Acid-Base Balance

Zehra Eren,M.D.

LEARNİNG OBJECTİVES•explain normal acid-base balance•explain buffers systems in regulation of pH•explain compensatory response to acid-base

disorders• recognize metabolic acidosis• recognize metabolic alkalosis• recognize respiratory acidosis and alkalosis

Normal Acid-Base Balance

•Daily net acid production: 1mEq hydrogen ions(H+) per kilogram

•H+: 0.0004 mEq/L (40nmol/L)= pH: 7.40

•Arterial pH:7.35-7.45• İntracellular pH:7.0-7.3

Buffer Systems in Regulation of pH

•Extracellular fluid:- bicarbonate ion (HCO3

-) /carbonic acid

H++HCO3-⇔H2CO3 H2O + CO2

- plasma proteins- phosphate ions- Ca2+ and HCO3

- release of bone

carbonic

anhydrase

Buffer Systems in Regulation of pH

• İntracellular fluid- hemoglobin- cellular proteins- organophosphate complexes- HCO3

- by the H+/ HCO3- transport

mechanism

Henderson-Hasselbach Equation

•pH=6.1+log

pH 7.00 7.40 7.70[H+]nmol/L 100 40 20

[HCO3- ] (mEq/L)

0.03XpCO2 (mm Hg)

Normal Levels•pH: 7.35-7.45

•pCO2: 37-45 mmHg

•HCO3- : 22-26 mEq/L

pH•Acidosis <7.35-7.45> Alkalosis

•HCO3- ↑↓ → Metabolic

•CO2 ↑↓ → Respiratory

Compensatory response to acid-base disorders

•Metabolic Acidosis/Alkalosis→reducing / increasing CO2

•Respiratory Acidosis/Alkalosis→renal secretion / reabsorption of HCO3

-/H+

Metabolic Acidosis

•Fall in HCO3- concentration witt fall in pH

•Compensatory response: fall in pH causes inreased respiration, reducing CO2

• 1.2 mmHg fall in arterial PCO2 for every 1 meq/L reduction in

the serum HCO3 concentration

Causes of Metabolic Acidosis

• İncreases acid load (H+)•HCO3

- loses- extrarenal: gastrointestinal- renal

• Decreased renal acid excretion

Serum Anion Gap

[Na+] - ([Cl-]+[HCO3- ])

9 ± 3 mEq/L (mmol/L)

Serum Anion Gap•Serum AG= Measured cations –

Measured anions

•Serum AG= Na - (Cl+HCO3)

•Serum AG= Unmeasured anions – Unmeasured cations

HIGH SERUM ANION GAP • increase in unmeasured anions

metabolic acidosis, hyperalbuminemia, hyperphosphatemia, or overproduction of an anionic paraprotein

•reduction in unmeasured cationshypokalemia, hypocalcemia, hypomagnesemia

LOW SERUM ANION GAP •Decrease in unmeasured anions

primarily due to hypoalbuminemia• Increase in unmeasured cations

hyperkalemia, hypercalcemia, hypermagnesemia, or severe litium intoxication

•Bromide ingestion•serum protein electrophoresis should be

obtained to look for a cationic paraprotein that is present in some patients with multiple myeloma

Urinary Anion Gap

UAG=( UNa + UK) – UCl

(-20) — (-50) mEq/L (NH4 +)

Metabolic Alkalosis

•Rise in HCO3- concentration with rise in pH

•Compensatory response:rise in pH causes decreased respiration, increasing CO2

• raise the PCO2 by 0.7 mmHg for every 1 meq/L elevation in the serum HCO3 concentration

GASTROINTESTINAL HYDROGEN LOSS

• Each meq of hydrogen lost generates one meq of bicarbonate: the hydrogen ion is derived from water, while the associated hydroxyl ion combines with carbon dioxide to form bicarbonate

Development and maintenance of metabolic alkalosis

•An elevation in the plasma bicarbonate concentration due to hydrogen loss in the urine or gastrointestinal tract, hydrogen movement into the cells, the administration of bicarbonate, or volume contraction around a relatively constant amount of extracellular bicarbonate (called a contraction alkalosis)

•A decrease in net renal bicarbonate excretion (due both to enhanced reabsorption and reduced secretion), since rapid excretion of the excess bicarbonate would normally correct the alkalosis

Factors responsible for the rise in net bicarbonate reabsorption •Effective circulating volume depletion,

including reduced tissue perfusion in edematous states such as congestive heart failure and cirrhosis

•Chloride depletion and hypochloremia

•Hypokalemia

EFFECTIVE VOLUME DEPLETION• Aldosterone directly enhances acidification by increasing the

activity of the H-ATPase pumps in the luminal membrane of the intercalated cells. This pump promotes the secretion of hydrogen ions into the tubular lumen, thereby increasing the reabsorption of bicarbonate.

• Aldosterone-stimulated sodium reabsorption in the adjacent principal cells makes the lumen electronegative due to the loss of cationic sodium. This potential minimizes the passive back-diffusion of hydrogen ions out of the lumen, allowing the urine to become much more acid than the plasma.

• Decreased chloride delivery diminishes bicarbonate secretion in the type B intercalated cells, which is thought to be an important component of the normal renal response to a bicarbonate load.

CHLORIDE DEPLETION•Vomiting •Diuretic therapy ->hydrogen and chloride loss•The hypochloremia can contribute to the

reduction in bicarbonate excretion by increasing distal reabsorption and reducing distal secretion; this effect of chloride may be more important than the associated volume depletion

HYPOKALEMIA•Hypokalemia directly increases

bicarbonate reabsorption

Respiratory Acidosis•Rise in CO- concentration with fall in pH

•Compensatory response:fall in pH causes increased renal H+ secretion, raising HCO3

- concentration

Causes of Respiratory Acidosis

• İnhibition of respiratory drive-opiates-anesthetics-sedatives-central sleep apnea-obesity-central nervous system lesions

Causes of Respiratory Acidosis 2•Disorders of respiratory muscles

1.Muscle weakness;-myastenia gaves-periodic paralysis-aminoglycosides-Guillan-Barre syndrom-spinal cord injury-acute lateral sclerosis-multiple sclersis

2.Kyphoscoliosis

Causes of Respiratory Acidosis 3•Upper airway obstruction

-obstructive sleep apnea-laryngospasm-aspiration

•Lung diseases -pneumonia -severe asthma -pneumothorax -acute respiratory disress syndrom -chronic obsructive pulnmonery disease -interstitial lung disease

Respiratory Alkalosis•Fall in CO- concentration with rise in pH

•Compensatory response:rise in pH causes diminished renal H+ secretion, lowering HCO3

- concentration

Causes of Respiratory Alkalosis•Hypoxemia

1.Pulmonary disease-pneumonia-interstitial fibrosis-emboli-edema

2.Congestive heart failure3.Anemia

Causes of Respiratory Alkalosis 2•Stimulation of the medullary respiratory

center-hyperventilation-hepatic failure-septicemia-salycilate intoxication-pregnancy-neurologic disordrs

•Mechanical ventilation

Suggested Reading•Goldman's Cecile Medicine, Goldman L, Schafer AI

•Case files Internal Medicine, Toy Patlan

•Current Medical Diagnosis and Treatment, Maxine A. Papadakis, Stephen J. McPhee, Eds. Michael W. Rabow, Associate Ed.

•Current Diagnosis & Treatment: Nephrology & Hypertension Edgar V. Lerma, Jeffrey S. Berns, Allen R. Nissenson