Hyperkalemia Flashcards
(25 cards)
define hyperkalemia
Small shifts in potassium concentration result in problems with muscle and nerve conduction, leading to potentially life-threatening disorders of the cardiac and neuromuscular systems. The normal plasma concentration of potassium is 3.5-5.5 mEq/L. Hyperkalemia is defined as a potassium level of >5.5 mEq/L. Further subdivision into mild moderate and sever forms follow:
Mild 5.5-5.9 mmol/l
Moderate 6.0-6.4 mmol/l
Severe > 6.5 mmol/l
physiology of K+
About 98% of total body potassium (K+) is Intracellular and off this, 75% is contained in skeletal muscle cells.
The remaining 2% extracellular component is maintained within a tight range of 3.5 to 5.5 mEq/L (1 mmol equals 1 mEq K+) by the body.
The main mechanism by which this trans-cellular ratio is maintained is through the sodium-potassium (Na-K) adenosine triphosphatase (ATPase) pump. It uses ATP to drive K+ into cells in exchange for sodium (Na).
The resulting K+ gradient creates a resting membrane potential that determines cardiac and neuromuscular cell excitability and signal conduction
Because the extracellular K+ level is proportionally so much less than the intracellular level, even a small change in the extracellular level significantly alters the resting membrane potential.
causes of high K+
Causes of hyperkalaemia can be broadly placed into three categories:
1) Imbalance between intake and excretion of K leading to total body excess
2) trans-cellular shifts/ excessive tissue release
3) measurement error.
causes of failed K+ excretion
Decreased glomerular filtration rate
Renal Injury
Type 4 renal tubular acidosis
Heart failure
Obstructive uropathy
Low aldosterone level
Adrenal insufficiency (Addison disease)
Low renin level
Medications that inhibit Na-K ATPase in the distal nephron = ACE-I
causes of transcellular shifts
Haemolysis
- Rhabdomyolysis
- Tumour lysis syndrome
- Haematoma reabsorption
Medications that inhibit Na-K ATPase pump
Insulin deficiency
- Diabetes mellitus
- Prolonged fasting
Hypertonicity
- Hyperglycaemia
- Hypernatremia
Acidosis
Hyperkalaemia periodic paralysis (mutation of skeletal muscle Na-K pump)
how does measurement error happen
> Haemolysis during blood draw
Prolonged tourniquet use
Small needle calibre
Excessive fist clenching
Excessive plunger force to pull blood into a syringe
> Haemolysis before laboratory analysis
Delay between blood draw and analysis
Aggressive sample shaking
> Hyperviscosity
Extreme leukocytosis
Extreme thrombocytosis
Polycythemia vera
patient presentation
Patients may experience palpitations or generalized fatigue and malaise
.
Muscle cramps, paresthesias, and weakness that can progress to a flaccid paralysis can occur.
Nausea, vomiting, and diarrhea are common GI complaint.
examination findings - see ECG
> bradycardia and/or irregular cardiac rhythm with frequent premature ventricular contractions.
Neurologic examination may show decreased deep tendon reflexes and decreased power. Sensation is, however, intact.
what is the mx of hyperkalemia based on?
(a) serum levels
(b) the presence or absence of ECG changes
(c) underlying renal function.
If the patient has ECG changes of hyperkalaemia…
10% calcium chloride or gluconate should be given in an initial 10 mL
> temporarily reverse potassium’s deleterious electrical effects. After membrane stabilization potassium is moved intracellularly (“shifted”) to lower the serum potassium level. It is however important to remember that this does not lower the total body potassium level and for that reason the final step in the management is always increasing potassium excretion.
NB: STOP ALL POTASSIUM CONTAINING FLUIDS AND DRUGS THAT MAY WORSEN HYPERKALAEMIA.
membrane stabilisation
10mL of 10% Ca2+ gluconate or chloride
Calcium chloride has higher bioavailability
The preferred treatment during cardiac resuscitation due to the ready availability of Ca2+
calcium gluconate = 2.2mmol of Ca2+ in 10mL
calcium chloride = 6.8mmol of Ca2+ in 10mL
> antagonises the membrane excitability of heart
does not lower serum K+
can cause: bradycardia, arrhythmias, tissue necrosis if extravasated
goals of rx
> membrane stabilisation
shift into cells
increase elimination
how to shift K+ into cells?
1 - insulin/dextrose
2 - salbutamol nebs
3 - bicarb infusion
use of insulin/dextrose
10U actrapid, 50mL of 50% dextrose
insulin increases uptake by stimulating the Na+/K+ ATPase
reduces K+ by around 0.65-1mmol/L/hr
risk in insulin use
hypoglycaemia
salbutamol use for shift
10mg Salbutamol in 4ml Saline nebs
binds to the beta-2-receptor -> stimulated adenylase cyclase converting ATP->cAMP -> stimulation of Na+/K+ ATPase with subsequent increase in intracellular K+
risk in salbutamol use for shift
tachyarryhmias, tremor, flushing
bicarb infusion use for shift
50 - 100mL of 8.4% over 30 min.
decreases the concentration of H+ in the extracellular fluid compartment -> increases intracellular Na+ via the Na+/H+ exchanger and facilitates K+ shift into cells via the Na+/K+ ATPase
ONLY IF ACIDOSIS PRESENT
risk in bicarb infusion
don’t administer in same line as Ca2+ - can cause precipitation
how to increase elimination of K+
> diuretics
dialysis
binders
diuretic use
Lasix 1-2mg/kg IVI slowly
dialysis use
Haemodialysis best (can remove 25-40mmol/hr -> 1mmol/L/hr)
faster if increase blood flow rate, dialysis flow rate, low K+ concentration in dialysate, high bicarbonate concentration
binders use
Sodium polysterene sulphonate (Kayexalate) 30g PO or PR
cation exchange resins
negatively charged polymers than exchange the cation for K+ across the intestinal wall
admission criteria
Hyperkalaemia persists despite treatment
Cardiac toxicity demonstrated (severe hyperkalaemia)
Underlying condition mandates admission (e.g. severe renal failure)
