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Respiratory > Lecture 9 - Respiratory and Urinary Unit Acid-Base Balance > Flashcards

Lecture 9 - Respiratory and Urinary Unit Acid-Base Balance Flashcards

1
Q
  • Kidneys and resp system work together to
A

maintain pH homeostasis

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2
Q
  • Lungs …………. responders
  • Kidneys ……….. ……….. homeostasis- takes days for full compensation
  • Both essential
A
  • Lungs rapid responders
  • Kidneys longer term homeostasis- takes days for full compensation
  • Both essential
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3
Q
  • pH homeostasis primarily determined by
A

CO2- bicarbonate system

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4
Q
  • ratio of[bicarbonate]: [CO2] must remail equal to
A

20/21/:1 – pH will remain 7.4

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5
Q
  • [CO2] determined by
A

lungs

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6
Q
  • [HCO3-] determined by
A

kidneys

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7
Q

how do the kdimeys control [HCO3-]

A
  • Absorption
  • Secretion
  • Synthesis
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8
Q

pH equation and how it relates to CO2 and bicarbonate

A

pH= 6.1 + log([HCO3-]/ 0.03x [pCO2])

if HCO3- conc gets smaller= pH will be lower

if pCO2 gets smaller= pH will be higher

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9
Q
  • Plasma pH must be maintained within a tight range
A
  • pH 7.35-7.45
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10
Q
  • Plasma pH greater than 7.45-
A
  • alkalosis
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11
Q

Plasma pH less than 7.35-

A

acidosis

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12
Q

which is most dangerpis alkalosis or acidosis

A

alkalosis

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13
Q

why is alkalosis more dangerous

A
  • Alkalaemia lowers free calcium by causing Ca2+ to come out of solution increases neuronal excitability
    • pH>7.45 leads to paraesthesia and tetany
    • Issue when affects lung muscles
  • 45% mortality if higher than 7.55
  • 80% if higher than 7.65
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14
Q

acidodis increases which plasma ion

A

potassium

  • Effected excitability
  • Due to increase in potassium conc
    • Particularly affects heart- arrhythmia
  • Increasing [H+] affects enzymes and proteins
    • Effects muscles contractility, glycolysis, hepatic function
  • Effects severe below pH 7.1
  • Life threatening below pH 7
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15
Q

plasma pH depends on

A
  • pH depends on ratio of [HCO3-] to pCO2
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16
Q
  • pCO2 determined by respiration but controlled by
A
  • controlled by chemoreceptors
  • disturbed by resp disease
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17
Q
  • [HCO3-] determined by the kidneys
    • Disturbed by
A

metabolic and renal disease

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18
Q

Henderson Hasselbach equation for plasma pH

A
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19
Q

how do the kidneys control plasma pH

A
  • Control pH- variable recovery of HCO3- and active secretion of hydrogen ions
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20
Q

how do the lungs control plasma pH

A
  • Alveolar ventilation allows diffusion of O2 into blood and CO2 out of blood- control pO2 and pCO2
  • Rate of ventilation controlled by chemoreceptors
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21
Q

pH of arterial blood

A
  • Determined by ratio of pCO2 and [HCO3-]
  • HCO3- made in RBC
  • But conc controlled by kidneys
  • Normal conc in arterial blood is around 25 mmol.-1
    • Range 22-26
    • Can be changed to maintain pH
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22
Q

why do we produe acid

A

due to metabolism

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23
Q

why does acid production due to metabolism not deplete HCO3-

A
  • We produce acid due to metabolism
  • This does not deplete HCO3- because
    • Kidneys recover all filtered HCO3-
    • Proximal tubule makes HCO3- from amino acids (glutamine), putting NH3 into urine
    • DCT make HCO3- from co2 and h2o
      • h+ is buffered by phosphate and ammonia in the urine
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24
Q

Renal control of HCO3-

A
  • HCO3- filtered at the glomerulus
  • Mostly recovered in PCT
  • H+ excretion linked to Na+ entry in PCT
  • H2CO3  carbonic anhydrase  HCO3- + H+)
  • H+ reacts with HCO3- in the lumen to form CO2 which enters cells
  • Converted back to HCO3- which enter ECF
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25
Q
  • Just recovery of HCO3- wont be enough-which amino acid is used to make more HCO3-?
A

glutamine –> alpha ketoglutate + NH4=

NH4–> NH3+ (excreted) + H+

alpha-ketoglutarate –> 2HCO3- (reabsorbed)

26
Q

H+ excretion

A
  • DCT and CD ducts also secrete H+ produced from reaction of CO2 with water
  • H+ ions are actively secreted
  • H+ buffered by ammonia and phosphate (titratable)
    • Produce NH4+ and H2PO4- which are excreted
  • No CO2 is formed to re-enter the cell
  • Allows HCO3- to enter the plasma
27
Q
  • Excretion of ………. is the major adaptive response to an increased acid load in healthy individuals
A
  • Ammonium generation from glutamine in PCT can be increased in response to low pH
  • NH4+ –> NH3 + H+ (PCT – major adaptive response to increase in H+)
    • NH3 freely moves into lumen and throughout interstitium
    • H+ actively pumped into lumen in the DCT and CT
    • H+ combines with NH3–> NH4+ (trapped in lumen forever)
    • NH4+ can also be taken up in the TAL and transported to interstitium and dissociated to H+ and NH3 –> lumen of collecting ducts
28
Q

minimum pH of urine is

A

4.5

29
Q

ions in urine

A
  • No HCO3- (all has been recovered)
  • Some H+ is buffered by phosphate (titratable)
  • Some has reacted with ammonia to form ammonium
  • Total acid excretion = 50-10-0 mmol H+ per day
  • This is needed to keep [HCO3-] normal
30
Q

acidosis leads to

A

hyperkalaemia

31
Q

how does acidosis lead to hypokalaemia

A
  • Hydrogen ions move into the cell
  • Potassium ions moves out of cells
  • Decreased potassium excretion in distal nephron
32
Q

alkalosis can lead to

A

hypokalamaeia

  • H+ moves out of cell
  • Potassium ions move into cell
  • Enhanced excretion of potassium in distal nephrons
33
Q

Acid base disturbances and potassium- hyperkalamia

A
  • Hyperkalaemia makes intracellular pH of tubular cells more alkaline (intracellular alkalosis)
    • H+ ions move out of the cells
    • This favours HCO3- excretion
      • Metabolic acidosis (in the plasma)
34
Q

Acid base disturbances and potassium- hypokalamia

A
  • Hypokalaemia makes the intracellular pH of tubular cells more acidic (intracellular alkalosis)
    • H+ ions move into the cells
    • This favour H+ excretion and hCO3- recovery
      • Metabolic alkalosis (in the plasma)
35
Q

effect of respiratory acidosis on the ABG

A
  • Hypoventilation –> hypercapnia (pCO2 rises)
  • Hypercapnia –> fall in plasma pH
  • Respiratory acidosis
  • Characterised by
    • High pCO2
    • Normal HCO3-
    • Low pH
36
Q

Respiratory alkalosis and the ABG

A
  • Hyperventilation  hypocapnia (fall in pCO2- blowing off CO2)
  • Hypocapnia  rise in pH
  • Resp alkalosis
  • Characterised by
    • Low pCO2
    • Normal HCO3-
37
Q
  1. Compensated respiratory acidosis
A
  • High pCO2 (due to hypoventilation)
  • Raised [HCO3-]–> kidneys help kicked in
  • Relatively normal pH (fully (if slightly compensated= partial compensation)
38
Q
  1. Compensated respiratory alkalosis
A
  • Low pCO2 (hyperventilating)
  • Lowered [HCO3-]
  • Relatively normal pH
  • Raised pH
39
Q
A
40
Q

Compensation

A
  • Plasma pH depends on ratio of [HCO3-] to pCO2 not on their absolute values
  • Changes in pCO2 can be compensated by changes in [HCO3-]
    • Kidneys increase [HCO3-] to compensate for resp acidosis
    • Kidneys decrease [HCO3-] to compensate for resp alkalosis
  • Takes time…. 2-3 days
41
Q

the anion gap

A
  • Difference between measured cations and anions
  • ([Na+] + [K+]) – ([Cl-] + [HCO3-])
  • Normally 10-18 mmol-1
    • Due to other anions that are not measured
  • This gap is increased if HCO3- is replaced by other anions
  • If metabolic acid (such as lactic acid) reacts with HCO3- the anion of the acid replaced HCO3-
42
Q

Renal causes of acidosis and the anion gap

A

will be unchanged

Not making enough HCO3- but this is replaced by Cl-

Renal problem when Cl- replaces the HCO3-

43
Q

Metabolic problem and anion gap

A
44
Q

Metabolic acidosis and ABG

A
  • Normal CO2 (no breathing problem)
  • Low HCO3- (problem with kidneys)
  • Low pH
  • Increased anion gap if HCO3- is replaced by another organic anion from an acid
  • BUT HCO3- normal anion gap if replaced by Cl-
45
Q

3. Compensated metabolic acidosis

A
  • Peripheral chemoreceptors (carotid bodies) detect pH drop
    • Stimulate ventilation
    • Leading to decrease pCO2
      • Characterised by:
        • Low HCO3-
        • Lowered pCO2
        • Nearer normal pH
46
Q

Metabolic alkalosis

A
  • If [HCO3] increases
    • Normal pCO2
    • Raised HCO3-
    • Increased pH
  • Cannot normally be compensated to a great extent by reducing breathing – need to maintain pO2
  • Should be easy for kidney to correct- see later
47
Q

Conditions leading to respiratory acidosis

A
  • Type 2 respiratory failure
48
Q
  • Type 2 respiratory failure
A
    • Low pO2 and High pCO2
      • The alveoli cannot be properly ventilated
      • Severe COPD, severe asthma, drug overdose, neuromuscular disease (myasthenia gravis)
  • Can be compensated for by increase in [HCO3-]
  • Chronic conditions can be well compensated such that pH near normal
49
Q

Conditions leading to respiratory alkalosis

  • *
A
  • Hyperventilation
    • Anxiety / panic attacks – acute setting – Low pCO2, rise in pH
  • Hyperventilation in response to long-term hypoxia – Type 1 respiratory failure
50
Q

Type 1 respiratory failure

A
  • cause of resp alkalosis
  • Low pCO2 with initial rise in pH
  • Chronic hyperventilation can be compensated for by fall in [HCO3-]
  • Can restore pH to near normal
51
Q

Conditions leading to metabolic acidosis

  • If anion gap is INCREASED
    *
A
  • – indicates a metabolic production of an acid
    • Keto-acidosis
      • diabetes
    • Lactic acidosis
      • Exercising to exhaustion
      • Poor tissue perfusion
    • Uraemic acidosis
      • Advanced renal failure – reduced acid secretion, build up of phosphate, sulphate, urate in blood
52
Q

metabolic acidosis

  • If anion gap is NORMAL
    *
A
  • HCO3- is replaced by Cl-
    • Renal tubular acidosis (rare)
      • Problem with transport mechanism in tubules
      • Type 1 (distal) RTA- inability to pump out H+
      • Type 2 (proximal) RTA (VERY RARE) – problems with HCO3- reabsorption
    • Severe persistent diarrhoea can also lead to metabolic acidosis due to loss of HCO3-
      • Replaced by Cl-
      • Therefore anion gap unaltered
53
Q

Metabolic acidosis and potassium

*

A
  • Non-renal causes of metabolic acidosis cause increase reabsorption of K+ by kidneys
  • And movement of K+ by kidneys
    • Hyperkalaemia
  • However in diabetic ketoacidosis may be due to total body depletion of K+
    • K+ moves out of cell (due to acidodis and lack of insulin)
    • But osmotic diuresis means K+ lost in urine
    • Give insulin and K+
54
Q

Conditions leading to metabolic alkalosis

A
  • In metabolic alkalosis HCO3- is retained in place of Cl-
  • Stomach major site of HCO3- production
    • By product of H+ secretion
    • Serve prolonged vomiting- loss of H+
    • Or mechanical drainage of stomach
  • Other causes
    • Potassium depletion/ mineralocorticoid excess
    • Certain diuretics (loop and thiazide)
55
Q

conditions leading to Metabolic alkalosis

  • *
A
  • [HCO3-] increase e.g. after persistent vomiting
    • This should be easy to correct
    • HCO3- can be excreted very rapidly following infusion of HCO3-
  • Corrected by
    • Rise in pH of tubular cells leads to fall in H+ excretion and reduction in HCO3- recovery
    • BUT
    • Problem if there is also volume depletion
      • Capacity to lose HCO3- is reduced because of high rate of Na+ recovery
      • Recovering Na+ favours H+ excretion and HCO3- recovery
56
Q

Metabolic alkalosis and potassium

A
  • Less H+ excretion in nephron leads to more K+ excreted
  • Alkalosis also causes movement of K+ ions into cells
  • This leads to hypokalaemia
57
Q
  • If pCO2 is not normal, [HCO3-] is normal and pH has changed in opp direction to pCO2
A

Respiratory acidosis/alkalosis

58
Q
  • If [HCO3-] is not normal, pCO2 is normal and pH has changed in the same direction as [HCO3-]
    *
A

Metabolic acidosis/alkalosis

59
Q
  • If pCO2 is high, [HCO3-] is raised and pH is relatively normal
    *
A
  • Compensated resp acidosis
  • This is only scenario as we cant compensate metabolic alkalosis
60
Q
A
61
Q
  • If [HCO3-] is low, pCO2 is low, pH is normal
    *
A
  • Could either be compensated respiratory alkalosis or compensated metabolic acidosis
    • Think history: if no resp disease or altitude, unlikely to be resp
    • GO CHECK ANION GAP- if increase it is metabolic acidosis

Respiratory (27 decks)

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