acid-base balance Flashcards
(29 cards)
acid and base
An acid donates H+
A base accepts H+
After donating H+ an acid becomes its conjugate base
Acid ↔ (Base)- + H+
H+ in solution
Intra – and extra – cellular fluids are complex solutions with multiple solutes existing in various degrees of ionisation
Free [H+] is very low (almost zero) – mostly complexed with water or other molecules.
pH or H+
pH is derived from the use of ion-selective electrode to measure H+
pH = -log10 H+
Change in H+ by factor of 2 lead to change in pH of 0.3
regulation of H+ matter
At physiological pH most biosynthetic and metabolic pathways involve
precursors that are ionised
This traps them within cells/organelles
Deviation of pH alters ionization states and equilibria thus hugely impairs cellular and metabolic function
effects of acid-base disorder
Depend on nature of disorder and cause but include:
Cardiovascular
BP, cardiac rhythm
Respiratory
Ventilation, resp rate
Metabolic
Protein wasting, bone
Renal
electrolytes
GI
Neurological
Confusion, seizures
threats to homeostasis
Generation of CO2 from aerobic respiration
Metabolism of foods generating acid or alkali
Metabolism of αα create acid load (e.g.lysine, arginine, methionine, cysteine) or alkali load (glutamate, aspartate)
- Protein rich “Western Diet” is acid-load
Incomplete respiration (anaerobic)
-Keto-acids, lactic acid
Loss of alkali in stool or loss of acid in vomiting
basic acid-base physiology
Maintenance of normal H+ (pH) crucial for normal cellular function
acid- base regulation
Buffering: avoids instantaneous shifts in H+, until….
Balance is restored through
Ventilation – control of CO2
Renal regulation of HCO3 and H+ secretion and reabsorption
Although acid/base may be transiently out of balance, homeostatic mechanisms quickly restore input/loss
Resulting maintenance of [H+] may be at the expense of other abnormal blood chemistry, e.g. HCO3, CO2
buffering
Buffers are weak acids, partially dissociated in solution
Acid ↔ Base + H+
[H+] = K [acid]/[base]
pH = pK + log [base]/[acid]
Buffers react poorly with water and are available to react with either H+ (base) or OH- (WA)
Concentration of acid/base»_space; [H+]
This allows consumption of WA/base and avoid big changes in [H+]
henderson- hasselbach equation
CO2 + H2O ↔ H2CO3 ↔ HCO3 + H+
Since CA catalyses conversion of H2CO3 v fast, [H2CO3] v low and we can simplify to:
CO2 + H2O ↔ HCO3 + H+
[H+] = Ka . [CO2] Henderson Equation
[HCO3]
If we use pH then we re-arrange to:
pH = pKa +log{[HCO3]} Henderson-Hasselbach Equation
[CO2]
physiological buffering
+
CO2- HCO3 system is the principle physiological buffer
CO2 + H2O ↔ H2CO3 ↔ HCO3 + H+
pH = 6.1 +log{[HCO3]/[CO2]}
Addition of H+ consumes
Maintenance of [H+] ≡ Maintenance of [HCO3]
buffer examples
Buffering can occur in ECF or ICF
Other than HCO3
Haemoglobin
Buffers CO2 in blood
Proteins
Important intracellular buffer
Bone
Long term buffer
PO4
Intracellular and urinary buffer
disorders of acid-base balance
Respiratory:
↑pCO2 →resp acidosis
↓pCO2 →resp alkalosis
Metabolic:
↓HCO3 →metabolic acidosis
↑HCO3 →metabolic alkalosis
respiratory system and changes in acid base balance
CO2 generated by aerobic “respiration”
Transported to lungs and ventilated
Thus 2 processes underlie contribution of respiratory system to maintaining acid-base balance:
-Control of alveolar ventilation
-Relationship between pCO2 and pH
regulation of ventilation
pCO2 is sensed by chemoreceptors
Chemoreceptors input to respiratory centre
Respiratory centre stimulates respiratory muscles
This is a “servo-controlled system”
role of respiratory system in acid bae homeostasis
Ventilate CO2 generated by aerobic metabolism
Compensate when there is a metabolic acid-base disorder
respiratory acidosis
Acid-base disorder in which the primary abnormality is ↑pCO2
↓ventilation
(↑CO2 in inspired air e.g rebreathing)
(↑CO2 production with fixed ventilation)
In practice almost always due to hypoventilation
May be associated with hypoxia
effects of respiratory acidosis
Mostly due to ↑pCO2
CO2 lipid soluble and easily enters cells in CNS
CV effects
Vasodilation, tachycardia (parasympathetic nervous system) , may cause arrythmia
compensation and buffering in respiratory acidosis
CO2/H2CO3/HCO3 system can’t buffer itself
Initial buffering by intracellular proteins, esp Hb
Mass action dictates ↑ HCO3, with H+ buffered intracellularly
Thereafter there is slow onset renal buffering due to renal retention of HCO3
The rise in HCO3 is predictable – roughly 4mmol/L rise for every 1.44kPa rise in pCO2
how does renal compensation work
Major mechanism for H+ entering tubule is Na/H anti-porter
For reach HCO3 ion reabsorbed 1 Na ion is also reabasorbed
assessment of respiratory acidosis
Clinical assessment – diagnosis usually obvious (COPD)
Beware of resp suppressing drugs – esp Opiates, BDZ
Consider trigger in susceptible patient
Need usual biochem, FBC, HCO3, CRP, CXR
ABG
Beware of co-existing resp acidosis in a patient with metabolic acidosis
management
Vast majority due to inadequate ventilation
Treat factors contributing to that
If COPD treat infection, bronchospasm, fluid overload etc
Sometimes mechanical ventilation may be required
respiratory alkalosis
Always due to increased (alveolar) ventilation
Why “alveolar”
- Ventilation of CO2 = RR x tidal volume
- If there is physiological dead space effective tidal vol is reduced so CO2 may not fall
