About electrolyte imbalances

1. Dr. Parantap Trivedi
3rd Year Resident
M.D. Anaesthesiology
Dept. of Anaesthesiology
GMC Bhavnagar

2. Potassium
• Chiefly intracellular, normal serum levels 3.5-5.0 meq/L
• Levels regulated through Renal excretion and Aldosterone.
• Excretion is increased by high aldosterone levels in Alkalosis
and Hyperkalemia.
• Physiologically, Insulin, circulating catecholamine level
regulate K+ levels in body.
• In metabolic Acidosis, K+ levels increase due to extracellular
shift of K+, while in Alkalosis K+ levels decrease.
• When body potassium increases, serum levels rise
proportionately, giving a direct idea of Total hyperkalemia
• While in case of Hypokalemia, serum levels do not directly
reflect the intracellular Hypokalemia due to shifting of K+
ectracellularly, causing Underestimation of K+ deficit.

4. Hyperkalemia
• When K+ more than 5.5 meq/l.
• Occurs due to
• Intercompartmental shifts: Acidosis-Rhabdomylosis-Excessive Exercise-
Succinylcholine
• Decreased Renal excretion: Renal failure, Aldosterone deficit, K+ sparing drugs,
NSAIDS, ACE Inhibitors
• Increased K+ uptake or release of K+ from Ischemic Organ.
• Pseudohyperkalemia is seen in elevated Hemolysis, improper drawing technique
like application of Torniquet for too long, and/or limb exercise before drawing
blood.

5. Clinical Considerations
• Hyperkalemia chiefly affects Skeletal and Cardiac Muscle.
• Skeletal Muscle paralysis is seen in levels above 8meq/l.
• Cardiac manifestations start when levels exceed 7meq/l.
• ECG Changes sequentially progress:
 Peak T waves
 widening of QRS
 prolongation of PR interval
 loss of P wave
 Loss of R wave
 ST Depression
 Sine wave pattern
 V fib, Asystole

6. Treatment
• When to start: At potassium level > 6.0 meq/l.
• Goal of treatment: To reverse Cardiac manifestations and Skeletal
muscle weakness.
• Things to consider before starting treatment: Wheter
Hyperkalemia due to Hyporaldosteronism/ due to drugs causing
Hyperkalemia/ K+ in IV fluids? / Metabolic Status/ Spurious values
possible?
How to start treatment? :
1. Stop K+ containing iv fluids/ oral intake/drugs causing K+ rise.
2. 10ml of 10% Calcium Gluconate in 100cc NS iv over 30 mins
helps in antagonizing cardiac effects of Hyperkalemia.
3. Definitive treatment: 10U of Pl. Insulin in D25 100ml iv over 1
hours, helps in cellular uptake of K+.
4. Nebulization with Salbutamol 8-10mg Nebulization (around 2
respules) every 2 hourly.

7. 5. Forced Diuresis with loop diuretic is effective in patients with
normal renal function.
6. Dialysis is definitive urgent treatment in patients with Renal
disease.
7. K+ Exchange polymers: Sodium Polystyrene, Kayxalate,
Patiromer are other modes of elimination.
8. Sodium Bicarbonate correction according to metabolic
status.
• In presence of Metalbolic Acidosis, iv Sodium Bicarbonate
correction promotes cellular uptake of K+ and can lead to
Hypokalemia so potassium correction needs to be given
accordingly.

8. ANAESTHETIC IMPLICATIONS
• Elective surgery should not be undertaken
in patients with significant Hyperkalemia.
• Management aims at lowering K+ levels
and stabilising Cardiac condititon.
• ECG monitoring closely.
• In emergency surgery, Succinylcholine is
contraindicated (100mg raises S. K+ by
0.5- 1 meq/l)
• Avoidance of Metabolic/Resp. Acidosis is
must, and so slight hyperventilation
under GA is desirable.
• Neuromuscular function should be closely
monitored as Hyperkalemia accentuates
the effect of Neuromuscular Blockers, so
use of PNS becomes handy.

10. Hypokalemia
• Serum K+ levels < 3.5 meq/l.
• Occurs due to:
• GI Losses: Vomitting, Secretory Diarrhea and excessive RT Suctioning, laxative
abuse.
• Increased K+ loss: Sweating
• Diuresis
• Chronic Alkalosis
• Renin excess (Renal HTN),
• Amphotericin B
• Renal Tubular Acidosis
• Aldosterone excess (Conn’s syndrome), pancreatic tumours, fistulae.
• Intracellular shift of K+: Alkalosis
• Insulin therapy
• B12 therapy
• rarely Thyrotoxicosis and Barium ingestion.

11. Clinical Considerations
1. Cardiac manifestations:
 Delayed ventricular
depolarisation
 T wave flattening and
inversion
 Increasingly prominent U
wave
 ST depression
 Increase P wave amplitude
prolongation of PR
interval.

12. 2. Neuromuscular: Skeletal muscle weakness, hyporeflexia,
muscle cramping, paralytic ileus, rarely flaccid paralysis or
rhabdomyloysis.
3. Hypokalemia due to diuretic overdose causes:
Loop Diuretic fluid loss  causes reabsorption of Na+ for
volume repletion  K+ and Cl- excreted  Bicarb
reabsorbed  Metabolic Alkalosis (due to Hypochloremia).
4. Hyperaldosternonism causes renal dysfunction due to
decreased urine concentration ability, causing Polyuria and
increasing level of Ammonia, which causes intracellular shift
of H+ ions to compensate for K+ loss resulting in Metabolic
Alkalosis and increase in Ammonia level causing
Encephalopathy in patients with liver disease. (cirrhosis
causes primary hyperaldosteronism.

13. • When to start:
- If S. K+ 3-3.5 meq/l: Correction in selected cases -CHF,
Digitalis Therapy, h/o IHD/MI) corrected by Oral K+
supplementation. (Syp. Potklor, Banana, Coconut Water)
- Syrup Potklor can be given in dose of 20meq TDS/QID.
- If S. K+ < 3 : Definitive Treatment Required.
• Principles of K+ correction via IV route:
- Amount of K+ correction is required to correct deficit cannot
be determined by a fix formula.
- If avg. deficit is 200-400meq, 50-100meq per day corrects
deficit slowly.
- In severe deficit and higher rate of ongoing loss, larger dose
and faster correction is required.
- Hypokalemia in serum levels shows much greater deficit in
Intracellular K+ levels, as shown in table:
Treatment

14. Serum K+ > 3.5 meq/l 3 2 <2
Total K+
Deficit
0 meq/l 300 450-600 >600
Table: K+ deficit at normal pH
- Correction is given by Infusion of Inj. KCL.
- Usually 10-20meq can be given per hour via peripheral line.
- At higher rates there high risk of vein thrombophlebitis.
- For faster and correction with higher dose, Central Vein
cannulation becomes necessary. Via central line corrections upto
30-40meq per hour can be given safely.
- Highest rate of correction should not be >240meq/day.
- Never given IV directly, causes sudden Cardiac Arrest.
- Treatment of Acidosis with with iv NaHCO3 precipitates
Hypokalemia so K+ correction should be given first.

15. • How to give KCL?
- Each ampoule contains
20meq/10ml solution.
- Clinically we can give Potassium
correction as 100meq (5amp) in
500cc NS which prepares
20meq/100ml.
- Given at rate of 100ml/hr, giving
20meq per hour correction.
- Which equals 1.6ml/min
- Which Also equals 26 drops/min.

16. • Things to keep in mind:
- Digitalis sensitises heart to K+ levels, and in presence of
Digitalis K+ entry in cells is slower, so Slow correction is required
otherwise there’s risk of transient Hyperkalemia.
- Patients on K+ sparing diuretics, Slow correction of K+ should
be slow otherwise risk of transient Hyperkalemia.
- Hypokalemia in Serum shows much greater deficit in
Intracellular K+ levels.
- Never given IV directly, causes sudden Cardiac Arrest.
- Never given IV directly, causes
sudden Cardiac Arrest.

17. • For how long? :
- Till cardiac rhythm comes to normal, respiratory muscle tone
returns normal, drip is tapered and stopped.

18. ANAESTHETIC IMPLICATIONS
• Elective surgery should not be undertaken in patients with K+ <3.0 or
<3.5 if patient on digoxin.
• Management aims at K+correction and stabilising Cardiac condititon.
• ECG monitoring closely.
• Avoid hyperventilation under GA.
• Neuromuscular function should be closely monitored as Hyperkalemia
increases the sensitivity to Neuromuscular Blockers.

19. Sodium
•Major Intracellular Cation.
•Hyponatremia management goes hand in hand with the
management of fluid status in the body.
•Classification:

20. HYPONATREMIA

22. Basic Fluid Compartments

23. • These compartments water moves freely between
intracellular and extracellular compartments, so if solute
concentration (Na+ in our case) is high in any one
compartment, water moves from low osmolarity to high
osmolarity till Na+ is distributed equally between
compartments.
• Hence measurement of Serum Na+ reflects the total Na+
status in body.

24. Hyponatremia Causes
• It’s simple.

25. • Dilutional Hyponatremia:
When we drink excessive water, the Na+ is diluted, causing
relative hyponatremia, called dilutional hyponatremia.
• Due to decreased Excretion:
ADH, causes reabsorption of water back into body through
reabsorption. In SIADH, excessive reabsorption, hence
Hyponatremia.
• Due to decreased intake:
Due to insufficient Na+ in diet. (Highly unlikely to happen).
• Due to increased excretion:
Increased loss via Diuretics, sweating, vomiting, Burns. In
Primary Adrenal insufficiency, there’s deficiency of
Aldosterone, which increased Na+ and decreases K+ in blood.
so it’s deficiency causes Hyponatremia.

26. Diagnosis
• 3 steps:
– Assess Serum Osmolality:
• Formula: 2 x Na+ + Glucose+ Urea
1. If Na+ = Low and S.Osmolality= Low it’s Hyponatremic
Hyponatremia. [ TRUE HYPONATREMIA]
2. If Na+ = Low and S.Osmolality= Normal it’s
Pseudohyponatremia, occurs due to increased increased
lipid and protein in blood causing relative hyponatremia.
(Hyperlipdemia and Multiple Myeloma)
3. If Na+= Low and S.Osmolality= High, it’s called
Hyperosmolar Hyperglycemic state (HHS) occurs in Type 2
DM. High amount of Glucose in blood and it’s excretion
through kidney causes alongwith removal of water and
sodium and thus hyponatremia.
2 and 3 have their own separate Medical Management

27. If Hyponatremic Hyponatremia: True
Hypnatremia which requires correction
– Check fluid status:
Hyponatremic
Hyponatremia
Dilutional
Hyponatremia
Dilutional
Hyponatremia

28. • Check Urine Osmolality:
High Na+ in urine shows the cause of
Hyponatremia is in kidenys.

29. Diagnostic Algorithm

30. • Because of increased ADH secretion, free water excretion
becomes difficult, retention of water causes dilutional
Hyponatremia and progressive expansion of intra and
extraceullular spaces.
• This leads to increased secretion of Atrial Natriuretic Peptide
(ANP) and decreased Aldosterone, stopping reabsorption of
Sodium and promotes excretion which increases Urine
Osmolality and inappropriately concentrated urine.

32. Treatment
• Principles:
 Patient with severe neurological symptoms due to
huponatremia need prompt treatment with Inj. 3% NaCl
100ml. So rapid correction (<48hours) is required if Na+ <
120 with severe Neurlogical symptoms
 If chronic and mild hponatremia are at lesser risk of
developing demyelination and most of the times correction
is not required and treatment by fluid restriction suffices.
 3% NaCl contains 513 meq/l, which equals 50meq in 100ml.
Correction given over 6hours require 16ml of fluid to be
infused per hour to finish at 6th hour.
 In 100ml there’s 50meq of sodium, in 16ml there’s roughly
8meq of sodium which is our Daily Goal to correct.

34. Definitive treatment
CHRONIC ASYMPTOMATIC
HYPONATREMIA
ACUTE SYMPTOMATIC HYPONATREMIA
• Targeted rate of correction is 0.5-
1meq/hr and less than 18meq/hour over
first two days.
•Maximum raise should be 8 meq/l on
first day and max. 18meq/l on first two
days.
•NO MORE THAN 8meq/L on any day of
treatment
•These patients require rapid correction.
•Rate should be 1.5-2 meq/hr till severe
symptoms of CNS improve.
•Correction should not increase more
than 8-10meq in 24hours.
•Patients with seizure require
anticonvulsants as well.
•TOO RAPID correction leads to swelling
of Brain cells called “Central Pontine
Myelinolysis” which causes Brain
herniation.
Sodium Deficit: TBW X (Desired Na+ - Present Na+)
TBW= 0.6 X Body weight in Young
0.4 X body weight in elderly

35. Central Pontine Myelinolysis
• Severe neurological disorder caused by
Too Rapid Correction of Sodium leading
swelling of Brain cells and herniation of
brain through foramen magnum.
• Symptoms: Dysarthria, dysphasia,
flaccid paralysis, Coma.
• Diagnosis by CT and MRI

36. ANAESTHETIC IMPLICATIONS
• Patients with Sodium imbalance usually present with Hypovolemia or
Hypervolemia, and both disturbances should be corrected before elective
procedures.
• Cardiac, Liver and Kidney functions should be carefully evaluated in presence
of HYPERNATREMIA.
• Hypovolemic patients are sensitive to Vasodilating and Negative inotropic
effects of Inhalational anesthetics, Propofol and drug induced Histamine
release. Dose requirements for this drug maybe reduced due to decrease in
their Volume of Distribution.
• Hypovolemic patients are also sensitive to Sympathetic blockade from Spinal
and Epidural anaesthesia. If GA must be administered prior to correction of
Hypovolemia, Etomidate or Ketamine are agents of choice.
• Hypervolemia is treated with diuretics. Major hazard of increased
Intracellular volume is impaired gas exchange due to pulmonary oedema,
pleural effusion or ascites.

38. Hypernatremia
• Causes:
– Excessive water loss: Sweating, vomitting, burns,
severe exercise, patient on ventilator, Diabetes
insipidus, Excessive Diuretics, uncontolled DM,
Diarrhea.
– Water deficit due to impaired thirst: Primary
hypodipsia, confused and comatose patient.
– Sodium Retention: Excessive 3% NaCl or NaHCO3

39. Treatment
• Hypernatremia is due to Water deficit and rarely due to Na+
overload.
• Treatment is to stop fluid loss and correct water deficit.

41. Magnesium
• Normal levels: 1.4-2.2 meq/l
• 60% in bone, 1% ECF and Rest in Cells
• Function: Neuromuscular function and maintaining
Cardiovascular tone.

42. ANAESTHETIC IMPLICATIONS
Hypermagnesemia Hypomagnesemia
•Presents with Neurologic, neuromuscular
and cardiac manifestations: Hyporeflexia,
Sedation, muscle weakness.
•Cardiac features: Bradycardia, Myocardial
depression, vasodilatation, prolongation
of PR Interval, widening of QRS.
•Severe hypermagnesemia leads to
respiratory and Cardiac arrest.
• Treatment by IV Calcium Gluconate in
acute toxicity followed by Loop diuretics.
•Close anesthetic monitoring reqd of
Cardiorespiratory parameters.
•Potentiation of NMB, Vasodilatory and
negative inotropic effects to be expected.
•Causes are IV MgSO4 therapy in Obsterics
and antacid abuse.
•Caused by renal wasting by Alcohol,
Amphotericin B, Theophylline, Diuretics
and Cyclosporine.
•Also associated with long term Proton
Pump inhibitor therapy.
•Symptoms include weakness,
fasiculations, paresthesia, confusion,
ataxia, seizures and Arrythmias and
potentiation of Digoxin toxicity.
•Frequently it is associated with
Hypokalemia and Hypocalcemia
•ECG changes: Atrial fibrillation and
prolongation of PR and QT interval.
•Treatment by Inj MgSO4 1-2g over
60mins.
•Anesthetic monitoring specifically for
Cardiac Arrhythmias and prophylactic
MgSO4 to be considered.

44. Calcium
• Normal value of S. Ca2+ : 10-10.5 mg/dl.
• 40% of it bound to Albumin and rest in ionized form.
• Ionized calcium is physiologically active and it’s value is
4.8mg/dl. Total serum calcium does not always reflect
ionized calcium.
• Hypoprotenemia leads to decreased serum calcium
levels, hence ionized calcium needs to be calculated to
prevent misdiagnosis of Hypocalcemia.

45. ANAESTHETIC IMPLICATIONS
Hypercalcemia Hypocalcemia
• Signifcant Hypercalcemia is a medical
emergency and should be corrected
before elective surgery and ionized
calcium levels closely monitored.
•In Emergency surgery, Fluids and saline
diuresis needs to be continued during
surgery taking care to prevent
hypovolemia.
•Serial K+ and Mg2+ also should be done to
view diuresis induced Hypkalemia and
Hypomagnesemia.
•Response to NMB is unclear, ventilation
should be controlled under GA.
•Acidosis to be avoided to not worsen
elevated plasma calcium.
•90% time cause is Malignancy or
Hyperparathyroidism
•Should be diagnosed only on basis of
plasma ionized calcium levels.
•Significant hypocalcemia to be corrected
before elective surgery by 10ml of 10%
Calcium Gluconate in 100ml NS iv over
30-45mins.
•Serum Ionized calcium levels to be
observed intraoperatively.
•IV Calcium maybe necessary following
rapid transfusion of blood products.
•Potentiation of Negative inotropic effects
of anesthetics to be expected.
•Response to NMB is variable
•Alkalosis avoided to prevent further
decrease in Ca2+ levels.
•Causes are Hypoparathyroidism, Vit D
deficiency, Pancreatitis, Chelation by
blood products.

47. Phosphorus
• Normal value 3-4.5mg/dl.
• Measured in fasting as it has diurnal variation
• Regulation by PTH: PTH release causes
increased Calcium and decreased Phosphorus
in blood.

48. ANAESTHETIC IMPLICATIONS
Hypophosphatemia Hyperphosphatemia
•Mild to moderate hypophosphatemia 1-2.5mg/dl is
asymptomatic.
But <1mg/dl causes life threatening complications.
•It causes Cardiomyopathy, impaired oxygen
delivery by increasing 2,3 DPG level, Hemolysis,
impaired WBC function, platelet dysfunction,
arrythmia, diaphagmatic weakness, skeletal
myopathy and Resp. failure.
•Some patient require Mechanical Ventilation
postoperatively due to muscle weakness.
•Causes include Resp. Alkalosis, large dose of
Antacids, Hyperparathyroidsm, Alcohol withdrawal,
inadequate supply during TPN.
•Treatment is mostly by Vit D supplementation and
Milk
•Significant Hyperphosphatemia
leads to decreased Serum
Calcium and it’s features.
•Causes include Phosphorus
containing laxative abuse.
•Treatment by avoidance of
Phosphorus and VitD rich
supplements and Phosphorus
binders like Aluminium Hydroxide
or Carbonate.