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Body Fluid Compartments
2/3 (65%) of TBW is intracellular (ICF)
1/3 extracellular water
25 % interstitial fluid (ISF)
5- 8 % in plasma (IVF intravascular fluid)
1- 2 % in transcellular fluids – CSF, intraocular fluids,
serous membranes, and in GI, respiratory and urinary
tracts (third space)
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Fluid compartments are separated by
membranes that are freely permeable to
water.
Movement of fluids due to:
hydrostatic pressure
osmotic pressure\
Capillary filtration (hydrostatic) pressure
Capillary colloid osmotic pressure
Interstitial hydrostatic pressure
Tissue colloid osmotic pressure
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Balance
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Solutes – dissolved particles
Electrolytes – charged particles
Cations – positively charged ions
Na+, K+ , Ca++, H+
Anions – negatively charged ions
Cl-, HCO3- , PO43-
Non-electrolytes - Uncharged
Proteins, urea, glucose, O2, CO2
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Body fluids are:
Electrically neutral
Osmotically maintained
Specific number of particles per
volume of fluid
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Homeostasis maintained
by:
Ion transport
Water movement
Kidney function
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Tonicity
Isotonic
Hypertonic
Hypotonic
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Cell in a
hypertonic
solution
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Cell in a
hypotonic
solution
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Movement of body fluids
“ Where sodium goes, water follows.”
rapid
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Makulay ang Buhay sa Sinabawang
Gulay
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Regulation of body water
ADH – antidiuretic hormone + thirst
Decreased amount of water in body
Increased amount of Na+ in the body
Increased blood osmolality
Decreased circulating blood volume
Stimulate osmoreceptors in
hypothalamus
ADH released from posterior pituitary
Increased thirst
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Result:
increased water consumption
increased water conservation
Increased water in body, increased
volume and decreased Na+ concentration
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Dysfunction or trauma can cause:
Decreased amount of water in body
Increased amount of Na+ in the body
Increased blood osmolality
Decreased circulating blood volume
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Edema is the accumulation of fluid within the
interstitial spaces.
Causes:
increased hydrostatic pressure
lowered plasma osmotic pressure
increased capillary membrane permeability
lymphatic channel obstruction
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Hydrostatic pressure increases due to:
Venous obstruction:
thrombophlebitis (inflammation of veins)
hepatic obstruction
tight clothing on extremities
prolonged standing
Salt or water retention
congestive heart failure
renal failure
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Decreased plasma osmotic pressure:
↓ plasma albumin (liver disease or
protein malnutrition)
plasma proteins lost in :
glomerular diseases of kidney
hemorrhage, burns, open wounds
and cirrhosis of liver
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Increased capillary permeability:
Inflammation
immune responses
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Fluid accumulation:
increases distance for diffusion
may impair blood flow
= slower healing
increased risk of infection
pressure sores over bony
prominences
Psychological effects
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Edema of specific organs can be life
threatening (larynx, brain, lung)
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Electrolyte balance
Na + (Sodium)
90 % of total ECF cations
135 -145 mEq / L
Pairs with Cl- , HCO3- to neutralize charge
Low in ICF
Most important ion in regulating water
balance
Important in nerve and muscle function
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Regulation of Sodium
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Potassium
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Regulation of Potassium
Through kidney
Aldosterone
Insulin
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Isotonic alterations in
water balance
Occur when TBW changes are
accompanied by = changes in
electrolytes
Loses plasma or ECF
Isotonic fluid loss
↓ECF volume, weight loss, dry skin
and mucous membranes, ↓ urine
output, and hypovolemia ( rapid
heart rate, flattened neck veins, and
normal or ↓ B.P. – shock)
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Isotonic fluid excess
Excess IV fluids
Hypersecretion of aldosterone
Effect of drugs – cortisone
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No Dandruff,Just Soft
Hair
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Electrolyte imbalances:
Sodium
Hypernatremia (high levels of
sodium)
Plasma Na+ > 145 mEq / L
Due to ↑ Na + or ↓ water
Water moves from ICF → ECF
Cells dehydrate
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Hypernatremia Due to:
Hypertonic IV soln.
Oversecretion of aldosterone
Loss of pure water
Long term sweating with chronic
fever
Respiratory infection → water vapor
loss
Diabetes – polyuria
Insufficient intake of water
(hypodipsia)
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Clinical manifestations
of Hypernatremia
Thirst
Lethargy
Neurological dysfunction due to
dehydration of brain cells
Decreased vascular volume
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Treatment of
Hypernatremia
Lower serum Na+
Isotonic salt-free IV fluid
Oral solutions preferable
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Hyponatremia
Overall decrease in Na+ in ECF
Two types: depletional and dilutional
Depletional Hyponatremia
Na+ loss:
diuretics, chronic vomiting
Chronic diarrhea
Decreased aldosterone
Decreased Na+ intake
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Dilutional Hyponatremia:
Renal dysfunction with ↑ intake of
hypotonic fluids
Excessive sweating→ increased thirst →
intake of excessive amounts of pure water
Syndrome of Inappropriate ADH (SIADH) or
oliguric renal failure, severe congestive
heart failure, cirrhosis all lead to:
Impaired renal excretion of water
Hyperglycemia – attracts water
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Clinical manifestations of
Hyponatremia
Neurological symptoms
Lethargy, headache, confusion, apprehension,
depressed reflexes, seizures and coma
Muscle symptoms
Cramps, weakness, fatigue
Gastrointestinal symptoms
Nausea, vomiting, abdominal cramps, and
diarrhea
Tx – limit water intake or discontinue meds
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Hypokalemia
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Causes of Hypokalemia
Decreased intake of K+
Increased K+ loss
Chronic diuretics
Acid/base imbalance
Trauma and stress
Increased aldosterone
Redistribution between ICF and
ECF
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Clinical manifestations of
Hypokalemia
Neuromuscular disorders
Weakness, flaccid paralysis,
respiratory arrest, constipation
Dysrhythmias, appearance of U wave
Postural hypotension
Cardiac arrest
Others – table 6-5
Treatment-
Increase K+ intake, but slowly, preferably by
foods
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Hyperkalemia
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Clinical manifestations of
Hyperkalemia
Early – hyperactive muscles ,
paresthesia
Late - Muscle weakness, flaccid
paralysis
Change in ECG pattern
Dysrhythmias
Bradycardia , heart block, cardiac
arrest
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Treatment of
Hyperkalemia
If time, decrease intake and increase
renal excretion
Insulin + glucose
Bicarbonate
Ca++ counters effect on heart
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Calcium Imbalances
Most in ECF
Regulated by:
Parathyroid hormone
↑Blood Ca++ by stimulating
osteoclasts
↑GI absorption and renal
retention
Calcitonin from the thyroid gland
Promotes bone formation
↑ renal excretion
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Love ko toh!
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Hypercalcemia
Results from:
Hyperparathyroidism
Hypothyroid states
Renal disease
Excessive intake of vitamin D
Milk-alkali syndrome
Certain drugs
Malignant tumors – hypercalcemia of malignancy
Tumor products promote bone breakdown
Tumor growth in bone causing Ca++ release
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Hypercalcemia
Usually also see hypophosphatemia
Effects:
Many nonspecific – fatigue, weakness, lethargy
Increases formation of kidney stones and
pancreatic stones
Muscle cramps
Bradycardia, cardiac arrest
Pain
GI activity also common
Nausea, abdominal cramps
Diarrhea / constipation
Metastatic calcification
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Hypocalcemia
Hyperactive neuromuscular reflexes and
tetany differentiate it from hypercalcemia
Convulsions in severe cases
Caused by:
Renal failure
Lack of vitamin D
Suppression of parathyroid function
Hypersecretion of calcitonin
Malabsorption states
Abnormal intestinal acidity and acid/ base bal.
Widespread infection or peritoneal
inflammation
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Hypocalcemia
Diagnosis:
Chvostek’s sign
Trousseau’s sign
Treatment
IV calcium for acute
Oral calcium and vitamin D for chronic
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Phosphate levels less than 1.7 mEq/L or less than
2.5 mg/dl or less than
0.8 mmol/L)
ETIOLOGY :
1. Decreased PO4 = Intake/Absorption:
A. Excessive or prolonged antacid use
(Antacids absorbs PO4)
B. Chronic LEM, Alcoholism
C. Malnutrition
D. Increased Vitamin D (increased Ca++ ,
decreased PO4)
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•Prevent Hypophosphatemia
2.Restore normal PO4 levels
Nursing Actions :
1. For mild PO4 = decreased
a. remove precipitated functions
b. give adequate PO4 in diet
2. For severe PO4 = decreased
a. PO4 = replacement IV - - - - K+ PO4
tablets
b. Watch out for PO4 toxicity
c. High PO4 = diet - - - - - carbonated
drinks, processed foods, milk, eggs, meats
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H Y P E R P H O S P H A TE M I A
DEFINITION : Phosphate Excess (Serum
PO4 = greater than 4.5 mg/dl or
Greater than 2.6 mEq/L or
Greater than 1.5 mmol/L
ETIOLOGY :
1. Increased PO4 = Intake/Absorption :
A. Excessive PO4 = therapy especially
IV
B. Excessive Fleets enema (Phospho
Soda and Neutra Phosphate)
2. Incresaed PO4 = Release from cells
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Decreased PO4 Intake
1. Low PO4 diet
* Avoid : milk, eggs, liver, nuts, kidney, sardines
any food with milk, poultry, legumes, hard cheese,
creams, whole grain cereals, dried fruits, dried
vegetables, sweetbreads.
2. Avoid PO4 continuing enemas, laxatives
3. Hydrate with Ca++ continuing IV solutions.
Diurese to eliminate excess PO4 =
4. Administer ALOH - gel in the form of antacids
(via GIT) called PO4 = binding agents
5. Dialysis for Renal failure
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HYPOMAGNESEMIA
DEFINITION : Magnesium Deficit (Serum Mg++ less than
1.5 mEq/L)
ETIOLOGY :
Decrease Mg++ Intake/Absorption
A. Prolonged malnutrition - Anorexis
nervosa,Bulimia
B. Starvation
C. IV therapy without Mg++
D. Malabsorption syndromes
E. Steatorrhea, Pancreatitis
F. Ileal resection
G. Chronic Alcoholism
H. Hypercalcemia
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Nursing Actions :
I. For Mild Mg++ Deficit :
* Dietary replacement of Mg++
- green vegetables
- nuts, legumes, peanuts
- chocolate , cocoa, tea and coffee
- fruits, bananas, grape fruits, orange
II. For Severe Mg++ Deficit :
* Mg++ SO4 = IV
Magnesium SO4 (Epson salt, Mg++ SO4=)
Dose : 15 gms. in1 glass H2O or other liquid.
1 - 5 gms. (25-50 % solution) up to 6x Daily
1 - 4 gms. (10-20% solution)IV
Toxicity :
: drowsiness
: tetany
: decreased or (-) deep tendon reflexes
: decreased BP, decreased RR,
decreased HR
: Flushing, sweating
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DEFINITION : Magnesium Excess (Serum Mg++ greater
than 2.5 mEq/L
Or greater than 3.0 mg%
Or greater than 1.25 mmol/L Or S.I.U.)
ETIOLOGY :
1.Increase Mg++ Intake or Absorption
1.Increase use Mg++ spontiniung antacids, cathartics
irrigating solutions
2.Increase IV infusion of MG++
3.Increase treatment with MgSO4
4.Aspiration of sea water (near drowning)
2. Increased Mg++ Retention
•Oliguria Renal Failure
•Adrenal Insufficiency (Addison’s)
•Severe Dehydration with Oliguria
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•Prevent administration of MG++ to patient with Renal Failure Check
urine output
•For seriously ill patients, check for Mg++ toxicity when administering
MgSO4
C. Avoid Mg++ rich foods :
•Whole grain cereals
•Dark green vegetables
•Dried peas and beans
•Soy products
•Nuts especially cashews and almonds
•Peanut butter
•Cocoa, chocolates
•Bananas, sea salt
•Egg yolk
2. Restore Mg++ at normal
•Hydrate with D5W
•Diureses with loop diuretics
•Avoid Mg++ containing antacids
•Administer I.V. Ca++ Gluconate 10 cc slow IV as antidote to Mg++
* Increase Ca++ - - - Decrease Mg++
•Dialysis for Renal Failure
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3. Prevent Complications :
•Be alert for s/s of respiratory difficulty related to
respiratory paralysis or laryngospasm
•Monitor for Cardiac Dysrythmias and abnormal vital
signs (decreased BP, decreased HR, decreased RR)
•EKG change : Increased T wave
: Increased PR interval
: Increased QRS complex
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No SUGAR
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By: Franco R. Ganacias
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SLUMDOG MILLIONAIRE
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Acid and Base Balance
and Imbalance
by: Franco R. Ganacias
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pH Review
pH = - log [H+]
H+ is really a proton
Range is from 0 - 14
If [H+] is high, the solution is acidic;
pH < 7
If [H+] is low, the solution is basic or
alkaline ; pH > 7
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Normal Blood Gas
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Arterial Blood Gas
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Acids are H+ donors.
Bases are H+ acceptors, or give up OH-
in solution.
Acids and bases can be:
Strong – dissociate completely in
solution
HCl, NaOH
Weak – dissociate only partially in
solution
Lactic acid, carbonic acid
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The Body and pH
Homeostasis of pH is tightly
controlled
Extracellular fluid = 7.4
Blood = 7.35 – 7.45
< 6.8 or > 8.0 death occurs
Acidosis (acidemia) below 7.35
Alkalosis (alkalemia) above 7.45
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Small changes in pH can
produce major disturbances
Most enzymes function only with
narrow pH ranges
Acid-base balance can also affect
electrolytes (Na+, K+, Cl-)
Can also affect hormones
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The body produces more
acids than bases
Acids take in with foods
Acids produced by metabolism of
lipids and proteins
Cellular metabolism produces CO2.
CO2 + H20 ↔ H2CO3 ↔ H+ + HCO3-
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Control of Acids
1. Buffer systems
Take up H+ or release H+ as
conditions change
Buffer pairs – weak acid and a base
Exchange a strong acid or base for a
weak one
Results in a much smaller pH change
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Bicarbonate buffer
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Phosphate buffer
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Protein Buffers
Includes hemoglobin, work in blood and ISF
Carboxyl group gives up H+
Amino Group accepts H+
Side chains that can buffer H+ are present
on 27 amino acids.
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2. Respiratory
mechanisms
Exhalation of carbon dioxide
Powerful, but only works with
volatile acids
Doesn’t affect fixed acids like lactic
acid
CO2 + H20 ↔ H2CO3 ↔ H+ + HCO3-
Body pH can be adjusted by
changing rate and depth of breathing
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3. Kidney excretion
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Rates of correction
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Acid-Base Imbalances
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Compensation
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Acidosis
Principal effect of acidosis is depression of
the CNS through ↓ in synaptic
transmission.
Generalized weakness
Deranged CNS function the greatest threat
Severe acidosis causes
Disorientation
coma
death
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Alkalosis
Alkalosis causes over excitability of the
central and peripheral nervous systems.
Numbness
Lightheadedness
It can cause :
Nervousness
muscle spasms or tetany
Convulsions
Loss of consciousness
Death
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Respiratory Acidosis
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Respiratory Acidosis
Acute conditons:
Adult Respiratory Distress Syndrome
Pulmonary edema
Pneumothorax
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Compensation for
Respiratory Acidosis
Kidneys eliminate hydrogen ion and
retain bicarbonate ion
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Signs and Symptoms of
Respiratory Acidosis
Breathlessness
Restlessness
Lethargy and disorientation
Tremors, convulsions, coma
Respiratory rate rapid, then gradually
depressed
Skin warm and flushed due to
vasodilation caused by excess CO2
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Treatment of Respiratory
Acidosis
Restore ventilation
IV lactate solution
Treat underlying dysfunction or
disease
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Respiratory Alkalosis
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Respiratory Alkalosis
Conditions that stimulate respiratory
center:
Oxygen deficiency at high altitudes
Pulmonary disease and Congestive heart
failure – caused by hypoxia
Acute anxiety
Fever, anemia
Early salicylate intoxication
Cirrhosis
Gram-negative sepsis
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Compensation of Respiratory
Alkalosis
Kidneys conserve hydrogen ion
Excrete bicarbonate ion
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Treatment of Respiratory
Alkalosis
Treat underlying cause
Breathe into a paper bag
IV Chloride containing solution – Cl-
ions replace lost bicarbonate ions
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Metabolic Acidosis
Bicarbonate deficit - blood
concentrations of bicarb drop below
22mEq/L
Causes:
Loss of bicarbonate through diarrhea or
renal dysfunction
Accumulation of acids (lactic acid or
ketones)
Failure of kidneys to excrete H+
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Symptoms of Metabolic
Acidosis
Headache, lethargy
Nausea, vomiting, diarrhea
Coma
Death
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Compensation for Metabolic
Acidosis
Increased ventilation
Renal excretion of hydrogen ions if
possible
K+ exchanges with excess H+ in ECF
( H+ into cells, K+ out of cells)
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Treatment of Metabolic
Acidosis
IV lactate solution
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Metabolic Alkalosis
Bicarbonate excess -
concentration in blood is greater
than 26 mEq/L
Causes:
Excess vomiting = loss of stomach acid
Excessive use of alkaline drugs
Certain diuretics
Endocrine disorders
Heavy ingestion of antacids
Severe dehydration
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Compensation for Metabolic
Alkalosis
Alkalosis most commonly occurs with
renal dysfunction, so can’t count on
kidneys
Respiratory compensation difficult –
hypoventilation limited by hypoxia
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Symptoms of Metabolic
Alkalosis
Respiration slow and shallow
Hyperactive reflexes ; tetany
Often related to depletion of
electrolytes
Atrial tachycardia
Dysrhythmias
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Treatment of Metabolic
Alkalosis
Electrolytes to replace those lost
IV chloride containing solution
Treat underlying disorder
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Diagnosis of Acid-Base
Imbalances
1. Note whether the pH is low
(acidosis) or high (alkalosis)
2. Decide which value, pCO2 or HCO3- ,
is outside the normal range and
could be the cause of the problem.
If the cause is a change in pCO2, the
problem is respiratory. If the cause
is HCO3- the problem is metabolic.
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3. Look at the value that doesn’t
correspond to the observed pH change.
If it is inside the normal range, there is
no compensation occurring. If it is
outside the normal range, the body is
partially compensating for the problem.
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Example
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Diagnosis
Metabolic acidosis
With compensation
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