Electrolyte Abnormalities: Sodium & Potassium Flashcards
1
Q
Define hyponatraemia
A
Serum sodium conc <135 mmol/L
Severe: <120 mmol/L
2
Q
What is serum osmolality?
A
The conc of solutes in the blood –> sodium is the most important determinant of serum osmolality.
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).
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
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.
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.
7
Q
Normal sodium range?
A
136-145 mmol/L
8
Q
Symptoms of hyponatraemia?
A
- asymptomatic
- lethargy
- headaches
- dizziness
severe:
- postural hypotension
- ataxia
- confusion
- psychosis
- seizures
- comas
9
Q
Calculation for osmolarity?
A
2xNa + glucose + urea (all measured in mmol/L)
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
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)
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)
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
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.
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.
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
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)
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.
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.
20
Q
After checking serum osmolarity in hyponatraemia and it is low (true hyponatraemia), what is the next step?
A
Check fluid status
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
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
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)
24
Q
What are the 3 key steps in the assessment of hyponatraemia?
A
1) Serum osmolarity
2) Fluid status
3) Urine sodium/osmolality
25
Patient is hyponatraemic and hypovolaemic.
What is cause of hyponatraemia?
DECREASED SODIUM
1) Sodium loss:
- renal loss
- loss from elsewhere e.g. GI, transdermal
2) Inadequate sodium intake (rare)
26
What is an important investigation in hypovolaemic hyponatraemia?
Urine sodium
27
In a normal functioning kidney, what should happen in serum sodium levels are low?
Sodium should be conserved in the urine if serum sodium levels are low.
28
In hypovolaemic hyponatraemia, what does a urinary sodium >20mmol/L (i.e. high) indicate?
Renal cause of sodium loss --> as the kidney is not conserving sodium.
29
In hypovolaemic hyponatraemia, what does a urinary sodium <20mmol/L (i.e. normal or low) indicate?
A non-renal cause of sodium loss: the kidney is conserving sodium, but the sodium is being lost from elsewhere.
30
Give some renal causes of sodium loss (urine sodium >20 mmol/L)
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
31
How does Addison's disease lead to hyponatraemia & hypokalaemia?
Reduced aldosterone/cortisol
32
Which diuretic is most likely to cause renal sodium loss?
Thiazide-like diuretics
33
what are the main 2 non-renal causes of sodium loss (urine sodium <20mmol/L)
1) GI losses: vomiting, diarrhoea, small bowel obstruction, fistulae
2) Skin: sweating, burns
34
Patient is hyponatraemic and hypervolaemic.
What is cause of hyponatraemia?
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.
35
What are the 4 main causes of hypervolaemia hyponatraemia?
1) Congestive cardiac failure
2) Liver cirrhosis (liver failure)
3) End-stage renal failure
4) Nephrotic syndrome
36
How can congestive cardiac failure lead to hypervolaemic hyponatraemia?
1) fluid retention (affecting RAAS)
2) increased venous capillary pressure, encouraging fluid extravasation as oedema
37
How can liver cirrhosis lead to hypervolaemic hyponatraemia?
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).
38
How can end stage renal failure lead to hypervolaemic hyponatraemia?
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).
39
How can nephrotic syndrome lead to hypervolaemic hyponatraemia?
Inappropriate loss of albumin through the glomerulus --> hypoalbuminaemia --> decreases plasma oncotic pressure --> fluid accumulates in the extracellular space.
40
Patient is hyponatraemic and euvolaemic.
What is cause of hyponatraemia?
The diagnosis is most commonly SIADH.
Other less common causes: primary polydipsia, severe endocrine disturbances (hypothyroidism/cortisol deficiency).
41
In euvolaemic hyponatraemia, what is it important to check?
Urine osmolality.
42
Under normal conditions, what should happen to urine osmolality when serum sodium (and serum osmolality) is low?
Urine osmolality should be decreased as the body attempts to conserve sodium by producing dilute urine.
43
In euvolaemic hyponatraemia, if the urine osmolality is raised (>300mOsm/kg), what is the diagnosis?
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.
44
In euvolaemic hyponatraemia, if the urine osmolality is decreased (<300mOsm/kg), what is the diagnosis?
Water intoxication may be the cause (primary polydipsia).
45
Who is primary polydipsia seen in?
- psychiatric disturbances
- use of ectasy
- severe hypothyroidism
- glucocorticoid deficiency.
46
The clinical features of hyponatraemia are primarily neurological.
Why is this?
Due to the effects of cerebral oedema, which can occur secondary to fluid shifts across the blood-brain-barrier.
47
Mild to moderate symptoms of hyponatraemia?
- anorexia
- headache
- N&V
- lethargy
- confusion
- ataxia
48
symptoms of severe hyponatraemia?
- seizures
- cerebral obtundation/coma
49
What is the key to clinical examination in hyponatraemia/
An accurate assessment of fluid/hydration status, as this will help to classify the likely cause of hyponatraemia and guide initial management.
50
What are some signs of hypovolaemia?
1) tachycardia, hypotension (late sign)
2) dry mucous membranes
3) reduced skin turgor
51
What are some signs of hypervolaemia?
1) peripheral oedema
2) raised JVP
3) bibasal lung field crepitations (pulmonary rales)
52
What are some neurological signs of severe hyponatraemia?
1) cognitive impairment
2) drowsiness
3) signs of seizure activity/brainstem herniation (indicate life-threatening hyponatraemia with cerebral oedema)
53
Relevant blood tests in hypontraemia?
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
How can serum glucose affect sodium?
Significant hyperglycaemia can cause hyponatraemia, often with raised serum osmolality.
55
Relevant urine tests in hyponatraemia?
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
Give 3 causes of pseudohyponatraemia
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
How can significant hyperglycaemia (e.g. DKA / HHS) affect sodium?
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
Manageemnt of acute hyponatraemia with severe neurological symptoms (e.g. seizures, severe drowsiness)?
Medical emergency
1) IV hypertonic saline bolus (100ml 3% NaCl)
2) Close monitoring of serum sodium
59
Management of hyponatraemia without severe neurological symptoms?
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
If the sodium is corrected too quickly in hyponatraemia, what is the patient at risk of?
Osmotic demyelination syndrome
61
Management of hypovolaemic hyponatraemia?
Rehydration with IV 0.9% normal saline, with regular monitoring of serum sodium.
62
Management of hypervolaemic hyponatraemia?
Fluid restriction (<1.5L/24h), with regular monitoring of serum sodium.
63
Management of euvolaemic hyponatraemia?
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
Complications of hyponatraemia?
1) gait disturbance & falls: particularly in elderly
2) cerebral oedema: brainstem herniation and death
3) osmotic demyelination syndrome
65
What is osmotic demyelination syndrome?
- 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
How does osmotic demyelination syndrome typically present?
Quadriplegia & pseudobulbar palsy
67
When does osmotic demyelination syndrome typically present?
2-4 days after treatment
68
Give 5 causes of SIADH
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
Give 3 drugs that can cause SIADH
1) carbamazepine
2) SSRIs
3) amitriptyline
70
What 4 lab investigations are indicated in SIADH?
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
What are the 6 features that must be present for a diagnosis of SIADH to be made?
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
Management of SIADH?
Fluid restriction
73
Name some drugs that require monitoring of U&Es
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
What is creatinine?
A waste product of muscle metabolism
75
What is creatinine excreted by?
Excreted entirely by the kidney
76
Who is serum creatinine level naturally higher in?
It is naturally higher in individuals with greater skeletal muscle mass (thus generally higher in males than females).
77
What is the primary determinant of serum creatinine?
The kidney's ability to filter creatinine from the bloodstream.
I.e. a raised creatinine level is an indicator of kidney dysfunction.
78
What is the Estimated Glomerular Filtration Rate (eGFR)?
The eGFR is a mathematically derived number based on a patient’s serum creatinine in conjunction with age, sex and race.
79
How does serum creatinine affect eGFR?
As the serum creatinine rises, the eGFR will decrease, indicating worsening kidney dysfunction.
80
Describe eGFR in stage 1 to 5 of CKD
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
What is urea?
Urea is a waste product of protein breakdown produced in the liver.
82
What is urea a breakdown product of?
Protein
83
What is creatinine a waste product of?
Muscle metabolism
84
What is urea excreted by?
The kidneys predominantly excrete urea, and it can be used as a surrogate marker of renal function.
85
is creatinine or urea a better marker for kidney function?
Serum creatinine is a more accurate assessment of renal function than urea; however, urea is increased earlier in renal disease.
86
Give some causes of a raised serum urea (uraemia)
1) renal dysfunction
2) dehydration
3) upper GI bleed
87
How can renal dysfunction result in uraemia?
Decreased excretion of urea in the urine
88
How can dehydration result in uraemia?
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
How can an upper GI bleed result in uraemia?
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
What is the main determinant of plasma osmolality?
Sodium
91
Define hypernatraemia
serum sodium level >146mmol/L.
92
What is hypernatraemia commonly caused by?
Dehydration (e.g. unreplaced skin or GI losses of hypotonic fluid)
93
What are some rarer causes of hypernatraemia?
- diabetes insipidus
- drugs e.g. loop diuretics
- osmotic diuresis e.g. in hyperglycemic states
- extreme levels of salt ingestion
94
Treatment of hypernatraemia?
Where there is a clear history implicating dehydration (e.g. vomiting/diarrhoea) --> gentle rehydration with IV hypotonic fluids (e.g. 5% dextrose).
95
What can correcting the hypernatraemia too rapidly cause?
Can lead to intracerebral fluid shifts and devastating consequences such as central pontine myelinolysis (also known as osmotic demyelination syndrome).
96
Under physiological conditions, where is potassium stored?
Intracellularly
97
How is potassium excreted?
By the kidneys
98
Define hyperkalaemia
>5.5 mmol/L
Mild: 5.5-5.9 mmol/L
Moderate: 6.0-6.4 mmol/L
Severe: >6.5 mmol/L
99
Give some causes of hyperkalaemia
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
What are the 3 cardinal features of hyperkalaemia on an ECG?
1) tall tented T waves
2) prolonged PR interval
3) widened QRS complexes
101
Renal impairment is one of the commonest causes of hyperkalaemia.
Give 3 renal causes of hyperkalaemia
1) AKI
2) CKD
3) Hyperkalaemic renal tubular acidosis
102
What medications can cause hyperkalaemia?
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
Give 3 iatrogenic causes of hyperkalaemia
1) Medications
2) IV fluids containing potassium
3) Blood transfusion
104
Give some causes of hyperkalaemia
1) Renal causes
2) Iatrogenic
3) Trauma & burns
4) DKA
5) Addison's
6) Pseudohyperkalaemia
105
How can trauma or burns lead to hyperkalaemia?
Tissue damage sustained secondary to trauma or burns results in the release of significant volumes of potassium from damaged cells.
106
How can DKA lead to hyperkalaemia?
In DKA, potassium shifts from the intracellular to the extracellular space due to a lack of insulin, resulting in hyperkalaemia.
107
How can Addison's lead to hyperkalaemia?
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
Give some causes of pseudohyperkalaemia
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
If there are concerns about pseudohyperkalaemia, what should you do?
a sample should be urgently repeated to check the validity of the result.
110
Symptoms of hyperkalaemia?
Typically vague:
- general weakness
- fatigue
Can get:
- palpitations
- chest pain
- SOB
111
Potential clinical signs of hyperkalaemia?
1) Bradycardia secondary to hyperkalaemia-induced atrioventricular block
2) Depressed or absent tendon reflexes
112
What blood test can be used to rapidly confirm hyperkalaemia?
Venous blood gas
113
Relevant bedside investigations in hyperkalaemia?
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
Lab investigations in hyperkalaemia?
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
3 steps in management of hyperkalaemia?
1) Stabilise the cardiac membrane (protect the heart)
2) Shift potassium intracellularly (reduce serum potassium)
3) Remove potassium from the body
116
What indicates urgent treatment (a medical emergency) in hyperkalaemia?
1) potassium level of >/= 6.5 mmol/L
2) hyperkalaemia-associated ECG changes
117
What is used to stabilise the cardiac membrane in hyperkalaemia?
IV calcium gluconate
118
Is the administration of calcium gluconate without hyperkalaemia-associated ECG changes recommended?
No
119
Role of IV calcium gluconate in hyperkalaemia?
Stabilises the myocardium and buys time but does NOT reduce potassium levels.
120
Give 2 options that can shift potassium intracellularly in hyperkalaemia
1) Insulin-glucose infusion
2) Salbutamol
121
Give 3 options that can remove potassium from the body in hyperkalaemia
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
Define hypokalaemia
serum potassium <3.5mmol/L.
123
What potassium level can destabilise the myocardium in hypokalaemia?
<3 mmol/L
124
ECG changes in hypokalaemia?
1) PR prolongation
2) widespread ST depression / T wave flattening
3) prominent U waves
125
Give some causes of hypokalaemia
1) GI potassium loss e.g. prolonged diarrhoea
2) Renal potassium loss
3) Intracellular potassium accumulation
126
Potassium loss in upper vs lower GI losses?
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
How can prolonged vomiting cause hypokalaemia?
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
Renal causes of hypokalaemia?
1) medications e.g. loop diuretics (e.g. furosemide) and thiazide diuretics (e.g. indapamide)
2) increased mineralocorticoid activity
129
Management of hyperkalaemia ?
1) IV or oral potassium replacement
2) Treatment of underlying cause
130
When is oral vs IV potassium replacement indicated in hypokalaemia?
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
