Regulation of K+ and Ca2+ Flashcards
Potassium balance
Input = diet, output = excretion, small amount by stool and sweat
Quantities of potassium
3000mmol in the body.
Mostly present in skeletal muscle, some in bone, liver and red blood cells
Plasma concentration = 3.5-5mmol.
Reasons for hyperkalaemia
Renal failure (including due to ACE inhibitors or spironolactone)
Crush injuries
Escape of intracellular K+ following acidosis
Haemolysis - eg in freshwater drowning.
Reasons for hypokalaemia
Excessive diuretics (particularly thiazide)
Severe GI disease
Severe burns
First sign of hyperkalaemia
On the ECG, shortened ST interval and T wave attenuating, as cardiac cells are most sensitive to changing K+. As action potential shortened due to activation of inward rectifier channels, so less time for Ca2+ entry and less CICR = impaired contraction.
Low K+ effect on the heart
De-activation of delayed rectifier K+ channels and other repolarising currents, so increased time for Ca influx (during plateau period), then stimulating the Ca/3Na pump, and have net positive charge into the cell. This is occasionally seen in middle aged men who drop dead due to high sympathetic and low K+ as moer Ca is driven into cells.
List of physiological factors which will alter K+ homeostasis
Insulin Catecholamines Acid-base status Hypoxia Exercise
Exercise changes to K+ homeostasis
Plasma K+ can rise to 9mmol/L, but drops immediately following conclusion of exercise. As muscle cells depolarise then there is a leak of K+ as the Na/K pump cannot keep up, so there is a net efflux into the plasma. On finishing exercise then sympathetic stimulation means that K+ is taken back up effectively.
May be the K+ which causes muscle pain in fatigue, as lactic acid production peaks two minutes AFTER finishing exercise, potentially increased K+ causes depolarisation of sensory nerve endings. Hyperventilation also drives hyperkalaemia?
Skeletal muscle fatigue
High K+ outside leads to depolarisation of cells, such that VG Na channels open but also are more frequency inactivated. This means that action potentials are much more sluggish, and high Na+ is negatively inotropic in muscle.
Myocardial stability in exercise
During exercise there is mutual antagonism between high levels of K+ and high levels of catecholamines, and on balance means increased inotropy and chronotropy, by increasing the action potential current of iCa-L. Exercise induces independent Ca pathways, particularly through angiotensin II?
Signs and symptoms of hyperkalaemia
Glucose intolerance Arrhythmias Orthostatic hypotension Vasodilation Constipation Muscle weakness/paralysus Oedema Reduced aldosterone Reduced GFR
Treatment of hyperkalaemia
Correction of cause.
In an emergency can give intravenous Ca2+ gluconate to maintain inotropic support to the heart, and give insulin and glucose which causes widespread reuptake.
Potential consequences of hypokalaemia
After depolarisation, as cardiac cell cannot deal with extra load of intracellular Ca2+, and attempt to compensate with Ca/3Na pump leads to net influx. Many extra depolarisations may cause the heart to contract prematurely before ventricular filling is complete. Reduced CO = collapse in arterial blood pressure and potential hypoxia.
Hypocalcaemia
Causes nerve hyperexcitability and muscle tetany due to decrease in threshold potential. Reduces myocardial contractility
Hypercalcaemia
Decreased excitability of nerves, causing long-term lethargy. Can often by chronic and generally less dangerous. In extreme situations arrests the heart in systole.
