Definition:

pH is defined as potential of H+ Ion concentration in body fluid. The amount of H+ ion concentration is so low in the body hence it is expressed as ve logarithm to base of the H+ ion concentration in mEq/lit. pH = log 1/ [H+ ] = - log [H+ ]

 Balance

of H conc. In ECF . To Achieve Homeostasis . Balance Between :

The H Intake or Production The H Removal

blood = 7.35 7.45 Can be explained as follows; Normal value of H+ ion conc. is about 40nEq/lit. 40 nEq/lit = 0.00000004 Eq/lit. Therefore pH = - log [0.00000004] = 7.4
Arterial

 Acidosis

= Decrease in arterial PH ( <7.35 ) Due to excess H+ Alkalosis = Elevation in Arterial PH ( >7.45) Due to excess base .

Molecules containing H atoms that can release (donate) H ions in solutions . Example : HCL . Hydrogen ions are the toxic end product of metabolism and they adversely affect all physical and biochemical cellular process in our body.

Strong acids : - Completely dissociate : (HCL , H2SO4 ) Weak acid : - Partially dissociate : ( H2CO3)

 An

Ion that accept a H ion . An example of a base is the Bicarbonate ( HCO3 ) .

 Substances

that Neutralize acids or bases. Chemical Reactions which Reduce the effect of adding acid or base to a solution H.

 Three 1) 2) 3)

Systems in the body : Buffers in blood . Respiration through the lungs . Excretion by the kidney .

 These

buffer systems serve as a first line of defense against changes in the acidbase balance : - HCO3(Regulated by Renal and Respiratory) . - Protein - Phosphate - Hemoglobin

 Acidic

and Basic Amino acid in plasma and cell protein act as buffers . HB is an important buffer , cant be regulated physiological .

 Both

Intra and Extra cellular phosphate act as a buffer . But its role is minor compared to HB or HCO3. Intracellular buffers are needed because H doesnt cross Plasma Membrane . Intracellular PH is more acidic . (7.2)

Hydrogen Ion Excretion in Kidney

Buffering of hydrogen ions in urine

Factors that increase or decrease H secretion and HCO3 Reabsorption by renal tubules :
Increase in H ion secretion and HCO3 ion reabsorption PCO2 H , HCO3 ECF volume Angiotensin II Decrease H ion secretion and HCO3 ion reabsorption PCO2 H , HCO3 ECF volume Angiotensin II

Aldosterone
Hypokalemia

Aldosterone
Hyperkalemia

 Maintaining

Normal PH by maintaining constant PCO2 . Normal gas Exchange and ventilation . Controlled by chemoreceptors . PCO2 PH

 Tubular

Mechanisms of H+ Tubular Reabsorption of HCO3 .

 Blood

PH Blood PCO2 Blood HCO3

Compensation -If underlying problem is metabolic : Hyperventilation and Hypoventilation mechanisms will help through Respiratory Compensation . -If the problem is Respiratory , Renal mechanisms , then Renal mechanisms will help through Metabolic Compensation .

Acidosis
-Principal effect of acidosis is Depression of the CNS through the decrease in synaptic transmission . - Generalized Weakness . - Deranged CNS is the greatest thread . - severe acidosis causes : 1- Disorientation 2- Coma 3- Death

Alkalosis
-Causes over excitability of the central and peripheral nervous systems . -Numbness - Lightheadedness It can cause : - nervousness . - muscle spasms or tetany . - convulsions - loss of consciousness - death .

Acid/base disorders

Primary change

Compensatory change

Timescale of compensat ory change Minute/hour s

Metabolic acidosis

Decrease in plasma bicarbonate concentration Increase in plasma bicarbonate concentration

Decrease in pCO2 (hyperventilation)

Metabolic alkalosis

Increase in pCO2 (hypoventilation)

Minute/hour s

Respiratory Increase in pCO2 Increase in renal bicarbonate acidosis reabsoption : increase in plasma bicarbonate concentration Respiratory Decrease in alkalosis pCO2 Decrease in renal bicarbonate reabsoption : decrease in plasma

Days

Days

 Metabolic acidosis Ketoacidosis Lactic acidosis Renal failure (inorganic acids) Severe diarrhea (loss of bicarbonate) Surgical drainage of intestine (loss of bicarbonate) Renal loss of bicarbonate (renal tubular acidosis

type 2) Impairment of renal H+ excretion (renal tubular acidosis type 1)

 Respiratory

acidosis

Chronic obstructive airways disease Severe asthma Cardiac arrest

Depression of respiratory center (opiats)

Weakness of respiratory muscles (poliomyelitis,

MS) Chest deformities Airway obstructive

 Metabolic

alkalosis

Vomitting (loss of hydrogen ion) NGT suction Hypoklaemia

IV administration of bicarbonate (after cardiac

arrest)

 Respiratory

alkalosis

Hyperventilation (anxiety, fever) Lung diseases associated with hyperventilation Anemia

Salicylate poisoning

Disorder

pH

pCO2 Decrease (respiratory compensation)

Bicarbonate Decrease (primary change)

Metabolic acidosis Decrease

Respiratory acidosis

Decrease

Increase (prymary Increase change) (metabolic compensation)

Mixed

Excessive decrease

Increase (respiratory acidosis)

Decrease (metabolic acidosis)

Disorder ory alkalosis) Metabolic alkalosis Respiratory alkalosis Mixed

pH Increase

pCO2 Increase (respiratory compensation) Decrease (primary change) Decrease (respiratory alkalosis)

Bicarbonate Increase (primary change) Decrease (metabolic compensation) Increase (metabolic acidosis)

Increase

Excessive increase