Fluid and Electrolyte Distubances Flashcards
Normal serum osmolality
280 -295 mOsm/kg
AVP secretion is stimulated as systemic osmolality increases above this threshold level
> ~285 mOsm/kg
Definition of hypovolemia
Hypovolemia generally refers to a state of combined salt and water loss, leading to contraction of the ECFV
Normal amount of insensible losses in healthy adults
500-650 ml/d
Signs of hypovolemia
Decreased JVP
orthostatic tachycardia
orthostatic hypotension
severe:
hypotension
tachycardia
peripheral vasoconstriction
peripheral hypoperfusion
Orthostatic tachycardia
an increase of >15-20 bpm upon standing
Orthostatic hypotension
a >10-20 mmHg drop in blood pressure on standing
Symptoms of hypovolemia
Fatigue
Weakness
Thirst
Postural dizziness
severe: oliguria, cyanosis, abd and chest pain, confusion or obtundation
Therapeutic goals in hypovolemia
restore normovolemia and replace ongoing fluid losses
The most appropriate resuscitation fluid for normonatremic or hyponatremic patients with severe hypovolemia
Isotonic normal saline (0.9% NaCl)
Hyponatremia
plasma Na+ concentration <135 mM
-almost always the result of an increased circulating AVP and/or increased renal sensitivity to AVP, combined with an intake of free water
Diagnostic approach to hyponatremia
Features suggestive of hypoaldosteronism
Hyperkalemia and hyponatremia in a hypotensive and or/hypovolemic patient with high urine Na concentration
A rare cause of hypovolemic hyponatremia, encompassing hyponatremia with clinical hypovolemia and inappropriate natriuresis in association with intracranial disease
Cerebral salt wasting
Conditions that may present with cerebral salt wasting
Subarachnoid hemorrhage
Traumatic brain injury
Craniotomy
Encephalitis
Meningitis
Most frequent cause of euvolemic hyponatremia
SIADH
Causes of acute hyponatremia
The time period that clinically defines chronic hyponatremia
> 48h
Overly rapid correction of hyponatremia
> 8-10 mM in 24h or 18 mM in 48h
Presentation of ODS (Central pontine myelinolysis)
Paraparesis or quadriparesis
Dysphagia
Dysarthria
Diplopia
“Locked-in syndrome’
Loss of consciousness
Pseudohyponatremia
defined as coexistence of hyponatremia with a normal or increased plasma tonicity
The ultimate “gold standard” for the diagnosis of hypovolemic hyponatremia
Demonstration that plasma Na+ concentration corrects after hydration with normal saline
Cornerstone of the therapy of chronic hyponatremia
Water deprivation
Urine-to- plasma electrolyte ratio
(Urinary Na + K)/ Plasma Na
a quick indicator of electrolyte-free water excretion
Ratio > 1 - should be aggresively restricted (<500 ml/d)
Ratio ~1 - should be restricted 500-700 ml/d
Ratio <1 should be restricted <1L/d
A potent inhibitor of principal ells and can be used in patients whose Na levels do not increase in response to furosemide and salt tablets
Demeclocycline
Highly effective in SIAD and in hypervolemic hyponatremia due to heart failure or cirrhosis, reliably increasing plasma Na concentration due to their “aquaretic” effects
AVP antagonists (vaptans)
Most appropriate for the management of significant and persistent SIAD that has not responded to water restriction and/or oral furosemide and salt tablets
Oral tolvaptan
Treatment of acute symptomatic hyponatremia
Hypertonic saline 3% (512 mM) to acutely increase plasma Na concentration 1-2 mM/h to a total of 4-6 mM
Na deficit
0.6 x BW x (target plasma Na concentration - starting plasma Na concentration)
Rate of correction of chronic hyponatremia
<8-10 in the first 24h and <18 mM in the first 48 hours
Given to patients with Na overcorrection
AVP agonist desmopressin acetate (DDAVP) and or administration of free water, typically IV D5W to prevent or reverse the development of ODS
Definition of hypernatremia
an increase in the plasma Na concentration to >145 mM
-result of combined water and electrolyte deficit
Individuals with highest risk of developing hypernatremia
Elderly individuals
-reduced thirst and/or diminished access to fluids
Most common gastrointestinal cause of hypernatremia
diarrhea
Gestational DI
a rare complication of late-term pregnancy wherein increased activity of a circulating placental protease with “vasopresssinase” activity leads to reduced circulating AVP and polyuria, often accompanied by hypernatremia
Treatment for gestational DI
Desmopressin acetate (DDAVP)
Diagnostic approach to hypernatremia
Management of hypernatremia
Hypokalemia
defined as plasma K concentration of <3.5 mM
Causes of hypokalemia
Relationship between hypomagnesemia and hypokalemia
Magnesium depletion:
-inhibitory effects on muscle Na+/ATPase activity
-secondary kaliuresis
-exagerrated K+ secretion by the distal nephron
**hypomagnesemic patients are clinically refractory to K+ replacement in the absence of Mg2+ repletion
Role of hypokalemia as a risk factor of digoxin toxicity
Reduced competition between K+ and digoxin for shared binding sites on cardiac Na+/K+-ATPase subunits
ECG findings of hypokalemia
Broad flat T waves, ST depression, and QT prolongation
Functional effects of hypokalemia on the kidney
NaCl and HCO3 retention
Polyuria
Phosphaturia
Hypocitraturia
Activation of renal ammoniagenesis
The diagnostic approach to hypokalemia
Goals of therapy in hypokalemia
Prevent life-threatening and/or serious chronic consequences, to replace the associated K+ deficit, and to correct the underlying cause and/or mitigate future hypokalemia
Mainstay of therapy in hypokalemia
Oral replacement of KCL
Peripheral intravenous dose of potassium correction
20-40 mmol of KCL per liter
Central vein intravenous dose of potassium correction
10-20 mmol/h
Absolute amount of K+ that should be administered to prevent inadvertent infusion of a large dose
20 mmol in 100 ml of saline solution
Strategies to minimize K+ losses
non-K+ sparing diuretics,
Restricting Na+ intake,
Using clinically appropriate combination of non-K+ sparing and K+ sparing medications
Definition of hyperkalemia
defined as a plasma potassium level of 5.5 mM, occurring in up to 10% of hospitalized patients
Most frequent underlying cause of hyperkalemia
Decrease in renal K+ excretion
Pseudohyperkalemia
an artifactual increase in serum K due to the release of K+ during or after venipuncture
Causes of hyperkalemia
Difference of hyperkalemic brugada’ sign and genetic brugada’s syndrome
Absence of P waves
Marked QRS widening
Abnormal QRS axis
Classic ECG manifestations in hyperkalemia
5.5-6.5 mM - tall peaked T waves
6.5-7.5 mM - loss of P waves
7.0-8.0 mM- widened QRS complex
> 8.0 mM - sine wave pattern
First priority in the management of hyperkalemia
Assess the need for emergency treatment, followed by a comprehensive workup to determine the cause
Diagnostic approach to hyperkalemia
Three stages of the treatment of hyperkalemia
- Immediate antagonisms of the cardiac effects of hyperkalemia
- Rapid reduction in plasma K+ concentration by redistribution into cells
- Removal of potassium
Most effective and reliable methods to reduce plasma K+ concentration
Hemodialysis
