Session 5 Flashcards
Explain depolarisation
If extracellular K+ rises, resting membrane potential is decreased
Na+ ions in
Explain repolarisation
If extracellular k+ falls, resting membrane potential is increased (hyperpolarised)
K+ ions out
ECG trace in hypokalaemia
Peaked P wave
Prolonged PR
ST depression
Shallow T wave
Prominent U wave
ECG trace in hyperkalaemia
Wide, flat P wave
prolonged PR
Decreased R wave amplitude
Widened QRS
Depressed ST segment
Tall, peaked T wave
Intra and Extra cellular concentrations of K+
Intra- 130-140 mEq/L
Extra- 3.5-5.5 mEq/L (due to Na+Ka+ATPase)
Distribution of body water
60% fluids (40% solids)
In 60% = 1/3 ECF, 2/3 ICF
In 1/3 ECF = 75% interstitial fluid, 25% plasma
How do the intercalated cells control pH of blood
Acidosis: secrete H+ into tubule, reabsorb K+ and HCO3- into blood
Alkalosis: secrete K+ and HCO3- into tubule, reabsorb H+ into blood
Clinical features of hyperkalaemia
Can be asymptomatic
Muscle weakness, cardiac arrhythmis (impacts nerve conduction)
Hyperkalaemia can result from
Lack of excretion - (kidneys failing, AKI/CKD, potassium sparing diuretics, ACE inhibitor, aldosterone problem)
Release from cells- acidosis, lysis
Excess administration- too much fluids, medications
When is emergency treatment of hyperkalaemia needed
When there is more than 6.5mlmol/L or ECG changes
Emergency treatment of hyperkalaemia
Calcium gluconate- Ca2+ stabilises the myocardium, preventing arrhythmias
Insulin- drives K+ into cells to lower plasma concentrations, given with glucose to avoid hypoglycaemia
Calcium resonium- removes K+ by binding to it and increasing excretion. Only way to remove K+ without renal replacement therapy
Clinical effects of hypokalaemia
Muscle weakness, cramps and tetany (starts in lower extremities)
Vasoconstriction and cardiac arrhythmias
Impaired ADH action causing thirst, polyuria and no concentration of urine
Metabolic alkalosis due to increase in intracellular H+ concentration
Long term control of hyperkalaemia
Low potassium diet
Stop offending medications
Furosemide- enhances potassium loss in urine
Dialysis?
Causes of hypokalaemia
Reduced dietary intake (anorexia nervosa)
Increased entry into cells (alkalosis or noradrenaline release due to stress perhaps)
Increased GI losses
Increased urine loss
Treatment for hypokalaemia
Treat cause- diuretics, diarrhoea, poor oral intake
Give replacement:
Oral- banana, orange, Sando-K
IV- add KCL to IV bags
Potassium sparing diuretics= spironolactone, amiloride
K+ too high or low will cause
Nerve dysfunction and cardiac arrest
Excretion of K+
Kidneys excrete 80% of K+, bowel 20%
Insulin will decrease k+ for appprox
6 hours
What is osmolality
Particles of solute per kg of solvent
What is osmolarity
Particles of solute per litre of solution
What is tonicity
Effective osmotic pressure gradient of two solutions separated by a semi permeable membrane
Differences in movement between intracellular and extracellular
Intracellular: potassium is major cation, Cell membrane limits transport
Extracellular: Sodium is major cation, concentration gradients allow movement
What is the TBW of a newborn baby
75%
What is TBW in elderly
45%
Why do patients need fluids
Nil by mouth
Malfunctioning gastro-intestinal tract
Dehydration
Fluid losses
Abnormal electrolytes
What to think about when giving fluids
Maintenance fluids- day to day requirements
Has patient lost any additional fluids
What happens when you give dextrose
Glucose taken up by cells rapidly (intracellular), H20 reduces osmolarity of all compartments equally
Movement of ions between spaces
Extracellular: Na+ can move between interstitial and intravascular (plasma and interstitium)
Na+ K+ ATPase allows transport of Na+ out of intracellular space and K+ in
What happens when you give saline
Na+ remains in ECF, no change in osmolarity (no drive to move intracellular)
What happens when you give Hartman’s
Majority retained in extracellular space as osmolarity maintained with effective osmoles sodium, potassium and calcium
What happens when you give dextrose and saline
H20 reduces osmolarity of all compartments
Saline remains in ECF
Dextrose drawn into ICF
Why are maintained requirements different in hospital patients
Vasopressin (ADH) differences (drugs, pain, nausea, low ECV)
Generally not sweating much
RAAS, catecholamines, reduced caloric expenditure (stress response)
NICE guidelines for fluids
25-30ml/kg/day of water
1 mmol/kg/day of potassium, sodium and chloride
50-110g/day of glucose to limit starvation ketosis
What happens when you give a patient saline that isn’t needed
Expanded ECF
What happens when a patient drinks too much water
Water expands ECF
Dilutes ECF (osmolarity decreased)
Water moves from ECF to ICF due to difference in osmolarity until new eq. Reached
What happens to the fluid volumes of a bleeding person
Losing volume from ECF
What happens to fluid volumes in a patient vomiting
ECF decreases
Osmolarity increases as more dehydrated
Water moves from ICF to ECF
What happens to the fluid volumes of someone who drinks salt water in large volume
ECF volume increases
Osmolarity increases
Water moves from ICF to ECF
What would you give a 96kg man who is NBM
1 x Hartman’s
2 x 5% dextrose (+40 mmol KCL)
What would you give a 65kg person who is NBM
2L 0.18 NaCl, 4% dextrose with KCL added to the bags
What would you give a 65kg person who is vomiting
1L saline, 2L 5% dextrose with KCL added
So saline can go ECF and dextrose can go ICF
