Unit 2 Electrolytes

Question 1

Hyponatremia

Answer 1

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

Question 2

Hyponatremia S/S

Answer 2

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

Question 3

Hyponatremia Anesthesia implications

Answer 3

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

Question 4

Correction of Hyponatremia

Answer 4

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

Question 5

Hypernatremia

Answer 5

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

Question 6

Hypernatremia S/S

Answer 6

Most S/S are related to Na’s role in neurological tissue.

Tremors
Weakness
Irritability
Confusion
Seizures/Coma
Hypovolemia
Renal insufficiency
Diabetes insipidus

Question 7

Hypovolemia with Hypernatremia

Answer 7

Due to water loss exceeding Na loss

Question 8

Hypovolemia with Hypernatremia causes

Answer 8

Diarrhea, vomiting, osmotic diuresis (mannitol administration or hyperglycemia), inadequate intake, fever, burns, exposed surgical areas, prolonged positive pressure ventilation w/o humidity

Question 9

Hypovolemia with Hypernatremia S/S

Answer 9

Hypotension, decreased CVP, decreased UOP, decreased skin turgid, increased HR

Question 10

Hypovolemia with hypernatremia treatment

Answer 10

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)

Question 11

Hypervolemia with hypernatremia causes

Answer 11

Due to Na overload.

Dialysis with hypertonic saline solutions
Treatment with hypertonic saline
NaHCO3 administration

Question 12

Hypervolemia with Hypernatremia treatment

Answer 12

Excess Na removed by dialysis or diuretics, and water deficits replaced with D5W

Question 13

Potassium

Answer 13

Principal intracellular cation
Essential for maintains resting membrane potentials and in generating action potentials in neuro and cardiac tissue.

Question 14

Hypokalmeia definition and etiology

Answer 14

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

Question 15

Hypokalmeia redistribution etiology

Answer 15

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.

Question 16

Hypokalmeia S/S

Answer 16

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

Question 17

Other study technique for this stuff

Answer 17

Copy pictures from PPt to a notability file to review.

Question 18

Hypokalmeia Anesthetic considerations

Answer 18

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

Question 19

Hypokalemia treatment

Answer 19

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

Question 20

Hyperkalemia

Answer 20

Plasma level > 5.5 mEq/L
Most dangerous >7 mEq/L

Question 21

Hyperkalemia S/S

Answer 21

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.

Question 22

Hyperkalemia Etiology

Answer 22

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.

Question 23

Hyperkalemia Anesthetic considerations

Answer 23

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)

Question 24

Hyperkalemia treatment

Answer 24

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.

Question 25

Hyperkalmeia Anesthetic considerations

Answer 25

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

Question 26

Magnesium

Answer 26

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

Question 27

Hypmagnesemia

Answer 27

Plasma level < 1.5mEq/L

Question 28

Hypomagnesemia etiology

Answer 28

Inadequate intake
Protracted vomiting/diarrhea
Renal insufficiency

Question 29

Hypomagnesemia S/S

Answer 29

Skeletal muscle spasms and weakness
CNS irritability
Seizures, hyper reflexes, confusion, ataxia, cardiac irritability

Question 30

Hypomagnesemia treatment

Answer 30

Bolus with MgSO4 over 15-20min, monitor VS and reflexes
infusion rate no greater than 1mEq/min???

Question 31

Hypomagnesemia anesthetic considerations

Answer 31

Look for other associate disturbances with may be present like hypokalemia, hyponatremia, hypocalcemia

This frequently occurs in alcoholic patients

Question 32

Hypermagnesemia

Answer 32

Plasma level > 2.5 mEq/L

Question 33

Hypermagnesemia etiology

Answer 33

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).

Question 34

Hypermagnesemia S/S

Answer 34

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)

Question 35

Hypermagnesemia Treatment

Answer 35

Stop Mg intake
Increase excretion
Antagonize CV of NM toxicity with CaCl or Cagluconate

Question 36

Hypermagnesemia Anesthetic Considerations

Answer 36

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.

Question 37

Calcium Measurements

Answer 37

1mg/dL = 0.25mmol/L = 0.5mEq/L

Question 38

Calcium background info

Answer 38

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

Question 39

Hypocalcemia

Answer 39

Serum Ca < 8.5 mg/do
Ionized Ca < 2.0 mEq/L

Question 40

Hypocalcemia etiology

Answer 40

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

Question 41

Hypocalcemia S/S

Answer 41

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

Question 42

Hypocalcemia Anesthesia considerations

Answer 42

Avoid alkalosis, which drives Ca into the cells
Monitor ionized Ca levels and VS during replacement

Question 43

Hypocalcemia treatment

Answer 43

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

Question 44

Hypercalcemia

Answer 44

Total Ca++ level > 8.5 mg/dL or 10.5 mg/dL
Ionized Ca++ above 2.25 mEq/L or 2.46 mEq/L

Question 45

Hypercalcemia etiology

Answer 45

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

Question 46

Hypercalcemia S/S

Answer 46

Muscle weakness
CNS depression
NEphrolithiasis (kidney stones)
Increased sensitivity to digoxin
HTN
Prolonged PR/wide QRS

Question 47

Hypercalcemia Treatment

Answer 47

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

Question 48

Hypercalcemia Anesthetic considerations

Answer 48

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

Question 49

Anion Gap

Answer 49

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.

Question 50

Importance of Anion Gap

Answer 50

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.