Acid Base Balance & Arterial Blood Gases Flashcards

1
Q

buffers that exist in the body

A

proteins
haemoglobin
Carbonic acid/bicarbonate

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2
Q

what are the three situations in which a acid-base disturbance would occur

A
  • There is a problem with ventilation
  • There is a problem with renal function
  • Overwhelming acid or base load the body can’t handle
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3
Q

what is standard bicarbonate

A

calculated from the actual bicarbonate but assuming 370C and a paCO2 of 5.3kPa

this reflects the metabolic component of acid base balance

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4
Q

base excess

A

value calculated from blood pH & pCO2. Defined as the amount of acid required to restore a litre of blood to its normal pH at a PCO2 of 5.3. Normal range -2 - +2mmol/L. Becomes more negative in metabolic acidosis

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5
Q

Metabolic problems

A

overwhelming acid load
• Bodies own production (endogenous)
• Ingestion (exogenous source)
• Failure of excretion/ regeneration bicarb by the kidneys

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6
Q

condition causing hypoperfusion

A

– Of the whole body: shock (cardiogenic, septic, hypovolaemic, anaphylactic)
– Or part of the body: femoral artery embolism

increased anaerobic metabolism with
subsequent increased production of lactic acid Lactic acidaemia

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7
Q

Lactic acid

A

• Product of anaerobic metabolism
• In health lactate is metabolised in liver and overall there is no NET
production of acid
HOWEVER this process needs oxygen so therefore

Production increases whenO2 delivery falls AND consumption of lactate by the liver falls

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8
Q

Other causes of lactic acidaemia

A
  • Severe acute hypoxia
  • Severe convulsions (resp arrest)
  • Strenuous exercise (dehydration
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9
Q

lactate normal marker

A

> 2mmol/L marker of concern

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10
Q

Situa􏰀ons of ↓ insulin & ↑ glucagon

A

–Uncontrolled diabetes mellitus (severe, life- threatening)
– Alcoholic ketoacidosis (common clinically)
– Starvation ketoacidosis (mild)
Ketoacidosis

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11
Q

Monitoring response to treatment: KDA

A

bedside measurement of capillary blood ketones
• Venous blood should be used rather than arterial (unless respiratory problems dictate otherwise) in blood gas analysers

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12
Q

Exogenous acid load

A

Accidental / deliberate ingestion

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

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13
Q

Renal causes of metabolic acidosis (variable anion gap)

A

Functions of the kidney re: bicarbonate
• Reabsorbs filtered bicarbonate
• Regenerates bicarbonate consumed by buffering
• Renal failure both acute and chronic (↑gap) • Renal tubular acidosis (normal gap)

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14
Q

Gastrointestinal causes of metabolic acidosis (normal anion gap)

A
  • Much of gut below pylorus secretes bicarbonate into gut lumen
  • For every bicarb ion into gut a H+ ion enters ECF
  • Diarrhoea this process increases
  • AND volume depletion renin/angiotensin/aldosterone axis stimulated retaining chloride
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15
Q

Compensation for metabolic problems

A

Slow metabolic (renal) compensation correction
–Secrete more acid (therefore also make NEW bicarbonate)
– plasma H+ decreases (pH rises) and plasma bicarbonate rises to normal
BUT ONLY IF :
1. The metabolic acidaemia is of non-renal origin
2. The kidneys are functioning effectively.

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16
Q

To compensate for a metabolic acidosis…

A

pCO2 must fall, therefore minute volume must increase
• 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

17
Q

• Kussmaul respiration

A

a laboured deep, rapid pattern of breathing

18
Q

Metabolic alkalosis (alkalaemia)

A
  • 2 processes have to happen:
  • An initiating process
  • A maintaining process
19
Q

Most common initiating process of metabolic alkalosis

A

Loss of H+ ions
From the gut (above the pylorus)
–From the kidney ( furosemide & thiazide)

20
Q

Maintenance of the alkalosis

A
  • A process which impairs the kidneys ability to excrete bicarbonate
  • Hypokalaemia
  • Aldosterone Excess
  • Volume & chloride depletion group