Electrolytes Flashcards
Potassium
general
In kidneys, the majority of filtered K+ is resorbed in the proximal tubular system
Selective secretion or absorption in the distal tubule determines net K+
Limit of renal K+ excretion 10 mEq/ L
Excretion affected by circulating Aldosterone, cellular and extracellular K+, tubular urine flow rates, & acid-base disturbances
potassium
normal range
3.5-5.0 mEq/L
Potassium
Function
NA+/K+-ATPase
Nerve transmission
Skeletal muscle contraction
Cardiac muscle function
Renal and fluid ion balance
Potassium channels
Nerve action potentials
Hypokalemia
causes
K level < 3.5 mEq/L
Hypokalemia occurs from one of 3 pathologic mechanisms:
Deficient intake
Anorexia, alcohol use disorder
Increase excretion
Diuretics, Hyperglycemia, 1° or 2° Aldosteronism, Elevated ACTH, Corticosteroid excess
GI loss
Colon, rectum- high K content
Gastric- hypokalemic hypochloremic met. Alkalosis
Other: Licorice, Acute Leukemia, Iatrogenic
Hypokalemia
Clinical Symptoms
Skeletal muscle weakness/malaise
Fatigue
Weakness/cramps
Paresthesias
Paralysis (flaccid paralysis if severe)
N/V/C – paralytic ileus
Polydipsia
Polyuria/Nocturia
Usually asymptomatic until < 3.0 mEq/L
Hypokalemia
Clinical Signs
hypotension
Diminished/ absent DTRs
Cardiac abnormalities-EKG changes
Ventricular arrhythmias, flatten T waves, U waves, depressed ST segments, and ventricular ectopy, cardiac arrest
May be acidotic
Usually asymptomatic until < 3.0 mEq/L
hypokalemia
ECG changes
Although the ECG is a fairly good indicator of hyperkalemia, it is not reliable for detecting hypokalemia. However, when ECG changes are seen they tend to be those that are shown in this figure.
A : normal
B : shows flattening of the T wave, which is the earliest change
C and D :A “U wave” then develops, associated with ST-T wave flattening and sometimes slight ST depression. A “pseudo P-pulmonale” pattern may be seen.
E and F : ST depression is more noticeable and the U wave increases in amplitude until ultimately the U wave overtakes the T wave. At this point distinguishing between the T wave and U wave may be almost impossible (“Q-U” prolongation).
Note - The ECG changes of hypomagnesemia are identical to those of hypokalemia.
with K think t wave
Hypokalemia
Treatment
Replace potassium (10 mEq of KCl will increase serum K approximately 0.1 mEq/L)
Orally (preferred)
Normal renal fxn
Do not exceed 40 mEq/h
IV (if emergent)
Do not exceed 10 mEq/h
Repeat as often as necessary
ECG monitor, mandatory if rate > 10 mEq/h
Avoid dextrose solutions-will drop K level
Rapid correction
Hyperkalemia
Arrhythmias
Make sure Mg is normal. If not, correct hypomagnesemia (K+ will normalize)
Correct hypocalcemia and hypokalemia together
hypokalemia
if oral - should take 4 hours for K/ 24 hours for Mg
if IV - should take 1 hour for K/
Hyperkalemia
general and causes
K level > 5.2 mEq/L
Physiologic Response
Rapid urinary excretion
Etiology
Impaired renal potassium excretion
Hypoaldosteronism
Shift from inside cells to extracellular fluid
Medications : ACE/ARB/Spironolactone
Laboratory error:
Hemolysis
Patients with hyperkalemia and no kidney injury/disease who are not taking medications that cause hyperkalemia should have repeat blood draw to rule out spurious hyperkalemia
Hyperkalemia
Clinical Manifestations
Peripheral muscle weakness and fatigue
SOB/Respiratory paralysis
CARDIAC abnormalities
EKG with peaked T waves at K of 6.0-7.0
flat p wave
increased PR interval
decreased QT interval
wide QRS
depressed ST segment
K of 8.0 or higher the QRS merge with T , V-fib, cardiac arrest
hyperkalemia
A: normalB: shows peaking of the T wave, which is the earliest change (K+ about 6-7 mEq/L)
C: The T wave becomes taller and more peaked (K+ about 7-8 mEq/L); it almost looks like the Empire State building (tall, peaked, with a narrow base). Contrast with the T wave that is sometimes seen in healthy individuals as a normal variant (shaded box) in which the T wave is rounded, its sides are not symmetric, and it has a broad base.
D: P wave amplitude decreases, the PR interval lengthens, and the QRS widens (K+ >8 mEq/L).
E: P waves disappear (sino- ventricular rhythm) and the QRS becomes sinusoid (K+ >10 mEq/L).V Fib usually follows.
Hyperkalemia-
work up
Labs – to determine cause
To determine potential cause (Electrolytes and EKG done)
Renal function assessment for renal failure
Urine K, Na, and osmolality
CBC (low Hg, Hct, or abnormal red cell suggests hemolysis/severe leukocytosis or a questions if it is pseudo-hyperkalemia
Metabolic panel – low bicarb (metabolic acidosis), hyperglycemia, elevated LDH, uric acid, phosphate, ALT, CK (rhabdomyolysis)
Serum cortisol, renin, aldosterone (adrenal insuff.)
check Mg as well
Hyperkalemia
Treatment
mild/moderate vs severe
Mild to Moderate (no cardiac abnormalities)
Restrict K+ intake, stop K+ sparing diuretics, address volume or acid-base disorders
Give K+ wasting diuretics
Severe or if cardiac abnormalities present
10% calcium gluconate IV over 5 min to reduce muscle excitability
Use 10 to 30 mL, action is quick (1-2 min)
Redistribute potassium from extracellular space to intracellular space
Using rapid-acting insulin (5 to 10 U) drives K+ into the cells
Given with 25 g glucose 50% IV over 5 min
Sodium bicarb IV (helpful if acidotic)
β₂-adrenergic agonist (Albuterol) 0.5% 20 mg in 4mL normal saline by nebulizer (onset is 15-30 min)
Dialysis (Decrease total body potassium level)
Identify and treat correctable causes
Kayexalate by mouth or enema binds and removes K- gives diarrhea
Hypochloremia
General and Causes
Normal serum chloride 98-110 mEq/L
Hypochloremia < 98 mEq/L
Due to
Loss of gastric contents (N/V, NGT)
Excess extracellular water (hypotonic fluid admin., SIADH)
Renal losses caused by diuretics
Renal failure
During respiratory acidosis (kidneys resorb bicarb, Cl- excreted)
Hypochloremia
Clinical Sx and Tx
No specific S/S
(typically co-exist with Na def – Na and Cl stick together)
TX: NaCl or KCl (if K def too)
Hyperchloremia
general and causes
Sx / Tx
Serum Cl- >110 mEq/L
Uncommon in the surgical pt
Most commonly caused by administration of chloride rich IV fluids (0.9% NaCl)
In association with hyperchloremic metabolic acidosis, RTA, hypernatremia, iatrogenic,
No specific s/s
Treat underlying disorder. Used balanced solutions.
Calcium
general
Normal serum calcium 8.5-10.5 mEq/L (ionized 4.75-5.30mg/dL)
Hypocalcemia < 8.5 mEq/L (corrected for albumin)
Hypercalcemia >11 mEq/L
Most found in hydroxyapatite crystals in bone
40% bound to plasma protein (albumin)
Correct serum Ca++ in hypoalbuminemic pts
Corrected serum Ca++ = measure Ca++ + (0.8 X [4-measured albumin in g/dL])
50% ionized and physiologically active
Resorption Increased by
PTH or metabolic alkalosis
Half of serum calcium is free while the other half is bound to albumin
calcium
function
Neural signaling
Bone mineralization
Cardiac function
Skeletal muscle contraction
Digestive system function
Physiology of Calcium
Stimulates osteoclasts to break down bone – releasing calcium and phosphorus
Increases reabsorption of calcium by kidneys
Blocks reabsorption of phosphate by kidneys, leading to urinary phosphate loss.
Increases conversion of inactive to active 1,25 vitamin D (which then increases calcium absorption from gut)
Hypocalcemia
general and causes
Serum calcium < 8.5 mg/dL
Normal physiologic Response
Etiology
Malabsorption
Decreased intake
Vitamin D deficiency
Bowel surgery
Hypoparathyroidism
Decreased serum albumin
Chronic kidney disease
Decreased calcitriol
Hyperphosphatemia
Often seen in surgical patient/hospitalized patients
May be acute or chronic
Acute pancreatitis
Hypoparathyroidism
Severe soft tissue infections (necrotizing fasciitis)
Renal Insufficiency
Malabsorption syndromes
Chronic Diarrhea
Vitamin D def.
Hypomagnesemia
Hyperphosphatemia
Blood transfusion
Adverse effects of drugs
rhabdomyolysis
Tumor lysis syndrome
rickets
Genetic disorders
Chronic Diarrhea
Osteoblastic metastases
Prostate and breast cancer
DiGeorge syndrome
IBD
Fluid loss from pancreatic/ intestinal fistulas
hypocalcemia
Clinical Manifestations
Circumoral tingling
Numbness/ tingling of fingertips
Muscle cramps
Wheezing/Dyspnea
Seizures
Palpitations/Chest pain
Confusion
Depression
Trousseau’s Sign :Carpal spasm elicited by inflation of BP cuff to 20 mmHg above systolic pressure for 3 min
Chvostek Sign :Twitching of circumoral muscles in response to tapping facial nerve anterior to ear
Wheezing
Irregular heart rhythm
Hyperactive DTRs
Tetany
Prolonged QT on EKG
Hypocalcemia
Diagnostic evaluation
Serum Calcium or ionized Calcium
Identify cause:
Serum albumin, K, Mg, Phos, Alk, Vit D, PTH, Cr, CK
Urinary calcium
Hypercalcemia
general and causes
Serum Ca > 10.5 mEq/L
No formal classification, but may be described as mild, moderate, or severe
Mild < 12
Moderate 12-14
Severe > 14
Occurs from one of three mechanisms:
1) increased bone resorption (example, lytic bone lesions)
2) Increased GI absorption of Ca (excessive PTH effects on 1,25 (OH)2D
3) Decreased renal Ca excretion (thiazide diuretics)
May be classified if PTH are elevated or reduced
PTH elevated: primary or tertiary hyperparathyroidism
PTH reduced: malignancy, excess Vit. D, Drugs (thiazides. Lithium, estrogens/testosterone, milk-alkali syndrome, thyrotoxicosis, pheochromocytoma, acute adrenal insuf.
Most common causes are primary hyperparathyroidism and malignancy.
Hypercalcemia
clinical manifestations
Asymptomatic
Symptomatic:
Gastrointestinal
Constipation
Anorexia
Renal
Nephrolithiasis
Neurologic
Anxiety, lethargy
Cardiac
Arrhythmia – Short QT interval
“moans, groans, pains, and stones”
Calcium
Hypercalcemia
treatment
Restrict Ca++
Hydrate- IV ½ NS or NS
Enhances urinary calcium excretion
Saline diuresis lead to hypokalemia, hypomagnesemia, or other electrolyte imbalance
Avoid fluid overload
If severe, use bisphosphonates. (not used if hyperparathyroid)
Drugs of choice are pamidronate and zoledronic acid.
Corticosteroid-used long term to suppress calcium release from bone but take 1-2 weeks to show results
Treat underlying cause
Magnesium
general and function
2nd most abundant cation of the intracellular fluid
Mg++ is tightly regulated by the gut, kidney, and bone.
Function
Activates enzymes
ATP function in combination with phosphate
Signal transduction pathways
Nerve transmission
Hypomagnesemia
general and cause
mild/mod/severe
Normal 1.8-2.1 mg/dL
Mild 1.5-1.8 mg/dL
Moderate 1-1.4 mg/dL
Severe < 1mg/dL
Common in critically ill pts
Etiology
Diminished absorption or intake
Increased renal loss
hypomagnesemia
Cardiac Arrhythmias
(variety of atrial and ventricular arrhythmias – flattened T waves, prolonged QT interval, ST depression, and widened QRS complexes)
Hypomagnesemia
Treatment
TX: oral, IV magnesium sulfate, hydration-watch in renal failure
Management
Chronic, asymptomatic
PO Magnesium oxide
Symptomatic
IV Magnesium sulfate in 5% dextrose or normal saline
Calcium and potassium replacement may be required, but patients with hypokalemia and hypocalcemia do not recover without magnesium supplementation
Dose adjustments for patients with advanced chronic kidney disease
hyperphosphatemia
Treatment
If acute, asymptomatic, and normal renal function, hyperphosphatemia will most likely resolve spontaneously.
If symptomatic and impaired renal function, extracorporeal therapy to remove excess phosphate.
Chronic
Minimize dietary phosphorus intake
Phosphate binders (calcium salts, lanthanum carbonate, or sevelamer)
Aluminum hydroxide effective phosphate binder, but prolonged use leads to aluminum accumulation. (may cause encephalopathy and osteomalacia)
hemodialysis
