RESPIRATORY ACIDOSIS

 pH < 7.35,  PaCO2 > 45

 Hydrogen increases

Causes= retained CO2, Hypoventilation, COPD, opioids, atelectasis, pneumonia

Interventions= Bronchodialators, deep breathing

RESPIRATORY ALKALOSIS

 pH > 7.45,  PaCO2 < 35

Decreased Hydrogen

Causes= Exhaled CO2, Hyperventilation Hysteria, anxiety, pain, overdose ASA

Interventions= Rebreather mask, paper bag, sedation

METABOLIC ACIDOSIS

 pH < 7.35,  HCO3 < 22

Increased Hydrogen

Causes= DKA, sever diarrhea, kidney failure, increased lactic acid, high fat diet

Interventions; IV HCO3, dialysis

METABOLIC ALKALOSIS

 pH > 7.45,  HCO3 > 26

Decreased Hydrogen

Causes= Vomiting, GI suctioning, Hypokalemia (body compesates by raising ions which raises K+)

Interventions= Repalce K+, decrease HCO3, monitor labs

COMPENSATORY

RESPIRATORY ACIDOSIS

 Kidney increases HCO3 and excretion of H+

absent= pH abnormal, one component abnormal, second component within normal range

partial= abnormal pH, one component abnormal, second component begining to change

complete= pH within normal range, one component abnormal, second component changed to move pH within normal range

COMPENSATORY

RESPIRATORY ALKALOSIS

 Kidneys decrease HCO3 and excretion of H+

absent= pH abnormal, one component abnormal, second component within normal range

partial= abnormal pH, one component abnormal, second component begining to change

complete= pH within normal range, one component abnormal, second component changed to move pH within normal range

COMPENSATORY

METABOLIC ACIDOSIS

Hyperventilation to increase CO2 elimination

absent= pH abnormal, one component abnormal, second component within normal range

partial= abnormal pH, one component abnormal, second component begining to change

complete= pH within normal range, one component abnormal, second component changed to move pH within normal range

COMPENSATORY

METABOLIC ALKALOSIS

Hypoventilation to decrease CO2 elimination

absent= pH abnormal, one component abnormal, second component within normal range

partial= abnormal pH, one component abnormal, second component begining to change

complete= pH within normal range, one component abnormal, second component changed to move pH within normal range

Osmolarity

The measure of concentration of electrolytes in a fluid

"pulling power" of a solution

Normal concentration of electrolytes in body fluids is between 275-295 mOsm/L

Isotonic solution

concentration is the same as body fluids

285 mOsm/L

Hypertonic solutions

Concentration is >275 mOsm/L

Draws water into circulation

Increases blood volume

Hypotonic solutions

Concentration is <275mOsm/L

Draws water into cells

Decreases Blood volume

ECF

fluid in Vascular and Tissue

provides nourishment

receives wastes

infants have more

Diffusion

Tendency for solutes to move freely throughout a solution.

From a higher concentration to a lower.

O2 and CO2 move by diffusion in th lungs.

Filtration

passage of fluid through a semipermeable membrane

higher concentration to lower

ie. Arterial pressure- hydrostatic pressure

*when pressure inside capillaries are less than the pressure in the interstitial space.

Reabsorbstion

Acts to prevent too much fluid from leaving the capillaries- no matter how much hydrostatic pressure.

*Plasma protein Albumin facillitates reabsorption by pulling fluid back into capillaries.

Colloid Osmotic Pressure

Oncotic pressure, or colloid osmotic pressure, is a form of osmotic pressure exerted by proteins in blood plasma that usually tends to pull water into the circulatory system.

Fluid Balance

Adult intake ranges from 1500-3500ml

average= 2500-2600ml daily

Intake should approximate Output

Sensible Water Losses

Urine, Feces, Persipitation

Insensible Water Losses

Inperceptable ie. water exhaled from lungs, water evaporated from skin

Homeostatic role of Parathyroid

Regulates calcium and phosphorus.

Parathyroid hormone helps pull calcium from bones, kidneys, and intestines into the blood.

Nervous System's Homeostatic Role

Chief regulator of sodium and water intake and excretion.

Thirst Center

Hypothalmus

Neurons/osmoreceptors sensitive to concentration in ECF communicates with ADH

Acid

Substance containing hydrogen that can release the H+ ions= Carbonic Acid

Base

Substance that can accept or trap H+ ions= Bicarbonate

Three buffering systems

Protein

Phosphorus

Bicarbonate

pH of Urine

Typically= 4.5-8.2

Hypovalemia

Isotonic fluid loss

Decreased water/solutes in ECF

Fluid volume defecit

*Hydrostatic/Osmotic pressure force interstitial fluid into intravascular space to compensate for volume loss in blood vessels

*As interstitial space is depleted it's fluid bcomes hypertonic- cellular fluid is then sucked into interstitial space

Third Spacing

Body fluids shifts into pleural spaces, peritoneal, or pericardial areas

Severe Burns, Bowel Obstruction, Hypo-albuminemia

Hypervolemia

Excess water/sodium in ECF

Excess Isotonic fluid

*Kidney Malfunction

Causes edema

Hyponatremia

<135 mEq/L

Caused by decreased NACL or increased H2O

Low sodium causes fluid to move from ECF to ICF

Swelling of cells, cerebral edema, Sz, and permanent brain damage can occur

Hypernatremia

145>mEq/L

Excess water loss or increased sodium

Increases extracellular osmotic pressure- Fluids move out of cells

Can cause neurological impairment

Hypokalemia

K+=<3.5

causes; K wasting diuretics (Lasix), GI fluid loss (vomiting/diarrhea, suctioning), excessive sweating, steroids

S/S; Anorexia, N/V, dysrhythmias, muscle weakness fatigue

Interventions; replace K+, Monitor ECG

Hyperkalemia

K+=>5.0

Causes; Renal Failure, severe burns, K+ sparing diuretics (spironolactone), overuse of K+ salt substitutes

S/S; Tall T waves, muscle weakness, hypotension, Paresthesia (pins/needles)

Interventions; Monitor ECG, increase fluidintake for excretion

Hypocalcemia

<8.5

Causes; bone cancer, parathyroidectomy, hypoparathyroidism, malaborption of Ca+, vitamin D deficiency

S/S; Tetany, Positive trousseau, Positive Chvostek, paresthesia, larangeal spasms, Sz, dysrhythmias

Interventions; Calcium gluconate solution at bedside for pt.s w/ parathyroidectomy

Positive Trousseau

Trousseau sign of latent tetany, observed in patients with low calcium while checking BP with a manual cuff.

Postive Chvostek

Abnormal reaction to the stimualtion of facial nerve caused by low calcium levels

Hypercalcemia

>10.5

Causes; Prolonged immobilization, hyperparathyroidism, bone disease, excess vitamin D

S/S; Muscular weakness, constipation, polyuria, polydipsia, renal calculi, dysrhythmias

Interventions; Monitor I/O, increase fluid intake, increase mobilization, avoid Ca+ based antacids

Hypomagnesium

<1.3

Causes; Chronic alcoholism, malaborption, diarrhea, diuretics, prolonged gastric suction

S/S; Hyperactive reflexes, Sz, Tachyarhythmias, Insomnia, twitching, tremors

Interventions; avoid ETOH use, monitor I/O, Sz precautions

Hypermagnesium

>2.1

 Causes; RARE, Renal failure, Mg+ containing laxitives

S/S; Flushing/Sweating, hypotension, Muscle weakness

Intervention; monitor I/O, BP, and RR, monitor reflexes

Blood Buffers

Main line defence to pH imbalance

Protein

Phosphate

BiCarb

Respiratory pH Balance

Second line defence against pH imbalance

Lungs control carbonic acid supply

CO2 (a bi-product of carbonic acid) is excreted by lungs

Lungs either expell CO2 or conserve it

Intermittent IV Device

"PRN Lock"

Keeps IV reay for use

Meds/KVO(TKO)

Not attached to IV line

Mut be flushed Q8 w/2ml

Infusion Pump

Mandatory for:

• 
  TPN
• Heparin
• Insulin
• CV meds
• Chemotherapy

Central line and PICC

disadvantages

infection

bleeding

air embolism

Central or PICC

how long?

6-8 weeks

Huber Needle

Used for implanted infusion ports

Peripheral IV Sites

Must be checked at least once an hour

Cephalic, Bailic, antebrachial, ad back of hand most common

Phlebitis

Inflammation of the vein

S/S= Erythema, Sclerosis, Warmth, Edema, Tender

Tx= D/C, Warm Compress, Elevate

Thrombophlebitis

Inflammation of veins with blood clots inside the veins.

S/S= Sclerosis, Warmth, Erythema, Tender

Tx= D/C, Restart, Notify practicioner

Hematoma

Infiltration of blood into tissue.

(Can be starting point for thrombophelbitis)

S/S= Ecchymosis, Swelling, Resistance to flush

Tx= Apply pressure, Ice, Elevate

Infiltration

Infiltration is the diffusion or accumulation (in a tissue or cells) of substances not normal to it or in amounts in excess of the normal.

S/S= Cool to touch, edema, pale appearance

Tx= D/C, Restart, Elevate

Extravasation

Infiltration of vesicant med into tissue.

S/S= Pain, Erythema, Necrosis (if severe)

Tx= D/C immediately, Notify physician

*Use large vein w/ high blood flow for vesicant meds

Infection r/t Infusion

S/S= Warmth, Fever, Chills, Swelling, Tenderness

Tx= D/C infusion, notify physician

Prevention= Sterile Technique

Septicemia

Presence of bacteia in the blood.

Can be cused by breaks in sterile technique, cannula insertion, bag or tubing change

S/S= Fever/Chills, Fatigue, Pain, HA, N/V

Circulatory Overload

Excessive Rapid Infusion

S/S= Increased BP, Distended neck veins, Dyspnea, Crackles

Tx= Decrease infusion rate, Notify physician, Elevate HOB, Assess for edema

Gravity Infusion

Adults tolerate-

Adults tolerte 20-60 gt/min

or

80-150mL/hr

Macrodrip(s)

Baxter= 10gtts/mL

Abbott= 15gtts/mL

Microdrip

60gtts/mL

Formula for calculating rate of gravity infusion

amount of solution in mL X DF of tubing

time in minutes

250mg of medication in a solution to be infused at 125ml/hr using Abbott tubing

250 X 15 = 1875= 31gtt/min 

                       60           60   

Formula for calculating rate of gravity infusion

Amount of solution in mL X DF of tubing

time in minutes

Order= 35mL of solution per hour for a child using microdrip tubing

35mL X 60gtt/mL = 2100gtt = 35gtt/min

                      60                  60

IV Therapy Protocols

• Tubing must be changed every 24 hours
• IV bags should not be used for more than 24hours
• peripheral cannulas  and tubing is changed every 48-72hours
• If complication occurs w/ 72 hours interval should be limited to every 48 hours

Hydrostatic Pressure

A pushing pressure at the arterial end of the capillary bed. Forces H2O, Oxygen, an nutrients through capillary walls into interstitial spaces.

Forces fluids out of capillaries.

Changes in hydrostatic pressure will change fluid movement out of the blood.

Colloid Osmotic

Oncotic Pressure

Pressure created by plasma proteins.

This pressure pulls fluid back into capillaries.

Pulls fluid back into blood vessels at venous end of the capillary bed.

Colloid osmotic pressure is like cooking a hot dog in water. The protein attracts water and the hot dog swells. 

Colloid Osmotic pressure exists at both arterial and venous ends of capillary bed but is higher at venous end.

The osmotic gradient pulls fluid back into blood vessels from the interstitial space at the venous end of the capillary bed.

Dominate Cation inside Cell

K+

Potassium

Dominate Cation outside Cell

Na+

Sodium

All cell membranes are permeable to water, but the cell membrane is relatively impermeable to Na+

Sodium Potassium Pump

• A form of Active Transport
• Requires O2 and Glucose
• Powered by energy from metabolism and ATP
• Pumps Na+ out of the cell and K+ into the cell

Cellular mechanism of Hypoxia

Decrease in O2 decreases amount of ATP. Na+ stays in the cell and the cell swell.

Causes of Decreased Oncotic Pressure

Burns

Malnutrition

Nephrosis

Liver Disease

Increased Capillary Permeability

 Protein molecules are too large to pass through the capillary membrane unless the permeability is changed. With protein molecules in the interstitial space, water is attracted and edema results.

Damage to blood vessels, (trauma/burns), proteins leak into interstitial space. The osmotic pull or gradient that would ordinarily pull water back into the blood vessel is reduced. 

Fluid is then pulled from intravascular space into interstitial space= Third Spacing (possibly the abdominal cavity)

Result= Tissue Edema (protein in the interstitial space attracts water)

Lymph Obstruction

When lymph nodes are removed, or in cancer metastasis, fluid and protein are retained in interstitial spaces. The increase in interstitial protein reduces the osmotic gradient and causes water to be held in the interstitial space.

Obstruction to lymph capillaries creates external pressure which forces the lymph fluid out into the interstitial space, causing edema.

Hypervolemia

caused by ▼ of sodium r/t water retention or the effects of ADH

Congestive Heart Failure

Renal Failure

Cirrhosis of the Liver

Cushing's Syndrome

Corticosteroids

Excessive use of salt

Excessive amounts f sodium-containing IV fluids

Hypervolemia's S/S

Weight Gain

Peripheral Edema

Distended Neck Veins

Bounding Pulse

Polyuria

Pulmonary Edema (Moist Rales)

Ascites~ Pleural Effusion

Elevated CVP

Serum Sodium = Normal or Decreased

Hematocrit Decreased

Low BUN (blood urea nitrogen)

Managing Hypervolemia

Tx the problem

Limit fluid intake

Diuretics to promote fluid and sodium loss

Restrict sodium intake to reduce thirs

Hypovolemia

Results in low cardiac output, reduced pressure and decreased renal blood flow. ADH secretion increases and the renin-aldosterone-angiotensin mechanism is triggered.

Reduced renal blood flow=▼glomerular filtration rate

Activates the renin-angiotensis-aldosterone mechanism

The lower blood volume reduces the stretch on the carotid baroreceptors which then triggers ADH release from the pituitary gland.

sodium and water are retained to restore water volume to the vascular bed, and oliguria might be seen.

Third Spacing

A shift of fluid from the vascular bed to the interstitial space. The vascular volume is reduced, but the person will have edematous tissue r/t:

1. lymph obstruction

2. ▲capillary hydrostatic pressure forces more liquid into interstitial space

3. ▲capillary permeability = proteins in interstital space holding fluid there

4. ▼plasma proteins reduce the vascular oncotic pressure and ability to pull water into the vascular bed. Due to - Malnutrition, protein loss from burns, kidney malfunction, inflammation, or liver disease = inability to make albumin

Causes of Hypovolimia

blood loss

reduced fluid intake

excessive water loss

fluid lost in interstitial space

loss of excessive water and sodium from the GI tract or via the urine or skin

Indications of Fluid Deficit

<30ml/hr in urine

drop in BP

weak and rapid pulse

▲Hematocrit

▲BUN

dry mucous membrane - furrow in tongue

drop in body temp

cold clammy skin

oliguria

weight loss

weight gain in 3rd spacing

drop in CVP 

flat neck veins

slow filling hand veins

Tx for Hypovolemia

Determine Renal Function

Isotonic electrolytes (LR) followed by Hypotonic solution (half strength saline)

continue with fluids

Evaluate lung sounds and BP for Fluid Overload

Monitor renal output/function

Cations

Sodium

Potasium

Calcium

Magnisium

Anions

Chloride

Bicarbonate

Phosphate

Protein

Electrolytes in ECF

The ECF has large amounts of sodium, chloride, and bicarbonate.

Electrolytes in ICF

The ICF has large amounts of potassium, phosphate, sulfate, and protein

Increased K+

stimulate aldosterone release from the adrenal gland-

in turn promotes K+ loss from urine

movement of K+ is influenced by:

Changes in pH

Insulin

Adrenal Hormones

Changes in serum sodium

Potassium Functions

Neuromuscular irritability

Cardia impulse conduction and muscle contration

ICF osmolarity

Regulation of acid-base balance

Activation of enzyme reactions

Kidney functions

Hypokalemia occurs from:

• Excessive fluid loss from diarrhea, vomiting, NG suction
• Diuretics (esp. loop diuretics like Lasix)
• Draining wounds/fistulas
• Loss of K= in urine when kidney does not reabsorb K+
• Diuresis in uncontrolled DM = polyuria
• excess aldosterone secretion (hyperaldosteronism)
• Nakabsorption syndromes, malnutrition
• Acid-base- imbalances
• Heart failure (as Na+ and H2O is retained - K+ is lost)
• Laxative abuse
• K+ free IV fluids while pt. is NPO
• Trauma w/ loss of K+ in urine
• IV insulin and glucose
• Stress reaction (excess adrenocortical hormone secretion) 

Hypokalemia S/S

Serum K+ <3.5

Generalized muscle weakness & malaise

Parasthesias - loss of sensation

Cardia dysrhythmias

Enhanced effects of digitalis (Digitalis toxicity)

Decrease or absent reflexes (begins in lower extremities)

Abdominal pain, N/V

Reduced intestinal peristalsis 

Decreased BP

Metabolic alkalosis

Polyuria

Hypovolemic Cardiac S/S

Forceful contraction

Weak pulse

Electrocardiogram = flat/inverted T-wave, U wave present, depressed ST segment, Tall P-waves, prolonged P-R interval, wide QRS interval

V-fib and cardia arrest

supraventricular and ventricular eptoic beats

Tx for Hypokalemia 

• correct cause
• Oral or intravenous admin of K+ (do not use K+ if urine is <600 per day)
• Foods high in K+ + bananas, pear, resh dried apricots, meat, fish, chocolate...

Tx for Hyperkalemia

• Calcium to counteract effect of K+ on heart muscle
• Sodium Bicarbonate to alkalinize body fluids (causes K+ to shift from ECF to ICF)
• Hemodialysis or peritoneal dialysis
• Cation exchange resins (Kayexalate) by mouth or enema pulls K+ and water into intestines)
• Small dose of regular insulin and 50% glucose IV to aid transfer of glucose and K+ into the cells

Aldosterone and K+

Aldosterone promotes K+ loss or gain depending on the serum level of K+

Burns and Hypokalemia

Initially after a thermal burn, K+ will be high since the K+ moves out of the injured cells. However, after a few days, the K+ drops as the excess is eliminated by the kidneys and some begins to move back into cells.

Na+ is regulated by:

Aldosterone

Renal Blood flow

Renin secretion

ADH (due to it's effect on water)

Estrogens

Carbonic Anhydrase Enzyme

Aldosterone

 hormone secreted by the adrenal gland that increases the reabsorption of sodium and water and the release (secretion) of potassium in the kidneys. This increases blood volume and, therefore, increases blood pressure.

Na+ physiological functions

Neuromuscular irritability

Conduction of nerve impulses and muscle Contraction

Osmotic pressure of the ECF

Acid-base balance

Water balance

Gland secretions

Which electrolyte determines tonicity of blood

Na+

Hyperosmolar

an increase of Na+ in blood

Hypo-osmolar

Decrease of Na+ in blood

Excess intake of water/forcing hypotonic fluids

Inability of kidneys to excrete water (renal failure)

Retention of water (as in heart failure or cirrhosis of the liver)

Excess tap water enema

Excess IV fluids of dextrose in water

SIADH (syndrome of inappropriate antidiuretic hormone secretion)

Hyponatremia

• Diuretic therapy
• Burn wounds or wound drainage
• Cystic fibrosis
• Adrenal insufficiency 
• Fluid loss replaced by water only
• Excessive GI loss (loss of bile, NG suction w/ ice chips or water by mouth, using water only for NG tube irrigations)

Hyponatremia

• Serum Na+ < 1.35 mEq/l
• Mental confusion, headache
• Altered level of consciousness, coma
• Hyper-irritability, anxiety
• Tremors, Seizures
• Hyperreflexia, muscle weakness, twitching
• N/V; abdominal cramps
• Edema and weight gain

Manifestations of Hyponatremia

• Hypotension
• Tachycardia
• Cold, clammy skin
• Decreased skin turgor
• Dry mucous membranes
• Weight loss
• Seizures, hyper-irritability 
• Serum Na+ <1.35

Clinical findings of HYPONATREMIA w/ dehydration (w/ Hypovolemia)

Hyperosmolar

Too much sodium in relation to the amount of water. There will either be a deficit of body fluid w/ hypernatremia or hypernatremia in excess of the amount of water.

Decreased water intake due to:

• inability to swallow
• mental confusion, loss of consciousness
• debilitated state
• anorexia, depressed thirst mechanism
• inability to communicate need for water

Excessive water loss, w/out sodium loss; burns sweating, mechanical ventilation, coughing, polyuria

Failure of kidney to reabsorb water

Diabetes Insipidus

Cushing's Syndrome

Excessive use of osmotic diuretics

Causes for Hyperosmolar/Hypernateremia

• Intense thirst
• Flushed, dry skin, poor skin turgor
• Low grade fever
• Weakness, lethargy
• Irritability, agitation, convulsions, tremors
• Increased deep tendon reflexes, Nuchal rigidity
• Dry, sticky mucous membranes, dry rough, red tongue
• Oliguria
• Circulatory overload, shock, resp. distress if condition continues

Indication of Hyperosmolar/Hypernatremia 

Tx for Hypernatremia/Hyperosmolar condition

• Gradual reduction of serum Na+ to prevent cerebral edema
• Use D5/.25% or .45% saline solution (avoid overcorrection causing deficit)
• Monitor urine output and serum sodium levels
• Administer fluids cautiously
• Restrict sodium intake

Calcium Level

8.4 - 10.6 mEq/l

• Parathyroid hormone
• Calcitonin
• Vitamin D
• Estrogens and androgens
• Carbohydrate and lactose

Factors that influence Calcium levels

• Hypoparathyroidism, injury to parathyroid glands during thyroidectomy
• Impaired intestinal absorption from diarrhea, overuse of laxatives or enemas containing phosphorous
• Chronic malabsorption syndromes
• Hyperphosphatemia (occurs in renal failure)
• Alkalosis
• Hyperproteinemia- excess protein in blood
• Chronic renal failure
• Cushing's syndrome (excess adrenal hormones)
• Hypermagnesemia
• Sepsis
• Burns
• Hyperventalation

Causes for Hypocalcemia

• Hypotension
• Altered blood clotting, bleeding (if -- is very low)
• Cardiac dysrhythmias, arrest
• Bradycardia, decreased cardia contractility 
• Tonic/clonic seizures
• Muscle spasms, twitching, cramping

Hypocalcemia

<8.4mEq/l

Tx hypocalcemia

• Oral or intravenous calcium
• Give oral calcium 30 minutes before other meds/meals to aid absorption
• Encourage dietary intake of calcium-e.g. milk, cheese, broccoli
• Careful use of laxatives, antacids and phosphate enemas
• Monitor serum calcium, albumin and clotting levels
• Avoid hyperventilation/respiratory alkalosis

• Prolonged immobility
• Hyperparathyroidism
• Alkalosis
• Thyrotoxicosis (hyperactivity of thyroid)
• Addison's disease (adrenal insufficiency)
• Acute renal failure
• Prolonged use of thiazide diuretics 
• Hypophosphatemia
• Osteoporosis

Causes of Hypercalcemia 

• Hypertension
• Renal calculi accompanied by flank pain
• Polyuria, polydipsia
• Abdominal pain
• Anorexia, N/V, constipation
• Digitalis Toxicity
• Increased cardiac contractility
• Heart block or cardiac arrest w/ large excess of --
• Lethargy, drowsiness
• Pathologic fractures
• Confusion, personality change, depression

S/S of Hypercalcemia

Tx of Hypercalemia

• Encourage weight bearing and physical activity if possible
• Loop diuretics may be used to increase urine output and C++ loss
• Corticosteroids
• Proper use of supplemental vitamins
• Encourage fluid intake
• Monitor for urinary calculi
• Tx malignancies if present
• Hemodialysis
• Meds which inhibit bone resorption

Magnesium

Normal Mg++ = 1.5 - 2.5 mEq/l

about 1/3 of Mg++ is bound to protein

The other 2/3 is free in plasma

Second highest electrolyte in ICF (K+ is 1st)

Mg++ and Ca++ are tied together in function

Functions of Mg++

• Affects skeletal muscles by depressing acetylcholine release at synaptic junctions
• Regulates neuromuscular irritability
• Aids absorption of calcium from the intestine
• Aids calcium metabolism
• Affects parathyroid hormone secretion and therefore intracellular calcium
• Aids transport of K+ and Na+ across cell membranes
• Is required for use of ATP as a source of energy-- Na+ & K+ pump is effected by decreased Mg++
• Activates enzymes which influence protein and nucleic acid synthesis
• Assists in cell metabolism
• Regulates ICF concentration of K+, Ca+, and PO (phosphate)
• Aids in blood clotting

• Hyperirritibility
• tetany, foot and leg cramps, hyperactive reflexes, tremors
• Paresthesia of the legs and feet
• Positive Chvostek's sign
• Vasodilation w/ hypotension and dizziness
• Insomnia, lethargy
• Dyshythmias-- tachycardia, PVCs, V-fib
• ECG changes w/ mild-severe deficits
• Digitalis toxicity
• N/V; anorexia
• Low serum Ca+ and K+
• Low serum calcium that does not improve after Ca+ gluconate
• Serum Mg++ <1.5 mEq/l

S/S of Hypomagnesium

Tx for Hypomagnesium 

• Slow (to prevent cardiac arrest) IV infustion of Mg+ sulfate
• Oral or IM Mg+ sulfate
• Dietary intake of Mg+
• Reduce auditory, visual, mechanical stimulation
• Monitor cardia and neurologic status
• Teach the need to avoid laxative and antacid abuse

• Chronic renal failure
• Aspiration of sea water
• Adrenal insufficiency 
• Hyperparathyroidism
• Hypothyroidism
• Untreated DKA
• Dehydration
• Excessive intake of laxatives or anatacids containing --

Causes of Hypermagnesemia

• Hypotension
• Feeling of warmth and sweating w/ severe depression
• Bradycardia
• ECG changes; prolonged QT interval, heart block
• Cardiac arrest (w/ very high -- levels)
• Lethargy, drowsiness
• Tremors, hyporeflexia
• Muscle weakness
• Flaccid paralysis; respiratory muscle paralysis
• serum -- >2.5 mEq/l

S/S of Hypermagnesemia

Tx for Hypermagnesemia

• Monitor cardiac and respiratory function
• Calcium gluconate IV
• Dialysis for the person who has renal failure
• Stop antacids and laxatives containing Mg+
• Increase fluids

Chloride

95-108 mEq/l

Found in GI fluids

Chloride competes w/ HCO³ to combine w/ Na+

• Metabolic alkalosis
• Heart Failure
• Untreated DKA
• Heat exhaustion
• Ulcerative colitis
• Excessive H+ loss
• Prolonged use of D5 
• Use of HCO³, Lasix, thiazide diuretics, ethacrynic acid
• Acute nfections
• Adrenal insufficiency (Addison's disease)
• Sever Burns

Causes of Hypochloremia

• serum -- level <95mEq/l
• pH >7.45 (kidneys respond to -- drop by reabsorbing HCO³) ~ Hyperirritability, tetany, depressed respirations
• Low K+ and Na+

S/S of Hypochloremia

Tx of Hypochloremia

• IV NaCl
• Ammonium chloride
• Tx the cause

• Cardiac decompensation
• Primary hyperparathyroidism
• Metabolic acidosis (HCO³ excreted, replaced w/ --)
• Respiratory alkalosis
• Drop in ECF HCO³
• Use of Boric acid
• Hyperventilation
• Anemia
• Cushing's syndrome

Causes of Hyperchloremia

• Serum -- level >108mEq/l
• pH <7.35 (a drop in HCO³ causes an ↑in --)
• Symptoms associated w/ metabolic acidosis
• ECG changes
• Stupor, coma
• Deep-rapid breathing (Kussmaul breathing)
• weakness

S/S of Hyperchloremia

Tx of Hyperchloremia

Prevention

Tx the cause

Phosphorus

1.7 - 2.6 mEq/l

The most abundant anion in ICF

Regulated by parathyroid hormone (PTH)

PTH causes PO3−
4  to move from bone to plasma

PO3−
4 enters cell w/ glucose and is lowered after

carb ingestion

Inverse relationship with CA+

An increase in Ca+ will cause the kidney to

excrete the other

• Formationof bone
• Acid-base balance
• Storage and transfer of energy from one site to another

Functions of 

PO3−
4

• Hyperinsulinism
• Continuous administration of IV glucose (in non-diabetic)
• Tx of DKA
• Prolonged respiratory alkalosis
• Excessive use of -- containing antacids
• Malabsorption syndromes
• Hyperalimentation w/ inadequate amounts of --
  
• Alcoholism
• Hyperparathyroidism (serum Ca+ will be elevated)

Causes of Hypophosphatemia 

• Serum -- level <1.2 mEq/l
• Unequal pupils
• Paresthesia
• Muscle weakness; tremors
• Ataxia
• Confusion
• Sz.
• Long Bone Pain
• Shallow respirations
• Dysphagia
• Nystagmus (rapid lateral eye movement)

S/S of Hypophosphatemia

Tx of Hypophosphatemia

• Oral phosphate supplements (mild to moderate deficiencies)
• IV Phosphate for sever deficiencies
• Monitor serum Ca+ closely

• Renal insufficiency or renal failure
• Hypoparathyroidism (w/ increased --, decreased Ca+ and normal renal function)
• Hypocalcemia
• Excessive intake of alkali (e.g. baking soda)
• Excessive intake of vitamin D
• Healing Fx
• Bone tumors
• Addison's disease (adrenal insufficiency)
• LYmphomas
• Increased catabolism states
• use of laxatives on enemas containing large amounts of --

Causes of Hyperphosphatemia

• Serum -- level >3.0 mEq/l
• Tetany (short term)
• Soft tissue calcification (long term)
• Serum Ca+ <4.5mEq/l
• Cardia dysrhythmias and muscle twitching (w/ rapid increase of --, th Ca+ drops, which effects muscles)
• Excess -- will cause grief for the heart muscle, and serum calcium will be low

S/S of Hyperphosphatemia

Tx of Hyperphosphatemia

• A thorough pt. Hx to help find the cause
• Restrict' dietary intake of PO
• Give Rx to bind PO (certain antacids) if ordered
• Monitor serum Ca+ levels
• Observe tetany and cardia dysrhythmias