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ELECTROLYTE IMBALANCE
only k+ and Mg+2
DR. M.ANEEQUE ALAM KHAN
DEPARTMENT OF ANAESTHESIA, SICU
AND PAIN MANAGEMENT
CIVIL HOSPITAL KARACHI / DOW
UNIVERSITY OF HEALTH SCIENCES
aneeque86@gmail.com
HYPOKALEMIA
HYPOKALEMIA
• Hypokalemia defined as plasma K+ less
than 3.5 mEq/L.
• A decrease in plasma K+ from 4 mEq/L to
3 mEq/L usually represents a 100- to 200-
mEq deficit,
• whereas plasma K+ below 3 mEq/L can
represent a deficit anywhere between 200
mEq and 400 mEq.
CAUSES
Renal tubular acidosis
EXCESS RENAL LOSS
Mineralocorticoid excess
Primary hyperaldosteronism (Conn’s syndrome)
Renin excess
Renovascular hypertension
Diuresis
Chronic metabolic alkalosis
G.I LOSS
Vomiting
Diarrhea,
ECF → ICF shifts
Acute alkalosis
Hypokalemic periodic paralysis
Barium ingestion
Insulin therapy
CLINICAL MANIFESTATION
 Most patients are asymptomatic until
plasma [K +] falls below 3 mEq/L.
 Cardiovascular effects are most
prominent includes
 an abnormal ECG
 arrhythmias,
 decreased cardiac contractility,
 labile arterial blood pressure due to
autonomic dysfunction.
 ECG manifestations are primarily due to
delayed ventricular repolarization and
includes
 T-wave flattening and inversion
 prominent U wave
 ST- segment depression
 increased P- wave amplitude
 prolongation of P–R interval
TREATMENT
 Safest method is oral replacement by KCL 60-80 mEq/day
over several days
 peripheral intravenous replacement should not exceed
8 mEq/h.
 More rapid intravenous potassium replacement (10–20
mEq/h) requires central venous administration and
close monitoring of the ECG.
 Intravenous replacement should generally not exceed
240 mEq/d
ANESTHETIC
CONSIDERATION
 The decision to proceed with elective
surgery is often based on lower plasma K+
limits somewhere between 3 and 3.5
mEq/L.
 In general, chronic mild hypokalemia (3–
3.5 mEq/L) without ECG changes does
not substantially increase anesthetic risk.
 Increased sensitivity to neuromuscular
blockers (NMBs) may be seen
 dosages of NMBs should be reduced
25– 50%
HYPERKALEMIA
HYPERKALEMIA
 Hyperkalemia exists when plasma K
exceeds 5.5 mEq/L.
 kidneys can excrete as much as 500
mEq of K per day.
 So hyperkalemia rarely occurs in
normal individuals
CLINICAL MANIFESTATION
 Important effects of hyperkalemia are on
skeletal and cardiac muscle.
 Skeletal muscle weakness is generally
not seen until plasma K+ is greater
than 8 mEq/L,
 Cardiac manifestations are primarily due
to delayed depolarization, and are
consistently present when plasma K+ is
greater than 7 mEq/L.
ECG changes
 peaked T waves
 widening of the QRS complex
 prolongation of the P–R interval
 loss of the P wave
 loss of R wave amplitude
 ST-segment depression
 an ECG that resembles a sine wave,
 before progression to ventricular fibrillation and
asystole.
TREATMENT
 Hyperkalemia exceeding 6 mEq/L should always
be corrected.
 Treatment is directed to reversal of cardiac
manifestations and skeletal muscle weakness, and to
restoration of normal plasma K+
 Calcium (5–10 mL of 10% calcium gluconate or 3–5
mL of 10% calcium chloride) partially antagonizes
the cardiac effects of hyperkalemia and is useful in
patients with marked hyperkalemia
 When metabolic acidosis is present, intravenous sodium
bicarbonate (usually 45 mEq) will promote cellular
uptake of potassium and can decrease plasma [K+]
within 15 min
 Βeta agonists promote cellular uptake of potassium and
may be useful in acute hyperkalemia associated with
massive transfusions
 An intravenous infusion of glucose and insulin (30–50 g
of glucose with 10 units of insulin) is also effective in
promoting cellular uptake of potassium and lowering
plasma K+ but may take up to 1 h for peak effect.
 Kayexalate resin 30-60 gm PO or PR
 Dialysis is indicated in symptomatic patients with
severe or refractory hyperkalemia
ANESTHETIC
CONSIDERATION
 Elective surgery should not be
undertaken in patients with significant
hyperkalemia.
 Succinylcholine is contraindicated,
 the use of any potassium containing
intravenous solutions such as lactated
Ringer’s injection.
 avoidance of metabolic or respiratory
acidosis
MAGNESIUM
• Serum level 1.7-2.4 mg/dl or 1.4-2.0 mEq/l
INDICATIONS
• Pre-eclampsia, eclampsia
• Tetanus
• Torsades de pointes
• Status asthmaticus
• Digoxin induce tachyarrhythmias
• Decrease anesthetic requirements
• Attenuate nociception
• Blunt response of laryngoscopy & intubation
• Potentiate NMBs
Mechanism of action
• Antagonize calcium
• Adrenal medullary catecholamine release
• Alter CNS neurotransmitter release
HYPERMAGNESEMIA
Plasma magnesium concentration more than
• 4 to 6 mEq/L or
• 4.8 to 7.2 mg/dL or
• 2 to 3 mmol/L
CAUSES
• Excessive intake
• Hemolysis
• Renal insufficiency
• Diabetic ketoacidosis
• Hyperparathyroidism
• Adrenal insufficiency
• Lithium intoxication
TREATMENT
• Intraveneous calcium temporarily anatagonize
• Loop diuretic with fluid replacement
• dialysis
Toxicity
HYPOMAGNESEMIA
TREATMENT
Electrolyte imbalance

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Electrolyte imbalance

  • 1. ELECTROLYTE IMBALANCE only k+ and Mg+2 DR. M.ANEEQUE ALAM KHAN DEPARTMENT OF ANAESTHESIA, SICU AND PAIN MANAGEMENT CIVIL HOSPITAL KARACHI / DOW UNIVERSITY OF HEALTH SCIENCES aneeque86@gmail.com
  • 3. HYPOKALEMIA • Hypokalemia defined as plasma K+ less than 3.5 mEq/L. • A decrease in plasma K+ from 4 mEq/L to 3 mEq/L usually represents a 100- to 200- mEq deficit, • whereas plasma K+ below 3 mEq/L can represent a deficit anywhere between 200 mEq and 400 mEq.
  • 4. CAUSES Renal tubular acidosis EXCESS RENAL LOSS Mineralocorticoid excess Primary hyperaldosteronism (Conn’s syndrome) Renin excess Renovascular hypertension Diuresis Chronic metabolic alkalosis G.I LOSS Vomiting Diarrhea, ECF → ICF shifts Acute alkalosis Hypokalemic periodic paralysis Barium ingestion Insulin therapy
  • 5. CLINICAL MANIFESTATION  Most patients are asymptomatic until plasma [K +] falls below 3 mEq/L.  Cardiovascular effects are most prominent includes  an abnormal ECG  arrhythmias,  decreased cardiac contractility,  labile arterial blood pressure due to autonomic dysfunction.
  • 6.  ECG manifestations are primarily due to delayed ventricular repolarization and includes  T-wave flattening and inversion  prominent U wave  ST- segment depression  increased P- wave amplitude  prolongation of P–R interval
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  • 8.
  • 9. TREATMENT  Safest method is oral replacement by KCL 60-80 mEq/day over several days  peripheral intravenous replacement should not exceed 8 mEq/h.  More rapid intravenous potassium replacement (10–20 mEq/h) requires central venous administration and close monitoring of the ECG.  Intravenous replacement should generally not exceed 240 mEq/d
  • 10. ANESTHETIC CONSIDERATION  The decision to proceed with elective surgery is often based on lower plasma K+ limits somewhere between 3 and 3.5 mEq/L.  In general, chronic mild hypokalemia (3– 3.5 mEq/L) without ECG changes does not substantially increase anesthetic risk.
  • 11.  Increased sensitivity to neuromuscular blockers (NMBs) may be seen  dosages of NMBs should be reduced 25– 50%
  • 13. HYPERKALEMIA  Hyperkalemia exists when plasma K exceeds 5.5 mEq/L.  kidneys can excrete as much as 500 mEq of K per day.  So hyperkalemia rarely occurs in normal individuals
  • 14.
  • 15. CLINICAL MANIFESTATION  Important effects of hyperkalemia are on skeletal and cardiac muscle.  Skeletal muscle weakness is generally not seen until plasma K+ is greater than 8 mEq/L,  Cardiac manifestations are primarily due to delayed depolarization, and are consistently present when plasma K+ is greater than 7 mEq/L.
  • 16. ECG changes  peaked T waves  widening of the QRS complex  prolongation of the P–R interval  loss of the P wave  loss of R wave amplitude  ST-segment depression  an ECG that resembles a sine wave,  before progression to ventricular fibrillation and asystole.
  • 17.
  • 18. TREATMENT  Hyperkalemia exceeding 6 mEq/L should always be corrected.  Treatment is directed to reversal of cardiac manifestations and skeletal muscle weakness, and to restoration of normal plasma K+  Calcium (5–10 mL of 10% calcium gluconate or 3–5 mL of 10% calcium chloride) partially antagonizes the cardiac effects of hyperkalemia and is useful in patients with marked hyperkalemia
  • 19.  When metabolic acidosis is present, intravenous sodium bicarbonate (usually 45 mEq) will promote cellular uptake of potassium and can decrease plasma [K+] within 15 min  Βeta agonists promote cellular uptake of potassium and may be useful in acute hyperkalemia associated with massive transfusions
  • 20.  An intravenous infusion of glucose and insulin (30–50 g of glucose with 10 units of insulin) is also effective in promoting cellular uptake of potassium and lowering plasma K+ but may take up to 1 h for peak effect.  Kayexalate resin 30-60 gm PO or PR  Dialysis is indicated in symptomatic patients with severe or refractory hyperkalemia
  • 21. ANESTHETIC CONSIDERATION  Elective surgery should not be undertaken in patients with significant hyperkalemia.  Succinylcholine is contraindicated,  the use of any potassium containing intravenous solutions such as lactated Ringer’s injection.  avoidance of metabolic or respiratory acidosis
  • 22. MAGNESIUM • Serum level 1.7-2.4 mg/dl or 1.4-2.0 mEq/l INDICATIONS • Pre-eclampsia, eclampsia • Tetanus • Torsades de pointes • Status asthmaticus • Digoxin induce tachyarrhythmias
  • 23. • Decrease anesthetic requirements • Attenuate nociception • Blunt response of laryngoscopy & intubation • Potentiate NMBs
  • 24. Mechanism of action • Antagonize calcium • Adrenal medullary catecholamine release • Alter CNS neurotransmitter release
  • 25. HYPERMAGNESEMIA Plasma magnesium concentration more than • 4 to 6 mEq/L or • 4.8 to 7.2 mg/dL or • 2 to 3 mmol/L
  • 26. CAUSES • Excessive intake • Hemolysis • Renal insufficiency • Diabetic ketoacidosis • Hyperparathyroidism • Adrenal insufficiency • Lithium intoxication
  • 27. TREATMENT • Intraveneous calcium temporarily anatagonize • Loop diuretic with fluid replacement • dialysis
  • 30.