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Year 2 semester 3 respiratory system > Session 5 > Flashcards

Session 5 Flashcards

1
Q

Acid-Base Balance

A
  • Plasma pH must be maintained within a tight range
  • pH 7.35 –7.45
  • Very low but tightly regulated concentration of H+ ions – 44.5 –35.5 nmol.l-1
  • Plasma pH greater than 7.45 -Alkalaemia
  • Plasma pH less than 7.35 - Acidaemia
  • Dissolved CO2 reacts with water to form H+ and HCO3– Reversible reaction
  • Net direction depends on the concentrations of reactants and products
  • pH depends on how much CO2 reacts to form H+

– [CO2] dissolved pushes reaction to right

– [HCO3-] pushes reaction to left

CO2 + H2O ⇔ H+ + HCO3-

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2
Q

Alkalaemia

A

• Alkalaemia lowers free calcium by causing Ca2+ ions to come out of solution – Increases neuronal excitability

Normally bivalent cations are involved in charge shielding which is important with excitable membranes as this protects them and prevents them from getting too excitable. If you lower Ca concentration then the tissues become more excitable.

  • pH > 7.45 leads to paraesthesia and tetany
  • Alkalaemia can be very serious
  • 45% mortality if pH rises to 7.55
  • 80% mortality at pH 7.65
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3
Q

Acidaemia

A
  • Increases plasma potassium ion concentration – Effects excitability (particularly cardiac muscle)
  • arrhythmia
  • Increasing [H+] affect many enzymes
  • Denatures proteins
  • Effects muscle contractility, glycolysis, hepatic function
  • Effects severe below pH 7.1
  • Life threatening below pH 7.0
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4
Q

Plasma pH

A
  • pH depends on ratio of [HCO3-] to pCO2
  • pCO2 determined by respiration – Controlled by chemoreceptors – Disturbed by respiratory disease
  • [HCO3-] determined by the kidneys – Controlled by the kidney – Disturbed by metabolic and renal disease
  • pH = pK + Log ([HCO3-] /(pCO2 x 0.23))
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5
Q

How do the kidneys and lungs work together to control plasma pH?

A

Kidneys

• Control pH – variable recovery of hydrogen carbonate and active secretion of hydrogen ions

Lungs

  • 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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6
Q

pH of arterial blood

A
  • Determined by:
  • Ratio of pCO2 and [HCO3-]
  • HCO3- is made in red blood cells
  • But the concentration present is CONTROLLED by the kidneys
  • Normal concentration in arterial blood ~ 25 mmol.l-1

– Range 22 –26 mmol.l-1

– But can be changed to maintain pH

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7
Q

Acid production

A
  • Normally we produce acid due to metabolism
  • This does not deplete HCO3- because:

– The kidneys recover all filtered HCO3-

– Proximal tubule makes HCO3- from amino acids, putting NH4+ into urine

– Distal tubule makes HCO3- from CO2 and H2O; the H+ is buffered by phosphate and ammonia in the urine

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8
Q

Renal control of HCO3-

and creation of HCO3- in the PCT and DCT

A
  • HCO3- filtered at the glomerulus
  • Mostly recovered in PCT:

H+ excretion linked to Na+ entry in PCT - NaK ATPase creates concentartion gradient of sodium as it pumps it into the ECF allowing Na to enter the cell from the lumen in exchange for H+ ions.

Within the tubular cell there is Co2 and water which react to form H+ and HCO3- ,. The hydrogen ion is pumped into the lumen in the dosium hydrogen exchanger and the HCO3 leaves the cell into the ECF with a sodium via a sodium HCO3- cotransporter. The H+ that enters the lumen will react with HCO3 in the lumen to from CO2 and water which will both enter the cell from the lumen and be converted back into HCO3- which enters ECF

Creation of HCO3- in proximal tubule

•Glutamine → αketoglutarate – Produces HCO3- and ammonium (NH4+) – HCO3-enters ECF – NH4+ enters lumen (urine)

H+ buffering in kidney

  • 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 (‘titratable’) – Produce NH4+ and H2PO4- which are excreted
  • No CO2 is formed to re-enter the cell
  • Allows HCO3- to enter plasma

This takes place in alpha-intercalated cells of the DCT

  • Excretion of ammonium is the major adaptive response to an increased acid load in healthy individuals
  • Ammonium generation from glutamine in proximal tubule can be increased in response to low pH
  • NH4+ → NH3 + H+

– NH3 freely moves into lumen and throughout interstitium

– H+ actively pumped into lumen in DCT and CT

– H+ combines with NH3 → NH4+ (trapped in lumen)

– NH4+ can also be taken up in TAL and transported to interstitium and dissociates to H+ and NH3 → lumen of collecting ducts

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9
Q

H+ buffering systems in kidney

A

slide 13 lec 1

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10
Q

Acid Excretion

A
  • The minimum pH of urine is 4.5 (≈ 0.04mmol.l-1 H+)
  • No HCO3- (has all been recovered)
  • Some H+ is buffered by phosphate (titratable)
  • Some has reacted with ammonia to form ammonium
  • Total acid excretion = 50 – 100mmol H+ per day
  • This is needed to keep [HCO3-] normal
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11
Q

Relationship between H+ and potassium

A

• Acidosis → hyperkalaemia

– Potassium ions move out of cells

– Decreased potassium excretion in distal nephron

• Alkalosis → hypokalaemia

– Potassium ions move into cells

– Enhanced excretion of potassium in distal nephron

  • Hyperkalaemia makes intracellular pH of tubular cells more alkaline – H+ ions move out of the cells – This favours HCO3- excretion
  • Metabolic acidosis
  • Hypokalaemia makes the intracellular pH of tubular cells more acidic – H+ ions move into the cells – This favours H+ excretion and HCO3- recovery
  • Metabolic alkalosis
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12
Q

Things that disrupt acid-base balance

A

Ventilation and acid base balance

  • Hypoventilation → hypercapnia (pCO2 rises)
  • Hypercapnia → fall in plasma pH
  • That is respiratory acidosis (acidaemia)
  • Characterised by: – High pCO2 – Normal HCO3– Low pH
  • Hyperventilation → hypocapnia (fall in pCO2)
  • Hypocapnia → rise in pH
  • This is respiratory alkalosis (alkalaemia)
  • Characterised by: – Low pCO2 – Normal HCO3– Raised pH
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13
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-]
  • The kidneys increase [HCO3-] to compensate for respiratory acidosis
  • The kidneys decrease [HCO3-] to compensate for respiratory alkalosis
  • But takes time, 2-3 days
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14
Q

Compensated respiratory acidosis

A

• Characterised by: • High pCO2 • Raised [HCO3-] • Relatively normal pH

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15
Q

Compensated respiratory alkalosis

A

• Characterised by: • Low pCO2 • Lowered [HCO3-] • Relatively normal pH

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16
Q

Metabolic acid

A
  • If the tissues produce acid, this reacts with and removes HCO3
  • There is a fall in [HCO3-] → fall in pH
  • This is metabolic acidosis
  • Note the extra CO2 produced is breathed off at the lungs so there is no increase in arterial pCO2
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17
Q

The anion gap

A
  • Difference between measured cations and anions
  • ([Na+] + [K+]) – ([Cl-] + [HCO3-])
  • Normally 10 – 18 mmol.l-1

– Due to other anions that are not measured

  • This gap is increased if HCO3- is replaced by other anions
  • If a metabolic acid (such as lactic acid) reacts with HCO3- the anion of the acid replaces HCO3
  • In renal causes of acidosis anion gap will be unchanged – Not making enough HCO3- but this is replaced by Cl
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18
Q

Metabolic acidosis

A

• Initially characterised by – 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- replaced by Cl

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19
Q

Compensating metabolic acidosis

A
  • Peripheral chemoreceptor (carotid bodies) detect pH drop – Stimulate ventilation – Leading to decrease pCO2
  • Compensated metabolic acidosis is characterised by: – Low HCO3– Lowered pCO2 – Nearer normal pH
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20
Q

Metabolic alkalosis

A
  • If [HCO3-] increases this is metabolic alkalosis
  • Therefore will have: – 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 although not always possible
21
Q

Conditions leading to respiratory acidosis

A
  • Type 2 respiratory failure – Low pO2 and High pCO2 – The alveoli cannot be properly ventilated – Severe COPD, severe asthma, drug overdose, neuromuscular disease
  • Can be compensated for by increase in [HCO3-]
  • Chronic conditions can be well compensated such that pH near normal
22
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

– Low pCO2 with initial rise in pH

– Chronic hyperventilation can be compensated for by fall in [HCO3-]

– Can restore pH to near normal

23
Q

Conditions leading to metabolic acidosis

A

• If anion gap is INCREASED – indicates a metabolic production of an acid

– Keto-acidosis • diabetes

– Lactic acidosis • Exercising to exhaustion • Poor tissue perfusion

– Uraemicacidosis • Advanced renal failure – reduced acid secretion, build up of phosphate, sulphate, urate in blood

Conditions leading to metabolic acidosis with a normal anion gap

  • If anion gap is normal HCO3- is replaced by Cl
  • Renal tubular acidosis (This is a rare condition) – Problems with transport mechanisms in the 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

24
Q

Metabolic acidosis and potassium

A
  • Non-renal causes of metabolic acidosis cause increased reabsorption of K+ by kidneys
  • And movement of K+ out of cells → hyperkalaemia
  • However in diabetic ketoacidosis may be a total body depletion of K+ – K+ moves out of cells (due to acidosis and lack of insulin) – But osmotic diuresis means K+ lost in urine so need to give portassium and insulin
25
Q

Conditions leading to metabolic alkalosis

A
  • In metabolic alkalosis HCO3- is retained in place of Cl
  • Stomach is a major site of HCO3- production

– By-product of H+ secretion

– Severe prolonged vomiting - loss of H+

– Or mechanical drainage of stomach

• Other causes:

– Potassium depletion / mineralocorticoid excess

– Certain diuretics (loop and thiazide)

26
Q

Metabolic alkalosis correction

A

• [HCO3-] increase eg after persistent vomiting

– This should be very 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 HCO3recovery
  • 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

27
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
28
Q

How to interpret the values

A
  • If pCO2 is not normal, [HCO3-] is normal and pH has changed in opposite direction to pCO2 – Respiratory acidosis / alkalosis
  • If [HCO3-] is not normal, pCO2 is normal and pH has changed in the same direction as [HCO3-] – Metabolic acidosis / alkalosis
  • If pCO2 is high, [HCO3-] is raised and pH is relatively normal
  • Compensated respiratory acidosis
  • This is only scenario as we can’t compensate metabolic alkalosis
  • If [HCO3-] is low, pCO2 is low, pH is relatively normal
  • Could be either compensated respiratory alkalosis or compensated metabolic acidosis
  • If no respiratory disease or altitude exposure – unlikely to be respiratory
  • Check anion gap –if increased is metabolic acidosis
29
Q

Interpreting APG

A

use panopto slide 2 lec 2

30
Q

pH= 7.33 (7.35 – 7.45); PaCO2 = 7.6 kPa ( 4.7 – 6.0 kPa), HCO3- = 29.4 mmol.l-1 (22 -26) PaO2= 7.8 kPa (9.3-13.3) State his acid base status

A

(i) Respiratory acidosis (ii) compensation has started - because HCO3- is slightly elevated at 29.4 mmol.l-1 (iii) Partially compensated respiratory acidosis because pH is still low (despite compensation having started This is a patient with COPD with chronic type 2 respiratory failure. (

31
Q

pH= 7.5 (7.35 – 7.45); PaCO2 = 4.5 kPa ( 4.7 – 6.0 kPa), HCO3- = 26 mmol.l-1 (22 -26) PaO2= 13.3 kPa (9.3-13.3) State his acid base status

A

(i) Respiratory alkalosis (ii) No compensation yet - HCO3- is still in normal range (iii) Uncompensated respiratory alkalosis This is a patient with hyperventilation due to anxiety

32
Q

A 61 year-old man has vomiting and colicky central abdominal pain. On examination the abdomen is distended and increased bowel sounds are heard on auscultation. An abdominal x-ray suggests small bowel obstruction. ABG results: pH = 7.47 (7.35 – 7.45) PaO2 = 11.2 kPa (9.3-13.3) PaCO2 = 5.5 kPa (4.7-6.0) HCO3- = 29 mmol/L (22-26) What is this patients acid base status?

A

Metabolic alkalosis

33
Q

A 61 year-old man has vomiting and colicky central abdominal pain. On examination the abdomen is distended and increased bowel sounds are heard on auscultation. An abdominal x-ray suggests small bowel obstruction. ABG results: pH = 7.47 (7.35 – 7.45) PaO2 = 11.2 kPa (9.3-13.3) PaCO2 = 5.5 kPa (4.7-6.0) HCO3- = 29 mmol/L (22-26) What is the most likely cause of the acid base disturbance?

A

Vomiting → loss of H+ ions in vomitus

34
Q

A 18-year-old man is brought to the emergency department by his parents. He has recent weight loss, and has been vomiting in the last 24 hours. On examination he is confused. Heart rate = 110 bpm, BP = 80/ 60, Respiratory rate 20/min. He is clinically dehydrated. ABG results: pH = 7.3 (7.18) (7.35 – 7.45) PaO2 = 13 kPa (9.3-13.3) PaCO2 = 4.1 kPa (4.7) (4.7-6.0) HCO3- = 13 mmol/L (22-26) What is this patient’s acid base status?

A

C. Metabolic acidosis 

35
Q

A 18-year-old man is brought to the emergency department by his parents. He has recent weight loss, and has been vomiting in the last 24 hours. On examination he is confused. Heart rate = 110 bpm, BP = 80/ 60, Respiratory rate 20/min. He is clinically dehydrated. ABG results: pH = 7.3 (7.35 – 7.45) PaO2 = 13 kPa (9.3-13.3) PaCO2 = 4.1 kPa (4.7-6.0) HCO3- = 13 mmol/L (22-26) What is the most likely cause of his acid base status?

A

B. Diabetic ketoacidosis → ketoacids in the blood C. Dehydration →Hypotension → poor tissue perfusion → lactic acid production Both B and C are possible, need to measure random blood glucose plasma ketones and check urine for sugar and ketones

36
Q

A 72-year-old woman is admitted for treatment of a severe pneumonia. She is confused, heart rate = 120 bpm, BP is 70/50 mmHg. ABG results: pH = 7.29 (7.35 – 7.45) PaO2 = 8.8 kPa (9.3-13.3) PaCO2 = 5.5 kPa (4.7-6.0) HCO3- = 15 mmol/L (22-26) What is this patient’s acid base status?

A

Metabolic acidosis 

37
Q

An 72-year-old woman is admitted for treatment of a severe pneumonia. She is confused, heart rate = 120 bpm, BP is 70/50 mmHg. ABG results: pH = 7.29 (7.35 – 7.45) PaO2 = 8.8 kPa (9.3-13.3) PaCO2 = 5.5 kPa (4.7-6.0) HCO3- = 15 mmol/L (22-26) What is the most likely cause of her acid base status?

A

sepsis leads to hypotension so she gets poor tissue perfusion leading to higher lactic acid production

38
Q

A 32-year-old woman has sudden onset breathlessness and pleuritic chest pain. She returned from a holiday in Thailand 2 weeks ago. Apart from the oral contraceptive pill she is not on any medication. Examination: HR = 112 bpm, BP = 120/80, Respiratory rate = 32 /minute. ABG results: pH = 7.5 (7.35 – 7.45) PaO2 = 8.0 kPa (9.3-13.3) PaCO2 = 3.1 kPa (4.7-6.0) HCO3- = 21 mmol/L (22-26) What is this patient’s acid base status?

A

Partially compensated Respiratory alkalosis

39
Q

A 32-year-old woman has sudden onset breathlessness and pleuritic chest pain. She returned from a holiday in Thailand 2 weeks ago. Apart from the oral contraceptive pill she is not on any medication. Examination: HR = 112 bpm, BP = 120/80, Respiratory rate = 32 /minute. ABG results: pH = 7.56 (7.35 – 7.45) PaO2 = 8.0 kPa (9.3-13.3) PaCO2 = 3.1 kPa (4.7-6.0) HCO3- = 21 mmol/L (22-26) What is the most likely cause of her Acid base status?

A

Pulmonary embolism →Hypoxia → hyperventilation → low pCO2 

40
Q

A 26 year old man has severe diarrhoea due to food poisoning. On examination he appears mildly dehydrated. HR = 88 bpm, BP 120/80. Temp =370 C, abdominal examination is normal ABG results: pH = 7.3 (7.35 – 7.45) PaO2 = 13.3 kPa (9.3-13.3) PaCO2 = 4.1 kPa (4.7-6.0) HCO3- = 13 mmol/L (22-26) What is this patient’s acid base status?

A

C. Partially compensated Metabolic acidosis

41
Q

A 26 year old man has severe diarrhoea due to food poisoning. On examination he appears mildly dehydrated. HR = 88 bpm, BP 120/80. Temp 37°C, abdominal examination is normal ABG results: pH = 7.3 (7.35 – 7.45) PaO2 = 13.3 kPa (9.3-13.3) PaCO2 = 4.1 kPa (4.7-6.0) HCO3- = 13 mmol/L (22-26) What is the most likely cause of his acid base status

A

Diarrhoea → loss of HCO3 in stools

42
Q

A 22-year-old previously healthy woman is seen in the emergency department with breathlessness. ABG results: pH = 7.49 (7.35 – 7.45) PaO2 = 14 kPa (9.3-13.3) PaCO2 = 3.2 kPa (4.7-6.0) HCO3- = 22 mmol/L (22-26) What is this patient’s acid base status?

A

Uncompensated Respiratory alkalosis

43
Q

A 65-year-old man has shortness of breath of several months duration. He is a heavy smoker. On examination he is breathless. The chest is barrel shaped, and he is using accessory muscles of inspiration. ABG results: pH = 7.38 (7.35 – 7.45) PaO2 = 7.8 kPa (9.3-13.3) PaCO2 = 6.6 kPa (4.7-6.0) HCO3- = 28 mmol/L (22-26) What is this patient’s acid base status?

A

Compensated Respiratory acidosis

44
Q

Summarise CO2 in blood

A

• pH is determined by the ratio of [HCO3-]: [CO2] in the plasma • This ratio is 25mmol: 1.2 mmol (20:1) • There is 20 times more HCO3- in plasma than dissolved CO2 • Most of the extra x 20 amount of HCO3- was generated by the reaction of CO2 inside RBCs • the H+ produced inside RBC was mopped up by Hb, • The HCO3- enters the plasma establishing the 20:1 ratio • It is the 20:1 ratio that gives plasma its normal alkaline pH of 7.4

45
Q

Summarise respiratory acidosis

A

Respiratory acidosis • When CO2 retention occurs due to Hypoventilation (type 2 resp failure) The CO2 + H2O → carbonic acid → dissociates to generate H+ and HCO3• To keep pH the same, each extra CO2 molecule must be matched by 20 extra HCO3- ions. (This does not happen immediately) • the rise in [CO2] causes pH to drop. This is respiratory acidosis • The kidney starts to compensate by reabsorbing HCO3-and generating HCO3(for each H+ ion excreted, a HCO3- ion enters the blood) • the ratio returns towards 20:1, returning the pH towards normal (though now both CO2 & HCO3- are high)

46
Q

Summarise metabolic acidosis with respiratory compensation

A

• When lactic acid is added, HCO3- ions used up to buffer H+ ions. • Equation shifts to left. More CO2 formed • Not enough HCO3- to keep the [HCO3-]: [CO2] ratio at 20:1 → hence the pH will fall. • Acidosis (H+ ions) stimulates peripheral chemoreceptors and ↑pCO2 stimulates central chemoreceptors • Hyperventilation → CO2 breathed out slide 20 lec 2

47
Q

Renal compensation of respiratory acidosis is by recovery and creation of HCO3

A

slide 21 lec 2

48
Q

Summarise The anion gap

A

• Total anions = Total cations • But not all anions and cations are measured • Difference between measured cations and anions = the anion gap • ([Na+] + [K+]) – ([Cl-] + [HCO3-]) = Normally 10 – 18 mmol/L Example: Na+ =140, Cl-=110 K+ =4, HCO3-= 24 Then (140 + 4) – (110 + 24) = 10 mmol/L This 10 mmol/L are unmeasured anions like SO4–, phosphate, lactate, & protein anions present in the blood. • Increased anion gap seen in metabolic acidosis (some types) • where extra acid is generated (or added to the body) e.g. • In DKA – Ketoacids ( anion: acetoacetate ) • In hypoxia –lactic acid ( anion: lactate) • total cations = total anions • Also, the metabolic acid (e.g. lactic acid) reacts with HCO3- , so HCO3 level drops. • Example: patient with hypoxia, with extra lactate in blood • cations (148 + 5) = anions (110 + 15 + A- ) A- = all unmeasured anions • 153 – 125 = anion gap is 28 (higher than normal, because extra lactate is included) • In some renal causes of acidosis (renal tubular acidosis) the anion gap is unchanged HCO3- is low but this is replaced by Cl- (HCO3- low, but Cl- high)

Year 2 semester 3 respiratory system (13 decks)

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