Hyperkalaemia Flashcards
function of potassium
Potassium (K+) is involved in maintaining the resting cell membrane potential
problems caused by small shifts in potassium concentration
problems with muscle and nerve conduction, leading to potentially life-threatening disorders of the cardiac and neuromuscular systems
normal plasma concentration of potassium
3.5-5.5 mEq/L
definition of hyperkalemia
Hyperkalemia is defined as a potassium level of >5.5 mEq/L
mild hyperkalemia
5.5-5.9 mmol/l
moderate hyperkalemia
6.0-6.4 mmol/l
severe hyperkaelemia
> 6.5 mmol/l
pathophysiology of hyperkaelemia
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.
This leads to decrease muscle contractile strength, evident in the typical clinical presentation
categories’ of the causes of hyperkalemia
- Imbalance between intake and excretion of K leading to total body excess
- trans-cellular shifts/ excessive tissue release
- measurement error.
number one cause of hyperkalaemia
spurious elevation
other common causes of hyperkalemia
Chronic renal failure (the true number one cause of hyperkalaemia)
Acidosis (potassium moves out of the cell as the pH falls)
Drug induced (including nonsteroidal anti-inflammatory drugs, potassium-sparing diuretics, digoxin, angiotensin-converting enzyme inhibitors, and administration of intravenous potassium chloride)
Cell death (when potassium comes out of injured muscle or red cells); including burns, crush injuries, rhabdomyolysis, tumour lysis syndrome, and intravascular haemolysis.
Much less common causes of hyperkalaemia include adrenal insufficiency, hyperkalaemic periodic paralysis, and hematologic malignancies.
disorders causing hyperkalaemia
- failure of excretion
- transcellular shifts (Na-K ATPase pump)
- measurement error (pseudohyperkalemia)
- large, rapid potassium load
failure of excretion
-Decreased glomerular filtration rate
^^Renal Injury
-Heart failure
-Obstructive uropathy
-Low aldosterone level
^^Adrenal insufficiency (Addison disease)
^^Low renin level
-Type 4 renal tubular acidosis
-Medications that inhibit Na-K ATPase in the distal nephron
transcellular shifts (Na- K ATPase pump)
-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)
measurement error (pseudohyperkalemia)
-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
large, rapid potassium load
-Massive blood transfusion protocol
-High-dose potassium penicillin
-Poisoning/ingestion
Recognizing the patient with hyperkalaemia
-Most patients presenting with isolated hyperkalaemia are asymptomatic, until very severe, and the diagnosis is only made after potassium levels are drawn.
-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.
-Physical examination findings include 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.
diagnosis: ECG
-An ECG is the first step in the workup of a patient with hyperkalaemia.
-Hyperkalaemia increases myocyte sensitivity in different areas of the heart progressively as K+ levels rise:
^^Atria
^^Ventricles
^^Bundle of His
^^Sinoatrial node
^^Interatrial tracts
-Therefore, the ECG progresses through several phases that are loosely correlated with absolute serum K+ levels and with the rate of increase in serum K+ levels.
^^The first and most common sign is tall, “peaked” T waves with a narrow base. These occur most frequently in the precordial leads V2-V4. A sensitive sign is if the amplitude of the T exceeds the amplitude of the R. This loosely correlates with potassium levels between 5.5 and 6.5 mEq/dL.. The most dangerous ECG finding
is widening of the QRS, which may merge
with the abnormal T wave and create a sine-wave-appearing ventricular tachycardia.
^^As the atria are affected the PR interval lengthens, and as the ventricles are affected the QRS widens.
^^When hyperkalemia affects the conduction system, the P waves decrease in amplitude until the ECG develops a “nodal” rhythm with absent P waves (Corrolated loosely with potassium levels between 6.5 and 7.5 mEq/dL.)
^^The QRS continues to widen until the S and T waves merge into a “sine wave” pattern (generally associated with levels of 8.0 mEq/dL) The sine wave pattern usually shortly precedes ventricular fibrillation (VFib) and cardiac arrest.
-Confirm with serum potassium level
serum K: <2.5 mEq/L
depressed ST segment
diphasic T wave
Prominent U wave
serum K: normal
normal ECG
serum K: > 6.0 mEq/L
tall T waves
serum K: > 7.5 mEq/L
long PR interval
Wide QRS duration
tall T wave
serum K: > 9.0 mEq/L
absent P wave
sinusiodal wave
what is treatment based on
(a) serum levels,
(b) the presence or absence of ECG changes, and
(c) underlying renal function
management
f the patient has ECG changes of hyperkalaemia
10% calcium chloride or gluconate should be given in an initial 10 mL to 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 stabilization
calcium
-10mL of 10% Ca2+ gluconate or chloride
*Calcium chloride has higher bioavailability, but is prone to cause tissue necrosis. It is however, 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
shift K+ into cells
insulin/ dextrose
salbutamol nebulisation
HCO3- infusion
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
-watch out for hypoglycaemia
salbutamol nebulisation
-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+
-can cause: tachyarrhythmias, tremor, anxiety and flushing
HCO3- infusion
-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 consider if metabolic acidosis present.
-don’t administer in same line as Ca2+ - can cause precipitation
increase K+ elimination
diuretics
dialysis
resonium- K+ binders
diuretics
Lasix 1-2mg/kg IVI slowly
dialysis
-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
resonium- K+ binders
-Sodium polysterene sulphonate (Kayexalate) 30g PO or PR
-cation exchange resins
-negatively charged polymers than exchange the cation for K+ across the intestinal wall
what is important to consider
treat the underling cause
disposition: admission criteria
-Hyperkalaemia persists despite treatment
-Cardiac toxicity demonstrated (severe hyperkalaemia)
-Underlying condition mandates admission (e.g. severe renal failure)
disposition: discharge criteria
-Potassium corrected to normal levels
-Underlying cause has been found and treated
-Drugs that are causative have been stopped
-Out-patients follow-up has been arranged
