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Flashcards in Sodium Deck (25)
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What is a major extracellular cation?



What is the importance of Sodium?

It maintained ECF and therefore maintains effective circulatory volume


Where does the majority of sodium balancing occur?

In the kidneys:
-they change the filtration if there are fluctuations in GFRs
-low pressure baroreceptors in the atrium and pulmonary vessels and high pressure baroreceptors in the aorta and carotid sinus senses fluid vol. changes
-renal receptors respond by activating the renin-angiotensin-aldosterone system
-the Decreased perfusion causes renin to cleave to angiotensin converting it to angiotensin I and then to angiotensin II by angiotensin converting enzyme (ACE) in the lungs, which stimulates aldosterone release causing increased sodium reabsorption.


What is defined as hypernatraemia?

Sodium levels of >155mEq/L
Patients are also classified as Hyperosmolar and Hypertonic in ECF


What causes Hypernatraemia?

*Lack of water to consume
*Loss of free water
*Loss of hypotonic fluids
*Excessive gains in sodium


What are the clinical signs of Hypernatraemia?

At Na >170mg/L:
-Neuro: disorientation, behavior, seizures, coma due to water moving out of brain cells

Other signs: anorexia, vomiting, lethargy and ataxia

Chronic: osmolytes produced in the brain to prevent dehydration of brain

Acute: signs of vol. depletion / shock, pulmonary edema


What is the most common cause of Hypernatraemia?

Hypotonic water loss:
-vomiting, diarrhea, small intestinal obstruction, third spacing, burns, diabetes mellitus, mannitol, diuretic administration, chronic renal failure, non-oliguric acute renal failure, post obstructive diuresis

There will be signs of vol. depletion:
-Tachycardia, prolonged CRT, weak pulses

If losses are isotonic to ECF:
-no water movement
-entire loss by ECF compartment resulting in SHOCK


What are the uncommon causes of hypernatraemia?

Pure water loss:
-lack of drinking water, fever, high environmental tempt, central or neurogenic diabetes insipidus
-ECF becomes hypertonic compared to ICF causing fluid to move from ICF to ECF
-No sign of volume depletion

Excessive sodium gain:
-salt poisoning (neuro signs if acute) and administration of hypertonic fluid (hypertonic saline, sodium bicarbonate), TPN, sodium phosphate enemas, hyperaldosteronism (causes increase sodium reabsorption), hyperadrenocorticism

2 mechanism understood here:
1. Excessive addition of Na to ECF
2. Gain of a non-sodium impermeant solute (glucose and mannitol)
-draws water in ECF but causes osmotic diuresis where the solutes replaces Na in the urine which leaves Na in ECF leading to hypernatraemia


Treatment of hypernatraemia

*Replace water deficit and restore electrolyte balance
*Calculate free water deficit:
0.6 x BW kg X (1-140/serum Na) = L free water required

*Serum Na levels should not be lowered too quickly
-No more than 0.5mEq/L to minimize risk of neurologic problems
-Takes about 48-72 hours to correct water deficit


What fluids can be used to treat Hypernatraemia?

D5W (0)
0.45% NaCl with or without 2.5%dextrose (77)
LRS (130)
Normosol-R (140)
0.9% NaCl (154)


How to determine what type of fluids to use to treat HyperNatraemia?

1. If hyperNa present for more than 3 days: use 0.45 % or 0.9% NaCl

2. In pure water deficits
-acute vs chronic matters
-5% dextrose (D5W): 1L D5W = 1L free water
-do not restore free water too quickly = cerebral oedema

3. Hypotonic fluid losses
-isotonic fluids

4. Impermanet solute gains
-5% dextrose
-caution as ECF may already be expanded: normal patients will induce diuretics whereas diseased patients (renal or cardiac) may need loop diuretic

***Restore water deficits slowly over 48 hours***


What is defined as hyponatraemia?

Na < 135mg/dL


What disease processes causes hyponatraemia?

Hyperlipemia, hyperproteinemia, hyperglycaemia, mannitol, liver disease, CHF, nephritic syndrome, ADH secretion, antidiuretic drugs, myxedema coma (hypothyroid), hypotonic fluid administration, vomiting and diarrhoea, third spacing, burns, hypoadrenocorticism (due to lack of aldosterone) and the administration of diuretics


What are the clinical signs of hyponatraemia?

*Depends on how rapid the loss is
*Serum Na should not drop at a rate faster than 0.5 mEq/L/hr
*Not allowed to drop less than 120mg/dL
*Cerebral oedema and water intoxication
*Mild: lethargy and nausea, vomiting, depression which progresses to in coordination, seizures, coma and death
*Chronic: CNS has had time to adjust so signs will be absent


Hyponatraemia with normal plasma osmolality

*Due to abnormally high lipid content or protein in the serum
-results in pseudohyponatraemia (PHN) due to machine’s inability to read properly
*can be suspected when there is a normal osmolal gap with normal measured plasma osmolality


Hyponatraemia with increased plasma osmolality

Most commonly seen in hyperglycaemia or mannitol administration
-impermeable solutes causes fluids to move from ICF to ECF and increased osmolality of both
-Na becomes diluted = hypoNa
*Diabetes: each 100mg/dL increase in BG = decrease of 1.6 mEq/L Na
*Mannitol: concurrent increase in osmoloal gap


Hyponatraemia with decreased plasma osmolality

*must estimate total body sodium content and ECF vol.
*patients may have normal, decreased or increased sodium and ECF vol.
*Hx: find out fluid loss, Physical examination: hydration status and 3rd spacing, and diagnostics (PCV, TP, systemic BP and CVP)


HypoNa + plasma osmolality + vol. depletion= LARGE total body deficit of Na

-losses through: kidneys, GIT, 3rd spacing
*HypoNa with hypovolemia:
-CHF, severe liver dz, nephrotic syndrome
-perceived loss due to decreased effective circulatory vol.
-renin-angiotensin system activated = increased Na retention=impairs water excretion
-causes dilution of retained Na


Liver cirrhosis and nephrotic syndrome

*IVF vol. may decrease initially due to hypoalbuminemia
*low oncotic pressure
-vasopressin and renin-angiotensin system stimulated



Low CO=perceived low circulatory vol. = release of vasopressin


HypoNa with normovolemia

Due to:
* psychogenic polydipsia = low vasopressin release (syndrome of inappropriate antidiuretic hormone secretion - SIADH)
*administration of hypotonic fluids or anti diuretic drugs
*drugs that stimulate ADH secretion
*myxedema coma from severe hypothyroidism



1. Diagnose underlying dz or processes
2. Increase serum Na content I and plasma osmolality
3. Normalising fluid vol.


Tx for chronic hypoNa

*Tx is more dangerous than imbalance
*Brain dehydration that may result in osmotic demyelination (too rapid correction)


Tx of acute Na

*<24-48 hrs
*need prompt tx
*correct Na at a rate of <10-20 mEq/L/day (0.5 mEq/L/hr)


Tx of hypoNa

*Fluids: Isotonic replacement fluids (Normosol-R, LRS, and 0.9%NaCl)

*Serial Na serum measurements

*Restrict water in normovolemic patients
*Stop diuretic drugs
*Hypervolemic patients
-fed diets restricted in Na content
-use loop diuretics
*Administer ACE inhibitor
-improves SV and CO
-therefore decreases vasopressin secretion = increase water excretion