27. Investigation of Salt & Water & Acid/Base Balance Flashcards
What are water and sodium balance determined by?
WATER •Intake - Dietary intake (Thirst) •Output - Obligatory losses - Skin - Lungs - Controlled losses – these depend on: - Renal function - Vasopressin/ADH (anti-diuretic hormone) - Gut (main role of the colon) •Redistribution
SODIUM •Intake - Dietary (unless vegan and doesn’t add salt) - Western diet 100-200 mmol/day •Output - Obligatory loss - Skin - Controlled losses / excretion - Kidneys - Aldosterone - GFR - Gut - most sodium is reabsorbed; loss is pathological
What are the hormones involved in water and salt balance?
•Sodium
- 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
- 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
How does osmotic pressure affect water movement?
Osmotically active substances in the blood may result in water redistribution to maintain osmotic balance but cause changes in other measured solutes
It 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 cells shrink (dehydrate)
What are the physiological responses to water loss?
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
How would you assess a patient with possible fluid/electrolyte disturbance?
History
- Fluid intake / output
- Vomiting/diarrhoea
- Past history
- Medication
Examination - Assess volume status
- Lying and standing BP
- Pulse
- Oedema
- Skin turgor/Tongue
- JVP / CVP
Why do we need to properly manage fluid/electrolyte problems?
- Hyponatraemia - Over-rapid correction may lead to central pontine myelinolysis
- Hypernatraemia - Over rapid correction may lead to cerebral oedema
What are some key laboratory investigations used in investigating salt and water balance?
Urea/creatinine ratio is useful
- Urea up a lot = dehydration
Serum osmolality
- Indicates if other osmotically active substances are present
Urinary sodium – ignore the reference interval
- <20 mmol/L = conservation
- > 20 mmol/L = loss
Urinary osmolality - ignore the reference interval
- Relate to the serum osmolality
Urine /serum osmolality
- > 1 = water conservation
- < 1 = water loss
Why do we need to investigate acid-base balance?
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. ~ depends on the relative balance between acid production and excretion
- carbon dioxide production and excretion (respiration)
- hydrogen ion production and excretion (renal)
How does the body compensate when acid/base balance is disrupted?
Attempt to return acid / base status to normal
- 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 - Compensation
- Diametric opposite of original abnormality
- Never overcompensates
- Delayed and limited - Treatment
- By reversal of precipitating situation
How fast do different acid/base compensations occur?
•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
What are some pitfalls of the ABG?
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 OK at room temp for ̴ 30mins
- Ice not required
- Need to ensure no clot in syringe tip
List some cause of respiratory acidosis
• 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
Describe the compensation, correction and features of respiratory acidosis.
•COMPENSATION:
- Increased renal acid excretion (metabolic alkalosis, 36-72 hrs delay)
•CORRECTION:
- Requires return of normal gas exchange
•FEATURES:
- acute: ↓pH (↑[H+]), ↑pCO2, normal HCO3-], ~ ie. no compensation
- chronic: ↓pH (↑[H+]), ↑pCO2, ↑[HCO3-], ~ ie. compensation
List some causes of respiratory alkalosis
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
Describe the compensation, correction and features of respiratory alkalosis.
•Compensation
- Increased renal bicarbonate excretion (metabolic acidosis, 36-72 hrs delay)
• Correction
- Of cause
•FEATURES:
- acute: high pH, low [H+], n[HCO3-], low pCO2 – no compensation
- chronic: high pH, low [H+], low [HCO3-], low pCO2
