Fluid & Electrolytes Flashcards
What are the symptoms and signs of hypokalaemia?
MUSCLE –> weakness, myalgia
CARDIAC –> arrhythmia, palpitations, syncope
ECG progresses from T wave flattening –> T wave inversion + ST depression –> U waves appear –> U waves become larger than T waves.
Arrhythmias that can occur:
- Ectopic atrial and ventricular beats
- Sinus bradycardia
- Atrial tachycardia
- AV block
- VT
- VF
RENAL –> hypokalaemia leads to impaired urinary concentrating ability and eventually nephropathy –> polyuria, nephrogenic DI
What causes hypokalaemia?
INADEQUATE INTAKE - needs to be extreme dietary insufficiency to cause hypokalaemia - e.g. anorexia nervosa
INTRACELLULAR SHIFT -
K shifts into cells is stimulated by insulin and adrenaline
LOSSES -
GIT: diarrhoea, vomiting
RENAL: K-wasting diuretics, Conn syndrome (excess aldosterone), tubular disease (Bartter and Gitelman syndromes), RTA
OTHER: burns, excessive sweating
How would you treat hypokalaemia?
For mild hypoK (i.e. K 3.0-3.5)
Oral supplementation with KCl
For more severe hypoK (i.e. <3.0) or cannot tolerate oral intake –> IV KCl with normal saline + continuous ECG monitoring.
+ correct any other electrolyte disorders
+ correct any dehydration
+ investigate and treat underlying cause
What are the symptoms and signs of hyperkalaemia?
MSK --> - Weakness (starts in lower limbs) - Muscle cramps CARDIAC --> - Palpitations - Arrhythmia ECG changes: First (usually at 5.5-6.5 mmol/L): - Peaked T waves - Prolonged PR interval Then, as K continues to rise: - Loss of P waves - Widened QRS - Sine wave pattern - Asystole
What causes hyperkalaemia?
The 2 main underlying causes are:
- Impaired renal K excretion - could be due to:
- CKD
- AKI
- Drugs: ACE-I, ARB, K-sparing diuretic
- Aldosterone deficiency: Addison’s disease - Shifts of K out of cells
- Cell breakdown: rhabdomyolysis, trauma
- Drugs: B-blocker
- Insulin deficiency: e.g. in DKA
How would you treat hyperkalaemia?
CARDIAC MONITORING
IV ACCESS
- Prevent arrhythmia –> Give IV calcium
- Drive K into cells –> Give insulin + dextrose infusion, B2-agonist (nebulised albuterol)
- Remove K from body –> loop diuretic (if not volume depleted), intestinal K-binders, or dialysis
- Identify and treat cause
What are the 2 main organ systems affected by K abnormalities?
Both HYPOKALAEMIA and HYPERKALAEMIA can cause:
MSK –> weakness, myalgia
CARDIAC –> arrhythmia, palpitations
What is the daily recommended fluid intake?
Men = approx. 3.7L/day Women = approx. 2.7L/day
How would you assess volume/fluid status?
VITALS: tachycardia, orthostatic hypotension, hypotension
WEIGHT
URINE OUTPUT
SKIN & MUCOUS MEMBRANES:
Skin - temperature, turgor, capillary refill (normal = <2 sec)
Mucous membranes - dry or moist
JVP (height = cm above angle of sternum measured vertically. Considered elevated if > 3cm at 45 degrees)
OEDEMA/EFFUSION
Pulmonary oedema - SOB, crackles
Ascites
Peripheral oedema
Fluid management strategies: Hypovolemic shock? Dehydration without shock? NBM? Ongoing losses?
HYPOVOLEMIC SHOCK - GIVE FLUID BOLUS
- UNSTABLE –> stat bolus of 1L 0.9% normal saline or bolus of 10-20mL/kg NS; watch response and repeat if necessary +/- vasopressors
DEHYDRATION W/O SHOCK - FLUID RESUSCITATION with CHALLENGE
Possible approach: fluid challenge = stat bolus of 250mL 0.9% normal saline; watch response –> if partially rectifies issue - repeat with further 250mL 0.9%NS stat then slow to 1L/8-10 hours.
OR, if only mildly dehydrated –>
1L NS over 4 hours, then
1L NS over 6 hours, then
1L NS over 8 hours –> then normal maintenance if required
NIL BY MOUTH –> MAINTENANCE FLUIDS
Possible approach: 3L/24 hours = 1L/8 hourly 0.9% normal saline.
If NBM for 24+ hours –> add 30mmol KCl to 2 of the bags of NS.
Alternatively, use Hartmann’s instead of NS –> reduced risk of metabolic acidosis. Still need to add 30mmol KCl to 2 of the bags.
ONGOING LOSSES –> MAINTENANCE + REPLACE ONGOING LOSSES.
What causes hypercalcemia?
PTH-MEDIATED HYPERCA
- Primary hyperparathyroidism: hyperplasia, adenoma
- Tertiary hyperparathyroidism from CKD
NON-PTH-MEDIATED HYPERCA
- Malignancy:
From paraneoplastic production of PTHrP
From osteolytic metastases
- Granulomatous disease e.g. TB
From activated mononuclear cells –> have hydroxylase activity –> increased active vitamin D - Mediations:
Thiazide - reduce renal calcium excretion
Vitamin D excess
Calcium supplementation
Vitamin A excess
Lithium - reduces renal calcium excretion and alters PTH secretion set point
Milk-Alkali syndrome - Thyrotoxicosis
From T3/T4 –> stimulation of osteoclasts - Immobilization –> stimulation of osteoclasts
What are the symptoms and signs of hypercalcemia?
BONES, STONES, Abdominal GROANS, Psychic MOANS and CARDIAC
BONES:
Bone pain
Muscle weakness, especially proximal myopathy
Fracture
STONES:
Kidney stones
GROANS: N&V Anorexia Constipation PUD Pancreatitis
MOANS: Fatigue Inability to concentrate Depression --> confusion --> coma
CARDIAC: Bradycardia 1st degree AV block Short QT Arrhythmia
How would you treat hypercalcaemia?
- Evaluate patient:
DRSABCD, Vitals, LOC, stable/unstable
Obtain ECG/ cardiac monitoring
IV access - Initial IX for underlying aetiology:
FBC, EUC, CMP, ALP
PTH, vitamin D
Further IX depending on suspected cause. - Appropriate hydration & diuresis
(hypercalcemia may cause N&V + will dilute calcium)
IV fluids with 0.9% NS - may require a lot of fluid e.g. 5-10L over 24 hours
Loop diuretic if volume overloaded - Avoid medications that aggravate hypercalcaemia (thiazide, lithium, vitamin D, calcium)
- Mild –> as above + monitor with serial CMP; arrange consultation e.g. endocrinology, nephrology
- Moderate/ Severe –> as above + consider:
Rapid onset, short-term control of hyperca –> calcitonin
Slower onset, long-term control of hyperca –> Bisphosphonates
Dialysis
Monitor - serial CMP, ECG
