Acid Base Balance 2 Flashcards
What can an acid or base load do if renal or respiratory function is abnormal?
Overwhelm the body and a change in pH occurs
What is a decrease in pH called?
Acidosis
What is an increase in pH called?
Alkalosis
What do respiratory disorders affect that leads to a change in pH?
PCO2
What do renal disorders affect that leads to a change in pH?
[bicarbonate]
What is respiratory acidosis?
pH fallen due to respiratory change, so PCO2 must have increased:
- Results from reduced ventilation and therefore retention of CO2
What are some causes of respiratory acidosis?
- Acute
- Drugs which depress the medullary respiratory centres, such as barbiturates and opiates
- Obstruction of major airways
- Chronic
- Lung disease such as bronchitis, emphysema, asthma
What is the bodies response to respiratory acidosis?
The response is need to protect pH so need to increase [HCO3-]:
- Increase in PCO2 will increase secretion of H and HCO3-
- Acid conditions stimulate renal glutaminase to get more NH3 produced, but it takes time
- So there is generation of new HCO3- as well as increased reabsorption, because having generated more HCO3- the increase in PCO2 will also increase the ability to reabsorb it
The bodies response to respiratory acidosis is to increase [bicarbonate] which will protect the pH. However, what does this not correct?
The original disturbance that caused the increase in PCO2 that causes respiratory acidosis
In respiratory acidosis, what will correct the primary disturbance?
Restoration of normal ventilation
When patients have lung diseases the pH can be protected by the kidneys maintaining high [bicarbonate]. When do problems arise?
When patients with lung disease develop renal dysfunction
What is respiratory alkalosis due to?
Due to fall in PCO2 and can only occur through increased ventilation and CO2 blow-off
What are some causes of respiratory alkalosis?
- Acute
- Voluntary hyperventilation
- Aspirin
- First ascent to altitude
- Chronic
- Long term residence at altitude
- Decreased PO2 to <60mmHg (8kPa) stimulates chemoreceptors to increase ventilation
What does the body do to protect pH during respiratory alkalosis?
[HCO3-] should decrease
What mechanism deals with alkaline conditions in the body?
Bicarbonate absorptive mechanism
What is required to fix the original disturbance that causes respiratory alkalosis?
Restoration of normal veniltation
How does an increase in PCO2 impact H secretion and bicarbonate reabsorption?
Increased H secretion
Increased bicarbonate reabsorption
How does a decrease in PCO2 impact H secretion and bicarbonate reabsorption?
Decreased H secretion
Decreased bicarbonate reabsorption, more lost in urine
What is metabolic acidosis due to?
Decrease in [bicarbonate]
A decrease in [bicarbonate] causes respiratory acidosis. What can this be due to?
Increasing buffering of H or direct loss of bicarbonate
What does the body do to protect pH during metabolic acidosis?
PCO2 must be decreased
What are some causes of metabolic acidosis?
- Increased H production, as in ketoacidosis of a diabetic or in lactic acidosis
- Failure to excrete the normal dietary load of H as in renal failure
- Loss of HCO3- as in diarrhoea
- Ie failure to reabsorb HCO3-
How does the body decrease PCO2 to maintain pH during metabolic acidosis?
- Increase in ventilation is in depth rather than rate, reaching a maximum of 30L/min compared to normal 5-6L/min when arterial pH falls to 7
What is the maximum degree of hyperventilating to try and maintain the pH during metabolic acidosis known as?
Kussmaul breathing
What is Kussmaul breathing a sign of?
Renal failure or diabetic ketoacidosis
How can ventilation change in L/min to try and maintain pH during metabolic acidosis?
Can reach a maximum of 30L/min compared to normal 5-6L/min
What normally occurs to fix the orginal disturbance that caused metabolic acidosis?
The kidneys restore [bicarbonate] and get rid of H ions
But a problem is the source of H ions is the carbonic acid from CO2, but the respiratory compensation lowers the PCO2 to protect the pH
Explain what happens when there is an increase in metabolic H within the body?
- Immediate buffering in ECF and then ICF
- Respiratory compensation within minutes
- Renal correction of disturbances takes longer to develop the full response to increased H excretion and generate new HCO3- because renal glutaminase takes 4-5 days to reach maximum
- As HCO3- starts to increase, respiratory compensation begins to wear off until eventually get rid of all excess H
- So respiratory compensation delays the renal correction, but protects the pH which is much more important
What is the explanation that explains how the kidneys are able to correct metabolic acidosis by restoring [bicarbonate] and getting rid of H ions although the source of the H ions is carbonic acid from CO2 (which is reduced due to respiratory compensation lowering PCO2 to protect the pH)?
- Compensation for A/B disturbances are always in the same direction as initial disturbance, remember pH is defined as ratio of [HCO3-]/ PCO2, however they are never quite to the same extend so pH is not restored to 7.4
- Complete compensation would remove the drive to correct the original disturbance
- Because of the decrease in PCO2 the total amount of H secreted by renal tubule will be less than normal but because the plasma [HCO3-] and therefore filtered load of HCO3- is reduced to an even greater extent, a smaller fraction of total H is needed to HCO3- reabsorption and therefore a greater proportion is available for excretion in the form of titratable acid and NH4+
Why does renal correction of disturbances for metabolic acidosis take longer than respiratory compensation?
Renal glutaminase takes 4-5 days to reach maximum
How does respiratory compensation impact renal correction of metabolic acidosis?
Respiratory compensation delays the renal correction, but protects the pH which is much more important
What occurs in metabolic alkalosis?
[HCO3-] must have increased and PCO2 will increase to protect pH
What is the bodies response to protect pH in metabolic alkalosis?
Increase PCO2
What are some causes of metabolic alkalosis?
- Increase H ion loss, such as vomiting loss of gastric secretions
- Increase in renal H loss, such as due to aldosterone excess or excess liquorice ingestion
- Excess administration of HCO3- is unlikely to produce alkalosis in subjects with normal renal function, but may do so in renal impairment
- Massive blood transfusions can lead to metabolic alkalosis because bank blood contains citrate to prevent coagulation, which is converted to HCO3-
- Needs at least 8 units to have this effect
In respiratory acidosis, how is: H and pH changed, what is the initial disturbance, and what is done to compensate?
In respiratory alkalosis, how is: H and pH changed, what is the initial disturbance, and what is done to compensate?
In metabolic acidosis, how is: H and pH changed, what is the initial disturbance, and what is done to compensate?
In metabolic alkalosis, how is: H and pH changed, what is the initial disturbance, and what is done to compensate?
Changes in [bicarbonate] or PCO2 can be the primary disturbance, or the bodies response to compensate. What does this mean clinically?
It is important to distinguish between cause and effect, look at the pH
What can an increase in pH be due to in terms of [bicarbonate] and PCO2?
Increased [bicarbonate]
Decreased PCO2
What can a decrease in pH be due to in terms of [bicarbonate] and PCO2?
Decrease in [bicarbonate]
Increase in PCO2
For any given PCO2 is does the decrease in pH change between chronic and acute acidosis?
- Small decrease in pH in chronic respiratory acidosis than in acute
- Due to mechanisms used to raise [HCO3-]
- NH3 production takes 4-5 days to be fully turned on, so initially can only raise [HCO3-] by titratable acid so is limited. With time can use NH3 production which has a considerable capacity to raise [HCO3-]
- Similar difference seen between acute and chronic respiratory alkalosis because of the delay in turning of NH3 production, in contrast to renal compensation which need time to reach completion, respiratory compensations occur in minutes so no difference
What are the 2 main ways of increasing [bicarbonate]?
1) Ammonium excretion
2) Titratable acid
What is an example of putting acid/base balanc einto practive?
Example is a badly controlled diabetic in ketoacidosis:
- So has metabolic acidosis
- Also has always smoked so has chronic bronchitis cause respiratory acidosis
- And has haemorrhage so has lactic acidosis
So combined has metabolic and respiratory acidosis
How do you manage a patient who combined has metabolic and respiratory acidosis?
- Release high acidity will cause hyperkalaemia as H ions are buffered intracellularly in exchange for K ions
- Danger of ventricular fibrillation
- Management
- Insulin (plus glucose if non-diabetic), stimulates cellular uptake of K
- Also for hyperkalaemia, calcium resonium which exchanges Ca ions for K ion
- Ca gluconate (IV) decreases excitability of heart, stabilises cardiac muscle cell membranes
What must be considered about ketoacidosis management in relation to K?
Patient wil have hyperkalaemia as H ions are buffered intracellularly in exchange for K ions, so there is a danger of ventricular fibrillation
As well as acid/base balancing, what else are the kidneys important for?
Regulating ECF volume and composition
This can cause problems when fixing one compromises another
What is an example of something that challenges the kidneys ability to balance acids/bases and also regulate ECF volume and composiiton?
Consider a bad case of vomiting:
- Loss of NaCl and water causes hypovolaemia
- Loss of HCl causes metabolic alkalosis
What is the bodies response to a bad case of vomiting?
The hypervolemia will stimulate aldosterone to increase distal tubule reabsorption of Na:
- Under conditions of avid Na reabsorption (and due to loss of Cl) the main ion exchanged for Na is H
- The respiratory compensation for the metabolic alkalosis ie increase in PCO2 helps drive the H secretion and exacerbates the metabolic alkalosis by adding yet more CHO3- to the plasma
Shows that restoration of volume takes precedence over correction of metabolic acidosis
Which of restoring volume and metabolic alkalosis takes precedence?
Restoring volume
How does the bodies response to a case of bad vomiting exacerbate the metabolic alkalosis that the vomiting causes?
The bodies response to fix volume causes the loss of more H, which exacerbates the metabolic alkalosis
Why in vomiting, although you lose acids and alkalis, why do you become alkalotic and what is this called?
“Contraction alkalosis”
Due to decrease in ECF volume causing an increase in aldosterone
What is an example of a sweetie that can cause metabolic alkalosis?
Liquorice contains glycyrrhizic acid, which is very similar to aldosterone, so that excess ingestion can cause metabolic alkalosis
What is the anion gap?
Difference between the sum of the principle cations (Na and K) and the principle anions in the plasma (Cl and HCO3), is normally 14-18mmol/L (ie (140 +4) – (104 +24) =16mmoles/L, (due to plasma proteins))
What is an anion?
Negatively charged molecule
What are cations?
Positively charged ions
What are the principle cations of the body?
Na+ and K+
What are the principle anions of the body?
What is the anion grap normally?
14-18mmol/L (ie (140 +4) – (104 +24) =16mmoles/L, (due to plasma proteins))
When is it useful to measure the anion gap?
In metabolic acidosis:
- There are 2 patterns of metabolic acidosis in terms of anion gap
- In one there is no change from normal
- In other the anion gap increases
What are the 2 patterns of metabolic acidosis in terms of anion gap?
- In one there is no change from normal
- In other the anion gap increases
Explain how in some metabolic acidosis there is no change in anion gap from normal, whereas in others the anion gap increases?
If the acidosis is due to for example a loss of bicarbonate from the gut then the reduction of bicarbonate is compensated by an increase in chloride so there is no change in anion gap, however in lactic acid or diabetic acidosis the reduction in bicarbonate is made up by other anions such as lactate, acetoacetate, b-OH butyrate and so the anion gap is increased
