ight © 2004 Pearson Education, Inc., publishing as Benjamin Cummings FLUIDS AND ELECTROLYTES ACID-BASE BALANCE
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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
Figure 26.2
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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
InterActive Physiology®: Fluid, Electrolyte, and Acid/Base Balance: Introduction to Body FluidsPLAYPLAY
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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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Figure 26.6
Mechanisms and Consequences of ADH Release
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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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Figure 26.7a
Disorders of Water Balance: Dehydration
Excessive loss of H2O from ECF
1 2 3ECF osmotic pressure rises
Cells lose H2O to ECF by osmosis; cells shrink
(a) Mechanism of dehydration
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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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HYPERVOLEMIASigns 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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HYPOVOLEMIAInterventions
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
Provide effective skin care
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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
Disorders of Water Balance: Hypotonic Hydration
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Figure 26.7b
Disorders of Water Balance: Hypotonic Hydration
Excessive H2O enters the ECF
1 2 ECF osmotic pressure falls
3 H2O moves into cells by osmosis; cells swell
(b) Mechanism of hypotonic hydration
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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
<135 mEq/L
>145 mEq/L
Normal
Hyponatremia
Hypernatremia
SIADH
Diabetes Insipidus
Serum K 3.5 – 5mEq/L
<3.5 mEq/L
>5 mEq/L
Normal
Hypokalemia
Hyperkalemia
Diarrhea
Burns & renal failure
Total serum calcium
8.9-10.1 mg/dL
<8.9 mg/dL
>10.1 mg/dL
Normal
Hypocalcemia
hypercalcemia
Acute pancreatitis
Hyperparathyrodism
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Electrolyte
Results Implications Common Causes
Ionized Ca 4.5-5.1 mg/dL
<4.5 mg/dL
>5.2 mg/dL
Normal
Hypocalcemia
Hypercalcemia
Massive transfusion
Acidosis
Serum Phosphates
2.5–4.5 mg/dL
<2.5 mg/dL
>4.5 mg/dL
Normal
Hypophosphatemia
hyperphosphatemia
Diabetic ketoacidosis
Renal insufficiency
Serum Mg 1.5-2.5 mEq/L
<1.5 mEq/L
>2.5 mEq/L
Normal
Hypomagnesemia
Hypermagnesemia
Malnutrition
Renal Failure
Serum Cl 96-106 mEq/L
<96 mEq/L
>106 mEq/L
Normal
Hypochloremia
Hyperchloremia
Prolonged vomiting
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
Figure 26.8
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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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Figure 26.10
Mechanisms and Consequences of ANP Release
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Estrogens:
Enhance NaCl reabsorption by renal tubules
May cause water retention during menstrual cycles
Are responsible for edema during pregnancy
Influence of Other Hormones on Sodium Balance
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Progesterone:
Decreases sodium reabsorption
Acts as a diuretic, promoting sodium and water loss
Glucocorticoids – enhance reabsorption of sodium and promote edema
Influence of Other Hormones on Sodium Balance
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ELECTROLYTE IMBALANCES
Interventions:
Monitor & record vsCarefully record I and OAssess skin and MM for signs of breakdown and infectionMonitor patient’s serum electrolyte levelsRestrict oral intake, as neededGive oral hydration, as neededGive supplemental feedings, as neededAssist with oral hygienePrevent complicationsAdminister 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
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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 glandDepends on what’s eaten & how it’s absorbed by the intestinesIncreased Na intake: increased ECF fluid volumeDecreased Na intake: decreased ECF fluid volumeIncreased 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 LOCHeadache Muscle twitchingNausea Dry MMHypertension Poor skin turgorTachycardia Weight gainRapid, bounding pulse
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Hyponatremia
Interventions:Monitor and record vs, esp. BP and pusleMonitor neurologic status frequentlyAccurately measure I and OWeigh the ptAssess skin turgorWatch for & report extreme serum Na levels changesRestrict fluid intake as orderedAdminister oral sodium supplementsMaintain patent IV lineMaintain 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 flushedAgitationLow-grade feverThirst
Interventions:Assess…Replenish…Restore…
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HYPOKALEMIA (<3.5 mEq/L)
Signs & symptoms:
Skeletal muscle weaknessU waveConstipation, ileusToxic effects of digoxin (from hypokalemia)Irregular, weak pulseOrthostatic hypotensionNumbness (paresthesia)
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Hypokalemia
Interventions:Monitor vsCheck heart rate and rhythmMonitor serum K levelsAsess for signs of hypokalemiaMonitor and document I and OObserve proper guidelines in IV K administration
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HYPERKALEMIA (>5 mEq/L)
Signs & symptoms:
Abdominal cramping diarrheaEKG changes hypotensionIrregular pulse rate irritabilityMuscle weakness nauseaparesthesia
-Most dangerous of the electrolyte disorders
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Hypokalemia
Interventions:Monitor vsMonitor and document I and OPrepare to administer a slow calcium gluconate IV infusionKeep in mind that when giving Kayexalate,, serum Na levels may riseMonitor bowel sounds & the number of BMMonitor serum K levels
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HYPOCALCEMIA (<8.9 mg/dL)
Signs & symptoms:
Trousseau’s signChvostek’s signAnxiety ConfusionDecreased CO ArrhythmiasFractures IrritabilityMuscle cramps TetanyTremors twitching
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Hypocalcemia
Interventions:Monitor vs, cardiac status; observe for Chvostek’s and Trousseau’s signsMonitor for arrhythmiasInsert and maintain IV line for Ca therapyAdminister oral replacements as orderedMonitor pertinent lab test resultsTake safety and seizure precautionsDocument pertinent info
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HYPERCALCEMIA (>10.1 mg/dL)
Signs & symptoms:Abdominal pain, constipationAnorexiaBehavioral changesBone painDecreased DTRsExtreme thirstHypertensionLethargyMuscle weaknessNauseaPolyuriaVomiting
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Hypocalcemia
Interventions:Monitor vsMonitor for arrhythmiasInsert and maintain IV lineAdminister a diureticStrain the urine for calculiWatch for signs/symptoms of digitalis toxicityProvide a safe env’t.Provide safety
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HYPOPHOSPHATEMIA (<2.5 mg/dL)
Signs & symptoms:
HypotensionDecreased COCardiomyopathyRhabdomyolysisCyanosisRespiratory failure
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Hypophosphatemia
Interventions:
Monitor vsAssess the pt’s LOCMonitor the rate and depth of respirationsMonitor the pt for evidence of heart failureMonitor temp frequentlyAssess for evidence of decreasing muscle strength
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HYPERPHOSPHATEMIA (>10.1 mg/dL)
Signs & symptoms:AnorexiaChvostek’s/ Trousseau’s signsConjuntivitis, visual impairmentDecreased mental statusHyperreflexiaMuscle weakness, cramps, spasmNausea & vomitingPapular eruptionsParesthesiaTetany
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Hyperphosphatemia
Interventions:Monitor vsMonitor for arrhythmiasInsert and maintain IV lineAdminister a diureticStrain the urine for calculiWatch for signs/symptoms of digitalis toxicityProvide a safe env’t.Provide safety
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HYPOCHLOREMIA (<96 meQ/L)
Signs & symptoms:
Hyperactive DTRsMuscle hypertonicitys/sx pf acid-base imbalancestetany
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Hypochloremia
Interventions:
Monitor vs & LOCMonitor serum electrolyte levelsOffer food high in chlorideInsert and maintain a patent IV lineAccurately measure I and OUse NSS to flush NGTProvide a safe and quiet env’t.
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HYPERCHLOREMIA (>106 mEq/L)
Signs & symptoms:
ArrhythmiasDecreased CODecreased LOC that may progress to coma
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Hyperchloremia
Interventions:Monitor vs including cardiac rhythmProvide safetyLook for changes in respiratory patternInsert and IV and maintain patencyRestrict fluids, Na, and Cl as neededMonitor serum & electrolyte levels and ABG resultsMonitor I and O
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HYPOMAGNESEMIA (<1.5 meQ/L)
Signs & symptoms:
Altered LOC, confusion, hallucinationsMuscular weakness, leg and foot cramps, Hyperactive DTRs, tetany, Chvostek’s & trousseau’s signsTachycardia, hypertensionDysphagia, anorexia, nausea, vomiting
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Hypomagnesemia
Interventions:
Monitor vs & LOCMonitor serum electrolyte levelsOffer food high in magnesiumInsert and maintain a patent IV lineAccurately measure I and OProvide a safe and quiet env’t.
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HYPERMAGNESEMIA (>2.5 mEq/L)
Signs & symptoms:
Decreased muscle and nerve activityHypoactive DTRsGeneralized weakness, drowsiness, lethargyNausea, vomitingSlow, shallow, respirationsRespiratory arrestECG changesVasodilation
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Hyperchloremia
Interventions:Monitor vs including cardiac rhythmProvide safetyLook for changes in respiratory patternInsert and IV and maintain patencyRestrict fluids, Na, and Cl as neededMonitor serum & electrolyte levels and ABG resultsMonitor 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
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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Proximal tubule secretion and reabsorption of filtered HCO3-
Kidney Hydrogen Ion Balancing: Proximal TubuleKidney Hydrogen Ion Balancing: Proximal Tubule
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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 Figure 26.13
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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®: Fluid, Electrolyte, and Acid/Base Balance: Acid/Base HomeostasisPLAYPLAY
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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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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
Problems with Fluid, Electrolyte, and Acid-Base Balance
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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 pHNormal: 7.35 - 7.45Acidemia: <7.35Alkalemia: >7.45
Step 2: Assess PaCO2 Normal: 35- 45 mm HgRespiratory acidosis: >45 mm HgRespiratory alkalosis: <35 mm Hg
Step 3: Assess HCO3-
Normal: 22-26 mEq/LMetabolic acidosis: <22 mEq/LMetabolic alkalosis: >26 mEq/L
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Step 4: Determine Presence of CompensationCompensation 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 PossibleIf 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
UncompensatedCompensated
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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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
Pathophysiology
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
apprehensionconfusiondecreased deep-tendon reflexesdiaphoresisdyspnea, with rapid, shallow respirationsnausea or vomitingrestlessnesstachycardiatremorswarm, 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 orderedPerform tracheal suctioning, incentive spirometry, postural drainage, & coughing & deep breathing, as indicated
- Make sure the pt takes in enough fluids, both oral & IV, & maintain accurate I & O records
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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
- need for increased caloric intake, if appropriate
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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 anemia, pulmonary embolus, & hypotension
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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
- Stay with pt during periods of extreme stress & anxiety
- Institute safety measures & seizure precautions
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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
UncompensatedCompensated
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
Poisoning or toxic drug reaction
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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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HCO3- accumulation in the body
Pathophysiology (diagram here)
Chemical buffers bind w/ ions
Excess HCO3 that don’t bind w/ chemical buffers
Elevated serum pH level
Depressed respiratory system
pH >7.45
HCO3 >26
mEq/L
Slow, shallow resp.
Excess HCO3- excreted via the kidneys (>28 mEq/L)
Alkaline urine &
pH
Near normal
HCO3 level
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Na, H2O, & HCO3- excretion via the kidneys
Ions shifting ( K and H)
Decreased Ca ionization
Nerve cells’ increased permeability to Na ions
polyuria
Hypovolemia s/sx
tetany
belligerence
irritability
Hypokalemia s/sx: anorexia, muscle weakness, etc.
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