Potassium

Question 1

Which fluid compartment is potassium a primary cation in?

Answer 1

The intracellular fluid compartment. Levels are ~140mEq/L.

Plasma levels do not reflect intracellular levels.

Question 2

Why is potassium important?

Answer 2

*Normal K concentrations in both the ECF and ICF are vital to maintain proper resting membrane potential of muscle cells

Question 3

HyperK

Answer 3

• Uncommon in patients with normal renal functions
• Unlikely due to excessive intake
• K+ is quickly redistributed by insulin into cells until kidneys can excrete excess
• iatrogenic is possible
• Metabolic acidosis
• K+ shifts from cells into serum to exchange for H+ ions for buffering
• most common causes:
• Acute, anuric or oliguric renal failure
• urinary obstruction, urinary bladder rupture
• hypoadrenocorticism, GI dz, primary hypoaldosteronism
• DKA with hyperosmolality due to lack of insulin and acidosis present

Question 4

What are the drugs most likely to cause HyperK+?

Answer 4

• ACE inhibitors (Enalapril)
• Angiotensin receptor blockers
• Cyclosporine
• Potassium sparing diuretics (Spironolactone)
• NSAIDs
• Heparin
• Trimethoprim

Question 5

Clinical signs of HyperK

Answer 5

*>8.0mEq/L
*Muscle weakness and ECG signs
*Changes in resting membrane potential of muscle cells
-the higher the potassium concentration, the less negative the resting potential
-if severe enough, resting potential can drop below threshold = cells unable to depolarise or contract I.e. think cardiac muscles
*ECG: peaked, narrow, height T waves (Not seen in 40% of hyperK)
:Prolongation of PR interval
: Shortening of QT interval
: Changes with T waves and QT interval
- due to rapid repolarisation at mild increased K+ levels
*Worsening hyperK
:prolonged PR interval + widening of QRS due to slowed atroventricular system conduction

*Progressively worsening hyperK
:flattening and widening of P wave
:until they disappear completely due to cessation of atrial conduction

*Bradycardia
:with sinoventricular rhythm = atrial standstill
:then ventricular fibrillation or asystole may occur

*Other signs
:diarrhoea, abdo pain and flaccid paralysis

Question 6

Tx of hyperK

Answer 6

*Treat underlying cause I.e. relieving urinary obstruction
*Non-life threatening
:6.0-8.0mEq/L
:treat with IVF and underlying cause is enough usually

*K > 8.0
:when cardiac signs noted
:IVF, calcium gluconate 10%, dextrose / insulin administration and sodium bicarbonate

Question 7

Calcium gluconate for HyperK

Answer 7

• 1/2 ml/kg slow IV
• 50-100mg/kg over 10-20 mins
• if bradycardia occurs, stop
• works by antagonising toxic effect by normalising distance between resting and threshold
• has no effect on K levels and only last 1 hour

Question 8

How does giving glucose help hyperK?

Answer 8

• Stimulates insulin secretion
• Moves glucose with K into cells
• 0.5-1gm/kg
• If hyperglycaemic already
• give insulin 0.5-1.1 U/kg
• Glucose alone will aid in lowering K levels within an hour
• Adding insulin will result in more of an immediate effect

Question 9

How does giving sodium bicarbonate help in HyperK?

Answer 9

• shifts K into body cells as they replace H ions moving out of cells to be buffered by HCO3-
• works within 1 hour with effects continuing for several hours
• 0.5-2 mEq/kg IV
• with metabolic acidosis use:

Measured base deficit x BW kg X 0.3

• low dose bogus over 10-15 mins
• can be repeated
• reassess K, ECG, acid/base status after each dose
• care with renal patients
• can add loop diuretic (non-potassium sparing)

Question 10

What are the causes of HypoK?

Answer 10

• Dietary, losses through GI or renal, intro Elul are translocation, iatrogenic (lack of sup during IVF), metabolic alkalosis (K translocation into cells causing low serum K), hypothermia, overdose on albuterol, post obstructive diuretics, dialysis, hyperadrenocorticism (high levels of cortisol stimulates tubules in kidneys to excrete more K)
• Drugs: loop diuretic, thiazine diuretics, amphotericin B, penicillins
• Rattlesnake envenomation

Question 11

Clinical signs of HypoK

Answer 11

• Muscle weakness K<3
• Ventroflexion of neck (most common)
• Weakness in HL or stiff gait
• elevated creatinine kinase levels if K <2.5mEq/L
• Rhabdomyolysis (muscle breakdown) when K<2.0

Question 12

What happens when K levels are low?

Answer 12

• Negative resting membrane potential
• Increases distance between resting and threshold potential
• cells have decreased excitability
• repolarisation becomes prolonged

Question 13

What are the ECG changes seen in HypoK?

Answer 13

• Depression of the ST segment
• Low amplitude of T waves
• Prolongation of QT intervals
• Development of ventricular and supraventricular arrhythmias
• If cardiac muscle are unresponsive to class I antiarrhythmic drugs (Lidocaine and procainamide) = check K levels!!

Question 14

Treatment for HypoK

Answer 14

Supplement orally with potassium gluconate Mild) or for 7-14 days at 2-3mEq/day (Dogs) and 2.5-5mEq/day (Cats) IV

*Once balance corrected
:maintenance dose of 1-2mEq/day
:felines with renal failure 2-4mEq/day

*KCL supplementation IVF
\:should not exceed 0.5mEq/kg/hr
\:must be diluted
\:undiluted allowed if K very low but
-do not exceed 0.5mEq/kg/hr
-check hourly K levels with continuous ECG monitoring
-discontinue when K>3.5mEq/L