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
Classifications of mild vs severe
Mild
Calcium level of 8.5-8.0
asymptomatic
Severe
Calcium level below 7.6
Symptomatic at any level below normal
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
Hypocalcemia
Tx
Treatment depends on severity, how acutely it developed, and the degree of neuromuscular irritability.
Treatment given to:
Asymptomatic patients with calcium < 7.6 mg/dL
Symptomatic pts
Preferred tx: Calcium gluconate 10 mL 10% (slow injection over 5 min)
Calcium gluconate diluted in 50 mL of 5% dextrose or 0.9% NaCl
Monitor calcium levels. If persistent, may give calcium gluconate infusion
1.2 to 1.6 mg/kg of elemental Ca infused over 4 to 6 hrs increases serum Ca by 2 to 3 mg/dL
If Ca persists (or likely to), give oral Vitamin D supplementation.
If pt is also hypomagnesemic, must correct Mg first.
If Chronic, give supplemental Ca with Vit D.
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
Clinical Manifestations
Most frequently, asymptomatic
Clinical manifestations appear with more severe symptoms:
N/V
Anorexia
Weakness
Lethargy
Cramps
Fasciculations, tetany
Carpopedal spasm
Paresthesias
Irritability, inattention
Confusion
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
Hypermagnesemia
general and causes
Serum magnesium > 2.2 mg/dL
Rare
However, magnesium toxicity is potentially fatal.
Persistent hypermagnesemia most often seen in chronic renal insufficiency.
These patients are taking large amounts of magnesium.
May occur in patients given large doses of IV magnesium (ie, preeclampsia)
May be seen in oral supplementation; however, the kidney is typically able to excrete excess magnesium.
May be caused by:
Eclampsia treatment
Renal failure
Rhabdomyolysis
Dehydration
Severe metabolic acidosis
Adrenal Insufficiency
Antacids
Hypermagnesemia
Clinical Findings
Impaired neurologic function
Muscle weakness
Decreased deep tendon reflexes
Obtundation, confusion
Flaccid paralysis
Impaired gastrointestinal function
Ileus
Cardiac abnormalities
Prolonged QT interval
Severe
Respiratory paralysis
Hypotension, cardiac arrest
Hypermagnesemia
Tx
Discontinue exogenous sources
Antacids, laxatives
IV Calcium chloride
Antagonizes magnesium
Avoid use of magnesium in advanced chronic kidney disease
Hemodialysis
Phosphorus
general and function
Normal 3 to 4.5 mg/dL
Total body content: 85% in bone, 14% intracellular, and 1% extracellular
Daily intake is 800 to 1500 mg
Present in many foods: dairy products, meats, grains
Kidney secretes phosphorus
Most filtered at the glomerulus
PTH increases renal phosphate excretion
Vitamin D enhances intestinal phosphate absorption
Hypophosphatemia
etiology
Caused by :
Decreased intake
Impaired intestinal absorption
Antacid use, TPN, Vit D. def
Redistribution into cells or bone
Hyperparathryoidism, cancer, steroids
Renal losses
Diuretics, hyperaldosteronism, burns, renal transplant, resp. alkalosis, SIADH, steroids
Frequently depleted in alcoholism
poor diet and renal loss
Common in surgical pt
Associated with Potassium and Magnesium losses
Hypophosphatemia
clin man
Clinical Manifestations:
Only observed if severe (< 1 mg/dL)
Encephalopathy, dilated cardiomyopathy, generalized muscle weakness, rhabdomyolysis, and hemolysis.
hypophospatemia
Dx
often done with history and physical exam
Can measure 24 hr urine or fractional excretion in spot urine for phosphate
normal response is for kidneys to reduce phosphate excretion to less than 100 mg/day
hypophosphatemia
Tx
Treatment:
If mild, no treatment – decrease intake.
If symptomatic or having ongoing loss,
Oral repletion: Na or KPO4 salts or skimmed milk
IV phosphorus
If on dialysis, use phosphate-containing dialysate
Hyperphosphatemia
general and causes
Common
Caused by:
Excessive phosphate intake
Increased intestinal absorption
Laxatives and enemas, intoxication with Vit. D
Redistribution from intracellular stores
Massive cell lysis (rhabdomyolysis, tumor lysis syndrome), DKA
Impaired renal excretion
Acute or chronic renal failure, primary hypoparathyroidism
Pseudohyperphosphatemia may occur in hemolytic specimens or hyperglobulinemic states (ie, multiple myeloma)
Hyperphosphatemia
clin man
May cause Acute Renal Failure.
Can cause hypocalcemia – tetany, hypotension, seizures, & cardiac arrhythmias
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
- Which of the following electrolyte abnormalities is commonly associated with hypomagnesemia?
a. Hypercalcemia
b. Hypernatremia
c. Hypochloremia
d. Hypokalemia
d. Hypokalemia
- Which of the following electrocardiogram findings is most associated with hypercalcemia?
a. Elevated ST segment
b. Increased QRS voltage
c. Lengthened PR interval
d. Short QT interval
e. Widened T-waves
d. Short QT interval
- Which of the following is the most appropriate initial treatment of cardiac arrhythmia in a patient with hyperkalemia?
a. Calcium gluconate
b. Furosemide (Lasix)
c. Insulin with glucose
d. Sodium polystyrene (Kayexalate)
e. Triamterene (Dyrenium)
a. Calcium gluconate
Which of the following mediations is most likely to cause hyperkalemia?
a. Acetazolamide (Diamox)
b. Eplerenone (Inspra)
c. Furosemide (Lasix)
d. Hydrochlorothiazide (Microzide)
b. Eplerenone (Inspra)
A 72-year old man is hospitalized for severe malnutrition. The patient is started on total parenteral nutrition. Which of the following electrolyte abnormalities should you be monitoring vigilantly?
a.-hyperkalemia
b. Hypermagnesemia
c. Hypocalcemia
d. hypophosphatemia
all of them
Which of the following electrolyte abnormalities is associated with diuretic therapy ?
a. Hyperkalemia
b. Hypermagnesemia
c. Hypomagnesemia
d. hyperchloremia
c. Hypomagnesemia
A 75-year-old man is admitted with congestive heart failure. His home medications include furosemide 80 mg daily and digoxin 0.125 mg daily. His admitting ECG reveals flattened T waves and the prescence of U wave. Which of the following serum electrolyte abnormalities is most likely for this patient?
a. K 2.4 mEq/L
b. K 5.7 mEq/L
c. Calcium 12mg/dL
d. Magnesium 1.2
a. K 2.4 mEq/L
A 57-year-old woman presents to clinic with weight loss, fatigue, and recurrent nephrolithiasis. Her physical exam is unremarkable. Her laboratory evaluations reveals normal renal and hepatic function, ESR of 52 mm/h, TSH of 2.0, and a serum calcium of 17mg/dL.
Which of the following is the most likely cause of the patient’s hypercalcemia?
a. Thyrotoxicosis
b. Hyperparathyroidism
c. Excessive calcium supplements
d. malignancy
d. malignancy
stones, bones, abdominal moans
