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HYPOKALEMIA
Presenter – Dr Sudha.P
Moderator- Dr. MAHADEVAIAH
Introduction
 Normal potassium levels are 3.5-5 mEq/L
 Hypokalemia is defined as plasma K levels <3.5mEq/L
 Plasma potassium levels correlate poorly with the total
potassium deficit.
 Potassium is essential for Muscles, cardiovascular system,
Central nervous system, respiratory system.
 Maintain osmolarity of ECF and ICF and hence cellular
volume
 Regulation of acid base balance along with cellular growth,
protein synthesis and hormonal secretion
 Vital for cell excitability and muscle contraction
 Maintenance of transmembrane electric potential.
Physiology
 98% of total body K+ is intracellular and chiefly in muscles.
 In a healthy individual steady state K+ excreted 90% in urine
and 10% in feces.
 K+ absorbs from small intestine; through duodenum, jejunum
and ileum.
 K+ mainly required for the below mentioned channels’
 K+ ATPase: almost all cells contains this pump; required for
maintenance of ICF and ECF through electromechanical gradient
(3 Na+ out & 2 K+ in)
 H+K+ATPase: In GI cells and renal tubules (H+ out and K+
in)
 Na+K+Cl- co transport: in salivary gland, GI tract and
Renal tubules; brings 1 Na+, 1 K+ & 2 Cl- inside cell
 K+CI- Co transport: plays role in maintaining volume of
erythrocytes.
 Potassium homeostasis is mainly done by renal system.
 In case of hypokalemia it reabsorbs the filtered K+ and in
hyperkalemia it promotes secretion of K+ by principle
cells.
Classification of Hypokalemia
Etiology of Hypokalemia
 There are 2 main causes of hypokalemia:
Transcellular K' shifts from ECF to ICF:
Iatrogenic causes:
 Insulin therapy
 Lithium therapy
 Vitamin B therapy
 Barium ingestion
 Exogenous catecholamines:
 Epinephrine
 Ritodrine, terbutaline
 Stress related catecholamine release
 Acute alkalosis
 Hypothermia
 Hypokalemic periodic paralysis
 Thyrotoxicosis (rarely)
Potassium depletion:
 Insufficient intake:
 Anorexia nervosa, geophagia
 Starvation, primary aldosteronism
 Alcoholism, secondary aldosteronism
Increased losses:
 GI losses:
 Vomiting, malabsorption
 NG suction
 Diarrhea (especially secretory diarrhea)
 Ureterosigmoidostomy
 Villous adenomas
 Enteric fistulas
Renal losses:
 Primary hyperaldosteronism (Conns syndrome)
 Bartters syndrome
 Liddles syndrome
 Chronic metabolic acidosis
 Renal tubular acidosis
 Reno vascular hypertension
 Excessive tobacco chewing
 Drugs:
 Carbenicillin
 Gentamicin
 Amphotericin B
 Levodopa
 Lithium
 Theophylline
 Chloroquine
Pathophysiology
 K+ is the principle intracellular cation, 98% of K in body is
intracellular
 Extracellular K+ is found mainly in muscles
 Hypokalemia results in a reduction of the extracellular
potassium levels
 Reduction in ECF K+ leads to a reduction in the resting
membrane potential (RMP)
 This causes reduced responsiveness to sodium shifts into
the cell
 Therefore, cellular excitability reduces
 Chronic K+ loss causes ratio of ICF: ECF K+ to remain
stable
 Acute K+ loss causes redistribution from ECF to ICF,
causing changes in RMP
 This causes hyperpolarization of cardiac cell resulting in:
 Ventricular premature ectopics.
 Re-entrant phenomenon
 Ectopic tachycardia
Clinical features
Cardiovascular system:
 Hypertension
 Autonomic neuropathy
 Orthostatic hypotension
 ECG changes :
 U waves
 T wave inversion
 ST depression
 QT shortening
 Dysrhythmias: ventricular ectopics and AF most commonly
 Myocardial dysfunction
Neuromuscular:
 Malaise
 fatigue
 Skeletal muscle weakness
 Hyporeflexia
 Cramps, paralysis, tetany
 Paresthesia, rhabdomyolysis
Gastrointestinal:
 Nausea, vomiting
 Abdominal distension Paralytic ileus
Renal:
 Metabolic alkalosis
 Paradoxical aciduria
 Nephrogenic diabetes insipidus
 Increased ammonia production
 Low GFR
 Chronic intestitial damage
Metabolic:
 Encephalopathy in patients with liver disease
Endocrine:
 Glucose intolerance due to decreased insulin secretion
 Decreased aldosterone secretion
Ecg changes that do not correlate with
severity of Hypokalemia
Changes include:
 Narrow QRS complexes
 ST depression > 0.5 mm
 QT prolongation
 T wave inversion and flattening
 U wave amplitude> 1 mm
 U wave amplitude greater than T wave amplitude inthe
same lead
 These patients are predisposed to serious ventricular
arrhythmias such as:
 Ventricular tachycardia
 Torsades de-pointes
 Ventricular fibrillation.
Therapeutic goals
1. Prevention of hypokalemia
2. To prevent life threatening complications. (arrhythmia
and respiratory failure)
3. To correct the potassium deficit
4. To minimize on-going losses
5. To treat underlying etiology
Prevention of potassium depletion
 Normal potassium intake of about 60 mEq/day is sufficient to
prevent hypokalemia.
 But patients receiving digitalis, long term diuretics or large
doses of steroids should receive potassium supplement.
Conditions where prevention of hypokalemia is of special
importance are digitalis therapy, hepatic failure, previous
myocardial infarction or IHD and diabetes mellitus.
 Postoperative patients on parenteral fluid therapy should
receive40-50 mEq/day of potassium to prevent hypokalemia.
How much total body potassium deficit
occurs in hypokalemia?
 The degree of total body potassium depletion does not
correlate with serum potassium.
 Roughly 1 mEq/L fall in serum potassium 200-400 mEq
total body potassium deficit.
When to treat hypokalemia? – Treatment
guidelines
3.5 to 4 mEq/L:
 No potassium supplement. Increased oral intake of potassium rich
food ,Add potassium sparing diuretics or decrease dose of diuretics
3 to 3.5 mEq/L:
 Treatment in selected high risk patients(Risk of arrhythmia e.g.
CHF, digitalis therapy, history of acute myocradial infarction or
IHD.)
< 3 mEq/L :
 Needs definitive treatment
How much potassium to give
 The amount of potassium required to correct potassium deficit
cannot be determined by any fixed formula.
 When the average deficit of potassium is about 200-400 mEq,
50 - 100 mEq/day of potassium slowly given & it adequately
corrects deficit.
 With severe hypokalemia or with high rate of ongoing loss,
larger dose may be required.
 The deficit should be corrected slowly over a period of days. It
may take weeks to correct severe potassium loss.
 Failure to increase serum potassium after sufficient dose and
duration of potassium supplement raises the possibility of
associated magnesium deficiency.
Selection of Potassium preparations
 Potassium chloride (KCI) is usually the preparation of choice and
will promote correction of hypokalemia as well as of metabolic
alkalosis (vomiting and diuretics lead to both hypokalemia and
alkalosis).
 Potassium bicarbonate and citrate tend to alkalinize the patient
and would be more appropriate for hypokalemia associated with
chronic diarrhoea or distal RTA.
 Oral potassium administration is safer than I.V. route because I.V.
route carries high risk of hyperkalemia.
 Inj. Potassium chloride: Most widely available and used is
inj. KCI 15%, 10 ml ampoule.
 10 ml of 15% KCI = 1.5 gm KCI = 20 mEq of potassium,1 ml
of 15% KCI = 2 mEq of potassium
Oral K+ Supplementation
 Oral potassium is a safer mode of correction of hypokalemia's
 In mild to moderate hypokalemia (serum potassium 3 to 3.5 mEq/L)
average dose of potassium chloride is 60 to 80 mEq/day (20 mEq, 3-
4 times) along with treatment of underlying disorder (such as
vomiting or diarrhoea).
 In severe or symptomatic hypokalemia more rapid replacement is
needed and can be most easily done by oral replacement.
 In severe cases (serum potassium 2 mEq/L or less) it can be
increased upto 40 mEq 6 hourly under close ECG monitoring.
 Potassium chloride solution, available in the market
contains 20 mEq potassium per 15 ml solution (1gm
KCl=13.4 mEq of potassium).
 KCI tablets available contain 8 mEq potassium per tablet.
 Oral potassium preparation may frequently cause G.I.
irritation and therefore the patient is advised to take
potassium chloride solution with proper dilution in a glass
of water, after food.
 Esophageal or small bowel erosion and stricture are
uncommon side effects.
Potassium rich food:
 Fruit juices, coconut water, banana, juicy fruits, dry
fruits, chocolate, coffee, soup, salt substitutes e.g. Lona
salt.
Iv potassium therapy
 I.V. potassium supplementation carries higher risk of
hyperkalemia.
 So I.V. potassium supplementation should be reserved for
severe symptomatic hypokalemia (K* <3 mEq/L) or for patients
who cannot ingest oral potassium
 common guidelines for I.V. potassium therapy are as follows:
 Always monitor I.V. potassium therapy closely with continuous ECG
monitoring and frequent serum potassium estimation.
 Avoid I.V. potassium, till urine output is established
 Don't give 10-20 mEq/hour.
 Don't give> 40 mEq/Litre.
 Don't give > 240 mEq/day.
 Never give inj. KCI directly intravenously, it can cause
sudden hyperkalemia and instant death from cardiac
arrest.
 Never add KCI to Isolyte-M.
 Remember that hypokalemia is safer than hyperkalemia.
 Rapid I.V. correction can cause dangerous hyperkalemia
even in potassium depleted patients.
 Treatment of acidosis with I.V. NaHCO, may aggravate or
precipitate hypokalemia (due to intracellular shift of
potassium
How long to give
 As soon as cardiac rhythm returns to normal or the
respiratory muscle strength is restored to normal, I.V.
potassium drip is gradually tapered and discontinued and
oral KCI is initiated.
Infusion rate and method:
(Body weight) x (Potassium deficit) 1
KCL required in mL = _____________________________ x ___
2 3
 Maximum rate is 0.5 mEq/kg/hr or 250 mEq/day
 20 mEq K is added to 100 mL of NS and infused over 1 hour
 Maximum rate of infusion is usually set at 20 mEq/hr
Anaesthetic considerations
Pre-operative considerations
 Patients with ESRD should undergo dialysis except during
emergency surgery
 Plasma K+ levels measured 1-3 days before surgery
 0.2-0.8 mEq/L higher than if measured immediately before
surgery
 Beta blockers like propranolol can be used to prevent this effect
 Prevent hypokalemia from anxiety induced hyperventilation by
premedication with dexmedetomidine/clonidine
INTRA-OPERATIVE CONSIDERATIONS
 Glucose free intravenous fluids are used
 No change in anesthetic requirements immediately in
perioperative period
 Avoid hyperventilation as it aggravates hypokalemia by causing
respiratory alkalosis
 Increased sensitivity to NMBAs may be seen
 This may necessitate:
 Reduction in dosage of NMBAS
 Monitoring with nerve stimulator
 Prolonged NMB action expected post-surgery: delayed recovery.
Following factors should be considered
before postponement of Sx
 Urgency of surgery
 Concomitant medications given (digitalis toxicity with
serum K<4 mEq/L)
 Acid base balance
 Sudden of development of hypokalemia
 All patients undergoing elective surgery to have normal K+
level
 Postponement of surgery not required if K+ >3 mEq/l.
 Thank you

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Hypokalemia.pptx

  • 1. HYPOKALEMIA Presenter – Dr Sudha.P Moderator- Dr. MAHADEVAIAH
  • 2. Introduction  Normal potassium levels are 3.5-5 mEq/L  Hypokalemia is defined as plasma K levels <3.5mEq/L  Plasma potassium levels correlate poorly with the total potassium deficit.  Potassium is essential for Muscles, cardiovascular system, Central nervous system, respiratory system.  Maintain osmolarity of ECF and ICF and hence cellular volume
  • 3.  Regulation of acid base balance along with cellular growth, protein synthesis and hormonal secretion  Vital for cell excitability and muscle contraction  Maintenance of transmembrane electric potential.
  • 4. Physiology  98% of total body K+ is intracellular and chiefly in muscles.  In a healthy individual steady state K+ excreted 90% in urine and 10% in feces.  K+ absorbs from small intestine; through duodenum, jejunum and ileum.  K+ mainly required for the below mentioned channels’  K+ ATPase: almost all cells contains this pump; required for maintenance of ICF and ECF through electromechanical gradient (3 Na+ out & 2 K+ in)
  • 5.  H+K+ATPase: In GI cells and renal tubules (H+ out and K+ in)  Na+K+Cl- co transport: in salivary gland, GI tract and Renal tubules; brings 1 Na+, 1 K+ & 2 Cl- inside cell  K+CI- Co transport: plays role in maintaining volume of erythrocytes.
  • 6.  Potassium homeostasis is mainly done by renal system.  In case of hypokalemia it reabsorbs the filtered K+ and in hyperkalemia it promotes secretion of K+ by principle cells.
  • 8. Etiology of Hypokalemia  There are 2 main causes of hypokalemia: Transcellular K' shifts from ECF to ICF: Iatrogenic causes:  Insulin therapy  Lithium therapy  Vitamin B therapy  Barium ingestion  Exogenous catecholamines:  Epinephrine  Ritodrine, terbutaline
  • 9.  Stress related catecholamine release  Acute alkalosis  Hypothermia  Hypokalemic periodic paralysis  Thyrotoxicosis (rarely) Potassium depletion:  Insufficient intake:  Anorexia nervosa, geophagia  Starvation, primary aldosteronism  Alcoholism, secondary aldosteronism
  • 10. Increased losses:  GI losses:  Vomiting, malabsorption  NG suction  Diarrhea (especially secretory diarrhea)  Ureterosigmoidostomy  Villous adenomas  Enteric fistulas
  • 11. Renal losses:  Primary hyperaldosteronism (Conns syndrome)  Bartters syndrome  Liddles syndrome  Chronic metabolic acidosis  Renal tubular acidosis  Reno vascular hypertension  Excessive tobacco chewing
  • 12.  Drugs:  Carbenicillin  Gentamicin  Amphotericin B  Levodopa  Lithium  Theophylline  Chloroquine
  • 13. Pathophysiology  K+ is the principle intracellular cation, 98% of K in body is intracellular  Extracellular K+ is found mainly in muscles  Hypokalemia results in a reduction of the extracellular potassium levels  Reduction in ECF K+ leads to a reduction in the resting membrane potential (RMP)  This causes reduced responsiveness to sodium shifts into the cell
  • 14.  Therefore, cellular excitability reduces  Chronic K+ loss causes ratio of ICF: ECF K+ to remain stable  Acute K+ loss causes redistribution from ECF to ICF, causing changes in RMP  This causes hyperpolarization of cardiac cell resulting in:  Ventricular premature ectopics.  Re-entrant phenomenon  Ectopic tachycardia
  • 15. Clinical features Cardiovascular system:  Hypertension  Autonomic neuropathy  Orthostatic hypotension  ECG changes :  U waves  T wave inversion  ST depression  QT shortening
  • 16.  Dysrhythmias: ventricular ectopics and AF most commonly  Myocardial dysfunction Neuromuscular:  Malaise  fatigue  Skeletal muscle weakness  Hyporeflexia  Cramps, paralysis, tetany  Paresthesia, rhabdomyolysis
  • 17. Gastrointestinal:  Nausea, vomiting  Abdominal distension Paralytic ileus Renal:  Metabolic alkalosis  Paradoxical aciduria  Nephrogenic diabetes insipidus  Increased ammonia production  Low GFR  Chronic intestitial damage
  • 18. Metabolic:  Encephalopathy in patients with liver disease Endocrine:  Glucose intolerance due to decreased insulin secretion  Decreased aldosterone secretion
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  • 23. Ecg changes that do not correlate with severity of Hypokalemia Changes include:  Narrow QRS complexes  ST depression > 0.5 mm  QT prolongation  T wave inversion and flattening  U wave amplitude> 1 mm  U wave amplitude greater than T wave amplitude inthe same lead
  • 24.  These patients are predisposed to serious ventricular arrhythmias such as:  Ventricular tachycardia  Torsades de-pointes  Ventricular fibrillation.
  • 25. Therapeutic goals 1. Prevention of hypokalemia 2. To prevent life threatening complications. (arrhythmia and respiratory failure) 3. To correct the potassium deficit 4. To minimize on-going losses 5. To treat underlying etiology
  • 26. Prevention of potassium depletion  Normal potassium intake of about 60 mEq/day is sufficient to prevent hypokalemia.  But patients receiving digitalis, long term diuretics or large doses of steroids should receive potassium supplement. Conditions where prevention of hypokalemia is of special importance are digitalis therapy, hepatic failure, previous myocardial infarction or IHD and diabetes mellitus.  Postoperative patients on parenteral fluid therapy should receive40-50 mEq/day of potassium to prevent hypokalemia.
  • 27. How much total body potassium deficit occurs in hypokalemia?  The degree of total body potassium depletion does not correlate with serum potassium.  Roughly 1 mEq/L fall in serum potassium 200-400 mEq total body potassium deficit.
  • 28. When to treat hypokalemia? – Treatment guidelines 3.5 to 4 mEq/L:  No potassium supplement. Increased oral intake of potassium rich food ,Add potassium sparing diuretics or decrease dose of diuretics 3 to 3.5 mEq/L:  Treatment in selected high risk patients(Risk of arrhythmia e.g. CHF, digitalis therapy, history of acute myocradial infarction or IHD.) < 3 mEq/L :  Needs definitive treatment
  • 29. How much potassium to give  The amount of potassium required to correct potassium deficit cannot be determined by any fixed formula.  When the average deficit of potassium is about 200-400 mEq, 50 - 100 mEq/day of potassium slowly given & it adequately corrects deficit.  With severe hypokalemia or with high rate of ongoing loss, larger dose may be required.  The deficit should be corrected slowly over a period of days. It may take weeks to correct severe potassium loss.  Failure to increase serum potassium after sufficient dose and duration of potassium supplement raises the possibility of associated magnesium deficiency.
  • 30. Selection of Potassium preparations  Potassium chloride (KCI) is usually the preparation of choice and will promote correction of hypokalemia as well as of metabolic alkalosis (vomiting and diuretics lead to both hypokalemia and alkalosis).  Potassium bicarbonate and citrate tend to alkalinize the patient and would be more appropriate for hypokalemia associated with chronic diarrhoea or distal RTA.  Oral potassium administration is safer than I.V. route because I.V. route carries high risk of hyperkalemia.
  • 31.  Inj. Potassium chloride: Most widely available and used is inj. KCI 15%, 10 ml ampoule.  10 ml of 15% KCI = 1.5 gm KCI = 20 mEq of potassium,1 ml of 15% KCI = 2 mEq of potassium
  • 32. Oral K+ Supplementation  Oral potassium is a safer mode of correction of hypokalemia's  In mild to moderate hypokalemia (serum potassium 3 to 3.5 mEq/L) average dose of potassium chloride is 60 to 80 mEq/day (20 mEq, 3- 4 times) along with treatment of underlying disorder (such as vomiting or diarrhoea).  In severe or symptomatic hypokalemia more rapid replacement is needed and can be most easily done by oral replacement.  In severe cases (serum potassium 2 mEq/L or less) it can be increased upto 40 mEq 6 hourly under close ECG monitoring.
  • 33.  Potassium chloride solution, available in the market contains 20 mEq potassium per 15 ml solution (1gm KCl=13.4 mEq of potassium).  KCI tablets available contain 8 mEq potassium per tablet.  Oral potassium preparation may frequently cause G.I. irritation and therefore the patient is advised to take potassium chloride solution with proper dilution in a glass of water, after food.  Esophageal or small bowel erosion and stricture are uncommon side effects.
  • 34. Potassium rich food:  Fruit juices, coconut water, banana, juicy fruits, dry fruits, chocolate, coffee, soup, salt substitutes e.g. Lona salt.
  • 35. Iv potassium therapy  I.V. potassium supplementation carries higher risk of hyperkalemia.  So I.V. potassium supplementation should be reserved for severe symptomatic hypokalemia (K* <3 mEq/L) or for patients who cannot ingest oral potassium  common guidelines for I.V. potassium therapy are as follows:  Always monitor I.V. potassium therapy closely with continuous ECG monitoring and frequent serum potassium estimation.  Avoid I.V. potassium, till urine output is established
  • 36.  Don't give 10-20 mEq/hour.  Don't give> 40 mEq/Litre.  Don't give > 240 mEq/day.  Never give inj. KCI directly intravenously, it can cause sudden hyperkalemia and instant death from cardiac arrest.  Never add KCI to Isolyte-M.  Remember that hypokalemia is safer than hyperkalemia.
  • 37.  Rapid I.V. correction can cause dangerous hyperkalemia even in potassium depleted patients.  Treatment of acidosis with I.V. NaHCO, may aggravate or precipitate hypokalemia (due to intracellular shift of potassium
  • 38. How long to give  As soon as cardiac rhythm returns to normal or the respiratory muscle strength is restored to normal, I.V. potassium drip is gradually tapered and discontinued and oral KCI is initiated.
  • 39. Infusion rate and method: (Body weight) x (Potassium deficit) 1 KCL required in mL = _____________________________ x ___ 2 3  Maximum rate is 0.5 mEq/kg/hr or 250 mEq/day  20 mEq K is added to 100 mL of NS and infused over 1 hour  Maximum rate of infusion is usually set at 20 mEq/hr
  • 41. Pre-operative considerations  Patients with ESRD should undergo dialysis except during emergency surgery  Plasma K+ levels measured 1-3 days before surgery  0.2-0.8 mEq/L higher than if measured immediately before surgery  Beta blockers like propranolol can be used to prevent this effect  Prevent hypokalemia from anxiety induced hyperventilation by premedication with dexmedetomidine/clonidine
  • 42. INTRA-OPERATIVE CONSIDERATIONS  Glucose free intravenous fluids are used  No change in anesthetic requirements immediately in perioperative period  Avoid hyperventilation as it aggravates hypokalemia by causing respiratory alkalosis  Increased sensitivity to NMBAs may be seen  This may necessitate:  Reduction in dosage of NMBAS  Monitoring with nerve stimulator  Prolonged NMB action expected post-surgery: delayed recovery.
  • 43. Following factors should be considered before postponement of Sx  Urgency of surgery  Concomitant medications given (digitalis toxicity with serum K<4 mEq/L)  Acid base balance  Sudden of development of hypokalemia  All patients undergoing elective surgery to have normal K+ level  Postponement of surgery not required if K+ >3 mEq/l.