Hyperkalaemia Flashcards
Definition?
Hyperkalemia (high serum potassium) is a common and potentially life-threatening disorder of potassium balance.
ddx?
psuedo-poor sample collection
tumour lysis syndrome-hyperuricemia and hypocalcaemia
CKD-low urine output and uraemic signs
Digitalis toxicity-drug screen
injuries-history
malignant hyperthermia-history of anaesthetic use and febrile and tachycardia
Epidemology?
Age: Infants/older
Sex:
Ethnicity:
P: 5% general pop and 10% hospitalised
Aetiology?
potassium excess
extracellular shift
pseudohyperkalaemia
potassium excess?
- Reduced excretion:acuteandchronic kidney disease
- Endocrine causes:hypocortisolism,hypoaldosteronism
- Drugs:potassium-sparing diuretics,ACE inhibitors,angiotensin receptor blockers,NSAIDs, andtrimethoprim-sulfamethoxazole[4]
- GI absorption: increased intake ofhigh-potassiumfoods (e.g., fresh fruits, dried fruits and legumes, vegetables, nuts, seeds, bran products, milk, and dairy products)
- Type IVrenal tubular acidosis
- Release from cells:myolysis,tumorlysis,hemolysis
extracellular shift?
• Acidosis→↑ extracellular H+→inhibitionof theNa+/H+antiporter→↓ intracellular Na+→↓ sodiumgradient inhibits theNa+/K+-ATPase→↑ extracellular K+concentration
○ Hyperkalemia→↑ extracellular K+concentration →↑ potassiumgradientstimulatestheNa+/K+-ATPase→↑ extracellular Na+→↑ sodiumgradient stimulates theNa+/H+antiporter→↑ extracellular H+→acidosis
○ Exception: Inrenal tubular acidosis, findings includehypokalemiaandmetabolic acidosis.
• Hyperosmolality
• Insulindeficiency(manifests withhyperglycemia)
• Release from cells:rhabdomyolysis,tumor lysis syndrome,hemolysis
• Drugs
○ Beta-blockers
○ Succinylcholine: (esp. when given with preexistingburnsand/or muscle trauma),
○ Digoxin: inhibits theNa+/K+-ATPase→↑ extracellular K+concentration
psuedo?
• Pseudohyperkalemia: due to the release of potassium fromred blood celllysis
• Blood drawn from the side of IV infusion or acentral linewithout previousflushing
• Prolonged use of a tourniquet
• Fist clenching during blood withdrawal
Delayed sample analysis
CP
Symptoms usually occur if serum potassium levels are> 7.0 mEq/Lor they change rapidly.
• Cardiac arrhythmias(e.g.,atrioventricular block,ventricular fibrillation)
• Muscle weakness, paralysis,paresthesia
• ↓ Deeptendon reflexes
• Nausea, vomiting,diarrhea
Pathophys
- Higher than normal potassium levels in the blood >5.5mmo/L
- IC- most
- EC-less-includes venous and lymphatic space
- Carries charge-electrochemical gradient across membranes
- Maintained by Na/K pump-2K in for 3Na out
- Sets resting membrane potential for contraction of smooth, cardiac and skeletal muscle
• External balance-intake matches output-excreted in urine and insensible losses
- External balance shift-less K excreted-increased in blood
- Internal balance shift-K moves out of cells and increased in blood
- Insulin deficiency-cant bind to cells and be taken up from the blood
- Acidosis-H/K transporter overworks-more deposited into blood-compensation-metabolic only as CO2 diffuses readily into cells
- Same if lactic or ketoacidosis
- B2 and A receptors-stimulates pump or Ca-dependent pump-Beta blockers and alpha agonists increases in blood
- Hyperosmolality-water out of cells into ECF-increases K conc in cell-moves out of cell down gradient into blood
- Cell lysis-released into blood-burns, rhabdomyolysis and tumour lysis
- Exercise-more ATP used-opens K-more out-made worse if on drugs
- External Balance Shift
- If rapid and excessive intake-IVF
- Usually filtered in PCT, ALoH, a-intercalated cells (absorption) and principal cells (secretion)
- Aldosterone-more potassium secretion into tubule-insufficiency-less removal of K
- Drugs-renin, ACE, AR, selective aldosterone, K-sparing inhibitors/diuretics
- AKI-less blood is filtered-less K removed form blood as less water is being reabsorbed from the tubule
Investigations-first line?
• Serum electrolytes and glucose, creatinine
• Glucose: If very high, consider spurious hyperkalemia secondary tohyperglycemic crisis.
• Serum electrolytes
○ Na+: normal or can be ↓ inadrenal insufficiency(see “Diagnostics” in “Adrenal insufficiency”)
○ K+: Repeat to confirm the diagnosis and rule outpseudohyperkalemia(see “Etiology”).
• Kidney function tests: often show renal impairment[12]
• CBC: can showhemolytic anemiaorthrombocytosis[13]
• Liver chemistries: may be abnormal inhemolysisortumor lysis syndrome
• Blood gases(venous or arterial):often showmetabolic acidosis
ECG
ECG findings?
Thecorrelationbetween serum K+levels and the severity ofECGchanges is loose. Findings are more likely to occur withrapid-onsethyperkalemia.
• Mild hyperkalemia:5.5–6.4 mEq/L
• Tall,peakedT waves
• Moderate hyperkalemia:6.5–8.0 mEq/L
• Lengtheningof QRS interval(QRS complexwidening)
• Widening andflatteningofP wave, which eventually disappears
• Severe hyperkalemia:> 8.0 mEq/L
• AbsentP wave
• Intraventricular conduction block
• Unusual QRS morphology
• Sine wave pattern: a sinusoidal pattern with absentP wavesand a wideQRS complexthat merges with theT wave; a marker of impending V-Fib andasystole
• Cardiac arrhythmias(e.g.,V-tach,V-fib),asystole
Investigation-second line?
Depending on symptoms andrisk factors,further testing may be appropriate, particularly if renal function is normal.
• Creatine kinase: ↑ inrhabdomyolysis
• LDH: ↑ intumor lysis syndromeorhemolysis
• Renin-angiotensin-aldosterone system
• ↑Aldosterone: suggests e.g.,pseudohypoaldosteronism, nephropathy due tosickle cell disease, andtype 1 RTA
• ↓Aldosterone: Assessrenin.
○ Normal or↑renin: suggests e.g.,hypoaldosteronism(e.g., due toAddison disease)orcongenital adrenal hyperplasia
○ ↓Renin: suggests e.g.,AIN,diabetic nephropathy
• Cortisol: can be ↓ inprimary adrenal insufficiency
• Urineelectrolytes: rarely indicated
Management-risk scoring?
• The risk ofhyperkalemic emergency(acute severe elevation requiring urgent lowering) is elevated if any of the following are present:
○ Clinical manifestations: e.g.,cardiotoxicity(see “ECG changes in hyperkalemia”), muscle weakness, paralysis
○ Serum K+> 6.0–6.5 mEq/L[24]
○ Comorbidities that affect ongoing K+influx and elimination: e.g.,AKI,ESRD,GI bleeding,rhabdomyolysis,TLS
• Less urgent hyperkalemia (typically chronic elevations that can be lowered more slowly)is more likely in the following cases:
○ Asymptomatic patient
○ Serum K+=5.5–6.0 mEq/L
Nohigh-riskcomorbidities
Cardiac membrane stabilisation?
Calcium salts reduce cardiac irritability.
• Indication: signs of cardiotoxicity (see “ECG changes in hyperkalemia”)
• Options
• 10%calcium gluconate[23]
• 10% calciumchloride(preferably given in a central ordeep vein)[15]
• Considerations[10]
• Ensurecontinuous cardiac monitoringthroughout to detect potentialarrhythmias.
• Effects last only30–60 minutes; additional dosing may be required.
IC K shifting?
These drugs should be given in tandem with calcium salts (if calcium is indicated).
• Insulinand glucose: preferred acute noninvasive K+-lowering treatment;short-actinginsulincombined with50% dextrose
• Patients with glucose levels> 250 mg/dLshould not receive D50W.
• Monitor all patients forhypoglycemiahourly for at least2 hoursafter administration.
InhaledSABAs: e.g.,nebulizedalbuterol(off-label); to consider as an adjunct toinsulin(not effective as a monotherapy)
