ELECTROLYTES

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 - ,

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

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-

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

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 : 3.5 -4.5 mmol/l

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

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

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

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

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 10 -20 meq / hr : prevent hyperkalaemia and rthus prevent cardiac arrest

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 : 135- 145 mmol/l

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

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

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.

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.

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

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

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

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

Hypocalcaemia Eating disorder Lack of parathyroid hormone

Hypercalcaemia Hyper parathyroid hormone Vitamin D overdose Prolonged immobilisation

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

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

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