alkalosis is metabolic or respiratory.

Other blood tests may be needed to determine the cause of the alkalosis.

Other tests may be needed to determine the cause of the alkalosis. These may include:

Chest x-ray

Urinalysis

Urine pH

Treatment

To treat alkalosis, your provider needs to first find the underlying cause.

For alkalosis caused by hyperventilation, breathing into a paper bag allows you to keep more carbon dioxide in your body, which improves the alkalosis. If your oxygen level is low, you may receive oxygen.

Medicines may be needed to correct chemical loss (such as chloride and potassium). Your provider will monitor your vital signs (temperature, pulse, rate of breathing, and blood pressure).

Outlook (Prognosis)

Most cases of alkalosis respond well to treatment.

When to Contact a Medical Professional

Contact your provider if you become confused, unable to concentrate, or unable to “catch your breath.”

Go to the emergency room or call 911 or the local emergency number if there is:

Loss of consciousness

Rapidly worsening symptoms of alkalosis

Seizures

Severe breathing difficulties

Prevention

Prevention depends on the cause of the alkalosis. People with healthy kidneys and lungs do not usually have serious alkalosis.

Alternative Names

Metabolic alkalosis; Respiratory alkalosis

Images

Kidneys

References

Kliegman RM, St. Geme JW, Blum NJ, et al. Electrolyte and acid-base disorders. In: Kliegman RM, St. Geme JW, Blum NJ, et al, eds. Nelson Textbook of Pediatrics. 22nd ed. Philadelphia, PA: Elsevier; 2025:chap 73.

Oh MS, Briefel G, Pincus MR. Evaluation of renal function, water, electrolytes, and acid-base balance. In: McPherson RA, Pincus MR, eds. Henry’s Clinical Diagnosis and Management by Laboratory Methods. 24th ed. Philadelphia, PA: Elsevier; 2022:chap 15.

Sanghavi S, Albert TJ, Swenson ER. Acid-base balance. In: Broaddus VC, Ernst JD, King TE, et al, eds. Murray and Nadel’s Textbook of Respiratory Medicine. 7th ed. Philadelphia, PA: Elsevier; 2022:chap 12.

Seifter JL. Acid-base disorders. In: Goldman L, Cooney KA, eds. Goldman-Cecil Medicine. 27th ed. Philadelphia, PA: Elsevier; 2024:chap 104.

Review Date 11/6/2025

Updated by: Jacob Berman, MD, MPH, Associate Professor of Medicine, Division of General Internal Medicine, University of Washington School of Medicine, Seattle, WA. Also reviewed by David C. Dugdale, MD, Medical Director, Brenda Conaway, Editorial Director, and the A.D.A.M. Editorial team.

DERIVATIONS of alkalosis

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Med roots Appendix A Prefixes Appendix B Combining Forms Appendix C Suffixes Appendix D Suffix forms

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alkalosis

🏥 ICD-10-CM CODES

Primary Diagnosis — Alkalosis (E87.3)

Commonly Associated / Co-Diagnosis Codes (Code Additionally)

🔧 COMMON CPT CODES (Evaluation & Laboratory Diagnostics)

Arterial Blood Gas (ABG) — Primary Diagnostic Tool

Urine Studies

Treatment-Related CPT Codes

Modifiers Commonly Used

Causes

Exams and Tests

Treatment

Outlook (Prognosis)

When to Contact a Medical Professional

Prevention

Alternative Names

Images

References

Review Date 11/6/2025

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