Transcript NURS 2140 Fluid and Electrolytes Acid Base and IV Therapy

NURS 2140
Fluid and Electrolytes Acid Base
and IV Therapy
Teresa Champion, RN MSN
Metropolitan Community College
Winter 2012
BODY COMPOSITION AND FUNCTION
• PRIMARY FLUID = Water
– 60% total body weight (1 L = 2.2 lbs)
– 2 – 2.5 L of water per day
• TWO PRIMARY FLUID COMPARTMENTS
– Intracellular (ICF)
– Extracellular (ECF)
• FUNCTIONS:
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Transporting
Removing
Regulation
Lubricating
Food Digestion
Intake = Output
Regulation of Body Fluid
• Osmosis – movement of water from lower
particle concentration to higher particle
concentration
• Diffusion – movement of molecules from higher
to lower concentration (simple or facilitated)
• Filtration – movement of molecules through a
semi-permeable membrane from higher
concentration to lower concentration as a result
of hydrostatic pressure
There are two ways
in which substances
can enter or leave a
cell:
1) Passive
a) Simple
Diffusion
b) Facilitated
Diffusion
(carrier)
c) Osmosis (water
only)
2) Active
a) Molecules
b) Particles
Oncotic vs Hydrostatic Pressure
• Filtration is directly opposed by the oncotic pressure of
plasma proteins, especially Albumin in the blood stream.
• Arteriole – high hydrostatic pressure - (~32mmHg)
• Venus – low hydrostatic pressure – (~15 mmHg)
• Plasma oncotic pressure – (~22mmHg)
• http://www.youtube.com/watch?v=VMvD29-Agtg
• http://www.youtube.com/watch?v=mpg7ON2CfFE
• http://www.youtube.com/watch?v=dAO8igIysaA
• Homeostasis - thus in a steady state ECF = ICF
OSMOLALITY
• Number of molecules of solute per kg of water
• NORMAL OSMOLALITY of blood is 275 – 295
milliosmoles per kg (mOsm/kg) of body weight
– Isotonic Fluids - same osmolality as blood plasma)
– Hypotonic Fluids - less concentration than blood plasma
(< 275 mOsm/kg)
– Hypertonic Fluids - greater concentration than blood
plasma (>295 mOsm/kg)
Homeostatic Mechanisms
• Fluid Balance - regulated by:
– Osmoreceptors of the hypothalamus - stimulates release
of ADH and stimulates thirst.
– Baroreceptors (pressure sensitive cells) in carotids and
aorta also stimulate the release of ADH
– Baroreceptors in glomerular arterioles in kidney will
secrete Renin and start the Renin-Angiotension (RAA)
cascade thus resulting in release of aldosterone from
the adrenal glands and cause sodium retention = fluid
retention (water follows sodium)
Role of the Heart
• Atrial Natriuretic Peptide: (ANP): secreted
from atrial cells of heart (in response to too
much volume in the blood)
– acts as diuretic
– inhibits thirst mechanism
– suppresses the RAA cascade
Role of the Kidneys
• Filter approx 180 Liters of blood per day; GFR
(glomerular filtration rate)
• Produces urine between 1-2 Liters/day
• If loss of 1% to 2% of body water, will conserve
water by reabsorbing more water from
filtrate; urine will be more concentrated
• If gain of excess body water, will excrete more
water from filtrate; urine will be more diluted
Lab Tests for Evaluating Fluid Balance
SERUM
Normal Levels
Osmolality
275-295 mOsm/kg of
water
Hematocrit
40-50%*
BUN
5-20 mg/dl
URINE
Normal
Levels
Specific Gravity
1.005 – 1.030
Osmolality
50-1200 mOsm/kg
of water
Sodium
135 – 145 mEq/L
Potassium
3.5 – 5.0 mEq/L
Sodium
40-220 mEq/day
Chloride
95-108 mEq/L
Potassium
25-100 mEq/day
Bicarbonate
(CO2)
22-28 mEq/L -Arteriole
24-30 mEq/L -Venous
Evaluation of Fluid Status
• Normal serum hematocrit
– 40 – 50%
• Dilute serum
– Low hematocrit and electrolyte levels
• Concentrated serum
– Elevated hematocrit and electrolyte levels
Clinical Manifestations of
Overhydration and Dehydration
OVERHYDRATION
DEHYDRATION
Crackles in lungs
Dry mouth and tongue, mucous membranes
S3 Heart Sound
Tachycardia
Dyspnea
Severe thirst (maybe not in elderly)
Reduced blood oxygen levels and increased
CO2 levels – respiratory acidosis
Increased temperature (may rise 1 or 2 degrees)
Bounding pulses
Weak pulses
Increased blood pressure
Orthostatic Hypotension, systemic hypotension
Increased edema, ascites
“tenting” skin
Increased neck swelling – jugular vein
distension
Flat neck veins
Decreases in HCT, Serum Osmolality, Serum
Sodium, Potassium, Chloride, Bicarbonate,
BUN; Urine Specific Gravity < 1.005; Urine
Osmolality >1,200 mOsm/kg
Increases in HCT, Serum Osmolality, Serum
Sodium, Potassium, Chloride, Bicarbonate, BUN,
Creatinine; Urine specific Gravity >1.030; Urine
Osmolality < 50 mOsm/kg
Nursing Considerations
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Assess for headache, dizziness, syncope
CHF-SOB, dyspnea, activity intolerance
Maintaining accurate I & O
Daily weights
Monitoring Lab values
Frequency and consistency of stools
Meals include adequate fluid intake
Dehydration in the Elderly
Increased risks for dehydration:
•Decrease in thirst
•Lack of fluid replacement
•Use of diuretic medications for
high BP
•Susceptibility to contagious
diseases
Nursing Care Plan
Dehydration
• Risk for imbalanced Fluid
Volume Related to excessive
fluid loss/inability to take in
fluids AEB ….
Overhydration
• Risk for Imbalanced Fluid
Volume Related to excessive
fluid intake/decreased
urination AEB ….
Electrolytes
– Substance that develops an electrical charge when
dissolved in water
• Cation - positive charged
• Anion - negative charged
• Examples of cations: Sodium, Potassium,
Magnesium, Calcium
• Examples of anions: Chloride, Bicarbonate,
Phosphorous
Sodium
Normal serum values
135-145 mEq/L
• Most abundant cation in ECF
• Functions
– ECF volume – water balance
– Acid-base balance
– Nerve impulse control – sodium potassium pump
– Levels below 115 mEq/L – brain damage, seizures
– Sodium is primarily excreted through the kidneys, but
other avenues are GI Secretions and sweat.
Sodium Deficit - Levels < 135 mEq/L
Hyponatremia
• Loss through GI tract, skin or kidneys
• An increased amount of sodium shift into the
cells when there is a potassium deficit
• An excessive ADH release (SIADH) causing
Water retention and sodium deficit
• Inadequate sodium intake, increased water
intake
• Excessive use of 5% dextrose solution
• Levels below 115 mEq/L – brain damage
Pathophysiology of decreased sodium
imbalances
• CNS – excess water moves into the cerebral
tissues – increased intracranial pressure
• GI – loss causes acid base imbalances
• Kidneys – renal dysfunction promotes sodium
and water retention resulting in diluted
sodium level (fluid overload)
• Cellular activity - decrease in Na-K pump
Causes of Hyponatremia
• Dietary changes – low sodium intake, excessive water
intake, “fad diets”/fasting, anorexia nervosa, prolonged
use of IV D5W
• GI Losses – vomiting, diarrhea, GI Suctioning, Tap water
enemas, GI surgery, Bulimia.
• Renal Loses – Salt wasting kidney disease, diuretics.
• Hormonal Influences - ADH, SIADH.
• Decreased adrenocortical hormone: Addison’s disease.
• Altered Cellular Function – Hypervolemic state: heart
failure, cirrhosis
• Burns
• Skin
Sodium Excess - Levels > 145 mEq/L
Hypernatremia
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Excessive secretion of aldosterone or cortisol
Excessive sodium intake
Decreased water intake
GI disorders
Decreased renal function
Pathophysiology of increased sodium
imbalances
• Overproduction of adrenal hormones –
excessive secretions of aldosterone and
cotrisol promote an increase in the sodium
level
• Cellular activity – increases the sodium pump
action, causes cellular irritability.
Causes of Hypernatremia
• Dietary Changes – Increased sodium intake, decreased
water intake, Administration of 3% saline solutions
• GI Disorders – severe vomiting, Diarrhea
• Decreased Renal Function – reduced glomerular
filtration
• Environmental Changes – Increased temperature and
humidity, water loss
• Hormonal Influence – Increased adrenocortical
hormone production: oral or IV cortisone or Cushing's
syndrome.
• Altered Cellular Function – Heart Failure, Renal
Diseases
• Trauma – Head injury
Clinical Manifestations of Sodium
Imbalances
Hyponatremia
• Nausea, vomiting, diarrhea,
abdominal cramps
• Tachycardia, hypotension
• Headaches, apprehension,
lethargy, confusion, depression,
seizures
• Muscle weakness
• Dry skin, pale dry mucus
membranes
• Serum Na <135 mEq/L
• Serum osmolality < 275 mOsm/kg
• Urine Specific Gravity <1.005
• Urine Sodium >220 mEq/day
Hypernatremia
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Nausea, vomiting, anorexia
Rough, dry tongue
Tachycardia, possible hypertension
Restlessness, agitation, stupor,
elevated body temperature
Muscular twitching, tremor,
hyperreflexia
Flushed, dry skin and dry sticky
membranes
Serum Na >145 mEq/L
Serum osmolality > 295 mOsm/kg
Urine Specific Gravity >1.030
Urine Sodium < 40 mEq/day
Chloride
Normal Levels
95-108 mEq/L
• Primary extracellular anion
• Creates electrical neutrality when combined with
sodium
• Body Water Balance
• Hydrochloric acid
• Buffers carbonic acid
• Anion gap - calculated AG = (Na + K) – (Cl + HC03
(metabolic acidosis)
Hypochloremia <95 mEq/L
• Causes
– Loss of gastric fluid
– Osmotic diuresis
• Manifestations
– Reflects alkalosis
– Paresthesias, muscle spasms, slow respirations
– Dehydration
Hyperchloremia > 108 mEq/L
• Causes
– Hyperparathyroidism, dehydration
– Respiratory acidosis
• Manifestations
– Lethargy, disorientation
– Increased rate and depth of respirations
Chloride
• Primary extracellular anion
• Creates electrical neutrality when combined
with sodium
• Hydrochloric acid
• Buffers carbonic acid
• Anion gap - calculated AG = (Na + K) – (Cl +
HC03 (metabolic acidosis)
Potassium
Normal serum values
3.5- 5.0 mEq/L
• Most abundant cation in ICF
• Functions
– Transmission and conduction of nerve impulses and the
contraction of skeletal, cardiac and smooth muscles (na-K
pump)
– Assists with regulation intracellular osmolality
– Enzyme production for cellular metabolism
– Maintains Acid-base Balance
– Levels less than 2.5 mEq/L and greater than 7.0 mEq/L can
cause cardiac arrest
– Potassium is excreted through the kidneys (80-90%) and
feces (10-20%)
Potassium Deficit - Levels < 3.5 mEq/L
Hypokalemia causes
• Dietary changes – decrease in dietary intake
• Cellular Potassium Loss – Tissue Injury, Muscle
contraction
• GI losses – vomiting, diarrhea, GI suctioning, intestinal
fistula, laxative abuse, bulimia, enemas
• Hormonal Influences – Aldosterone (Cushing
syndrome), licorice, Stress
• Drugs – adrenergic, epinephrine, decongestants,
amphotericin B, beta2 –adrenergic agonist,
aminoglycosides, large doses of penicillins, potassium
wasting diruetics, steroids
• Redistribution - Insulin, alkalotic states
• Electrolyte loss - Magnesium
Potassium Excess - Levels > 5.0 mEq/L
Hyperkalemia causes
• Dietary – excessive intake, supplements, salt
substitutes, herbal juices
• IV Potassium replacements – with poor renal function
• Decreased renal function – acute and chronic renal
failure
• Altered Cellular Function – injury, metabolic acidosis,
stored blood >1-3 weeks old
• Hormonal Deficiency – Addison’s disease
• Drugs – K-sparing diuretics, ACE inhibitors, beta
blockers
• Pseudohyperkalemia – poor blood samples
Clinical Manifestations of Potassium
Imbalances
Hypokalemia
• GI – anorexia, N/V, diarrhea,
abdominal distention, decreased
peristalsis or ileus
• Cardiac – dysrhythmias, vertigo
(dizziness), cardiac arrest
• ECG – Flat or inverted T waves,
depressed ST
• Renal – polyuria
• Neuromuscular – malaise,
drowsiness, muscular weakness,
confusion, mental depression,
diminished deep tendon reflexes,
respiratory paralysis
• Lab Values - <3.5 mEq/L
• Alkalosis
Hyperkalema
• GI – Nausea, Diarrhea, Abdominal
Cramps
• Cardiac – tachycardia, then
bradycardia and then cardiac
arrest
• ECG - Peaked T waves, shortened
QT interval, prolonged PR followed
by a disappearance of the P wave,
Prolonged QRS.
• Renal - oliguria or anuria
• Neuromuscular – weakness,
numbness or tingling sensation,
muscle cramps
• Lab Values - > 5.0 mEq/L
• Acidosis
Hypokalemia – flattened, inverted T
wave with a U wave sometimes
present
Hyperkalemia – peaked T Wave
CLINICAL MANAGEMENT OF
POTASSIUM IMBALANCES
Hypokalemia
• Oral supplements (tablets,
capsules, liquid)
– Oral potassium is very irritating to
the gastric mucosa and should be
given diluted and not on an empty
stomach
• IV Potassium DILUTED in an IV
Solution
– Never more than 10mEq of KCL per
hour
– Never given undiluted as a bolus
injection
– For life threatening hypokalemia
(<2.6 mEq/L) 30-40 mEq of KCL can
be diluted in 100 – 150 ml of IV
Fluid and administered in a central
line over an hour.
Hyperkalemia
• Potassium Restriction
• IV Sodium bicarbonate (NaHCO3)
– moves K back into the cells –
temporary tx
• 10% Calcium gluconate
– decreases irritability of myocardium,
does not promote K loss, use
cautiously with patients on digitalis
• Insulin and glucose – (10 units of
Insulin and 50% dextrose)
– Moves K back into the cells
• Kayexalate (sodium polystyrene)
and sorbitol 70%
– Cation exchange
• Dialysis
Drugs that effect Potassium Balances
Hypokalemia
• Laxatives and enemas
• Corticosteroids
• Antibiotics
• Potassium-wasting diuretics
• Beta2 agonists
Hyperkalemia
• Oral and intravenous K
• Central nervous system
agents
• Potassium sparing diuretics
• ACE inhibitors
• Beta blockers
• Heparin/Lovenox
• NSAIDS
Calcium
Normal serum values 8.5- 10.5 mg/dL
Ionized Calcium 4.0 – 5.0 mg/dL
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Cation found in both ECF and ICF, but greater concentration in ECF
Maintains cellular membrane stability
98% in bones and teeth, 2% in the serum
Of the 2% in serum - 45% is bound to albumin and 50% is ionized
calcium – physiologically active
Serum pH greatly affects calcium levels – metabolic acidosis
increases ionized calcium levels, alkalosis opposite effect
Normal ionized Ca levels are 4.0 to 5.0 mg/dL
Serum Ca levels are regulated by Vitamin D, calcitonin (thyroid
glad) and parathyroid hormone (PTH) from parathyroid gland
There is a direct relationship between Ca and Phosphorous, when
Ca is low Phosphorous is high and vise versa.
Calcium Regulation
When serum Calcium is low:
• PARATHYROID GLAND
releases PTH. PTH mobilizes
calcium from the bone,
increases renal
reabsorption of calcium and
promotes calcium
absorption in the intestines
in the presence of Vitamin
D to increase serum
Calcium levels
When serum Calcium is High:
• THYROID GLAND – releases
Calcitonin. Calcitonin
increases calcium return to
the bone and decreases
serum Calcium levels
Functions of Calcium
• Neuromuscular
– normal nerve and muscle activity, causes transmission of nerve
impulses and contraction of skeletal muscles.
• Cardiac
– contraction of the myocardium (heart muscle)
• Cellular and Blood
– maintenance of normal cellular permeability - decreased
calcium increases cellular permeability
– Coagulation of blood. Promotes clotting by converting
prothrombin into thrombin
• Bone and teeth construction
– Calcium along with phosphorous forms bones and teeth make
them strong and durable
Calcium Deficit - Levels < 8.5 mg/dL
and Ionized Ca is <4.0 mg/dL
Hypocalemia causes
• Dietary changes – lack of calcium intake (rare), inadequate
Vitamin D, inadequate protein intake, hypoalbuminemia*,
chronic diarrhea
• Hormone and electrolyte influence – decreased PTH (thyroid
surgeries), increased serum phosphorous, decreased
magnesium
• Calcium Binders or Chelators - citrated blood transfusions
• Alkalosis
• Increased serum albumin* (low ionized Ca)
• Renal Failure – decreases phosphorous excretion and results
in excessive Ca Loss
• GI Surgery, Pancreatitis and Small Bowel disease
Calcium Excess - Levels >10.5 mg/dL
and Ionized Ca is >5.0 mg/dL
Hypercalemia causes
• Primary hyperparathyroidism
• Bone malignancy, fractures and immobility
• Drug toxicity (lithium carbonate, vitamin a and d,
thiazides)
• Excessive use of calcium supplements, anti-acids
and calcium salts
• Renal Impairment and diuretics (thiazides)
• Steroid therapy
• Decreased serum phosphorous
Clinical Manifestations of Calcium
Imbalances
HYPOCALCEMIA
• CNS and Muscular
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Anxiety, irritability
Tetany, muscle twitching (Chvostek’s sign)
Numbness and tingling
Carpopedal spasm (Trousseau’s sign)
Convulsions
Abdominal and muscle cramps
• Cardiac
– Weak contractions
– ECG/EKG lengthened ST segment and
prolonged QT interval
• Blood
– reduction in prothrombin (reduced
clotting)
• Bone
– With prolonged deficiency – fractures
occur easily
HYPERCALCEMIA
• CNS and Muscular
– Depression/apathy
– Weak, flabby muscles
• Cardiac
– Signs of heart block
– Cardiac arrest in systole
– Decreased or diminished ST
segment and shortened QT interval
• Bone
– Pathologic fracture
– Deep pain over bony areas
– Thinning of bones
• Renal
– Flank pain
– Calcium stones in kidney
Important Clinical tests for
Hypocalemia
Chvotsek’s Sign
• https://www.youtube.com/
watch?v=ep6IEqnyxJU
Trousseau’s Sign
• https://www.youtube.com/
watch?v=H13yn9AwtPY&fe
ature=relmfu
ECG changes with Calcium Imbalances
• Normal ST segment and
QT Interval
• Hypocalcemia – ST
segment is lengthened,
QT interval is prolonged
• Hypercalcemia – ST
segment is shortened,
QT interval is shortened
Clinical Management of Calcium
Imbalances
Hypocalcemia
• Oral supplements and IV
calcium diluted in D5W (not
normal saline)
– IV calcium should be given
slowly at 1-3ml/min
• Vitamin D supplements
Hypercalcemia
• Treat underlying cause
• IV Normal Saline
• Loop Diuretics
• Calcitonin SQ
• IV phosphates
• Others:
– Corticosteroids
– Antitumor antibiotics
MAGNESIUM
Normal serum values
1.4- 2.1 mg/dL
• Intracellular Cation (2nd most)
• Only 1% of body magnesium is in the blood serum the rest is
stored in muscle and bone
• Of the 1% - 2/3 is ionized (free) and 1/3 is bound to plasma
proteins
• When calcium absorption goes up magnesium absorption goes
down
• Alcohol decreases magnesium absorption
• Many of the same foods rich in potassium and also rich in
magnesium (green vegetable, whole grains, fish, seafood and
nuts).
• Mg deficiency is usually asymptomatic until <1.0 mg/dL
Functions of Magnesium
• Neuromuscular activity transmission
• Contracts the heart muscle
• Cellular
– Activates enzymes for carbohydrate and protein
metabolism
– Responsible for proper transportation of sodium and
potassium across cell membranes
– Influences utilization of K, Ca, and proteins
– Magnesium deficits are FREQUENTLY accompanied by
a Potassium and/or Calcium deficit
Magnesium deficit < 1.4 mg/dL
Hypomagnesemia Causes
• Dietary – inadequate intake, mal absorption, GI losses,
TPN, malnutrition, starvation, chronic alcoholism, GI
fistulas, chronic use of laxatives, chronic diarrhea
• Renal Dysfunction – diuresis in diabetic ketoacidosis
and in ARF in the diuretic phase
• Cardiac dysfunction – post MI, prolonged diuretic
therapy with CHF
• Electrolyte and Acid/Base Influences – hypocalcemia,
hypokacemia, metabolic alkalosis
• Drug influence – potassium wasting diuretics,
aminoglycosides, cortisone, amphotericin B, digitalis
Magnesium excess > 2.1 mg/dL
Hypermagnesemia Causes
• Dietary – prolonged use/excessive use of
magnesium-containing anta-acids (Maalox),
laxatives (MOM) and IV magnesium sulfate
• Renal Dysfunction – Renal insufficiency and
failure
• Severe Dehydration – Diabetic ketoacidosis
Clinical Manifestations of Magnesium
Imbalances
Hypomagnesemia
• Neuromuscular –
hyperirritability, tetany-like
symptoms, tremors,
twitching of the face,
spasticity, increased tendon
reflexes
• Cardiac – Hypertension,
cardiac dysrhythmias PVC’s, VT (Torsades), VF, and
flat or inverted T wave, ST
depression (like low K levels)
Hypermagnesemia
• Neuromuscular – CNS
depression, lethargy,
drowsiness, weakness,
paralysis, loss of deep tendon
reflexes
• Hypotension, Complete heart
block (3rd degree), bradycardia,
Widened QRS complex,
prolonged QT interval
• Others: Flushing, respiratory
depression
Hypomagnesemia
Clinical Management of Magnesium
Imbalances
Hypomagnesemia
• Oral or IV replacements
• Diet high in magnesium green vegetables, whole
grains, legumes, nuts
Hypermagnesemia
• Correct the underlying
cause
• IV saline or calcium
• Dialysis
Phosphorous
Normal levels
2.5 – 4.5 mg/dL
• Major Intracellular anion
• Needed for metabolism, nerve and muscle
function
• Part of energy units
• Component of phospholipids (cellular and
organelle membranes)
• Regulated by calcitonin, parathyroid hormone
AND Vitamin D
• Levels vary with acid-base balance
• Glucose, insulin or sugar-containing foods
temporarily shift phosphorous into the cells
Functions of Phosphorous
• Neuromuscular – normal nerve and muscle activity
• Bones and teeth – bone and teeth formation,
strength and durability
• Cellular
– forms high energy compounds (ATP, ADP, AMP), is the
backbone of nucleic acids and stores metabolic energy
– Formation of red blood cell enzyme (2,3diphosphoglycerate) that delivers oxygen to tissues
– Utilization of B vitamins
– Metabolism of fats, carbohydrates and proteins
– Maintenance of ACID BASE balance in body fluids
Phosphorous deficit < 2.5 mg/dL
Hypophosphatemia Causes
• Dietary - Vitamin D deficiency, chronic
alcoholism TPN
• GI – malabsorption, vomiting, diarrhea
• Hormonal Influence – Hyperparathyroidism
(increased PTH)
• Drugs – aluminum containing antacids (binders),
diuretics
• Cellular – Diabetic Ketoacidosis
• Acid-Base disorders – Respiratory alkalosis,
metabolic alkalosis
Phosphorous excess > 4.5 mg/dL
Hyperphosphatemia Causes
• Dietary – excessive administration of
phosphorous containing substances
• Hormonal – lack of PTH
• Renal Insufficiencies – Renal Failure (ARF, CRF)
• Drug – frequent use of phosphate laxatives
• Cellular destruction – chemo, radiation,
rhabdomyolsis (breakdown of striated muscle)
• Acid-Base disorders – Metabolic and Respiratory
Acidosis
Clinical Manifestations of Phosphorous
Imbalances
Hypophosphatemia
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Hyperphosphatemia
Neuromuscular – muscle
• Neuromuscular – Tetany (with
weakness, tremors,
decreased calcium),
paresthesia, bone pain,
hyporeflexia, seizures,
hyperreflexia, muscular
delirium, hallucinations,
weakness (more common with
ascending motor paralysis
hypophosphatemia), flaccid
Hematologic – tissue hypoxia,
paralysis
possible bleeding, possible
infection
• Cardiopulmonary –
Cardiopulmonary – weak
tachycardia
pulse, hyperventilation,
respiratory weakness
• GI- nausea, diarrhea,
GI – Anorexia, dysphagia
abdominal cramps
Clinical Management of Phosphorous
Imbalances
Hypophosphatemia
• Oral phosphorous
replacements
• Treat underlying causes
• Diet high in phosphorous
• Avoid phosphorous binding
antacids
• IV phosphorous (only when
levels are below 1 mg/dl)
dose 12-15 mmol/L diluted
in IV fluid
Hyperphosphatemia
• Phosphorous binding antacids
• Calcium based antacids are
preferred in renal failure to
avoid hypermagnesemia
• If hyperphosphatemia is
accompanied by hypocalcemia
correcting calcium level will
reduce phosphorous levels
• Administer Insulin and glucose
ACID BASE IMBALANCES
NURS 2140
Winter 2012
Teresa Champion, RN, MSN
ACID BASE BALANCE
• Hydrogen ions - Low concentrations but highly
reactive
– Concentration affects physiological functions, for
example:
• Alters protein and enzyme functioning
• Can cause cardiac, renal, respiratory abnormalities
• Alters blood clotting, metabolization of meds
Acid and Bases
• Acids – compounds that form hydrogen ion in a
solution
– Proton donors
– Strong acids give up their hydrogen ion easily
– Weak acids hold on to their hydrogen ion more tightly
• Bases – compounds that combine with hydrogen
ion in a solution
– Proton acceptors
– Neutralizes
• 20:1 ratio (20 parts bicarbonate to one part
carbonic acid)
The Basics explained:
• pH is a measurement of the acidity or alkalinity of
the blood.
• It is inversely proportional to the number of
hydrogen ions (H+) in the blood.
– The more H+ present, the lower the pH will be.
– The fewer H+ present, the higher the pH will be.
Plasma pH
• Inversely related to hydrogen ion
concentration
– ↑ hydrogen ion concentration, ↓ pH
– ↓ hydrogen ion concentration, ↑ pH
Body Acids
• Respiratory Acid - CO2 – eliminated by lungs (daily
~288L/day)
• Metabolic acids: (either excreted by kidney or
metabolized in liver and Production: 0.1 mol (100
mEq)/day. Eliminated more slowly than respiratory acid
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Lactic acids
Pyruvic acid
Ketoacids (DKA)
Acetoatic acids
Beta-hydrobutyric acids
Normal Blood pH
• The normal blood pH range is 7.35 to 7.45.
– Slightly alkalotic
– Must maintain this range for normal body
functions
• < 7.35 Blood pH is acidotic
• > 7.45 blood pH is alkalotic
• This is the FIRST step in interpretation of
Arterial Blood Gases and plasma pH.
BUFFER SYSTEMS
• Extracellular Buffers
– carbonic acid (lungs) and bicarbonate (kidneys)
• Intracellular Buffers
– Phosphate Buffer System
• Dihydrogen phosphate (H2PO4) – hydrogen donor
• Hydrogen phosphate (HPO4) – hydrogen acceptor
• Protein Buffers
– Plasma Proteins
– Hemoglobin – oxyhemoglobin and deoxygenated Hgb
• Bones
– Carbonate and phosphate salts in bone provide a long term
supply of buffer.
Role of the lungs
• Regulate plasma pH minute to minute by
regulating the level of Carbon Dioxide (CO2)
• Carbon Dioxide is measured as a partial
pressure of carbon dioxide in arterial blood –
PaCO2 35-45mmHg
• Lungs alter rate and depth of ventilations in
order to retain or excrete CO2
Minute Volume – Tidal Volume
• Ventilation is measured by how much air the lungs
move in one minute (minute ventilation)
• Minute Ventilation is the product of respiratory rate
and depth and is referred to as the TIDAL VOLUME
(Vt)
• NORMAL tidal volume at rest is about 500ml.
• Aveolar volume = tidal volume – anatomical dead
space
• Aveolar minute ventilation = respiratory rate x
alveolar volume
Terms for Respiration
• Hypercarbic Drive – increased PaCO2 levels raise
the level of H+ ions, lowering pH. Central
Chemorectptors (in CNS) stimulate the phrenic
nerve, increasing respiration
• Hypoxic Drive – peripheral chemoreceptors in
carotid arteries and arch of aorta are stimulated
by low PaO2 level (<60mmHg) increasing
respiratory rate.
• Hypocapnia – Low PaCO2 (<35)
• Hypercapnia – High PaCO2 (>45)
The role of the Kidneys
• Two main functions to maintain acid/base
– Secrete hydrogen ions
– Restore or reclaim bicarbonate
• Secretion – active process of moving substances from
blood into the tubular fluid against a concentrated
gradient, for example hydrogen ions.
• In high metabolic acidosis, the kidneys can excrete
ammonia as a urinary buffer.
• In alkalosis - the kidneys retain hydrogen ion and
excrete bicarbonate to correct the pH.
• In acidosis - the kidneys excrete hydrogen ion and
conserve bicarbonate to correct the pH.
Assessment of ACID BASE
• Arterial Blood Gases (ABG) most often and the most
accurate to assess acid base balances.
• Serum Electrolytes can help fine tune acid base
analysis
• NORMAL ABG VALUES:
• pH = 7.35 to 7.45
• PaCO2 = 35 – 45 mEq/L (40 mEq/L – middle range)
• HCO3 = 22 – 28 mEq/L
Steps to Interpret ABG’s
1. Assess the pH
2. Assess the respiratory component – PaCO2
3. Assess the metabolic component – HCO3,
base excess
4. Evaluate compensation
Respiratory Acidosis
• High PaCo2 (>45 mEq/L) with resultant drop in
in pH (<7.35 - acid)
• Respiratory system fails to eliminate the
appropriate amount of carbon dioxide to
maintain the normal acid-base balance
• Caused by pneumonia, drug overdose, head
injury, chest wall injury, obesity, asphyxiation,
drowning, or acute respiratory failure
• Medical treatment
– Improve ventilation, which restores partial pressure
of carbon dioxide in arterial blood (Paco2) to normal
Respiratory Acidosis
• Nursing care
– Assess Paco2 levels in the arterial blood, and pH.
– Observe for signs of respiratory distress:
restlessness, anxiety, confusion, tachycardia
• Intervention
– Encourage fluid intake
– Position patients with head elevated 30 degrees
Respiratory Alkalosis
• Low PaCO2 (< 35 mEq/L) with a resultant rise in pH
(>7.45 – alkalotic)
– Most common cause of respiratory alkalosis is
hyperventilation – usually caused by pain, anxiety
• Medical treatment
• Major goal of therapy: treat underlying cause of condition; sedation
may be ordered for the anxious patient
• Nursing care
– Intervention
• In addition to giving sedatives as ordered, reassure the patient to
relieve anxiety
• Encourage patient to breathe slowly, which will retain carbon dioxide
in the body
Metabolic Acidosis
• Body retains too many hydrogen ions or loses too
many bicarbonate ions; with too much acid and
too little base, blood pH falls (pH <7.35)
• Causes are starvation, dehydration, diarrhea,
shock, renal failure, and diabetic ketoacidosis
• Signs and symptoms: changing levels of
consciousness, headache, vomiting and diarrhea,
anorexia, muscle weakness, cardiac dysrhythmias
• Medical treatment: treat the underlying disorder
Metabolic Acidosis cont’d
• Nursing care
– Assessment of the patient in metabolic acidosis
should focus on vital signs, mental status, and
neurologic status
– Emergency measures to restore acid-base balance.
Administer drugs and intravenous fluids as
prescribed. Reassure and orient confused patients
Metabolic Alkalosis
• Increase in bicarbonate levels or a loss of hydrogen
ions and increases pH (>7.45)
• Causes:
– Loss of hydrogen ions may be from prolonged
nasogastric suctioning, excessive vomiting, diuretics, and
electrolyte disturbances
• Signs and symptoms:
– headache; irritability; lethargy; changes in level of
consciousness; confusion; changes in heart rate; slow,
shallow respirations with periods of apnea; nausea and
vomiting; hyperactive reflexes; and numbness of the
extremities
• Medical treatment
– Depends on the underlying cause and severity of the
condition
Metabolic Alkalosis
• Nursing care
– Assessment
• Take vital signs and daily weight; monitor heart rate, respirations,
and fluid gains and losses
• Keep accurate intake and output records, including the amount of
fluid removed by suction
• Assess motor function and sensation in the extremities; monitor
laboratory values, especially pH and serum bicarbonate levels
• Intervention
– To prevent metabolic alkalosis, use isotonic saline solutions
rather than water for irrigating nasogastric tubes because
the use of water for irrigation can result in a loss of
electrolytes