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Flashcards in Potassium Deck (22):


Hypokalaemia: features

- muscle weakness, hypotonia
- hypokalaemia predisposes patients to digoxin toxicity care should be taken if patients are also on diuretics



ECG features:
U waves
small or absent T waves
prolonged PR interval
ST depression
Long QT

In Hypokalaemia U have no Pot and no T but a long PR and a long QT

The U wave is a small (0.5 mm) deflection immediately following the T wave
U wave is usually in the same direction as the T wave.
U wave is best seen in leads V2 and V3.


HYPOKALAEMIA with ACIDOSIS - Differentials

Hypokalaemia with acidosis
- Diarrhoea
- Renal tubular acidosis Types 1 and 2
- Acetazolamide
- Partially treated diabetic ketoacidosis
- Theophylline Toxicity



Hypokalaemia with alkalosis:
- vomiting
- diuretics
- Cushing's syndrome
- Conn's syndrome (primary hyperaldosteronism)

- Bartter's
- Gitelman's
- Liddle's


Potassium and Magnesium

Magnesium deficiency may also cause hypokalaemia. In such cases, normalizing the potassium level may be difficult until the magnesium deficiency has been corrected


Drugs causing Hyperkalaemia

Potassium sparing diuretics eg Spironolactone

ACE Inhibitors




Beta-blockers (NB Beta-agonists used in emergency Mx of Hyperkalaemia)


Hypokalaemia and HTN

For exams it is useful to be able to classify the causes of hypokalaemia in to those associated with hypertension, and those which are not

Hypokalaemia with hypertension
Cushing's syndrome (Low Renin, High Aldosterone)
Conn's syndrome (Low Renin, High Aldosterone)
Liddle's syndrome (Low Renin, Low Aldosterone)
11-beta hydroxylase deficiency*
Renal artery stenosis (High Renin, High Aldosterone)

Ix to differentiate = Plasma Renin and Aldosterone

Carbenoxolone, an anti-ulcer drug, and liquorice excess can potentially cause hypokalaemia associated with hypertension

*21-hydroxylase deficiency, which accounts for 90% of congenital adrenal hyperplasia cases, is not associated with hypertension


Hypokalaemia WITHOUT HTN

Hypokalaemia without hypertension

GI loss (e.g. Diarrhoea, vomiting)
renal tubular acidosis (type 1 and 2**)
Bartter's syndrome
Gitelman syndrome

**type 4 renal tubular acidosis is associated with hyperkalaemia


Hypokalaemic Periodic Paralysis

Hypokalaemic periodic paralysis

Hypokalaemic periodic paralysis is a rare autosomal dominant disorder characterised by episodes of paralysis, typically occur at night. The underlying defect is a mutation in muscle voltage-gated calcium channels. Attacks may be precipitated by carbohydrate meals

lifelong potassium supplementation

Example Question:

A 17 year old girl is brought into A&E by her mother. The patient appears terrified after she experienced an episode on waking earlier in the morning when she could not move at all for 2 hours. This was her second episode. She reports no loss of consciousness and was aware throughout the episode. She has no other past medical history documented. She is not aware of a previous episode of epilepsy. On examination, her heart sounds and breath sounds are unremarkable. Neurological examination demonstrated no abnormalities. She normal dentition and her BMI is 19.5. A 12 lead ECG demonstrated a jerky baseline with flat T waves. What is the diagnosis?

Partial or absence seizures
Guillain Barre syndrome
Botulinum toxicity
Myasthenia gravis
> Hypokalaemia

The patient describes episode of periodic paralysis and the ECG characteristics are consistent with that of hypokaelamia. The underlying diagnosis is a rare familial condition of skeletal muscle ion channels called hypokaelamc periodic paralysis, onset most commonly in childhood and adolescents. Attacks last hours and neurological examination is normally unremarkable in between attacks. The average K+ on diagnosis is 2.4 mmol/L1. Diagnosis is often made clinically in association with low potassium but genetic testing can help if known mutations are present.

1. Miller TM, Dias da Silva MR, Miller HA et al. Correlating phenotype and genotype in the periodic paralyses. Neurology. 2004;63(9):1647.


Hypokalaemic Alkalosis - Example Question

A 32 year-old man is referred by his GP after collapsing while at work. He does not remember the episode but witnesses say that there was no incontinence or fitting and the patient does not have a sore mouth or tongue. This is the first time this has happened and the patient does not have any other past medical history of note and takes no regular medication.

Examination reveals a blood pressure of 162/95 mmHg, a pulse of 74 beats per minute, a respiratory rate of 16 and a temperature of 37.4ºC. Heart sounds 1 and 2 are present with no added sounds, the lung fields are clear and his abdomen is soft and non-tender.

Blood tests performed and reveal:

Na+ 143 mmol/l
K+ 3.0 mmol/l
Urea 5.6 mmol/l
Creatinine 76 µmol/l
Bicarbonate 31 mmol/l
Renin low
Aldosterone low

Which of the following is the best treatment?

> Amiloride
ACE inhibitor
Angiotensin II receptor blocker

This man has Liddle's syndrome, an autosomal dominant disorder characterised by hypertension associated with hypokalaemic metabolic alkalosis, low plasma renin activity, and suppressed aldosterone secretion. Amiloride is the best treatment for the hypertension and hypokalaemia as it acts on the sodium channels directly, as opposed to spironolactone, which acts on mineralocorticoid receptors.

Liddle's syndrome is a rare autosomal dominant condition that causes hypertension and hypokalaemic alkalosis. It is thought to be caused by disordered sodium channels in the distal tubules leading to increased reabsorption of sodium.

Treatment is with either amiloride or triamterene


Hypokalaemic Periodic Paralysis - Example Question

A 19 year old gentleman with a background history of asthma presents to the Emergency Department complaining of leg weakness and the inability to walk. He had run a marathon the day before. On examination there is 3/5 weakness of the leg extensors bilaterally. Tone, reflexes and coordination are unimpaired and plantars are downgoing bilaterally. Straight leg raise and sensation to light touch and pain stimulus are unimpaired.

Blood tests show the following:

Hb 13.4g/dl
WBC 6.2 x 109/l
Na+ 136mmol/l
K+ 2.9mmol/l
Urea 6.8mmol/l
Creatinine 104µmol/l

What is the most appropriate treatment in this case?

Oral potassium and encourage bed rest
Hourly forced vital capacity measurements and plasma exchange
> Oral potassium and encourage gentle exercise
Hourly forced vital capacity measurements and IV immunoglobulin
Plasma exchange and oral potassium supplementation

Hypokalaemic periodic paralysis is a rare autosomal dominant periodic paralysis but can also occur as a result of a spontaneous mutation (a third of cases have no family history). Attacks often occur in the morning with a history of strenuous exercise or a high carbohydrate meal the day before or may be provoked by stress eg. infections, lack of sleep. Weakness can range from an isolated muscle group to generalised weakness and tends to affect proximal muscles first.

Serum potassium decreases during attacks but may not necessarily fall below the normal range (3.5 -5mmol/l).

The mainstay of treatment for an acute attack is oral potassium supplementation and encouragement of gentle exercise. Intravenous potassium is reserved for those unable to swallow or with cardiac arrhythmias. Acetozolamide or dichlorphenamide are used as first line prophylactic agents.


Hypokalaemia Diagnosis - Example Question

A 27-year-old female was seen in the general medicine outpatient clinic following a referral by her GP. She had presented to her GP feeling generally tired for the last few months. Her GP organised a blood screen revealing no abnormalities except the presence of a potassium level of 2.8 mmol/l. Her GP subsequently repeated the test four weeks later revealing a level of 2.6 mmol/l, leading to the referral to the clinic. Other than the tiredness she was well in herself, denying all other symptoms. She denied specifically the presence of any cardiovascular and muscular symptoms and had never collapsed. Her past medical history was unremarkable and she was taking no prescribed medication. There was no family history of note.

Examination revealed a well 27-year-old lady. Her blood pressure was 108/78 mmHg, heart rate 82 bpm and BMI 23kg/m². Examination of her cardiovascular and respiratory systems revealed the presence of normal heart sounds, a JVP of 3cm and warm well perfused peripheries. Examination of her gastrointestinal and neurological systems was unremarkable.

Investigations conducted at the clinic revealed the following results:

Hb 122 g/l
Platelets 242 * 109/l
WBC 7.8 * 109/l

Na+ 132 mmol/l
K+ 2.5 mmol/l
Urea 7.2 mmol/l
Creatinine 68 µmol/l
Bicarbonate 37 mmol/l

Serum renin 824 (NR 100-500 pmol/l)
Serum aldosterone 82 (NR 55-250 pmol/l)
TSH 1.2 mu/l

24 hour urine result:

Na+ 28 (NR <20mmol/L if hyponatraemia)
K+ 45 (NR <10mmol/l if hypokalaemic)
Calcium 0.8 (NR <7.5 mmol/24hrs)

What is the most likely diagnosis?

Addison's disease
> Gitelman's syndrome
Conn's disease
Bartter's syndrome
Laxative abuse

Gitelman's syndrome is an autosomal recessive disorder resulting in a normotensive hypokalaemic metabolic alkalosis with hypocalciuria and is often accompanied with hypomagnesaemia. The defect is in the thiazide-sensitive sodium chloride symporter within the distal convoluted tubules, in contrast to Bartter's syndrome which presents in the same way but with hypercalciuria owing to a defect within the ascending loop of Henle. Patients with both conditions are often asymptomatic or may complain of fatigue, cramps and weakness. Conn's disease is associated with hypertension and in this instance the aldosterone level is normal with an elevated renin, making this diagnosis unlikely. Both Addison's disease and laxative abuse are associated with a metabolic acidosis; in Addison's serum potassium also tends to be elevated. The best answer is, therefore, Gitelman's syndrome.


Hypokalaemia - Example Question

A 23 year old with known ulcerative colitis presents for the fourth time in 6 months with a severe flare. On examination, he has a distended and generally tender abdomen. He was treated with intravenous hydrocortisone, standard 0.9% saline intravenous fluids and thromboprophylaxis. Although AXR demonstrated dilated large bowel loops, no operation was deemed necessary after surgical. The same treatment continued for 3 days. On day 3 of his admission, he reports chest pain with palpations. A 12 lead ECG was taken:


What is the underlying diagnosis?


Hypokaelamia is a common consequence following extensive GI losses, in addition to bicarbonate and chloride losses. In this case, lack of potassium replacement resulted in tachyarrhythmia with U waves (see extra complex after the T wave). The patient may well be intravenously dry as well but while this may result in tachycardia, it does not explain U waves.


Patient presenting with Hypokalaemia, metabolic alkalosis and a normal-high BP - Differentials?!

- Diuretic Abuse
- Gitelman's syndrome
- Bartter's syndrome

Diuretic abuse:
NB: Of these three, the most common cause is diuretic abuse, especially in young women, and can be ruled out with a urine diuretic assay.

Bartter's syndrome:
Bartter's syndrome presents early in life, with classical features of triangular facies, polyuria, polydipsia and renal failure. Serum renin and aldosterone levels are high despite a low or normal blood pressure. Urine calcium may be raised, and renal stones are a common feature.

In Gitelman's syndrome patients may present later on in adulthood, but have a milder disease course or may be asymptomatic compared to patients with Bartter's syndrome.
NB: Hypomagnesaemia and hypocalciuria differentiates Gitelman's syndrome from Bartter's syndrome.


Hypokalaemia - Example Question

A 19-year-old girl was seen in clinic with lethargy, weakness worsening over the past 4 weeks. She also complains of recurrent muscle cramps in her legs, causing her to have trouble sleeping. On further questioning she admits to urinary frequency, passing urine up to ten times a day, and feels dehydrated all the time. She also mentions that her periods which were usually irregular, have stopped 4 months ago.

On examination, she is thin, with a body mass index of 17kg/m². Her heart rate is 88 bpm and blood pressure is 108/86 mmHg.

C Reactive protein 2mg/l
Haemoglobin 158 g/l
White cell count 7.6 x 10^9/L
Na+ 136 mmol/l
K+ 2.9 mmol/l
Urea 7.2 mmol/l
Creatinine 108 µmol/l
Corrected calcium 2.42 mmol/l

Venous blood gas result

pH 7.532
Bicarbonate 37mmol/l

What would be the next most useful investigation?

Transvaginal ultrasound (TVUS) of the ovaries
Urine diuretic assay
Early morning cortisol
Serum renin and aldosterone levels
Fasting blood glucose levels

Patients with hypokalaemia, metabolic alkalosis and a normal - low blood pressure the following differentials should be considered - diuretic abuse, Bartter's syndrome, Gitelman's syndrome. Of the three, the most common cause is diuretic abuse, especially in young women, and can be ruled out with a urine diuretic assay.

Bartter's syndrome presents early in life, with classical features of triangular facies, polyuria, polydipsia and renal failure. Serum renin and aldosterone levels are high despite a low or normal blood pressure. Urine calcium may be raised, and renal stones are a common feature. In Gitelman's syndrome patients may present later on in adulthood, but have a milder disease course or may be asymptomatic compared to patients with Bartter's syndrome. Hypomagnesaemia and hypocalciuria differentiates Gitelman's syndrome from Bartter's syndrome.

This patient may need other further investigations such as a TVUS, early morning cortisol and fasting blood glucose tests to rule out other conditions, but in view of her biochemistry profile, a urine diuretic assay would be the most useful next investigation to perform.


Potassium and Acidosis

Potassium and hydrogen can be thought of as competitors. Hyperkalaemia tends to be associated with acidosis because as potassium levels rise fewer hydrogen ions can enter the cells



= Rise in serum K+ that occurs due to excessive leakage of potassium from cells during or after blood is taken

= Laboratory artefact = doesn't represent true serum K+ conc (for accurate lab result, use heparin tube and request slow spin on centrifuge) Majority of K+ is intracellular so leakage from cells can cause significant impact on serum levels

- Haemolysis during venepuncture (excessive vacuum of blood drawing or too fine a needle to gauge)
- Delay in processing of blood specimen
- Abnormally high numbers of platelets (e.g. thrombocytosis - large numbers of platelets aggregate and degranulate releasing K+), leukocytes, erythrocytes
- Familial causes

ABG = Quick and accurate measure of true serum K+


Hyperkalaemia - Mx


Untreated Hyperkalaemia - can cause life threatening arrhythmias

Precipitating Factors:
- Acute Renal F - address
- Aggravating Drugs e.g. ACEI - Stop

- IV Calcium Gluconate
NB Some guidelines only recommend if K+ over 7.0 or ECG changes but should be priority over lowering the serum potassium in first instance

- Combined insulin/dextrose infusion
- Nebulised Salbutamol

- Calcium Resonium (orally or enema)
- Loop Diuretics
- Dialysis



Plasma K+ levels are regulated by a number of factors inc Aldosterone, Acid-Base balance, and insulin levels

eg metabolic acidosis is assoc with increased K+ because K+ and H+ ions compete with each other for exchange with Na+ ions across cell membranes and in distal tubule


Hyperkalaemia - Causes

- Acute Renal F
- DRUGS: Spironolactone (and other potassium sparing diuretics), ACEIs, Cyclosporin, Heparin (both UFH and LWMH), ARBs
- Metabolic Acidosis
- Addison's
- Rhabdomyolysis
- Massive blood transfusion
- Beta blockers (Beta agonists used in Mx of Hyperkalaemia!)


Foods high in K+

- Salt substitutes (contain K+ instead of Na+)
- Bananas
- Oranges
- Kiwi fruit
- Avocado
- Spinach
- Tomatoes

NB Pts with CKD need to eat these in moderation


Hyperkalaemia - ECG Changes

K+ > 5.5 = Peaked T waves, usually earliest sign (repolarisation abnormalities)

K+ > 6.5 = P wave flattens, PR segment lengthens, P waves eventually disappear (progressive paralysis of the atria)

K+ > 7.0 = Prolonged QRS (wide) w bizarre morphology , High grade AV block, Sinus bradycardia/Slow AF, Development of sine wave appearance (pre-terminal rhythm)
(conduction abnormalities and bradycardia)

K+ > 9 = Cardiac arrest 2dry to A-systole/VF/PEA

Suspect hyperkalaemia in any patient with a new bradyarrhythmia or AV block, especially patients with renal failure, on haemodialysis or taking any combination of ACE inhibitors, potassium-sparing diuretics and potassium supplements.