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 Acid-base 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

• 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 - Symptoms

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 (0.1-0.2mg/dL) can lead to acute hemolytic anemia, platelet dysfunction with petechial hemorrhages, Rhabdomyolysis, encephalopathy

• Other Manifestations include: irritability, confusion, dysarthia, seiqures, coma

• 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

Hypophosphatemia

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

• 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

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

• 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

Hyperkalemia

• Findings– Muscle weakness– Abdominal distention– Diarrhea– Rare finding – flaccid paralysis

• 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

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

• 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 – Emergent TX

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

• Common findings– Muscular weakness– Muscle cramps– Fatigue– Constipation or ileus

Hypokalemia - Signs

• In severe Cases– Flaccid paralysis– Hyporeflexia– Hypercapnia– Tetany– Rhabdomyolysis

Hypokalemia- Signs

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 – plasma sodium levels under <135 mmol x L(-1).

• SEVERE HYPONATREMIA – 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, third-spacing)

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

Serum osmolality

Low(< 280 mosm/kg

Normal (280-295 mosm/kg

High(> 295 mosm/kg

Isotonic hyponatremia1. Hyperproteinemia2. Hyperlipidemia (chylomicrons, 3. triglycerides)

Hypotonic hyponataremia

Hypertonic hyponatremia1. Hperglycemia2. Mannitol, sorbitol, glycerol, maltose3. Radiocontrast agents

Continued next slide

Hyponatremia

Hypotonic hyponatremia

Volume Status

HypovolemicEuvolemic

Hypervolemic

Edematous states1. CHF2. Liver Disease3. Nephrotic syndrome (rare)4. Advanced renal failure

1. SIADH2. Post-op hyponatremia3. Hypothyroidism4. Psychogenic polydipsia5. Beer potomania6. Idiosyncratic drug reaction7. Endurance exercise

UNa+ < 10meq/LExtrarenal salt loss1. Dehydration2. Diarrhea3. Vomiting

UNa+> 20meq/LRenal salt loss1. Diuretics

2. Ace inhibitors3. Nephropathies

4. Mineralocorticoid deficiency5. Cerebral sodium wasting syndrome

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

• 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.

Hypertonic hyponatremia

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

• 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

Hypernatremia- TX

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

• 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

• 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 – Lab Findings

• 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

Hypomagnesemia - TX

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

• 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

Hypermagnesemia

THE END