Electrolyte disorders Flashcards
Discuss how sodium and water balance are regulated
There are receptors in the hypothalamus (hypothalamic osmorecpetors) that detect changes in osmolality and induce compensatory mechanisms to return plasma to its hypothalamic setpoint. Two major mechanisms are the… ADH system and THIRST!
ADH system
Small peptide secreted by posterior pituitary gland
Two main stimuli for release (elevated plasma osmolality and dec. effective circulating volume)
Inc. plasma osmolality -> shrinks the osmoreceptors (special cells) in the hypothalamus , they send an impulse via nerve afferents to the posterior pituitary -> ADH release
Low effective circulating volume -> baroreceptor cells in the aortic arch and carotid bodies send neural impulses to the pituitary gland -> ADH release
ADH acts on the renal tubular collecting cells , activates V2 receptors on the renal collecting tubular cell and aquaporin-2 molecules are inserted into the cells luminal membrane.
Aquaporins are channels that allow movement of water molecules into the renal tubular cell. Water molecules cross through, into the hyperosmolar renal medulla down their osmotic gradient.
If the kidney is unable to generate a hyperosmolar renal medulla because of disease or diuretic admin, then water will not be reabsorbed, even with high conc of ADH. circulating ADH concentration and its normal effect on the kidney are prime physiologic determinants of free water retention and excretion.
Thirst
Hyperosmolality and decreased effective circulating volume also stimulate thirst. Similar to the mechanisms that stimulate ADH release. Thirst and resultant water consumption are the main physiologic determinants of free water intake
Plasma sodium is the MAIN determinant of plasma osmolality as shown below
Osmolality (mOsm/L) = 2[Na+] + [Glucose]/18 + [ BUN ]/2.8
(Gluc and BUN divided to convert them from mg/dl to mmol/L, and Na x 2 because it is considered that as Na major extracellular cation, that the sum of natraemia is equal to all the anions combined)
Understand the effects of osmolality on intracellular and extracellular fluid volume
Under normal physiological conditions, the RAAS monitors and fine-tunes effective circulating volume, and the ADH system maintains normal plasma osmolality.
Effective circulating volume is ALWAYS prioritised over plasma osmolality.
So a patient with poor effective circulating volume will have increased thirst and ADH release regardless of their osmolality. The free water intake (from drinking) and water retention(from ADH action at level of kidney) can lead to hypoNa (and therefore hypoosmolality) in patient with poor effective circulating volume. E.G patients with chronic CHF that present with hyponatraemia.
Total body sodium content vs plasma sodium concentration
TBS = total number of Na osmoles in the body, regardless of ratio Na:H20
Na content determines hydration status of an animal
Hydration used clinically is a misnomer, as skin tenting and moist mm are reflections of BOTH Na and water that the Na hold in the IS space.
If animal has increased TBS , and increased quantity of fluid is held within the IS and the animal appears overhydrated, regardless of the plasma sodium concentration. This may manifest clinically as ventral pitting oedema, excessive nasal discharge, gelatinous subcutis
If an animal has decreased TBS, a lower quantity of fluid is held within the IS and the animal appears dehydrated , regardless of the plasma sodium concentration. Patients with dehydration can become hypovolaemic as fluid shifts from the IV space into the IS space as a result of decreased IS hydrostatic pressure.
SO the sodium/water ratio is independent of the total body sodium content
A patient may be euhydrated, dehydrated, or overhydrated (normal, decreased or increased total body sodium content) and have a normal plasma sodium concentration, hypernatraemia OR hyponatreamia…FUN!)
List the common causes of hypernatremia and explain the mechanisms contributing to the development of sodium imbalance in each case
Most dogs and cats with hyperNa have excessive free water loss rather than increased sodium intake or retention.
Free water deficit
Denied water for extended periods
Vomiting, diarrhoea or polyuria of low-sodium urine
Activated charcoal containing a cathartic (cathartic draws electrolyte-free water into GI tract)
Mannitol (osmotic diuresis)
DI , when they do not drink water, because they cannot reabsorb free water in the renal collecting duct.
Hypodipsic hypernatraemia - associated with hypothalamic granulomatous meningoencephalitis, hydrocephalus and other CNS issues
Sodium excess - seawater, beef jerky, dough, hypertonic saline admin,
List the common causes of hyponatremia and explain the mechanisms contributing to the development of sodium imbalance in each case
Almost always free water retention in excess of sodium retention, may have sodium loss as well
Decreased effective circulating volume
-leads to ADH release, water intake increases, dec plasma sodium conc
Hypoadrenocortism
Decreased sodium retention (caused by hypoaldosteronism) combined with inc. water drinking and retention in defense of inadequate circulating ovlume
Also in atypical addisons as although their aldosterone production and release are normal, they have low circulating cortisol which increases ADH release and increased water retention regardless of intravascular volume status.
Diuretic
Three methods -
1. Induce hypovolaemia,
2. hypokalemia, that causes intracellular shuft of sodium in exchange for K+
3. inability to dilute urine
**Renal failure can cause hyponatreamia by similar methods. **
Discuss the management of hypernatremia, including the potential adverse effects of treatment
Have a free water deficit, so free water is replaced in the form of fluid with a lower effective osmolality than that of the patient
Must be cautious treatment
All cells affected that have Na/K - ATPase pumps (shrink) BUT because neurons are the least tolerant to this change in cell volume, we see neuro signs most commonly.
If patient develops hyperNa slowly they are often asymptomatic. Because of the physiologic adaptation discussed below…
Initial stages of hyperNa (early mins to hours) fluid is drawn from CSF into brain interstitium , then plasma osmolality rises, and Na and Cl move rapidly from CSF into cerebral tissue. This helps minimise brain volume loss by increasing neuronal osmolality and drawing water back into the IC space.
Within 24 hrs the neurons begin to accumulate organic solutes to increase intracellular osmolality and shift lost water back to the IC space. Full compensation can take 2-7 days, important to consider during treatment for hyper.
Can also be associated with hyperlipidaemia poss as a result of inhibition of lipoprotein lipase.
Clinical impact of this on correction of Hypernatraemia
Mild - moderate hypernatraemia
<180mEq/L , decrease Na no more rapidly than 1mEq/L/hr
Severe hypernatraemia
>180mEq/L , decrease no more rapidly than 0.5mEq/L/hr,
important to prevent cellular swelling.
Idiogenic osmoles are broken down slowly
If rapid drop in plasma Na (and therefore plasma osmolality) , then free water will move back in to the relatively hyperosmolar intracellular space and can lead to neuronal oedema.
Need to calculate the free water deficit , this is the total volume of free water that needs to be replaced.
This volume is usually given as 5% dextrose in water, infused over the number of hours calculated for safe reestablishment of normal plasma sodium concentration. Can be given IV or orally on an hourly schedule in animals that are alert, willing to drink and not vomiting.
Free water replacement along will not correct clinical dehydration or hypovolaemia , because it does not provide the sodium required to correct these problems.
Free water replacement in hypernatraemic animals is relatively safe, even in animals with cardiac or renal disease because two thirds of the volume administered will enter the cells.
the rate of free water replacement may be inadequate in cases of ongoing free water loss , as seen with diuresis of electrolyte-free water in DI or unregulated DM, but it is a safe starting point in most cases*
Monitor plasma sodium concentration at least every 4 hours
CNS status should be monitored continuously for signs of obtundation , seizures or other abnormalities.
Goal of tx = drop of plasma sodium conc. No greater than 1mEq/hr and no clinical signs of cerebral oedema.
Complications of therapy for hypernatraemia
Cerebral oedema ( obtundation, head pressing, coma, seizures)
If happens, immediately stop admin of any fluid that has a lower sodium conc than the patient and disallow drinking.
Re-measure plasma sodium conc. To confirm it is lower than when treatment was instituted. (important BECAUSE worsening hyperna can look similar to cerebral oedema) -> IF decreased , even if less than 1mEq/L/hr consider cerebral oedema
Cerebral oedema is treated with a dose of mannitol at 0.5/1g/kg IV over 20-30 mins , should be admin via a central vein if possible, but may be diluted 1:1 in sterile water and given through a peripheral vein in emergency
If mannitol not available or ig single dose doesnt improve signs, consider dose of 7.2% NaCl at 3-5ml/kg over 20 mins , similar admin to mannitol. Dont give as a rapid bolus as can cause vasodilation.
Discuss the management of hyponatremia, including the potential adverse effects of treatment
Plasma or serum sodium below reference interval (not total body sodium!)
Clinically detrimental hypona is uncommon in critically ill dogs and cats
Almost always have free water retention in excess of sodium retention, may have sodium loss as well. Usually requires water intake in addition to decreased water excretion.
Decreased effective circulating volume is a common cause -> ADH release, inc water intake to defend intravascular volume, -> decreased plasma sodium concentration
Possible causes -> CHF, excessive GI loss, excessive urinary loss, body cavity effusions, edematous states.
CHF - patient has increased total body sodium (is overhydrated) because of activation of RAAS , yet is hyponatraemic because of increased water retention in excess of sodium retention.
Excessive urinary or GI loss -> patient is total body sodium depleted (dehydrated) and is hyponatraemic as a result of compensatory water drinking and retention to maintain effective circulating volume.
Correction of hypo
Limit of 10mE2/l over first 24 hours then no more than 18 over 48 , total more important than the rate at any one period
If neuro signs during tx, stop admin of any fluid that is hyperosmolar to the patient (mannitol, hper or isotonic fluids)
Check serum na to see if it has truly increased, as worsening hypona can look similar .
Requires admin of free water, very difficult , could consider loop diuretic such as furosemide to clamp urine osmolality and replace water simultaneously.
Watch for myelinosis of the thalamus , delayed many days after intervention so not at the time
discuss pseudohyponatraemia
PSEUDOHYPONATRAEMIA
Hyponatraemia in a patient with normal or elevated plasma osmolality
Most commonly caused by hyperglycaemia (glucose is an effective osmole - cannot cross readily)
In hyperglycaemia, excess glucose molecules cause an increase in ECF water, filkuting sodium to a lower concentration. For each 100mg/dl increase in blood glucose, sodium conc drops by approx 1.6mEq/L , but the effect is non-linear
No specific treatment required, as hyperglycaemia resolves, water moves back into the cells and sodium concentration will increase
VOLUME EXPANSION IN HYPO OR HYPER NATRAEMIC PATIENT
Resusc with a fluid that has a sodium conentration that matches the patient
HYPO -> 130 or maintenance that has NAcL added to match the patient
HYPER -> balanced solution with NaCl added
Simplest way is to add 23.4% nacl to the bag, contains 4mEq NaCL/ml and so adds significant sodium in a small volume. (available in nz??)
Explain the effects of serum calcium and potassium on membrane potentials of cardiac cells
Serum calcium alters the threshold potential required for cell depolarisation. Ionized hypocalcaemia lowers the threshold potential, so makes cells more easily excitable (less depolarisation from Na influx required to tip them over the edge, for the self-perpetuating cycle to begin). Hypercalcaemia requires a greater than normal depolarisation for the threshold potential to be reached.
Potassium alters the resting potential.
Hypokalaemia increases the resting potential , which makes it more negative and hyperpolarises the cell.
Hyperkalaemia means that there are more potassium ions in the ECF than normal. This means that less K+ ions diffuse out of ICF along the concentration gradient, and the cell becomes more positive.
This causes a decrease in the resting potential, making it more excitable initially. Clinically we might see this in a blocked cat with a HR of 230bpm, but it is not often seen as this is the early stages of hyperkalaemia.
As hyperkalemia worsens, and the ECF conc increases further, the RM potential falls even further and goes BEYOND the threshold potential which leaves the cell in a permanent state of depolarisation.
a.k.a
Once the resting potential is decreased to below the threshold potential, the cell depolarises and is not repolarised, and the cell is no longer excitable.
So with lack of conduction and muscle contraction we see the cardinal signs of hyperK
-muscle weakness
- bradycardia
- slowed cardiac conduction
-hypotension
Action potential and cell excitability is important for skeletal muscle, cardiac muscle, nerves and transporting epithelia.
As a cells membrane potential changes, so too does its permeability to ions. If an area of a cell suddenly becomes more permeable to sodium, then it will RUSH in along its concentration gradient and make that area more positive.
In excitable cells there is a gradual movement of ions which makes the ICF less negative, so from -90 to -60.
-60 = threshold potential, once this is reached the cell is very permeable to sodium, it rushes in, and makes the ICF suddenly positive.this is called DEPOLARISATION and is the beginning of the action potential. Then everything either flows or gets pumped back to where it should be and the cell charge returns to its resting potential. This is called REPOLARISATION
Excitability = how easily a cell can be depolarised. Depends on the difference between the resting and threshold potential (less difference = more excitable)
List the electrocardiographic changes seen with hyperkalaemia
Initial stages just a bradycardia. Then see a gradual loss of P wave size until no P wave present and a gradual increase in T wave “tenting”
Initial stages could see higher amplitude T waves and shortening of the QT due to increased repolarisation. The slower repolarisation is because there is a smaller concentration gradient of K+ than normal (higher K+ ECF), so the normally rapid efflux of K+ out of the ICF is prolonged.
Later on see prolonged PR interval and widening of the QRS complex due to slowing of the conduction through the AV complex. As hyperkalemia worsens, conduction through the atria is impaired so we see a decrease in amplitude and widening of the P wave.
In advanced cases see cessation of atrial conduction, so no P wave, pronounced bradycardia and a sinoventricular rhythm may be observed. In extreme cases the QRS complex merges with the T wave which can create a sinus pattern, which then progresses to ventricular fibrillation or asystole.
In cats can also see wide-complex tachycardia without identifiable P waves
So basically
Atrial inexitability
Depressed conduction through the specialized tissues and ventricular muscle
Lead to axis deviations, widening of QRS complex and v.asystole or v.fib
List the common causes of hyperkalaemia and explain the mechanism(s) contributing to potassium imbalance in each case
Decreased urine excretion
Urethral obstruction
Ruptured bladder
Anuric or oliguric renal failure
Hypoadrenocorticism
Translocation (ICF->ECF)
Acute mineral acidosis (HCL, NH4Cl)
The h+ concentration goes up, then it is pumped into cells, and K+ flows OUT to maintain electroneutrality. The ECF K+ goes up.
NOTE - organic acidosis (lactic or keto) do NOT cause this transcellular shift most likely because they are transported into cells along with H+ And don’t change electroneutrality that would lead to K+ wanting to exit to fix
Insulin deficiency (dka) RARE, because diabetics havemore going on that causes K+ to fall
Reperfusion of extremities in cats with thromboembolism and DCM
Blockade of B2 receptors can cause ECF K+ to increase
List the common causes of hypokalaemia and hyperkalaemia and explain the mechanism(s) contributing to potassium imbalance in each case
(depletion OR redistribution)
Decreased intake
Admin of potassium-free fluids over several days
Translocation (ECF -> ICF)
Alkalaemia
Insulin/ glucose-containing fluids
Hypothermia
Refeeding syndrome
Increased loss
GI loss (vomiting or diarrhoea)
Urinary loss
Chronic acidosis leads to H+ into ICF, K+ gets kicked out to maintain electroneutrality, but then continual loss from ICF , over time this is excreted , so net loss of k+ from the body.
Chronic renal failure in cats
Post-obstructive diuresis
Mineralocorticoid excess (hyperadrenocorticism)
Loop diuretics
DKA
Discuss the management of hyperkalaemia, including the mechanism by which each management strategy affects potassium concentration or clinical condition
Iv fluids
Dilutes K+
Restores blood volume
Promotes renal excretion of K+
Nacl or LRS fine (4mmol/L in there so not too much to affect them plus bonus of helping with acidosis which reduces K) if you have to wait a long time before correcting the cause then go for NaCL
Calcium gluconate
Immediate onset , cardioprotectvie action (no effect on K+ conc)
Lasts 20-30 mins , can give a second dose if deteriorates again
50-100mg/kg IV (0.5-1ML/kg of 10%)
Give 1ml/min without ecg, faster if ecg
Calcium makes threshold membrane less negative , so increases the diff between resting and threshold, allowing action potential to be generated
Sidenote - hypocalcaemia will make the threshold potential more negative, decreasing the difference between resting and threshold, and make the cells unable to repolarise and generate another action potential. So we see weakness, bradycardia, similar signs to kyperK
Dextrose +/- insulin
Onset within the hour
Lasts a few hours
Regular (soluble) insulin 0.25-0.5IU/kg IV
2g dextrose per UNIT of insulin as a bolus at time
And add 2.5% dextrose to iv fluids (for next 12 hours or so)
Insulin pushes glucose into cells via NaK pump, so glucose goes IN and so too does K+, reducing ECF K+.
If they dont have ECG abnormalities, you could just give glucose, and let the body’s natural insulin push it in, but if they have abnormal ecg then give insulin also
DO NOT GIVE if hypovolaemia, correct this first otherwise arrhythmias and death
Soluble insulin iv is supposed to only last 4 hours but can last longer, so make sure to keep the dextrose going for 8 hours (monitor that their k+ doesnt go too low though)
Sodium Bicarb
Works by reducing ECF [H+] , so H+ flows out of the cell, and K+ flows IN to maintain electroneutrality.
Onset within the hour and lasts a few hours
Not first line treatment, go for calcium first!
1-2mEq/kg IV (or ⅓ of the SBE on blood gas) slowww over 10 mins
SIDE EFFECTS
Hypernatraemia
Hyperosmolality
Acute CV collapse if given rapidly
Paradoxical intracellular and CSF acidosis
Diuretics and peritoneal dialysis
Diuretics for severe oliguric/anuric renal failure only
Dialysis for uroabdomen and anuric renal failure
Giving calcium to increase the resting potential, buys time while treat the initial cause
Understand how chloride concentration affects acid base balance
Chloride and bicarbonate ions are the two most common anions in the body that have a single negative charge. This means when chloride concentration increases, bicarbonate is excreted, and a metabolic acidosis results.
When chloride concentration decreases, bicarbonate is reabsorbed, so a metabolic alkalosis develops
Be able to calculate a corrected chloride concentration and use this to guide therapy
