Acid – base balance

Acid – base balance. -Ali Ghazla -Ashfaq Aleesha -Noor Sibgha -SamaSamaaad -Khan Azam -Hussain Habib.

Acids vs. Bases. definition: Bronsted-Lowry (1923) normal A:B ratio  1:20 strength is defined in terms of the tendency to donate (or accept) the hydrogen ion to (from) the solvent (i.e. water in biological systems).

pH. pH is and indirect measure of [H + ] CAVE! Hydrogen ions (i.e. protons) do not exist free in solution but are linked to adjacent water molecules by hydrogen bonds (H 3 O + )  [H + ] by a factor of 2 causes a  pH of 0.3 neutral vs. normal plasma pH pH 7.4 (7.36-7.44)  normal pH 7.0  neutral but fatal!!!.

Buffers. extracellular carbonic acid / bicarbonate (H 2 CO 3 / HCO 3 - ) haemoglobin.

Organs involved in the regulation of A-B-balance.

Organs involved in the regulation of A-B-balance.

pH is constantly “impaired” by metabolism. METABOLISM continuous production of acids obc c: au y cds dissolved H,c03 * goo,'e co,+Hzo —(CA)» Hac03 C02 H*+HC03 = 24 x (pcoz / [HC03]).

Why is pH so important ?. All the known low molecular weight and water soluble biosynthetic intermediates possess groups that are essentially completely ionised at neutral pH’ pH-dependent ionisation (i.e. charge) serves to an efficient intracellular trapping of ionised compounds within the cell and its organelles Exceptions: macromolecules (proteins) mostly charged anyway or size-trapping or hydrophobic lipids those needed intarcellularly are protein-bound waste products pH has an effects on protein function.

The most important pH for the body is the intracellular pH.

The most important pH for the body is the intracellular pH.

Respiratory system - CO 2. differences in the stimulation of respiration by pCO 2 , H + and pO 2 alveolar ventilation disturbances acidemia  respiratory centre of the brain   alveolar ventilation   CO 2 alkalemia  respiratory centre of the brain   alveolar ventilation   CO 2.

Renal system – fixed H + & HCO 3 -. Proximal tubular mechanisms: reabsorption of HCO 3 - filtered at the glomerulus production of NH 4 +.

Assessment of A-B balance. Arterial blood Mixed venous blood range range pH 7.40 7.35-7.45 pH 7.33-7.43 pCO 40 mmHg 35 – 45 pCO 2 41 – 51 pO 2 95 mmHg 80 – 95 pO 2 35 – 49 Saturation 95 % 80 – 95 Saturation 70 – 75 BE 2 BE HCO 3 - 24 mEq/l 22 - 26 HCO 3 - 24 - 28.

Disorders of A-B balance. Acidosis: abnormal condition lowering arterial pH before secondary changes in response to the primary aetiological factor Alkalosis: abnormal condition raising arterial pH before secondary changes in response to the primary aetiological factor Simple A-B disorders: there is a single primary aetiological acid-base disorder Mixed A-B disorders: more primary aetiological disorders are present simultaneously.

Causes. Respiratory abnormal processes which tend to alter pH because of a primary change in pCO 2 levels acidosis alkalosis Metabolic abnormal processes which tend to alter pH because of a primary change in [HCO 3 - ] acidosis alkalosis.

Respiratory acidosis (RA). primary disorder is a pH due to Pa CO 2 (>40 mmHg), i.e. hypercapnia time course: acute (  pH) chronic (  pH or normalisation of pH) renal compensation – retention of HCO 3 - , 3-4 days causes: decreased alveolar ventilation (presence of excess CO 2 in the inspired gas) (increased production of CO 2 by the body).

Most cases of RA are due to decreased alveolar ventilation !!!!.

RA - inadequate alveolar ventilation. Central respiratory depression & other CNS problems drug depression of respiratory center (e.g. by opiates, sedatives, anaesthetics) CNS trauma, infarct, haemorrhage or tumour hypoventilation of obesity (e.g. Pickwick syndrome) cervical cord trauma or lesions (at or above C4 level) high central neural blockade poliomyelitis tetanus cardiac arrest with cerebral hypoxia Nerve or muscle disorders Guillain-Barre syndrome Myasthenia gravis muscle relaxant drugs toxins e.g. organophosphates, snake venom various myopathies.

RA - rare causes. Over-production of CO 2 in hypercatabolic disorders malignant hyperthermia sepsis Increased intake of CO 2 re-breathing of CO 2 -containing expired gas addition of CO 2 to inspired gas insufflation of CO 2 into body cavity (e.g. for laparoscopic surgery).

RA - metabolic effects ( hypercapnia! ). depression of intracellular metabolism cerebral effects cardiovascular system extremely high hypercapnia: anaesthetic effects (pCO 2 >100mmHg) hypoxaemia.

RA - compensation. Acute RA - buffering only! about 99% of this buffering occurs intracellularly proteins (haemoglobin and phosphates) are the most important intravascular buffers for CO2 but their concentration is low relative to the amount of carbon dioxide requiring buffering the bicarbonate system is not responsible for any buffering of a respiratory acid-base disorder - system cannot buffer itself.

RA - correction (i.e. treatment). the pCO 2 rapidly returns to normal with restoration of adequate alveolar ventilation treatment needs to be directed to correction of the primary cause if this is possible rapid fall in pCO 2 (especially if the RA has been present for some time) can result in: severe hypotension ‘post hypercapnic alkalosis’.

Metabolic acidosis (MA). primary disorder is a pH due to HCO 3 - :  fixed [H + ] = high anion gap loss or  reabsorption of HCO 3 - = normal anion gap.

MA - causes. ketoacidosis diabetic, alcoholic, starvation lactic acidosis acute renal failure toxins.

MA - metabolic effects. respiratory hyperventilation shift of haemoglobin dissociation curve to the right decreased 2,3 DPG levels in red cells (shifting the ODC back to the left) cardiovascular others increased bone resorption (chronic acidosis only) shift of K + out of cells causing hyperkalaemia.