Electrolyte disorders Flashcards
Ions in ICF and ECF
- ICF: K, Mg, PO4, proteins
- ECF: Na, Cl, HCO3
causes of dehydration and clinical presentation
- cause: Insufficient oral intake, impaired renal concentrating mechanisms
- pres: Excessive thirst, decreased skin turgor, elevated serum Na and osmolality
Causes and clinical presentation of hypovolemia
- causes: External fluid losses (burns, hemorrhoage, diuresis)
- pres: dizziness, decreased urine output, hypovolemic shock
fluid management strategies
- Resuscitation: rapid & aggressive fluid replacement to maintain oral perfusion (more so for hypovolemia)
- Replacement: replace volume loss in addition to maintenance
- Maintenance: basal fluid requirements, prevent dehydration
symptoms of hyponatremia
- Moderate: headache, lethargy, disorientation, restlessness
- Severe: seizures, coma, respiratory arrest
- Other (depends on etiology): dry mucous membranes, tachycardia, hypotension, reduced/increased urine output
cause of hypertonic hyponatremia
- caused by hyperglycemia
- treat hyperglycemia
cause of isotonic hyponatremia
caused by presence of markedly elevated serum lipids or proteins
types of hypotonic hyponatremia
- hypervolemic: Excess of TBW and Na but excess TBW > excess Na
- euvolemic: Excess of TBW but total body Na is normal
- hypovolemic: Deficit of TBW and Na but deficit in Na > deficit in TBW
causes and treatment of euvolemic hypotonic hyponatremia
- cause: syndrome of inappropriate ADH secretion (SIADH)
- treatment: Fluid restriction, treat underlying cause, ADH receptor antagonist
Causes and treatment of hypervolemic hypotonic hyponatremia
- cause: HF, liver cirrhosis, nephrotic syndrome
- treatment: Na & fluid restriction, diuretics, treat underlying cause
causes and treatment of hypovolemic hypotonic hyponatremia
- causes:
- Renal losses e.g. diuretic use.
- Extrarenal losses e.g. GI, skin & lungs
- treatment: Isotonic &/or hypertonic fluids
- need to correct both Na and TBW deficit -> hence use NS (0.9% NaCl)
causes of SIADH
- Carcinomas in lung or pancreas
- Pulmonary disorders e.g. pneumonias, tb
- CNS disorders e.g. meningitis, shock, trauma, tumor
- Medications -> stimulate the release of ADH from pituitary gland causing water retention and dilution of body’s Na stores.
meds can incl: (e.g. sulfonylureas, barbiturates, antipsychotics, tricyclic antidepressants, selective serotonin reuptake inhibitors, dopamine agonist)
General treatment for all the hyponatremia
- Treat underlying cause
- use hypertonic saline (3% NaCl) to inc tonicity
- Acute: increase serum Na by 6-12mmol/L in 24h
- Chronic: increase serum Na by 6-8mmol/L in 24h
- Change in serum Na = (infusate Na – serum Na)/(TBW+1)
- Too rapid correction -> central pontine myelinolysis (damage to regions of the brain) so rate is impt
causes and signs and symptoms for hypernatremia
- S&S: mental slowing, confusion, hallucinations, intracranial bleeding, coma
- Causes: dehydration, diabetics insipidus (decreased ADH secretion, opposite condition of SIADH), Na overload
treatment of hypernatremia
- Free water deficit = TBW x ((current Na/desired Na)-1)
- Administer hypotonic fluids
- Desmopressin for diabetics insipidus
How is K homeostasis regulated externally
- dietary intake,
- renal excretion
- ## extrarenal losses (GI, sweat)
o Renal excretion: K is freely filtered, mostly passively reabsorbed at PCT, secreted in DCT and CD. Regulated by aldosterone
how is K homeostasis regulated internally
- Internal: Na-K-ATPase and K+ leak channels.
Affected by:
- Insulin :stimulates Na-K-ATPase to drive K into cells
- Catecholamines
- acid-base disorders
- hyperosmolarity -> drags water out of cell
- exercise
- in metabolic acidosis, there is high plasma H+ so exchange with K+ in cells to maintain electrical neutrality -> hyperkalemia.
- In metabolic alkalosis, CO2 is removed via respiration so there will not be exchange of H+ and K+ -> no hypokalemia
Etiology of hypokalemia
- Insufficient dietary intake, excessive renal and GI losses e.g. diarrhoea and vomiting, drug-induced, hypomagnesemia
- Shift of K+ into ICF
- Aldosterone inhibit Na reabsorption, K secretion (Na, K exchanger)
- diuretics inhibit upstream Na reabsorption –> reabsorb Na downstream and secrete K+
CLinical presentation of hypokalemia
Mild: often asymptomatic.
Moderate-severe: cramp, weakness, malaise, myalgia
- Signs: can show as ST-segment depression in ECG (for severe), low serum K
treatment of hypokalemia
by severity
- Mild: Initiate pharmacologic therapies depending on S&S
- Moderate: PO K supplement
- Severe: IV K supplement, correct hypomagnesemia if present (can increase renal excretion of K+)
dosage of oral KCl supplement
how much to take
- PO:600mg SR tablets (8mmol) and 500mg/5ml solution (6.7mmol/5ml)
- Mild-mod hypoK: 10-20mmol 2-4 times daily
o Prevention: 20mmol daily
o Total daily dose divided into 2-4 doses to avoid GI irritation
o Starting dose is lower for renally impaired
o Prevention: 20mmol daily
o Total daily dose divided into 2-4 doses to avoid GI irritation
o Starting dose is lower for renally impaired
dosage for IV KCl
how much to take
- IV: 10mmol in 100ml of NS/water infusion via peripheral line. Avoid dilution in dextrose-containing solution.
- For severe hypoK, pts who cannot tolerate oral therapy or exhibiting S&S
- Monitoring of ECG, serum K and if any phlebitis and pain at site of infusion recommended
etiology of hyperkalemia
- increased K intake,
- decreased renal excretion of K,
- tubular unresponsiveness to aldosterone (sickle cell anemia, SLE, amyloidosis),
- redistribution of K into ECF (metabolic acidosis, DM, CKD)
- Falsely elevated serum K can occur due to extravascular hemolysis of RBC
clinical presentation of hyperkalemia
heart palpitations, ECG ST elevation, serum K
treatment of hyperkalemia flow of thinking
- if abnormal ecg –> calcium gluconate (if not then monitor)
- if hyperglycemia: give insulin, if not give insulin and glucose
- consider albuterol
- bicarbonate if acidic
- exchange resis/consider dialysis
- follow K every 2h until < 5mEq/L
drugs that shift K into cells
- insulin IV and dextrose (inc NA K ATPase activity, with dextrose to avoid hypoglycemia)
- NaHCO3 IV (for metabolic acidosis, but can cause hyperna and overload)
- Salbutamol IV / nebulisation (stimulate NaKATPase)
Drugs that increase K elimination
- Sodium polystyrene (SPS) (Resonium)
- MOA: ion (Na and K) exchange resin in large intestine, PO/rectal, 4h prn
- SE: Na load, intestinal necrosis
- Sodium zirconium cyclosilicate (Lokelma)
- Exchanges Na for K throughout entire GIT
- Administered PO
- Separated from other PO medications that exhibit pH-dependent solubility for at least 2h
- SE: edema from Na exchange
etiology of hypomagnesemia
- GI: Reduced intake, reduced absorption (e.g. PPI when used in long run), increased loss (e.g. vomiting, diarrhoea)
- Renal: primary tubular disorders, drug-induced (e.g. AGs, ampho B, diuretics, cyclosporin etc.), primary HPT, aldosteronism
Magenesium supplement dosings
PO and IV
- PO: for mild(Mg>0.5). Most common SE: diarrhoea
- IV: for symptomatic (< 0.5). Often given as 2-4g in 50-100ml infused over 1h
- Dose is reduced in renally impaired pts
Etiology and treatment of hypermagnesemia
- decreased renal excretion (e.g. AKI), excessive intake, others such as Lithium therapy
- treatment: reduce Mg intake, increase elimination, calcium gluconate to reduce symptoms
