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FLUIDS AND

ELECTROLYTES

ACID-BASE BALANCE

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Body Water Content

 Infants have low body fat, low bone mass, and


are 73% or more water
 Total water content declines throughout life
 Healthy males are about 60% water; healthy
females are around 50%
 This difference reflects females’:
 Higher body fat
 Smaller amount of skeletal muscle
 In old age, only about 45% of body weight is
water
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Fluid Compartments
 Water occupies two main fluid compartments
 Intracellular fluid (ICF) – about two thirds by
volume, contained in cells
 Extracellular fluid (ECF) – consists of two major
subdivisions
 Plasma – the fluid portion of the blood
 Interstitial fluid (IF) – fluid in spaces
between cells
 Other ECF – lymph, cerebrospinal fluid, eye
humors, synovial fluid, serous fluid, and
gastrointestinal secretions
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Fluid Compartments

Figure 26.1
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Composition of Body Fluids

 Water is the universal solvent

 Solutes are broadly classified into:

 Electrolytes – inorganic salts, all acids and


bases, and some proteins
 Nonelectrolytes – examples include glucose,
lipids, creatinine, and urea
 Electrolytes have greater osmotic power than
nonelectrolytes
 Water moves according to osmotic gradients
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Electrolyte Concentration

 Expressed in milliequivalents per liter (mEq/L), a


measure of the number of electrical charges in
one liter of solution
 mEq/L = (concentration of ion in [mg/L]/the
atomic weight of ion) × number of electrical
charges on one ion
 For single charged ions, 1 mEq = 1 mOsm

 For bivalent ions, 1 mEq = 1/2 mOsm

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CELLS AND TONICITY

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FLUID& ELECTROLYTE TRANSPORT

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FLUID& ELECTROLYTE TRANSPORT

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Extracellular and Intracellular Fluids

 Each fluid compartment of the body has a


distinctive pattern of electrolytes
 Extracellular fluids are similar (except for the
high protein content of plasma)
 Sodium is the chief cation

 Chloride is the major anion

 Intracellular fluids have low sodium and chloride

 Potassium is the chief cation

 Phosphate is the chief anion


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Extracellular and Intracellular Fluids

 Sodium and potassium concentrations in extra-


and intracellular fluids are nearly opposites
 This reflects the activity of cellular ATP-
dependent sodium-potassium pumps
 Electrolytes determine the chemical and
physical reactions of fluids

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Extracellular and Intracellular Fluids

 Proteins, phospholipids, cholesterol, and neutral


fats account for:
 90% of the mass of solutes in plasma

 60% of the mass of solutes in interstitial


fluid
 97% of the mass of solutes in the
intracellular compartment

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Electrolyte Composition of Body Fluids

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Fluid Movement Among Compartments

 Compartmental exchange is regulated by


osmotic and hydrostatic pressures
 Net leakage of fluid from the blood is picked up
by lymphatic vessels and returned to the
bloodstream
 Exchanges between interstitial and intracellular
fluids are complex due to the selective
permeability of the cellular membranes
 Two-way water flow is substantial

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Extracellular and Intracellular Fluids
 Ion fluxes are restricted and move selectively
by active transport
 Nutrients, respiratory gases, and wastes move
unidirectionally
 Osmolalities of all body fluids are equal; changes
in solute concentrations are quickly followed by
osmotic changes

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Continuous Mixing of Body Fluids

Figure 26.3
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Water Balance and ECF Osmolality

 To remain properly hydrated, water intake must


equal water output
 Water intake sources

 Ingested fluid (60%) and solid food (30%)

 Metabolic water or water of oxidation (10%)

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Normal I and O (insert here)

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Water Balance and ECF Osmolality

 Water output

 Urine (60%) and feces (4%)

 Insensible losses (28%), sweat (8%)

 Increases in plasma osmolality trigger thirst and


release of antidiuretic hormone (ADH)

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Water Intake and Output

Figure 26.4
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Regulation of Water Intake

 The hypothalamic thirst center is stimulated:

 By a decline in plasma volume of 10%–15%

 By increases in plasma osmolality of 1–2%

 Via baroreceptor input, angiotensin II, and


other stimuli

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Regulation of Water Intake

 Thirst is quenched as soon as we begin to drink


water
 Feedback signals that inhibit the thirst centers
include:
 Moistening of the mucosa of the mouth and
throat
 Activation of stomach and intestinal stretch
receptors

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Regulation of Water Intake: Thirst Mechanism

Figure 26.5
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Insert angiotensin-aldosterone system

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Insert ADH regulation here

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Regulation of Water Output

 Obligatory water losses include:

 Insensible water losses from lungs and skin

 Water that accompanies undigested food


residues in feces
 Obligatory water loss reflects the fact that:

 Kidneys excrete 900-1200 mOsm of solutes


to maintain blood homeostasis
 Urine solutes must be flushed out of the body
in water
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Influence and Regulation of ADH
 Water reabsorption in collecting ducts is
proportional to ADH release
 Low ADH levels produce dilute urine and
reduced volume of body fluids
 High ADH levels produce concentrated urine

 Hypothalamic osmoreceptors trigger or inhibit


ADH release
 Factors that specifically trigger ADH release
include prolonged fever; excessive sweating,
vomiting, or diarrhea; severe blood loss; and
traumatic burns
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Mechanisms and Consequences of ADH Release

Figure 26.6
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Disorders of Water Balance: Dehydration

 Water loss exceeds water intake and the body


is in negative fluid balance
 Causes include: hemorrhage, severe burns,
prolonged vomiting or diarrhea, profuse
sweating, water deprivation, and diuretic abuse
 Signs and symptoms: cottonmouth, thirst, dry
flushed skin, and oliguria
 Prolonged dehydration may lead to weight loss,
fever, and mental confusion
 Other consequences include hypovolemic shock
and loss of electrolytes
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Disorders of Water Balance: Dehydration

1 Excessive loss of H2O from 2 ECF osmotic 3 Cells lose H2O


ECF pressure rises to ECF by
osmosis; cells
shrink

(a) Mechanism of dehydration

Figure 26.7a
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Interventions
 Monitor s/sx closely

 Record I and O

 Maintain IV access as ordered. Monitor IV infusions

 Monitor serum Na levels, urine osmolality, & urine specific


gravity
 Insert a urinary catheter as ordered

 Initiate safety precautions

 Obtain daily weights

 Provide skin & mouth care

 Assess pt for diaphoresis

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HYPOVOLEMIA
 -isotonic fluid loss from the extracellular space

Etiology:

-abdl. Surgery DM

Excessive diuretic therapy excessive laxative use

Excessive sweating fever

Fistulas hemorrhage

NG drainage Vomiting & diarrhea

renal failure w/ increased urination

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HYPOVOLEMIA

Etiology (third-space shift):

-acute intestinal obstruction

-acute peritonitis

-burns

-crush injuries

-hip fracture

-hypoalbuminemia

-pleural effusion

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HYPERVOLEMIA
Signs and Symptoms
Tachypnea

Dyspnea

Crackles

Rapid, bounding pulse

Hypertension

Increased CVP, PAP, and PAWP

Distended neck and hand veins

Acute weight gain

Edema

S3 gallop
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HYPOVOLEMIA
Interventions
Ensure patent airway
Apply and adjust O2 therapy as ordered
Lower the head of the bed to slow a declining BP
Stop bleeding, as needed
Maintain patent IV access
Administer IV fluid, a vasopressor, and blood as prescribed
Draw blood for typing and crossmatching, as ordered
Closely monitor the pt’s mental status and vs
Monitor the quality of peripheral pulses
Obtain & record results of lab test results
Offer emo support to pt and family
Give health teaching
Auscultate for breath sounds
Prevent complications
Weigh pt daily
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Disorders of Water Balance:
Hypotonic Hydration
 Renal insufficiency or an extraordinary amount
of water ingested quickly can lead to cellular
overhydration, or water intoxication
 ECF is diluted – sodium content is normal but
excess water is present
 The resulting hyponatremia promotes net
osmosis into tissue cells, causing swelling
 These events must be quickly reversed to
prevent severe metabolic disturbances,
particularly in neurons
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Disorders of Water Balance:
Hypotonic Hydration

1 2 ECF osmotic 3 H2O moves into


Excessive H2O
pressure falls cells by osmosis;
enters the ECF cells swell

(b) Mechanism of hypotonic hydration

Figure 26.7b
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HYPERVOLEMIA

-excess of isotonic fluid in the ECF

-mild to moderate fluid gain: 5% to 10% wt increase

-severe fluid gain: more than 10% wt increase

-prolonged or severe or in pts with poor heart function: can lead


to heart failure or pulmonary edema

-elderly pts & pts with impaired renal or cardiovascular function:


increased susceptibility

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Disorders of Water Balance: Edema
 Atypical accumulation of fluid in the interstitial
space, leading to tissue swelling
 Caused by anything that increases flow of fluids
out of the bloodstream or hinders their return
 Factors that accelerate fluid loss include:
 Increased blood pressure, capillary
permeability
 Incompetent venous valves, localized blood
vessel blockage
 Congestive heart failure, hypertension, high
blood volume
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Edema

 Hindered fluid return usually reflects an


imbalance in colloid osmotic pressures
 Hypoproteinemia – low levels of plasma proteins

 Forces fluids out of capillary beds at the


arterial ends
 Fluids fail to return at the venous ends

 Results from protein malnutrition, liver


disease, or glomerulonephritis

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Edema
 Blocked (or surgically removed) lymph vessels:

 Cause leaked proteins to accumulate in


interstitial fluid
 Exert increasing colloid osmotic pressure,
which draws fluid from the blood
 Interstitial fluid accumulation results in low
blood pressure and severely impaired circulation

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PITTING EDEMA

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Signs of hypo / hypervolemia:

Volume depletion Volume overload


Postural hypotension Hypertension
Tachycardia Tachycardia
Absence of JVP @ 45o Raised JVP / gallop rhythm
Decreased skin turgor Edema
Dry mucosae Pleural effusions
Supine hypotension Pulmonary edema
Oliguria Ascites
Organ failure Organ failure

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ELECTROLYTES

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Electrolyte Results Implications Common Causes

Serum Na 135-145 mEq/L Normal


<135 mEq/L Hyponatremia SIADH
>145 mEq/L Hypernatremia Diabetes Insipidus

Serum K 3.5 – 5mEq/L Normal

<3.5 mEq/L Hypokalemia Diarrhea

>5 mEq/L Hyperkalemia Burns & renal failure

Total serum 8.9-10.1 mg/dL Normal


calcium
<8.9 mg/dL Hypocalcemia Acute pancreatitis

>10.1 mg/dL hypercalcemia Hyperparathyrodism


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Electrolyte Results Implications Common Causes

Ionized Ca 4.5-5.1 mg/dL Normal

<4.5 mg/dL Hypocalcemia Massive transfusion

>5.2 mg/dL Hypercalcemia Acidosis

Serum 2.5–4.5 mg/dL Normal


Phosphates
<2.5 mg/dL Hypophosphatemia Diabetic ketoacidosis

>4.5 mg/dL hyperphosphatemia Renal insufficiency

Serum Mg 1.5-2.5 mEq/L Normal

<1.5 mEq/L Hypomagnesemia Malnutrition

>2.5 mEq/L Hypermagnesemia Renal Failure

Serum Cl 96-106 mEq/L Normal

<96 mEq/L Hypochloremia Prolonged vomiting

>106 mEq/L Hyperchloremia Hypernatremia


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Electrolyte Balance

 Electrolytes are salts, acids, and bases, but


electrolyte balance usually refers only to salt
balance
 Salts are important for:
 Neuromuscular excitability
 Secretory activity
 Membrane permeability
 Controlling fluid movements
 Salts enter the body by ingestion and are lost via
perspiration, feces, and urine
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SODIUM
 Sodium holds a central position in fluid and
electrolyte balance
 Sodium salts:
 Account for 90-95% of all solutes in the ECF
 Contribute 280 mOsm of the total 300 mOsm
ECF solute concentration
 Sodium is the single most abundant cation in the
ECF
 Sodium is the only cation exerting significant
osmotic pressure
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Sodium in Fluid and Electrolyte Balance

 The role of sodium in controlling ECF volume and


water distribution in the body is a result of:
 Sodium being the only cation to exert
significant osmotic pressure
 Sodium ions leaking into cells and being
pumped out against their electrochemical
gradient
 Sodium concentration in the ECF normally
remains stable

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Sodium in Fluid and Electrolyte Balance

 Changes in plasma sodium levels affect:

 Plasma volume, blood pressure

 ICF and interstitial fluid volumes

 Renal acid-base control mechanisms are coupled


to sodium ion transport

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Regulation of Sodium Balance: Aldosterone

 Sodium reabsorption

 65% of sodium in filtrate is reabsorbed in the


proximal tubules
 25% is reclaimed in the loops of Henle

 When aldosterone levels are high, all remaining


Na+ is actively reabsorbed
 Water follows sodium if tubule permeability has
been increased with ADH

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Regulation of Sodium Balance: Aldosterone
 The renin-angiotensin mechanism triggers the
release of aldosterone
 This is mediated by the juxtaglomerular
apparatus, which releases renin in response to:
 Sympathetic nervous system stimulation

 Decreased filtrate osmolality

 Decreased stretch (due to decreased blood


pressure)
 Renin catalyzes the production of angiotensin
II, which prompts aldosterone release
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Regulation of Sodium Balance: Aldosterone

 Adrenal cortical cells are directly stimulated


to release aldosterone by elevated K+ levels in
the ECF
 Aldosterone brings about its effects
(diminished urine output and increased blood
volume) slowly

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Regulation of Sodium Balance: Aldosterone

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Cardiovascular System Baroreceptors

 Baroreceptors alert the brain of increases in


blood volume (hence increased blood pressure)
 Sympathetic nervous system impulses to the
kidneys decline
 Afferent arterioles dilate

 Glomerular filtration rate rises

 Sodium and water output increase

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Cardiovascular System Baroreceptors

 This phenomenon, called pressure diuresis,


decreases blood pressure
 Drops in systemic blood pressure lead to
opposite actions and systemic blood pressure
increases
 Since sodium ion concentration determines fluid
volume, baroreceptors can be viewed as “sodium
receptors”

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Maintenance of Blood Pressure Homeostasis

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Atrial Natriuretic Peptide (ANP)

 Reduces blood pressure and blood volume by


inhibiting:
 Events that promote vasoconstriction
 Na+ and water retention
 Is released in the heart atria as a response to
stretch (elevated blood pressure)
 Has potent diuretic and natriuretic effects
 Promotes excretion of sodium and water
 Inhibits angiotensin II production
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Mechanisms and Consequences of ANP Release

Figure 26.10
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Influence of Other Hormones on Sodium
Balance

 Estrogens:

 Enhance NaCl reabsorption by renal tubules

 May cause water retention during menstrual


cycles
 Are responsible for edema during pregnancy

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Influence of Other Hormones on Sodium
Balance

 Progesterone:

 Decreases sodium reabsorption

 Acts as a diuretic, promoting sodium and


water loss
 Glucocorticoids – enhance reabsorption of
sodium and promote edema

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ELECTROLYTE IMBALANCES

Interventions:

Monitor & record vs


Carefully record I and O
Assess skin and MM for signs of breakdown and
infection
Monitor patient’s serum electrolyte levels
Restrict oral intake, as needed
Give oral hydration, as needed
Give supplemental feedings, as needed
Assist with oral hygiene
Prevent complications
Administer prescribed meds and monitor the pt for
their effectiveness
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Regulation of Potassium Balance

 Relative ICF-ECF potassium ion concentration


affects a cell’s resting membrane potential
 Excessive ECF potassium decreases
membrane potential
 Too little K+ causes hyperpolarization and
nonresponsiveness

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Regulation of Potassium Balance

 Hyperkalemia and hypokalemia can:

 Disrupt electrical conduction in the heart

 Lead to sudden death

 Hydrogen ions shift in and out of cells

 Leads to corresponding shifts in potassium in


the opposite direction
 Interferes with activity of excitable cells

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Regulatory Site: Cortical Collecting Ducts

 Less than 15% of filtered K+ is lost to urine


regardless of need
 K+ balance is controlled in the cortical collecting
ducts by changing the amount of potassium
secreted into filtrate
 Excessive K+ is excreted over basal levels by
cortical collecting ducts
 When K+ levels are low, the amount of secretion
and excretion is kept to a minimum
 Type A intercalated cells can reabsorb some K+
left in the filtrate
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Influence of Plasma Potassium Concentration

 High K+ content of ECF favors principal cells to


secrete K+
 Low K+ or accelerated K+ loss depresses its
secretion by the collecting ducts

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Influence of Aldosterone
 Aldosterone stimulates potassium ion secretion
by principal cells
 In cortical collecting ducts, for each Na+
reabsorbed, a K+ is secreted
 Increased K+ in the ECF around the adrenal
cortex causes:
 Release of aldosterone

 Potassium secretion

 Potassium controls its own ECF concentration via


feedback regulation of aldosterone release
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Regulation of Calcium

 Ionic calcium in ECF is important for:

 Blood clotting

 Cell membrane permeability

 Secretory behavior

 Hypocalcemia:

 Increases excitability

 Causes muscle tetany

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Regulation of Calcium
 Hypercalcemia:
 Inhibits neurons and muscle cells
 May cause heart arrhythmias
 Loss of appetite
 Weight loss
 Nausea
 Vomiting
 Thirst
 Fatigue
 Muscle weakness
 Restlessness
 Confusion
 Elevated blood calcium level

Calcium balance is controlled by parathyroid hormone (PTH) and calcitonin


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Regulation of Calcium and Phosphate
 PTH promotes increase in calcium levels by
targeting:
 Bones – PTH activates osteoclasts to break
down bone matrix
 Small intestine – PTH enhances intestinal
absorption of calcium
 Kidneys – PTH enhances calcium reabsorption
and decreases phosphate reabsorption
 Calcium reabsorption and phosphate excretion
go hand in hand
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Regulation of Calcium and Phosphate
 Filtered phosphate is actively reabsorbed in the
proximal tubules
 In the absence of PTH, phosphate reabsorption
is regulated by its transport maximum and
excesses are excreted in urine
 High or normal ECF calcium levels inhibit PTH
secretion
 Release of calcium from bone is inhibited
 Larger amounts of calcium are lost in feces
and urine
 More phosphate is retained
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Influence of Calcitonin

 Released in response to rising blood calcium


levels
 Calcitonin is a PTH antagonist, but its
contribution to calcium and phosphate
homeostasis is minor to negligible

InterActive Physiology®:
PLAY
Fluid, Electrolyte, and Acid/Base Balance: Electrolyte Homeostasis

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Regulation of Anions

 Chloride is the major anion accompanying sodium


in the ECF
 99% of chloride is reabsorbed under normal pH
conditions
 When acidosis occurs, fewer chloride ions are
reabsorbed
 Other anions have transport maximums and
excesses are excreted in urine

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HYPONATREMIA (<135 mEq/L)
-Maintained by ADH secreted from the posterior pituitary
gland
Depends on what’s eaten & how it’s absorbed by the
intestines
Increased Na intake: increased ECF fluid volume
Decreased Na intake: decreased ECF fluid volume
Increased Na levels: increased thirst, release of ADH,
retention of H2O by the kidneys, dilution of blood
-Decreased Na levels: suppression of thirst, suppression of
ADH secretion, excretion of H2O by the kidneys

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Hyponatremia

Signs & symptoms:


Abdominal cramps Altered LOC
Headache Muscle twitching
Nausea Dry MM
Hypertension Poor skin turgor
Tachycardia Weight gain
Rapid, bounding pulse

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Hyponatremia

Interventions:
Monitor and record vs, esp. BP and pusle
Monitor neurologic status frequently
Accurately measure I and O
Weigh the pt
Assess skin turgor
Watch for & report extreme serum Na levels
changes
Restrict fluid intake as ordered
Administer oral sodium supplements
Maintain patent IV line
Maintain safety

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HYPERNATREMIA (>145 mEq/L)

-Caused by water loss, inadequate water intake, or Na gain on


what’s eaten & how it’s absorbed by the intestines

- Increased risk for infants, immobile, and comatose pts

- Always results in increased osmolality

- Fluid shifts out of cells

- Must be corrected slowly to prevent a rapid shift of water


back into the cells, which couls cause cerebral edema

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Hypernatremia

Signs & symptoms:


Skin flushed
Agitation
Low-grade fever
Thirst
Interventions:
Assess…
Replenish…
Restore…

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HYPOKALEMIA (<3.5 mEq/L)

Signs & symptoms:

Skeletal muscle weakness


U wave
Constipation, ileus
Toxic effects of digoxin (from hypokalemia)
Irregular, weak pulse
Orthostatic hypotension
Numbness (paresthesia)

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Hypokalemia

Interventions:
Monitor vs
Check heart rate and rhythm
Monitor serum K levels
Asess for signs of hypokalemia
Monitor and document I and O
Observe proper guidelines in IV K administration

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HYPERKALEMIA (>5 mEq/L)

-Most dangerous of the electrolyte disorders

Signs & symptoms:

Abdominal cramping diarrhea


EKG changes hypotension
Irregular pulse rate irritability
Muscle weakness nausea
paresthesia

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Hypokalemia

Interventions:
Monitor vs
Monitor and document I and O
Prepare to administer a slow calcium gluconate IV
infusion
Keep in mind that when giving Kayexalate,, serum
Na levels may rise
Monitor bowel sounds & the number of BM
Monitor serum K levels

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HYPOCALCEMIA (<8.9 mg/dL)

Signs & symptoms:

Trousseau’s sign Chvostek’s sign


Anxiety Confusion
Decreased CO Arrhythmias
Fractures Irritability
Muscle cramps Tetany
Tremors twitching

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Hypocalcemia

Interventions:
Monitor vs, cardiac status; observe for Chvostek’s
and Trousseau’s signs
Monitor for arrhythmias
Insert and maintain IV line for Ca therapy
Administer oral replacements as ordered
Monitor pertinent lab test results
Take safety and seizure precautions
Document pertinent info

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HYPERCALCEMIA (>10.1 mg/dL)

Signs & symptoms:


Abdominal pain, constipation
Anorexia
Behavioral changes
Bone pain
Decreased DTRs
Extreme thirst
Hypertension
Lethargy
Muscle weakness
Nausea
Polyuria
Vomiting
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Hypocalcemia

Interventions:
Monitor vs
Monitor for arrhythmias
Insert and maintain IV line
Administer a diuretic
Strain the urine for calculi
Watch for signs/symptoms of digitalis toxicity
Provide a safe env’t.
Provide safety

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HYPOPHOSPHATEMIA (<2.5 mg/dL)

Signs & symptoms:

Hypotension
Decreased CO
Cardiomyopathy
Rhabdomyolysis
Cyanosis
Respiratory failure

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Hypophosphatemia

Interventions:

Monitor vs
Assess the pt’s LOC
Monitor the rate and depth of respirations
Monitor the pt for evidence of heart failure
Monitor temp frequently
Assess for evidence of decreasing muscle strength

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HYPERPHOSPHATEMIA (>10.1 mg/dL)

Signs & symptoms:


Anorexia
Chvostek’s/ Trousseau’s signs
Conjuntivitis, visual impairment
Decreased mental status
Hyperreflexia
Muscle weakness, cramps, spasm
Nausea & vomiting
Papular eruptions
Paresthesia
Tetany

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Hyperphosphatemia

Interventions:
Monitor vs
Monitor for arrhythmias
Insert and maintain IV line
Administer a diuretic
Strain the urine for calculi
Watch for signs/symptoms of digitalis toxicity
Provide a safe env’t.
Provide safety

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HYPOCHLOREMIA (<96 meQ/L)

Signs & symptoms:

Hyperactive DTRs
Muscle hypertonicity
s/sx pf acid-base imbalances
tetany

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Hypochloremia

Interventions:

Monitor vs & LOC


Monitor serum electrolyte levels
Offer food high in chloride
Insert and maintain a patent IV line
Accurately measure I and O
Use NSS to flush NGT
Provide a safe and quiet env’t.

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HYPERCHLOREMIA (>106 mEq/L)

Signs & symptoms:

Arrhythmias
Decreased CO
Decreased LOC that may progress to coma

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Hyperchloremia

Interventions:
Monitor vs including cardiac rhythm
Provide safety
Look for changes in respiratory pattern
Insert and IV and maintain patency
Restrict fluids, Na, and Cl as needed
Monitor serum & electrolyte levels and ABG results
Monitor I and O

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HYPOMAGNESEMIA (<1.5 meQ/L)

Signs & symptoms:

Altered LOC, confusion, hallucinations


Muscular weakness, leg and foot cramps,
Hyperactive DTRs, tetany, Chvostek’s & trousseau’s
signs
Tachycardia, hypertension
Dysphagia, anorexia, nausea, vomiting

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Hypomagnesemia

Interventions:

Monitor vs & LOC


Monitor serum electrolyte levels
Offer food high in magnesium
Insert and maintain a patent IV line
Accurately measure I and O
Provide a safe and quiet env’t.

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HYPERMAGNESEMIA (>2.5 mEq/L)

Signs & symptoms:

Decreased muscle and nerve activity


Hypoactive DTRs
Generalized weakness, drowsiness, lethargy
Nausea, vomiting
Slow, shallow, respirations
Respiratory arrest
ECG changes
Vasodilation

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Hyperchloremia

Interventions:
Monitor vs including cardiac rhythm
Provide safety
Look for changes in respiratory pattern
Insert and IV and maintain patency
Restrict fluids, Na, and Cl as needed
Monitor serum & electrolyte levels and ABG results
Monitor I and O

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ACID-BASE BALANCE

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Acid-Base Balance
 Normal pH of body fluids

 Arterial blood is 7.4

 Venous blood and interstitial fluid is 7.35

 Intracellular fluid is 7.0

 Alkalosis or alkalemia – arterial blood pH rises


above 7.45
 Acidosis or acidemia – arterial pH drops below
7.35 (physiological acidosis)
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Sources of Hydrogen Ions
 Most hydrogen ions originate from cellular
metabolism
 Breakdown of phosphorus-containing proteins
releases phosphoric acid into the ECF
 Anaerobic respiration of glucose produces
lactic acid
 Fat metabolism yields organic acids and
ketone bodies
 Transporting carbon dioxide as bicarbonate
releases hydrogen ions
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Hydrogen Ion Regulation

 Concentration of hydrogen ions is regulated


sequentially by:
 Chemical buffer systems – act within seconds

 The respiratory center in the brain stem –


acts within 1-3 minutes
 Renal mechanisms – require hours to days to
effect pH changes

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Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings
Chemical Buffer Systems

 Strong acids – all their H+ is dissociated


completely in water
 Weak acids – dissociate partially in water and
are efficient at preventing pH changes
 Strong bases – dissociate easily in water and
quickly tie up H+
 Weak bases – accept H+ more slowly (e.g., HCO3¯
and NH3)

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Chemical Buffer Systems

 One or two molecules that act to resist pH


changes when strong acid or base is added
 Three major chemical buffer systems

 Bicarbonate buffer system

 Phosphate buffer system

 Protein buffer system

 Any drifts in pH are resisted by the entire


chemical buffering system
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Bicarbonate Buffer System

 A mixture of carbonic acid (H2CO3) and its salt,


sodium bicarbonate (NaHCO3) (potassium or
magnesium bicarbonates work as well)
 If strong acid is added:

 Hydrogen ions released combine with the


bicarbonate ions and form carbonic acid (a
weak acid)
 The pH of the solution decreases only slightly

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Bicarbonate Buffer System

 If strong base is added:

 It reacts with the carbonic acid to form


sodium bicarbonate (a weak base)
 The pH of the solution rises only slightly

 This system is the only important ECF buffer

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Phosphate Buffer System

 Nearly identical to the bicarbonate system

 Its components are:

 Sodium salts of dihydrogen phosphate


(H2PO4¯), a weak acid

 Monohydrogen phosphate (HPO42¯), a weak


base
 This system is an effective buffer in urine and
intracellular fluid

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Protein Buffer System
 Plasma and intracellular proteins are the body’s
most plentiful and powerful buffers
 Some amino acids of proteins have:

 Free organic acid groups (weak acids)

 Groups that act as weak bases (e.g., amino


groups)
 Amphoteric molecules are protein molecules
that can function as both a weak acid and a weak
base
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Physiological Buffer Systems

 The respiratory system regulation of acid-base


balance is a physiological buffering system
 There is a reversible equilibrium between:

 Dissolved carbon dioxide and water

 Carbonic acid and the hydrogen and


bicarbonate ions

CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3¯

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Physiological Buffer Systems
 During carbon dioxide unloading, hydrogen ions are
incorporated into water
 When hypercapnia or rising plasma H+ occurs:
 Deeper and more rapid breathing expels more
carbon dioxide
 Hydrogen ion concentration is reduced
 Alkalosis causes slower, more shallow breathing,
causing H+ to increase
 Respiratory system impairment causes acid-base
imbalance (respiratory acidosis or respiratory
alkalosis)
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Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings
Renal Mechanisms of Acid-Base Balance

 Chemical buffers can tie up excess acids or


bases, but they cannot eliminate them from the
body
 The lungs can eliminate carbonic acid by
eliminating carbon dioxide
 Only the kidneys can rid the body of metabolic
acids (phosphoric, uric, and lactic acids and
ketones) and prevent metabolic acidosis
 The ultimate acid-base regulatory organs are
the kidneys
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Renal Mechanisms of Acid-Base Balance

 The most important renal mechanisms for


regulating acid-base balance are:
 Conserving (reabsorbing) or generating new
bicarbonate ions
 Excreting bicarbonate ions

 Losing a bicarbonate ion is the same as gaining a


hydrogen ion; reabsorbing a bicarbonate ion is
the same as losing a hydrogen ion

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Renal Mechanisms of Acid-Base Balance

 Hydrogen ion secretion occurs in the PCT and in


type A intercalated cells
 Hydrogen ions come from the dissociation of
carbonic acid

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Reabsorption of Bicarbonate

 Carbon dioxide combines with water in tubule


cells, forming carbonic acid
 Carbonic acid splits into hydrogen ions and
bicarbonate ions
 For each hydrogen ion secreted, a sodium ion and
a bicarbonate ion are reabsorbed by the PCT cells
 Secreted hydrogen ions form carbonic acid; thus,
bicarbonate disappears from filtrate at the same
rate that it enters the peritubular capillary blood

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Kidney Hydrogen Ion Balancing: Proximal Tubule

Proximal tubule secretion and reabsorption of filtered HCO3-


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Generating New Bicarbonate Ions

 Two mechanisms carried out by type A


intercalated cells generate new bicarbonate ions
 Both involve renal excretion of acid via
secretion and excretion of hydrogen ions or
ammonium ions (NH4+)

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Hydrogen Ion Excretion

 Dietary hydrogen ions must be counteracted by


generating new bicarbonate
 The excreted hydrogen ions must bind to buffers
in the urine (phosphate buffer system)
 Intercalated cells actively secrete hydrogen ions
into urine, which is buffered and excreted
 Bicarbonate generated is:
 Moved into the interstitial space via a
cotransport system
 Passively moved into the peritubular capillary
blood
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Hydrogen Ion Excretion

 In response to
acidosis:
 Kidneys
generate
bicarbonate ions
and add them to
the blood
 An equal amount
of hydrogen
ions are added
to the urine
Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Figure 26.13
Ammonium Ion Excretion

 This method uses ammonium ions produced by


the metabolism of glutamine in PCT cells
 Each glutamine metabolized produces two
ammonium ions and two bicarbonate ions
 Bicarbonate moves to the blood and ammonium
ions are excreted in urine

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Ammonium Ion Excretion

Figure 26.14
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Bicarbonate Ion Secretion
 When the body is in alkalosis, type B
intercalated cells:
 Exhibit bicarbonate ion secretion

 Reclaim hydrogen ions and acidify the blood

 The mechanism is the opposite of type A


intercalated cells and the bicarbonate ion
reabsorption process
 Even during alkalosis, the nephrons and
collecting ducts excrete fewer bicarbonate ions
than they conserve
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Respiratory Acidosis and Alkalosis
 Result from failure of the respiratory system to
balance pH
 PCO2 is the single most important indicator of
respiratory inadequacy
 PCO2 levels

 Normal PCO2 fluctuates between 35 and 45 mm Hg

 Values above 45 mm Hg signal respiratory


acidosis
 Values below 35 mm Hg indicate respiratory
alkalosis
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Respiratory Acidosis and Alkalosis

 Respiratory acidosis is the most common cause


of acid-base imbalance
 Occurs when a person breathes shallowly, or
gas exchange is hampered by diseases such as
pneumonia, cystic fibrosis, or emphysema
 Respiratory alkalosis is a common result of
hyperventilation

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Metabolic Acidosis
 All pH imbalances except those caused by
abnormal blood carbon dioxide levels
 Metabolic acid-base imbalance – bicarbonate ion
levels above or below normal (22-26 mEq/L)
 Metabolic acidosis is the second most common
cause of acid-base imbalance
 Typical causes are ingestion of too much
alcohol and excessive loss of bicarbonate ions
 Other causes include accumulation of lactic
acid, shock, ketosis in diabetic crisis,
starvation, and kidney failure
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Metabolic Alkalosis

 Rising blood pH and bicarbonate levels indicate


metabolic alkalosis
 Typical causes are:

 Vomiting of the acid contents of the stomach

 Intake of excess base (e.g., from antacids)

 Constipation, in which excessive bicarbonate


is reabsorbed

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Respiratory and Renal Compensations

 Acid-base imbalance due to inadequacy of a


physiological buffer system is compensated for
by the other system
 The respiratory system will attempt to
correct metabolic acid-base imbalances
 The kidneys will work to correct imbalances
caused by respiratory disease

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Respiratory Compensation
 In metabolic acidosis:

 The rate and depth of breathing are elevated

 Blood pH is below 7.35 and bicarbonate level


is low
 As carbon dioxide is eliminated by the
respiratory system, PCO2 falls below normal

 In respiratory acidosis, the respiratory rate is


often depressed and is the immediate cause of
the acidosis
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Respiratory Compensation

 In metabolic alkalosis:

 Compensation exhibits slow, shallow


breathing, allowing carbon dioxide to
accumulate in the blood
 Correction is revealed by:

 High pH (over 7.45) and elevated bicarbonate


ion levels
 Rising PCO2

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Renal Compensation

 To correct respiratory acid-base imbalance,


renal mechanisms are stepped up
 Acidosis has high PCO2 and high bicarbonate
levels
 The high PCO2 is the cause of acidosis

 The high bicarbonate levels indicate the


kidneys are retaining bicarbonate to offset
the acidosis

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Renal Compensation

 Alkalosis has Low PCO2 and high pH

 The kidneys eliminate bicarbonate from the


body by failing to reclaim it or by actively
secreting it

InterActive Physiology®:
PLAY
Fluid, Electrolyte, and Acid/Base Balance: Acid/Base Homeostasis

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Developmental Aspects
 Water content of the body is greatest at birth (70-
80%) and declines until adulthood, when it is about
58%
 At puberty, sexual differences in body water
content arise as males develop greater muscle mass
 Homeostatic mechanisms slow down with age
 Elders may be unresponsive to thirst clues and are
at risk of dehydration
 The very young and the very old are the most
frequent victims of fluid, acid-base, and electrolyte
imbalances
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Problems with Fluid, Electrolyte, and Acid-Base
Balance
 Occur in the young, reflecting:

 Low residual lung volume

 High rate of fluid intake and output

 High metabolic rate yielding more metabolic


wastes
 High rate of insensible water loss

 Inefficiency of kidneys in infants

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ABG Analysis

pH 7.35 - 7. 45

PaCO2 35 - 45 mm Hg

HCO3- 22 - 26 mEq/L

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Step 1: Classify the pH
Normal: 7.35 - 7.45
Acidemia: <7.35
Alkalemia: >7.45

Step 2: Assess PaCO2


Normal: 35- 45 mm Hg
Respiratory acidosis: >45 mm Hg
Respiratory alkalosis: <35 mm Hg
Step 3: Assess HCO3-
Normal: 22-26 mEq/L
Metabolic acidosis: <22 mEq/L
Metabolic alkalosis: >26 mEq/L

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Step 4: Determine Presence of Compensation
Compensation present PaCO2 and HCO3- are abnormal (or
nearly so) in opposite directions; that is, one is acidotic and the
other alkalotic

Step 5: Identify Primary Disorder, If Possible


If pH is clearly abnormal: The acid-base component most
consistent with the pH disturbance is the primary disorder.
If pH is normal or near-normal: The more deviant component is
probably primary. Also note whether pH is on acidotic or alkalotic
side of 7.4. The more deviant component should be consistent
with this pH

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RESPIRATORY ACIDOSIS

Uncompensated Compensated

pH < 7.35 Normal

PaCO2 (mmHg) < 45 > 45

HCO3- (mEq/L) Normal > 26

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Causes

Hypoventilation from CNS trauma or tumor that


depresses respiratory center

Neuromuscular diseases that affect respiratory drive

Lung diseases that decrease amount of surface area


available for gas exchange

Airway obstruction

Chest-wall trauma

Certain drugs that depress repiratory center primary hypoventilation

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Pathophysiology

When pulmonary ventilation decreases, retained CO2 combines with H2O to


form H2CO3. The carbonic acid dissociates to release free H ions and HCO3
ions. The excessive carbonic acid causes a drop in pH.
Look for PaCO2 level above 45 mm H g and a pH level below 7.35

As the pH level falls, 2,3-diphosphoglycerate (2,3-DPG) increases in the RBC


and causes a change in Hb that makes the Hb release O2. The altered Hb now
strongly alkaline picks up H ions and CO2, thus eliminating some of the free H
ions and excess CO2.
Look for decreased arterial oxygen saturation

Whenever PaCO2 increases, CO2 builds up in all tissues and fluids, including
CSF & the respiratory ctr. in the medulla. The CO2 reacts with H20 to form
H2CO3, which then breaks into free H ions & HCO3- ions. The increased
amount of CO2 & free H ions stimulate the respiratory center to increase the
respiratory rate. An increased respiratory rate expels more CO2 & helps to
reduce the CO2 level in the blood & other tissues.
Look for rapid, shallow respirations & a decreasing PaCO2
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Eventually, CO2 and H ions cause cerebral blood vessels to dilate, which
increases blood flow to the brain. That increased flow can cause cerebral
edema and depress CNS activity
Look for headache, confusion, lethargy, nausea, or vomiting

As respiratory mechanisms fail, the increasing PsCO2 stimulates the


kidneys to conserve HCO3- and Na ions & to excrete H ions, some in the
form of NH4. The additional HCO3- & Na combine to form extra
NaHCO3, which is then able to buffer more free H ions.
Look for increased acid content in the urine, increasing serum pH & HCO3-
levels, & shallow, depressed respirations

As the concentration of H ions overwhelms the body’s compensatory


mechanisms, the H ions move into the cells, and K ions move out. A
comncurrent lack of oxygen causes an increase in the anaerobic production
of lactic acid, which further skews the acid-base balance & critically
depresses neurologic & cardiac functions.
Look for hyperkalemia, arrhythmias, increased PaCO2, decreased PaO2,
decreased pH, & decreased LOC
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Signs and Symptoms

apprehension
confusion
decreased deep-tendon reflexes
diaphoresis
dyspnea, with rapid, shallow respirations
nausea or vomiting
restlessness
tachycardia
tremors
warm, flushed skin

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Nursing Management

- Monitor vs & assess cardiac rhythm

- Continue to assess respiratory patterns & report changes quickly

- Monitor the pt’s neurologic status, & report significant changes

- Report any variations in ABG, pulse oximetry, or serum electrolyte


levels

- Give meds (antibiotic & bronchodilators) as ordered

- Administer O2 as ordered
Perform tracheal suctioning, incentive spirometry, postural drainage, &
coughing & deep breathing, as indicated

- Make sure the pt takes in enough fluids, both oral & IV, & maintain
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Treatment

- bronchodilators

-supplemental oxygen, prn

-drug therapy for hyperkalemia

-antibiotic for infection

-chest physiotherapy

-removal of a foreign body from the pt’s airway, if needed

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Health Teaching

- description of the condition & how to prevent it

- reasons for repeated ABG analyses

- deep-breathing exercises

- prescribed meds

- home oxygentaion therapy, if indicated

- warning signs & symptoms & when to report them

- proper techniques for using bronchodilators, if appropriate

- need for frequent rest


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RESPIRATORY ALKALOSIS

Uncompensated Compensated

pH > 7.45 Normal

PaCO2 (mmHg) < 35 < 35

HCO3- (mEq/L) Normal < 22

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Causes

Any condition that increases respiratory rate & depth

Hyperventilation

Hypercapnia

Hypermetabolic states

Liver failure

Certain drugs

Conditions that affect brain’s respiratory control center

Acute hypoxia 2o to high altitude, pulmonary disease, severe


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Nursing Management

- Monitor pts at risk for developing respiratory alkalosis

- Allay anxiety whenever possible

- Monitor vs. Report changes in neurologic, neuromuscular, or


cardiovascular functioning

- Monitor ABG & serum electrolyte levels, & immediately report any
variations

- Pts with MV: check settings frequently

- Provide undisturbed rest periods after the pt’s respiratory rate


returns to normal
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Treatment

- focus is on removing the underlying cause

- oxygen therapy

- sedative/anxiolytic

-breathing into a paper bag

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Health Teaching

- explanation of the condition & its treatment

- warning signs & symptoms & when to report them

- anxiety-reducing techniques, if appropriate

-controlled-breathing exercises, if appropriate

-prescribed medications

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METABOLIC ACIDOSIS

Uncompensated Compensated

pH < 7.35 Normal

PaCO2 (mmHg) Normal < 35

HCO3- (mEq/L) < 22 <22

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Causes

Loss of HCO3-

Accumulation of metabolic acids

Overproduction of ketone bodies

Decreased ability of kidneys to excrete acids

Excessive GI losses from diarrhea, intestinal malabsorption, or


urinary diversion to the ileum

Hyperaldosteronism

Use of K-sparing diuretics


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Signs and Symptoms

confusion dull headache

decreased DT reflexes hyperkalemic s/sx

hypotension Kussmaul’s respirations

lethargy warm, dry skin

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Nursing Management

-Monitor vs and assess cardiac rhythm


-Prepare for mechanical ventilation or dialysis, as required
-Monitor the pt’s neurologic status closely
-Insert an IV line, as ordered, and maintain patent IV access
-Administer NaHCO3 as ordered
-Position the pt to promote chest expansion & facilitate breathing
-Take steps to help eliminate the underlying cause
-Watch for any 2o changes, such as declining BP
-Monitor pt’s renal function through I & O
-Watch for changes in the serum electrolyte levels; continuously
monitor ABG results
-Orient the pt as needed
-Investigate reasons for pt’s ingestion of toxic substances

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Treatment

-adjust the K

-Replace the HCO3-

-Ventilatory support

-Dialysis

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Health Teaching

- basics of the condition & its treatment

- testing of blood glucose levels, if indicated

- need for strict adherence to antidiabetic therapy, if


appropriate

- avoidance of alcohol

- warning s/sx & when to report them

-prescribed meds

-avoidance of ingestion of toxic substances


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METABOLIC ALKALOSIS

Uncompensated Compensated

pH > 7.45 Normal

PaCO2 (mmHg) Normal > 45

HCO3- (mEq/L) > 22 <26

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Causes

Excessive acid loss from the GIT

Diuretic therapy

Cushing’s dse.

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Pathophysiology (diagram here)

HCO3- accumulation in the body Chemical buffers bind w/ ions

Excess HCO3 that don’t bind w/


chemical buffers
pH >7.45

Elevated serum pH level HCO3


>26
mEq/L
Depressed respiratory system
Slow,
shallow
resp.
Excess HCO3- excreted via the Alkaline
kidneys (>28 mEq/L) urine &
pH

Near
normal
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polyuria
Na, H2O, & HCO3- excretion via the
kidneys
Hypovolemia
s/sx

Ions shifting ( K and H)


Hypokalemia s/sx:
anorexia, muscle
weakness, etc.

Decreased Ca ionization

tetany
Nerve cells’ increased permeability to
Na ions
belligerence

irritability

disorientation

seizures
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Signs and Symptoms

anorexia apathy

confusion cyanosis

hypotension loss of reflexes

muscle twitching nausea

paresthesia polyuria

vomiting weakness

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Nursing Management

-Monitor vs & assess cardiac rhythm & monitor resp. pattern


-Assess LOC
-Administer O2, as ordered
-Institute seizure precautions; explain to pt and family
-Maintain patent IV access as ordered
-Administer diluted K solutions w/ an infusion device
-Monitor I & O
- Infuse 0.9% ammonium chloride no faster than 1 L over 4 hrs.
-Irrigate NG tube w/ NSS
-Assess lab test results; inform doctor of any changes
-Watch closely for signs of muscle weakness, tetany, or
decreased activity
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Health Teaching

- basics of the condition & its treatment

- need to avoid overuse of alkaline agents & diuretics

- prescribed meds, esp. adverse rxns of K-wasting


diuretics or KCl supplements

- warning signs & symptoms & when to report them

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