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Resp > Lecture 9 - Acid base balance > Flashcards

Lecture 9 - Acid base balance Flashcards

1
Q

Plasma pH

A

7.35 - 7.45

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2
Q

H+ ion concentration

A

Low an tightly regulated

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3
Q

pH greater than 7.45

A

Alkaemia

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4
Q

pH lower than 7.35

A

Acidaemia

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5
Q

Alkaemia

A

Lowers free calcium - dangerous

  1. Less H+ ions bound to plasma proteins
  2. More -vely charged sites are available on the plasma protein
  3. Ionised free Ca2+ binds to plasma proteins (chelated) therefore less Ca2+ available
  4. Ca2+ also binds to bone and leaves the ECF causing hypocalcaemia
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6
Q

Hypocalcaemia

A

Increases neurone excitablity

  • Tetany
  • Paraesthesia
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7
Q

pH 7.55

A

45% mortality

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8
Q

pH 7.65

A

80% mortality

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9
Q

Acideamia

A

Increases plasma K+ ion concentration - hyperkaleamia

Denatures proteins therefore impaired:

  • muscle contraction
  • glycolysis
  • hepatic function
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10
Q

pH 7.1

A

Severe effects and life threatening below 7.0

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11
Q

Buffer system

A

CO2 + H20 –> H2CO3- –> H+ + HCO3-

Using carbonic anhydrase
pH dependent on how much CO2 is converted to H+

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12
Q

Increased CO2

A

Pushes reaction to the right producing more H+

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13
Q

Increased HCO3-

A

Pushes reaction to the left producing more CO2 which is breathed away

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14
Q

What determines plasma pH

A

Determined by the HCO3- : pCO2 ratio (20:1)

HCO3- controlled by kidneys

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15
Q

pCO2

A

Detected by chemoreceptors Controlled by ventilation

Disrupted by respiratory disease

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16
Q

HCO3-

A

HCO3- made in RBC
Controlled by kidneys
Disturebed by metabolic and renal disease

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17
Q

Kidneys

A

Produces and recovers HCO3-

Excretes H+

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18
Q

Lungs

A

Alveloar ventilation diffuses CO2 out of blood to maintain concentration gradient

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19
Q

HCO3- concentration in RBC

A

25 mmol/L

22-26 mmol/L
Can change to maintain pH

20
Q

HCO3- production and recovery

A

Kidneys recover all HCO3-

PCT makes 2HCO3- from glutamine and excreting NH4+ into urine

DCT makes 2 HCO3- from CO2 and H2O
(H+ bufffered by phosphate and ammonia in the urine)

21
Q

PCT HCO3- recovery

A

80 - 90% recovered by PCT

  1. NHE excretes H+ into the lumen for every Na+ into the cell
  2. HCO3- filtered in the glomerulus into the lumen binds to H+ to form CO2
  3. CO2 diffuses into the cell transcellularly
  4. CO2 is converted to H+ (which is excreted again) and HCO3-
  5. HCO3- enters plasma via Na+/HCO3- co transporter therefore Na+dependent
22
Q

PCT HCO3- production

A
  1. Glutamine is converted to alpha ketoglutarate and ammonium (NH4+)
  2. Ammonium is converted to ammonia (NH3) which freely diffuses into the lumen and H+ which is secreted into the lumen using NHE
  3. NH3 + H+ -> NH4 in lumen as ammonia acts as buffer
  4. Alpha ketoglutarate produces 2 HCO3- molecules
  5. HCO3- molecules diffuse into the blood via Na+/HCO3- channel
23
Q

DCT and CT

A
  1. Alpha intercalated cells actively secret H+ into the lumen using H+ ATPase
  2. Ammonia and hydrogen phosphate buffer the H+ in the lumen
  3. CO2 and water (from metabolism) inside the intercalated cell produce HCO3-
  4. HCO3- enters the blood via HCO3-/ Cl- antiporter therfore non Na+ dependent
24
Q

Increased acid load and low pH in healthy individual

A

Increased excretion of ammonium in urine as ammonia buffers H+

Ammonium generation from glutamine is increased in the PCT

NH3 freely moves in urine and interstitium as not charged

25
Q

NH4+ in thick ascending limb

A

Can be taken up by thick ascending limb where it travels to the collecting ducts.

Dissociates into NH3 and H+ where it can be excreted into the lumen

26
Q

Minimum pH of urine

A

4.5

Due to H+ buffering system excreting H+
No HCO3- as also reabsorbed

27
Q

Hyperkalaemia

A

Caused by metabolic acidosis
H+ moves into body cells and K+ moves out into blood

In nephron cells, H+ is excreted into lumen and K+ is taken up

Causes cardiac arrythmias

28
Q

Hypokalaemia

A

Caused by metaboloc alkalosis

H+ moves out of cells and K+ moves in

In distal nephron, H+ is absorbed and K+ is excreted

29
Q

Hypoventilation

A

Causes hypercapnia

Increased CO2
Decreases pH
Respiratory acidosis

30
Q

Hyperventilation

A

Causes hypocapnia

Decreased CO2
High pH
Respiratory alkalosis

31
Q

Compensation of respiratory acidosis and alkalosis

A

Acidosis - Kidneys produce more [HCO3-]

Alkalosis - Kidneys decrease [HCO3-]

Takes 2-3 days so gradual respiratory disease is well compensated but acute cases are not

32
Q

Metabolic acidosis

A

Tissues produce acid e.g. lactic acid and ketoacidosis

Acids react with HCO3- decreasing the concentration

Decreases pH

33
Q

Compensation of respiratory metabolic acidosis

A

Peripheral chemoreceptors detect pH drop in the carotid body

Stimulates an increase in ventilation proportional to HCO3- loss

34
Q

Anion gap

A

([Na+] + [K+]) - ([Cl-] + [HCO3-])

Other anions are not measured e.g. proteins

Gap increased if HCO3- is replaced by other anions e.g. lactate

Tissues produce e.g. lactic acid in MI that reacts with HCO3- and replaces it with another anion. HCO3- decreases therefore the anion gap increases

35
Q

Renal cause of metabolic acidosis

A

Anion gap is unchanged

As HCO3- produced less
But Cl- produced instead

36
Q

metabolic alkalosis

A

Increase in HCO3-

Cannot be compensated efficiently as body must preserve oxygen supply to brain so can’t hypoventilate proportionally

Therefore kidney excretes HCO3-

37
Q

Type 2 respiratory failure

A

Low O2
High pCO2

Compensated by increase of HCO3-

38
Q

Causes of type 2 resp failure

A 
Hypoventilation
Severe COPD
Severe asthma
Drug overdose 
Neuromuscular disease
39
Q

Conditions causing respiratory alkalosis

A

Hyperventilation
Panic attacks
Anxiety

40
Q

Type 1 respiratory failure

A

Low O2
Low CO2

Hyperventilation in repsonse to long term hypoxia
Initial rise in pH
Compensated for by fall in HCO3-

41
Q

Conditions causing metabolic acidosis with increased anion gap

A
  • Ketoacidosis - diabetes
  • Lactic acidosis - exercise to exhaustion
  • Poor tissue perfusion - MI releases lactic acid
  • Uraemic acidosis - advanced renal failure causes a decrease in H+ secretion
42
Q

Uraemic acidosis

A

Build up in blood of :

  • phosphate
  • H+
  • sulfate
  • urate
43
Q

Conditions causing metabolic acidosis with normal anion gap

A

Renal tubular acidosis

  • Type 1 - distal inability to pump out H+
  • Type 2 - proximal problems with HCO3- reabsorption

Severe persistant diarrhoea - loss of HCO3- replaced by Cl-

44
Q

Diabetic ketoacidosis

A

Normally get hyperkalaemia however, total body depletion of K+

  • K+ moves out of body cells due to acidosis and lack of insulin
  • Osmotic diuresis due to less Na+ reabsorption means K+ lost in urine
45
Q

Conditions causing metabolic alkalosis

A

Vomiting - loss of H+

Mechanical drainage of stomach into duodenum - lack of secretion of HCO3- to neutralise H+ as no H+

46
Q

Volume deplete

A

Normally easy to correct metabolic alkalosis as downregulate NHE

However, if volume deplete can’t downregulate as need to retain water with Na+ absorption

Resp (22 decks)

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