S5) Acid Base Balance Flashcards
What is alkalaemia?
Alkalaemia is a plasma pH greater than 7.45
What is acidaemia?
Acidaemia is a plasma pH less than 7.35
Which conditions can arise from alkalaemia?
- Paraesthesia
- Tetany
Why does alkalaemia lead to paraesthesia and tetany?
- Free calcium is lowered by causing Ca2+ to come out of solution
- This increases neuronal excitability
Describe the mortality associated with alkalaemia
- 45% mortality - pH rises to 7.55
- 80% mortality - pH rises to 7.65
Describe the effect of acidaemia on excitability in the body
- Increases plasma [K+]
- Affects excitability (particularly cardiac muscle) which causes arrhythmias
Describe the effect of acidaemia on enzymes
- Increasing [H+] affects many enzymes and denatures proteins
- This affects muscle contractility, glycolysis, hepatic function
Describe the mortality associated with acidaemia
- Severe effects – below pH 7.1
- Life threatening – below pH 7.0
pCO2 is determined by respiration.
Identify the factors which disturb and control pCO2
- Controlled by chemoreceptors
- Disturbed by respiratory disease
[HCO3-] is determined by the kidneys.
Identify the factors which disturb and control [HCO3-]
- Controlled by the kidney
- Disturbed by metabolic and renal disease
Why does metabolic acid not deplete hydrogen carbonate?
- The kidneys recover all filtered HCO3-
- PCT makes HCO3- from AA, putting NH4+ into urine
- DCT makes HCO3- from CO2 and H2O (H+ is buffered by phosphate and ammonia in the urine)
Describe the renal control of hydrogen carbonate
- HCO3- filtered at the glomerulus & recovered in PCT
- H+ excretion linked to Na+ entry in PCT
- H+ reacts with HCO3- (lumen) to form CO2 which enters cell and is converted back to HCO3- which enters ECF
Describe the role of glutamine in the creation of hydrogen carbonate in th PCT
- Glutamine breaks down and forms α-ketoglutarate
- HCO3- and ammonium are produced
- HCO3- enters ECF and NH4+ enters lumen (urine)
Describe the renal control of hydrogen carbonate in the distal tubule and collecting duct
- DCT and CD also actively secrete H+
- H+ buffered by ammonia and phosphate to produce NH4+ and H2PO4- which are excreted
- HCO3- now can enter plasma
Excretion of ammonium is the major adaptive response to an increased acid load.
Describe the role of ammonium in the renal control of HCO3-
NH4+ ⇒ NH3 + H+
- NH3 freely moves into lumen and throughout interstitium
- H+ actively pumped into lumen in DCT and CT
- H+ combines with NH3 to form NH4+ (trapped in lumen)
What is the pH of urine?
The minimum pH of urine is 4.5
How much acid is secreted per day and why?
- Total acid excretion = 50 – 100mmol H+ per day
- Needed to keep normal [HCO3-]
Explain how acidosis leads to hyperkalaemia
- K+ move out of cells
- Decreased K+ excretion in distal nephron
Explain how alkalosis leads to hypokalaemia
- K+ move into cells
- Enhanced excretion of K+ in distal nephron
Explain how hyperkalaemia can lead to metabolic acidosis
- Hyperkalaemia makes pHi of tubular cells more alkaline
- H+ move out of the cells which favours HCO3- excretion
Explain how hypokalaemia can lead to metabolic alkalosis
- Hypokalaemia makes pHi of tubular cells more acidic
- H+ move into the cells which favours H+ excretion and HCO3- recovery
How does hypoventilation lead to respiratory acidosis (acidaemia)?
- Hypoventilation → hypercapnia (pCO2 rises)
- Hypercapnia → fall in plasma pH
Identify 3 factors which characterise respiratory acidosis
- High pCO2
- Normal HCO3-
- Low pH
How does hyperventilation lead to respiratory alkalosis (alkalaemia)?
- Hyperventilation → hypocapnia (fall in pCO2)
- Hypocapnia → rise in pH
Identify 3 factors which characterise respiratory alkalosis
- Low pCO2
- Normal HCO3-
- Raised pH
How do kidneys compensate for respiratory acidosis?
The kidneys increase [HCO3-] to compensate for respiratory acidosis
How do kidneys compensate for respiratory alkalosis?
The kidneys decrease [HCO3-] to compensate for respiratory alkalosis
Identify 3 factors which characterise compensated respiratory acidosis
- High pCO2
- Raised [HCO3-]
- Relatively normal pH
Identify 3 factors which characterise compensated respiratory alkalosis
- Low pCO2
- Lowered [HCO3-]
- Relatively normal pH
What is the anion gap?
The anion gap is the difference between measured cations and anions
([Na+] + [K+]) – ([Cl-] + [HCO3-])
What is the normal value for the anion gap and why?
Normally 10 – 18 mmol.l-1 due to other anions that are not measured
How can the anion gap be increased?
Increased if HCO3- is replaced by other anions:
E.g. If a metabolic acid (such as lactic acid) reacts with HCO3- the anion of the acid replaces HCO3-
In renal causes of acidosis, the anion gap will be unchanged.
Why?
Not making enough HCO3- but this is replaced by Cl-
In terms of the anion gap, identify 2 factors which characterise metabolic acidosis
- Increased anion gap if HCO3- is replaced by another organic anion from an acid
- Normal anion gap if HCO3- replaced by Cl-
Explain how carotid bodies compensate for metabolic acidosis
- Peripheral chemoreceptor (carotid bodies) detect pH drop
- Ventilation is stimulated which leads to a decrease in pCO2
Identify 3 factors which characterise compensated metabolic acidosis
- Low HCO3-
- Lowered pCO2
- Nearer normal pH
What is observed in Type II Respiratory Failure?
- Low pO2 and high pCO2
- Alveoli cannot be properly ventilated
Identify 4 clinical conditions in Type II respiratory failure which lead to respiratory acidosis
- Severe COPD
- Severe asthma
- Drug overdose
- Neuromuscular disease
How can respiratory acidosis be compensated for?
Increase [HCO3-]
What is observed in Type I Respiratory Failure (hyperventilation in response to long term hypoxia)?
Low pCO2 with initial rise in pH
Identify 2 clinical conditions in Type I respiratory failure which cause respiratory alkalosis
- Chronic hyperventilation
- Anxiety/panic attacks
How can respiratory alkalosis be compensated for?
Decrease [HCO3-]
Identify and describe 3 clinical conditions which can cause metabolic acidosis
- Keto-acidosis: seen in diabetes
- Lactic acidosis: exercising to exhaustion leading to poor tissue perfusion
- Uraemic acidosis: advanced renal failure leading to reduced acid secretion & build up of plasma phosphate, sulphate, urate
Identify 2 clinical conditions which lead to metabolic acidosis with a normal anion gap
- Renal tubular acidosis
- Severe persistent diarrhoea
Renal tubular acidosis involves problems with transport mechanisms in the tubules.
Identify and describe its 2 forms
- Type 1 RTA (distal) involves the inability to pump out H+
- Type 2 RTA (proximal) involves problems with HCO3- reabsorption
Identify 3 clinical states which lead to metabolic alkalosis
- Severe prolonged vomiting (loss of H+ from stomach)
- Potassium depletion
- Mineralocorticoid excess
Certain diuretics can also cause metabolic alkalosis.
Identify 2
- Loop diuretic
- Thiazide diuretic
What process is occuring in the following:
Abnormal pCO2, normal [HCO3-] and pH has changed in opposite direction to pCO2
Respiratory acidosis / alkalosis
What process is occurring in the following:
Abnormal [HCO3-], normal pCO2 and pH has changed in the same direction as [HCO3-]
Metabolic acidosis / alkalosis
What process is occurring in the following:
High pCO2, raised [HCO3-] and pH is relatively normal
Compensated respiratory acidosis
What process is occurring in the following:
Low [HCO3-], low pCO2 and pH is relatively normal
Compensated respiratory alkalosis / compensated metabolic acidosis (check anion gap)
Describe the form of acidosis/alkalosis happening in the patient:
- pH = 7.22 (7.35 - 7.45)
- pCO2 = 8.1 (4.7 - 6.0)
- HCO3- = 24 (22 - 26)
- pO2 = 8.9 (9.3 - 13.3)
Uncompensated respiratory acidosis
Describe the form of acidosis/alkalosis happening in the patient:
- pH = 7.22 (7.35 - 7.45)
- pCO2 = 4.5 (4.7 - 6.0)
- HCO3- = 13 (22 - 26)
- pO2 = 12.4 (9.3 - 13.3)
Partially compensated metabolic acidosis
Describe the form of acidosis/alkalosis happening in the patient:
- pH = 7.46 (7.35 - 7.45)
- pCO2 = 3.3 (4.7 - 6.0)
- HCO3- = 17 (22 - 26)
- pO2 = 13.3 (9.3 - 13.3)
Partially compensated respiratory alkalosis
Describe the form of acidosis/alkalosis happening in the patient:
- pH = 7.22 (7.35 - 7.45)
- pCO2 = 4.8 (4.7 - 6.0)
- HCO3- = 14 (22 - 26)
- pO2 = 11.8 (9.3 - 13.3)
Uncompensated metabolic acidosis
Describe the form of acidosis/alkalosis happening in the patient:
- pH = 7.28 (7.35 - 7.45)
- pCO2 = 8.6 (4.7 - 6.0)
- HCO3- = 30 (22 - 26)
- pO2 = 8.6 (9.3 - 13.3)
Partially compensated respiratory acidosis
Describe the form of acidosis/alkalosis happening in the patient:
- pH = 7.46 (7.35 - 7.45)
- pCO2 = 5.6 (4.7 - 6.0)
- HCO3- = 29 (22 - 26)
- pO2 = 10.1 (9.3 - 13.3)
Uncompensated metabolic alkalosis
Describe the form of acidosis/alkalosis happening in the patient:
- pH = 7.35 (7.35 - 7.45)
- pCO2 = 7 (4.7 - 6.0)
- HCO3- = 28 (22 - 26)
- pO2 = 8.6 (9.3 - 13.3)
Fully compensated respiratory acidosis
Describe the form of acidosis/alkalosis happening in the patient:
- pH = 7.35 (7.35 - 7.45)
- pCO2 = 4.1 (4.7 - 6.0)
- HCO3- = 17 (22 - 26)
- pO2 = 13.0 (9.3 - 13.3)
Fully compensated metabolic acidosis
Describe the form of acidosis/alkalosis happening in the patient:
- pH = 7.5 (7.35 - 7.45)
- pCO2 = 4.5 (4.7 - 6.0)
- HCO3- = 26 (22 - 26)
- pO2 = 13.0 (9.3 - 13.3)
Uncompensated respiratory alkalosis
