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Kofi: Pure Clinical Sem 3 > Resp: pH syndromes > Flashcards

Resp: pH syndromes Flashcards

1
Q

What is the main role of CO2 in blood?

A

-Acts as part of the pH buffering system

Only 8% of the total CO2 is transported

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2
Q

What is hypercapnia?

A

Rise in pCO2

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3
Q

What is hypocapnia?

A

Fall in pCO2

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4
Q

How does exercise affect the partial pressure of CO2 and O2?

A
  • pO2 drops and pCO2 rises

- Breathing more will restore both

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5
Q

What is hyperventilation?

A

Ventilation increase without change in metabolsim

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6
Q

What is hypoventilation?

A

-Ventilation decrease without change in metabolism

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7
Q

What happens to pCO2 and pO2 in hyperventilation?

A
  • pO2 will rise

- pCO2 will fall

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8
Q

What happens to pCO2 and pO2 in hypoventilation?

A
  • pO2 will fall

- pCO2 will rise

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9
Q

What happens if the pO2 changes without a change in CO2?

A

Correction of the pO2 will cause the pCO2 to drop

This leads to hypocapnia

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10
Q

Control system are in place to prevent marked hypoxia. True/False

A

True

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11
Q

What is the effect of CO2 on plasma pH if bicarbonate remains unchanged?

A
  • If pCO2 increase then pH falls
  • If pCO2 decreases then pH rises

Small changes in pCO2 lead to large changes in pH.

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12
Q

What are the effects of pH falling and pH rising?

A
  • If pH falls below 7.0 then enzymes become denatured

- If pH rises above 7.6 free calcium concentration drops leading to tetany

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13
Q

What are the effects of hypercapnia on plasma pH?

A

-Respiratory acidosis due to fall in plasma pH

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14
Q

What are the effects of hypocapnia on plasma pH?

A

-Respiratory alkalosis due to rise in plasma pH

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15
Q

How does the kidney compensate for respiratory acidosis?

A
  • Kidneys increase reabsorption of HCO3-
  • This compensate for the the increase in pCO2

(can take 2-3 days)

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16
Q

How does the kidney compensate for respiratory alkalosis?

A
  • Kidneys decrease reabsorption of HCO3-
  • This compensates for the decrease in pCO2

(can take 2-3 days)

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17
Q

How does metabolic acidosis occur?

A
  • If tissues produce acid, this reacts with HCO3-
  • Fall in [HCO3-] leads to fall in pH
  • This causes metabolic acidosis
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18
Q

How is metabolic acidosis compensated for?

A
  • Compensated for by changing ventilation
  • Increased ventilation lowers pCO2
  • Restores pH towards normal
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19
Q

How does metabolic alkalosis occur?

A
  • If the plasma HCO3- rises
  • Plasma pH rises
  • Causes metabolic alkalosis
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20
Q

How is metabolic alkalosis compensated for?

A

-Decreasing ventilation so that pO2 falls and pCO2 increases

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21
Q

How are the respiratory pathways controlled?

A
  • Sensors located in CNS and the periphery feed information back to the control centre for processing
  • Ventilation is adjusted as necessary
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22
Q

What are the examples of peripheral chemoreceptors?

A

Carotid and aortic bodies

Sensitive to O2

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23
Q

What stimulates the peripheral chemoreceptors and what does it lead to?

A

Large falls in pO2 stimulate the peripheral chemoreceptors. This leads to

  • Increased breathing
  • Changes in the heart rate
  • Changes in blood flow distribution which increases the flow to the brain and kidneys
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24
Q

What is the sensitivity of the peripheral chemoreceptors to the pCO2?

A

Relatively insensitive to pCO2

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25
Q

What is the sensitivity of the central chemoreceptors to the pCO2?

A

Sensitive to the pCO2

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26
Q

Where are the central chemoreceptors found?

A

Medulla of the brain

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27
Q

Why isn’t the central chemoreceptor affected by bicarbonate ions and H+ but it is affected by CO2?

A
  • The ECF and CSF is impermeable to HCO3- and H+ due to the blood brain barrier
  • The blood brain barrier is selective permeable to CO2 however
28
Q

How do the central chemoreceptors work?

A
  • Respond to changes in the pH of cerebrospinal-spinal fluid
  • CSF is operated from blood by the blood brain barrier
  • CSF [HCO3-] is controlled by choroid plexus cells
  • CSF pCO2 is determined by arterial pCO2
29
Q

How is CSF pH determined?

A
  • Determined by ratio of [HCO3-] to pCO2
  • [HCO3-] fixed in the short term as the blood brain barrier is impermeable to HCO3-
  • Falls in pCO2 lead to rise in CSF pH
  • Rises in pCO2 lead to falls in CSF pH
  • Persisting changes in pH corrected by choroid plexus cells which change the [HCO3-]
30
Q

How do the central chemoreceptors counteract an increase in the pCO2?

A
  • Elevated pCO2 drives the CO2 into the CSF across the blood brain barrier
  • CSF [HCO3-] is initially constant
  • CSF pH falls
  • Fall in CSF pH detected by central chemoreceptors
  • Drives increased ventilation
  • This lowers the pCO2 to restore the CSF pH
31
Q

What is the action of the choroid plexus?

A
  • Determine what is normal
  • CSF [HCO3-] determine which pCO2 is associated with normal CSF pH.
  • CSF [HCO3-] therefore sets the control system to a particular pCO2
  • Can be reset by changing CSF [HCO3-] with persistent hypercapnia
32
Q

How does persisting hypoxia affect the central chemoreceptors?

A
  • Hypoxia is detected by the peripheral chemoreceptors which will trigger increase in ventilation
  • pCO2 will fall further and this causes decrease in ventilation
  • CSF composition compensates for the altered pCO2
  • Choroid plexus cells selectively add H+ or HCO3- into the CSF
  • Central chemoreceptors accept the pCO2 as normal
33
Q

How does persisting hypoxia and hypercapnia affect the central chemoreceptors?

A
  • Hypoxia and hypercapnia lead to respiratory acidosis
  • Decreased pH of CSF
  • Peripheral and central chemoreceptors stimulate breathing
  • CO2 diffuses into CSF and CSF pH drops
  • Persistently CSF acidity harmful to neurons
  • Low CSF pH corrected by choroid plexus cells which secrete HCO3- in to CSF

  • The CSF pH returns to normal; central chemoreceptors no longer stimulated
  • pCO2 in the blood is still high but central chemoreceptors now unresponsive to this pCO2 i.e. Central chemoreceptors have ‘reset’ to a new higher CO2 level
  • The persistent hypoxia stimulates peripheral chemoreceptors

  • Respiratory drive is now driven by hypoxia (via peripheral chemoreceptors)
34
Q

What is alkalaemia and acidaemia?

A 
Alkalaemia = >7.45
Acidaemia = <7.35
35
Q

What is the effect of alkalaemia?

A
  • Lower free calcium by causing Ca2+ to come out of solution
  • This increase neuronal excitability
  • Can lead to paraesthesia and tetany

Higher mortality compared to acidaemia

36
Q

What is the effect of acidaemia?

A
  • Causes an increase plasma potassium ion concentration affects excitability particularly in heart muscle and can cause arrhythmia
  • Can denature enzymes high can affect muscle contractility, glycolysis and hepatic function
  • Severe effect below 7.1 and life threatening below 7
37
Q

How are pCO2 and HCO3- disturbed ?

A

pCO2 is disturbed by respiratory disease

HCO3- is disturbed by metabolic and renal disease

38
Q

Why doesn’t acid produced by metabolism deplete HCO3-?

A
  • Kidney recovers all filtered HCO3-
  • Proximal tubule make HCO3- from amino acids, putting NH4+ in the urine
  • Distal tubule makes HCO3- from CO2 and H2O. The H+ is buffered by phosphate and ammonia in the urine when excreted
39
Q

What is the process for recovery of HCO3-?

A
  • HCO3- filtered at the glomerulus
  • Mostly recovered in PCT
  • H+ excretion is linked to Na+ entry in PCT
  • H+ react with HCO3- in the lumen to form CO2 which enters the cell
  • CO2 converted back to HCO3- which enters the ECF
40
Q

Describe the creation of HCO3- in the proximal tubule?

A
  • Glutamine is convert to alpha ketoglutarate
  • Produces HCO3- and ammonium
  • HCO3- enters the ECF
  • NH4+ enters lumen
41
Q

Describe the formation of HCO3- in the distal tubule

A
  • Distal tubule and collecting ducts also secrete H+ produced from reaction of CO2 with water
  • H+ ions are actively secreted
  • H+ buffered by ammonia and phosphate. NH4+ and H2PO4- created
  • No CO2 is formed to re-enter the cell
  • Allows HCO3- to enter plasma
42
Q

What is the kidney response to an increased acid load in an individual?

A
  • Ammonium generation from glutamine in proximal tubule can be increased in response to low pH
  • Ammonium splits to form NH3
  • NH3 moves into lumen and throughout the interstitum
  • H+ actively pumped into lumen in DCT and CT
  • H+ combines with NH3 to form NH4+. This is trapped in lumen
  • Ammonium can’t move back into the cell
  • Increased excretion of ammonium as a result

-NH4+ can also be taken up in TAL and transported to interstitum and dissociated to H+ and NH3. This moves into the lumen of collecting ducts

43
Q

What are the features of urine in terms of cations and anions?

A
  • Minimum pH is 4.5
  • No HCO3-
  • Some H+ is buffered by phosphate
  • Some H+ has reacted with ammonia to form ammonium
44
Q

What is the effect of acidosis on potassium?

A
  • Potassium ions move out of cells
  • Decreased potassium excretion in distal nephron
  • Hyperkalaemia
45
Q

What is the effect of alkalosis on potassium?

A
  • Potassium ions move into cells
  • Enhanced excretion of potassium in distal nephron
  • Hypokalaemia
46
Q

What is the effect of hypokalaemia on intracellular pH of tubular cells?

A
  • H+ move into the cells
  • Favours K+ excretion and HCO3- recovery
  • Metabolic alkalosis
47
Q

What is the effect of hyperkalaemia on intracellular pH of tubular cells?

A
  • H+ ions move out of the cells
  • This favours HCO3- excretion
  • Metabolic acidosis
48
Q

What are the characteristics of uncompensated respiratory acidosis?

A
  • High CO2
  • Normal HCO3-
  • Low pH
49
Q

What are the characteristics of uncompensated respiratory alkalosis?

A
  • Low pCO2
  • Normal HCO3-
  • Raised pH
50
Q

What are the characteristics of compensated respiratory acidosis?

A
  • High pCO2
  • Raised HCO3-
  • Relatively normal pH
51
Q

What are the characteristics of compensated respiratory alkalosis?

A
  • Low pCO2
  • Lowered HCO3-
  • Relatively normal pH
52
Q

What is the anion gap?

A
  • Difference in measured anions and cations

- Normally 10-18 mmol/l

53
Q

When is the anion gap increased?

A
  • If HCO3- is replaced by other anions

- If a metabolic acid reacts with HCO3-, the anion of the acid replaces HCO3-

54
Q

What is the effect of Renal causes of acidosis on the anion gap?

A
  • In renal causes of acidosis anion gap will be unchanged

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

55
Q

What are the features of uncompensated metabolic acidosis?

A
  • Normal pCO2
  • Low HCO3-
  • Low pH
  • Increased anion gap if HCO3- is replaced by another organic anion from an acid
  • Normal anion gap if HCO3- is replaced by Cl-
56
Q

What are the characteristics of compensated metabolic acidosis?

A
  • Low HCO3-
  • Lowered pCO2
  • Nearer normal pH
57
Q

What are the characteristics of uncompensated metabolic alkalosis?

A
  • Normal pCO2
  • Raised HCO3-
  • Increased pH
58
Q

What is type 2 respiratory failure?

A
  • Low pO2 and High pCO2

- Alveoli cannot be properly ventilated

59
Q

What are causes of type 2 respiratory failure?

A
  • Severe COPD
  • Severe asthma
  • Drug overdose
  • Neuromuscular disease
60
Q

How can type 2 respiratory failure be compensated for?

A

Increase in HCO3-

-Chronic conditions can be well compensated to the near normal

61
Q

What are conditions that can cause respiratory alkalosis?

A

Hyperventilation caused by Anxiety/panic attacks (acute setting)

Hyper ventilation in response to long-term hypoxia (type 1 respiratory failure)

62
Q

What are conditions that cause metabolic acidosis?

A
  • Keto acidosis in diabetes
  • Lactic acidosis (exercising to exhaustion, poor tissue perfusion)
  • Uraemic acidosis (advanced renal failure)
63
Q

What are conditions leading to metabolic acidosis with a normal anion gap?

A
  • Renal tubular acidosis. Problems with transport mechanism in the tubules
  • Severe persistent diarrhoea which can lead to metabolic acidosis due to loss of HCO3-. Replaced by Cl-
64
Q

What happens in diabetic acidosis to potassium?

A
  • K+ moves out of cells
  • Osmotic diuresis means K+ is lost in urine
  • Total body depletion of K+
65
Q

What are conditions leading to metabolic alkalosis?

A
  • Severe prolonged vomiting or mechanical drainage of the the stomach leads to loss of H+. Stomach secretes more H+ and produces HCO3- in this process.
  • Potassium depletion/mineralcoritcoid excess
  • Certain diuretics
66
Q

How is metabolic alkalosis corrected?

A
  • Rise in pH of tubular cells leads to fall in H+ excretion and reduction in HCO3- recovery
  • Problems can occur is there is also volume depletion
67
Q

Why can problems occur with correction of metabolic alkalosis if there is volume depletion?

A
  • High Na+ recovery rate so capacity to loss HCO3- is reduced
  • Recovering Na+ favours H+ excretion and HCO3- recovery

Kofi: Pure Clinical Sem 3 (44 decks)

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