Treatment For Hyperkalemia

TREATMENT FOR HYPERKALEMIA

Q. 1

Hyperkalemia without ECG changes may be treated with all except ‑

 A

Calcium gluconate

 B

Salbutamol

 C

Na bicarbonate

 D

Insulin with dextrose

Q. 1

Hyperkalemia without ECG changes may be treated with all except ‑

 A

Calcium gluconate

 B

Salbutamol

 C

Na bicarbonate

 D

Insulin with dextrose

Ans. B

Explanation:

Calcium gluconate [Ref Harrison 17/c p. 284]

  • Calcium gluconate is the fastest acting agent used in t/t of hyperkalemia.
  • In acts within minutes but an important point to note is that it does not cause transcellular movement of potassium, instead it acts on cell membrane.

– it stabilizes the cardiac: cell membrane and reduces chances of cardiac anyhthmia…

– Thus it has no use when there are no E.C.G.. features.

NaHCO3

  • NaHCO3 has been routinely used in the treatment of hyperkalemia.
  • It was believed that NaHCO3 caused movement of potassium inside the cells by causing alkalosis.
  • But studies do not support this

– They claim that NaHCO3 do not cause movement of potassium inside the cells in acute cases of hyperkalemia. – It only decreases potassium when there is coexisting acidosis.

– NaHCO3 can decrease potassium level in chronic hyperkalemia. It increases potassium delivery to the kidney.

  • But the use of NaHCO3 still continues in most hospitals and institutes across the world.

– It is now hypothesized that NaHCO3 does not cause r entry inside the cell by mechanism earlier believed to he, but by another mechanism.

  • The question does not say anything about acidosis.
  • Don’t think that acidosis occurs only in severe hyperkalemia.
  • Most patients with C.R.F. present with acidosis and mild moderate hyperkalemia.

In hyperkalemia with no E.C.G. feature, calcium prophylaxis is not indicated

– Calcium gluconate is administered to stabilize the cardiac membrane

– Instability of the cardiac membrane is indicated by E.C.G. changes

– Absence of E.C.G. changes suggest that the cardiac membrane is stable. In these cases there is no use of calcium administration.

  • Prophylactic calcium gluconate is of no use.


Q. 2

A girl presented with severe hyperkalemia and peaked T waves on ECG. Fastest way of shifting potassium intracellularly is ‑

 A

Calcium gluconate IV

 B

Oral resins

 C

Insulin + glucose

 D

Sodium bicarbonate

Q. 2

A girl presented with severe hyperkalemia and peaked T waves on ECG. Fastest way of shifting potassium intracellularly is ‑

 A

Calcium gluconate IV

 B

Oral resins

 C

Insulin + glucose

 D

Sodium bicarbonate

Ans. C

Explanation:

Insulin + glucose [Ref : Harrison 17th/e p. 284]

  • Tall T waves on ECG indicate cardiac manifestation of hyperkalemia.

– Intravenous calcium gluconate is the first drug to be administered in a patient with hyperkalemia having E.C.G. abnormalities. – It stabilizes the myocardium immediately. – It acts within minutes and is characterized by improvement in E.C.G. appearance.

But an important point to note

It does not affect transcellular movement of potassium. Thus it won’t help in reducing the hyperkalemia. Among the agents which cause transcellular (intracellular) movement of potassium.

“Intravenous insulin is the fastest way to lower serum potassium levels”.

The goals of the therapy for the tit of acute hyperkalemia in chronological order are as follows:?

i)   Antagonize the affect of IC on excitable cell membranes

ii)  Redistribution of extracellular potassium into cells

iii)   Enhance elimination of potassium from the body

i) Antagonize the effect of potassium on excitable cell membrane

  • Calcium directly antagonizes the myocardial effect of hyperkalemia.
  • It does so by reducing the threshold potential of cardiac myocytes.
  • Calcium. for injection is available as chloride or gluconate salt.
  • The preferred agent is the gluconate salt since it is less likely than calcium chloride to cause tissue necrosis.
  • The onset of action is < 3 minutes.
  • The duration of action is 30-60 minutes during which time further measures may be undertaken to lower p1{.

ii) Redistribution of potassium into cells 😕

Insulin

  • Insulin shifts potassium into cells.
  • Potassium shift inside the cells is mediated by Na+ IC ATPase.
  • I.V. insulin is the fastest way to lower serum potassium levelr2.
  • The onset of action is < 15 minutes and the effect is maximal b/w 30-60 minutes.
  • Dextrose is given along with insulin to prevent hypoglycemia.
  • It was believed that administration of dextrose alone, can cause shift of potassium inside the cells by promoting insulin release. •

The administration of hypertonic dextrose alone for hyperkalemia is not recommended for two reasons:­- Endogenous insulin levels are unlikely to rise to the level necessary for a therapeutic effect.

– There is a risk of exacerbating hyperkalemia by inducing hypertonicity.

5′ adrenoceptor agonists

  • These drugs can also cause movement of potassium inside the cell.
  • High dose albuterol shows their effect in 30 minutes and persists for at least 2 hours.
  • The effect of insulin is additive with that of albuterol.

Patients taking nonselective 18 adrenoceptor blockers will be unlikely to manifest the hypokalemic effects of albuterol.

– Even among patients not taking ft blockers as many as 40% seem to be resistant to the hypokalemic effect of albuterol.

– The mechanism .for this resistance is unknown and currently, there is no basis for predicting which patients will respond.

– For this reason albuterol should never be used as a single agent for the treatment of urgent hyperkalemia. Bicarbonate

  • Bicarbonate (as a bolus injection) was used in the emergency t/t of hyperkalemia. Ironically this dogma was based on studies using a prolonged (4-6 hrs) infusion of bicarbonate.
  • It has now been demonstrated that short term bicarbonate infusion does not reduce pK in patients with dialysis dependent kidney failure, implying that it does not cause IC+ shift into cells.
  • Sodium bicarbonate seems to have no effect to shift IC into cells even after several hours.
  • It is likely to be effective especially in combination with a diuretic drug in enhancing urinary IC’ elimination in patients with some kidney. function, although it use for this purpose has not been evaluated.

iii) Elimination of potassium from the body

  • Hyperkalemia occurs most often in patients with renal insufficiency.

– However renal potassium excretion may be enhanced even in patients with significant renal impairment by increasing the delivery of solute to the distal nephron.

Sodium bicarbonate

  • A sodium bicarbonate infusion administered during 4-6 hrs at a rate designed to alkalinize the urine may enhance urinary K+ excretion and would be desirable especially in patients with metabolic acidosis.
  • The risk of volume expansion with the bicarbonate infusion can be mitigated by use of loop acting diuretics which would, be likely to enhance the kaliuresis.

Exchange resin

  • Sodium polysterene sulfonate is a cation exchange resin.
  • In the lumen of intestine it exchanges sodium for secreted potassium.
  • Most of this exchange takes place in the colon, the site of most potassium secretion in the gut.

There are two concerns with the use of resin in the t/t of urgent hyperkalemia

  • The first is its slow effect

– When given orally, the onset of action is at least 2 hrs and the maximum effect may not be seen for more than 6 hrs.

  • The second is its adverse effect

– It can cause intestinal necrosis

Dialysis

-“Hemodialysis is the method of choice for removing potassium from the body”.

– The rate of potassium removed with peritoneal dialysis is much slower than with hemodialysis.


Q. 3

Hyperkalemia with no ECG finding. The drug that should not be used is‑

 A

Sodium bicarbonate

 B

Calcium gluconate

 C

Glucose with insulin

 D

Resins

Q. 3

Hyperkalemia with no ECG finding. The drug that should not be used is‑

 A

Sodium bicarbonate

 B

Calcium gluconate

 C

Glucose with insulin

 D

Resins

Ans. B

Explanation:

Calcium gluconate [Ref: Harrison 17th/e p. 284] (Also see AIIMS May 2010)

Calcium gluconate is the fastest acting agent used in t/t of hyperkalemia.

In acts within nzinutes but an important point to note is that it does not cause transcellular movement of potassium, instead it acts on cell membrane.

– It stabilizes the cardiac cell membrane and reduces chances of cardiac arryhthmia.

– Thus it has no use when there are no E.C.G. features.

NaHCO3

  • NaHCO3 has been routinely used in the treatment of hyperkalemia.
  • It was believed that NaHCO3 caused movement of potassium inside the cells by causing alkalosis.
  • But studies do not support this

– They claim that NaHCO3 do not cause movement of potassium inside the cells in acute cases of hyperkalemia.

– It only decreases potassium when there is coexisting acidosis.

– NaHCO3 can decrease potassium level in chronic hyperkalemia. It increases potassium delivery to the kidney.

  • But the use of NaHCO3 still continues in most hospitals and institutes across the world.

– It is now hypothesized that NaHCO3 does not cause IC* entry inside the cell by mechanism earlier believed to be, but by another mechanism.

  • The question does not say anything about acidosis.
  • Don’t think that acidosis occurs only in severe hyperkalemia.
  • Most patients with C.R. F. present with acidosis and mild moderate hyperkalemia.

In hyperkalemia with no E.C.G. feature, calcium prophylaxis is not indicated

– Calcium gluconate is administered to stabilize the cardiac membrane

– Instability of the cardiac membrane is indicated by E.C.G. changes

– Absence of E.C.G. changes suggest that the cardiac membrane is stable. In these cases there is no use of calcium administration.

  • Prophylactic calcium gluconate is of no use.

Quiz In Between


Q. 4

All are used in hyperkalemia except

 A

50 ml of 50% dextrose

 B

Sodium bicarbonate

 C

Salbutamol

 D

Salbutamol

Q. 4

All are used in hyperkalemia except

 A

50 ml of 50% dextrose

 B

Sodium bicarbonate

 C

Salbutamol

 D

Salbutamol

Ans. A

Explanation:

50 ml of 50% dextrose [Ref: Harrison I7th/e p. 284-285]

Dextrose alone

  • It was earlier believed that administration of dextrose alone can cause shift of potassium inside the cells by promoting insulin releases.
  • The administration of hypertonic dextrone alone for hyperkalemia is not recommended for two reasons. – Endogenous insulin levels are unlikely to rise to the level necessary for therapeutic effect.

– There is a risk of exacerbating hyperkalemia by inducing hypertonicity.

Sodium Biarbonate

  • Sodium bicarbonate was earlier believed to cause movement of potassium inside the cells.
  • It has now been demonstrated that Na Bicarbonate does not cause movement of potassium inside the cells even when infused for 4-6 hrs.
  • Instead.

Sodium bicarbonate causes excretion of potassium from the body.

When sodium bicarbonate is administered at a rate designed to alkalinize the urine it enhances urinary K+ excretion. This also benefits in metabolic acidosis.


Q. 5

Drugs not used for treatment of acute hyperkalemia ‑

 A

Insulin + glucose

 B

Potassium exchange resins

 C

Calcium carbonate

 D

Sodium bicarbonate

Q. 5

Drugs not used for treatment of acute hyperkalemia ‑

 A

Insulin + glucose

 B

Potassium exchange resins

 C

Calcium carbonate

 D

Sodium bicarbonate

Ans. B

Explanation:

Potassium exchange resins [Ref : Harrison 17’Ve p. 84; CMDT 2007 p. 899] Repeat from May 10 Q no. 101.

EMERGENCY

Modality

Mechanism of action

Onset

Duration

Calcium

gluconate

Antagonizes cardiac

conduction abnormalities

0-5 minutes

1 hour

Sodium

Bicarbonate

Distributes K+ into cells (only

indicated with acidosis )

15-30 minutes

1-2 hours

Insulin

Distributes K+ into cells

15-60 minutes

4-6 hours

Albuterol

Distributes K+ into cells

15-30 minutes

2-4 hours

NONEMERGENCY

Modality

Mechanism of action

Duration of treatment

Loop diuretic

I Renal K+ excretion

0.5-2 hours

Sodium polystyrene

sulfonate (kayexalate)

Ion-exchange resin binds K+

1-3 hours

Hemodialysis

Extracorporeal K+ removal

48 hours

Peritoneal dialysis

Peritoneal K+ removal

48 hours


Q. 6

Patient presents with hyperkalemia with no ECG changes. All are used for treatment, EXCEPT:

 A

Glucose + Insulin

 B

Sodium bicarbonate

 C

Calcium gluconate

 D

Resins

Q. 6

Patient presents with hyperkalemia with no ECG changes. All are used for treatment, EXCEPT:

 A

Glucose + Insulin

 B

Sodium bicarbonate

 C

Calcium gluconate

 D

Resins

Ans. C

Explanation:

Prompt treatment is essential for hyperkalemia without ECG changes to prevent cardiac irregularities. It consists of strategies that, 

  • Promote potassium redistribution into cells (with glucose, insulin, and beta2-agonist medications)
  • Increase potassium removal (through sodium polystyrene sulfonate, loop diuretics, or hemodialysis).
  • Calcium gluconate administration is indicated when there is ECG changes like arrhythmias. 
Must know:
 
Hyperkalemia is defined as a serum potassium level >5.5 mmol/L (>5.5 meq/L).
Classical ECG manifestations of hyperkalemia:
  • Tall peaked T waves
  • Loss of P waves
  • Widened QRS complex
  • Sine wave pattern
Cardiac arrhythmias associated with hyperkalemia include,
  • Sinus bradycardia
  • Sinus arrest
  • Slow idioventricular rythms
  • Ventricular tachycardia
  • Ventricular fibrillation
  • Asystole
Ref: Josephson S.A., Samuels M.A. (2012). Chapter e47. Special Issues in Inpatient Neurologic Consultation. In D.L. Longo, A.S. Fauci, D.L. Kasper, S.L. Hauser, J.L. Jameson, J. Loscalzo (Eds), Harrison’s Principles of Internal Medicine, 18e.

Quiz In Between


Q. 7

All the following drugs may cause hyperkalemia except-

 A

Cyclosporine

 B

Amphotericin B

 C

Heparin

 D

NSAIDs

Q. 7

All the following drugs may cause hyperkalemia except-

 A

Cyclosporine

 B

Amphotericin B

 C

Heparin

 D

NSAIDs

Ans. B

Explanation:

Ans. is ‘b’ Amphotericin B

Important drugs causing hvperkalemia

o ACE inhibitors           o Trimethoprim            o Succinylcholine            o K+ sparing diuretic        o Heparin

o NSAIDS                   o Pentamidine              o Lithium.                    o Cyclosporine


Q. 8

A girl aged 8 years has been admitted for dialysis.

She has serum K of 7.5 meq/1, which is the fastest way to reduce the hyperkalemia?

 A

Kayexalate enema

 B

Infusion of insulin + glucose

 C

IV calcium gluconate

 D

IV NaHCO3

Q. 8

A girl aged 8 years has been admitted for dialysis.

She has serum K of 7.5 meq/1, which is the fastest way to reduce the hyperkalemia?

 A

Kayexalate enema

 B

Infusion of insulin + glucose

 C

IV calcium gluconate

 D

IV NaHCO3

Ans. B

Explanation:

Answer is B (Infusion of insulin and glucose):

‘Intravenous insulin is the fastest way to lower serum potassium levels’

Reduce serum levels by shifting Remove excess potassium from the body K+ from extracellular to intracellular fluid


Q. 9

All of the following are used for treatment of hyperkalaemia except :

 A

Calcium gluconate

 B

Sodium bicarbonate

 C

Intravenous infusion of glucose with insulin

 D

Beta blockers

Q. 9

All of the following are used for treatment of hyperkalaemia except :

 A

Calcium gluconate

 B

Sodium bicarbonate

 C

Intravenous infusion of glucose with insulin

 D

Beta blockers

Ans. D

Explanation:

Answer is D (Beta blocker)

Beta blockers have no role in management of hyperkalemia

Parenteral or Nebulrized Beta 2 agonist may be useful by promoting cellular uptake of IC .

Calcium gluconate provides cardiac protection by decreasing membrane excitability, white Insulin and Sodium bicarbonate decrease plasma IC concentration by shifting IC+ into cells.

Quiz In Between


Q. 10

All of the following are used in the management of hyperkalemia except:  

March 2007

 A

Calcium gluconate

 B

Sodium bicarbonate

 C

I.V. infusion with glucose and insulin

 D

I.V. KC1 infusion

Q. 10

All of the following are used in the management of hyperkalemia except:  

March 2007

 A

Calcium gluconate

 B

Sodium bicarbonate

 C

I.V. infusion with glucose and insulin

 D

I.V. KC1 infusion

Ans. D

Explanation:

Ans. D: I.V. KC1 infusion

Causes of hyperkalemia include:

  • Ineffective elimination from the body

Renal insufficiency

– Medication that interferes with urinary excretion:

  • ACE inhibitors and angiotensin receptor blockers
  • Potassium-sparing diuretics (e.g. amiloride and spironolactone)
  • NSAIDs such as ibuprofen, naproxen, or celecoxib
  • The calcineurin inhibitor immunosuppressants cyclosporin
  • Trimethoprim
  • Pentamidine

– Mineralocorticoid deficiency or resistance, such as:

  • Addison’s disease
  • Aldosterone deficiency
  • Congenital adrenal hyperplasia
  • Type IV renal tubular acidosis (resistance of renal tubules to aldosterone)

– Gordon’s syndrome (“familial hypertension with hyperkalemia”)

Excessive release from cells

– Rhabdomyolysis, burns or any cause of rapid tissue necrosis, including tumour lysis syndrome

Massive blood transfusion or massive hemolysis

– Shifts/transport out of cells caused by acidosis, low insulin levels, beta-blocker therapy, digoxin overdose, or the paralyzing anesthetic succinylcholine

Excessive intake

– Intoxication with salt-substitute, potassium-containing dietary supplements, or potassium chloride (KC1) infusion.

ECG findings:

With mild to moderate hyperkalemia, there is reduction of the size of the P wave and development of peaked T waves. Severe hyperkalemia results in a widening of the QRS complex, and the EKG complex can evolve to a sinusoidal shape.

Treatment

  • Calcium supplementation (calcium gluconate)
  • Insulin intravenous injection along with dextrose to prevent hypoglycemia, will lead to a shift of potassium ions into cells, secondary to increased activity of the sodium-potassium ATPase.
  • Bicarbonate therapy
  • Salbutamol
  • Sodium Polystyrene sulfonate.

Q. 11

Hyperkalemia is caused by ‑

 A

Amphotiricin B

 B

Beta agonists

 C

Gentamycin

 D

Succinylcholine

Q. 11

Hyperkalemia is caused by ‑

 A

Amphotiricin B

 B

Beta agonists

 C

Gentamycin

 D

Succinylcholine

Ans. D

Explanation:

Ans. is ‘d’ i.e., Succinylcholine

Drugs causing hypokalemia

  • β agonist
  • Licorice                     
  • Penicillin derivatives 
  • Amphotericin B 
  • Theophylline
  • Steroids
  • α Blockers 
  • Toluene abuse
  • Gentamicin
  • Insulin
  • Vitamin B12
  • Diuretics
  • Carbenoxalone

Important drugs causing hyperkalemia

  • ACE inhibitors
  • Trimethoprim
  • Succinylcholine            
  • K+ sparing diuretic      
  • Hep.
  • NSAIDS
  • Pentamidine 
  • Lithium.                          
  • Cyclosporine

Q. 12

The drug of choice for acute condition as shown in the photograph below is? 

 A

PTU.

 B

Propranolol.

 C

Calcium gluconate.

 D

Alkaline diuresis.

Q. 12

The drug of choice for acute condition as shown in the photograph below is? 

 A

PTU.

 B

Propranolol.

 C

Calcium gluconate.

 D

Alkaline diuresis.

Ans. C

Explanation:

Ans:C.)Calcium gluconate.

The condition shown above is Hyperkalemia.

Hyperkalemia

Hyperkalemia
ECG:
Early ECG changes of hyperkalemia(serum potassium level of 5.5-6.5 mEq/L):

    • Tall, peaked T waves with a narrow base, best seen in precordial leads
    • Shortened QT interval
    • ST-segment depression
  • At a serum potassium level of 6.5-8.0 mEq/L, the ECG typically shows the following:
  • Peaked T waves
    • Prolonged PR interval
    • Decreased or disappearing P wave
    • Widening of the QRS
    • Amplified R wave
  • At a serum potassium level higher than 8.0 mEq/L, the ECG shows the following:
    • Absence of P wave
    • Progressive QRS widening
    • Intraventricular/fascicular/bundle branch blocks
    • The progressively widened QRS eventually merges with the T wave, forming a sine wave pattern.

Treatment is as follows:

  • IV calcium to ameliorate cardiac toxicity, if present
  • Calcium (calcium chloride or calcium gluconate) increases threshold potential thus restoring normal gradient between threshold potential and resting membrane potential, which is elevated abnormally in hyperkalemia.
  • Identify and remove sources of potassium intake
  • IV glucose and insulin infusion to enhance potassium uptake by cells
  • Correct severe metabolic acidosis with sodium bicarbonate
  • Consider beta-adrenergic agonist therapy in patients with renal failure
  • Increase potassium excretion
  • Emergency dialysis for patients with potentially lethal hyperkalemia


Quiz In Between


Q. 13

The treatment of choice in acute hyperkalemia of life threatening to cardiac myocytes is

 A

Infusion of calcium gluconate

 B

Oral resins

 C

Intravenous infusion of insulin

 D

β blocker

Q. 13

The treatment of choice in acute hyperkalemia of life threatening to cardiac myocytes is

 A

Infusion of calcium gluconate

 B

Oral resins

 C

Intravenous infusion of insulin

 D

β blocker

Ans. A

Explanation:

Ans. is `a’ i.e. Infusion of calcium gluconate


Q. 14

Succinylcholine causes hyperkalemia in patients with ‑

 A

Burn

 B

Severe infection

 C

High velocity trauma

 D

All of the above

Q. 14

Succinylcholine causes hyperkalemia in patients with ‑

 A

Burn

 B

Severe infection

 C

High velocity trauma

 D

All of the above

Ans. D

Explanation:

Ans. is’d’  i.e., All of the above

Quiz In Between



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