lab investigations - salt/water/acid Flashcards
body fluids make up how much of our body weight?
60%
40% = Intracellular Fluid Compartment 20% = Extracellular Fluid Compartment
20% of our fluid is in the Extracellular Fluid Compartment - what is this made up of?
Interstitial
Intravascular
Transcellular
H2O in connective tissue
water and sodium balance are determined by what?
input
output (obligatory and controlled losses)
obligatory and controlled losses of water?
Obligatory losses
- Skin
- Lungs
Controlled losses – these depend on:
- Renal function
- Vasopressin/ADH (anti-diuretic hormone)
- Gut (main role of the colon)
obligatory and controlled losses of sodium?
Obligatory loss
-Skin
Controlled losses / excretion
- Kidneys
- Aldosterone
- GFR
- Gut - most sodium is reabsorbed; loss is pathological
what do controlled losses depend on?
depend on renal function
where does the majority of water get reabsorbed?
in the gut (colon)
where is majority of sodium lost?
kidney
hormones involved in sodium balance?
aldosterone
- produced in the adrenal cortex
- regulates sodium and potassium homeostasis
natriuretic hormones
- ANP cardiac atria, BNP cardiac ventricles
- promotes sodium excretion and decreases blood pressure
hormones involved in water balance?
ADH/vasopressin
- synthesised in hypothalamus
- stored in posterior pituitary
- release causes increase in water absorption in collecting ducts
Aquaporins
- AQP1 - proximal tubule, not under control of ADh
- AQP2 and 3 - collecting duct, under control of ADH
how does water move?
- moves across a semi-permeable membrane
- moves from a more diluted area to a more concentrated area, in order to maintain an osmotic balance across the membrane
what effect do osmotically active substances have?
osmotically active substances in the blood will result in water redistribution to maintain osmotic balance
water loss causes an increase in ECF osmolality - what happens as a result?
- stimulation of VP release
- stimulation of hypothalamic thirst centre
- redistribution of water from ICF
sodium reabsorption in the renal tubules
- majority of Na reabsorbed in PCT
- fine tuning in DCT, under the influence of aldosterone
- ADH acts in collecting duct to stimulate water reabsorption
sodium depletion will have what effect?
- will have a positive effect on JGC’s within the kidney
- JGC’s will produce renin
- Renin converts angiotensinogen to angiotensin I
- Angiotensin I stimulates the adrenal cortex to produce aldosterone
- ACE in the lungs converts angiotensin I to angiotensin II
what converts Ang I to Ang II?
ACE in the lungs
angiotensin converting enzyme
what is osmometry?
measuring the osmotic strength of a solution
Freezing point depression
- Uses colligative properties of a solution
- More solute – lower the freezing point
how is sodium measured in the body?
Indirect Ion selective electrodes (main lab analysers)
Direct Ion selective electrodes (Blood gas analyser)
increased water gain (and sodium loss), will cause what?
hyponatraemia
increased sodium gain can cause what?
hypernatraemia
how do 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
Fluid chart
explain the importance of managing fluid/electrolyte problems?
important to not do over rapid correction
-Important to correct sodium at the same speed, no more than 10mmol/L per 24 hours sodium change
over rapid correction of hyponatraemia can cause what?
central pontine myelinolysis
-rapid rise in sodium concentration is accompanied by the movement of small molecules and pulls water from brain cells
over rapid correction of hypernatraemia can cause what?
may lead to cerebral oedema
if your brain expands very rapidly, what happens?
it has nowhere to go except down through the base of the skull
if there are labs done on paired serum and urine osmolality and electrolytes, what is measured and what do the results mean?
Urea/creatinine ratio is useful
-Urea up a lot = dehydration
Serum osmolality
-Indicates if other osmotically active substances are present
Urinary sodium
Urinary osmolality
Urine /serum osmolality
>1 = water conservation
< 1 = water loss
Calculated Serum osmolality
2 x Na + urea + glucose (+/- 10)
290 = (2 x 140 = 280) + 5 + 5
how is blood pressure/volume sensed?
Baroreceptors
Renal perfusion pressure
what are actions that occur at the DCT?
Sodium reabsorption
Loss of H+/K+
what is an inevitable by product of ATP production?
large amounts of protons/hydrogen ions
why is maintenance of extracellular [H+]/pH essential?
to maintain correct protein/enzyme function
extracellular [H+]/pH level depend on what?
- relative balance between acid production and excretion
- carbon dioxide production and excretion (respiration)
- hydrogen ion production and excretion (renal)
H+ production and H+ excretion?
production
-carbonic acid and non-carbonic acids
excretion
-lungs and kidneys
pH = ?
-log10[H+]
ratio of HCO3/CO2
Henderson Hasselbalch equation
CO2 + H20 -> H2CO3 -> HCO3- + H+
all arrows are reversible
metabolic acidosis?
rate of H+ generation > excretion
respiratory acidosis?
rate of CO2 generation > excretion
how can alkalosis occur?
increased renal excretion of H+, regeneration of HCO3
how can acidosis occur?
increased retention of CO2
how does the body 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 do compensation speeds vary?
Respiratory compensation for a primary metabolic disturbance can occur very rapidly
Metabolic compensation for primary respiratory abnormalities take 36-72 hours to occur
how does respiratory compensation for a primary metabolic disturbance occur?
occurs very rapidly
example:
Kussmaul breathing (respiratory alkalosis) in response to DKA (diabetic ketoacidosis)
-deep and laboredbreathingpattern
how does metabolic compensation for primary respiratory abnormalities occur?
36-72 hours
requires enzyme induction from increased genetic transcription and translation
no compensation seen in acute respiratory acidosis such as asthma
requires more chronic scenario to include compensation mechanism
Mechanism of renal bicarbonate regeneration
renal lumen exchanges sodium for potassium, so sodium enters the tubular cell and H+ also leaves with potassium
tubular cell generates bicarbonate
what is ABG’s
arterial blood gases
Pitfalls of ABG?
Errors in blood gas analysis are dependent more on the clinician than on the analyser
- Expel air
- Mix sample
- Analyse ASAP
- Plastic syringes are ok at room temp for 30 mins
- Ice not required
- Ensure no clot in syringe tip
interpreting ABG’s - what do we look at?
pO2 remember to check FiO2
pH – ? Normal or does it show an acidosis or alkalosis
pCO2 – primary respiratory or compensatory response
HCO3 – metabolic component
what are the causes of respiratory acidosis (co2 retention)?
airway obstruction
-Bronchospasm (Acute), COPD (Chronic), Aspiration, Strangulation
respiratory centre depression
-anaesthetics, sedatives, tumours
neuromuscular disease
-Motor Neurone Disease
pulmonary disease
-Pulmonary fibrosis, pneumonia, Respiratory Distress Syndrome
extrapulmonary thoracic disease
-Flail chest
Respiratory acidosis - how to fix it
Increased renal acid excretion
-Requires return of normal gas exchange
what are the 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
Respiratory alkalosis - how to fix it
Increased renal bicarbonate excretion (metabolic acidosis, 36-72 hrs delay)
what are the causes of metabolic acidosis?
-Increased H+ formation
Ketoacidosis
Lactic acidosis
-Acid ingestion
Acid poisoning (methanol, ethanol)
XS parenteral administration of amino acids e.g. arginine
Decreased H+ excretion
- Renal tubular acidosis
- Renal failure
- Carbonic dehydratase inhibitors
Loss of bicarbonate
- Diarrhoea
- Pancreatic, intestinal or biliary fistulae/drainage
metabolic acidosis - how to fix it
Compensation
-hyperventilation, hence low pCO2
Correction
- of cause
- increased renal acid excretion
Features
-low pH, high [H+], low [HCO3-], low pCO2
what are the causes of metabolic alkalosis?
-Increased addition of HCO3-
-Increased loss of H+
GI loss, Gastric aspiration, vomiting with pyloric stenosis
-decreased excretion of HCO3-
metabolic alkalosis - how to fix it
Compensation
-hypoventilation with CO2 retention (respiratory acidosis)
Correction
- increased renal bicarbonate excretion
- reduce renal proton loss
Features
-high pH, low [H+], high [HCO3-], N/highpCO2
what is acidosis associated with?
Hyperkalaemia
Acidemia will tend to shift K+ out of cells and cause hyperkalemia
