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Yr 4 - ACC > Electrolyte Abnormalities: Sodium & Potassium > Flashcards

Electrolyte Abnormalities: Sodium & Potassium Flashcards

1
Q

Define hyponatraemia

A

Serum sodium conc <135 mmol/L

Severe: <120 mmol/L

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2
Q

What is serum osmolality?

A

The conc of solutes in the blood –> sodium is the most important determinant of serum osmolality.

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3
Q

How does changes in sodium affect water movement?

A

Any alteration in sodium concentration will affect serum osmolality, ultimately leading to shifts in water (osmotic shifts) between the intracellular and extracellular compartments.

I.e. if there is a lot of sodium in the blood, water will move out of cells and into the blood (intra to extracellular shift).

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4
Q

What complex homeostatic mechanism maintains serum sodium regulation?

A

1) Thirst
2) Anti-diuretic hormone (ADH)
3) Renin-angiotensin-aldosterone system (RAAS)
4) Renal sodium excretion

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5
Q

What is ADH released in response to?

A

Increased serum osmolality (i.e. more concentrated) –> this leads to increased water retention in the collecting ducts of the kidneys.

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6
Q

How does water ingestion not lead to hyponatraemia?

A

As the fall in osmolality leads to suppression of ADH secretion, allowing water to be excreted in dilute urine.

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7
Q

Normal sodium range?

A

136-145 mmol/L

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8
Q

Symptoms of hyponatraemia?

A
  • asymptomatic
  • lethargy
  • headaches
  • dizziness

severe:
- postural hypotension
- ataxia
- confusion
- psychosis
- seizures
- comas

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9
Q

Calculation for osmolarity?

A

2xNa + glucose + urea (all measured in mmol/L)

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10
Q

Mechanisms of hyponatraemia:

A

1) Increased water:
- increased water intake
- increased water reabsorption (i.e. more ADH)

2) Inadequate sodium intake (rare)

3) Excess sodium loss:
- kidneys
- other areas e.g. sweating, vomiting, diarrhoea, burns

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11
Q

Describe the RAAS system in the management of serum osmolality in healthy individuals

A

1) Hypothalamus: detects increased serum osmolality (i.e. blood more conc)

2) Posterior pituitary: releases ADH in response to increased serum osmolality

3) Kidneys: ADH travels to kidneys where it binds to ADH receptors on the distal convoluted tubules –> causes reabsorption of water out of the collecting ducts and back into the bloodstream

4) This results in increased urine osmolality and decreased urine volume

5) This results in decreased serum osmolality (and increased serum volume)

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12
Q

What are the 2 main ways that sodium is lost through the kidneys?

A

1) Medications e.g. diuretics

2) Shortage of steroid hormone e.g. aldosterone, cortisol (to a lesser extent)

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13
Q

How does aldosterone (and cortisol to a lesser extent) affect sodium and potassium?

A

Causes sodium reabsorption and potassium excretion in the kidneys

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14
Q

How can primary adrenal insufficiency (Addison’s disease) cause hyponatraemia?

A

There is a deficiency in steroid hormones (aldosterone & cortisol) –> prevents adequate reabsorption of sodium.

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15
Q

Which 3 medications can lead to hyponatraemia?

A

1) loop diuretics
2) thiazide diuretics
3) potassium sparing diuretics

These all act to prevent sodium reabsorption.

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16
Q

1st step in assessment of hyponatraemia?

A

Determine if it is a true hyponatraemia or not –> calculate the serum osmolality.

Calculated osmolarity = 2xNa + glucose + urea

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17
Q

How can calculated serum osmolarity determine if it is a true hyponatraemia or not?

A

1) Low sodium and low serum osmolarity –> genuine hyponatraemia (as low sodium is causing low osmolarity).

2) Low sodium and normal osmolarity –> pseudohyponatraemia

3) Low sodium and hig osmolarity –> usually caused by very high levels of glucose (hyperosmolar hyperglycaemic state/HHS)

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18
Q

What happens in a pseudohyponatraemia?

A

There is a high level of lipids (e.g. in hyperlipidaemia) or proteins (e.g. myeloma) take up a high proportion of the blood volume.

The blood analyser thinks that there is a low sodium but there is not.

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19
Q

How does HHS cause low sodium and high osmolarity?

A

Blodo glucose goes up very high –> glucose leaks into urine –> water & sodium follows –> concentrates glucose in blood.

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20
Q

After checking serum osmolarity in hyponatraemia and it is low (true hyponatraemia), what is the next step?

A

Check fluid status

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21
Q

How to check fluid status in hyponatraemia?

i.e. 3 different types

A

Are they:

1) dehydrated (i.e. hypovolaemic) –> due to decreased soium:
- indaequate intake
- increased loss

2) euvolaemia –> due to increased water
- increased intake (drinking)
- reduced loss through kidneys

3) oedematous (i.e. hypervolaemic)
- congestive cardiac failure
- hypoalbuminaeima 2ary to liver disease or nephrotic syndrome

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22
Q

After checking fluid status in hyponatraemia, what is the next step?

A

Check the urine sodium/osmolality –> tells you if cause of hyponatraemia is in kidneys or somewhere else

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23
Q

How can the urine sodium/osmolality tell you if the cause of the hyponatraemia is in the kidneys?

A

If urine sodium/osmolality is high –> problem in kidneys

If low/normal –> problem is someone else (as kidneys working normally)

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24
Q

What are the 3 key steps in the assessment of hyponatraemia?

A

1) Serum osmolarity

2) Fluid status

3) Urine sodium/osmolality

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25
Q

Patient is hyponatraemic and hypovolaemic.

What is cause of hyponatraemia?

A

DECREASED SODIUM

1) Sodium loss:
- renal loss
- loss from elsewhere e.g. GI, transdermal

2) Inadequate sodium intake (rare)

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26
Q

What is an important investigation in hypovolaemic hyponatraemia?

A

Urine sodium

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27
Q

In a normal functioning kidney, what should happen in serum sodium levels are low?

A

Sodium should be conserved in the urine if serum sodium levels are low.

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28
Q

In hypovolaemic hyponatraemia, what does a urinary sodium >20mmol/L (i.e. high) indicate?

A

Renal cause of sodium loss –> as the kidney is not conserving sodium.

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29
Q

In hypovolaemic hyponatraemia, what does a urinary sodium <20mmol/L (i.e. normal or low) indicate?

A

A non-renal cause of sodium loss: the kidney is conserving sodium, but the sodium is being lost from elsewhere.

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30
Q

Give some renal causes of sodium loss (urine sodium >20 mmol/L)

A

1) Renal failure: creatinine will be increased, eGFR decreased

2) Addison’s disease: associated with hyperkalaemia

3) Excess diuretics: particularly thiazide like diuretics

4) Osmotic diuresis: severe hyperglycaemia

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31
Q

How does Addison’s disease lead to hyponatraemia & hypokalaemia?

A

Reduced aldosterone/cortisol

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32
Q

Which diuretic is most likely to cause renal sodium loss?

A

Thiazide-like diuretics

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33
Q

what are the main 2 non-renal causes of sodium loss (urine sodium <20mmol/L)

A

1) GI losses: vomiting, diarrhoea, small bowel obstruction, fistulae

2) Skin: sweating, burns

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34
Q

Patient is hyponatraemic and hypervolaemic.

What is cause of hyponatraemia?

A

In a fluid overloaded patient, fluid accumulates in the extracellular (‘third’) space. This extra fluid causes a dilutional effect on serum sodium, causing hyponatraemia.

I.e. more water than sodium, leading to a relative sodium deficiency.

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35
Q

What are the 4 main causes of hypervolaemia hyponatraemia?

A

1) Congestive cardiac failure

2) Liver cirrhosis (liver failure)

3) End-stage renal failure

4) Nephrotic syndrome

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36
Q

How can congestive cardiac failure lead to hypervolaemic hyponatraemia?

A

1) fluid retention (affecting RAAS)

2) increased venous capillary pressure, encouraging fluid extravasation as oedema

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37
Q

How can liver cirrhosis lead to hypervolaemic hyponatraemia?

A

1) Decreased albumin synthesis leads to hypoalbuminaemia –> causes reduced oncotic pressure in the bloodstream, leading to fluid loss into the extracellular space.

2) Increased pressure in the portal venous system (portal hypertension) leads to fluid accumulation in the peritoneal space (ascites).

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38
Q

How can end stage renal failure lead to hypervolaemic hyponatraemia?

A

Kidney loses ability to effectively act as a filter from the bloodstream and urine output decreases –> significant fluid retention.

BUT eGFR must be severely reduced for this to be the cause of oedema (end-stage renal failure).

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39
Q

How can nephrotic syndrome lead to hypervolaemic hyponatraemia?

A

Inappropriate loss of albumin through the glomerulus –> hypoalbuminaemia –> decreases plasma oncotic pressure –> fluid accumulates in the extracellular space.

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40
Q

Patient is hyponatraemic and euvolaemic.

What is cause of hyponatraemia?

A

The diagnosis is most commonly SIADH.

Other less common causes: primary polydipsia, severe endocrine disturbances (hypothyroidism/cortisol deficiency).

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41
Q

In euvolaemic hyponatraemia, what is it important to check?

A

Urine osmolality.

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42
Q

Under normal conditions, what should happen to urine osmolality when serum sodium (and serum osmolality) is low?

A

Urine osmolality should be decreased as the body attempts to conserve sodium by producing dilute urine.

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43
Q

In euvolaemic hyponatraemia, if the urine osmolality is raised (>300mOsm/kg), what is the diagnosis?

A

SIADH.

A raised urine osmolality in the presence of low serum osmolality suggests SIADH, as the kidney is inappropriately producing concentrated urine despite low serum osmolality.

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44
Q

In euvolaemic hyponatraemia, if the urine osmolality is decreased (<300mOsm/kg), what is the diagnosis?

A

Water intoxication may be the cause (primary polydipsia).

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45
Q

Who is primary polydipsia seen in?

A
  • psychiatric disturbances
  • use of ectasy
  • severe hypothyroidism
  • glucocorticoid deficiency.
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46
Q

The clinical features of hyponatraemia are primarily neurological.

Why is this?

A

Due to the effects of cerebral oedema, which can occur secondary to fluid shifts across the blood-brain-barrier.

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47
Q

Mild to moderate symptoms of hyponatraemia?

A
  • anorexia
  • headache
  • N&V
  • lethargy
  • confusion
  • ataxia
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48
Q

symptoms of severe hyponatraemia?

A
  • seizures
  • cerebral obtundation/coma
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49
Q

What is the key to clinical examination in hyponatraemia/

A

An accurate assessment of fluid/hydration status, as this will help to classify the likely cause of hyponatraemia and guide initial management.

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50
Q

What are some signs of hypovolaemia?

A

1) tachycardia, hypotension (late sign)
2) dry mucous membranes
3) reduced skin turgor

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51
Q

What are some signs of hypervolaemia?

A

1) peripheral oedema
2) raised JVP
3) bibasal lung field crepitations (pulmonary rales)

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52
Q

What are some neurological signs of severe hyponatraemia?

A

1) cognitive impairment
2) drowsiness
3) signs of seizure activity/brainstem herniation (indicate life-threatening hyponatraemia with cerebral oedema)

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53
Q

Relevant blood tests in hypontraemia?

A

1) U&Es: to confirm hyponatraemia, assess renal function and potassium levels.

2) Serum osmolality: usually decreased in hyponatraemia; if normal consider pseudohyponatraemia, if raised consider hyperglycaemia.

3) LFTs: assess the albumin levels in hypervolaemic hyponatraemia, and exclude obstructive jaundice if pseudohyponatraemia is suspected.

4) Serum lipids: to assess for lipaemia if pseudohyponatraemia is suspected.

5) Serum glucose: significant hyperglycaemia can cause hyponatraemia, often with raised serum osmolality.

6) Serum cortisol/thyroid function tests: exclude Addison’s (low cortisol level) / severe hypothyroidism (high TSH, low T3) as rare causes of euvolaemic hyponatraemia.

54
Q

How can serum glucose affect sodium?

A

Significant hyperglycaemia can cause hyponatraemia, often with raised serum osmolality.

55
Q

Relevant urine tests in hyponatraemia?

A

1) urine osmolality: required to confirm a diagnosis of SIADH (a raised urine osmolality in the presence of low serum osmolality suggests SIADH)

2) urine sodium: useful to differentiate renal vs extrarenal cases of sodium loss in hypovolaemic hyponatraemia.

56
Q

Give 3 causes of pseudohyponatraemia

A

1) hyperlipidaemia

2) hyperproteinaemia

3) hyperbilirubinaemia (2ary to obstructive jaundice)

These can interrupt some laboratory analysis methods of measuring serum sodium, leading to falsely low readings.

57
Q

How can significant hyperglycaemia (e.g. DKA / HHS) affect sodium?

A

In patients with significant hyperglycaemia (e.g. DKA / HHS), the increase in serum glucose raises serum tonicity, pulling water out of cells and expanding the extracellular space, causing a dilutional effect on serum sodium concentrations.

In this case, total body sodium remains unchanged, and sodium concentration will generally correct with the correction of the hyperglycaemia.

58
Q

Manageemnt of acute hyponatraemia with severe neurological symptoms (e.g. seizures, severe drowsiness)?

A

Medical emergency

1) IV hypertonic saline bolus (100ml 3% NaCl)

2) Close monitoring of serum sodium

59
Q

Management of hyponatraemia without severe neurological symptoms?

A

A cautious approach to management is taken –> if the sodium is corrected too quickly, patients are at risk of severe complications (osmotic demyelination syndrome).

Goal –> to correct by no more than 6mmol/L in the first 6 hours and no more than 10mmol/L in the first 24 hours.1

60
Q

If the sodium is corrected too quickly in hyponatraemia, what is the patient at risk of?

A

Osmotic demyelination syndrome

61
Q

Management of hypovolaemic hyponatraemia?

A

Rehydration with IV 0.9% normal saline, with regular monitoring of serum sodium.

62
Q

Management of hypervolaemic hyponatraemia?

A

Fluid restriction (<1.5L/24h), with regular monitoring of serum sodium.

63
Q

Management of euvolaemic hyponatraemia?

A

1) Fluid restriction (1.5L/24h), with regular monitoring of serum sodium.

2) Oral salt tablets may be required if fluid restriction alone is ineffective.

64
Q

Complications of hyponatraemia?

A

1) gait disturbance & falls: particularly in elderly

2) cerebral oedema: brainstem herniation and death

3) osmotic demyelination syndrome

65
Q

What is osmotic demyelination syndrome?

A
  • Severe and often irreversible neurological deficits secondary to intracerebral fluid shifts caused by the rapid correction of hyponatraemia
  • Classically occurs 2-4 days after the treatment
  • Typically presenting with quadriplegia and pseudobulbar palsy.
66
Q

How does osmotic demyelination syndrome typically present?

A

Quadriplegia & pseudobulbar palsy

67
Q

When does osmotic demyelination syndrome typically present?

A

2-4 days after treatment

68
Q

Give 5 causes of SIADH

A

1) primary brain injury e.g. meningitis, subarachnoid haemorrhage

2) malignancy e.g. small cell lung cancer

3) drugs e.g. carbamazepine, SSRIs, amitriptyline)

4) infectious e.g. atypical pneumonia, cerebral abscess

5) hypothyroidism

69
Q

Give 3 drugs that can cause SIADH

A

1) carbamazepine
2) SSRIs
3) amitriptyline

70
Q

What 4 lab investigations are indicated in SIADH?

A

1) U&Es: serum sodium is low in SIADH (<130 mmol/L).

2) Plasma osmolality: reduced in SIADH (due to low serum sodium).

3) TFTs: hypothyroidism is potential cause

4) Serum cortisol: checked to rule out Addison’s disease as a cause of hyponatraemia

71
Q

What are the 6 features that must be present for a diagnosis of SIADH to be made?

A

1) hyponatraemia

2) low plasma osmolality

3) euvolaemia

4) inappropriately elevated urine osmolality (i.e. greater than plasma osmolality)

5) urine [Na+] >40 mmol/L despite normal salt intake

6) normal thyroid and adrenal function

72
Q

Management of SIADH?

A

Fluid restriction

73
Q

Name some drugs that require monitoring of U&Es

A

1) ACEi and ARBs

2) Diuretics: spironolactone, thiazide diuretics (e.g. indapamide), loop diuretics (e.g. furosemide)

3) DOACs

4) Carbamazepine

5) Lithium

6) Digoxin

74
Q

What is creatinine?

A

A waste product of muscle metabolism

75
Q

What is creatinine excreted by?

A

Excreted entirely by the kidney

76
Q

Who is serum creatinine level naturally higher in?

A

It is naturally higher in individuals with greater skeletal muscle mass (thus generally higher in males than females).

77
Q

What is the primary determinant of serum creatinine?

A

The kidney’s ability to filter creatinine from the bloodstream.

I.e. a raised creatinine level is an indicator of kidney dysfunction.

78
Q

What is the Estimated Glomerular Filtration Rate (eGFR)?

A

The eGFR is a mathematically derived number based on a patient’s serum creatinine in conjunction with age, sex and race.

79
Q

How does serum creatinine affect eGFR?

A

As the serum creatinine rises, the eGFR will decrease, indicating worsening kidney dysfunction.

80
Q

Describe eGFR in stage 1 to 5 of CKD

A

Stage 1: eGFR >90 (normal), with other tests showing signs of kidney damage (e.g. proteinuria)

Stage 2: eGFR of 60 to 89 ml/min, with other tests showing signs of kidney damage (e.g. proteinuria

Stage 3a: eGFR of 45 to 59 ml/min

Stage 3b: eGFR of 30 to 44 ml/min

Stage 4: eGFR of 15 to 29 ml/min

Stage 5: eGFR <15 ml/min

81
Q

What is urea?

A

Urea is a waste product of protein breakdown produced in the liver.

82
Q

What is urea a breakdown product of?

A

Protein

83
Q

What is creatinine a waste product of?

A

Muscle metabolism

84
Q

What is urea excreted by?

A

The kidneys predominantly excrete urea, and it can be used as a surrogate marker of renal function.

85
Q

is creatinine or urea a better marker for kidney function?

A

Serum creatinine is a more accurate assessment of renal function than urea; however, urea is increased earlier in renal disease.

86
Q

Give some causes of a raised serum urea (uraemia)

A

1) renal dysfunction

2) dehydration

3) upper GI bleed

87
Q

How can renal dysfunction result in uraemia?

A

Decreased excretion of urea in the urine

88
Q

How can dehydration result in uraemia?

A

Urea rises quickly in dehydration, even in the presence of normally functioning kidneys.

This is physiologically mediated by anti-diuretic hormone (ADH), released from the posterior pituitary gland in response to intravascular volume depletion. ADH increases urea and water reabsorption in the collecting ducts.

89
Q

How can an upper GI bleed result in uraemia?

A

Blood in the upper GI tract is broken down into proteins, which are transported to the liver via the portal vein and metabolised into urea - ‘high protein meal’

90
Q

What is the main determinant of plasma osmolality?

A

Sodium

91
Q

Define hypernatraemia

A

serum sodium level >146mmol/L.

92
Q

What is hypernatraemia commonly caused by?

A

Dehydration (e.g. unreplaced skin or GI losses of hypotonic fluid)

93
Q

What are some rarer causes of hypernatraemia?

A
  • diabetes insipidus
  • drugs e.g. loop diuretics
  • osmotic diuresis e.g. in hyperglycemic states
  • extreme levels of salt ingestion
94
Q

Treatment of hypernatraemia?

A

Where there is a clear history implicating dehydration (e.g. vomiting/diarrhoea) –> gentle rehydration with IV hypotonic fluids (e.g. 5% dextrose).

95
Q

What can correcting the hypernatraemia too rapidly cause?

A

Can lead to intracerebral fluid shifts and devastating consequences such as central pontine myelinolysis (also known as osmotic demyelination syndrome).

96
Q

Under physiological conditions, where is potassium stored?

A

Intracellularly

97
Q

How is potassium excreted?

A

By the kidneys

98
Q

Define hyperkalaemia

A

> 5.5 mmol/L

Mild: 5.5-5.9 mmol/L
Moderate: 6.0-6.4 mmol/L
Severe: >6.5 mmol/L

99
Q

Give some causes of hyperkalaemia

A

1) renal: decreased renal excretion (e.g. AKI or CKD)

2) medications: ACEi, potassium sparing diuretics, potassium supplements

3) Tissue damage: burns, rhabdomyolysis

4) Metabolic: DKA

5) Endocrine: Addison’s

100
Q

What are the 3 cardinal features of hyperkalaemia on an ECG?

A

1) tall tented T waves

2) prolonged PR interval

3) widened QRS complexes

101
Q

Renal impairment is one of the commonest causes of hyperkalaemia.

Give 3 renal causes of hyperkalaemia

A

1) AKI

2) CKD

3) Hyperkalaemic renal tubular acidosis

102
Q

What medications can cause hyperkalaemia?

A

1) ACEi
2) ARBs
3) Potassium-sparing diuretics
4) NSAIDs/COX 2 inhibitors
5) Digoxin (in toxicity)
6) Trimethoprim
7) Beta-blockers – selective and non-selective can cause it
8) Nicorandil
9) Heparin - UH and LMWH
10) Potassium supplements
11) Tacrolimus

103
Q

Give 3 iatrogenic causes of hyperkalaemia

A

1) Medications

2) IV fluids containing potassium

3) Blood transfusion

104
Q

Give some causes of hyperkalaemia

A

1) Renal causes

2) Iatrogenic

3) Trauma & burns

4) DKA

5) Addison’s

6) Pseudohyperkalaemia

105
Q

How can trauma or burns lead to hyperkalaemia?

A

Tissue damage sustained secondary to trauma or burns results in the release of significant volumes of potassium from damaged cells.

106
Q

How can DKA lead to hyperkalaemia?

A

In DKA, potassium shifts from the intracellular to the extracellular space due to a lack of insulin, resulting in hyperkalaemia.

107
Q

How can Addison’s lead to hyperkalaemia?

A

Aldosterone promotes the excretion of potassium by the kidneys.

In Addison’s disease, the adrenal glands cannot produce adequate aldosterone levels, which results in reduced renal excretion of potassium.

108
Q

Give some causes of pseudohyperkalaemia

A

1) Haemolysis: e.g. prolonged tourniquet time, prolonged sample transport time, use of incorrect blood bottles

2) Blood sample being taken from a limb receiving IV fluids containing potassium

3) Leukocytosis and thrombocytosis

109
Q

If there are concerns about pseudohyperkalaemia, what should you do?

A

a sample should be urgently repeated to check the validity of the result.

110
Q

Symptoms of hyperkalaemia?

A

Typically vague:
- general weakness
- fatigue

Can get:
- palpitations
- chest pain
- SOB

111
Q

Potential clinical signs of hyperkalaemia?

A

1) Bradycardia secondary to hyperkalaemia-induced atrioventricular block

2) Depressed or absent tendon reflexes

112
Q

What blood test can be used to rapidly confirm hyperkalaemia?

A

Venous blood gas

113
Q

Relevant bedside investigations in hyperkalaemia?

A

1) ECG

2) Blood glucose: exclude hyperglycaemia (e.g. DKA)

3) Blood gas (ABG or VGB): to exclude metabolic acidosis (e.g. hyperkalaemic renal tubular acidosis or DKA) and rapidly check serum potassium

114
Q

Lab investigations in hyperkalaemia?

A

1) U&E: a repeat U&E sample should be sent

2) FBC: to exclude haemolysis (e.g. normocytic normochromic anaemia) and leukocytosis or thrombocytosis

3) Serum cortisol: to exclude Addison’s disease (low serum cortisol is found in Addison’s)

4) Digoxin level: to exclude toxicity (if relevant)

115
Q

3 steps in management of hyperkalaemia?

A

1) Stabilise the cardiac membrane (protect the heart)

2) Shift potassium intracellularly (reduce serum potassium)

3) Remove potassium from the body

116
Q

What indicates urgent treatment (a medical emergency) in hyperkalaemia?

A

1) potassium level of >/= 6.5 mmol/L

2) hyperkalaemia-associated ECG changes

117
Q

What is used to stabilise the cardiac membrane in hyperkalaemia?

A

IV calcium gluconate

118
Q

Is the administration of calcium gluconate without hyperkalaemia-associated ECG changes recommended?

A

No

119
Q

Role of IV calcium gluconate in hyperkalaemia?

A

Stabilises the myocardium and buys time but does NOT reduce potassium levels.

120
Q

Give 2 options that can shift potassium intracellularly in hyperkalaemia

A

1) Insulin-glucose infusion

2) Salbutamol

121
Q

Give 3 options that can remove potassium from the body in hyperkalaemia

A

1) Calcium polystyrene sulfonate resin (Calcium resonium)

2) Correction of the underlying cause: kidneys should then resume their normal function of excreting adequate volumes of potassium via the urine.

3) Haemodialysis: invasive treatment reserved as a last resort for resistant hyperkalaemia that has failed to respond to all other therapies.

122
Q

Define hypokalaemia

A

serum potassium <3.5mmol/L.

123
Q

What potassium level can destabilise the myocardium in hypokalaemia?

A

<3 mmol/L

124
Q

ECG changes in hypokalaemia?

A

1) PR prolongation
2) widespread ST depression / T wave flattening
3) prominent U waves

125
Q

Give some causes of hypokalaemia

A

1) GI potassium loss e.g. prolonged diarrhoea

2) Renal potassium loss

3) Intracellular potassium accumulation

126
Q

Potassium loss in upper vs lower GI losses?

A

Lower gastrointestinal losses are relatively high in potassium e.g. prolonged diarrhoea

Upper gastrointestinal losses are relatively low in potassium –> BUT prolonged vomiting can lead to hypokalaemia

127
Q

How can prolonged vomiting cause hypokalaemia?

A

This occurs due to metabolic alkalosis secondary to gastric acid loss.

Excess potassium is excreted from the kidney as part of the renal compensatory mechanism to correct the alkalosis.

128
Q

Renal causes of hypokalaemia?

A

1) medications e.g. loop diuretics (e.g. furosemide) and thiazide diuretics (e.g. indapamide)

2) increased mineralocorticoid activity

129
Q

Management of hyperkalaemia ?

A

1) IV or oral potassium replacement

2) Treatment of underlying cause

130
Q

When is oral vs IV potassium replacement indicated in hypokalaemia?

A

1) If potassium is >3mmol/L, the patient is asymptomatic, and there are no ECG changes –> oral potassium replacement can be given.

2) If potassium is <3mmol/L (severe hypokalaemia) or ECG changes are present –> IV potassium replacement is indicated.

131
Q
A

Yr 4 - ACC (73 decks)

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