IOD Fluid and Electrolytes Flashcards
Hypernatremia?
sodium gain or water loss
Hyponatremia?
Sodium loss or water gain
What determines thirst?
osmoreceptors-changes i ECM
Low pressure baroreceptors-great veins and RA of heart
High pressure-carotid sinus and aorta
Ang ii –renin-renal hypotension
Water intake and output?
Intake Dietary intake (Thirst) Output Obligatory losses Skin Lungs Controlled losses – these depend on: Renal function Gut (main role of the colon) Vasopressin/ADH (anti-diuretic hormone) Redistribution
Osmotic pressure?
Osmotically active substances in the blood may result in water redistribution to maintain osmotic balance but cause changes in other measured solutes
hyperosmolality-cells shrink
hyposmolality-cells swell
ADH?
ADH acts on renal collecting ducts to make them permeable to water
allows free water absorption and production of a concentrated urine controlling ECF osmolality
only ADH concs urine
Factors of ADH secretion?
Secretion stimulated by:
Increase in plasma osmolality (v. sensitive 1-2% change)
Pain, stress, nausea, drugs, lung and CNS lesions, ectopic
Decrease in plasma volume (>5-8%)
Secretion decreased by:
Decrease in plasma osmolality (plasma dilution)
Increase in plasma volume
Ethanol (resulting in diuresis)
main factor of adh?
ecf vol
responses to water deficiency?
high ECF osmolality
ADH-renal water retention
HT thirst centre-increased water-restoration of ECF
redistribution of water from ICF-increased ECF water
Sodium intake vs excretion?
Intake Dietary (unless vegan do not add salt) Western diet 100-200 mmol/day Output Obligatory loss Skin Controlled excretion Kidneys Aldosterone GFR Gut - most sodium is reabsorbed; loss is pathological
Renal sodium absorption?
PCT-most sodium reabsorbed, increases as sodium reabsorption does, water absorbed is isoosmotic
loop of henle-just sodium
DCT-secretion of K and H
RAAS-increases sodium reabsorption
How much Sodium is reabsorbed renally?
95-98%
sodium balance
Blood pressure/volume sensed- Baroreceptors- Renal perfusion pressure Aldosterone produced- Adrenal cortex Action at Kidney- Sodium reabsorption Loss of H+/K+
Important sodium values?
ref range-135-145 mmol/L
Life threatening-<115 >160 mmol/L
Assessing pts with fluid and electrolyte disturbances?
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
urea and creatinine?
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
urine/serum osmolality?
> 1 = water conservation
< 1 = water loss
when another molecule is present?
Calculated Serum osmolality = 2 x Na + urea + glucose (+/- 10)
5 for u and g if unknown
move water out of cells to balance osmolality so seems like hyponatremia but amount of sodium is the same
Potassium?
Mostly excreted
increased IC factors?
insulin-stimulates ATPase
B receptors
alkalosis
decreased IC factors?
a receptors
acidosis
osmolality-leakage
how is H linked to K?
pump exchanges H in and K out of cells in acidosis
Acidosis & Hyperkalaemia
Alkalosis & Hypokalaemia
Renal control of K?
Most K absorbed in PCT and LoH
Control in DCT and CD
aldosterone causes pump of sodium into cells linig tubule-depolarisation so K into tubule lumen
increased intake of K?
parenteral acidosis low insulin tissue damage artefactual
decreased loss?
Reduced GFR
Reduced tubular loss (potassium
sparing diuretics
anti-inflammatories, ACEIs,
mineralocorticoid deficiencyincreased loss?
Gut (diarrhoea, laxatives)
Kidney (diuretics,
magnesium deficiency,
mineralocorticoid XS
renal tubular abnormalities)
alkalosis
insulin
B agonistsdecreased intake?
alcohol
anorexia
artefact causes
Not using vacutainers
Narrow needles
Injecting blood through narrow needles into vacutainers
cause cell rupture or high EDTA/Mg levels increase K levels
types of hyponatremia?
Hypertonic hyponatraemia - glu (high plasma osmolality) Hypotonic hyponatraemia : volume status (low plasma osmolality) PseudohypoNa - trigs protein (normal plasma osmolality)
Hypovolaemia?
urine more than 20-
extra-renal salt loss
urine o less than 20-renal salt loss
causes of extra renal salt loss?
GI loss (replacement with hypotonic fluid) Vomiting Diarrhoea Skin loss Burns sweating Haemorrhage
renal salt loss causes?
Addison’s Diuretic Rx Salt losing nephritis Solute diuresis Cerebral Salt wasting
euvolaemia?
urine o more than 20- Acute H20 overload XS intake urine o less than 20- Chronic H20 overload Impaired excretion
Acute H20
overload
XS intake causes?
Psychogenic
Beer potomania
Iatrogenic
Chronic H20
overload
Impaired excretion causes?
SIADH Hypothyroid
Glucocorticoid deficiency
hypervolaemia?
urine o less than 20-oedema
oedema causes?
Cirrhosis Cardiac failure Nephrotic syndrome
usually + diuretic Rx
Control of sodium?
IV vol control-RAAS
SIADH
Euvolaemia ie. no evidence of volume depletion or oedema
Hyponatraemia and hypo-osmolality
Inappropriately high urine osmolality & excessive renal excretion of Na
Normal renal, adrenal, pituitary, thyroid
Not on any drugs (diuretics, antidiuretics)
DIAGNOSIS OF EXCLUSION !!
Clinical and biochemical improvement with fluid restriction
causes-Small cell carcinoma, TB or pneumonia
drugs increasing ADH?
Anticonvulsants : carbamazepine
Antineoplastics : cyclophosphamide
Hypoglycaemics : chlorpropamide
Narcotics : morphine
drugs potentiate ADH?
Tricyclics
SSRI’s : Prozac
Paracetamol
Indomethacin
Diuretics?
Thiazides,
frusemide,
K+ sparing (amiloride, spironolactone)
ineffective plasma vol causes?
low albumin diuretics increased fluid loss-oedema, ascites, facial oedema RAAS- sodium retention portal hypertension and splanchnic VD thirst water from ICF ADH -volume overrides osmolar controls so increased water hypovolaemic dilutional hyponatremia
Sodium can be found in?
Antibiotics and IV fluids
colloid (gelofusine and haemacel) and crystalloids (Hartmanns and saline)
Distribution of IV fluids?
colloid-plasma
saline/balanced crystalloids-interstitial and lymphatic
sodium chloride and glucose-IC and all
glucose-IC and all
hyponatremia management issues?
Over-rapid correction may lead to central pontine myelinolysis-rapid sodium uptake causes water movement out of cells so myelin destoyed-lockedin or death
hypernatremia management issues?
over rapid correction leads to cerebral oedema
water into plasma and csf into cells but witholding sodium causes water movement into cells-swelling
