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Acid-base Balance and its Disorders. Prof. Dr. Meltem Pekpak. For optimal functioning of cells. Acids and bases in the body must be in balance. We all consume every day food and drinks which contain acids, metabolism produces also acids. Body pH Balance. Chemical blood buffers: Lungs,

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Acid base balance and its disorders

Acid-base Balance and its Disorders

Prof. Dr. Meltem Pekpak

For optimal functioning of cells
For optimal functioning of cells..

  • Acids and bases in the body must be in balance.

  • We all consume every day food and drinks which contain acids, metabolism produces also acids...

Body ph balance
Body pH Balance

  • Chemical blood buffers:

  • Lungs,

  • Cells,

  • Kidneys

  • Defences against changes in hydrogen concentration (getting acidotic..)

You get acidotic every day
You get acidotic every day !

  • While living, eating and drinking...there is..

  • Production of 1 mmol of fixed acid/kg body weight per day (60 kg=60 mmol/day)


  • Extracellular:

  • Hemoglobin

    • (‘Chloride shift’-for each chloride leaving the cell-one bicarbonate ion enters)

  • Plasma protein

    • (with the liver, varying the amount of H-ions in the protein structure)

  • Bicarbonate system:

    • Normal acid to base ratio is 20:1

    • 20 parts bicarbonate to 1 part carbonic acid (H2CO3=CO2),

    • Neutralizing a strong acid bicarb. will be lost

Human acid base homeostasis
Human Acid-baseHomeostasis

  • Tight regulation:

  • CO2 tension

    • by respiratory excretion (of volatile acids)

  • Plasma bicarbonate [HCO3-]

    • By renal HCO3- reabsorption and

    • Elimination of protons produced by metabolism

  • pH is determined by CO2 tension and [HCO3-]

Physiology of buffering
Physiology of Buffering:

  • Ability of a solution containing a weak or poorly dissociated acid and its anion (a base) to resist change in pH when strong acid or alkali is added

  • 1 ml of 0.1 M HCl to 9 ml distilled water =

  • [H+]from 10 -7 M to 10 -2 M= pH from 7 to 2

  • 1 ml of 0.1 M HCl to 9 ml of phosphate buffer: dissoc. H+combines with [HPO42-] = (H2PO4-)

  • pH fall of only 0.1= to 6.9

Bicarbonate buffer
Bicarbonate Buffer

  • Extracellular most important buffer

  • Proteins and phosphate buffer less important

  • Intracellularphosphate- most important b.

  • Equilibrium conditions because abundant carbonic anhydrase in blood

  • H+ + HCO3- H2CO3  H2O + CO2

  • [H+ ]= Keq x [H2CO3 ]/[HCO3-]


  • H+ + HCO3- H2CO3  H2O + CO2

  • Equilibrium

  • [H+ ]= Keq x [H2CO3 ]/[HCO3-]

Total acid base metabolism henderson hasselbalch 1909 1916
Total Acid- base Metabolism Henderson-Hasselbalch 1909,1916

Altered by


Primarily Altered

in Metabolic Disorders


  • pH = pK + log ------------


Metabolic comp.






Altered by Respiratory

Compensation for

Metabolic Disorders

Result of Metabolic

and Respiratory


Normal values
Normal Values

  • [HCO3-] ~ 24 mM

  • PaCO2 = 38 torr

  • pH ~ 7.42

  • Plasma HCO3- regulation by

    • reclaiming filtered HCO3- and

    • generating new HCO3- (carboanhydrase)

    • ( to replace the lost internally titrating metabolic acid and externally from the GI tract)

  • Production of 1 mmol of acid/kg body weight per day (60 kg=60 mmol/day)

Renal acid base handling
Renal Acid -base Handling

  • Two seperate functions:

  • Bicarbonate reabsorption

  • Net acid secretion

Proximal tubular bicarbonate reclamation process 90
Proximal Tubular BicarbonateReclamation Process (90 %)

Two vehicles for apical H+ secretion (Na+/H+ exchanger), H+ATPase.

Basolateral ion pumps: Na+/K+ ATPase, (Na+HCO3-)symporter,HCO3-/Cl-

Exchanger. The role of carbonic anhydrase (CA) in tubular cell and

brush border

Net acid excretion
Net Acid Excretion

  • Urine is acid = pH~ 4.5

  • Buffer salts are in the tubular fluid

  • Phosphate is the most important buffer in urine:

    HPO42- + H+ = H2PO4-

  • Nonvolatile (fixed) acids (anions= sulfates, phosphates) must be accompanied in the urine by equivalent cations (Na +, K +, Ca + +) for maintenance of electrical neutrality

  • In acid urine ammonium helps to keep

    [H+ ] (ammonia NH3+ to NH4+)

Clinical evaluation
Clinical Evaluation

  • Patient history

  • Clinical presentation

  • Acidemia Hyperventilation

  • Alkalemia Paresthesias and Tetany

  • Laboratory: Blood acid-base status:

  • Blood pH (4 º C, with anticoagulant, promptly),

  • Urine pH

  • Plasma and urine electrolyte concentration

  • Lactate concentration


  • Clinical effects of severe acidosis: pH <7.2

  • Cardiovascular system effects:

  • Decreased myocardial contractility

  • Decreased cardiac output

  • Cardiac failure

  • Hypotension

  • Decreased hepatic and renal blood flow

  • Centralization of effective blood volume

  • Tissue hypoxia

  • Pulmonary edema

Metabolic acidosis
Metabolic acidosis

  • Hallmark is [HCO3-]

  • 1. Acid production  net acid intake 

    above net renal excretion

    (ketoacidosis, lactic acidosis, ammonium chloride loading)

  • 2. failure of renal net excretion

    (chronic renal failure, renal tubular acidosis)

  • 3. Bicarbonate loss via the gastroinestinal tract (diarrhea, gastrointestinal fistula)

  • 4. Nonbicarbonate solutions added to ECF (dilutional acidosis)

Steps of evaluation
Steps of evaluation

  • 1.Examine pH= Reduction ( 7.2)  Acidosis

  • Increase (7.5) Alkalosis

  • 2. Examine directional change of PCO2

  • and [HCO3-] ,

  • pH acid, HCO3- low  Metabolic acidosis

  • pH alkal., HCO3- high  Metabolic alkalosis

  • 3. Assess degree of compensation: Mixed acid-base disorder?

  • Metabolic acidosis  PCO2 

  • Metabolic alkalosis  PCO2

  • Failure of respiratory compenstion= primary respiratory acid-base disorder

  • Never to initial pH through compensation !!

Steps of evaluation1
Steps of evaluation

  • 4. Calculate the serum anion gap

  • Is the acid-base disorder organic or mineral in origin??

  • We use venous sample blood electrolytes:

  • Electroneutrality demands:

  • Serum anion gap, that means:

  • [Na+] + [UC]= [Cl-] +[Total CO2] + [UA]

  • (U means: unmeasured)

Normally the serum anion gap is about 9 (6-12 mEq/l), a major increase in

Anion gap > 26 mEq/l always implies existence of an organic acidosis

Differential diagnosis of metabolic acidosis
Differential Diagnosis of Metabolic Acidosis major increase in

  • Normal anion gap Increased anion gap

  • (hyperchloemic) (organic)_________

  • GI loss ofHCO3- acid production

  • Diarrhea Lactic acidosis

  • Renal tub. Acidosis Diab. Ketoacidosis

  • Parenteral alimentation Toxic alcohol,salicy.

  • Carbonic anhydr. İnh. Acute renal failure

  • K-sparing diuretics Chronic renal failure

Increased anion gap metabolic acidosis
Increased anion gap major increase inMetabolic acidosis

  • Ketoacidosis (diabetic)

  • Uremia (renal failure)

  • Salicylate intoxication

  • Starvation

  • Methanol intoxication

  • Alcohol ketoacidosis

  • Unmeasured osmoles (intoxication)

  • Lactic acidosis

Simple decompensated acid base disorders
Simple decompensated major increase inAcid-base Disorders

  • Acid Base Dis.: pH pCO2 HCO3-

  • Metabolic acidosis   

  • Respiratory acidosis   

  • Metabolic alkalosis   

  • Respiratory alkalosis   

Compensatory response
Compensatory Response major increase in

one half of acid load is buffered by nonbicarbonate buffers= Bone, protein, red cells..

  • PCO2  (Kussmaul)

  • compensatory response after 15-30 minutes,

  • 5 days up to maximal

  • Kidney:

  • Metabolic acidosis

  •  processing of glutamine into NH4+ (ammonia to ammonium for better H-excretion)


  • Bicarbonate generation (and reclaiming)

Respiratory acidosis
Respiratory Acidosis major increase in

  • Acute increase in pCO2

  • Buffered primarily by intracellular buffers

  • Chronic state:

  • Kidneys compensation:

  • Increase net acid excretion,

  • (48 hours for fully development)

  • Underlying cause:

  • Central nervous system disease,

  • lung (COPD)and heart disease,

  • sedatives and opiates depressing the respiratory center

  • Hypercapnic encephalopathy can develop

Metabolic alkalosis
Metabolic Alkalosis major increase in

  • Plasma bicarbonate [HCO3-]  = pH 

  • 1) H+ GI loss or shift into cells

  • 2) Excess HCO3-

    Administration of  bicarbonate, or precursors:  lactate, acetate, citrate or

    Failure to excrete: mineralocorticoid effect

  • 3) Loss of fluid with

    Diuretic therapy

    [Cl-], [K+] and [H+] loss from plasma-

    extracellular volume contraction

Alkalosis major increase in

Volume depletion and metabolic alkalosis
Volume Depletion and Metabolic Alkalosis major increase in

  • Absolute volume depletion:

  • Loss of salt by bleeding or vomitting or

  • Effective volume depletion:

  • Heart failure, cirrhosis, nephrotic syndrome  whenever

  •   GFR

  •  Tubular HCO3- reabsorption

  • Because proximal tubule reabsorption is enhanced for

    Na and water

Compensatory respiratory response
Compensatory Respiratory Response major increase in

  • Alveolar hypoventilation(hypercapnia)

  • (limited pCO2riseto 50-60 mm Hg)

  • Kidneys:

  • Excretion of HCO3-proportional to GFR


Respiratory alkalosis
Respiratory Alkalosis major increase in

pCO2 , pH  due to:

Hypoxia (compensatory hyperventilation)

  • Acute: pulmonary edema or emboli, pneumonia,

  • Chronic: severe anemia, high altitude, hypotension

    Respiratory center stimulation

  • Pregnancy, Anxiety, Fever, heat stroke, sepsis, salisylate intox., cerebral disease, hepatic cirrhosis,

    Increased mechanical ventilation

Respiratory alkalosis1
Respiratory Alkalosis major increase in

  • Most common acid-base disorder

  • Physiologic in pregnancy and high altitude

  • Bad prognosisin critically ill patients

    (the higher hypocapnia, the higher mortality)

  • Hyperventilation,

  • Perioral and extremity paresthesias,

  • Light-headedness,

  • Muscle cramps,

  • Hyperreflexia, seizures,  ionized Ca  tetany

Metabolic alkalosis with and without volume depletion
Metabolic Alkalosis major increase inwith and without Volume Depletion

  • Volume depleted- Chloride responsive metabolic acidosis:

  • Urine chloride is low (<10 mmol/l)

  • Due to:

  • Gastric fluid losses

  • Stool losses

  • Diuretic therapy

Metabolic alkalosis excessive mineralocorticoids
Metabolic Alkalosis major increase inExcessive Mineralocorticoids

  • Mineralocorticoidsstimulatehydrogenionsecretion

  • And thisbicarbonate reabsorption

  • Urinary chloride is normal (<20 mmol/l)

  • Hypokalemia

  • Primary aldosteronizm,

  • Bartter’s Syndrome,

  • Cushing Syndrome

  • Renovascular hypertension

Proximal Tubular Bicarbonate Reclamation Process (90 %) major increase in

The proximal tubulus cells form carbonic acid from carbon dioxide and water

under the influence of the enzyme carboanhydrase (CA). Carbonic acid

ionizes to yield hydrogen and bicarbonate . Hydrogen formed in the cell

exchanges with sodium in the tubular fluid (dashed circle). As a net effect

Sodium bicarbonate is reabsorbed, and the hydrogen ion secreted into the

tubular lumen is buffered by filtered bicarbonate.

Henderson hasselbach 1909 1916
Henderson-Hasselbach major increase in1909,1916

  • H2CO3 = p CO2 +solubility in physiol. Fluids

  • [H+ ]= K x [S x pCO2 ]/[HCO3-]

    Antilog of both sides:

    pH= pK + log10 [HCO3-] / [S x PCO2]

    In blood at 37º C, pK =6.1 and S is 0.03

    pH= 6.1+ log10 [HCO3-] / [0.03 x PaCO2]