Acid base balance and its disorders
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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

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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)


Buffers

Buffers

  • 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-]


Equations

Equations

  • 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

Buffering

Primarily Altered

in Metabolic Disorders

HCO3-

  • pH = pK + log ------------

    PaCO2

Metabolic comp.

Respiratory

component

Primary

Respiratory

Disorders

Altered by Respiratory

Compensation for

Metabolic Disorders

Result of Metabolic

and Respiratory

Interplay


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


Acidosis

Acidosis

  • 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)


Acid base balance and its disorders

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

  • Normal anion gap Increased anion gap

  • (hyperchloemic) (organic)_________

  • GI loss ofHCO3- acid production

  • Diarrhea Lactic acidosis

  • Renal tub. Acidosis Diab. Ketoacidosis

  • Parenteral alimentationToxic alcohol,salicy.

  • Carbonic anhydr. İnh. Acute renal failure

  • K-sparing diureticsChronic renal failure


Increased anion gap metabolic acidosis

Increased anion gap Metabolic acidosis

  • Ketoacidosis (diabetic)

  • Uremia (renal failure)

  • Salicylate intoxication

  • Starvation

  • Methanol intoxication

  • Alcohol ketoacidosis

  • Unmeasured osmoles (intoxication)

  • Lactic acidosis


Simple decompensated acid base disorders

Simple decompensatedAcid-base Disorders

  • Acid Base Dis.: pH pCO2HCO3-

  • Metabolic acidosis   

  • Respiratory acidosis  

  • Metabolic alkalosis   

  • Respiratory alkalosis  


Compensatory response

Compensatory Response

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)

    and

  • Bicarbonate generation (and reclaiming)


Respiratory acidosis

Respiratory Acidosis

  • 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

  • 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

Alkalosis


Volume depletion and metabolic alkalosis

Volume Depletion and Metabolic Alkalosis

  • 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

  • Alveolar hypoventilation(hypercapnia)

  • (limited pCO2riseto 50-60 mm Hg)

  • Kidneys:

  • Excretion of HCO3-proportional to GFR

    (excessive)


Respiratory alkalosis

Respiratory Alkalosis

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

  • 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 Alkalosiswith 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 AlkalosisExcessive Mineralocorticoids

  • Mineralocorticoidsstimulatehydrogenionsecretion

  • And thisbicarbonate reabsorption

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

  • Hypokalemia

  • Primary aldosteronizm,

  • Bartter’s Syndrome,

  • Cushing Syndrome

  • Renovascular hypertension


Acid base balance and its disorders

Proximal Tubular Bicarbonate Reclamation Process (90 %)

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 1909,1916

  • 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]


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