Transcript Importance of Homeostasis

Electrolyte Imbalance
Victor Politi, M.D., FACP,
Medical Director, SVCMC,
St. Anthony’s School of Allied Health
Professions, PA Program
Importance of Homeostasis
• Fluid and electrolyte and Acidbase balance are critical to health
and well-being
– Maintained by intake and output
– Regulation by renal and pulmonary
systems
Imbalances Result From:
• Illness
• Altered fluid intake
• Prolonged vomiting or diarrhea
Imbalances Affect:
•
•
•
Respiration
Metabolism
Function of Central Nervous System
Distribution of Body Fluids
• Water is the largest single component of the
body
– 60% of adult’s weight is water
• Healthy people can regulate balance
Compartments
• Intracellular
– Within the cells
• Contains dissolved solutes essential to
balance
• Extracellular
– Outside of the cell
• Interstitial
– Between and around the cells
• Intravascular
• Also lymph and organ fluids
– Within the blood vessels
» Plasma
Composition of Body Fluids
• Water
• Electrolytes
– Separates into ions when dissolved
• Carries an electrical charge
– Positive charge – CATIONS
» Sodium, Potassium, Calcium
– Negative charge – ANION
» Bicarbonate, Chloride
Electrolytes
• Measured in Milliequivalents per liter
– mEq/L
• How many grams of electrolyte (solute) in a liter of
plasma (solution)
– Solution is the solvent
Minerals
• Constituents of all body tissues and fluids
• Important in maintaining physiological
processes
– Act as catalysts in:
• Nerve conduction
• Muscle contraction
• Metabolism of nutrients
– Regulate electrolyte balance and hormone
production
– Strengthen skeletal structures
Movement of Body Fluids
• Cell membranes are selectively
permeable
– Water passes through easily
– Most ions and molecules move
through much slower
Osmosis
• Moving a liquid through the membrane
from lesser to greater solute
concentration
– Rate depends on concentration
– Temperature
– Electrical charges
– Differences between osmotic pressures
• Works at equalizing concentration
Osmotic Pressure (Osmolarity)
• Pulling power for water
– Depends on number of molecules in solution
• Higher the concentration, greater pulling power
– (higher osmotic pressure)
• Rate is quicker
– Continues until equilibrium is reached
Osmolarity
• Hypertonic
– Higher osmotic pressure as RBC’s
• Pulls fluid from cells
– Shrinks cell
• Isotonic
– Same osmotic pressure as RBC’s
• No fluid shift
• Hypotonic
– Lower osmotic pressure thanRBC’s
• Fluid moves into cells
– Enlarges cell
Osmotic Pressure (cont)
• Affected by plasma proteins
– Albumin
• Keeps fluid in intravascular compartment using
osmotic pressure
• Hydrostatic pressure draws fluid back into
capillaries
– Force of fluid pressure outward against surface
Diffusion
• Moving a solid across the semipermeable
membrane
– From higher concentration to lower
• To reach equilibrium
• Difference between the two is concentration
gradient
Filtration
• Both water and solids move
together in response to fluid
pressure
– Seen in capillary beds
– ACTIVE Transport
• Requires energy
– Moves against gradient
» Sodium and potassium pump
– Uses carrier molecule
• Glucose entering cell
Regulation of Body Fluids
• To maintain homeostasis, fluids are
regulated by:
– Fluid intake
– Hormonal controls
– Fluid output
Fluid Intake
• Regulated primarily by thirst mechanism
– In the hypothalamus
• Osmoreceptors monitor serum osmotic pressure
– Hypothalamus stimulated when osmolarlity increases
– Thirst mechanism stimulated
» With decreased oral intake
» Intake of hypertonic fluids
» Loss of excess fluid
» Stimulation of renin-angiotensisn-aldosterone
mechanism
» Potassium depletion
» Psychological factors
» Oropharyngeal dryness
Fluid Intake (cont)
• Average adult intake
– 2200-2700 cc/day
• Oral – 1100-1400
• Solid foods – 800-1000
• Oxidative metabolism – 300
– By-product of cellular metabolism of ingested foods
Fluid Intake (cont)
•
•
•
•
Must be alert
Able to perceive mechanism
Able to respond to mechanism
**At risk for dehydration:
– Elderly
– Very young
– Neurological disorders
– Psychological disorders
Hormonal regulation
• ADH
– Stored in posterior pituitary gland
• Released in response to changes in blood
osmolarity
• Makes tubules and collecting ducts more permeable
to water
– Water returns the systemic circulation
» Dilutes the blood
– Decreases urinary output
Hormonal regulation (cont)
• Aldosterone
– Released by adrenal cortex
• In response to increased plasma potassium
• Or as part of renin-angiotensin-aldosterone
mechanism
– Acts on distal tubules to increase reabsorption of
sodium and water
– Excretion of potassium and hydrogen
Hormonal regulation (cont)
• Renin
– Secreted by kidneys
• Responds to decreased renal perfusion
• Acts to produce angiotensin I
– Causes vasoconstriction
• Converts to Angiotensin II
– Massive selective vasoconstriction
» Relocates and increases the blood flow to kidney,
improving renal perfusion
– Stimulates release of aldosterone with low sodium
Fluid Output Regulation
• Kidneys
– Major regulatory organ
• Receive about 180 liters of blood/day to filter
• Produce 1200-1500 cc of urine
• Skin
– Regulated by sympathetic nervous system
• Activates sweat glands
– Sensible or insensible-500-600 cc/day
» Directly related to stimulation of sweat glands
• Respiration
– Insensible
• Increases with rate and depth of respirations, oxygen delivery
– About 400 cc/day
• Gastrointestinal tract
– In stool
– Average about 100-200
» GI disorders may increase or decrease it.
Regulation and Movement
of Sodium
• Most abundant cation in ECF
– Major contributor to maintaining water
balance
• By effect on serum osmolality, nerve impulse
transmission, regulation of acid-base balance
and participation in chemical reactions
– Regulated by dietary intake and
aldosterone
– Normal level : 135-145
Regulation and Movement
of Potassium
• Major cation in intracellular compartments
– Regulates metabolic activities, necessary for
glycogen deposits in liver and skeletal muscle,
transmission and conduction of nerve
impulses, normal cardiac conduction and
skeletal and smooth muscle contraction
– Regulated by dietary intake and renal
excretion
– Normal level – 3.5-5.0
• Body conserves potassium poorly
– Increased urine output decreased serum potassium
Movement and Regulation
of Calcium
• Stored in bone, plasma and body cells
(Cation)
– 90% in bones
– 1% in ECF
• In plasma, binds with albumin
– Necessary for bone and teeth formation, blood
clotting, hormone secretion, cell membrane
integrity, cardiac conduction, transmission of nerve
impulses, and muscle contraction
– Normal level – 8.5-10.5
– Regulated by bone resorption
Movement and Regulation
of Magnesium
• Cation
– Normal 1.5-2.5
– Regulated by dietary, renal and PTH
Movement and Regulation
of Chloride
• Major anion in ECF
– Normal level – 95-108
• Follows sodium
– Regulated by dietary intake and
the kidneys
Movement and Regulation
of Bicarbonate
• Major chemical base buffer in the body
– Carbonic acid-Bicarbonate buffering system
• Needed for acid-base balance
– Normal level 22-26
– Regulated by kidneys
Movement and Regulation
of Phosphate
• Buffer anion found mainly in ICF
– Assists in acid-base balance
• Inversely proportional to calcium
– Helps maintain healthy bones and teeth,
neuromuscular activity, and CHO metabolism
– Absorbed through GI tract
– Normal level 2.5-4.5
– Regulated by dietary intake, renal excretion, intestinal
absorption and PTH
Acid-Base Balance
• pH measures amount of Hydrogen ion
concentration
– Greater the concentration, lower the pH
• 7 is neutral; <7 acidic; >7 basic or alkaline
– Needed to maintain cell membrane integrity
and speed of cellular enzymatic actions
– Normal range – 7.35-7.45
– Regulated by buffers
Buffer
• Substance or group of substances that
can absorb or release hydrogen ions to
correct an acid-base imbalance
• Processes to regulate acid-base balance
– Chemical
– Biological
– Physiological
Chemical Buffers
(Acid-base Regulators)
• Carbonic acid-bicarbonate buffer system
– First to respond to changes in ECF
• Acts within seconds
– Increased carbon dioxide increases hydrogen
ions
• Carbon dioxide is excreted through lungs
– Breathe faster if too high, slower if low
• Hydrogen and bicarbonate ion excretion is controlled
through kidneys
Biological Regulation (Buffers)
• When hydrogen ions are absorbed or
released by cells
– Occurs in 2-4 hours
• Hydrogen is positively charged, must change
places with other cation, usually Potassium
– With excess acid (low pH) hydrogen enters cell,
potassium leaves and enters ECF
» High K+
» Diabetic ketoacidosis, starvation
– Chloride shift
» With oxygenation of blood in the lungs,
» bicarbonate diffuses into the cells;
» chloride goes from hemoglobin to plasma
»
anion shift
Physiological Regulation
(Buffer)
• Lungs and Kidneys
– Lungs adapt fast
• Try to correct pH before biological buffers kick in
– Hydrogen and carbon dioxide levels provide stimulus for
respirations
» Lungs alter depth and rate according to hydrogen
concentration
– With metabolic acidosis, respirations increase to exhale more
carbon dioxide
– Metabolic alkalosis, lungs retain carbon dioxide by decreasing
respiraitons
– Kidneys take from a few hours to several days
• Reabsorb bicarbonate in case of acid excess; excrete it in
cases of acid deficit
Common Disturbances
Electrolyte Balance
• Sodium
– Hypernatremia (Na > 145, sp gravity < 1.010)
• Caused by excess water loss or overall sodium excess
– Excess salt intake, hypertonic solutions, excess
aldosterone, diabetes insipidus, increased s water loss,
water deprivation
– S&S: thirst, dry, flushed skin, dry, stick tongue and mucous
membranes
– Hyponatremia (Na < 135, sp gravity > 1.030)
• Occurs with net loss of sodium or net water excess
– Kidney disease with salt wasting, adrenal insufficiency, GI
losses, increased sweating, diuretics, SIADH
– S&S: personality change, postural hypotension, postural
dizziness, abd cramping, n&v, diarrhea, tachycardia,
convulsions and coma
Common Disturbances
Electrolyte Balance
• Potassium
– Hyperkalemia (K > 5.3; EKG irregularities-bradycardia,
heart block, wide QRS pattern-cardiac arrest)
• Primary cause: renal failure; major symptom: cardiac
irregularity
– Fluid volume deficit, massive cell damage, excess K+ given,
adrenal insufficiency, acidosis, rapid infusion of stored blood,
potassium-sparing diuretics
– S&S: dysrhythmias, paresthesia
– Hypokalemia (K < 3.5; EKG irregularities-ventricular)
• Most common electrolyte imbalance; affects cardiac
conduction and function. Most common cause: potassium
wasting diuretics
– Diarrhea, vomiting, alkalosis, excess aldosterone secretion,
polyruia, extreme sweating, insulin to treat diabetic ketoacidosis
– S&S: weakness, ventricular dysrhythmias, irregular pulse
Common Disturbances
Electrolyte Balance
• Calcium
– Hypercalcemia (Ca > 5; x-rays show calcium loss,
cardiac irregularities)
• Frequently symptom of underlying disease with excess
bond resorption and release of calcium
– Hyperparathyroidism, malignant neoplastic disease,
Paget’s disease, Osteoporosis, prolonged immobization,
acidosis
– S&S: anorexia, nausea and vomiting, weakness, kidney
stones
– Hypocalcemia (Ca < 4.0, EKG abnormalities)
• Seen in severe illness
– Rapid blood transfusion with citrate, hypoalbuminemia,
hypoparathyroidism, Vitamin D deficiency, Pancreatitis,
Alkalosis
– S&S: numbness and tingling, hyperactive reflexes, positive
Trousseau’s sign (wrist), positive Chvostek’s sign (cheek),
tetany, muscle cramps, pathological fracture
Common Disturbances
Electrolyte Balance
• Chloride
• Usually seen with acid-base imbalance
– Hyperchloremia (Na >145, Bicarb <22)
• Serum bicarbonate values fall or sodium rises
– Hypochloremia (pH > 7.45)
• Excess vomiting or N/G drainage; loop of
thiazide diuretics because of sodium excretion
– Leads to metabolic alkalosis due to reabsorption of
bicarbonate to maintain electrical neutrality
Common Disturbances
Fluid Balance
• Isotonic imbalances
– When water and electrolytes are gained or
lost in equal proportions
• Osmolar imbalances
– Loss or gain of only water
• Osmolality is affected
Isotonic imbalances
• Fluid volume deficit (Sp Gravity > 1.025, Hct >50%,
BUN > 25)
– GI losses, loss of plasma or whole blood, excess perspiration, fever,
decreased intake, diuretics
– S&S: postural hypotension, tachycardia, dry mucous membranes,
poor skin turgor, thirst, confusion, rapid weight loss, slow vein filling,
lethargy, oliguria, weak pulse, sunken, dry conjunctiva
• Fluid volume excess (Hct < 38%, BUN < 10
– Congestive heart failure, renal failure, cirrhosis, increased
aldosterone and steroid levels, excess sodium intake
– S&S: rapid weight gain, edema, hypertension, polyuria, neck vein
distention, increased venous pressure, crackles in lungs
Osmolar Imbalances
• Dehydration (Hyperosmolar imbalance)
(Na > 145)
– Diabetes insipidus, neurological damage to block
thirst drive, diabetic ketoacidosis, osmotic diuresis,
hypertonic IV fluids of tube feedings
– S&S: dry, sticky mucous membranes, flushed and
dry skin, thirst, elevated temp
• Water Excess (Hypoosmolar imbalance)
(Na < 135)
– SIADH, excess water intake
– S&S: decreased level of consciousness,
convulsions, coma
Acid Base Balance
• Arterial blood gas is best measure
– pH
• Measures hydrogen ion concentration
– 7.35-7.45
– PaCO2
• Measures carbon dioxide (pulmonary ventilation)
– 35-45
< hyperventilation; > hypoventilation
– PaO2
• Oxygen in arterial blood
– 80-100
– Oxygen Saturation
• How much hemoglobin is carrying oxygen
– 95-99%
– Base Excess
• How much blood buffer is present
– High – alkalosis Caused from: Antacids, rapid blood transfusion, IV bicarb
– Low – acidosis Caused from: Diarrhea
– Bicarbonate
• Major renal component of acid-base balance
– Excreted and reproduced by kidneys
• 22-26; 20 times the level of carbonic acid : low is metabolic acidosis, high alkalosis
Common Disturbances
in Acid-Base Balance
• Respiratory acidosis (pH <7.35; CO2> 45;)
– Increased carbon dioxide, excess carbonic
acid, increased hydrogen ion concentration
• Causes: HYPOVENTILIATION
– Atelectasis, pneumonia, cystic fibrosis, respiratory failure,
airway obstruction, chest wall injury, overdose, paralysis of
respiratory muscles, head injury, obesity
– S&S: neurological changes and respiratory depression
» Confusion, dizziness, lethargy, headache, ventricular
dysrhythmias, warm flushed skin, muscular twitching
Common Disturbances
in Acid-Base Balance
• Respiratory alkalosis (pH > 7.45; CO2 < 35;)
– Decreased carbon dioxide, decreased hydrogen
ions
• Causes: hyperventilation
– asthma, pneumonia, inappropriate ventilator settings, anxiety,
hypermetabolic state, CNS disorder, salicylate overdose
– S&S: dizziness, confusion, dysrhythmia, tachypnea,
numbness and tingling, convulsions, coma
Common Disturbances
in Acid-Base Balance
• Metabolic acidosis (pH < 7>35; Bicarb < 22)
– Increased acid (hydrogen ions, decreased
sodium bicarbonate
• High Anion Gap (Sodium minus Chlorine + Bicarb)
– Causes: starvation, diabetic ketoacidosis, renal failure, lactic
acidosis, drug use (paraldehyde, aspirin)
– S&S: tachypnea with deep respirations, headache, lethargy,
anorexia, abdominal cramps
Common Disturbances
in Acid-Base Balance
• Metabolic alkalosis
– Loss of acid (hydrogen ions) or increase
bicarbonate
• Most common cause: vomiting and gastric
secretions
– Hypokalemia, hypercalcemia, excess aldosterone,
use of drugs (steroids, bicarb, diuretics)
– S&S: numbness and tingling, tetany, muscle cramps
Variables Affecting Normal Fluid, Electrolyte
and Acid-Base Imbalances
•
•
•
•
Age
Orientation status
Mobility level
Prolonged illness
– Cancer, CHF, endocrine disease, COPD
• Medications
– Diuretics, steroids, IV therapy, TPN
• Gastrointestinal losses
Clinical Assessment for Fluid,
Electrolyte and Acid-Base Imbalances
• History
– Pre-existing disease processes
• Cancer, cardiovascular, renal, GI
– Age
• Infants have higher % water- loss felt faster
• Elderly –kidneys decreased filtration rate, less functioning nephrons,
don’t excrete mediations as fast, lung changes may lead to respiratory
acidosis
– Acute illness
• Surgery, burns, respiratory disorders, head injury
– Environmental
• Vigorous exercise, temperature extremes
– Diet
• Fluids and electrolytes gained through diet
– Lifestyle
• Smoking or alcohol
– Medications
• Side-effects may cause fluid and/or electrolyte imbalances
Medications Likely to Cause
F&E Imbalances
• Diuretics
– Metabolic alkalosis, hyperkalemia, hypokalemia
• Steroids
– Metabolic alkalosis
• Potassium supplements
– GI disturbances
• Respiratory center depressants (narcotic analgesics)
– Respiratory acidosis
• Antibiotics
– Nephrotoxicity, hyperkalemia, hypernatremia
• Calcium carbonate (TUMS)
– Metabolic alkalosis
• Magnesium hydroxide (Milk of Mag)
– hypokalemia
Assessment (cont)
• Physical assessment
• Intake and Output
– May need fluid restrictions
• Daily Weight
Lab Studies associated with
Fluid, Electrolyte and Acid-Base
Imbalances
• Serum and urinary electrolyte levels
• Hematocrit
– If no anemia, can indicate hydration status
• Blood creatinine
– Measure kidney function
• Excreted at constant level if no kidney disease
• BUN
– Indicates kidney function
• May be affected by cell destruction or steroid therapy
– Decrease may indicate malnutrition or hepatic damage
• Urine specific gravity
• ABG’s
Assessing Blood Gases
• 1st look at pH
– Over 7.45 Alkalosis
– Below 7.35 Acidosis
• 2nd check CO2
– Should move in opposite direction as pH
• if abnormal, respiratory cause
• if normal, metabolic
• 3rd evaluate bicarbonate
– Should move in same direction as pH
• If so, metabolic cause
• if not, respiratory cause
• 4th both CO2 and bicarbonate abnormal?
– Which more closely corresponds to pH and deviates more
from normal?
• Shows likely cause, other is trying to compensate
Interventions for Fluid, Electrolyte
and Acid-Base Imbalances
• Identify the cause and treat it
– Collaborate
– Always be aware of clinical condition
• Teach
– Risk factors
– Signs and symptoms to seek treatment for
• Maintain functioning IV site
• Check orders frequently, may change
quickly depending on ABG’s
Hypercalcemia
Hypercalcemia
• Most common causes (90% of cases):
– Malignancy associated hypercalcemia
• Tumor production of PTH-related protein is the
commonest paraneoplastic endocrine syndrome,
accounting for most cases of hypocalcemia in
inpatients
– Primary hyperparathyroidism
• Most common cause in ambulatory patients
Hypercalemia
• Chronic hypercalemia > 6 months or a
manifestation such as nephrolithiasis
suggest a benign cause.
Hypercalcemia - symptoms
• Symptoms
• (usually occur if serum calcium is > 12mg/dl and
tend to be more severe if hypercalcemia develops
acutely)
– Constipation
– Polyuria
– Heart
• Ventricular extrasystoles and idioventricular rhythm
– Neurologic symptoms
• Stupor, coma, azotemia in severe cases
Hypercalcemia - Labs
• Labs
– Significant elevation serum calcium
– ECG – shortened QT interval
– Measurements of PTH and PTH related
protein (PTHrP) help distinguish between
hyperparathyroidism (elevated PTH) and
malignancy associated hypercalemia
(elevated PTHrP)
Hypercalcemia - Investigations
• Establish hypercalcemia is real: check
renal function
• Measure serum PTH, 25-OH-vitamin D,
PTHrp, T4, ACE as appropriate
• Radiological investigations
– Basic – eg. Hands, KUB, CXR
– Localization
Hypercalcemia - TX
• Treatment
– Ultimate goal – locate primary disease
process & control
– Treatment of hypercalcemia of malignancy
• Bisphosponates – effective in 95% of cases
– Emergency tx of choice
• Saline & furosemide (prevent volume overload and
enhances Ca2+ excretion)
Hypocalcemia
Hypocalcemia
• Often mistaken as a neurological disorder
• Most common cause
– renal failure
• Other causes:
–
–
–
–
–
Malabsorption
Vitamin D deficit
Alcoholism
Diuretic therapy
Endocrine disease
Hypocalcemia - Symptoms
• Hypocalcemia increase excitation of nerve
and muscle cells, primarily affecting the
neuromuscular and cardiovascular
systems
Hypocalcemia - Symptoms
• Symptoms:
– Muscle cramps and tetany
– Laryngospasm w/stridor
– Convulsions
– Paresthesias of lips & extremities
– Abdominal pain
Hypocalcemia - Symptoms
• Chvostek’s & Trousseau’s signs are
usually readily elicited
– Chvostek’s sign
• Contraction of the facial muscle in response to
tapping the facial nerve anterior to the ear
– Trousseau’s sign
• Carpal spasm occurring after occlusion of the
brachial artery with a bp cuff for 3 minutes
Hypocalcemia - Labs
• ECG:
– Prolonged QT interval
• Serum calcium concentration:
– < 9mg/dl
• Serum magnesium
– usually low
• Serum phosphate level
– usually elevated in hypoparathyroidism or end-stage
renal failure
– Suppressed in early stage renal failure or vitamin D
deficiency
Hypocalcemia - Tx
• Severe, symptomatic hypocalcemia
– 10-15 milligrams of calcium per kilogram of body
weight, or 6-8 10-ml vials of 10% calcium gluconate
(558-744mg of calcium) added to 1 liter of D5W and
infused over 4-6hrs. Adjust infusion rate to maintain
serum calcium level at 7-8.5mg/dL
– In presence of tetany, arrhythmias or seizures
• Calcium gluconate 10% (10-20 ml) IV over 10-15min
Hypocalcemia - Tx
• Asymptomatic Hypocalcemia
– Oral calcium 1-2g and vitamin D preparations
are used
Hypophosphatemia
Hypophosphatemia
• Severe hypophosphatemia may cause tissue
hypooxygenation and rhabdomylosis
• Severe hypophosphatemia is common and multifactorial
in alcoholic patients (reversible after a month of
abstinence)
• Vomiting, diarrhea and poor dietary intake are
contributing factors for hypophosphatemia
• Patients with COPD and asthma commonly have
hypophosphatemia
Hypophosphatemia
• Renal loss of phosphate can be recognized by urinary
phosphate excretion (calculating the TmP/GFR
• Pi = serum phosphate concentration
• UPi= urine phosphate concentration
• UV= urine volume
Tmp
Serum Pi- (UPi x UV
=
GFR
GFR
Hypophosphatemia
• Acute, severe hypophosphatemia (0.10.2mg/dL) can lead to acute hemolytic
anemia, platelet dysfunction with petechial
hemorrhages, Rhabdomyolysis,
encephalopathy
• Other Manifestations include: irritability,
confusion, dysarthia, seiqures, coma
Hypophosphatemia
• Treatment is prophylaxis by including phosphate
in repletion and maintenance fluids
• A rapid decline in calcium levels can occur with
parenteral phosphate, therefore, when possible,
oral replacement is preferred
– Serum creatinine and calcium levels must be
monitored to guard against hypocalcemia
Hyperphosphatemia
Hyperphosphatemia
• Most common cause – renal insufficiency
• Clinical manifestations – those of
underlying disorders (eg, chronic renal
failure, hypoparathyroidism)
• Treatment is directed at underlying
disorder and of associated hypocalcemia if
present
Hyperphosphatemia
• In acute and chronic renal failure dialysis
with reduce serum phosphate
• Absorption can be reduced by calcium
carbonate 0.5-1.5 g 3x daily with meals
Hyperkalemia
Hyperkalemia
• Many cases associated with acidosis
• Pseudohyperkalemia – result of lysis of
red cells releasing potassium into the
serum
Hyperkalemia
• Serum potassium concentration rises
about 0.7 meq/L for every decrease of 0.1
pH unit during acidosis
• Potassium movement out of cells occurs
primarily in metabolic acidosis due to the
accumulation of minerals such as NH4Cl
or HCl.
Hyperkalemia
• ECG may show peaked T waves, widened
QRS & biphasic QRS-T complexes or may
even be normal despite life threatening
hyperkalemia
Hyperkalemia
• Associated With:
– HIV
– diabetic ketoacidosis
– Medications
•
•
•
•
Surgical Med - Aminocaproic acid
Ace Inhibitors
Trimethoprim
Immunosuppressive medications
Hyperkalemia
• Commonly seen in HIV infected patients
• Attributed to impaired renal excretion of
potassium due to the use of pentamidine
or trimethoprim-sulfamethoxazole or to
hyporeninemic hypoaldosteronism
Hyperkalemia
• The hyperkalemia frequently seen in diabetic
ketoacidosis is due to a combination of the
hyperosmolaity and deficiency of insulin,
catrecholamines, and aldosterone.
• Aminocaproic acid, (synthetic amino acid
struturally related to lysine and arginine) used
for the prevention of operative blood loss, may
induce shift of potassium.
Hyperkalemia
• Ace inhibitors or angiotensin receptor
blockers commonly used to treat CHF or
renal insufficiency may cause
hyperkalemia.
Hyperkalemia
• Findings
– Muscle weakness
– Abdominal distention
– Diarrhea
– Rare finding – flaccid paralysis
Hyperkalemia
• Heart rate may be slow, V-Fib & cardiac
arrest may occur
• ECG changes include:
– Peaked T waves, widening of QRS, biphasic
QRS-T complexes
• Note:nearly 50% of cases with serum levels 6.5meq/L or
greater will not exhibit ECG changes
Hyperkalemia - TX
• Confirm elevated level of serum potassium
(measure in plasma rather than serum)
• Tx consists of witholding potassium and
giving cation exchange resins by mouth or
enema
– Sodium polystyrene sulfonate 40-80g/d
Hyperkalemia – Emergent TX
• Indicated if cardiac toxicity or muscular
paralysis present or if hyperkalemia
severe > 6.5-7 meq/L
– Calcium gluconate 10% 5-30ml IV
– NaHCO3 44-88 meq (1-2 ampules) IV
– Insulin 5-10 units, IV plus glucose 50% 25g,1
ampule, IV
– Nebulized albuterol 10-20mg in 4 ml normal
saline inhaled over 10 min
Hyperkalemia – Nonemergent Tx
• Loop diuretic (Furosemide) 40-160mg IV
or orally w or w/o NaHCO3, 0.5-3 meq/kg
daily
• Sodium polystyrene sulfonate
(Kayexalate) oral: 15-30g in 20% sorbitol
(50-100mL) rectal: 50g in 20% sorbitol
• Hemodialysis
• Peritoneal Dialysis
Hypokalemia
Hypokalemia
• Severe hypokalemia may induce dangerous
arrhythmias or rhabdomyolysis
• Self limited hypokalemia occurs in 50-60% of
trauma patients (possibly related to enhanced
release of epinephrine)
• Hypokalemia in the presence of acidosis
suggests profound potassium depletion and
requires urgent tx
Hypokalemia - Signs
• Common findings
– Muscular weakness
– Muscle cramps
– Fatigue
– Constipation or ileus
Hypokalemia- Signs
• In severe Cases
– Flaccid paralysis
– Hyporeflexia
– Hypercapnia
– Tetany
– Rhabdomyolysis
Hypokalemia - Labs
•
•
•
•
•
•
ECG
Decreased amplitude
T wave broadening
Prominent U waves
PVCs
Depressed ST segment
Hypokalemia – Causes
Several Causes of Hypokalemia
– Decreased potassium intake
– Potassium shift into the cell
• trauma
– Renal potassium loss
•
•
•
•
•
Primary hyperaldosteronism
Renovascular HTN
Cushing’s Syndrome
Bartter’s Syndrome
Metabolic acidosis
– Extrarenal potassium loss
• Vomiting, diarrhea, laxative abuse,
• Zollinger-Ellison syndrome
Hypokalemia
• TTKG Gradient (transtubular K+ gradient)
provides a simple and rapid evaluation of
net potassium secretion
• TTKG=
Urine K+/Plasma K+
Urine osm/Plasma osm
Hypokalemia- Tx
• Mild to moderate deficiency
– Oral potassium
• 20 meq/L to prevent hypokalemia,
• 40-100 meq/L over a period of days to weeks to
treat hypokalemia and fully replete potassium
stores
Hypokalemia - TX
• Moderate to severe
– Peripheral IV should not exceed 40meq/L at
rates up to 40 meq/L/h
– Continuous ECG monitoring indicated
– Check serum potassium q 3-6 hours
– Correct magnesium deficiency
•
Hyponatremia
Hyponatremia
•
MILD HYPONATREMIA
–
•
SEVERE HYPONATREMIA
–
•
plasma sodium levels under <135 mmol x L(-1).
plasma sodium levels below < 130 mmol x L(-1)
compromising health and performance.
CRITICAL HYPONATREMIA
–
plasma sodium levels below 120 mmol x L(-1)
(may be fatal).
Hyponatremia
• Defined as serum sodium concentration
less than 130 meq/L
• Most common electrolyte abnormality
observed in hospitalized patient population
• Most cases of hyponatremia result from
water imbalance not sodium imbalance.
Hyponatremia
• Initial approach is to determine serum
osmolality
• Normal (280-295 mosm/kg)
• Low (< 280 mosm/kg)
• High (> 295 mosm/kg)
Hyponatremia
• Measurement of urine sodium helps distinguish
renal from non-renal causes
– Urine sodium > 20 meq/L
• consistent with renal salt wasting (diuretics, ACE inhibitors,
mineralocorticoid deficiency, salf-losing nephropathy)
– Urine sodium < 10meq/L or fractional excretion of
sodium < 1%
• implies sodium retention by kidney to compensate for
extrarenal fluid loss (vomiting, diarrhea, sweating, thirdspacing)
Hyponatremia
• Isotonic & Hypertonic hyponatremia can
be ruled out by determining serum
osmolality, blood lipids, and blood glucose
• Osmolality = 2 (Na+ meq/L) +
Glucose mg/dL + BUN mg/dL
18
2.8
Hyponatremia
Serum osmolality
Normal
(280-295 mosm/kg
Low
(< 280 mosm/kg
High
(> 295 mosm/kg
Hypotonic
hyponataremia
Isotonic hyponatremia
1. Hyperproteinemia
2. Hyperlipidemia (chylomicrons,
3. triglycerides)
Hypertonic hyponatremia
1. Hperglycemia
2. Mannitol, sorbitol, glycerol, maltose
3. Radiocontrast agents
Continued next slide
Hypotonic hyponatremia
Volume Status
Hypervolemic
Hypovolemic
Euvolemic
UNa+ < 10meq/L
Extrarenal salt loss
1. Dehydration
2. Diarrhea
3. Vomiting
UNa+> 20meq/L
Renal salt loss
1. Diuretics
2. Ace inhibitors
3. Nephropathies
4. Mineralocorticoid deficiency
5. Cerebral sodium wasting syndrome
1. SIADH
2. Post-op hyponatremia
3. Hypothyroidism
4. Psychogenic polydipsia
5. Beer potomania
6. Idiosyncratic drug reaction
7. Endurance exercise
Edematous states
1. CHF
2. Liver Disease
3. Nephrotic syndrome (rare)
4. Advanced renal failure
Isotonic Hyponatremia
• Seen in cases of hyperlipidemia & hyperproteinemia
– The marked increases in lipids and proteins (>10g/gL) occupy a
disproportionately large portion of the plasma volume.
– Plasma osmolality remains normal because its measurement is
unaffected by the lipids or proteins.
– A decreased volume of water results, so that the sodium
concentration in total plasma volume is decreased.
– Because the sodium concentration in the plasma water is
actually normal, hyperlipidemia and hyperproteinemia cause
pseudohyponatremia
Hypertonic hyponatremia
• Most commonly seen with hyperglycemia
• When blood glucose becomes acutely elevated,
water is drawn form the cells into the
extracellular space, diluting the serum sodium.
• The plasma sodium levels falls 2 meq/L for
every 100 mg/dL rise when the glucose
concentration is between 200 & 400 mg/dL
Hypertonic hyponatremia
• If the glucose concentration is above
400mg/dL, the plasma sodium
concentration falls 4meq/L for every
100mg/dL rise in glucose
• This dilutional hyponatremia is not
pseudohyponatremia, since the sodium
concentration does fall.
Hypotonic Hyponatremia
• Retention of electrolyte fee water nearly
always occurs because of impaired
excretion (renal failure, inappropriate ADH
excess, etc.)
Hypovolemic
• UNa+ < 10meq/L
• Extrarenal salt loss
– Dehydration
– Diarrhea
– Vomiting
• UNa+ > 20 meq/L
• Renal salt loss
–
–
–
–
Diuretics
ACE inhibitors
Nephropathies
Mineralocorticoid
deficiency
– Cerebral sodium
wasting syndrome
Euvolemic
•
•
•
•
•
•
SIADH
Postoperative hyponatremia
Hypothyroidism
Psychogenic polydipsia
Beer potomania
Idiosyncratic drug reaction (thiazide
diuretics, ACE inhibitors
• Endurance exercise
Hypervolemic
• Edematous states
– CHF
– Liver Dx
– Nephrotic Syndrome (rare)
– Advanced renal failure
Hyponatremia - Symptoms
• Swollen hands/feet, headache,
personality change, postural
hypotension, postural dizziness,
abdominal cramping, nausea &
vomiting, diarrhea, tachycardia,
convulsions and coma
Hyponatremia in AIDS
• Seen in up to 50% of patients hospitalized
for AIDS and in 20% of ambulatory AIDs
patients
Hyponatremia - Tx
•
•
•
•
Treatment of underlying condition
Water restriction
Diuretics
Hypertonic 3% saline
– Dangerous in volume
overloaded states, not
routinely recommended
– Emergency dialysis
Hypernatremia
Hypernatremia
– Na > 145, sp gravity < 1.010
• An intact thirst mechanism usually prevents
hypernatremia
• Excess water loss can cause hypernatremia only
when adequate water intake is not possible, as
with unconscious patients
• Rarely, excessive sodium intake may cause
hypernatremia
Hypernatremia - Symptoms
• Typical Findings include;
– orthostatic hypotension, oliguria
• In severe cases:
– hyperthermia, delirium, and coma
Hypernatremia
• Urine osmolality > 400mosm/kg
• Nonrenal losses:
– Water ingestion fails to keep up with hypotonic losses
• Excessive sweating, exertional losses from respiratory tract,
or through stool water
• Renal losses:
– Progressive volume depletion from the osmotic
diuresis of glycosuria can result in true hypernatremia
Hypernatremia
• Urine osmolality < 250 mosm/kg
– Characteristic of central and nephrogenic
diabetes insipidus
• Seen with lithium or demeclocycline therapy, after
relief of prolonged urinary tract obstruction or with
interstitial nephritis, results from renal insensitivity
to ADH
Hypernatremia- TX
• Treatment directed at correcting the cause
of fluid loss and replacing water and as
needed, electrolytes
• If hypernatremia is corrected too rapidly,
the osmotic imbalance may cause water to
preferentially enter brain cells causing
cerebral edema and potentially severe
neurologic impairment
Hypernatremia- TX
• Fluid therapy should be administered over
48hours, aiming for a decrease is serum
sodium 1 meq/L/h
• Potassium and phosphate may be added
as indicated by serum levels
Hypomagnesemia
Hypomagnesemia
• Common causes include:
– Diminished absorption or intake
• malabsorption, chronic diarrhea, laxative abuse
– Increased renal loss
• diuretic therapy, drugs, tubulointerstitial disease,
hypercalcemia, volume expansion
– Other Causes
• Diabetes, pregnancy, respiratory alkalosis
Hypomagnesemia
• Symptoms include:
– Weakness, muscle cramps, tremor
– Marked neuromuscular & central nervous
system hyperirritability with tremors, athetoid
movements, jerking, nystagmus, and a
positive Babinski response
– HTN, tachycardia, ventricular arrhythmias
– Prominent features - confusion and
disorientation
Hypomagnesemia – Lab Findings
• Urinary excretion of magnesium exceeding
10-30 mg/d or a fractional > 2%
• ECG – prolonged QT interval, due to
lengthening of the ST segment
• Parathyroid hormone secretion often
suppressed
Hypomagnesemia - TX
• If severe –
– IV fluids containing magnesium as chloride or sulfate,
240-1200 mg/d (10-50 mmol/d) followed by 120mg/d
(5mmol/d) for maintanence
• IM 200-800mg/d (8-33mmol/d) in four divided
doses
• Serum levels must be monitored to keep
concentration form rising > 2.5mmol/L
Hypomagnesemia - TX
• Chronic hypomagnesemia –
– Magensium oxide, 250-500 mg PO 2-4 x day
Hypermagnesemia
Hypermagnesemia
• Almost always the result of renal
insufficiency and the inability to excrete
what has been taken if from food or drugs,
especially antacids and laxatives
Hypermagnesemia
• General Symptoms
– Muscle weakness, decreased deep tendon
reflexes,
• Characteristic findings –
– mental obtundation and confusion
Hypermagnesemia
• Serum Mg2+ elevated
• ECG shows increased PR interval,
broadening of QRS complexes, peaked T
waves
Hypermagnesemia
• Treatment is directed at alleviating renal
insufficiency
• Calcium acts as an antagonist to Mg2+ and
may be given IV as calcium chloride,
500mg or more at a rate of 100mg
(4.5mmol/min)
• Hemodialysis or peritoneal dialysis may be
indicated
THE END