Bienvenidos!

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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

 Fluid and electrolyte homeostasis is

maintained in the body
 Neutral balance: input = output
 Positive balance: input > output
 Negative balance: input < output

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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.”

Diffusion – movement of particles down a

concentration gradient.

Osmosis – diffusion of water across a

selectively permeable membrane

Active transport – movement of particles up

a concentration gradient ; requires energy
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ICF to ECF – osmolality changes in ICF not

rapid

IVF → ISF → IVF happens constantly due to

changes in fluid pressures and osmotic forces
at the arterial and venous ends of capillaries

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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

Lymphatic channels blocked:

surgical removal
infection involving lymphatics
lymphedema

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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)

Water is trapped, unavailable for metabolic

processes. Can result in dehydration
and shock. (severe burns)

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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

 Renal tubule reabsorption affected

by hormones:
 Aldosterone
 Renin/angiotensin
 Atrial Natriuretic Peptide (ANP)

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Potassium

 Major intracellular cation

 ICF conc. =3.5-5.5 mEq/L
 Resting membrane potential
 Regulates fluid, ion balance inside
cell
 pH balance

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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

Get hypervolemia – weight gain,

decreased hematocrit, diluted plasma
proteins, distended neck veins, ↑ B.P.
Can lead to edema (↑ capillary
hydrostatic pressure) pulmonary
edema and heart failure

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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

 Serum K+ < 3.5 mEq /L

 Beware if diabetic
 Insulin gets K+ into cell
 Ketoacidosis – H+ replaces K+,
which is lost in urine
 β – adrenergic drugs or
epinephrine

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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

 Serum K+ > 5.5 mEq / L

 Check for renal disease
 Massive cellular trauma
 Insulin deficiency
 Addison’s disease
 Potassium sparing diuretics
 Decreased blood pH
 Exercise causes K+ to move out of cells

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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

 Partial pressure of oxygen (PaO2) - 75

- 100 mmHg
 Partial pressure of carbon dioxide
(PaCO2) - 35 - 45 mmHg
 A pH of 7.35 - 7.45
 Oxygen saturation (SaO2) - 94 - 100%
 Bicarbonate - (HCO3) - 22 - 26 mEq/L

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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

 Sodium Bicarbonate (NaHCO3) and

carbonic acid (H2CO3)
 Maintain a 20:1 ratio : HCO3- : H2CO3

HCl + NaHCO3 ↔ H2CO3 + NaCl

NaOH + H2CO3 ↔ NaHCO3 + H2O

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Phosphate buffer

 Major intracellular buffer

 H+ + HPO42- ↔ H2PO4-

 OH- + H2PO4- ↔ H2O + H2PO42-

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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

 Can eliminate large amounts of acid

 Can also excrete base
 Can conserve and produce bicarb
ions
 Most effective regulator of pH
 If kidneys fail, pH balance fails

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Rates of correction

 Buffers function almost

instantaneously
 Respiratory mechanisms take
several minutes to hours
 Renal mechanisms may take several
hours to days

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Acid-Base Imbalances

 pH< 7.35 acidosis

 pH > 7.45 alkalosis
 The body response to acid-base
imbalance is called compensation
 May be complete if brought back
within normal limits
 Partial compensation if range is
still outside norms.

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Compensation

 If underlying problem is metabolic,

hyperventilation or hypoventilation
can help : respiratory
compensation.
 If problem is respiratory, renal
mechanisms can bring about
metabolic 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

 Carbonic acid excess caused by

blood levels of CO2 above 45 mm Hg.
 Hypercapnia – high levels of CO2 in
blood
 Chronic conditions:
 Depression of respiratory center in brain
that controls breathing rate – drugs or
head trauma
 Paralysis of respiratory or chest muscles
 Emphysema

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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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103
Respiratory Alkalosis

 Carbonic acid deficit

 pCO2 less than 35 mm Hg
(hypocapnea)
 Most common acid-base imbalance
 Primary cause is hyperventilation

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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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108
 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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113
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

116
Treatment of Metabolic
Alkalosis
 Electrolytes to replace those lost
 IV chloride containing solution
 Treat underlying disorder

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118
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

 A patient is in intensive care because

he suffered a severe myocardial
infarction 3 days ago. The lab reports
the following values from an arterial
blood sample:
 pH 7.3
 HCO3- = 20 mEq / L ( 22 - 26)
 pCO2 = 32 mm Hg (35 - 45)

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Diagnosis

 Metabolic acidosis
 With compensation

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