Acid-Base Balance & Disorders Flashcards
A patient presents with:
- dyspnoea (SOB)
- confusion,
- headache (vasodilation),
- warm & flushed,
- tachycardia (“bounding pulse”)
on taking an ABG etc how do you compensate for this and how do you Rx correct it?
this is Respiratory Acidosis (retaining CO2)
Compensation: increased renal acid excretion
-> want metabolic alkalosis to oppose it –> metabolic = 36-72hrs delay though
Correction: requires return of normal gas exchange
A patient has ↓H+,
–> Ca2+ has gone into their cells from the blood &
hypocalcaemia = syx of
- tingling,
- paraesthesia,
- tetany,
- convulsions
What type of acid-base balance problem causes this?
- Alkalosis causes low blood calcium concentration.
- As the blood pH increases, blood transport proteins, such as albumin, become more ionized into anions.
- This causes the free calcium present in blood to bind more strongly with albumin.–> decrease Ca2+ If severe, it may cause tetany.
- [NB: hypercalcaemia = stones (kidney), bones, abdominal groans, thrones and psychic overtones]
- So overall if dc H+ and Ca into cells can be metabolic or resp alkalosis (as long as alkalosis)
What type of acid-base balance disorder does
- Hypoxia
- pulmonary disease
- mechanical overventilation
- increased respiratory drive
cause?
Respiratory alkalosis
AKA: the rate of CO2 excretion > generation - low CO2 –> potentially T1 resp failue (below 8 PaO2 and normal/low PaCO2)
Hypoxia, pulmonary disease, mechanical overcentilation and increased respiratory drive all lead to resp alkalosis aka: the rate of CO2 excretion > generation.
What casues of hypoxia and pulmonary disease are there?
Hypoxia: High altitude, Severe anaemia, Pulmonary disease
Pulmonary disease: PE, Pulmonary oedema
Hypoxia, pulmonary disease, mechanical overcentilation and increased respiratory drive all lead to resp alkalosis aka: the rate of CO2 excretion > generation.
What casues of increased respiratory drive are there?
- Respiratory stimulants eg salicylates
- Cerebral disturbance
- eg trauma, infection and tumours
- Hepatic failure
- G-ve septicaemia
- Primary hyperventilation syndrome
- Voluntary hyperventilation
Respiratory Alkalosis
SSx: ↓H+, Ca into cells (tingling, paraesthesia, tetany, convulsions
–> how does the body compensate and correct for this?
Compensation: increased renal bicarbonate excretion (metabolic acidosis, 36-72h delay)
Correction: of cause aka the hypoxia, pulm disease, mech overventilation, increased resp drive (hepatic failure, cerebral disturbance, hyperventilation etc)
What are the possible causes of this?
SSx: SOIB/dyspnoea, confusion, headache (vasodilation), warm & flushed, tachycardia (“bounding pulse”)
Respiratory acidosis aka the rate of CO2 excretion < generation (high O2)
e.g. all potentially cause T2 resp failure!
- Airway obstruction:
- Bronchospasm (Acute),
- COPD (Chronic),
- Aspiration,
- Strangulation
- obstructive sleep apnoea
- Respiratory centre depression:
- Anaesthetics,
- Sedatives,
- Cerebral trauma,
- Tumours
- Neuromuscular disease:
- Guillain-Barre Syndrome,
- Motor Neurone Disease
- Pulmonary disease:
- Pulmonary fibrosis,
- Respiratory Distress Syndrome,
- Pneumonia
- Extra-pulmonary thoracic disease:
- Flail chest / kyphosis
What are the possible causes of T1 resp failure?
e.g. PaO2 < 8 & low CO2 - respiratory alkalosis causes
- PE
- atelectasis/lung collapse
- pneumonia
- asthma
- pulm oedema
e.g. hypoxia - cant get O2 in
What are the possible causes of T2 resp failure?
PaO2 <8 and Co2 that is high (abnormal too) aka respiratory acidosis
- airway obstruction - COPD, sleep apnoea
- Neuromuscular disease - MND
- extra-pulm thoracic disease - kyphosis
- resp centre depression (anaesthetics, sedatives etc)
- pulm disease e.g. fibrosis
An unwell patient comes in with hyperventilation, what is this type of breathing known as and in what clinical scenarios would this happen?
An unwell patient hyperventilating = kussmauls breathing
- a sign of metabolic acidosis – trying to get rid of the excess acid by lowering CO2 by blowing it off
Clinical scenarios of metabolic acidosis:
- acid ingestion
- increased acid production
- reduced acid excretion
- compensation for respiratory alkalosis
What are the causes of metabolic acidosis (unwell patient, hyperventilating/kussmauls breathing)?
- rate of H+ generation > excretion e.g.
- increased addition of acid
- decreased H+ excretion
- loss of bicarbonate
causes of metabolic acidosis include:
- increased addition of acid
- decreased H+ excretion
- loss of bicarbonate
How would you get increased addition of acid?
Increased H+ formation:
- Ketoacidosis,
- Lactic acidosis,
- Poisoning (methanol, ethanol, ethylene glycol, salicylate),
- Inherited organic acidosis
Acid ingestion:
- Acid poisoning,
- excess parenteral administration of amino acids eg arginine
causes of metabolic acidosis include:
- increased addition of acid
- decreased H+ excretion
- loss of bicarbonate
How would you get decreased H+ excretion?
DECREASED H+ EXCRETION
- Renal tubular acidosis (from kidneys not appropriately acidifying the urine)
- Renal failure
- Carbonic dehydratase inhibitors (akak carbonic anhydrase inhib = no coversion of H+ and bicarb to CO2)
-
Addison’s (low cortisol e.g. pt taking steroids) - low Na, high K (+ low glucose), metab acidosis
- [as Na and H+ exchange e.g. if want to get rid of H+ out of kidneys need to retiain sodium]
causes of metabolic acidosis include:
increased addition of acid
decreased H+ excretion
loss of bicarbonate
How would you get LOSS OF BICARBONATE?
- Diarrhoea
- Pancreatic, intestinal or biliary fistulae/drainage
e.g. things running out of the lower GI tract means a loss of bicarb??
How do you compensate and correct an unwell pt, hyperventilating (“Kussmaul’s breathing”)?
aka: metabolic acidosis
Compensation: hyperventilation & low PCO2
Correction: of cause, increased renal acid excretion
What does the anion gap (aka negatively charged molecules) being increased point towards?
anion gaps refer to metabolic acidosis
An increased anion gap = increased production of organic acids
aka:
Lactic acid from SHOCK
Urate from renal failure
Ketones - DM/alcohol
Drugs (salicylates - aspirin)
What does a normal anion gap (aka negatively charged molecules) in acidosis point towards?
normal anion gap =
loss of HCO2 / ingestion of H+
(not increased production of the bodys own organic acids)
- Renal tubular acidosis (inc H+)
- Addison’s (retaining of H+)
- Diarrhoea (loss of HCO3)
- Pancreatic failure (no HCO3 released/made)
- Ammonium chloride ingestion
- Drugs (acetazolamide)
What are the causes of metabolic alkalosis?
ssyx = like respiratory alkalosis, both alkalosis types presents w/SSx: ↓H+, Ca into cells (tingling, paraesthesia, tetany, convulsions)
What causes of metabolic alkalosis are there?
- [Alkalosis causes low blood calcium concentration.*
- As the blood pH increases, blood transport proteins, such as albumin, become more ionized into anions (neg atoms)*
- This causes the free calcium present in blood to bind more strongly with albumin.–> decrease Ca2+ If severe, it may cause tetany.]*
-
Increased addition of base:
- Inappropriate Rx of acidotic states,
- Chronic alkali ingestion
- Decreased elimination of base:
- Increased loss of acid:
How do you get increased loss of acid in metabolic alkalosis?
- GI loss:
- Gastric aspiration,
- Vomiting with pyloric stenosis
- Renal loss:
- Diuretic Rx (not-K+sparing)
- Potassium depletion
- Mineralocorticoid excess- Cushing’s (at high levels cortisol acts like aldosterone), Conn’s (hyperaldosteronism) - bothe get inc Na (HTN), decreased K and H…
- Drugs with mineralocorticoid activity – carbenoxolone
In persistent vomiting you get hypovolaemia, that does this cause?
- loss of HCl (H+)
- loss of potassium
- loss of fluid
What drug can cause chronic K+ depletion?
diuretics!
e.g. only spironolactone, eplerenone, triamterene and amiloride are actually K+ sparing
(K+ sparing act on DCT where secretion of the ions into urine takes place, independently of Na+ after the blood has taken what is needed in the rest of the nephron)
what causes reabsorption (to blood) of NaCl/H2O at the distal convoluted tubule in the kidney in exchange for K+/H+?
what clinical scenario would stimulate this and what type of metabolic disturbance does it give?
aldosterone cacuses reabsorption of NaCl/H20 at the DCT in kidney in exhcange for K+/H+ (into the urine)
this aldosterone activation occurs in response to fluid loss in the body
loss of H+ e.g. acid loss (in exchange for water retaining Na+) gives a metabolic alkalosis
How does the body compensate and correct for a metabolic alkalosis?
Compensation:
- hypoventilation & CO2 retention –> respiratory acidosis
Correction:
- increased renal bicarbonate excretion,
- reduce renal proton (H+) loss
What electrolyte imbalances cause increased bicarbonate resorption into the blood?
When would these situations occur?
Low chloride and low potassium both = resorb more bicarbonate (into blood) –> metabolic alkalosis
e.g. as these are negative ions and they are low so recruit bicarb as another negative charge
Low Chloride:
- GI losses e.g. vomiting, adenoma
- Drugs e.g. diuretics
- Cystic fibrosis
Low potassium:
- Renal tubular disorders
- Drugs e.g. laxatives
- Hyper-aldosteronism (primary, secondary to liquorice ingestion) [gives ic Na, dc K+, dc H+)
Why is maintaianing extracellular [H+]/pH essential?
to maintain protein/enzyme function
between acid production and excreation –>
- CO2 production and excretion (respiration);
- H+ production and exretion (renal)
- NB: pH is a logarithmic scale; for every fall of 0.3 in pH the [H+] doubles
- What does this describe? rate H+ generation > excretion
- What does this describe? rate of CO2 excretion < generation
1 = metabolic acidosis
2 = respiratory acidosis
Bicarbonate is a buffer in serum. What is the mechanism of renal bicarbonate regeneration?
In the renal tubular cell (in the tubules):
H2O + CO2 <–> H2CO3 <–> H+ and HCO3-
the HCO3- is regenerated and reclaimed bicarbonate
the H+ then goes into the renal lumen to be excreted
Bicarbonate is a buffer in serum. What are the other 3 buffers?
- Phosphate in urine
-
skeleton
- maintains blood hydrogen ion concentrations
- intracellular accumulation/loss of H+ ions
What Ix do you do for acid/base balance disorders?
ABG: tells you…
- O2,
- CO2,
- H+,
- lactate
- (don’t measure bicarb - HCO3 - calculated using Hendleson-Hasselbach equation; which estimates the pH of a buffer solution and finds the equilibrium pH)
Compensation = Diametric opposite of original abnormality; delayed & limited
Respiratory compensation = quick e.g. Kussmaul breathing in response to DKA
Metabolic compensation = slow, can take 36-72hrs
Why is metabolic compensation slow?
- Requires enzyme induction from increased genetic transcription & translation etc.
- e.g. No compensation seen in acute respiratory acidosis such as asthma
- –>Requires more chronic scenario to include compensation mechanism
NB: Rx is by reversal of precipitating situation
