Unit 2 Electrolytes Flashcards
Hyponatremia
Most common electrolyte disorder in hospitalized patients
Typically from a excess to TBW
S/S depend on the rate and severity to decrease in Na
Hyponatremia S/S
CARDIAC SYMPTOMS:
Arterial hypertension (due to excess TBW)
^ CVP
Pulmonary edema > decreased cardiac function
Arrhythmias
NEURO SYMPTOMS:
Malaise
Headache
Lethargy
Seizure/coma
Background on neuro symptoms: BBB not permeable to Na, but it is to H20 so rapid decrease in plasma Na causes rapid in brain water and swelling
Hyponatremia Anesthesia implications
Surgery is postponed based on symptoms and urgency of symptoms
Manage the underlying cause
Can it be resolved in a timely manner?
Plasma Na >130 is safe for GA.
Also consider whether the Hyponatremia is chronic or acute
Specific Surgery Considerations:
TURP: uses large volume of hypotonic fluids, venous sinuses in prostate are open so large ammount of hypotonic fluid can get into the plasma.
Make sure you use isotonic fluids during surgery instead of hypotonic
Correction of Hyponatremia
Goal is to correct it to an acceptable level, not to a normal level
Done slowly to avoid pontine demyelination
Replace 1/2 of deficit in first 8 hours, then remainder over 24-72hrs if s/s resolved
Use 0.9 NS with loop diuretic
Monitor Na levels
Emergency? - Use hypertonic saline
Na should be raised slowly, to about 120-125mEq/L in order to avoid CNS complications
<1-2mEq/hr or > 8mEq/day
Hypernatremia
Absolute or relative TBW deficit to Na
Plasma Na >145 cause water loss from the cell and cremation
Geriatric patients are greatest risk, they have decreased ability to concentrate urine and decreased thirst
Hypernatremia S/S
Most S/S are related to Na’s role in neurological tissue.
Tremors
Weakness
Irritability
Confusion
Seizures/Coma
Hypovolemia
Renal insufficiency
Diabetes insipidus
Hypovolemia with Hypernatremia
Due to water loss exceeding Na loss
Hypovolemia with Hypernatremia causes
Diarrhea, vomiting, osmotic diuresis (mannitol administration or hyperglycemia), inadequate intake, fever, burns, exposed surgical areas, prolonged positive pressure ventilation w/o humidity
Hypovolemia with Hypernatremia S/S
Hypotension, decreased CVP, decreased UOP, decreased skin turgid, increased HR
Hypovolemia with hypernatremia treatment
If hemodynamically unstable:
initial replace Mtn with 0.45% or 0.9% saline
After replenishment, remaining free water deficit is replaced with D5W (hypotonic fluids)
Hypervolemia with hypernatremia causes
Due to Na overload.
Dialysis with hypertonic saline solutions
Treatment with hypertonic saline
NaHCO3 administration
Hypervolemia with Hypernatremia treatment
Excess Na removed by dialysis or diuretics, and water deficits replaced with D5W
Potassium
Principal intracellular cation
Essential for maintains resting membrane potentials and in generating action potentials in neuro and cardiac tissue.
Hypokalmeia definition and etiology
Plasma level < 3.5 mEq/L
Etiology - redistribution from ECF to ICV, total body K deficit, or decreased intake
Redistribution fro ECF to ICF: Alkalemia, insulin, beta2 agonists, hypercalcemia, hypomagnesemia Total body K deficit: vomiting, diarrhea, NG suction, billows adenoma of colon, diuresis, hyperaldosteronism, excess cortisol, surgical trauma
Hypokalmeia redistribution etiology
From increased activity to Na/K pump moving it from extra cellular to intracellular. Aldosterone causes K to be excreted, and hypomagnesemia impairs retention of K in kidneys resulting in increased secretion of K in urine.
Hypokalmeia S/S
Rarely appear unless K < 3mEq or a very rapid fall in Na level
Neuro symptoms
weakness
decreased cardiac contraction Ty
augmentation of neuromuscular block (Non-depolarizing NMB)
ECG changes
flattened T/U waves, increased PR/QT, ST depression, atrial and or ventricular arrhythmias
Other study technique for this stuff
Copy pictures from PPt to a notability file to review.
Hypokalmeia Anesthetic considerations
Avoid glucose IV fluids (this causes ^ secretion of insulin which can ^ K moving into the cell)
Avoid hyperventilation
Rapid correction of an acidosis which may lead to a fatal Hypokalmeia (must monitor K with rapid acidosis correction)
Consider also replacing magnesium
Hypokalemia treatment
Typically, no need to correct in chronic Hypokalmeia unless K < 2.5 mEq/L prior to induction UNLESS digitalis (digoxin) therapy
IV replacement recommended less than or equal to 10mEq/hour
Slow, PO correction is the safest
Hyperkalemia
Plasma level > 5.5 mEq/L
Most dangerous >7 mEq/L
Hyperkalemia S/S
Neuro symptoms:
Muscle weakness, especially in legs and respiratory system
Paresthesia
Cardiac conduction changes
Prolonged PR interval, loss of P, wide QRS, peaked T, vibration/arrest. If this changes occurs quickly they
will move through these phases very quickly.
Hyperkalemia Etiology
Decreased excretion
Intracellular to extracellular shift
Artificial elevation seen with hemolysis of blood sample
Hypoaldoseronism
K sparing diuretics acting as aldosterone antagonists
Caution with:
Penicillin VK in renal failure, NSAIDS, ACEI, CSA (last three affect kidney’s ability to secrete K)
Acidosis
0.1 unit decrease in arterial pH (10mmHg increase of PaCO2) can increase plasma potassium by about 0.5mEq/L
Upregulation of receptors following burns, stroke, parapalegia, prolonged bed rest.immobility. This upregulation becomes a big risk with use of succinylcholine
Administration of succinylcholine
Hyperventilation before admin may provide some degree of protection (careful with this though, and avoid sux at all costs unless you really have to use it.
Hyperkalemia Anesthetic considerations
Patient History:
medical hx, medications, renal issues, any meds that decrease cardiac function with ^ in K?
Consider canceling the case for elective surgery K>5.5 (consider chronic vs acute though, if chronic probably okay to proceed)
Always treat K levels above 6 mEq/L
Avoid hypoventilation
Avoid Succinylcholine use
Remove K from IV fluids. (Not really a huge issue with LR since it only has 4mEq/L, issue related to volume not the fluid)
Hyperkalemia treatment
Life threatening Hyperkalemia present?
ECG changes?
K > 6.5?
If all three, proceed to treatment.
Step 1. Stabilize myocardium with IV calcium chloride/calcium gluconate (1 amp or 10ml of 10% solution)
Step 2. Shift K into cells IV humulin 10-20 units % IV glucose 25-50g. Can also use inhaled beta 2 agonist
Step 3. Enhance elimination of K
Volume status low, give 0.9% NS
Volume normal to high, loop diuretic if they have UOP, if not, dialysis. If no response to diuretic, proceed to dialysis anyway.
Hyperkalmeia Anesthetic considerations
Have emergency drugs available
Muscle relaxants
Responses to NDMR in hyperkalmeia are unclear.
presence of skeletal muscle weakness preoperatively suggests possibility for decreased muscle relaxant requirements intraoperativley
Titrate muscle relaxants until desired effect
Know what is in your fluids, only 4 mEq/L of K in LR
Magnesium
Primarily intracellular; <1% in plasma
NMDA receptor antagonist
Essential co-factor for many enzymatic reactions, e.g. DNA and protein synthesis, energy metabolism, glucose utilization, FFA synthesis and break down
Controls K reabsorption in the renal tubules
Stabilize membranes: influence release of neurotransmitters at the NMJ
inhibit entry of Ca into presynaptic nerve terminals, so it is an endogenous Ca antagonist
Hypmagnesemia
Plasma level < 1.5mEq/L
Hypomagnesemia etiology
Inadequate intake
Protracted vomiting/diarrhea
Renal insufficiency
Hypomagnesemia S/S
Skeletal muscle spasms and weakness
CNS irritability
Seizures, hyper reflexes, confusion, ataxia, cardiac irritability
Hypomagnesemia treatment
Bolus with MgSO4 over 15-20min, monitor VS and reflexes
infusion rate no greater than 1mEq/min???
Hypomagnesemia anesthetic considerations
Look for other associate disturbances with may be present like hypokalemia, hyponatremia, hypocalcemia
This frequently occurs in alcoholic patients
Hypermagnesemia
Plasma level > 2.5 mEq/L
Hypermagnesemia etiology
Associated with:
acute or chronic renal failure
toxemia from Mg therapy (OB patients to stop uterine contractions)
over-administration of Mg containing compounds like antacids and cathartics (laxatives).
Hypermagnesemia S/S
Skeletal muscle weakness, can lead to respiratory arrest
Vasodilation with myocardial depression and hypotension
complete heart block, cardiac arrest
Hypo reflex is
diminished DTRs
Sedation (somnolence)
Hypermagnesemia Treatment
Stop Mg intake
Increase excretion
Antagonize CV of NM toxicity with CaCl or Cagluconate
Hypermagnesemia Anesthetic Considerations
Intubation of OB patients if become respiratory reflex compromised
Potentiates the action of NDMRs, so they will last way longer than normal and can be an issue when you want to extubate.
Also this is usually seen with Mg given too quickly to too much to correct hypomagnesemia.
Calcium Measurements
1mg/dL = 0.25mmol/L = 0.5mEq/L
Calcium background info
Found primarily in bone then in extracellular fluid
Approx 50% of serum Ca++ is ionized
only ionized calcium is physiologically active
4-45% is protein bound (to albumin)
Regulated by calcitonin and parathyroid hormone
Essential for all movement; normal excitation-contraction coupling in both skeletal and cardiac muscle
Neurtransmitter release
Influences second messenger systems, E.g. CAMP
Cardiac pacemaker activity
primary ion responsible for plateau phase
Hypocalcemia
Serum Ca < 8.5 mg/do
Ionized Ca < 2.0 mEq/L
Hypocalcemia etiology
Malabsorption
Increased excretion from chronic renal insufficiency
Hypoparathyroidism
Chelation from citrate in blood transfusions
transient and negligible unless renal/hepatic failure or hypothermia
Shift into cell with alkalemia
Hypocalcemia S/S
CNS: paresthesias, especially circumoral, confusion, seizures
CV: decreased myocardial contractility, hypotension, cardiac failure, arrhythmias
NM: twitching, cramping, trousseau’s sign, chvostek’s sign, convulsions, laryngospasm
EKG: prolonged cQTC
Hypocalcemia Anesthesia considerations
Avoid alkalosis, which drives Ca into the cells
Monitor ionized Ca levels and VS during replacement
Hypocalcemia treatment
CaCl2 3-5ml of 10% solution
CaGluc 10-20 ml of 10% solution
CaCl2 contains 13.6 mEq/gram versus CaGluc contains 4.65mEq/gram
Treat hypomagnesemia and or hyperphophatemia if present
Caution: if Hypokalemia is treated without treating hypocalcemia it may precipitate tetany
May antagonize effects of CCB - monitor for hypertension
CaCl2 is very irritating to the veins
Hypercalcemia
Total Ca++ level > 8.5 mg/dL or 10.5 mg/dL
Ionized Ca++ above 2.25 mEq/L or 2.46 mEq/L
Hypercalcemia etiology
Most common: > 90% of cases
Decreased renal excretion from hyperparathyroidism
Bone malignancies
Other:
Immobility (shift from bone cells)
Increased intake of antacids or Vit D
Hypercalcemia S/S
Muscle weakness
CNS depression
NEphrolithiasis (kidney stones)
Increased sensitivity to digoxin
HTN
Prolonged PR/wide QRS
Hypercalcemia Treatment
Hydration with NS plus oasis to inhibit renal reabsorption and promote Ca++ excretion
Dialysis
Chelations (phosphates, EDTA)
Biphosphonates: inhibit bone breakdown, relatively slow onset but long duration of action
Calcitonin: faster onset but short duration, so used in conjunction with biphosphonates
Hypercalcemia Anesthetic considerations
Careful use of phosphates (not used very often)
Lower doses of NDMR if skeletal muscle weakness exists (if any electrolyte disturbance that causes skeletal muscle weakness is present be careful before you extubate, make sure they have sufficient strength to protect the airway/maintain respirations)
Invasive monitors recommended if decreased cardiac function exists
Avoid Acute academia as it increases ionized Ca++
Caution with EDTA IV, can cause significant hypocalcemia
Anion Gap
Buffers, or total bicarbonate should be examined in relation to the other measured electrolytes
AG is [Na] - (total HCO3 + Cl-)
Normal is 8-12 mEq/L
If all serum anions and cations were measured anions would equal cations and their would be no anion gap.
Importance of Anion Gap
Help diagnosis reason for metabolic acidosis.
The higher the AG the more likely it reflects an organic acidosis E.g. lactic acidosis or ketoacidosis (regardless of pH)
Normal AG in a patient with metabolic acidosis indicates hyperchloremic acidosis, most commonly from renal or gastrointestinal bicarbonate loss, e.g. renal tubular acidosis or diarrhea.
