Unit 2 Electrolytes Flashcards

Question

Hyperkalmeia Anesthetic considerations

Answer 1

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

Answer 2

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

Answer 3

Plasma level < 1.5mEq/L

Answer 4

Inadequate intake Protracted vomiting/diarrhea Renal insufficiency

Answer 5

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

Answer 6

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

Answer 7

Look for other associate disturbances with may be present like hypokalemia, hyponatremia, hypocalcemia This frequently occurs in alcoholic patients

Answer 8

Plasma level > 2.5 mEq/L

Answer 9

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).

Answer 10

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)

Answer 11

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

Answer 12

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.

Answer 13

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

Answer 14

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

Answer 15

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

Answer 16

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

Answer 17

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

Answer 18

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

Answer 19

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

Answer 20

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

Answer 21

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

Answer 22

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

Answer 23

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

Answer 24

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

Answer 25

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.

Answer 26

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.