CC Labs Flashcards
Potassium
-Regulation of bone metabolism
-Regulation of Erythropoiesis
-Regulation of Acid Base Balance
-Excretion of waste products
-Regulation of body volume
Where is K in our body?
-Muscle (2650 mEq)
-Liver (250 mEq)
-Intracellular (150mEq/L)-98% of K
-Extracellular (4 mEq/L)
How does the body keep K in check?
Acutely:
-Shifting of K between the intracellular and extracellular compartments (effect on pump, effect of acidemia/alkalemia)
Chronic
-Urine excretion
Factors that increase activity of the pump
-Insulin
-Albuterol
-Aldosterone (most important hormone that regulates K balance in the body)
-Bicarbonate
-Potassium levels in the blood
—-Increase activity of the pump > lower K level in the blood
Acid Base Problems Affect K Balance
-If you have acidemia, H+ goes inside the cell to correct acidemia & K+ goes outside the cell (Hyperkalemic)
-If you’re alkalemia, K+ goes inside the cell and H+ goes outside cell to correct alkalemia (Hypokalemic)
Factors that have to be present for the kidney to excrete potassium in urine
-Aldosterone
-Flow of urine
-Amount of Na in the urine
Risk factors for developing Hyperkalemia
-Male, non-black, DM, CVD, AKI, CKD, Acidosis, urinary obstruction, HF
-Medications: K supplements, Penicillin, Digoxin, NSAIDs, ACEI/ARBS, BB, Heparin, Trimethoprim, pentamidine
Why do we panic when we see hyperkalemia?
-Lowers resting cardiac membrane potential > cell depolarization (Peaked T waves in V2-V4 leads)
-Conduction delay (PR interval prolongs, QRS complex widens)
-Cardiac Excitability (VT or VF)
-Cardiac depression (Bradycardia, AV block, Asystole
Approach to Treatment with hyperkalemia
-If it’s an emergency: Stabilize the heart, shift K inside the cell and eliminate K from the body
-Is it not an emergency? Eliminate the K from the body
Treatment of Hyperkalemic emergency
-Ca gluconate for cardiac stabilization: 10 cc of 10% soln (1g): onset is 3-5 minutes, lasts up to 1 hr
-Insulin + D5W = 10-20U IV with D50 followed by D20 150ml infusion over 3 hrs. Onset is 10 min, peak 1 hr, lasts 6hrs
-NaHCO3 = 50-100 mEq IV: Avoid if giving Ca, risk of precipitation
-Albuterol= 10-20 mg in 4mL saline nebulized: onset is 30 minutes, lasts up to 90-120 minutes.
Bicarbonate Solution in Hyperkalemia
-Isotonic bicarb (150mEq or 3 amps mixed in sterile water or D5W)
——–Monitor HCO3 closely (high risk of alkalemia with large volume resuscitation)
-1.5 amps of bicarbonate (75mEq) mixed with ½ normal saline (77mEq)
Diuretics and hyperkalemia management
-Loop > Thiazides
-Diuretics: Increase urine flow, increase urine sodium which enhances urinary K losses
-Which patients: Volume overloaded, hypertensive, volume replete but with underlying CKD, volume replete and on maintenance diuretics
Sodium Polystyrene
-Ion exchange binding resin (exchanges K for Na)
-Effect is delayed for 2 hrs
-Avoid in patients w/ recent surgery, h/o ischemic bowel, intestinal dysfunction
-Never use as monotherapy
Patiromer (Veltassa) Approved in 2016
-Ion exchange binding resin (exchanges K for Ca)
-Mean decrease K was 0.5-1mEq/L
ZS-9 (Lokelma)-approved 2018
-Ion exchange binding resin (exchanges K for Na and H+)
-Lokelma 10g administered three times daily lowered serum potassiumby -0.7 mmol/L at 48 hours
-Side effects: edema, hypokalemia
The initial regimen in patients with acute salt poisoning or diabetes insipidus is: Acute Phase
HYPERNATREMIA
-D5W IV @ 3-6 mL/kg/hr
-Serum Na and glucose should be monitored Q2-3hr until serum Na is lowered below 145 mEq/L
-Once serum Na is reached 145 mEq/L, rate of infusion reduced to 1mL/kg/hr and continued till normonatremia (140)
-Goal is to lower serum Na by 1-2mEq/L/hr & to restore normonatremia <24hrs
-Pts with central DI will also require desmopressin therapy
Amiloride
-Decreases Na
-Mild potassium-sparing diuretic, lessens the need for potassium supplementation that is usually required when thiazides are used to treat polyuria
Three causes of polyuria
-primary polydipsia, central DI, and nephrogenic DI —
-associated with an increase in water output and the excretion of a relatively dilute urine.
Low plasma sodium concentration
Less than 137 meq/L with a low urine osmolality (eg, less than one-half the plasma osmolality) is usually indicative of water overload due to primary polydipsia.
High-normal plasma sodium concentration
-Greater than 142 meq/L, due to water loss points toward DI, particularly if the urine osmolality is less than the plasma osmolality.
DI
-High normal plasma sodium > 142 d/t water loss
-Urine osmo < plasma osmo
Primary Polydipsia
-low plasma sodium concentration <137
-Low urine osmo < 1/2 the plasma osmo
-Indicative to water overload and primary polydipsia
Normal plasma Na concentration
-Not helpful in dx
-But if associated with a urine osmo > 600 mosmol/kg, excludes a diagnosis of DI.
Hypernatremia causes
-Dehydration
-DI
-Cushings
-Osmotic diuresis/diarrhea (hyperglycemia, mannitol)
-Aggressive NS hydration
Treatment of Hypernatremia
-Treat underlying cause
-Administer dilute fluids
-D5W 3-6 mL/kg/hr in acute phase
-Free water
-Amiloride
Causes of Hyponatremia
-<135
-Severe <120 (risk of seizures)
-can be due to increase water intake (primary polydipsia)
-overhydration
-Dehydration
-SIADH
-Adrenal failure
-Pseudo hyperglycemia
-Polydipsia
-Ecstasy
-Cirrhosis
