Electrolyte disturbances and fluid imbalance Flashcards
What does a loop diuretic do?
Inhibits the Na-K-Cl co-transporter in the thick ascending limb of the loop of Henle preventing the reabsorption of NaCl
Indications for use of a loop diuretic?
Heart failure (acute and chronic) Resistant hypertension (esp. in renal impairment)
Side effects
Opposite of normal effects e.g. could lead to hypotension, hyponatraemia, hypokalaemia, hypocalcaemia, hypochloraemia causign alkalsosis
Gout
Hyperglycaemia (less common than thiazides)
Renal impairment (dehydration and toxicity)
Ototoxicity
What is the effect of activating the RAAS?
Release of renin from kidney due to stretch receptors in kidneys -> angiotensin II
Vasoconstriction
Release of aldosterone from adrenal cortex which increases reabsorption (also K and H excretion)
Release of ANP from the heart which increases the GFR
Release of BNP from the brain which decreases the release of renin and angiotensin II
> 3 days on fluids requires what?
Food via oral/enteral/paraenteral route
What is colloid?
Fluid that stay in the intravascular space and exert oncotic pressure due to large molecules e.g. blood, human albumin or synthetics like gelafusin
What are colloids used for?
Resuscitation
What is a crystalloid
A fluid that distributes itself to water compartments in the body and does not remain intravascular (a little) like glucose, NaCl and saline
Which compartment does glucose 5% go to?
Mainly intracellular
Interstitial and lymphatic
(a little to intravascular)
Which compartment does NaCl 0.18% and glucose 4% go to?
Intracellular
Interstitial and lymphatic
(a little to intravascular)
Which compartment does saline 0.8% go to?
Interstitial and lymphatic
a little to intravascular
Which compartment does balanced crystalloid go to?
Interstitial and lymphatic
a little to intravascular
Which compartment does colloid go to?
Intravascular
Daily maintenance fluids:
1L normal saline 0.9% + 2L 5% dextrose with added K
OR 3L dextrose saline with K
Who is glucose 5% a good fluid for?
Dehydrated patient who is hypernatraemic
Who gets a daily maintenance dose?
Patient who can’t meet fluid/electrolyte needs orally/enterally but has no complex replacement or distribution issues
OR post-successful resuscitation with no signs of shock
1st line resuscitation
IV bolus of crystalloid e.g. saline - should raise BP after 15-20 minutes if dehydrated
When will an immediate IV bolus of crystalloid not restore blood pressure?
Cardiogenic shock (after immediate bolus you should seek help)
After immediate bolus what do you do if there are no signs of shock?
Give boluses up to 2000ml then seek help
Protocols for raising serum Na?
Raise by 4-6 mmol/L over a few hours
Raise by no more than 8 mmol/L per day
What is the danger of raising Na too quickly?
Can cause central pontine myelinolysis
Example of a balanced crystalloid?
Hartmann’s
Treatment for chronic hypernatraemia?
Hypotonic fluid given slowly e.g. dextrose 5% lower by no more than 10 mmol/L/day
Treatment for acute hypernatraemia?
Lower by 1-2 mmol/L/hour to normalise in 24 hours
Treatment for hypervolaemic hyponatraemia?
Treat cause
Fluid restrict
ADH receptor antagonist
What is nephrogenic diabetes insipidus?
Renal water loss
What is central diabetes insipidus?
Lack of ADH
Hormonal cause of hypernatraemia?
Hyperaldosteronism (salt retention)
Treatment for hypovolaemic hyponatraemia?
Correct the volume depletion e.g. with IV 0.9% saline
ECG of hypokalaemia:
Slightly peaked P wave Prolonged PR ST depression Flat/shallow T wave U wave QT interval prolonged
Hypokalaemia treatment:
Correct Mg levels
K replacement 10-20mmol/hour + cardiac monitoring
Address cause
ECG of hyperkalaemia
Sine wave Tall tented T wave Shortened QT PR lengthened Widened QRS No P waves
Hyperkalaemia treatment
IV calcium gluconate - antagonises the membrane potential of high K
IV insulin with glucose to drive K into cells
NaCl or beta-agonists to drive K into cells
Loop diuretics, haemodialysis/filtration to remove excess K
Endocrine cause of hyperkalaemia?
Addison’s disease (aldosterone insufficiency)
What is Addison’s disease?
Auto-immune primary adrenal insufficiency
Deficiencies of cortisol and aldosterone
Clinical features of Addison’s disease?
Lethargy, weakness, anorexia, N+V, weight loss, salt craving
Hyperpigmentation esp. in palmar creases, vitiligo
Loss of pubic hair in women
Hypotension
Hypoglycaemia
Crisis: collapse, shock, pyrexia
Primary causes of hypoadrenalism:
TB Metastases (e.g. bronchial carcinoma) Meningococcal septicaemia (Waterhouse-Friederichson syndrome) HIV Anti-phospholipid syndrome
Secondary causes of hypoadrenalism:
Pituitary disorders (e.g. tumours, irrigation, infiltration)
Other cause of hypoadrenalism
Exogenous glucocorticoid therapy
Differential of Addison’s and secondary hypoadrenalism:
Primary Addison’s is associated with hyper pigmentation whereas secondary is not
Which drugs cause sexual dysfunction?
Thiazide diuretics
