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Flashcards in Electrolyte distrubance Deck (25)
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1
Q

Discuss the effects of hyperkalaemia on the ECG

A

Potassium is vital for normal electrical activity of the heart. Hyperkalaemia leads to mycocardial excitability while depressing pacemaker cells and conduction tissue

Leads to suprression of impulse by the SA and progressive blocking of the AV node and purkinjes leading to bradycardia and conduction blocks and ultimately cardiac arrest

K>5.5 peaked T waves
K>6.5 associated with progressive paralysis of the atria - P wave widens and flattens, PR sement lengthens and p wave eventually disappear
K>7 – Prolonged QRS with bizarre morphology, high grade AV block with slow junctional and AV escape rhythm - leads to any conduction block, slow AF, SINE wave preterminal
K> 9 - asystole, VF, PEA with bizarre wide complex rythym

2
Q

Discuss the effects of hypokalaemia on the ECG

A

Decreased extracellular potassium leads to an increase in hyperexcitability with the potential to develop re-entrant arryhthmias

ECG changes begin when K+ <2.7

  • Increased amplitude and width of the P wave
  • prolongation of the PR interval
  • T wave flattening and inversion
  • ST depression
  • Prominent u waves

Worsening hypokalaemia

  • Frequent supraventricular and ventricular ectopics
  • Supraventricular tachyarrhythmias: AF, atrial flutter, atrial tachycardia
  • Potential to develop life-threatening ventricular arrhythmias, e.g. VT, VF and Torsades de Pointes
3
Q

Discuss the effects of hypernatraemia and hyponatraemia on the ECG

A

NIL

4
Q

Discuss effects of hypocalcaemia on the ECG

A

-Hypocalcaemia causes QTc prolongation primarily by prolonging the ST segment.
-The T wave is typically left unchanged.
Dysrhythmias are uncommon, although atrial fibrillation has been reported.
-Torsades de pointes may occur, but is much less common than with hypokalaemia or hypomagnesaemia.

5
Q

Discuss effects of hypercalcaemia on the ECG

A
  • The main ECG abnormality seen with hypercalcaemia is shortening of the QT interval
  • In severe hypercalcaemia, Osborn waves (J waves) may be seen
  • Ventricular irritability and VF arrest has been reported with extreme hypercalcaemia
6
Q

Discuss effects hypomagnesiumia on the ECG

A
  • The primary ECG abnormality seen with hypomagnesaemia is a prolonged QTc.
  • Atrial and ventricular ectopy, atrial tachyarrhythmias and torsades de pointes are seen in the context of hypomagnesaemia, although whether this is a specific effect of low serum magnesium or due to concurrent hypokalaemia is uncertain.
  • Nevertheless, correction of serum magnesium to >1.0 mmol/L (with concurrent correction of serum potassium to >4.0 mmol/L) is often effective in suppressing ectopy and supraventricular tachyarrhythmias, while a rapid IV bolus of magnesium 2g is a standard emergency treatment for torsades de pointes
7
Q

List common reasons for hyperkalaemia to develop

A

Spurious- haemolysed sample

  • renal failure
  • acidosis
  • cell death
  • drugs
8
Q

Discuss management of hyperkalaemia

A

IV calcium stabilizes the cardiac membrane by restoring the electrical gradient - it increases the depolarization threshod and the calcium gradient across teh cardiac membrane

Intracellular shift can be achieved with insulin dextrose, salbutamol and normal saline

  • insulin onset at 15 minutes with a peak at 30-60 minutes
  • salbutamol high doses 15-20mg measureable effect at 15 minutes and lowers K by 0.5 to 1
  • saline infusion stimualte Na/k atpase pump leading to an inward shift of potassium

Removal
HD
resonium `

9
Q

Discuss hypokalaemia

A

Most common electrolyte abnormality
Moderate is defined as 2.5-3 and severe is less than 2.5

Causes

  • Renal loss (diuretic use, steroid, metabolic acidosis, RTA, hyperaldosteronism, DKA, alcohol)
  • Increased non renal losses - sweating diarrhoea vomiting laxative use
  • decreased intake
  • intracellular shift
  • endocrine (cushing, bartters, insulin
10
Q

Discuss management of hypokalaemia

A

As potassium is an intracellular cation a low serum potassium level almost alwasy reflects a signifaicnt total body K deficit

Most patient with mild to moderate hypokalaemia will need only oral replacement

  • chlorvescent which has 8mmol of chloride and 14mmol of K
  • Span K 8 and 8 mmol of K and CL

Can safely replace 10-20mmol of IV K an hour - if needing to go faster than this will require central access

Hypokalaemia is often associated with hypomagnesemia. Without Mg potassium will not move intracellulary and will be lost through excretion. Magnesium should be replaced along side K

11
Q

Discuss hypernatraemia

A

Serum sodium above 145
Rarely seen in previously healthy patients and usually portends a poor prognosis. It can be subdivided into three phssiological pairing
1) hypernatraemia with dehydration and low total body sodium
-Heat stroke
-increased insensible losses - burns sweating
- GIT loss
-osmotic diuresis

2) hypernatraemia with low total body water and normal total body sodium
- DI
- Neurogenic
- Elderly with rest osmostat
- hypothalamic dysfunction
- suprasella or infrasellar tumors
- renal disease
- Drugs

3) hypernatraemia with increased total body sodium
-Salt tablet ingestion
-salt water ingestion
-saline infusions
-IV sodium bicardb
-primary hyperaldosteronisms
-cushings
conns

12
Q

Discuss the management of hypernatremia

A

Three independent goals

1) quickly correct underlying shock, hypoperfusion or significant hypovoalemia with normal saline
2) Treat underlying cause of hypernatreamia
- Central DI can be treated with DDAVP (desmopressin) initial dose is 1-2 microg
3) Carefully lower the serum sodium level usually by replacement of TBW

Almost all patient with hypernatraemia will have chronci hypernatraemia

  • Na should be lowered no more than 0.5mmol/hr or 10-12 mmol/day
  • IV saline for initial fluid resus to correct 1 than either 0.45% saline or 5% dextrose to correct at the rate above
13
Q

List causes of diabetes insipidus

A

Central

  • Idiopathic
  • familial disease
  • paraneoplastic
  • hypoxic encephaloapthy
  • infiltravitive disorders
  • post SVT
  • Anorexia nervosa

Nephrogenic

  • CKD
  • PCKD
  • Lithium toxicity
  • Hypercalcaemia
  • hypokalaemia
  • Hereditary
  • sickle cell disease
14
Q

Discuss hyponatraemia

A

Most patients present asymptomatic
two groups of patient will require acute treatment in the ED
1) those with severe hyponatrameia with sodium level of 110 or lower
2) those with Na level below 120 who are symptomatic

When neurons are subjected to a hyponatremic environement they become depleted of sodium and potassium in an attempt to limite their own osmolarity to prevetn intracellular fluid shift that would lead to cerebral oedema. If fluid therapy raises extracellular sodium levels two quickly fluids shift out of the neurons and can cause diffuse demyelination. This can result in a flaccid paralysis and death due to central pontine myelinolysis

15
Q

List causes of hyponatraemia

A

Pseudohyponatraemia

  • hyperlipidaemia
  • hyperproteinemia
  • Hyperglycaemia* - dilutional hyponatreamia

Hypovolaemic

  • Body fluid losses - sweating, vomtiing, diarrhoea, gastrointestinal suction
  • Third spacing - bowel obsturction, burns, pancreatitis, rhabdo
  • Renal - diuretics, mineralocorticoid deficiency, osmotic diuresis,, RTA, salt wasting nephropathies

Hypervolaemic

  • heart failure
  • chornic renal failure
  • hepatic failure and cirrhosis

Euvolemic

  • SIADH
  • Drugs causing SIAHD (diuretics, barbiturates, carbamazepine, chlorpropmaide, clofibrate, opioids, tolbutamide, vincristine)
  • psychogenic polydipsia
  • beer potomaniea
  • hypothyroidism
  • adrenalin insufficiency
  • MDMA
  • Cerebral salt wasting
16
Q

Discuss clinical finding of hyponatraemia

A

Most commonly asymptomatic with chronic hyponatraemia

Acute can present with non-specific signs

  • nausea and malaise - found with NA levels of 125-130
  • headahce, lethargy, obtundation, and eventually seizures, coma and respiratory arrest can occyr if the serum sodium falls below 115-120 - non cardiogenic pulmonary oedema has also been described
17
Q

Discuss IX of hyponatreamia

A
FBC
U&E 
LFT 
Lipid 
TFT
Cortisol level

Paired urine and serum electrolytes and osmolality

1) Low urine sodium and osmolality
- –Polydipsia
- – large fluid intake combined with protein malnurtrition described primarily in beer drinkgers (potomania )
2) high urine sodium and osmolality
- SIADH - urinary sodium usually above 40mmol - frequently associated with low uric acid and BUN
- severe hypothyroidism
- cortisol defiency
3) low urinary sodium with high urine osmolality
- SIADH with cocurrent hypovolaemia – cna be differentiated with a saline load and observing resposne

18
Q

Discuss aetiology of SIADH

A

CNS disturbances

  • Stroke, haemorrhage, trauma
  • infection
  • psychosis
  • Mass

Pulmonary

  • pneumonia
  • Lung masses (cancer, abscess)

Drugs

  • thiazide
  • narcotics
  • oral hypoglyacmic agents
  • antineoplastics

Malignancies

19
Q

Discuss goals of therapy for hyponatraemia

A

1) Prevent further decline in serum sodium
- reduce amount of free water
- if SIADH caution with saline containing fluid due to phenomenon that has been called desalination

2) Prevent brain herniation
3) relieve symptoms of hyponatraeami

4) avoid overcorrection
- Overcorrection or too rapid correction can lead to ODS (osmotic demylination syndrome)
- those at high risk for ODS are (NA <105, hypokalaemia, alcoholism, malnutrition, liver disease and possibly hypophosphataemia)

5) goal of correction
- raise serum sodium concentration by 4-6mmol/L in a 24 hour period. - in symptoamtic patients or those with severe severe symptoms this goal should be achieved in 6 hours with it kept at this level for the next 24 hours
- max rate should be 8mmol in a 24 hour period
- in most patient 4-6 mmol is enough to reverse severe symptoms, ODS occurs when raied by more than 10-12 mmol in 24 hours

20
Q

Discuss management of acute hyponatreamia in the 1st six hours

A

Asymptomatic

  • if less than 130mmol treat with 50ml bolus of 3% saline to prevent from falling further
  • not required if autocorrection already taking palce

Symptomatic

  • acutely hyponatreamic patients with a serum sodium of <130 who have symptoms that migh be due to increased intracraial pressure (seizure, obtundation, coma, resp arrest, headache, nausea , vomiting, tremors gait or movement disturbances or confusion) treat with 100ml bolus of 3% followed by additioanl two boluses if symptoms persist
  • goal is to rapidaly increase Na by 4-6 mmol
21
Q

Discuss management of chronic hyponatraemia in the 1st six hours

A

Mild 130-134

  • nil hypertonic saline
  • general measures applicable to all hyponatreamic patients ( seek and treat cause, limit further intake of water)

Moderate <130
-asymptomtic moderate 120-130 –> general measures applicable to all hyponatreamic patients

Severe <120
-either 3% infusions at 15-30ml/hour or 1ml/kg 3% boluses every 6 hours as needed

Severe symptoms or cocurrent intracranial mass
- as per severe hyponatraemia

If cause of hyponatreamia is rapidly reversible ie:
-hyponatreamia due to true volume depletion
-due to adrenalin insufficiency
-SIADH
They are likley to develop water diuresis during the course of therapy putting them at risk of ODS - desmopressin can be given proactively at the beginning of therapy 1-2mcg TDS

22
Q

List common causes of symptomatic hypocalcaemia

A

Symptomatic

  • hyperventilation - anxiety, sympathomimetics
  • ethanol abuse, chronic malnutrition - hypoalbuminemia
  • Massive blood transfusions >10 units
  • Toxins: hydrofluoric acid, ethylene glycol
  • severe pancreatitis
  • TLS

Other (often asymptoamtic)

  • Hypoparathyroidism
  • hyperphoshataemia
  • Drugs - bisphosphonates, phenytoin
  • Rhabdo
  • hypomag
23
Q

Discuss clinical features of hypocalcaemia

A

CVS

  • CVS collapse
  • synccioe
  • dysrhythmias
  • CHF
  • angina
  • hypotension
  • QT prolongation

Resp
-Bronchospasms

Neuro

  • perioral or finger paraethesias
  • tetanic contraction

Chronic

  • cataracts
  • poor dentition
  • dry skin
  • coarse hair
  • pruritis

Chvosteks sign may be presnet - when the examiner taps the facial nerve facial or eye muscle twitiching will be elicited
Trousseaus sign: Bp cuff 20mmhg above systolic BP for 3 minutes carpal spasms will be induced due to increased excitability

24
Q

Discuss IX of calcium

A

Total serum calcium is approxiamtly 50% free (ionised) and 50% bound thus serum levels should be corrected when hypoalbuminemia exists.

Ionised calcium is not affected by albumin load and is sometimes considered more accurate

25
Q

Discuss management of hypocalcaemia

A

For mild can give oral such as calcium carbonate
For moderate to severe given IV calcium gluconate is preferred as safer to give peripherally contains 92 mg of elemental calcium