Potassium Flashcards
Why is potassium important?
Deranged potassium is assocaiated with what?
Where is potassium mostly lost from?
• Strict regulation is essential for vital physiologic processes:
o the resting cellular-membrane potential
o propagation of action potentials in neuronal, muscular, and cardiac tissue
o hormone secretion and action
o vascular tone o systemic blood-pressure control o gastrointestinal motility o acid–base homeostasis
o glucose and insulin metabolism
o mineralocorticoid action
o renal concentrating ability
Patients with hypokalaemia or hyperkalaemia have an increased rate of death from any cause.
• Deranged potassium levels associated with:
o progression of cardiac and kidney disease
o interstitial fibrosis.
o fluid and electrolyte balance
Potassium loss: Kidney (90%), Gut + Skin( 10%)
How much potassium is there in the extracellular fluid and intracellular fluid?
What is the serum potassium concentration norm?
3.5 – 5.3 mmol/L - serum potassium concentration
Rapid clearance by renal and extra-renal mechanisms reduce variation in plasma potassium to no more than 10%.
What happens after a potassium load?
How is the extracellular fluid potassium homeostasis occuring?
How is it handled in the kidney?
When do you urinate potassium more in the morning or evening?
You urinate more potassium around noon.
What hormones help to increase potassium levels in the blood?
What hormones help to decrease the potassium levels in the blood?
What is the net effect of aldosterone on potassium?
What conditions can cause overactive RAAS system and what happens to K+ due to it?
What happens due to an underactive RAAS to the K+?
What is the affect of insulin and catecholamines on potassium?
What is the effect of metabolic acidosis on K+ in plasma??
What is the affect of metabolic alkalosis on K+ in plasma?
Metabolic Acidosis - increasse plasma [K+]
o Inhibition of renal tubular K+ secretion
o Shift of K+ from ICF to ECF
• Metabolic Alkalosis - decrease plasma [K+]
Alkalosis (pH > 7.54) o In serum • H+ moves from cells to ECF as buffer • To preserve electrochemical neutrality K+ and Na+ enter the cell • ECF [K+] falls o In urine • Alkalosis renal K+ losses (ECF Na+ reduction in serum stimulates aldosterone)
What happens to the potassium in renal tubular acidosis?
Why is there no K+ loss due to lactic acids or ketoacids?
How does insulin deficiency increase serum potassium?
What happens to the potassium levels in urine if the fluid delivery to the lumen increases?
What causes increase in fluid delivery?
What is the definition of hyperkalemia?
What is the potassium high enough to cause electrical excitability
A potassium level of what is a medical emergency which can cause cardiac arrest and arrythmias?
What ECG changes would you see?
[K+] > 5.0 mmol/L o Hospital incidence = 4 – 6%
- Telephone calls [K+] >6.5 mmol/L or dependent on the rate of change of [K+]
- [K+] >6.5 – 7.0 mmol/L altered electrical excitability
- Medical Emergency [K+] >7.5 mmol/L o arrhythmias, cardiac Arrest
o ECG changes: tall T waves, wide QRS complex, wide PR interval.
What is causing these ECG changes potentially?
What are the causes of hyperkalemia?
What is the most common cause?
Hints:
What causes intake to increase?
What causes reduced excretion?
What causes altered distribution?
What are artificial causes?
What are some drugs which can cause it
- Increased Intake o Oral o IV Therapy
- Reduced excretion o Renal Failure o Mineralocorticoid deficiency (Addison’s) o Tubular defects
- Altered Distribution o Acidosis o Insulin deficiency o Crush injury, haemolysis tumour lysis o Hyperkalaemic periodic paralysis
- Factitious :
o Improper collection: check picture
o Haematological disorders
• Drugs o ACEi, ARBs o Potassium-sparing diuretics eg amiloride / aldosterone antagonists eg spironolactone o Potassium supplements
Common causes o Chronic kidney disease o Redistribution secondary to acidosis
Consequences of hyperkalemia?
o Neuromuscular - Weakness, parasthesia, paralysis
o Gastrointestinal - Nausea, vomiting, pain, ileus
o Cardiovascular - Conduction defects, arrhythmias, Cardiac arrest
Hyperkalaemia: Acute Treatment
Consider urgent treatment if K+ >6.5 mmol/L
o Cardioprotection • Calcium gluconate to increase threshold potentials • ECG monitor • Care with patients on digoxin
o Redistribution NB this is a temporary measure
- Glucose + insulin
- b-agonist (salbutamol)
- Bicarbonate (beware cardiac failure)
o Removal
- Loop diuretic eg furosemide, bumetanide
- Ion-exchange resins (0.5 to 1.0 K+ mmol/g resin)
- Dialysis/Haemofiltration
Causes of chronic hyperkalemia
Commonest cause is chronic kidney disease (late complication):
• Treatment of underlying cause • Low potassium diet • Correction of metabolic acidosis
Hypokalaemia: Causes
Losses from GI causes
Losses from renal causes
Inadequate intake causes?
Redistribution causes
What are 2 causes of hypokalaemic acidosis?
Losses:
o Gastrointestinal: • Fistula • Diarrhoea • purgative abuse • Villous adenoma*
o Renal: • Loop diuretics • Renal tubular acidosis * • Mineralocorticoid excess (Cushing’s, Conn’s)
- Inadequate intake o Usually only appears if superimposed on other losses, e.g. diuretics, diarrhoea
- Redistribution o Insulin o Alkalosis o Salbutamol o Hypokalaemic periodic paralysis o Familial periodic paralysis
Consequences of hypokalemia on
skeletal muscles
GI
Kidney
Cardiac
Skeletal muscle o Weakness o paralysis
- Gastrointestinal o Paralytic ileus
- Kidney o Impaired concentrating ability o Tubular defects
- Cardiac o Conduction defects o Arrhythmias o Digoxin toxicity
What does this ECG change show?
What features of the ECG indicate this?
Torsades de points(long qt with polymorphic vtach - multiple qrs interval) happens in hypomagnesiemia as well.
Torsades will cause SpO2 to be low and you will have low bp and high HR.
Polymorphic ventricular tachycardia (PVT) is a form of ventricular tachycardia in which there are multiple ventricular foci with the resultant QRS complexes varying in amplitude, axis and duration. The commonest cause of PVT is myocardial ischaemia.
Torsades de pointes (TdP) is a specific form of polymorphic ventricular tachycardia occurring in the context of QT prolongation; it has a characteristic morphology in which the QRS complexes “twist” around the isoelectric line.
For TdP to be diagnosed, the patient has to have evidence of both PVT and QT prolongation.
Hypokalemia treatment
What happens to serum potassium concentration in the following situations?
- Diabetic ketoacidosis
- Primary hyperaldosteronism
- Adrenal insufficiency
- Renal tubular acidosis
- Salbutamol infusion
- Rhabdomyolysis
- Delayed arrival (>8h) of sample to laboratory
- Diabetic ketoacidosis - insulin lacking so K+ increase
- Primary hyperaldosteronism - too much aldosterone - Na/K+ blocked so more K+ excreted = low potassium
- Adrenal insufficiency- not enough cortisol(similiar to aldosterone) causes K+ excrete less to = K+ increase
- Renal tubular acidosis - low potassium - due to messing up the bicarbonate. Bicarbonate lost along with potassium. Trapping chlorine. k+ decrease
- Salbutamol infusion - - k+ into cell like insulin - K+ decrease
- Rhabdomyolysis - breaking cell K+ increase
- Delayed arrival (>8h) of sample to laboratory - K+ increase
