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1.
2. , ma
Normal
Range
137-145 mEq/L
137-145 mmol/L
2.7-4.5 mg/dL in adults
0.8-1.3 mmol/L (inorganic phosphate)
Hypo-Na Hyper-Na Hypo-P Hyper-P
Etiology Water excess, Fluid loss, Renal disease,
Diuretics, SIADH, Congestive heart
failure, Cirrhosis, Nephrosis
Excess water loss , Ecxess sodium
intake, Diabetes insipidus,
Diuresis, Sweating, GI fistula, Burns
Intracellular shift of Pi, Increase in renal Pi loss
Decrease in gastrointestinal Pi absorption
Renal failure, inadequte renal excretion,
increased movement of Pi out of cells,
increased Pi or Vit D intake
Common
Signs/
symptoms
Lethargy, weakness, irritability, nausea,
restlessness, seizures, confusion,
somnolence, coma
Lethargy, anorexia, nausea,
emesis, fatigue, seizures, confusion,
coma
confusion, weakness, seizures, respiratory
failure, heart failure
Muscle cramps, perioral tingling,
paresthesia, ventricular arrythmias
Approach Water restriction
Sodium supplement
Hypertonic solution
Hypotonic solution, Sodium
restriction, Diuretics
mild: give enteral phosphorus replacement
severe: give parenteral phosphorus
replacement
Correction of associated hypocalcemia,
Restricting intake, Increasing urinary
excretion , Increasing GI losses
Treatment Free water restriction (<1L/day)
Increasing free water excretion with
loop diuretics
Increased sodium administration
[Na] <115 to 120mEq/L require
agressive therapy
Calculate the free water deficit, total
body water, free water replacement
Parenteral free water replacement
with goal:
1/2 of free water defeicit in first 24
hrs, Remaining over next 48 hrs
Mild: enteral
Severe (<1mg/Dl) Pi or symptomatic: IV
phosphate administration
Calcium Supplementation of
hyperphosphatemic hypocalcemic patients
should be delayed until serum phosphate
had fallen below 2mmol/L (6mg/dl)
Doses Severe: initially 1-2 mL/kg/hr to
increase plasma [Na] by 1-2 mEq/L/hr,
then slow down
Must not exceed 1-2 mEq/L in any 1
hour and above 8 mEq/L in 24 hours
Once plasma Na exceed 120-125
mEq/L, water restriction alone is
sufficient to normalize Na
Acute hypernatremia: < 1-2mEq/L/hr
for first few hours
Chronic hypernatremia (>48 hours):
<0.5 mEq/L/day
Maximum change of 8 to 10
mEq/L/day
Dose: 0.2 mM-0.68 mM/kg (5-6mg/kg) over 12
hours
If chronic hypoP: 7-15 mmol of phosphate can
be infused per hour, magnitude of infusion
must be roportional to the severity of
symptoms
Oral therapy can be a substitute for parenteral
Pi once the serum Pi levels exceed 2mg/dL.
Continued therapy with Pi supplements is
required for 5-10 days
Increasing urinary excretion
Saline
Acetazolamide (500mg every 6
hours)
Increasing GI losses
by enteric administration of
aluminum hydroxide (30-45mL every
6 hours)
Rapid increase in plasma sodium
concentration = Osmotic
Rapid correction may result in
cerebral edema and neurologic injury
Close monitoring of serum Pi, Ca, Mg, and K is
essential to avoid complications
3. Potassium abnormalities Calcium abnormalities Magnesium abnormalities
Normal
range
3.5-5.0 mEq/L
3.5-5.0 mmol/L
4.2-5.2 mg/dL (ionized)
1.05-1.30 mmol/L (ionized)
1.8-2.3mg/dL 1.5-1.9 mEq/L
0.75-0.95mmol/L
Hypo-K Hyper-K Hypo-Ca Hyper-Ca Hypo-Mg Hyper-Mg
Etiology GI losses
Poor nutrition or
starvation
Diuretics
Alkalosis
Increased intake
Renal dysfunction
Tissue trauma
Acidosis
Drugs
Decreased intake of vit D,
Hypoparathyroidism, Massive
transfusion,
Pancreatitis,Rhabdomyolysis,
Burns, Sepsis, Liver or kidney
disease
Hyperparathyroidism,
Thyrotoxicosis, Excess
intake of vitamin A and
vitamin D, Malignancy,
Granulomatous disease,
Immobilization
Alcoholism, GI losses,
hyperparathyroidism,
hyperaldosteronism,
intracellular shift of fluid,
Renal failure
hypothyroidism, renal
failure
Common
signs and
symptoms
cardiac arrhythmias,
ileus, fatigue, muscle
weakness and paralysis
Muscle weakness, confusion,
n/v,
Paralysis, areflexia, asystole,
Cardiac hypoexcitability, heart
block
Laryngospasm, apnea,
seizure, Muscle cramps,
Weakness, muscle spasm,
tetany, paresthesia,
numbness, Traouseau and
chvostek sign
Bones (bone pain)
Stones (kidney stone)
groans (constipation)
psychic moans (fatigue,
depression, confusion),
Renal and cardiac failure
Weakness, abdominal
cramping, hyperreflexia,
cardiac arrhtyhmias,
refractory hypokalmea and
hypocalcemia, seizures,
confusion, coma
sedation, areflexia,
diarrhea, paralysis,
coma, cardiac
arrhtyhmias,
complete heart block,
cardiac arrest, apnea
Approach Increase diet intake
No urgent need for K
replacement therapy in
asymptomatic mild-to-
moderate hypoK (3-
3.5mEq/L)
Stabilize mycardium, Move K
from ECF to ICF: insulin,
sodium bicarb, CaGluc, beta
agonist; enhance K elimination
Increased Ca and Vit D intake
Mild: dont overtreat, give
entereal
Severe: parenteral
Rehydration
Forced diuresis with loop
diuretic, Dialysis
Mild: enteral magnesium
severe: hypomagnesemia
([Mg2+] <1 mg/dL) , give
parenteral MgSO4
Stop all Mg containing
preparations
Increase urinary
excretion of Mg
Dialysis
Doses Mild Hypokalemia
([K+] >2 mEq/L):
IV KCl infusion </=
10mEq/hr
SevereHypokalemia
([K+] </=2 mEq/L,
paralysis or ECG
changes):
IV KCl infusion </=
40mEq/hr
Reverse Membrane Effects
Calcium (10ml of 10% CaCl) 1
ampule) IV over 10 minutes)
Transfer extracellular [K+] into
cells
Glucose and insuline (D10W +
5-10U regular insulin per 25-
50g glucose); NaHC3 (50-100
mEq over 5-10 minutes); B2
agonists
Remove potassium from body
Initial bolus “Rule of 10”
10mL of 10% Ca Gluc (93mg
elemental calcium) over 10
minutes
Followed by continuous
infusion of elemental Ca 0.3-
2.0 mg/kg/hr IV Ca
Once IoCa at range of 4-
5mg/dL (1-1.25mM), shift to
Infusion of 0.9% saline will
dilute the serum calicum,
promote renal excretion
and can reduce the total
serum calcium by 1.5-
3mg/dL
UO maintained at 200-
300ml/hr
([Mg2+] <1 mg/dL):
parenteral MgSO4 1 - 2 g (8-
16 mEq) of MgSo4 as IV
bolus over first hour
Followed by continuous
infusion of 2 - 4 mEq/hr
(250-500mg/hr MgSo4)
Rate should not exceed 1
mEq/min
Toxicity of hyperMg
can be acutely but
trasniently
antagonized:
IV calcium (5-10 mEq)
Inducing diuresis and
expanding ECV (saline
and furosemide)
4.
5.
6.
7.
8.
9. Treatment of hypernatremia
• To increase free water replacement
• Free water should be replaced initially at a speed dependent on the
severity of the symptoms
• If hemodynamically unstable, administer normal saline until
intravascular volume is corrected
10.
11. Hypernatremia approach
Dehydration, tachycardia, hypotension?
[Na] >150 mEq/L
Yes No
Hypovolemic Hypernatremia
= hypotonic / sodium loss
Normovolemic
Hypernatremia
= pure water deficit
Hypervolemic
Hypernatremia
= sodium gain / overload
Polyuria, polydipsia?
hyperglycemia, diuretics? severe burn?
Inappropriate
Renal loss
Appropriate
Renal loss
YES
Cutaneous loss
GI loss
vomiting, diarrhea?
Third space
loss
NO
YES NO
YES NO
YES NO
-Osmotic diuresis
(hyperglycemia,
mannitol)
-Chemical
Diuresis
(furosemide)
-Renal failure
-Post-obstructive
diuresis
-Burns
-Vomiting
-Diarrhea
-Small intestine
obstruction
-Pancreatitis
-Peritonitis
-Pancreatitis
-Inadequate access to
water
-Diabetes insipidus
-Primary hypodipsia
-Salt poisoning
-Hyperaldesteronism
-Hypertonic fluid
administration
Assess volume status
12.
13.
14.
15.
16.
17. Hypernatremia: evaluation
Plasma [Na] >150 mEq/L
Clinical assessment of extracellular volume
Hypovolemic
Sodium Depletion (Hypovolemia)
Euvolemic
Normal Total body sodium
(Euvolemia)
Hypervolemic
Sodium Overload (Hypervolemia)
Fluid Management
Hypovolemia correction
(0.9% saline)
Hypernatremia correction (hypotonic
fluids)
Glucose solutions
Fluid Management
Replace water deficit (hypotonic
fluids)
Control diabetes insipidus
*Central DI:
Desmopressin 10-20ug intranasally; 2-
4 ug SC
Aqueous vasopressin, 5U Q2-Q4h IM
or SC
* Nephrogenic DI:
Restrict sodium, water intake
Thiazide diuretics
Fluid Management
Enhance sodium removal (loop
diuretics, dialysis)
Replace water deficit (hypotonic
fluids)
21. Parenteral Sodium Replacement
• Example: 70 kgs male with [Na]= 120 using parenteral IVF to correct
acute hyponatremia
• Calculation does not consider ongoing losses
• Changes in Na will also dependent on serum Na and body weight
IV solution [Na] Effect of 1L IVF # L of IVF needed to correct [Na]
0.9% NaCl (NS) 154 + 0.79 25
1.5% NaCl 257 + 3.19 6.27
3% NaCl 513 + 9.14 2.19
22.
23.
24. Emergent treatment of hyperkalemia
• Reverse Membrane Effects
• If with significant ECG changes:
• Administer 10-20ml of CaCl2 IV over 10 minutes to stabilize the myocardial
membrane
• Institute emergent therapy to redistribute or remove potassium from the
body
25. Redistribution treatments
• Transfer extracellular [K+] into cells
• Therapies are able to reduce serum [K] by 0.5-1.0 mEq/L over short
duration (30-60 minutes)
• Administer insulin and glucose
• 10 units insulin and 50 g of 50% dextrose
• Administered inhaled beta-agonists (albuterol)
• Administered sodium bicarbonate (50mEq)
• May be repeated for concomitant acidosis
• May lead to hypernatremia
26. Remove potassium from body
• Therapies are able to reduce greater amounts of serum [K] but may
take longer (>60 minutes)
• Administer loop diuretics and isotonic fluids
• Furosemide 1-2mg/kg IV
• Administer sodium polystyrene sulfonate to increase GI potassium loss
• 30-60 gm PO
• or PR via retention enema
• Initiate dialysis
27. Summary for treatment of hyperkalemia
• Reverse Membrane Effects
• Calcium (10ml of 10% calcium chloride (1 ampule) IV over 10 minutes)
• Transfer extracellular [K+] into cells
• Glucose and insuline (D10W + 5-10U regular insulin per 25-50g glucose)
• Sodium bicarbonate (50-100 mEq over 5-10 minutes)
• B2 agonists
• Remove potassium from body
• Diuretics, proximal and loop
• Potassium-exchange resins (Sodium polysterene sulfonate)
• Hemodialysis
• Monitor ECG and Serum [K+] level
30. Hypokalemia treatment
• Removal of offending drugs
• Hypomagnesemia must also be corrected aggressively to ensure
hypokalemia is reversed
• If acidosis is present, correct [K] before correcting acidosis
• [K] repletion
31. Hypokalemia treatment
Correct precipitating factors Increased pH
Decreased Mg
Drugs
Mild Hypokalemia
[K+] >2 mEq/L
IV KCl infusion </= 10mEq/hr
Severe Hypokalemia
[K+] </=2 mEq/L, paralysis or ECG changes
IV KCl infusion </= 40mEq/hr
Continuous ECG monitoring
If life thretening, 5-6 mEq bolus
32.
33. Hypophosphatemia Treatment
• Correction must be proportion to severity of symptoms
• Dose is adjusted according to level of serum Phosphate levels
• Frequent re-evaluation of serum phosphorus levels is recommended
Editor's Notes
ECG changes in hypoK primarily due to delayed ventricular repolarization
https://academic.oup.com/view-large/3532588
WHAT ARE THE NORMAL VALUES
MEasurement of urinary soium and osmolality can help differentiate the various causes.
Hypotonic urine (osmolality <150 mOsm/kg) in the setting of hypertonicity and polyuria is diagnostic of DI
Treatment of hypernatremia produced by water loss requires repletion of water as well of associated deficits in the total body sodium and other electrolytes
Common errors in treating hypernatremia include:
-exessively rapid correction
-failing to appreiate the magnitude of the water deficit
-failing to account for ongoing maintenance requirements
-failing to account for continued fluid losses in planning therapy http://www.openanesthesia.org/electrolytes_anesthesia_text/
Hypovolemic hyperntremia (most common in general ICU’s): Causes: loss of hypotonic body fluids (diuresis, diarrhea, vomiting) Treatment: rapidly replace volume (NS vs 5% albumin), slowly replace free water (deficit (L) = [0.6 x IBW] x [(Na current/140 ) – 1]), 50% acutely and the remainder over 24-36 hours to minimize cerebral edema (ΔNa < 0.5 mEq/L/hr) Other
READ IV FLUIDS NOTES each soln avail has a diff sodium conc
in d5w no sodium conc, its 10% free water
clearly if u use d5w u'll replace free water much quickly than using 1/4, 1/2 or normal saline
normal Na = 140 (middle of the normal range)
First, assess volume – if invasive hemodynamic monitoring is available, analyze the filling pressures and cardiac output. If these are not available, look to clinical variables such as 1) weight loss
2) peripheral edema 3) [Na+]urine (< 10 mEq/L suggests decreased ECV) and lastly the “shock variables” such as heart rate, blood pressure, urine output, and mental status.
deficit (L) = [0.6 x IBW] x [(Na current/140 ) – 1]) IDEAL BODY WEIGHT??
here its assumed that for each liter of D5W given we will decrease the Na serum conc by approx -3.72 mmol/L (decreased of 0.93mmol/250ml)
therefore to stay on track of correcting the Acute hypernatremia by <1.0 mmol/L/hr, we give the D5W no more than 250ml/hr
changes in Na are dependent on serum Na and overall BW REMEMBER Sodium concentration should be measured frequently and therapy should be adjusted for optimal correction of [Na]
Acute hypernatremia: < 1-2mEq/L/hr for first few hours
Chronic hypernatremia (>48 hours): <0.5 mEq/L/hr
Maximum change of 8 to 10 mEq per L in a 24-hour period
To compute for # L of IVF needed fo correct Na (Actual [Na] - Desired [Na]) / computed effect per 1L
Example: (160-140) /3.72
= 5.37
listen at 10:00minutes
PAGE 1042 barash Rapid correction of hyponatremia may result in permanent CNS injury
Central Pontine Myelinolysis
Osmotic Demyelinating Syndrome
Frequent [Na] analysis is required when parenteral hypertonic saline is administered
Acute setting <12 mEq/L/day
Chronic setting <8 mEq/L/day
interrupt or slow the treatment when symptoms improve
frequent Na determinations are impt to prevent correction at a rate above 1-2 mEq/L in any 1 hour and above 8 mEq/L in 24 hours
initially plasma Na may be increased by 1-2mEq/L/Hr; however the rate of correction should then be slowed to avoid excessively rapid correction. HYPERNATREMIA SHOULD BE AVOIDED Once plasma Na exceed 120-125 mEq/L, water restriction alone is usually sufficient o normalize Na
As acute hyponatremia is corrected, CNS signs and symptoms usually improve within 24 hours, although 96 hours may be necessary for full recovery *** Long term pharma therapy of hyponatremia, vasopressin receptor antagonist is a current promising drug
emergent treatment of sever hyperkalemia
membrane excitability can be entagonized by translocating potassium from ECV to ICV, rmoving excess potassium or transsiently by infusing calcium chloride to depress the membrane threshold potential
REVERSAL 1. while waiting for definitive treatment, rapid infusion of CaCl (1g of CaCL2 over 3 minutes of 2-3 ampules of 10% Cagluconate over 5 minutes) may stabilize the cardiac rhythm
If no significant ECG changes
Monitor closely
Initiate therapy as appropriate
MODE OF ACTION OF THESE DRUGSSSS
when giving insulin, u give glucose to prevent severe symptomatic hypoglycemia
TRANSFER
2. insulin in a dose dependent fashion, cause cellular uptake of potassium by increasing the activity f the NA/K ATPase pump. Insulin increases cellular uptake of K best when high insulin levels are achieved by IV injection of 5-10units regular insulin, accompanied by 50ml of 50% glucose. larger doses of insulin ar eno more effective and risk hypoglycemia
3. B2-adrenergic drugs such as salbutamol and albuterol also increase potassium uptake by skeletal muscle and reduce plasma K, an action that may explain hpokalemia with severe acute illness.
**Salbutamol is a selective B2 agonist, decreased serum K acutely by 1mEq/L or more when given by inhalation or IV (Caution because cardiac dysrhythmias may complicate treatment with B2 agonists)
4. Sodium bicarbonate has been a part of hyperkalemia treatment, but bicarbonate when used alone is relatively ineffective and is no longer favored, except in patients with metabolic acidosis
if u administer loop diuretics u may need to continue giving isotonic fluids to prevent the patient going to hypovolemia REMOVAL remove via renal or GI routes
1. furosemide promotes kaliuresis in a dose dependent fashion.
2. Sodium Polystyrer can be given orallly (30-60g) or as a retention enema (50g i 200ml of 20% sorbitol)
however sodium overload and hypervolemia are potential risks
3. HEMODIALYSIS and continuous renal replacement therapy may be necessry for patients with AKI or chronic renal failure
PAGE 1055
REVERSAL MEMBRANE EFFECTS: rapid infusion of CaCl (1g of CaCL2 over 3 minutes of 2-3 ampules of 10% Cagluconate over 5 minutes)
TRANSFER: 10 units insulin and 50 g of 50% dextrose, inhaled beta-agonists (albuterol), sodium bicarbonate (50mEq)
ELIMINATION: loop diuretics (Furosemide 1-2mg/kg IV) and isotonic fluids, Administer sodium polystyrene sulfonate to increase GI potassium loss 30-60 gm PO or PR via retention enema
Initiate dialysis
drugs loop diuretics
Usually treated based on Na and K levels
Because K is primarily an intracellular ion, it is difficult to predict how much K will be necessary to increase serum K to an acceptable level
PAGE 1049
treatment consist of K repletion, correction of alkalemia, and removal of offending drugs
hypoK secondary only to acute redistribution (ex secondary to acute alkalemia) may not require treatment
NO URGENT need for K replacement therapy in mild-to-moderate hypoK (3-3.5mEq/L) in patients with no signs and symptoms
if total body K is decreased then oral K supplements is preferrable to IV
In patients who have DKA and are both hypoK and acidemic, K admin must precede corrrection of acidosis to avoid precipitous decrease in plasma K as pH increase
IV K repletion when necessary is performed cautiously: usual rate of 10-20mEq/hr
the plasma K and the ECG must be monitored during the rapid repletion (10-20meq/hr) to avoid hyperkalemic complications
** concurrent case in ptc with acidemia, type IV renal tubular acidosis, DM, and those receiving NSAIDS, ACEI, Beta 2 blockers ----> all of which delay movement of extracellular K into cells or predispose ptx to hyperK
BUT in patients with life threathening dysrhythmias sec to hypoK, serum K must be rapidly increased. (page 1050)
assuming that plasma volume of a 70kg adult is 3L, admin of 6mEq/L of potassium in 1 minute withh acutely increase plasma K by no more than 2 mE1/L; subsequent redistribution into the interstitial fluid and IVC will rapidly decerase plasma K
in hypoK with hyperaldosteronemia (Primary aldosteronisn, cushing syndrome) this responds favorable to reduced sodium intake and increased potassium intake
hypoMg if present aggravates the effect of hypokalemia, impairs potassium conservation and should be treated
K supplements and K sparing diuretics must be given CAUTIOUSLY in patient with DM or enal insuff
loop diuretics: __________ PAGE 1038 BARASH
Treatment includes:
Free water restriction (sufficient to decrease TBW by 0.5 to 1L/day); water restriction decreases ECV even if excessive AVP secretion continues. the resultant reduction in GFR enhance proximal tbular reabsorption of Na and H2O thereby decreasing free water generation and stimulates aldosterone secretion
Increasing free water excretion with loop diuretics (furosemide administration increases free water excretion)
Increased sodium administration
Enteral (salt)
Parenteral IV solutions
** HypoNa treatment, increases in plasma Na are determined both by the composition of the infused fluid and the rate of renal free water excretion
![, ma
Normal
Range
137-145 mEq/L
137-145 mmol/L
2.7-4.5 mg/dL in adults
0.8-1.3 mmol/L (inorganic phosphate)
Hypo-Na Hyper-Na Hypo-P Hyper-P
Etiology Water excess, Fluid loss, Renal disease,
Diuretics, SIADH, Congestive heart
failure, Cirrhosis, Nephrosis
Excess water loss , Ecxess sodium
intake, Diabetes insipidus,
Diuresis, Sweating, GI fistula, Burns
Intracellular shift of Pi, Increase in renal Pi loss
Decrease in gastrointestinal Pi absorption
Renal failure, inadequte renal excretion,
increased movement of Pi out of cells,
increased Pi or Vit D intake
Common
Signs/
symptoms
Lethargy, weakness, irritability, nausea,
restlessness, seizures, confusion,
somnolence, coma
Lethargy, anorexia, nausea,
emesis, fatigue, seizures, confusion,
coma
confusion, weakness, seizures, respiratory
failure, heart failure
Muscle cramps, perioral tingling,
paresthesia, ventricular arrythmias
Approach Water restriction
Sodium supplement
Hypertonic solution
Hypotonic solution, Sodium
restriction, Diuretics
mild: give enteral phosphorus replacement
severe: give parenteral phosphorus
replacement
Correction of associated hypocalcemia,
Restricting intake, Increasing urinary
excretion , Increasing GI losses
Treatment Free water restriction (<1L/day)
Increasing free water excretion with
loop diuretics
Increased sodium administration
[Na] <115 to 120mEq/L require
agressive therapy
Calculate the free water deficit, total
body water, free water replacement
Parenteral free water replacement
with goal:
1/2 of free water defeicit in first 24
hrs, Remaining over next 48 hrs
Mild: enteral
Severe (<1mg/Dl) Pi or symptomatic: IV
phosphate administration
Calcium Supplementation of
hyperphosphatemic hypocalcemic patients
should be delayed until serum phosphate
had fallen below 2mmol/L (6mg/dl)
Doses Severe: initially 1-2 mL/kg/hr to
increase plasma [Na] by 1-2 mEq/L/hr,
then slow down
Must not exceed 1-2 mEq/L in any 1
hour and above 8 mEq/L in 24 hours
Once plasma Na exceed 120-125
mEq/L, water restriction alone is
sufficient to normalize Na
Acute hypernatremia: < 1-2mEq/L/hr
for first few hours
Chronic hypernatremia (>48 hours):
<0.5 mEq/L/day
Maximum change of 8 to 10
mEq/L/day
Dose: 0.2 mM-0.68 mM/kg (5-6mg/kg) over 12
hours
If chronic hypoP: 7-15 mmol of phosphate can
be infused per hour, magnitude of infusion
must be roportional to the severity of
symptoms
Oral therapy can be a substitute for parenteral
Pi once the serum Pi levels exceed 2mg/dL.
Continued therapy with Pi supplements is
required for 5-10 days
Increasing urinary excretion
Saline
Acetazolamide (500mg every 6
hours)
Increasing GI losses
by enteric administration of
aluminum hydroxide (30-45mL every
6 hours)
Rapid increase in plasma sodium
concentration = Osmotic
Rapid correction may result in
cerebral edema and neurologic injury
Close monitoring of serum Pi, Ca, Mg, and K is
essential to avoid complications](data:image/gif;base64,R0lGODlhAQABAIAAAAAAAP///yH5BAEAAAAALAAAAAABAAEAAAIBRAA7)