SPR L18 Pathophysiology of Acid-Base Disorders Flashcards Preview

Physiology > SPR L18 Pathophysiology of Acid-Base Disorders > Flashcards

Flashcards in SPR L18 Pathophysiology of Acid-Base Disorders Deck (18)
Loading flashcards...

Pathophysiology of Acid-Base Disorders

Learning Outcomes

  • Principles of acid-base regulation
  • Assessment of acid-base balance
  • Acid-base disorders


Principles of acid-base regulation

  1. What is another way of expressing [H+]
  2. What are the two main sources of [H+] in the body?

  1. pH
  2. CO2 production by cell respiration (‘volatile acid’)        Metabolic production of ‘fixed acids'Physiological, e.g. from dietary amino-acids, Pathophysiological e.g. incomplete oxidation glucose (hypoxia) or fatty-acids (diabetes)


Principles of acid-base regulation

  1. What are pH changes limited by?
    1. Give examples of Extracellular reactions
    2. Give examples of Intracellular reactions
  2. What is the most important buffering system?
    1. Why is it the most important?

  1. buffering reactions
    1. Extracellular: plasma proteins, bicarbonate, ammonia, phosphates

    2. Intracellular: Hb, other proteins (over 99% of total buffering)

  2. CO2 + H2O = H2CO3 = H+ + HCO3-

    1. Rapid equilibration in presence of carbonic anhydrase (eg in erythrocytes). Most important buffering system because CO2 and HCO3- can be regulated.


Principles of acid-base regulation

​CO2 + H2O = H2CO3 = H+ + HCO3-

  1. What is another way of expressing [CO2]?
  2. What can PaCO2 be regulated by?


  1. PaCO2 - direct linear relationship of conc and pp
  2. by the respiratory system - central chemoreceptors in respiratory centre increase ventilation in response to and increase PaCO2 or decrease in pH


Principles of acid-base regulation

CO2 + H2O = H2CO3 = H+ + HCO3-

  1. What can HCO3- be regulated by?
  2. Outline Renal acid base control mechanisms

  1. the kidneys
  2. HCO3- reabsorption (no net H+ secretion proximal tubules)

    H+ secretion with HCO3- ‘generation’ (distal tubules/collecting duct; phosphate and NH4+ buffers

PCT - no net

DCT - net secretion of acid in exhange for additonal generation of bicarbonate. Luminal buffers - ammonia and biphosphate are important

(see picture)


Principles of acid-base regulation

CO2 + H2O = H2CO3 = H+ + HCO3-

  1. What does the diet usually generate?
  2. H+ is secreted by the kidney in exchange for what?

  3. What happens to filtered HCO3- normally?

    1. What happens in acidosis?

    2. In persistent acidosis?

    3. What does this depend upon?

    4. What happens in alkalosis?

  4. Outline urinary buffering of secreted H+


  1. an excess of acid  (70-100 mmol/day)
  2. HCO3-
  3. all reabsorbed
    1. acid urine excreted
    2.  additional HCO3- is generated (renal compensation)
    3. renal carbonic anhydrase
    4. alkaline urine containing excess HCO3- is   excreted
  4. Filtered phosphates

    NH4+ (synthesised in tubular cells)


Assessment of acid-base balance

Arterial blood sample

CO2 + H2O = H2CO3 = H+ + HCO3-

What do the following reflect?

  1. pH: 7.35 - 7.45 
  2. PaCO2: 4.8 – 6.1 kPa

  3. Plasma [HCO3-]: 22 – 26 mmol/l

  4. Base excess: -2 – +2 mmol/l  

  1. measure of overall acid-base status

  2. reflects respiratory contribution to acid-base balance or disorder

  3. reflects metabolic contribution (from HCO3-) to acid-base balance or disorder (standard bicarbonate)

  4. reflects total metabolic contribution to acid-base balance or disorder


Assessment of acid-base balance

Anion gap

  1. What should total anionic charge be equal to?
  2. When is this important to look at?
  3. What occurs in reality?
  4. What is the equation?
  5. What is the normal value?
  6. Give examples of unmeasured anions
  7. What will give rise to a larger gap?

  1. total cationic charge
  2. Important measure in metabolic acidosis
  3. Not all anions and cations are measured

    Measured [anions] < measured [cations]

  4. Anion gap = {[Na+]+[K+]} – {[Cl-]+[HCO3-]}

  5. Normal value 10 – 18 mmol/l

  6. Albumin, Lactate, Sulphate, Phosphate, Other organic acids/anions (HA = H+ + A-)

  7. More anions being present (unmeasured type)



Acid-base disorders

​  CO2 + H2O = H2CO3 = H+ + HCO3-

Respiratory Disorders

  1. What is Respiratory acidosis?

  2. Over time (up to a week), what may be seen? What does this indicate?

  1. hypoventilation causing CO2 retention (T2 respiratory failure                                        increased [CO2] => increased [H+]                      Blood gases: decreased pH; increased PaCO2
  2. Maybe renal compensation (HCO3- production) - increased [HCO3-] indicates chronic hypercapnia


Acid-base disorders

​  CO2 + H2O = H2CO3 = H+ + HCO3-

Respiratory Disorders

  1. What is Respiratory alkalosis caused by?
  2. Give examples
  3. Describe relevant markers
  4. Describe the renal compensation in this case

  5. What other symptoms may be present?

  1. hyperventilation causing CO2 reduction
  2. Panic attack, some forms of Type 1 respiratory failure, altitude

  3. decreased [CO2] => decreased [H+]

    Blood gases: increased pH; decreased PaCO2

  4. unlikely in acute alkalosis (short duration)

    decreased [HCO3-] (over 2-3 days)

  5. May be hypocalcaemic symptoms          decreased [H+] => decreased proton binding by plasma proteins => increased Ca2+ binding by plasma proteins => decreased free Ca2+

Increased spasms. Hyperactivity. May complain of pins and needles. Less is biologically active.


Acid-base disorders

​  CO2 + H2O = H2CO3 = H+ + HCO3-

Metabolic acidosis

  1. What is this a result of?
  2. Describe the blood gases
  3. What is common?
  4. Describe the anion gap

  1. Loss of base

    Addition/accumulation of acid (‘consumes’ HCO3- in buffering reaction)

  2. blood: decreased pH; decreased [HCO3-]

  3. Respiratory compensation (RAPID) is common (CO2 removal)- increased ventilation (air hunger, Kussmaul breathing) => decreased PaCO2

  4. Normal: no increase in organic acid load

    Increased: additional organic acid load 


Acid-Base Disorders

Metabolic acidosis with normal anion gap (no increase in organic ion load)

  1. What is HCO3- replaced with? 
  2. What can result in the increased loss of HCO3-?
  3. How can H+ accumulation come about?

  1. Cl- (hyperchloraemic acidoses)
  2. GIT: diarrhoea

    Renal: failure of HCO3- re-absorption


    Specific renal tubular defects

  3. Specific renal tubular defects

    increased HCl production (NH4Cl, lysine, arginine)


Acid-Base Disorders

Metabolic acidosis with increased anion gap: additonal organic anion load

  1. How does this come about generally?
  2. Give specific examples

  1. Addition/accumulation of acids which produce unmeasured anions. Much more common.


  • Renal failure: sulphate and phosphate
  • Lactic acidosis:
    • increased production, eg in hypoxic tissues (can be a feature of shock)
    • Reduced hepatic lactate metabolism
  • Ketoacidosis in diabetes: b(OH)butyric acid and   acetoacetic acid
  • Acid ingestion: salicylate (aspirin) poisoning


Acid-base disorders

​​Metabolic Alkalosis

Describe the intiation of this state



What does respiratory compensation lead to?

  • loss of acid

    • GIT: Vomiting, NG suction

    • Renal: thiazide and loop diuretics

      • Increased Na+ in distal tubule

      • increased K+ loss, increased H+ loss

  • addition of base
    • excess HCO3- (IV, Oral)
    • Increased pH, increased [HCO3-]


Respiratory compensation leads to underventilation and increased PaCO2


Acid- Base Disorders 

Metabolic alkalosis

Outline the Maintenance of this state (1)

  1. When is chronic alkalosis seen?
  2. Kidneys mightnt be able to reaborb HCO3- to maintain acid base balance as a result of Cl- depletion. Describe this.
  3. What does treatment require?

  1. only seen with impairment of renal HCO3-   excretion


  • Seen with persistent vomiting and diuretics
  • Reduced filtered Cl- available for renal re-absorption => increased HCO3- generated to balance cations
  • Urinary [Cl-] low (<10 mmol/l)

3. Treatment requires re-expansion of fluid volume and replacement of Cl- (IV saline) allowing HCO3- excretion


Acid- Base Disorders 

Metabolic alkalosis

Outline the Maintenance of this state (2)

  1. Aside from Cl- depletion, give another reason why there may be an excess of HC03-
  2. What is this usually associated with?
    1. Give examples


  1. K+ depletion (mechanism unclear)
  2. Usually associated with elevated mineralocorticoid action: stimulates renal K+ and H+ loss
  • 1˚ or 2˚ hyperaldosteronism
  • Cushing’s syndrome
  • Some diuretics
  • Excess liqorice (reduced breakdown cortisol)


  • Urinary [Cl-] normal (>20 mmol/l)
  • Treatment resistant to re-expansion with saline


Acid-base disorders

Give a simplified summary of interpretation of acid-base status from arterial sample


Decks in Physiology Class (46):