Investigation of Salt and Water and Acid/Base Balance Flashcards

1
Q

What are the hormones involved in water and salt balance?

A

SODIUM BALANCE:

  • Aldosterone produced in the adrenal cortex: regulates sodium and potassium homeostasis
  • Natriuretic hormones (ANP cardiac atria, BNP cardiac ventricles) promote sodium excretion and decrease blood pressure

WATER BALANCE

  • ADH/vasopressin: synthesised in hypothalamus and stored in posterior pituitary. Release causes increase in water absorption in collecting ducts
  • Aquaporins (AQP1 proximal tubule and not under control of ADP) AQP2 and 3 present in collecting duct and under control of ADH
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2
Q

How does osmotic pressure affect water movement?

A

Osmotically active substances in the blood may result in water redistribution to maintain osmotic balance but cause changes in other measured solutes.

If there is excess solute in the cell, the water enters it to maintain the balance, making the cell swell (oedema).

If there is excess solute outside of the cell, water leaves the cell to maintain the balance, making the cell shrink (dehydrate).

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3
Q

What are the physiological responses to water loss?

A

With water loss, there is increased ECF osmolality. This leads to:

  • stimulation of vasopressin release, which causes renal water retention
  • stimulation of the hypothalamic thirst centre, increasing water intake
  • redistribution of water from the ICF, to increase ECF water

The aim of all these responses is to restore ECF osmolality.

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4
Q

How would you assess a patient with possible fluid/electrolyte disturbance?

A

HISTORY:

  • Fluid intake / output
  • Vomiting/diarrhoea
  • Past history
  • Medication

EXAMINATION - ASSESS VOLUME STATUS:

  • Lying and standing BP
  • Pulse
  • Oedema
  • Skin turgor/Tongue
  • JVP / CVP

FLUID CHART

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5
Q

Why do we need to properly manage the timing of correcting fluid/electrolyte problems?

A

With hyponatraemia, there can be over-rapid correction which may lead to central pontine myelinolysis.

With hypernatraemia, over-rapid correction may lead to cerebral oedema.

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6
Q

What are some key laboratory investigations used in investigating salt and water balance?

A

Urea/creatinine ratio:
- Urea up a lot = dehydration

Serum osmolality:
- Indicates if other osmotically active substances are present

Urinary sodium:

  • <20 mmol/L = conservation
  • > 20 mmol/L = loss

Urinary osmolality:
- Relate to the serum osmolality

Urine /serum osmolality:

  • > 1 = water conservation
  • < 1 = water loss
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7
Q

Why do we need to investigate acid-base balance?

A

Large amounts of protons/hydrogen ions are an inevitable by-product of energy/ATP production.

Maintenance of extracellular [H+]/pH is essential to maintain protein/enzyme function.
It depends on the relative balance between acid production and excretion
carbon dioxide production and excretion (respiration)
hydrogen ion production and excretion (renal).

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8
Q

How does the body compensate when acid/base balance is disrupted?

A

It attempts to return the acid/base status to normal by:

  1. BUFFERING
    - bicarbonate buffer in serum, phosphate in urine (for excretion)
    - skeleton
    - intracellular accumulation/loss of H+ ions in exchange for K+ , proteins and phosphate act as buffers
  2. COMPENSATION:
    - diametric opposite of original abnormality
    - never overcompensates
    - delayed and limited
  3. TREATMENT
    - by reversal of precipitating situation
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9
Q

How fast do different acid/base compensations occur?

A

RESPIRATORY compensation for a primary metabolic disturbance can occur very rapidly:
- Kussmaul breathing (respiratory alkalosis) in response to DKA

METABOLIC compensation for primary respiratory abnormalities take 36-72 hours to occur:

  • requires enzyme induction from increased genetic transcription and translation etc.
  • no compensation seen in acute respiratory acidosis such as asthma
  • requires more chronic scenario to include compensation mechanism
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10
Q

What are some pitfalls of the ABG?

A

The errors in blood gas analysis are dependent more on the clinician than on the analyser.

  • need to expel air
  • need to mix sample
  • need to analyse ASAP
  • plastic syringes are okay at room temperature for about 30 mins only
  • ice is not required
  • need to ensure that there is no clot in the syringe tip
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11
Q

List some causes of respiratory acidosis.

A

We are looking at the retention of carbon dioxide.

AIRWAY OBSTRUCTION:

  • Bronchospasm (Acute)
  • COPD (Chronic)
  • Aspiration
  • Strangulation

RESPIRATORY CENTRE DEPRESSION:

  • Anaesthetics
  • Sedatives
  • Cerebral trauma
  • Tumours

NEUROMUSCULAR DISEASE:

  • Guillain-Barre Syndrome
  • Motor Neurone Disease

PULMONARY DISEASE:

  • Pulmonary fibrosis
  • Respiratory Distress Syndrome
  • Pneumonia

EXTRAPULMONARY THORACIC DISEASE:
- Flail chest

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12
Q

Describe the compensation, correction and features of respiratory acidosis.

A

COMPENSATION:
- Increased renal acid excretion (metabolic alkalosis, 36-72 hrs delay)

CORRECTION:
- Requires return of normal gas exchange

FEATURES:

  • acute: ↓ pH (↑ [H+]), ↑ pCO2, →[HCO3-],– ie. no compensation
  • chronic: ↓ pH (↑ [H+]), ↑ pCO2, ↑ [HCO3-],– ie. compensation
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13
Q

List some causes of respiratory alkalosis.

A

HYPOXIA:

  • High altitude
  • Severe anaemia
  • Pulmonary disease

PULMONARY DISEASE:

  • Pulmonary oedema
  • Pulmonary embolism

MECHANICAL OVERVENTILATION

INCREASED RESPIRATORY DRIVE

  • Respiratory stimulants eg salicylates
  • Cerebral disturbance eg trauma, infection and tumours
  • Hepatic failure
  • G-ve septicaemia
  • Primary hyperventilation syndrome
  • Voluntary hyperventilation
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14
Q

Describe the compensation, correction and features of respiratory alkalosis.

A

COMPENSATION:
- Increased renal bicarbonate excretion (metabolic acidosis, 36-72 hrs delay)

CORRECTION:
- Of cause

FEATURES:

  • acute: ↑ pH, ↓ [H+], n[HCO3-], ↓ pCO2 – no compensation
  • chronic: ↑ pH, ↓ [H+], ↓ [HCO3-], ↓ pCO2
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15
Q

List some causes of metabolic acidosis.

A

ADDITION OF ACID:
Increased H+ formation, which can we due to:
- ketoacidosis
- lactic acidosis
- poisoning – methanol, ethanol, ethylene glycol, salicylate
- inherited organic acidosis

Acid ingestion, which can be due to:

  • acid poisoning
  • XS parenteral administration of amino acids e.g. arginine

H+ EXCRETION:

  • Renal tubular acidosis
  • Renal failure
  • Carbonic dehydratase inhibitors

LOSS OF BICARBONATE:

  • Diarrhoea
  • Pancreatic, intestinal or biliary fistulae/drainage
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16
Q

Describe the compensation, correction and features of metabolic acidosis.

A

COMPENSATION:
- hyperventilation, hence low pCO2

CORRECTION:

  • of cause
  • increased renal acid excretion

FEATURES:
- ↓ pH, ↑ [H+], ↓ [HCO3-], ↓ pCO2

17
Q

List some causes of metabolic alkalosis.

A

INCREASED ADDITION OF BASE:

  • Inappropriate reaction of acidotic states
  • Chronic alkali ingestion

DECREASED ELIMINATION OF BASE

INCREASED LOSS OF ACID:

  • GI loss
  • Gastric aspiration
  • Vomiting with pyloric stenosis

RENAL:

  • Diuretic reaction (not-K+sparing)
  • Potassium depletion
  • Mineralocorticoid excess- Cushing’s, Conn’s
  • Drugs with mineralocorticoid activity – carbenoxolone
18
Q

Describe the compensation, correction and features of metabolic alkalosis.

A

COMPENSATION:
- hypoventilation with CO2 retention (respiratory acidosis)

CORRECTION:

  • increased renal bicarbonate excretion
  • reduce renal proton loss

FEATURES:
- ↑ pH, ↓ [H+], ↑ [HCO3-], N/highpCO2