Investigation of Salt & Water and Acid/Base Balance Flashcards
Total body fluids weight?
- Extracellular fluid compartment
- Interstitial
- Intravascular
- Transcellular
- H2O in connective tissue - Intracellular fluid compartment
60% of body weight
- 20%
- 15%
- 5%
- 1%
- <1%
- 40%
What determines the water and sodium balance?
- Intakes and Output of Water and Sodium
- Redistribution of water
Water intake
Dietary intake (Thirst)
Water output
Obligatory losses
- Skin
- Lungs - lose water when cold
Controlled losses - these depend on:
- Renal function
- Vasopressin/ADH - controls loss of water from kidneys
- Gut - the main role of the colon: lots of water secreted into gut then reabsorbed.
Sodium intake
- Dietary (unless vegan and doesn’t add salt)
- Western diet 100-200 mmol/day
Encouraged to take less salt a day
Sodium output
Obligatory loss
- Skin: lose water during the day due to sweat
Controlled losses/excretion:
- Kidneys
- Aldosterone (mineralocorticoid)
- GFR
- Gut: most sodium is reabsorbed; unless lost pathologically.
Hormones that are involved in the balance of sodium (with water)
- Aldosterone: produced in the adrenal cortex; regulates sodium and potassium homeostasis; if there is a disorder, it will have profound effects and the sodium levels of the body are affected.
- Natriuretic hormones (ANP and BNP): promote sodium excretion and decrease blood pressure
Hormones that are involved in the balance of water (with sodium)
- ADH/vasopressin: synthesized in the hypothalamus and stored in the posterior pituitary. release causes an increase in water absorption in collecting ducts
- Aquaporins (AQP1 proximal tubule and not under the control of ADP) AQP2 and 3 in the collecting duct and under control of ADH
Osmotic pressure and water movement
Water moves across a semi-permeable membrane from a low osmolality to a high osmolality down a concentration gradient.
Osmotically active substances in the blood may result in water redistribution to maintain osmotic balance but cause changes in other measured solutes.
3 Physiological responses to water loss
- a) Low water triggers the release of vasopressin
b) There is an increase in osmolality which triggers the brain
c) This increases water intake - ADH increases water absorption: most is reabsorbed in the kidneys and is dependent on the filtering rate of the kidneys
- Aldosterone mechanism that is dependent on the perfusion rate of the kidney
Where is most sodium reabsorbed?
In the kidney
The mechanism for a person with hypertension
- Positive action on the juxtaglomerular cells in the kidney.
- Renin is activated and converts angiotensinogen into angiotensin I then ACE converts into angiotensin 2 in the lungs
- Then this increases the release of aldosterone which affects the sodium levels.
Osmometry
- Used to see if someone has taken alcohol
- Freezing point depression is measured
- > If more salt = lower freezing point
- > Also vapor pressure ones, however, cannot be used to measure volatile substances
- > Uses colligative properties of a solution
- > More solute - lower the freezing point
What types of electrodes can be used to measure Sodium levels?
- Indirect ion-selective electrodes (main lab analyzers): dilution of the sample that enters the electrode and gets a result coming out
- Direct ion-selective electrodes (blood gas analyzers): measures activity of ions rather than concentration
Hypernatraemia
More water loss, more sodium gain
Hyponatraemia
More water gain, more sodium loss
Normal sodium
Water loss and Sodium Loss; Water gain and Sodium gain
How to assess a patient with possible fluid/electrolyte disturbance?
- History of: 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
What can over-rapid correction of hyponatremia cause?
Over-rapid correction may lead to central pontine myelinolysis (brain shrinks)
What can over-rapid correction of hypernatraemia cause?
Over-rapid correction may lead to cerebral oedema
- Limited scope, therefore, if it expands rapidly it could cause a lot of damage.
Why is it important to correct sodium at the same speed?
Important to correct sodium at the same speed no more than 10mmol/L per 24 hours sodium change
What investigations are used to look at serum and urine osmolality and electrolytes?
- Urea/creatinine ratio is useful
- Serum osmolality: indicates if other osmotically active substances are present
- Urinary sodium: < 20 mmol/L and > 20 mmol/L -> switch off sodium excretion to conserve
- Urinary osmolality: relates to serum osmolality -> concentrated urine -> water conservation
- Urine/serum osmolaltiy: >1 = water conservation and < 1 = water loss -> indicates if other osmotically active substances are present.
When is calculated serum osmolality used?
Only useful if you think something else is present
= 2 x Na + urea + glucose (+/- 10)
290 = (2 x 140 = 280) + 5 + 5
Hypertonic hyponatremia
High glucose
Pseudohyponatraemia
High triglycerides and high protein
- Looks like cream and lots of protein if someone has a myeloma
Hypotonic hyponatremia
Volume status
Hypovolaemic
- Low circulating volume = low BP
What happens if salt is below 20mM?
Look at urine sodium and if salt is below 20mM then there is extra-renal salt loss - can be through GI loss - vomiting, diarrhea, skin loss burns, sweating and haemorrhage
Euvolemic
Normal circulating volume + normal BP
- Below 20 mM: - acute water overload, excess intake; due to psychogenic polydipsia, a beer that is weak, polomania and ketogenic
- Above 20 mM: - due to chronic water overload - impaired excretion; no water loss - SIADH when producing vasopressin/ADH is appropriate, can also have hypothyroid and glucocorticoid deficiency
What happens if sodium levels are above 20mM?
- Then there is a renal salt loss.
- Addison’s disease: where you cannot produce cortisol, aldosterone and taking diuretics
What senses blood pressure/volume?
- Baroreceptors and renal perfusion pressure
What produces aldosterone?
Adrenal cortex
Action at DCT
Sodium reabsorption
Loss of H+/K+
What is a byproduct of energy/ATP production?
Large amounts of protons/hydrogen ions are an inevitable by-product. The body controls our blood levels at nanomolar amounts however, we produce millimolar amounts protons.
What is needed to maintain protein/enzyme function?
Maintained by extracellular [H+]/pH
- depends on the relative balance between acid production and excretion.
- dependent on how much acid you produce and how much acid you are able to excrete.
- > Carbon dioxide production and excretion (respiration)
- > Hydrogen ion production and excretion (renal)
What are some threats to the normal pH level?
H+ production:
- Carbonic acid (volatile) 15,000 mmol/Day
- Non-carbonic acids (non-volatile) 80 mmol/Day
H+ excretion:
- 15,000 mmol/Day from the lungs
- 80 mmol/Day from the kidneys
Make sure the extracellular fluid is 40 nmol/L and the pH is 7.4
pH and [H+]
The higer the pH; the lower the hydrogen ion concentration.
- pH is proportional to the carbonic acid
pH =-log10[H+]
Henderson Hasselbalch equation
Say it - google it
Metabolic acidosis
- Rate of H+ generation is more than excretion
- Buffering - consumption of HCO3 should be reduced
- Removal of CO2
Respiratory acidosis
- Rate of CO2 excretion is less than the generation
- Increased retention of CO2
- Increased renal excretion of H+ and regenerate HCO3
What is compensation?
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
- Someone who has renal failure will take up H+ into the skeleton
Compensation
- Diametric opposite of original abnormality
- Never overcompensates
- Delayed and limited -> takes time as you need to replenish proteins through transcription and translation
Treatment
- By reversal of the precipitating situation
- If you have metabolic acidosis, compensate by developing respiratory alkalosis
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 takes 36-72 hours to occur
- Requires enzyme induction from increased genetic transcription and translation etc
- No compensation see in acute respiratory acidosis such as asthma
- Requires more chronic scenario to include compensation mechanism
Mechanism of renal bicarbonate regeneration
- Takes place at the renal lumen - exchanges sodium for potassium
- The potassium is switched off into the urine.
- The buffer system - water and CO2 produces carbonic acid which will break down to hydrogen ions and bicarbonate.
- Depending on which part of the kidney:
- > proximal tubule - reclaiming part of the bicarbonate
- > distal tubule - regenerate bicarbonate
- The H+ is removed from the kidneys:
- > When removing H+, you can’t remove potassium as well.
- > Need electrical neutrality across the membrane; therefore either lose hydrogen or potassium.
- There is a reuptake of sodium and hydrogen is then lost.
How long does a blood gas machine run for and what is it used for?
Used for ABG readings and can run for 2 hours on a battery pack
Modulator of the blood gas machine
Blood gas components can measure sodium, potassium, creatinine, glucose, and iron etc.
How to carry out a blood gas reading?
- Expel air
- Mix sample
- Analyse ASAP
- Plastic syringes OK at room temp for 30 mins
- Ice is not required
- Ensure no clot in syringe tip
Pitfalls of ABG
Errors in blood gas analysis are dependent more on the clinician than on the analyser
How to interpret ABG readings?
- PO2 remember to check F1O2 -> influence the partial pressure concentration
- pH - Normal or does it show an acidosis or alkalosis
- PCO2 - primary respiratory or compensatory response
- HCO3 - metabolic component: calculated by using the H-H equation
Causes of respiratory acidosis through CO2 retention
Airway obstruction:
- Bronchospasm (Acute)
- COPD (chronic)
- Aspiration
- Strangulation
Respiratory centre depression:
- Anaesthetics
- Sedatives
- Cerebral trauma
- Tumours
Neuromuscular disease:
- Guillain-Bare syndrome
- Motor neurone disease
Pulmonary disease:
- Pulmonary fibrosis
- Respiratory distress syndrome
- Pneumonia
Extrapulmonary thoracic disease
- Flail chest
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: decrease in pH (increase in [H+]), increase in pCO2, no change [HCO3-], i.e. no compensation
- Chronic: decrease in pH (increase in [H+]), increase in pCO2, increase in [HCO3-], i.e. compensation
There is only an increase in bicarbonate when you have compensation
Causes of respiratory alkalosis: low pCO2 removing carbon dioxide
Hypoxia:
- High altitude
- Severe anaemia
- Pulmonary disease
Pulmonary disease:
- Pulmonary oedema
- Pulmonary embolism
Mechanical overventilation
Increased respiratory drive:
- Respiratory stimulants e.g. salicylates
- Cerebral disturbance e.g. trauma, infection and tumours
- Hepatic failure
- G -ve septicaemia
- Primary hyperventilation syndrome
- Voluntary hyperventilation
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 - compensation
Causes of metabolic acidosis: increased addition of acid
Increased H+ formation:
- Ketoacidosis
- Lactic acidosis
- Poisoning - methanol, ethanol, ethylene glycol, salicylate
- Inherited organic acidosis
Acid ingestion:
- Acid poisoning
- XS parenteral administration of amino acids e.g. arginine
Causes of metabolic acidosis: Decreased H+ excretion through the loss of bicarbonate
- Renal tubular acidosis
- Renal failure
- Carbonic dehydratase inhibitors
- Diarrhoea
- Pancreatic, intestinal or biliary fistulae/drainage
Compensation, Correction, and Features of Metabolic acidosis
Compensation:
- Hyperventilation, hence low pCO2
Correction:
- Of cause
- Increased renal acid excretion
Features:
- low pH, high [H+], low [HCO3-], low pCO2
Causes of metabolic alkalosis
Increased addition of base:
- Inappropriate Rx of acidotic states
- Chronic alkali ingestion
Decreased elimination of base
Increased loss of acid:
- GI loss
- > Gastric aspiration
- > Vomiting with pyloric stenosis: a lot can cause damage to the oesophagus and dissolve teeth
Renal:
- Diuretic Rx (not K+ sparing)
- Potassium depletion
- Mineralocorticoid excess-Cushing’s, Conn’s
- Drugs with mineralocorticoid activity - carbenoxolone
Compensation, Correction, and Features of Metabolic alkalosis
Compensation:
- Hypoventilation with Co2 retention (respiratory acidosis)
Correction:
- Increased renal bicarbonate excretion
- Reduce renal proton loss
Features:
- high pH, low [H+], high [HCO3-], N/high pCO2
Hypovolaemia from persistent vomiting - Metabolic alkalosis
Metabolic alkalosis
- Loss of HCl
- Loss of potassium
- Loss of fluid stimulates the RAAS system
- Try to reabsorb Na+ and water in exchange for potassium and H+ ions
Diuretics - Metabolic alkalosis
Chronic K+ depletion
Response to fluid loss is aldosterone activation - Metabolic alkalosis
Reabsorb NaCl/H2O at distal convoluted tubule in kidney in exchange for K+/H+
Why is it important to get rid of the hydrogen ions instead of the potassium ions?
To have:
- Redistribution: the potassium will redistribute between the intracellular and the extracellular fluid rapidly - will cause acidosis.
- This will cause artefactual hyperkalaemia.
Artefactual hyperkalaemia
False hyperkalaemia
