Hyper K+ class slides Flashcards
K+
Major intracellular cation
Helps regulate pH
Major role in conducting nerve impulses and maintaining electrical excitability
Critical for neurological function
Hypo K+
<2.5 normal 3.5-5
Suspect hyper K+ in
Renal failure (most common) Renal dialysis (pts develop hyper k+ quickly) Pts taking k+ supplements
Potential cause hyper K+
Psuedo hyper K+ (tourniquet on too long) Acidosis Heavy exercise Insulin deficiency Dig tox K+ supplements/IV K+ Renal failure K+ sparing diuretics Crush injuries MEdications (succ) Hypoaldosteronism
Dig tox
yellow vision
ECG changes hyper K+
Not predictable
50% over K+ over 6mEq/L do not show on ECG changes
Neuromuscular symptoms hyperk+
ECG changes/dysrhythmias Weakness Paraesthesia Tremors Areflexia Respiratory failure Ascending paralysis GI
ECG K+ 5.5-6mEq/L
Tented T waves
ECG K+ 6-6.5mEq/L
Increasing PR and QT interval
ECG K+ 6.5-7mEq/L
Flattened P waves widen and flatten, PR lengthens and P waves usually disappear
ECG K+ 7-7.5 mEq/L
Widening of QRS and bizarre QRS morphology, high grade AV blocks, any conduction block, sinus brad or slow AF
ECG K+ 7.5-8mEq/L
Merging of S and T waves, development of sine wave
ECG K+ 8-10mEq/L
Sine wave, idioventricular complexes, VT appearance
ECG K+ over 10mEq/L
PEA with bizarre wide complex rhythm VT/VF asystole
Bicarb/calcium around
7mEq - QRS changes, blocks, brads, slow AF
TXs
- Membrane stabilization (priority, can all be done sequentially)
- Shift potassium intracellularly
- Remove excess potassium
7 tx options for hyper K+
Calcium chloride - severe Sodium bicarb - moderate to severe Insulin/dextrose - moderate to severe Ventolin - moderate to severe Furosemide - moderate to severe Kayexalate - mild to severe Dialysis - pt dependent ***Fluid TX - 10mL/kg
Calcium Chloride
No effect on k+
Antagonizes toxic effects of K+ at myocardial membrane
Onset 1-3 minutes
Duration 30-50minutes
Calcium Chloride indications
QRS complex, arrythmias are indications for CaCl
Peaked t waves alone are not
Usually given at 7.5mEq > range
Dose 8-16mg/kg single max dose of 1g over 10 minutes
Insulin and dextrose
For moderate to severe hyper K+
Facilitates uptake of glucose into cell, brings K+ with it
Movement of glucose causes intracellular movement of K+ which decreases plasma K+
Onset 30 minutes, duration 4-6 hours
Dextrose dose
0.5g/kg max 25g with 10 units humulin R IV/IO (no insulin repeat)
D50 repeat 0.5g/kg max 25 q 10-15 minutes
Check BGL each time
Sodium Bicarb
Alkalinizing agent: Increases pH which results in temporary k+ shift from extracell to intracell, these agents enhance effectiveness of insulin in pts with acidosis
Onset 30 minutes
Duration 1-2 hours
Given in moderate & severe cases (6.5mEq/L - 10mEq/L(
Dose 50mEq IV/IO
B2 agonists ventolin
Increase reuptake of k+ back into skeletal muscle
B2 effect increase glucose production in skeletal muscle and increase insulin production in pancreas
Onset 15-30 minutes
Duration 2-4 hours
Normal TX guidelines apply can be given prn
Kayexalate (polystyrene sulfonate)
Exchanges sodium for K+ in the gut, decrease total amount of K+
Onset 1-2 hours duration 4-6 hours
30G PO/OG/NG or 50g PR no repeat dose
Diuretics for hyperK+
Lasix, not K+ sparing diuretic, so essentially it will cause potassium loss through the kidney
Consider not in renal failure and for prehospital
Onset and duration varies
40-80mg SIVP/IO if pt is already on lasix then double dose
Dialysis for hyperK+
Gold standard tx for pts with severe hyperK+
Onset minutes
Hypokalemia
Most common electrolyte distrubance
Decrease in total body K+ often secondary to diuretic therapy
Hypokalemia causes
Intracellular shifts + increase losses
- Inadequate intake
- GI losses - diarrhea, vomiting
- Diuretic Therapy (most common cause)
- Renal loss - diuretics
- Alkalosis
- Beta adrenergics
Hypokalemia S&S CVS
HTN, Orthostatic hypotension, dysrhythmias (usually tachy)
ECG changes
Neuromuscular S&S hypoK+
Weakness, Hyporeflexia, Parasthesia, paralysis
HypoK+ TX
Oral replacement Intravenous KCL (normally 10-20mEq/L)
