2. Clinical aspects of Acid-Base control Flashcards

1
Q

1kPa=

A

7.5mmHg

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2
Q

What are the main buffers that maintain body pH?

Excretion of acid by?

A

Proteins
Haemoglobin
Carbonic acid/ bicarbonate

Excretion by lungs and kidneys

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3
Q
Normal values for:
• pH
• pO2
• pCO2
• Bicarbonate
(standard)
A
  • pH = 7.35 – 7.45
  • pO2 = 12 -13 kPa
  • pCO2 = 4.5 – 5.6 kPa
  • Bicarbonate (standard) = 22 – 26 mmol/l
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4
Q

What is standard bicarbonate?

A

Standard bicarbonate is calculated from the actual bicarbonate but assuming 370C and a paCO2 of 5.3kPa.
It reflects the metabolic component of acid base balance

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5
Q

How is ABGs assessed?

A

Step 1: Assess pO2 and oxygenation
Step 2: Assess pH
Step 3: Determine primary problem
Step 4: Is compensation occurring?

Hint: If pH and pCO2 are changing in the same direction the primary problem is metabolic
If in opposite direction, the primary problem is respiratory

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6
Q

How is pO2 and oxygenation assessed?

A

PaO2/FiO2 ratio (P/F ratio)
If P/F ratio > 50 = Healthy
If P/F ratio < 40 = Acute lung injury
If P/F ratio < 26.7 = ARDS

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7
Q

What is 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

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8
Q

If pCO2 and bicarb are moving in the same direction compensation, what is happening?

A

Compensation

If moving in opposite direction, suspect a mixed disorder.

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9
Q

Anion gap:
What is it?
Calculated from?
Formula?

A

The sum of routinely measured cations (+ve) in venous blood minus routinely measured anions (-ve). Indicator for metabolic acidosis
Calculated from venous blood
Anion gap= ([Na+] + [K+]) - ([Cl-] +[HCO3-])

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10
Q

Increased anion gap signals?

A

Presence of metabolic acidosis

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11
Q

Normal value for anion gap?

A

16

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12
Q

Causes of increased anion gap (metabolic acidosis)

A

Bodies own production (lactic acidosis, ketoacidosis)
Ingestion (exogenous source)
Failure of excretion by the kidneys

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13
Q

How can the bodies own production of acid result in an increased anion gap and then lactic acidosis?

A

Any condition causing hypoperfusion

  • Of the whole body: Shock (carcinogenic, septic, hypovolaemic, anaphylactic)
  • Of part of the body: Femoral artery embolism

Results in increased anaerobic metabolism with subsequent increased production of lactic acid = LACTIC ACIDOSIS

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14
Q

What two processes result in lactic acid build up?

A

Fall in O2 delivery

Fall in the consumption of lactate by the liver

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15
Q

How can the bodies own production of acid result in an increased anion gap and then ketoacidosis?

A

Situations of decreased insulin and increased glucagon.
E.g.
-Uncontrolled diabetes mellitus (severe, life threatening)
-Alcoholic ketoacidosis (common clinically)
-Starvation ketoacidosis (mild)

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16
Q

How does exogenous acid load leads to an increased anion gap?

A

Accidental/deliberate ingestion of e.g.

  • Methanol (industrial solvent, windscreen wash)
  • Ethylene glycol (anti-freeze)
17
Q

What are the renal causes of metabolic acidosis? What are there affects on the anion gap?

A

Renal failure, both acute and chronic, increased gap

Renal tubular acidosis, leads to normal gap

18
Q

Why does the kidney function alter the anion gap?

A

As the kidneys:

  • Reabsorbs filtered bicarbonate
  • Regenerates bicarbonate consumed by buffering
19
Q

Two causes of a normal anion gap with metabolic acidosis?

A

Diarrhoea

Renal tubular acidosis

20
Q

GI causes of metabolic acidosis with normal anion gap?
Why?
What procedures lead to a similar pathology?

A

Diarrhoea and volume depletion (leading to RAAS and chloride retention)

Why? As gut below pylorus secretes bicarbonate into gut lumen. For every bicarbonate ion secretes, an H+ ion enters the ECF

Procedures? Ileostomy, colostomy

21
Q

Compensation for metabolic problems?
Accompanying slow metabolic correction?
Conditions for correction?

A

RESPIRATORY compensation: pCO2 must fall, so minute volume must increase

Metbalolic correction stages:
1. Leads to slow metabolic correction. Secretes more acid (therefore also makes NEW bicarbonate).
2. Plasma H+ decreases (pH rises)
3. Plasma bicarbonate rises to normal
Conditions:
-The metabolic acidaemia is of non-renal origin
-The kidneys are functioning effectively.

22
Q

How is the breathing described during compensation of metabolic acidosis?

A

Kussmaul respiration: A laboured deep, rapid pattern of breathing

23
Q

Maximal compensation for metabolic problems can take…
Limited by?
Upper range of resp volume

A

• Maximal compensation can take up to 24hrs
• Respiratory compensation is limited by the
work involved in breathing
• Can increase minute volume up to about 30l/min but difficult to maintain

24
Q

Where is carbonic anhydrase found?

A

RBC

Tubule cells

25
2 processes of metabolic alkalaemia:
Initiating: - Loss of H+ ions (from gut above pylorus in *pyloric stenosis*, from the kidney due to diuretics) - Gain of exogenous alkali Maintenance of the alkalosis: -Process which impairs the kidneys ability to excrete bicarbonate e.g. *chloride depletion group*, potassium depletion group
26
In which situation is exogenous alkali gained?
Massive blood transfusion
27
How does chloride depletion cause metabolic alkalaemia?
Chloride and bicarb are the only anions present in appreciable quantities in the ECF. If chloride is low in renal tubular fluid, bicarbonate must be reabsorbed to maintain electrical neutrality
28
Compensation for metabolic alkalis
* pH =  HCO3/pCO2 * pCO2 must increase minute volume must fall * Difficult to predict extent...
29
GO LOOK AT SLIDE 39 OF LECTURE
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