Clinical Aspects Of Acid-Base Control Flashcards

1
Q

What is 1kPa in mmHg?

A

7.5mmHg

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2
Q

Steps of assessing ABGs?

A

Step 1 - Assess pO2 and Oxygenation
Step 2 - Assess pH, acidaemia or alkalaemia?
Step 3 - Determine the primary problem (think about the patient)
Step 4 - Is compensation occurring?

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3
Q

PaO2/FiO2 ratio

A

P/F ratio > 50 = healthy
P/F ratio < 40 = acute lung injury
P/F ratio < 26.7 = ARDS

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4
Q

Compensation

A

Altering in function of the respiratory or renal system to change the secondary variable in an attempt to minimise an acid/base imbalance.

Body will never overcompensate.

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5
Q

Compensation is most likely occurring when…

A

pCO2 and bicarbonate are moving in the same direction - if going different directions suspect a mixed disorder.

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6
Q

Anion Gap

A
  • Sum of routinely measured cations in venous blood minus routinely measured anions. ([Na+] + [K+]) - ([Cl-] + [HCO3-])
  • Calculated from venous blood.
  • Should be equal - normal anion gap is 16
  • Increased anion gap signals the presence of a metabolic acidaemia, helps differentiate cause of it.
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7
Q

Lactic Acidaemia

A

Increased anaerobic metabolism with subsequent increased production of lactic acid.
Causes include any condition which causes hypoperfusion (shock, femoral artery embolism), severe acute hypoxia, severe convulsions, strenuous exercise/dehydration

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8
Q

Lactic Acidaemia

A

Increased anaerobic metabolism with subsequent increased production of lactic acid.
Causes include any condition which causes hypoperfusion (shock, femoral artery embolism), severe acute hypoxia, severe convulsions, strenuous exercise/dehydration.

Addition of lactic acid increases anion gap, HCO3- falls because it is used to buffer protons.

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9
Q

Lactate marker of concern

A

> 2mmol/L

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10
Q

Ketoacidosis

A
  • increased anion gap
  • decreased insulin and increased glucagon - uncontrolled diabetes mellitus, alcoholic ketoacidosis and starvation ketoacidosis
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11
Q

Ketone Blood Test Values

A
  • Below 0.6mmol/l - normal
  • 0.6 - 3mmol/L - follow sick day rules - ensure fluid intake adequate, additional short acting insulin, retest blood glucose and ketones in hour
  • Over 3.0mmol/l - Risk of DKA
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12
Q

Exogenous Acid Load

A
  • Accidental/deliberate ingestion will cause an increased anion gap.
  • Methanol and Ethylene Glycol
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13
Q

Renal Causes of Metabolic Acidosis

A
  • Renal failure (acute and chronic)

- Renal Tubular Acidosis

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14
Q

Normal Anion Gap Metabolic Acidosis

A
  • Diarrhoea

- Renal Tubular Acidosis

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15
Q

GI Causes of Metabolic Acidosis (normal anion gap)

A
  • much of gut below pylorus secretes bicarbonate into gut lumen
  • for every bicarbonate ion into gut a H+ ion enters ECF
  • diarrhoea this process increases
  • and volume depletion, therefore renin/angiotensin/aldosterone axis stimulated retaining chloride

similar pathology - laxative abuse, ileostomy and colostomy

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16
Q

Metabolic Acidosis with Normal Anion Gap

A

Decrease in HCO3-, increase in Cl-.

17
Q

To compensate for a metabolic alkalosis

A

pCO2 must increase therefore minute volume must fall

18
Q

To compensate for a metabolic acidosis..

A

pCO2 must fall, therefore minute volume must increase. Kussmaul respiration - a laboured deep rapid pattern of breathing.

Maximal compensation can take up to 24hrs. Respiratory comp is limited. Can increase minute volume to 30l/min.

19
Q

Compensation for metabolic acidaemia…..

A
  • Is respiratory!!!!!
  • Slow metabolic (renal) correction - secrete more acid (making new bicarbonate), plasma H+ decreases (pH rises) and plasma bicarbonate rises to normal. But only if: metabolic acidaemia is of non-renal origin and kidneys are fuctioning effectively.
20
Q

Metabolic Alkalaemia

A
  • Least common because the kidney is very good at excreting bicarbonate.
  • 2 processes have to happen - initiating process and maintaining process.
  • most common initiating process - loss of H+ ion from either gut (above pylorus) or from the kidney (due to furosemide and thiazide)
21
Q

Maintenance of the Alkalosis

A

Processes which impair the kidneys ability to excrete bicarbonate:

  • Hypokalaemia
  • Aldosterone Excess
  • Volume & chloride depletion group
22
Q

Pyloric Stenosis

A
  1. In health parietal cell secrete H+ into lumen of the stomach. The bicarbonate is secreted into the ECF.
  2. Gastric fluid also contains Na+, water and K+ (5-10mmol/l)
  3. Initially excess bicarbonate is spilled in the urine but accompanied by a cation.
  4. Worsening volume depletion results in aldosterone secretion (RAAS)
  5. Sodium and water retained exacerbating hypokalaemia - losing K+ through vomiting and kidneys.
22
Q

Pyloric Stenosis

A
  1. In health parietal cell secrete H+ into lumen of the stomach. The bicarbonate is secreted into the ECF.
  2. Gastric fluid also contains Na+, water and K+ (5-10mmol/l)
  3. Initially excess bicarbonate is spilled in the urine but accompanied by a cation.
  4. Worsening volume depletion results in aldosterone secretion (RAAS)
  5. Sodium and water retained exacerbating hypokalaemia - losing K+ through vomiting and kidneys.
22
Q

Pyloric Stenosis

A
  1. In health parietal cell secrete H+ into lumen of the stomach. The bicarbonate is secreted into the ECF.
  2. Gastric fluid also contains Na+, water and K+ (5-10mmol/l)
  3. Initially excess bicarbonate is spilled in the urine but accompanied by a cation.
  4. Worsening volume depletion results in aldosterone secretion (RAAS)
  5. Sodium and water retained exacerbating hypokalaemia - losing K+ through vomiting and kidneys.
22
Q

Pyloric Stenosis

A
  1. In health parietal cell secrete H+ into lumen of the stomach. The bicarbonate is secreted into the ECF.
  2. Gastric fluid also contains Na+, water and K+ (5-10mmol/l)
  3. Initially excess bicarbonate is spilled in the urine but accompanied by a cation.
  4. Worsening volume depletion results in aldosterone secretion (RAAS)
  5. Sodium and water retained exacerbating hypokalaemia - losing K+ through vomiting and kidneys.
22
Q

Pyloric Stenosis

A
  1. In health parietal cell secrete H+ into lumen of the stomach. The bicarbonate is secreted into the ECF.
  2. Gastric fluid also contains Na+, water and K+ (5-10mmol/l)
  3. Initially excess bicarbonate is spilled in the urine but accompanied by a cation.
  4. Worsening volume depletion results in aldosterone secretion (RAAS)
  5. Sodium and water retained exacerbating hypokalaemia - losing K+ through vomiting and kidneys.