1. ELECTROLYTES

2. What is an electrolyte?
Are particles that carry electrical charge and are present in blood, plasma and urine.
Substances whose molecules dissociate into ions when placed into water
cations- positively charged e.g Na+, K+, Mg++, Ca++
anions – negatively charged e.g Cl - ,

3. Electrolytes
Essential minerals necessary for nerve and muscle function
Maintain body fluid balance
Regulate acid base balance
Balance of electrolytes is constantly shifting due to fluctuating fluid levels . E.g when we sweat as a result of exercise and illness .. Electrlolytes level fall . Vomoting , diarrhoea further causes dehydration

4. Types of electrolytes Positive cations : Negative cations :
potassium K+, sodium Na +, magnesium Mg2+, calcium 2+
Negative cations :
phosphate PO4 3-, chloride Cl_
Buffer : bicarbonate HCO3-

5. Distribution Intracellular fluid (ICF) :- prevalent cation – K+, Mg++
prevalent anion - PO4- - -
Extracellular fluid ( ECF) :-
prevalent cation – Na+
prevalent anion - Cl-

6. POTASSIUM or K+
Transmission and conduction of nerve and muscle impulse
Required for repolarization of cell membrane to a resting state after an action potential
Maintenance of cardiac rhythms
Acid base balance
Normal : mmol/l

7. Hyperkalaemia High serum K caused by :- massive intake
impaired renal secretion
shift from ICF to ECF : massive cell destruction e.g brain injury, crush injury

8. Hyperkalaemia Manifestation : Weak or paralysed skeletal muscles
VF or cardiac standstill
Small P waves and high peaked T waves
REMEMBER ALS GUIDELINES

9. Hyperkalaemia CORRECTION increase elimination ( diuretics, dialysis)
Force K+ from ECF to ICF by IV insulin with dextrose or sodium bicarbonate
reverse membrane effects of elevated ECF K+ by administrating Calcium Gluconate IV
Insulin will cause shift of potasium into the cells

10. HYPOKALAEMIA CAUSES : Kidney malfunction Diabetic ketoacidosis
Gastrointestinal tract losses : vomiting, diarrhoea
Mg deficiency : alcohol abuse
Metabolic alkalosis
2. Polyuria due to diabtetes .. Loss of K
3. Causes breakdown of muscle fibres resultiong in K release into blood stream . MG also regulates amt of K

11. HYPOKALAEMIA Clinical signs / Correction
Cardiac arrthymias : gradual sagging ST segment, flattening of T waves , appearance of U wave
Severe muscle weakness
shallow respiration : threatening respiratory function
Correction : oral or IV
Iv should not excced meq / hr : prevent hyperkalaemia and rthus prevent cardiac arrest

12. SODIUM or Na+ Most prevalent cation in ECF Plays a major role :-
ECF volume and concentration : retain body water
Generation and transmission of nerve impulse
pH balance
Normal concentration : mmol/l

13. Hypernatraemia Elevated serum sodium: mostly water deficit
causes hyper osmolality lead to cellular dehydration
Primary protection: thirst mechanism from hypothalamus
Water deficit : excess sweating

14. Hypernatraemia Clinical signs
Seizures, coma leading to irreversible brain damage
Correction :
not with WATER !!
Giving NaCl solution or with addition to dextrose: gradually reduced to avoid cerebral oedema
Rapidly lowering the sodium concentration with free water, once this adaptation has occurred, causes water to flow into brain cells and causes them to swell. This can lead to cerebral edema, potentially resulting in seizures, permanent brain damage, or death

15. Hyponatremia
Causes:
Low Na in plasma caused by liver failure, kidney failure and overhydration .
Proportional to excess water :SIADH (syndrome of inappropriate anti-diuretic hormone secretion)
Manifestation :
nausea, vomiting, headache, confusion, lethargy , restlessness, muscle weakness, spasms, cramps, seizures, coma .
Non cardiogenic pulmonary oedema .
sodium loss can lead to a state of volume depletion (loss of blood volume in the body), with volume depletion serving as a signal for the release of ADH (anti-diuretic hormone).[citation needed] As a result of ADH-stimulated water retention (too much water in the body), blood sodium becomes diluted and hyponatremia results.

16. Hyponatremia Correction :- Find the cause
Hypervolemia : both water and sodium level high
liver cirrhosis, CHF,
correction :- address liver and cardiac function
Euvolaemic hyponatremia: excess water but body Na+ level is same
Hypothoridism , steroid (glucosteroid deficiency )
Correction : water restriction
Hypovolaemic hyponatraemia : both water and sodium low
prolonged vomiting, severe diarrhoea, decreased oral intake , diuretic use
Correction : administration of NaCl.

17. Magnesium 2nd most abundant cation in ICF
Energy metabolism : glucose utilisation , fatty acid synthesis, muscle contraction
Na+ – K + pump
Affects Ca ++ homeostasis
Release and action of PTH
Ca channels are dependent on Mg , whn intracellular Mg conc. Is high Ca transport into the cells . In mg deficinciecy reverse occurs, Ca rises Mg

18. Hypomagnesaemia Malabsorption : inflammatory bowel disease Alcoholism
Following parathyrodiectomy
Hypercalaemia
Correction : IV MgSO4
2. Increase urinary Mg wasting
3. Drop in Ca, MG , k

19. Hypermagnesaemia Block synaptic transmission : deep tendon reflexes
Effect on smooth muscles : ileus and urinary retention
Bradycardia and hypotension : effects on Ca++ & K +
Correction:
IV Ca++
Renal patient : dialysis I

20. CALCIUM Transmission of nerve impulse Muscle contraction :Myocardial
Blood clotting
Formation of bones and teeth
Balance controlled by :
parathyroid hormone
Calcitonin
Vitamin D
While calcitonin promotes Ca level intake parathyroid hormone does opposite

21. Hypocalcaemia
Eating disorder
Lack of parathyroid hormone

22. Hypercalcaemia Hyper parathyroid hormone Vitamin D overdose
Prolonged immobilisation

23. Clinical symptoms Decreased memory Confusion , fatigue Constipation
Correction :- excretion of excess Ca++ with loop diuretics
Hydration with isotonic saline

24. Bicarbonates HCO3_ Maintains acid-base status Kidney regulation
Good indictors of acid-base balance

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